Sonodynamic therapy (SDT) is an emerging approach involving low-intensity ultrasound and specialized chemical agents known as sonosensitizers. It releases harmful reactive oxygen species (ROS) at the tumor site.

Cancer cells can activate antioxidant defense systems to counteract it, so the treatment is not considered very effective.

Scientists reported breaching these defenses using CRISPR/Cas9 gene editing in a new study. CRISPR/Cas9 gene-editing allows sonodynamic therapy to shrink tumors in a mouse model of liver cancer effectively.

Cancer cells can quickly overcome sonodynamic therapy by activating a nuclear factor erythroid 2-related factor 2 (NFE2L2) gene. The NFE2L2 deploys the cells detoxification and antioxidant enzyme defenses. Cas9 gene-editing technology is known for breaking down gene expression in the lab.

Hence, scientists wondered if they could increase sonodynamic therapys effectiveness by using this technology to reduce NFE2L2 expression.

Scientists started with encapsulating the CRISPR/Cas9 system and a ROS precursor molecule in lipid nanoparticles. They then treated hepatocellular carcinoma cells in a petri dish with the nanoparticles.

The cells lysosomes then took the lipid nanoparticles. ROS formation caused by ultrasound treatment ruptures lysosomes. It also enables the CRISPR/Cas9 system to enter the nucleus and break down NFE2L2 gene expression. The ROS also damaged other cellular components.

As a result, the therapy kills more cancer cells without NFE2L2 gene editing.

Scientists injected the nanoparticle treatment into mice with implanted human hepatocellular carcinoma tumors. After 15 days of follow-up, scientists did not find any tumor in the mice. The tumors in the mice disappeared and didnt come back.

Scientists acknowledged, Mice treated with sonodynamic therapy alone had fewer tumors than untreated mice, but the addition of the CRISPR/Cas9 gene-editing significantly improved the therapys effectiveness. Because gene editing occurs only in tumor tissues under ultrasound irradiation, it wont cause gene mutations in healthy tissues.

Journal Reference:

Read more:
CRISPR/Cas9 gene-editing increases the effectiveness of ultrasound cancer therapy - Tech Explorist

Recommendation and review posted by Bethany Smith

Bacteria get a bad rap, and often deservedly so: Different strains cause a range of infections and diseases, including pneumonia, strep throat, and tuberculosis. However, any well-researched health food advocate can list the many benefits of the bacteria present in yogurt, and your local pub would be doomed without the strains integral to crafting their signature brews. What might be even more surprising is that a recent, revolutionary gene-editing technology, once exclusively the subject of science fiction, is based on the bacterial genome.

Bacteria and archaea, the original hosts of the CRISPR-Cas9 system, use this DNA-protein system to defend themselves from viruses. CRISPRs are DNA sequences that repeat in the genome of a bacterium, interspersed with fragments of genetic code from past viral invaders. When a virus enters a bacterial cell, the remnants of that same virus held in the bacterias DNA help identify and eliminate the virus. Once a virus is identified by a bacterium, Cas9 proteins try to figure out whether the new viral intruder matches any of the genetic information contained in the CRISPRs sequences of their DNA. If the virus matches the stored genetic information, the Cas9 protein will cleave it into pieces.

In 2011, researchers, including Nobel laureates Jennifer Doudna and Emmanuelle Charpentier, discovered that Cas9 proteins can be used to cut genomes that do not contain viral information, inspiring a plethora of research projects that have widened the scope of biotechnological possibility.

One such project is spearheaded by Daniel Sapozhnikov, a PhD candidate in the Department of Pharmacology and Therapeutics at McGill, and Moshe Szyf, a professor in the same department. The project aims to develop a way to remove methyl groupsone carbon atom bonded to three hydrogensfrom genes. Many diseases and disorders are dependent on whether specific genes are expressed, or turned on. Since varying amounts of methylation are associated with whether or not a gene is active, then being able to remove methyl groups could have important consequences for gene manipulation in scientific studies.

Since the 1980s, its been shown that [] genes with less [methylation] tend to be expressed [more] and genes with more tend to be expressed [less], Sapozhnikov said in an interview with The McGill Tribune. Thats basically the same conclusion that we have been stuck with in 2020. Without the ability to manipulate the DNA methylation levels at specific genes, there is really not much causational evidence for how DNA methylation and gene expression interact.

In order to better understand the relationship between methylation and gene expression, Sapozhnikov and Szyf developed a technique to demethylate select regions of a cells DNA.

CRISPR-Cas9 plays an integral role in the demethylation technique developed by Sapozhnikov and Szyf. By using guide RNA and Cas9 to block the methylation of genes, the effect of DNA demethylation can be evaluated in different cases. The specific system of CRISPR-Cas9 the team used is known as dCas9, which is CRISPR-Cas9 with a modified protein that prevents the cutting of DNAa potentially lethal consequencewhile retaining the important function of gene targeting. Once the dCas9 protein reaches the desired target of a genome, it binds to the site, preventing methylation of whatever it is attached to by physically blocking the process.

Although other teams have developed techniques for demethylation, Sapozhnikov believes that their method is the most exact.

There have been other tools that have been made that do similar things, but we argue that our tool is better from a causational perspective because [] it has fewer other activities, Sapozhnikov said.

The technique developed by Sapozhnikov and Szyf only works to remove methyl groups. Understanding the correlation between demethylation and gene expression could help the development of therapies to treat the numerous problems that arise from the improper functioning of gene expression.

CRISPR-Cas9 is still a very new technology, and it can often have unforeseen consequences in the cells it is used onnot to mention the ethical concerns raised by editing someones DNA, which is a topic of heavy debate and even outrage amongst the scientific community. Despite the many unanswered questions, CRISPR-Cas9 represents an incredible step toward revolutionary gene therapy, and with research like that of Sapozhnikov and Szyf, important new uses will continue to be explored.

Read more:
CRISPR-Cas9, the unwitting revolutionary - McGill Tribune

Recommendation and review posted by Bethany Smith

Agreement with Corteva Agriscience and Broad Institute of MIT and Harvard grants FuturaGene access to gene editing technology to research and develop varieties of eucalyptus that are adapted to climate change

SAO PAULO, Brazil, December 08, 2021--(BUSINESS WIRE)--FuturaGene, a wholly owned subsidiary of world-leading eucalyptus pulp producer, Suzano, will use patented genome editing technology from global pure-play agriculture company, Corteva Agriscience, and non-profit research organization, the Broad Institute of MIT and Harvard, to develop new, improved eucalyptus varieties.

FuturaGene intends to apply the gene editing technology to research and develop new varieties of eucalyptus that are more productive, resistant to diseases and pests and have improved fiber properties. In addition, the company aims for the new varieties to be more resilient to climate change and to serve as an alternative to products derived from fossil fuels. FuturaGene has the option to convert the worldwide research license to cover commercial applications.

Dr. Stanley Hirsch, CEO of FuturaGene, commented: "With our extensive experience and growing pipeline, FuturaGene is well placed to apply gene editing technology from our licensors to develop eucalyptus varieties that can help the world meet the growing demand for renewable wood-based products. This includes fibers and the potential to replace carbon-intensive fossil fuel-based materials, such as plastics, in a sustainable way.

"Our ability to share the benefits of this major enabling technology with small farmers within our supply chain, royalty free, was an important part of our negotiations with the licensors. This commitment is strongly aligned with Suzanos sustainability goal to mitigate income inequality and help lift people out of poverty. FuturaGene has always seen shared value as a vital part of our purpose".

The multi-institutional license covers CRISPR-Cas9 patent rights owned by a collection of leading universities and institutes.

Story continues

The licensed genome editing technology gives scientists the ability to edit an organism's DNA by altering and silencing genes or adding genetic material at specific locations in a highly targeted way. This can potentially be used to change wood properties, ablate susceptibilities to disease or chemical agents, or select for and instill desirable traits. The technology therefore has huge potential in forestry to help farmers optimize productivity.

- Ends -

About FuturaGene

FuturaGene is a leader in plant genetic research and development for increasing productivity and resilience in the global renewable forestry sector. With facilities in Brazil and Israel, the company develops sustainable, ecologically sound technology to meet the ever-increasing demands for fiber, alternatives to fossil fuel-based products such as plastics and energy crops in the face of declining land and water resources and climate change. In April 2015, FuturaGene became the first company in the world to obtain regulatory approval to commercially deploy a yield enhanced genetically modified eucalyptus variety. Since July 2010, FuturaGene has been a wholly owned subsidiary of Suzano S.A., the worlds leading eucalyptus pulp producer and one of Latin Americas largest paper producers.

For more information, visit http://www.futuragene.com.

View source version on businesswire.com: https://www.businesswire.com/news/home/20211208005555/en/

Contacts

For additional information please contact: FuturaGene Sara El Kadri+55 11 997398249Global Communications and Public Affairs Manager, FuturaGenesara.kadri@futuragene.com

Agnes Stephens+44 207 457 2002Media relations, Instinctif Partnersfuturagene@instinctif.com

Read more:
FuturaGene Secures License to CRISPR-Cas9 Technology to Develop Sustainable Varieties of Eucalyptus with Improved Productivity, Stress Resistance and...

Recommendation and review posted by Bethany Smith

Gene editing techniques like CRISPR could revolutionize the poultry industry in the future, improving yield, resistance to disease and leading to better welfare.

Gene editing itself has become a topic of much research and great interest in the academic and in the commercial work, Mark Fife, Ph.D., head of biotechnology, Aviagen, said during the Poultry Tech Webinar Series.

CRISPR functions like a pair of molecular scissors. The technique can cut DNA from a specific location at the gene, deleting the sequence entirely or replacing it with an alternative sequence.

It has several applications from medical to plants to livestock and aquaculture and micro-organisms. The bulk of the stories in the news refer to potential breakthroughs in human medicine, such as cancer treatments and genetic disorders.

In livestock, much of the discussion about gene editing currently applies to disease resistance, yield and quality, welfare and sex determination. For example, in cows, CRISPR has been used to create polled cattle and heat tolerant cattle, which can be beneficial to both welfare and management.

Poultry require a slightly different gene editing approach compared to other livestock. For mammals, a technique called somatic cell nucleic transfer (SCNT) is used, but it requires access to the developing embryo.

In chickens, thats obviously a different story because we cant access the embryo to implant the edit, Fife explained,

Instead, the process used for avian species makes genetic edits to primordial germ cells, the progenitors for sperm and ovum cells in the chicken.

What we do is we get into the developing embryo at a very early stage, about two and a half days into embryonic development. We then isolate the primordial germ cells, he added.

Researchers can perform various gene edits on the primordial germ cells, which continue to grow and develop in cell culture. At HH stage 14-17 of the chick development, the primordial germ cells are reinserted into the embryo, resulting in a chimeric chicken.

As you can see, not only is it very different from somatic cell nuclear transfer, it also takes a very long time, said Fife.

Recent advancements in this gene editing technique have resulted in poultry resisted to the avian leukosis virus and avian influenza.

Gene editing currently faces regulatory hurdles throughout much of the world. In the U.S., gene editing is highly regulated by the Food and Drug Administration (FDA). Meanwhile, the process is completely prohibited in Europe, although a post-Brexit UK is currently looking at deregulating gene edited crops.

Although everyone is incredibly excited by this at the moment, the gene editing peak is probably at a max and we are talking about food security, sustainability and animal welfare. But often what happens with technology is we hit this trough of disillusionment, Fife said.

Hopefully, this technology will clear regulatory hurdles and enter the sight of the slope of enlightenment and the plateau of productivity, he added.

Aviagens breeding techniques are exclusively based on traditional and established selection methods, Fife said, and although the company also recognizes its potential value as a research tool, there are no plans to introduce gene editing or any other genetic modification technique for commercial breeding purposes.

For more on the technologies set to advance the poultry industry, join industry-changing innovators, researchers, entrepreneurs, technology experts, investors and leading poultry producers at the Poultry Tech Webinar Series, scheduled for November 2, 4, 10, 11, 17, 30 and December 2.

During the webinar series, industry experts will preview whats coming next from prospective solutions to developing technology for the poultry industry.

This webinar series is proudly sponsored by: Arm & Hammer, Aviagen, Baader, Boehringer Ingelheim, Cargill, Ceva, Chore-Time, Cobb, Evonik, Marel, Phibro Animal Health, Staubli and Zoetis.

Visit our website for more details on the webinar series, topics and speakers.

Register for free today and join us for a glimpse at the future of the poultry industry.

Read more here:
Will CRISPR transform the poultry industry? | WATTPoultry - WATTAgNet Industry News & Trends

Recommendation and review posted by Bethany Smith

One 2021 study looked at the genome of Solanum sitiens a wild tomato species which grows in the extremely harsh environment of the Atacama Desert in Chile, and can be found at altitudes as high as 3,300m (10,826ft). The study identified several genes related to drought-resistance in Solanum sitiens, including one aptly named YUCCA7 (yucca are draught-resistant shrubs and trees popular as houseplants).

They are far from the only genes that could be used to give the humble tomato a boost. In 2020 Chinese and American scientists performed a genome-wide association study of 369tomato cultivars, breeding lines and landraces, and pinpointed a gene called SlHAK20 as crucial for salt tolerance.

Once the climate-smart genes such as these are identified, they can be targeted using Crispr to delete certain unwanted genes, to tune others or insert new ones. This has recently been done with salt tolerance, resistance to various tomato pathogens, and even to create dwarf plants which could withstand strong winds (another side effect of climate change). However, scientists such as Cermak go even further and start at the roots they are using Crispr to domesticate wild plant species from scratch, "de novo" in science speak. Not only can they achieve in a single generation what previously took thousands of years, but also with a much greater precision.

De novo domestication of Solanum pimpinellifolium was how Cermak and his colleagues at the University of Minnesota arrived at their 2018 plant. They targeted five genes in the wild species to obtain a tomato that would be still resistant to various stresses, yet more adapted to modern commercial farming more compact for easier mechanical harvesting, for example. The new plant also had larger fruits than the wild original.

"The size and weight was about double," Cermak says. Yet this still wasn't the ideal tomato he strives to obtain for that more work needs to be done. "By adding additional genes, we could make the fruit even bigger and more abundant, increase the amount of sugar to improve taste, and the concentration of antioxidants, vitamin C and other nutrients," he says. And, of course, resistance to various forms of stress, from heat and pests to draught and salinity.

Excerpt from:
The tomatoes at the forefront of a food revolution - BBC News

Recommendation and review posted by Bethany Smith

EMERYVILLE, Calif.--(BUSINESS WIRE)--Metagenomi, a genetic medicines company with a versatile portfolio of next-generation gene editing tools, today announced that the company will share data related to their novel, compact, and hypo-immune gene editing systems at the 63rd Annual Meeting and Exposition of the American Society of Hematology (ASH), which is taking place in Atlanta, GA and virtually, December 1114.

The development of CAR T therapies and other genetically engineered cell therapies in recent years has resulted in significant benefits for patients, yet there remains a large unmet need for gene editing systems that can be used to develop novel immunotherapy approaches to treat blood cancers, said Brian C. Thomas, PhD, CEO and Co-Founder of Metagenomi. At ASH, we are presenting data on our novel nucleases that display highly efficient and specific gene editing both in vivo and ex vivo and hold significant potential to drive the development of new and efficacious therapies for patients.

In a poster titled A Novel Type V CRISPR System with Potential for Genome Editing in the Liver, it is shown that Metagenomis novel Type V CRISPR-associated nuclease was highly active in the liver of mice when systemically administered via lipid nanoparticles (LNP). The nuclease was derived from a unique natural environment and is phylogenetically distinct from previously identified Type V systems. Moreover, no antibodies to the nuclease were detected in serum from 50 healthy human donors, while between one third and half of the same serum samples contained antibodies that bind to spCas9, which is derived from a Streptococcus bacteria that commonly infects humans. In summary, this novel Type V CRISPR-associated nuclease is a promising new gene editing system for in vivo editing of the liver.

In a separate poster titled Novel CRISPR-Associated Gene Editing Systems Discovered in Metagenomic Samples Enable Efficient and Specific Genomic Engineering for Cell Therapy Development, three novel gene editing systems were used to make reproducible and efficient edits to human immune cells, demonstrating utility for the next generation of cell therapy development for blood cancers. Metagenomis novel gene editing systems were used to disrupt the T cell receptor alpha-chain constant region and the T cell receptor beta-chain constant region in approximately 90 percent of cells. Beta-2 microglobulin was edited in 95 percent of T cells. A chimeric antigen receptor (CAR) construct was also shown to be integrated in up to 60 percent of T cells. Novel gene editing systems were deployed in NK cells to disrupt CD38 a cell surface immune modulator that can be targeted in the development of cancer immunotherapy and to integrate a CAR construct that led to robust CAR-directed cellular cytotoxicity. B cell editing occurred in approximately 80% of target cells with successful transgene integration. Whats more, as these gene editing systems are taken from environmental samples as opposed to human pathogens, pre-existing immunity is expected to be rare. In summary, these novel systems were shown to result in highly efficient and specific gene edits in human immune cells and display the potential for use in cell therapy development.

Details of the presentations are below:

Presentation Title: A Novel Type V CRISPR System with Potential for Genome Editing in the LiverSession Title: 801. Gene Therapies: Poster IPresenting Author: Morayma Temoche-Diaz, PhDPublication Number: 1862 Session Time: Saturday, December 11, 5:30 p.m. ET

Presentation Title: Novel CRISPR-Associated Gene-Editing Systems Discovered in Metagenomic Samples Enable Efficient and Specific Genome Engineering for Cell Therapy DevelopmentSession Title: 801. Gene Therapies: Poster IIIPresenting Author: Gregory Cost, PhD, Vice President of Biology, MetagenomiPublication Number: 3984 Session Time: Monday, December 13, 6:00 8:00 p.m. ET

About Metagenomi

Metagenomi is a gene editing company committed to developing potentially curative therapeutics by leveraging a proprietary toolbox of next-generation gene editing systems to accurately edit DNA where current technologies cannot. Our metagenomics-powered discovery platform and analytical expertise reveal novel cellular machinery sourced from otherwise unknown organisms. We adapt and forge these naturally evolved systems into powerful gene editing systems that are ultra-small, extremely efficient, highly specific and have a decreased risk of immune response. These systems fuel our pipeline of novel medicines and can be leveraged by partners. Our goal is to revolutionize gene editing for the benefit of patients around the world. For more information, please visit https://metagenomi.co/.

See the original post:
Metagenomi to Present Preclinical In Vivo and Ex Vivo Gene-Editing Data at the 63rd American Society of Hematology (ASH) Annual Meeting - Business...

Recommendation and review posted by Bethany Smith

An enduring and persistent (albeit until now unresolved) issue in the patent interferences involving the Broad Institute, Harvard University, and MIT (collectively, "Broad") as Senior Party and the University of California/Berkeley, the University of Vienna, and Emmanuelle Charpentier (collectively, "CVC") as Junior Party has been the question of whether Broad had committed inequitable conduct in prosecuting its patents- and applications-in-interference. CVC raised the issue in its proposed motions in Interference No. 105,048 (see "CRISPR Interference Motions Set" and "PTAB Redeclares CRISPR Interference and Grants Leave for Some (But Not All) of Parties' Proposed Motions") and in this '115 Interference (see "CRISPR Interference Parties Propose Motions"). In both interferences, the Board denied CVC authorization to file its motions grounded in inequitable conduct as being premature but granted leave for CVC to file a motion for authorization to file their inequitable conduct motion at the end of the priority phase.

That day never came in the '048 Interference, because the Board granted Broad's motion that there was no interference-in-fact and the Broad prevailed (see "PTAB Decides CRISPR Interference -- No interference-in-fact"). In this '115 Interference, CVC made much the same allegations made in the earlier interference (see "CRISPR Interference Parties Propose Motions"). According to CVC, "Broad made at least one affirmative material misstatement during prosecution of each of Broad's involved patents, applications, or parent applications to which they claim priority" -- specifically, in a declaration by named inventor Zhang regarding actual reduction to practice of CRISPR-Cas9 in eukaryotic cells prior to May 2012. CVC asserted that these statements were untruthful because the CRISPR system did not comprise tracrRNA, which is necessary for CRISPR to be functional. CVC asserted that it was undisputed that tracrRNA is necessary for CRISPR function, using disclosure from U.S. Provisional Patent Application No. 61/736,527 as well as in the Broad's involved patents and independent prior art. CVC also asserted that Dr. Zhang's "conception" arose only after reading a Berkeley prior art disclosure. The proposal for this motion extensively analyzed purported evidence for actual reduction to practice to show the Broad's asserted failure, alleging that the Broad "cherry-picked data" that "intentionally omitted the context that shows his claims of successful DNA cleavage to be false." This motion applied to all the Broad's patents- and applications-in-interference because the alleged untruthful statements were submitted in all applications.

CVC also made similar allegations for another declaration submitted by a different inventor, which they contend evinced "a larger pattern of deception." These allegations were supported by an e-mail from a Zhang lab member and named inventor on the Broad's provisional application (albeit in a context where there seems to exist an axe to grind against Dr. Zhang):

The 15-page declaration of [Feng Zhang] and Le Cong's luciferase data is mis- and overstated to change the examiner's decision, which seems to be a joke. . . .

After seeing your in virto [sic, in vitro] paper, Feng Zhang and Le Cong quickly jumped to the project without letting me know. My lab notebooks, emails and other files like dropbox or gel pictures recorded every step of the lab's failure process. I am willing to give more details and records if you are interested or whoever is interested to clear the truth. . . .

We did not work it out before seeing your paper, it's really a pity.

It appears, however, that CVC's time may have come. On June 25th, CVC by e-mail requested leave to file its inequitable conduct motion which included an assertion that "there are new justifications for [the] requested motion" (which Broad opposed). The Board denied this request by Order under 37 C.F.R. 41.104(a) on July 8th. However, on November 12th, the Board entered an Order under 37 C.F.R. 41.104(a) granting CVC leave to file a paper of no more than five pages that listed its "additional justifications" for filing its inequitable conduce motion. On November 18th, in a Paper entitled "CVC's Additional Justifications Supporting Authorizing a Motion for Unpatentability due to Inequitable Conduct," CVC filed its list pursuant to the Board's November 12th Order. In that Paper, the CVC provided the following allegations:

1. That Dr. Zhang testified in the '115 Interference that "demonstrate[ed] that his 2014 Declaration [in the '048 Interference] knowingly mischaracterized his March 2011 experiments.

2. That "the record in this ['115] interference shows that Zhang's 2015 Declaration misrepresents his alleged possession of 'a single molecule' guide RNA."

Regarding the first allegation, CVC argues that statements made by Dr. Zhang in a Declaration dated January 30, 2014 were "knowingly false." The statement in question reads as follows:

Exhibit 7 [i.e., experiments conducted in March 2011, as first revealed in this interference] shows that prior to May 2012, I conceived and reduced to practice . . . [a]n engineered, programmable, non-naturally occurring Type II CRISPR-Cas system . . . . [Ex. 3424]

The bases for CVC's allegation of knowing falsehood include 1) that Dr. Zhang had "since conceded that those experiments did not include any tracrRNA, which he knew was a necessary component when he signed his 2014 Declaration"; (2) that Dr. Zhang in two instances (during cross-examination and in a 2020 inventor declaration) "admitted . . . , that he did not begin introducing any form of tracrRNA into his experiments until April of 2011," supported by his further admission that "he learned about the existence of tracrRNA only after reading Deltcheva et al. (Ex. 3214), which first published in Nature on March 30, 2011" made during his deposition and that he began adding "the native tracrRNA" on April 5, 2011. From this CVC drew the conclusion that because this was after the March 2011 experiments, Dr. Zhang had made a materially false statement in this regard in his earlier declaration. CVC then argues that this timeline and truthful testimony (after the fact) was consistent with the deposition testimony CVC elicited from Dr. Marraffini (see "CVC Files Motion in Opposition to Broad Priority Motion") regarding CVC's contention that "[Dr.] Zhang did not know that tracrRNA was part of the DNA-cleavage complex until June 26, 2012." Because "[b]y the time [Dr.] Zhang signed his 2014 Declaration, however, he did know that tracrRNA was a necessary part of the Type II CRISPR-Cas9 system" and "[Dr.] Zhang knew that his March 2011 experiments did not include any form of tracrRNA," CVC contends that "[i]t was therefore knowingly false to declare that these experiments 'describe and enable' and 'reduced to practice' the claimed Type II CRISPR-Cas9 system," which was Dr. Zhang's testimony in his 2014 declaration.

Accordingly, should the Board agree that Dr. Zhang's testimony amounts to a knowingly false statement, CVC argues that under Therasense, Inc. v. Becton, Dickinson & Co., 649 F.3d 1276, 1292 (Fed. Cir. 2011) (en banc), these statements would be material to patentability per se. Because Dr. Zhang's averments in his declaration were "for the purpose of removing prior art to obtain allowance of claims" (and indeed "the examiner expressly relied on Zhang's 2014 Declaration in her reasons for allowance in each of Broad's 13 involved patents and involved '551 application), CVC argues that an intent to deceive was an appropriate inference for the Board to draw (supported by Dr. Zhang's statement in his declaration that "I understand that . . . if I can show conception and actual reduction to practice prior to the filing dates of the [art] . . . then I have removed the [art] from being prior art . . . ." (emphasis added in CVC's brief).

Regarding the second allegation, CVC raises Dr. Zhang's 2015 declaration wherein "[Dr.] Zhang attests that Figure 4B in a 2012 grant proposal to the National Institutes of Health ("the NIH grant") showed that "a single RNA can be used as a guide in the CRISPR-Cas9 system." Ex. 3424. This testimony is inconsistent with Dr. Zhang's testimony (and Broad's arguments) in this interference, wherein "[Dr.] Zhang and Broad have represented in this proceeding that the same Figure 4B of the NIH grant shows a dual-molecule guide system and not a single-molecule guide system" (emphasis added). CVC adds Dr. Zhang's further assertions from his 2015 declaration:

Having generated the figure of part B in the above illustration from the January 12, 2012 R01 NIH grant application, prior to January 12, 2012, I appreciated the mammalian expression system illustrated could be constructed, and when introduced into a mammalian cell could express products and function in vivo for cleavage and genome editing, as illustrated above, and as actually done prior to November 30, 2011, with appreciation that a single RNA can be used as a guide in the CRISPR-Cas system, including as shown by . . . the illustration of the NIH R01 grant application . . . . [Ex. 3424]

CVC then cited the phrase "used as a guide" in this passage of Dr. Zhang's deposition testimony in contrast with Dr. Zhang's deposition testimony in this interference to refer to "RNA that's guiding Cas9 to the target" and consequently that "[Dr.] Zhang declared to the Office that Figure 4B 'show[ed]' that he appreciated that 'a single RNA can be used as a guide in the CRISPR-Cas system.'" Once again, CVC argues that this statement is "knowingly false" because here "[Dr.] Zhang has admitted in this proceeding [i.e., in his 2020 inventor declaration in this interference] that Figure 4B in fact shows a dual-molecule guide system." CVC also notes that Broad has taken this position (that Figure 4B shows a dual-molecule embodiment of CRISPR) in this interference, inter alia, "[i]n support of its motions to change the count and de-designate claims corresponding to the count (both of which the Board denied), citing several arguments in Broad's motions and replies to CVC's oppositions to these motions. Further, CVC argues that a proper interpretation of Figure 4B as not showing a single-molecule RNA-comprising embodiment of CRISPR is consistent with Dr. Maraffini's testimony "that he first conveyed such a system to Zhang on June 26, 2012, by showing him CVC's work" (neatly wrapping in CVC's arguments that if Df. Zhang had achieved a single-molecule RNA-comprising embodiment of CRISPR in eukaryotic cells he had done so by deriving the invention from CVC's inventors). Once again, CVC argues that Dr. Zhang's statements in this instance are "unmistakably false and thus per se material" and that the examiner relied upon these statements in allowing the '551 application. And, CVC argues, the Board can infer an intent to deceive in view of Dr. Zhang's participation inter alia in an examiner interview "that involved discussion of 'whether there need be consideration of interference [sic] as to [CVC] applications.'"

CVC further asserts that the Board should hear its motion before Final Judgment, based on circumstances where "the factual record is complete, no discovery is required, and resolution is in the public interest," citing McDonald v. Miyazaki, Interference No. 104,544, Paper 149. There, where "an inventor submitted a declaration during prosecution that misrepresented certain experiments and activities in an effort to antedate prior art," the Board entered judgment cancelling all involved claims on inequitable conduct grounds saying these circumstances were "the sort of over-reaching and truth-shaving that Rule 56 was enacted to prevent." According to CVC, Dr. Zhang's and Broad's inequitable conduct here has been "[e]ven more egregious and pervasive."

Under these circumstances, CVC asserts in support of its demand that the Board hears (and presumably decides this motion before Final Hearing) that "the PTAB has a duty to protect the public from inequitably procured patents and to enforce Rule 56 to prevent abuse of declaration practice, as the examining corps is not equipped to police such misconduct."

View original post here:
Inequitable Conduct by Senior Party Broad Alleged in Interference No. 106115 (and PTAB May Finally Hear Evidence About It) - JD Supra

Recommendation and review posted by Bethany Smith

For genes on autosomes, we all have two copiesone from each parent. The two copies may be the same, or they may be different. Different versions of the same gene are called alleles (uh-LEELZ). Genes code for proteins, and proteins make traits.* Importantly, its the two alleles working together that affect what we seealso called a phenotype.

Female pigeons (ZW) have just one Z chromosome, and therefore just one allele for each of the genes located there. One gene on the Z chromosome affects feather color; three different alleles make feathers blue, ash-red, or brown. In a female bird (ZW), her single color allele determines her feather color. But in males (ZZ), two alleles work together to determine feather color according to their dominance. That is, 'ash-red' is dominant to 'blue', which is dominant to 'brown'.

Having two copies of a gene can be important when one copy is broken or defective. A functional second copy can often work well enough on its own, acting as a sort of back-up to prevent problems. With sex-linked genes, male mammals (and female birds) have no back-up copy. In people, a number of genetic disorders are sex-linked, including Duchenne muscular dystrophy and hemophilia. These and other sex-inked disorders are much more common in boys than in girls.

Red/green colorblindness is also caused by a defective gene on the X-chromosome. You need at least one working copy of the gene to be able to see red and green. Since boys have just one X-chromosome, which they receive from their mother, inheriting one defective copy of the gene will render them colorblind. Girls have two X-chromosomes; to be colorblind they must inherit two defective copies, one from each parent. Consequently, red-green colorblindness is much more frequent in boys (1 in 12) than in girls (1 in 250).

*Some genes code for functional RNAs, which also influence our traits.

The differences in sex chromosomes between males and females leads to specific inheritance patterns for sex-linked genes. (Above) Female pigeons inherit their color allele from their father. Males inherit one allele from each parent. In humans (below), the pattern is reversed.

Here is the original post:
Sex Linkage - University of Utah

Recommendation and review posted by Bethany Smith

What Is It?

Hair loss can range from mild hair thinning to total baldness. Hair can fall out for many different reasons. Medically, hair loss falls into several categories, including:

We normally lose approximately 50 to 100 scalp hairs each day. If more than this is falling out, you may find unusually large amounts of hair in brushes, on clothing, and in the drains of sinks and tubs. You may also notice that your hair is generally thinner, that your part is wider, that your hairline has changed or that one or more bald patches have appeared.

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

Read the original here:
Hair Loss - Harvard Health

Recommendation and review posted by Bethany Smith

As males are unable to produce milk or lay eggs, the ability to breed cows and hens that produce all-female litters is likely to be high on most poultry and dairy farmers wish lists.

Now, scientists at the Francis Crick Institute and the University of Kent have come a step closer to realising this goal after successfully using CRISPR gene editing techniques to produce all-female or all-male litters of mice.

The technique could also be used to improve animal welfare in areas of scientific research in which only male or only female animals are required for studies, the researchers say.

To make the breakthrough the researchers took advantage of the fact that CRISPR consists of two parts the Cas9 enzyme, which cuts the DNA and enables scientists to alter specific regions of genes, and the guide RNA, which carries the Cas9 enzyme to the desired region on the genome.

They targeted the TOP1 gene, which is essential to DNA replication, and placed one part of CRISPR on the fathers X or Y chromosome, meaning that it will only be inherited by female or male embryos, and the other part on the mothers chromosomes, which will be inherited by all embryos.

This meant that when a sperm carrying the Cas9 enzyme on the fathers X or Y chromosome fertilised an egg carrying the guide RNA, the gene editing process was triggered in the resulting embryo and it was not able to develop beyond a very early stage.

Read more about genetic engineering:

This method works as we split the genome editing process in half, between a male and female, and it is only when the two halves meet in an embryo through breeding, that it is activated. Embryos with both halves cannot develop beyond very early cell stages, said Charlotte Douglas, first author and former PhD student and postdoctoral scientist at the Crick.

Weve also shown this process works successfully in different combinations introducing either the Cas9 or the guide RNA elements on to the mothers or fathers chromosomes.

Using this method, the researchers were able to control the sex of a litter with 100 per cent accuracy and found no harmful effects in the surviving animals.

Moreover, as the TOP1 gene is well conserved across mammals, these results may also be applicable to other animals such as livestock.

The implications of this work are potentially far-reaching when it comes to improving animal welfare, but should be considered at ethical and regulatory levels, said Dr Peter Ellis, author and senior lecturer in molecular genetics and reproduction at the University of Kent.

In particular, before any potential use in agriculture, there would need to be extensive public conversation and debate, as well as changes to legislation. On the scientific side, there is also much work to be done over a number of years. Further research is needed, first to develop the particular gene editing toolkits for different species, and then to check they are safe and effective.

More here:
Gene editing used to create all-male or all-female litters of mice - BBC Science Focus Magazine

Recommendation and review posted by Bethany Smith

A new systematic review of the validated monogenic causes of male infertility strengthens the evidence base for emerging gene-disease relationships; the review hopes to encourage more routine genetic testing in clinics and identify gaps in our knowledge of male infertility genetics.

In less than two years, the number of genes revealed in the literature as causative of male infertility phenotypes has increased from 78 (in 2019) to 104, an increase of 33%. All are supported by evidence of a direct gene-disease relationship and, say the authors of a new report, will provide the impetus for an update of existing guidelines, will inform novel evidence-based genetic testing strategies used in clinics, and will identify gaps in our knowledge of male infertility genetics.(1)

This latest report is an update on the first standardised clinical validity assessment of monogenic causes of male infertility published in 2019, and like that one this latest literature evaluation has been conducted with the International Male Infertility Genomics Consortium (IMIGC). The increase in the number of high-probability male infertility genes is not just a reflection of extended gene discovery but a function too of the recent rapid uptake of next generation sequencing in male infertility (with whole-exome sequencing described as the default sequencing approach) and research on clinical cohorts. The validation of these emerging genes will, say the authors, help give direction to which individual genes may be screened for and how they are relevant to certain types of infertility.

All 104 genes and their links to male infertility phenotypes are listed in a table, with organ effects noted in hypothalamic function, pituitary and adrenal gland dysfunction, vas deferens, reproductive organ development, Leydig cell, Sertoli-cell only syndrome, meiotic arrest, spermatogenesis and fertilisation.

As illustrated in a Campus meeting on the genetics of male infertility held online a few weeks ago, a wide range of phenotypes now appears to be largely genetic in origin.(2) Already, the genetic components of Klinefelter syndrome, Y-chromosome microdeletions and some monogenic causes of azoospermia are well recognised, but there remains a majority of male infertility cases (60-70%) without any clear diagnosis. Only 4% are actually diagnosed with a defined genetic cause. This updated systematic evaluation of all available evidence for published monogenic causes of isolated or syndrome male infertility will hopefully extend the limits for genetic testing and the diagnostic power for identifying the causes of male infertility; however, while NGS is now a cornerstone test in male infertility research, it is not, say the authors, extensively employed in clinical diagnosis.

The report notes that the diagnostic rate of genetic tests for all types of isolated male infertility currently lies between 4 and 9%. These are rates considerably behind those seen in other heterogeneous disorders with a large genetic contribution such as cardiomyopathies or developmental delay, where whole-exome and whole-genome sequencing are routinely applied. However, with reduced costs of NGS and better accessibility, the authors hope that the increased number of validated genes implicated in male infertility will lead to greater diagnostic implementation.

And this in turn will help in evaluating future health risks in which male infertility may be linked to other comorbidities in later life; for example, a number of multiple DNA repair genes linked to infertility are known to be involved in some cancers. There are also implications from genetic testing in male infertility for sons of men with Y-chromosome variants conceived by ART, who presumably will inherit the same infertility phenotype as their affected fathers - and thus may in turn require ART if wanting their own biological child.

1. Houston BJ, Riera-Escamilla A, Wyrwoll MJ, et al. A systematic review of the validated monogenic causes of human male infertility: 2020 update and a discussion of emerging genedisease relationships, Hum Reprod Update 2021; doi:10.1093/humupd/dmab0302. See https://www.focusonreproduction.eu/article/ESHRE-News-male

Read the original here:
The number of genotype-phenotype associations validated in male infertility continues to grow - ESHRE

Recommendation and review posted by Bethany Smith

Breadcrumb Trail Links

Author of the article:

The Calgary Zoo is planning for the arrival of a baby gorilla sometime in April or May 2022.

This advertisement has not loaded yet, but your article continues below.

The zoos 20-year-old western lowland gorilla Dossi is expecting her first baby. The father is the troops silverback leader, Jasiri.

We are cautiously optimistic as this is Dossis first baby, said Jamie Dorgan, director of animal care, health and welfare. Gorilla pregnancies are more likely to be unsuccessful the first time. There are lots of challenges ahead of us but the animal care, health and welfare team will be supporting Dossi every moment along the way.

Kim Walker, animal care manager for the Rainforest and South America sections at the Calgary Zoo, said the team working with Dossi will start a night watch in March, where technicians will be monitoring the troop 24/7.

(The night watch is necessary) because she could go into labour a little bit earlier, Walker said.

This advertisement has not loaded yet, but your article continues below.

Ongoing training is actively happening to ensure the process of Dossis pregnancy runs smoothly.

We are training her to pass the baby to us in case we have to supplement the bottle feed, Walker said. We also have another behaviour where shell put the newborn in a box and we can safely retrieve the baby in case veterinarians need to examine it any closer.

According to Walker, while the team is hoping for a successful birth, there is always the chance something can go wrong.

We are doing everything we can to support her and the troop for a successful birth and pregnancy, she said.

Issues arise within pregnancies due to the process being new for expecting mothers, Walker said. She added there was an unsuccessful birth earlier this year with 12-year-old Yewande.

This advertisement has not loaded yet, but your article continues below.

There was nothing wrong with the infant, it was just a very long labour for her, she said.

Zoo officials do not plan to intervene in the birth unless the health of the mother or baby is at risk.

The birth will mark a hopefully important milestone, as Walker said the wild gorilla population has declined by 80 per cent a grim statistic considering it comes from only the last 30 years.

There are dwindling numbers out there and we are doing everything we can to help, Walker said. If we have to, we may have to look at possible re-introductions into the wild if they do go extinct.

Through what Walker calls a dating service of sorts, also known as the Species Survival Program, members look at genetics and try to find the best match for a potential mother to ensure success in reproduction.

This advertisement has not loaded yet, but your article continues below.

Walker said after the loss of Kakinga in May 2016 , it took nearly three years to bring in Jasiri, due to the many factors that go into finding the right suitor.

They really have to look at what male would be best for the troop for the females to be safe, she said. We also have to find out if well have a good diversity of genetics if this male comes in to breed.

Kakinga, who died at age 37 after developing a large tear in his aorta, was successful in siring nine offspring while at the zoo.

He did leave a really good lineage, Walker said.

If Dossi successfully gives birth, it will be the first baby gorilla at the zoo since 2016, when baby Kimani was born.

This advertisement has not loaded yet, but your article continues below.

Sign up to receive daily headline news from the Calgary Herald, a division of Postmedia Network Inc.

A welcome email is on its way. If you don't see it, please check your junk folder.

The next issue of Calgary Herald Headline News will soon be in your inbox.

We encountered an issue signing you up. Please try again

Postmedia is committed to maintaining a lively but civil forum for discussion and encourage all readers to share their views on our articles. Comments may take up to an hour for moderation before appearing on the site. We ask you to keep your comments relevant and respectful. We have enabled email notificationsyou will now receive an email if you receive a reply to your comment, there is an update to a comment thread you follow or if a user you follow comments. Visit our Community Guidelines for more information and details on how to adjust your email settings.

Go here to read the rest:
Calgary Zoo gorilla 'Dossi' expecting her first baby in the spring - Calgary Herald

Recommendation and review posted by Bethany Smith

Fiona is turning 5. It's almost time to think about boys

Updated: 3:55 PM EST Dec 2, 2021

Hide TranscriptShow Transcript

>> THE CINCINNATYI ZOO HAS BEEN HERE A LONG TIME. AND WE'RE NOW FAMOUS, AS THE CINCINNATI ZOO AND BOTANICAL GARDENS. THAT LONG TRADITION, PARTICULARLY IN CINCINNATI WHERE EVERYBODY VALUES THE HISTORY IS VERY IMPORTANT. AS I SAY, CINCINNATI IS A ZOO TOWN. THIS TOWN STUCK WITH US. PEOPLE ARE STILL JOINING THE ZOO WITH, WE KNOW THAT YOU'RE NOT OPEN YET BUT WE KNOW YOU'RE GOING TO BE OPEN. WE WANT YOU TO MAKE IT. WE ARE A VERY SUPPORTIVE TOWN. >> FROM WLWT, THIS IS LET'S TALK CINCY IS PRESENTED BY WESTERN AND SOUTHERN FINANCIAL GROUP. PUT OUR FINANCIAL STRENGTH BEHIND YOU. COURTIS: ANYTIME SOMETHING IS CONSIDERED THE BEST, IT'S WORTH TALKING ABOUT. HELLO, EVERYONE. I'M COURTIS FULLER AND WELCOME TO LET'S TALK CINCY. THE CINCINNATI ZOO IS KNOWN AROUND THE WORLD AND IT IS NOW RANKED THE BEST ZOO IN AMERICA IN 2021, ACCORDING TO A POLL CONDUCTED BY USA TODAY'S 10 BEST. A PANEL OF TRAVEL EXPERTS PICKED THE INITIAL NOMINEES. THEN READERS SELECTED THE TOP 10 WINNERS BY POPULAR VOTE. THE ZOO'S RICH HISTORY BEGAN NEARLY 150 YEARS AGO IN 1873. ONE PERSON WHO KNOWS THE HISTORY AS WELL AS ANYONE, IS ZOO DIRECTOR THANE MAYNARD. THE ZOO HAS BEEN A BIG PART OF HIS LIFE FOR NEARLY A HALF CENTURY. >> THIS IS AN AMAZING PLACE, SECOND OLDEST ZOO IN THE COUNTRY. TALK ABOUT THE HISTORY OF THE ZOO. >> WELL, YOU KNOW, SINCE HE'S BEEN HERE A LONG TIME AND WE'RE NOW FAMOUS AS THE CINCINNATI ZOO AND BOTANICAL GARDEN. BUT THAT'S BEEN THE CASE ALL ALONG WITH ANDREW ERIC AND BRECKER AND THOSE GERMAN IMMIGRANTS STARTED THIS. THEY WANTED TO BRING WHAT THEY HAD HAD IN FRANKFURT AND STOOD GUARD TO CINCINNATI, WHICH WAS AN URBAN PARK, BEAUTIFUL PLANTINGS, EXOTIC ANIMALS AND CULTURAL EVENTS, AND OUR ORIGINAL TITLE WAS THE CINCINNATI ZOOLOGICAL' GARDEN. BUT IT'S A GARDEN ON STEROIDS NOW BECAUSE WE REALLY GET AFTER IT, THAT'S FOR SURE. BUT YOU KNOW THAT TRADITION. BACK THEN, YOU CAN IMAGINE HOW IMPORTANT THAT WAS. I MEAN, THERE WASN'T A LOT SHAKING IN THE 1870'S, AND SO HAVING A PLACE LIKE THAT WHERE YOU CAN GET OUT OF OVER THE RHINE OR DOWNTOWN, WHERE THERE REALLY NO PLANS AND COME UP TO A BEAUTIFUL GARDEN IS REALLY SIGNIFICANT. AND WE STILL PLAY THAT ROLE DAY RESPITE FROM THE CITY, A PLACE THAT'S SHADY AND SOFT AND LOTS AND LOTS OF CULTURAL EVENTS. YOU KNOW, WE'RE LIVING THAT SAME MISSION, BUT THAT LONG TRADITION, PARTICULARLY IN CINCINNATI WHERE EVERYBODY VALUES, THEIR, THE HISTORY IS VERY IMPORTANT. AS I SAY, CINCINNATI IS A ZOO TOWN. PEOPLE LOVE THIS. AND I GO, WHETHER I'M IN CLEAVES OR I'M ALL THE WAY UP TERRORIST PARK, OR I'M IN NORTHERN KENTUCKY, EVERYBODY MEET HAS A STORY ABOUT THEIR KIDS WENT ZOO CAMP, BECAME VETERINARIANS, WENT TO THE ZOO FOR 15 YEARS. IT'S FUN, THE ROLE THAT ZOO PLAYS IN FAMILIES LIVES HERE. THAT IS WHY WE ARE HERE. COURTIS: AND IT'S GOOD TO SEE SO MANY FAMILIES BACK OUT, ESPECIALLY AFTER THE YEAR WE'VE HAD. IT'S A REMINDER OF HOW IMPORTANT THIS ZOO IS TO GREATER CINCINNATI. >> IT IS TRUE, YOU KNOW, LAST YEAR WHEN THE PANDEMIC FIRST HIT AND THE GOVERNOR CLOSED THE ZOO. IT ENDED UP BEING THREE MONTHS BUT WE HAD NO IDEA, YOU KNOW. SOME OF THE ZOOS IN CALIFORNIA WERE CLOSED FOR OVER A YEAR, THE NATIONAL ZOO IN D.C. WAS CLOSED FOR OVER A YEAR. AND MAN, WE'D BE COMPLETELY BROKE IF THAT HAD BEEN THE CASE BECAUSE IT WAS EXPENSIVE, EVEN WHEN YOU'RE NOT OPENING. THE VETERINARIANS AND KEEPERS WE HAVE TO FEED ALL THE ANIMALS, BUT WE MADE IT THROUGH BETTER THAN ANYBODY WOULD HAVE THOUGHT. THIS TOWN STUCK WITH US. PEOPLE ARE STILL JOINING THE ZOO WITH, WE KNOW YOU ARE NOT OPEN YET BUT WE KNOW YOU'RE GONNA BE OPEN. WE WANT YOU TO MAKE IT. WE ARE IN A VERY SUPPORTIVE TOWN. COURTIS: 44 YEARS FOR YOU. >> I GOT OLD QUICK, COURTIS. I'M TELLING YOU. COURTIS: DON'T WE ALL. BUT TELL ME YOUR JOURNEY. HOW DID YOU START HERE AT THE ZOO AND, AND OBVIOUSLY 44 YEARS LATER. >> WELL 44 YEARS AGO, THERE , WASN'T AS GREAT AN INTEREST IN WORKING IN THE ZOO FIELD AS THERE IS TODAY. I MEAN, TODAY, IF A JOB CAME OPEN, WHETHER IT'S ZOOKEEPER OR ZOO EDUCATOR, WHICH IS HOW I STARTED THERE'D BE 100 QUALIFIED , KIDS APPLYING FOR THAT JOB. BUT THAT'S AFTER A COUPLE GENERATIONS, ZOO CAMPS AND THINGS WHERE PEOPLE REALLY, REALLY GOT INTO THIS FIELD. BACK THEN, FOR ME IT WAS JUST RIGHT PLACE AT THE RIGHT TIME. PROCTOR HAD FUNDED THE WORLD'S FIRST ZOO EDUCATION CENTER, WHICH IS THE WOODEN BUILDING WE NOW CALL TREE TOPS, AND WE USE IT FOR A WIDE VARIETY OF PURPOSES, BUT IT HAD FIVE CLASSROOMS. THERE'S NEVER BEEN ANYTHING LIKE IT. AND THEY NEEDED SOME PEOPLE TO HELP LEAD PROGRAMS, SO I WAS FORTUNATE. I'D GOTTEN OUT OF GRAD SCHOOL, AND MY WIFE'S FROM CINCINNATI, AND SHE HAD A JOB WRITING ANY CINCINNATI MAGAZINE. AND LIKE A LOT OF YOUNG GUYS COMING UP, I'D NEVER REALLY BEEN VERY THOUGHTFUL ABOUT MY CAREER. I THOUGHT I'D GO TO AFRICA OR SOMETHING, BANG AROUND FOR A FEW YEARS, BUT SUDDENLY I FOUND MYSELF MARRIED AND I'M LIKE, I SHOULD PROBABLY GET A JOB. AND SO, IT WAS FORTUNATE. JUST RIGHT PLACE, THE RIGHT TIME, SO I SPENT 25 YEARS, YEAH, WORKING IN THE ZOO EDUCATION DEPARTMENT. AND, YOU KNOW, HELPING THAT PHENOMENON GROW NOT JUST HERE , BUT AT OTHER INSTITUTIONS WHERE SO MANY FAMILIES TODAY. I MEAN, OUR ZOO CAMPS AND ZOO TROOP AND ALL THOSE , PARTICIPATORY PROGRAMS, VOLUNTEER PROGRAMS LIKE ZOO TEEN , THEY FILL UP INSTANTLY. FAMILIES REALLY WANT THEIR KIDS INVOLVED. COURTIS: YOU ARE A CINCINNATI CELEBRITY, A CINCINNATI LEGEND AND I SAY THAT WITH ALL SINCERITY. >> WELL, SOME OF THAT'S ATTRIBUTED TO WE ARE A NON-TOURIST TOWN, BUT DOESN'T TAKE MUCH TO BE A CELEBRITY HERE. IF THE ZOOKEEPER CAN BE, BUT DON'T FORGET MY FRIEND JACK HANNA, BECAUSE HE PUT HIS HOUSEHOLD NAME AND A DARN GOOD GUY. BUT THAT IS A REFLECTION OF A ZOO LIKE OURS, THAT HAS TREMENDOUS SUPPORT IN THE COMMUNITY INCLUDING ANNUAL PHILANTHROPY AND SPONSORSHIPS FOR OPERATIONS, AND ALL OF OUR CAPITAL IS PRIVATELY RAISED. THIS ZOO IS PLUGGED INTO THE COMMUNITY, SO WE'RE OUT THERE WE'RE PITCHING THE ZOO EVERY DAY YOU KNOW WHETHER IT'S ENCOURAGING PEOPLE TO GET OUT HERE FOR EVENTS LIKE YOU KNOW THE PNC FESTIVAL OF LIGHTS, ZOO BABIES OR IS TO GET SPONSORS TO WANT TO BE DIRECTLY INVOLVED WITH THE ZOO. AND AS A RESULT, I AND OTHERS WHO REPRESENT THE ZOO ARE OUT THERE WORKING AT PRETTY GOOD. YOU KNOW, THERE'S SOME TOWNS WHERE THE FUNDING IS DIFFERENT, AND THE ZOO IS NOT AS ENGAGED IN THE COMMUNITY. NATIONAL ZOO IN WASHINGTON IS PART OF THE SMITHSONIAN, THEY DON'T NEED TO HUSTLE AND OF COURSE THE SAN DIEGO ZOO IF YOU HAVE A ZOO IN SAN DIEGO WHERE THE WEATHER'S PERFECT AND THERE IS NOTHING BUT TOURISTS YOU OUGHT TO BE ABLE TO GET A , CROWD. WE'RE FORTUNATE WE'RE IN CINCINNATI STYLE ZOO, WE SORT OF DO IT PETE ROSE HEADFIRST SLIDE STYLE, LIKE COME ON. IF IT'S WORTH DOING WE OVERDO IT HERE. YEAH. COURTIS: UP NEXT, A BIG VISION. THE $150 MILLION FUNDRAISING CAMPAIGN LEADING TO THE LARGEST CONSTRUCTION PROJECT IN THE ZOO'S HISTORY. AN INSIDE LOOK, WHEN LET'S TALK CINCY CONTINUES. COURTIS: THE CINCINNATI ZOO HAS EMBARKED ON A JOURNEY LIKE NONE OTHER IN ITS HISTORY. THE PROJECT IS CALLED MORE HOME TO ROAM. IT IS A $150 MILLION CAPITAL CAMPAIGN THAT WAS LAUNCHED IN 2018 TO CREATE WHAT THE ZOO CALLS A PACHYDERM PARADISE. THE BIGGEST CONSTRUCTION PROJECT IN THE ZOO'S HISTORY. THANE MAYNARD SAID BIG DONATIONS HAVE MADE THE CROWN JEWEL OF THE PROJECT, ELEPHANT TREK, ALL POSSIBLE. WITH THE GROUNDBREAKING THIS YEAR, BUSINESS AND COMMUNITY LEADERS, HARRY AND LINDA FATH KICKED OFF THE CAMPAIGN IN 2018 WITH A MAJOR DONATION IN THE AMOUNT OF $50 MILLION. COURTIS: YOU WERE TALKING ABOUT HOW PEOPLE SUPPORT THE ZOO, THE PHILANTHROPY HERE. AND LET'S TALK ABOUT THE CAPITAL CAMPAIGN. THIS WAS $150 MILLION, A DREAM. THREE YEARS AGO, TALK A LITTLE BIT ABOUT THAT AND THE AMAZING SUPPORT THAT YOU RECEIVED ALREADY. >> WELL, CINCINNATI IS A GENEROUS TOWN. THAT IS THE TRUTH, NOT JUST OTHER CULTURAL GROUPS. I MEAN JUST REMARKABLE REALLY. I THINK WE HIT WAY ABOVE OUR WEIGHT. WHEN YOU HAVE GUESTS FROM OUT OF TOWN, YOU SHOW THEM THE ART MUSEUM MUSIC HALL AND ALL THE , DIFFERENT THINGS GOING ON IN THE CITY. I THINK THEY'RE REALLY IMPRESSED THAT OUR TOWN HAS ALL THAT, AND IT IS THANKS TO PRIVATE SUPPORT. A LOT OF TOWNS, SITES LIKE ST. LOUIS FUNDED THROUGH TAXES, BUT HERE, ALL THOSE THINGS I MENTIONED ARE FUNDED THROUGH PRIVATE SUPPORT. THAT'S PRETTY NEAT. OUR CAMPAIGN HAS GONE WELL. WE LAUNCHED IT IN THE SUMMER OF 2018 WITH THE INCREDIBLE LEADERSHIP GIFT FROM HARRY AND LINDA FATH, AND THAT GOT US A THIRD OF THE WAY THERE. THAT WAS UNPRECEDENTED, FRANKLY, IN OUR REGION, AND CERTAINLY UNPRECEDENTED IN THE HISTORY OF THE ZOO. WE HAVE A LONG HISTORY OF SUPPORT. THIS SINCE THAT TIME WE'VE BEEN GOING GANGBUSTERS AND WE'RE 80% OF THE WAY THERE, SO WE HAVE 30 MILLION MORE TO RAISE, AND THAT'S A LOT, BUT WE'RE GOING TO GET THERE. I COMPARE IT TO RUNNING THE FLYING PIG MARATHON WHICH I'VE DONE MANY YEARS, AND WE'RE AT ABOUT MILE 20. IT'S NO TIME TO STOP. IT'S GOT TO KEEP GOING. SO, IT'S BEEN GREAT, IT REALLY HAS. WE'VE HAD CERTAINLY MORE SUPPORT THAN EVER, AND A LOT OF ENTHUSIASM FOR WHERE WE'RE HEADED, BECAUSE, YES, THAT MONEYS FOR CAPITAL. BUT THAT CAPITAL IS REALLY THE FUTURE OF THE ZOO AND WHAT WE DO, SO IT IS CALLED MORE ROOM -- MORE HOME TO ROAM. BUT ARE OTHER ANIMALS, AS WELL WE'RE GONNA DOUBLE THE AMOUNT OF SPACE FOR BLACK RHINOS. WE'VE ALREADY MADE A TERRIFIC EXHIBIT FOR KANGAROOS, A LITTLE PENGUINS FROM AUSTRALIA, AND THAT AFFORDS US AN OPPORTUNITY TO DO A GREAT JOB WITH OUR GENERAL VISITORS AND MEMBERS BUT ALSO TO BE PARTICIPATING IN GLOBAL CONSERVATION PROGRAMS WITH EVERYTHING FROM ALL THOSE PIECES I MENTIONED FROM PENGUINS , IN THE WILD TO ASIAN ELEPHANTS IN INDIA. COURTIS: IT'S GOOD TO HEAR THAT IT IS GOING SO WELL. I CAN ONLY IMAGINE, IF WE REWIND A YEAR AGO, YOU WERE PROBABLY WONDERING HOW ARE WE GOING TO MAKE THIS HAPPEN IN THE MIDST OF THIS PANDEMIC? BUT AGAIN, SUPPORT KEPT COMING. DESPITE THE PANDEMIC. >> YEAH, I'M SURE ANYBODY THAT RUNS ANY BUSINESS ANYWHERE, TOOK A GREAT PAUSE IN MARCH OF 2020 BECAUSE BUSINESSES, WHETHER IT WAS, YOU KNOW, RESTAURANT, CLOSING DOWN. IN THE CASE OF THE ZOO, REALLY ANYWHERE THAT'S AN ATTRACTION, YOU WONDER WHAT THE FUTURE IS GOING TO LOOK LIKE. I THINK IT'S BEEN 100 YEARS SINCE OUR ZOO HAD EVER BEEN CLOSED AND THAT WAS FROM THE 1918 FLU, SO WE KNEW IT WAS SERIOUS, BUT IT TURNED AROUND FASTER THAN WE THOUGHT. AND PEOPLE DIDN'T STICK WITH US. THE FUNNY THING IS JUST AS WE CAME INTO THIS SUMMER, WE HAD MEETINGS AND SAID, GOSH, I DON'T KNOW IF PEOPLE ARE GONNA WANT TO GET IN BIG CROWDS AGAIN. AS SOON AS THE MASK MANDATE WENT DOWN, WE WERE SLAMMED. SO, WE'RE AN OUTDOOR PARK AND PEOPLE WANT TO BE HERE AND THEY WANT TO GET OUT. AND SO THAT'S BEEN VERY HEARTENING. WE'RE VERY FORTUNATE, YOU KNOW, ZOOS, BY THEIR NATURE AND POPULAR FAMILIES LOVE ANIMALS, BY OUR VERY HUMAN NATURE, WE'RE SORT OF INTERESTED IN ANIMALS AND INTERESTED IN NATURE. AND THAT CERTAINLY REFLECTS THE SUPPORT WE HAVE FOR OUR ZOO, AND IN THE CROWD, WE HAD LIKE, TODAY, IT'S A NICE DAY IN THE SUMMER, AND WE'RE PROBABLY ABOUT 10,000 PEOPLE HERE TODAY. COURTIS: UP NEXT, HOW TWO ANIMALS PUT THE ZOO IN THE INTERNATIONAL SPOTLIGHT IN A WAY NO ONE COULD EVER IMAGINE. A HIPPO NAMED FIONA. A GORRILLA NAMED HARAMBE. TWO DEFINING MOMENTS IN THE ZOO'S HISTORY, WHEN LET'S TALK CINCY CONTINUES. LACEY: WELCOME BACK, EVERYONE. I'M LACEY ROBERTS. JUST SAY THE NAME FIONA, AND YOU IMMEDIATELY THINK OF THE POPULAR AND LOVABLE HIPPO AT THE CINCINNATI ZOO. IN JANUARY 2017, THE FIRST NILE HIPPO WAS BORN AT THE ZOO IN 75 YEARS. FIONA WAS PREMATURE, WEIGHED LESS THAN 30 POUNDS. HER SURVIVAL DEPENDED ON SPECIAL CARE 24 HOURS, SEVEN DAYS A WEEK. HER STORY WENT VIRAL, AND AS THEY SAY, THE REST IS HISTORY. BUT AS YOU WILL SEE, THE ZOO MAY HAVE NEEDED FIONA AS MUCH AS SHE NEEDED THE ZOO, BECAUSE OF THE DEATH OF A SILVERBACK GORILLA NAMED HARAMBE. COURTIS CONTINUES HIS CONVERSATION WITH CINCINNATI ZOO DIRECTOR THANE MAYNARD. COURTIS: THE HIGH POINT, PROBABLY IN YOUR CAREER, YOU WOULD NEVER IMAGINE. FIONA. THIS THIS GIFT THAT BASICALLY WAS GIVEN TO YOU. JUST TALK ABOUT FIONA, HOW THIS ANIMAL HAS BECOME REALLY KNOWN AROUND THE WORLD. >> YOU KNOW, IT IS IMPOSSIBLE TO EXAGGERATE THE IMPACT SHE'S HAD AND THE POPULARITY SHE'S HAD. AND THINK OF THAT BECAUSE, OF COURSE, SHE IS A NILE HIPPOPOTAMUS, AND THAT'S NOT PRIOR ON ANYONE'S TOP 10 LISTS. YOU'VE COME TO ZOO AND THEY WANT TO SEE GIRAFFES AND TIGERS, ELEPHANTS, AND GORILLAS, AND EVEN WHEN YOU GO TO AFRICA AND YOU SEE HIPPOS, YOU KNOW, THEY'RE BIG AND THEY'RE LAYING IN THE WATER, BUT BOY, YOU SAY ONE, MAYBE PREMATURE HIPPO. SHE CHANGED THE WORLD. WHEN SHE WAS BORN, I'D NEVER SEEN ANYTHING LIKE IT, BECAUSE TYPICALLY, HIPPOS, AS HOOFED ANIMALS ARE VERY PRECOCIOUS, THEY'RE LARGE WHEN THEY'RE BORN. THEY WEIGH ABOUT 100 POUNDS, ABOUT THIS BIG. BORN UNDERWATER, CLIMB IN THEIR MOM'S BACK THE DAY THEY'RE BORN, NURSE UNDERWATER. WELL, SHE WAS ONLY 29 POUNDS. SHE LOOKED LIKE A LITTLE DEFLATED RUGBY BALL, AND WAS BORN JUST ON THAT STRAW. SHE WAS A NEW MOM AND CONFUSED BY IT. AND SHE WASN'T CAPABLE AND TAKE CARE OF HER. AND IT WORKED OUT, AND I MEAN IT TOOK HANDS ON DECK. WE HAD A GROUP BECAME TO BE KNOWN AS TEAM FIONA, WHICH WERE THE ANIMAL KEEPERS AND CAREGIVERS, BUT ALSO THE VET TEAM, THE NUTRITION TEAM AND , PEOPLE FROM ALL OVER THE CITY WHO WEIGHED IN AND WOULD SPEND THE NIGHT WITH HER AND TAKE CARE OF HER. TWO SPECIALIZED NURSES FROM CHILDREN'S HOSPITAL CAME WHEN SHE GOT DEHYDRATED, AS PREEMIES CAN, DIARRHEA AND THEN THEY NEED FLUIDS. WE COULDN'T HIT A VEIN AND THEY CAME OVER THERE. YEAH, THERE'S NEVER BEEN A THING WE HAVEN'T HAD, SO THEY PUT AN IV ENTER AND STEP BY STEP, THE NEXT THING YOU KNOW, WHEN SHE WAS A COUPLE MONTHS OLD. WE STARTED TO REALIZE, HEY, SHE'S GROWING, SHE'S GONNA MAKE IT. BUT THERE WERE A LOT OF NERVOUS TIMES THERE IN THE MIDDLE, BUT YEAH, IT'S FUNNY. WHEN SHE WAS A FEW MONTHS OLD, ONE OF OUR FORMER BOARD CHAIRS CALLED ME AND SAID THEY KNEW HOW TO GREET BB AGAIN, SO YOU CAN HAVE ANOTHER FIONA. SAID THERE'S NEVER GOING TO BE ANOTHER FIONA. THE WAY IT HIT REALLY WAS LIKE LIGHTNING IN A BOTTLE. THE SAVED FROM THE BRINK PREMATURE STORY WAS PART OF IT. THE PHENOMENON OF FACEBOOK AND OTHER SOCIAL MEDIA SITES, PEOPLE FOLLOWED HER ON, ON THE WEB. I MEAN THAT YEAR OF 2017, I TRAVELED A LOT. I WENT TO A COUNTRY IN THE OFFICIAL MIDDLE OF NOWHERE IN AFRICA. NEXT TO TOGO, AND I'M SITTING IN A TABLE, THERE'S PEOPLE EATING, AND SOMEONE SEES MY HATS AND CINCINNATI ZOO AND SAYS TO ME, ISN'T THAT WHERE FIONA'S FROM. AND I COULDN'T GET FARTHER AWAY FROM HERE. EARLIER THAT YEAR, I WAS DOWN IN BELIZE IN CENTRAL AMERICA BIRDWATCHING. I GET TO THIS VERY REMOTE SITE WHERE ONLY BIRDWATCHERS GO TO THIS ONE PLACE TO BE ABLE TO WATCH THESE VERY RARE BIRDS. SO, ALL THESE PEOPLE ARE THERE, THEY ARE ONLY INTERESTED IN ANYTHING BIRDS. AND I HEAR THESE TWO LADIES ON THIS BIRD BLIND, AND ONE LADY SAYS TO THE OTHER I'M GLAD THAT , GOT WI FI CUZ I GOTTA FOLLOW BABY FIONA. AND I WENT OVER AND INTRODUCED MYSELF AND SHE'S LIKE, I CAN'T EVEN BELIEVE IT, YOU KNOW, CUZ, YEAH, SHE TOOK OVER THE WORLD, NO DOUBT ABOUT IT. THE NUMBERS OF PEOPLE REACHED THROUGH ALL OF THAT ARE SO VAST THAT IT ALMOST SOUNDS LIKE MAKING IT UP. I MEAN, IN THE BILLIONS OF PEOPLE SAW THAT, YOU KNOW, ON HER PHONE, ON THEIR COMPUTER, SO YEAH, IT'S SOMETHING. COURTIS: IT'S ALMOST HARD TO SAY THAT THIS HIPPO HAS PERSONALITY. YOU KNOW, AND I SAY THAT AS THIS LAYMAN, BUT SHE HAS A LOT OF PERSONALITY. >> WELL, SHE WAS WHICH NEVER HAPPENED WITH AN ANIMAL LIKE A HIPPO, HAND RAISED. SO, SHE WAS SO SMALL, FOR MANY WEEKS, KEEPERS STAYED WITH HER, TO OBSERVE IT THEY LAID THERE HELD HER AND KEPT HER WARM, AND AS SHE GOT OLDER AND STARTED TO SWIM, SHE WOULD SWIM WITH PEOPLE, AND SHE WOULD REST ON THEIR SHOULDER. AND SO YEAH, SHE VERY MUCH IS HUMAN FOCUSED. NORMALLY, HOOFED ANIMALS LIKE A HIPPO OR A ZEBRA WOULDN'T CARE ABOUT PEOPLE. BUT SHE IS INTERESTED AND WILL GO UP TO YOU AND YOUR PHONE, SWIM UP TO YOU AND SAY, YOU MUST BE HERE TO SEE ME. COURTIS: SHE'S THE REAL THING, AND THE PARAPHERNALIA, I MEAN ALL THIS STUFF, THE MARKETING IS -- SHE'S THE NEW MICKEY MOUSE. >> IT'S BEEN NEAT I MEAN A TON OF COMPANIES HAVE SUPPORTED THE ZOO AND GET TO SHARE THAT, AND THAT'S TERRIFIC. IT HELPS OBVIOUSLY IN HER CARE AND CARE OF OTHER ANIMALS, HELPS IN OUR CONSERVATION PROGRAM SO IT'S IT'S BEEN NEAT ALL ALONG. IT IS ATTRIBUTED TO HELP PEOPLE LOVE HER. THAT FIRST YEAR WE HAD THE FIONA 1K AND IT WAS, IT WAS A WALK MORE THAN A RUN. AND IT WAS WHEN SHE TURNED 1000 POUNDS. I FORGET WHAT HER AGE WAS. HONEST TO GOODNESS, IT WAS DRIVING RAIN. I MEAN, DRIVING RAIN. THOUSANDS OF PEOPLE HERE WITH THE T-SHIRT ON. I'M COMING FOR THE FIONA THING SO IT'S, IT'S AMAZING. COURTIS: TERRIFYING MOMENTS AT THE ZOO, AND ONLY WLWT HAS VIDEO OF IT. COURTIS: SHE CAME AT A TIME THAT MIGHT HAVE BEEN THE ZOO'S LOWEST POINT. TALK A LITTLE BIT ABOUT GETTING THROUGH THAT. AND I THINK THAT WHOLE JOURNEY FROM HARAMBE TO FIONA IS SPEAKS VOLUMES ABOUT THE ZOO'S SUCCESS. >> IT DOES. THAT WAS CERTAINLY A LEARNING CURVE FOR ALL OF US BECAUSE THE ZOO WAS PACKED THAT UNFORTUNATE DAY THAT THE BOY GOT IN WITH HARAMBE, AND WE HAD TO SHOOT HIM. AND THAT WAS A DIFFICULT CALL BUT IT WAS A CALL WE WOULD MAKE AGAIN. WE HAVE TO MAKE SURE EVERYONE IS SAFE, BUT IT WAS A TERRIBLE LOSS. AND A TERRIBLE TRAGEDY SO YOU KNOW SOMETIMES TERRIBLE THINGS HAPPEN, BUT IT'S JUST THE TRUTH. I THINK WE GOT THROUGH IT BY BEING STRAIGHT WITH PEOPLE FROM THE FIRST DAY AND SAY THIS IS WHAT HAPPENED. AND NOBODY'S POINTING FINGERS, AND NOBODY'S SECOND GUESSING. WE DID OUR JOB. LACEY: UP NEXT, AS THE ZOO NEARS IT'S 150TH ANNIVERSARY THE FUTURE LOOKS BRIGHT. WHEN LET'S TALK CINCY CONTINUES. COURTIS: CONSIDER THIS. PRIOR TO THE PANDEMIC, THE CINCINNATI BUSINESS COURIER REPORTED ONLY KINGS ISLAND AND THE MUSEUM CENTER HAD A HIGHER ATTENDANCE. MORE THAN 1.7 MILLION PEOPLE MADE THE ZOO THEIR DESTINATION OF CHOICE IN 2019. THE ZOO IS POSITIONED TO SOAR IN THE FUTURE. >> 3, 2, 1. COURTIS: YOU BROKE GROUND IN JUNE. TALK A LITTLE BIT ABOUT THAT AND THE SECOND PART OF THAT IS JUST GIVE ME YOUR, YOUR VISION OF THE ZOO, GOING FORWARD. >> WELL, YEAH, THIS SUMMER IN JUNE, WE BROKE GROUND ON OUR BIGGEST EXHIBIT EVER ELEPHANT TREK, FIVE-ACRE FACILITY, BIG YARD FOR RELEVANCE. IT WILL ALLOW US TO DOUBLE THE SIZE OF OUR HERD. JUST GETTING STARTED. WE'LL TAKE BEFORE, WE HAVE FOUR NEW ONES THAT ARE FLYING HERE ON AN AIRPLANE NONSTOP ON DHL FROM THE DUBLIN ZOO IN IRELAND. WE HOPE THAT THE BARN -- JUST GOING TO BE VERY, VERY BIG IN THE YARD WILL BE READY IN 2023. AND WE'LL BE ABLE TO HAVE THAT. IT WON'T OPEN TO THE PUBLIC UNTIL 2024 BECAUSE THERE'S A NUMBER OF OTHER COMPONENTS. THERE'LL BE AN AREA FOR GIBBONS, WHICH ARE LESSER APES FROM SUMATRA AND BORNEO, THERE'LL BE ASIAN OTTERS, AND A LOT OF OTHER GREAT AMENITIES DOWN THERE. BUT IT'S AN EXCITING TIME AND IT'S A REFLECTION OF, AS I MENTIONED, THAT CAMPAIGN MORE HOME TO ROAM, GIVING ANIMALS MORE SPACE, BUT MORE IMPORTANTLY, IT'S A REFLECTION OF THE ZOOS COMMITMENT TO CONSERVATION. MANY OF THE SPECIES THAT WE HAVE HERE AT OUR ZOO ARE THE SAME SPECIES WE HAD WHEN I SHOWED UP. BUT THERE ARE MANY MORE ENDANGERED SPECIES IN THE WORLD THAN. SO, IN THE CASE OF ASIAN ELEPHANTS, THEY ARE UNDER PRESSURE, BUT WE'RE PARTNERING WITH REALLY GOOD PARTNERS IN NORTHEAST INDIA ON ELEPHANT CONSERVATION PROGRAMS, AND WE HELP TELL THAT STORY. WE HELP SUPPORT THEIR GOOD WORK, AND THERE'S STILL HOPE FOR ELEPHANTS, MUCH AS IN OUR COUNTRY, THERE HAVE BEEN A LOT OF COMEBACKS. YOU KNOW, BALD EAGLES, AMERICAN ALLIGATORS, PEREGRINE FALCONS, GRAY WOLVES, GRAY WHALES, ALL THEIR NUMBERS ARE BACK UP TO WHERE THEY WERE 100 YEARS AGO. AND SO, YOU CAN MAKE CONSERVATION WORK IF YOU REALLY GET AFTER IT. SO, ALL THESE AREAS WHERE THE ZOO IS ENLARGING, WE WERE ALSO INVOLVED, HANDS ON THE GROUND WITH CONSERVATION, WHETHER THAT'S IN AFRICA WITH GORILLAS AND CHEETAHS OR IT'S IN INDIA WITH ELEPHANTS. SO, THE BRICK AND MORTAR IS PART OF IT TO CELEBRATE WHERE THE ZOO IS NOW GROWING, BUT REALLY IT HELPS OUR WHOLE PROGRAM THRIVE. COURTIS: I THINK THE GREAT THING ABOUT THIS ZOO -- AND WE WERE TALKING ABOUT THIS EARLIER. IT JUST FILLS YOU WITH HOPE. YOU FEEL LIKE YOU ARE JUST WALKING THROUGH THEIR SPACE HERE AND THAT'S INTENTIONAL. >> RIGHT. AT OUR ZOO, WE ARE FORTUNATE WE HAVE A GREAT TEAM OF THE ANIMAL EXPERTS AND THE CURATORS WORKING WITH ARCHITECTS AND PLANNERS SAY ALRIGHT, HOW CAN WE TAKE WHAT WAS SAY, WE'RE RU GALLEONS THAT WAS A VERY THREADBARE PART OF THE ZOO CALLED WILDLIFE CANYON. ITS HEYDAY WAS BACK IN THE 1990S WHEN WE HAD SUMATRAN RHINOS. THEY WERE THE ONLY ZOO THAT EVER FIGURED OUT HOW TO FEED THEM AND BREED THEM, BUT ONCE THEY LEFT, IT WAS KIND OF THREADBARE, SO WE SCRAPED IT, PUT IN A TERRIFIC EXHIBIT AND IT'S ONE OF THOSE GOING FROM GOOD TO GREAT. BECAUSE MANY PARTS OF THIS ZOO WERE BUILT IN THE 1930S, AND THEY WERE REVOLUTIONARY THEN. YOU KNOW, OUR MONKEY ISLAND OR VALTTERI THE BEAR LINE, THE 90 YEARS LATER THEY'RE WORN OUT, SO A LOT OF OUR NEW EXHIBITS ARE DOING JUST THAT, SAYING LET'S REINVENT THIS AND FIGURE OUT HOW TO HAVE SOMETHING'S REALLY GREAT FOR THESE ANIMALS. COURTIS: THAT DOES IT FOR FOR THE PROGRAM. THANKS FOR JOINING US. WE WILL SEE YOU NEXT WEEK FOR ANOTHER EDITION OF "LET'S TALK CINCY."

Fiona is turning 5. It's almost time to think about boys

Updated: 3:55 PM EST Dec 2, 2021

They grow up so fast. World-famous Fiona the hippo the Cincinnati Zoos sassy heartthrob is just weeks away from her fifth birthday. Born Jan. 24, 2017, at the Cincinnati Zoo, the Nile hippopotamus has reached a certain level of maturity. When she turns 5, it could be time for Fiona to be a little more curious about boys. According to Wendy Rice, the head keeper at Cincinnati Zoo's Africa Department, Fiona needs to be at least 5 before she thinks about finding a boyfriend. And even 5 could be pushing it. Above video: An inside look at the Cincinnati Zoo, a WLWT special But what ultimately will decide Fiona's potential future romance?"The genetics are basically what's going to matter most," Rice said. "If and when Fiona were to get a breeding recommendation someday, it would be based entirely on who was genetically the best match for her that may or may not be Timothy."Fiona's genes are valuable in the world of Nile hippopotamuses. And eventually, Rice said the goal is to have Fiona breed if she can. But we're still talking a bit down the road. What happens then?RELATED: Fiona celebrating 5th birthday in January and you can be a part of the party"We obviously don't want her going anywhere," Rice said. "We love her. She's our baby and this hometown loves her. We're fairly certain people would riot if we said Fiona was leaving. We're hopeful that if she gets a breeding recommendation, that a male would be brought here for her so she wouldn't have to leave Cincinnati."Fiona the hippo was thrust into the spotlight due to her remarkable survival story.Born six weeks premature at the Cincinnati Zoo on Jan. 24, 2017, Fiona weighed only 29 pounds at birth 25 pounds less than the lowest recorded birth weight for her species. She survived because of her animal care team's tireless efforts to save her and has inspired many to care about her species and wildlife.Now weighing a healthy weight for a hippo her age, Fiona is remarkable for being unremarkable, just a 4-year-old hippo who almost didn't make it.It's her survival story and massive personality that made Fiona a worldwide phenomenon.She changed the world. When she was born, I had never seen anything like it," Cincinnati Zoo director Thane Maynard said. The way it hit was really like lightning in a bottle. The saved-from-the-brink premature story was part of it, and phenomenon of Facebook and other social media sites as people followed her on the web.She took over the world, no doubt about it, Maynard said. The number of people shes reached through all of that are so vast, its almost like youre making it up. I mean, in the billions of people!

They grow up so fast.

World-famous Fiona the hippo the Cincinnati Zoos sassy heartthrob is just weeks away from her fifth birthday.

Born Jan. 24, 2017, at the Cincinnati Zoo, the Nile hippopotamus has reached a certain level of maturity. When she turns 5, it could be time for Fiona to be a little more curious about boys.

According to Wendy Rice, the head keeper at Cincinnati Zoo's Africa Department, Fiona needs to be at least 5 before she thinks about finding a boyfriend. And even 5 could be pushing it.

Above video: An inside look at the Cincinnati Zoo, a WLWT special

But what ultimately will decide Fiona's potential future romance?

"The genetics are basically what's going to matter most," Rice said. "If and when Fiona were to get a breeding recommendation someday, it would be based entirely on who was genetically the best match for her that may or may not be Timothy."

Fiona's genes are valuable in the world of Nile hippopotamuses. And eventually, Rice said the goal is to have Fiona breed if she can. But we're still talking a bit down the road. What happens then?

RELATED: Fiona celebrating 5th birthday in January and you can be a part of the party

"We obviously don't want her going anywhere," Rice said. "We love her. She's our baby and this hometown loves her. We're fairly certain people would riot if we said Fiona was leaving. We're hopeful that if she gets a breeding recommendation, that a male would be brought here for her so she wouldn't have to leave Cincinnati."

Fiona the hippo was thrust into the spotlight due to her remarkable survival story.

Born six weeks premature at the Cincinnati Zoo on Jan. 24, 2017, Fiona weighed only 29 pounds at birth 25 pounds less than the lowest recorded birth weight for her species. She survived because of her animal care team's tireless efforts to save her and has inspired many to care about her species and wildlife.

Now weighing a healthy weight for a hippo her age, Fiona is remarkable for being unremarkable, just a 4-year-old hippo who almost didn't make it.

It's her survival story and massive personality that made Fiona a worldwide phenomenon.

She changed the world. When she was born, I had never seen anything like it," Cincinnati Zoo director Thane Maynard said. The way it hit was really like lightning in a bottle. The saved-from-the-brink premature story was part of it, and phenomenon of Facebook and other social media sites as people followed her on the web.

She took over the world, no doubt about it, Maynard said. The number of people shes reached through all of that are so vast, its almost like youre making it up. I mean, in the billions of people!

Originally posted here:
Fiona is turning 5. It's almost time to think about boys - WLWT Cincinnati

Recommendation and review posted by Bethany Smith

Nature is full of big questions that are easy to ask and hard to answer. With some good old-fashioned hard work and help from a humble, gilled vertebrate, though, Michigan State Universitys Sarah Fitzpatrick and Isabela Lima Borges have made headway on one of those mysteries.

MSU Assistant Professor Sarah Fitzpatrick

The Spartans helmed an extensive study of Trinidadian guppies to gather elusive data on relatively short swims. This information can help explain the larger mystery of why some individuals leave the safety of home to pursue life elsewhere.

Traveling can be dangerous and it takes energy. Given all the risks, why do things move around at all? said Fitzpatrick, an assistant professor of integrative biology in the College of Natural Science based at W. K. Kellogg Biological Station, or KBS. Its such a fundamental part of ecology that we know so little about.

Answers to this question relied largely on theories, but thanks to a new study published in the journal Ecology Letters on Nov. 25, the team provided concrete data to back these up.

MSU graduate student researcher Isabela Lima Borges

The data are also valuable from a conservation standpoint, said Borges, the first author of the new study and a graduate student researcher in the Department of Integrative Biology, also at KBS. By revealing more about an animals natural behavior, researchers can better spot when human activity starts to change it.

The team showed that although most guppies stayed put throughout their lives, males that ventured off were more likely to have offspring than their homebody counterparts. Females tended to move less and also saw no advantage to moving more. Still, there was a clear reward for males that swam the coop.

We get the chicken and the egg, said Borges. We see that males move more and that males benefit more from moving.

This wasnt a total surprise. Theory suggests that because staying in ones home is often safer for example, theres a lower risk of being eaten there must be an advantage to traveling. Otherwise, why leave? But the data to confirm the benefits were scant.

What we did was go further and track advantages for guppies that left home, said Fitzpatrick, who is also a core faculty member of MSUs Ecology, Evolution and Biology program and the coordinator of the KBS Molecular Ecology and Genomics Lab. Its cool to see a result that makes sense.

Female guppies, like the fish on the left, saw no reproductive advantage from leaving home. On the other hand, males, like the fish on the right, who moved more had more offspring. Credit: Emily Kane

Though the reproductive exploits of the unassuming guppy may not seem like big news, they can inform how other species answer the should-I-stay-or-should-I-go question.

Although this is a study of one species, there are many broader theories that can be informed by it, said Borges. For example, we expect to see this behavior in other species that dont have male parental care.

These broader implications are made possible by the Trinidadian guppys special place in science. The fish live in streams throughout Trinidad and each stream presents the guppies that call it home with slightly different conditions. Thus, the different streams are almost like different iterations of the same natural experiment, Borges said.

Because of this, scientists have studied the fish for decades and have established the guppy as a model organism. With a wealth of history and knowledge at their disposal, scientists can use what they learn about guppies to inform their understanding of larger motifs in the natural world.

Its similar to how scientists have long relied on fruit flies to test ideas about genetics and evolution in the lab, Fitzpatrick said, with a few notable differences. Guppies have backbones and scientists can study them in the wild with relative ease.

I tell people that guppies are the fruit fly of the vertebrate world, said Fitzpatrick, With them, we can study evolution in action in natural environments.

The team used butterfly nets to extract Trinidadian guppies from their home streams. Credit: Courtesy of the Fitzpatrick Lab

That said, the study was still intensive. This was super hard and this is an easy species to study, Borges said, which helps explain, in part, why such robust data hadnt been available before.

Working with collaborators at Colorado State University and the University of Texas at Austin, the researchers tattooed about 1,300 guppies. The researchers essentially color-coded individual fish with small injectable tags to track the guppies movements.

The team then fished the guppies out of their streams once a month for a year, noting their position, taking photographs and recording other measurements before returning the fish to the water.

The data showed that most fish stayed in the same pools they were born in, but others ventured dozens of meters away (moving more than 10 meters or about 33 feet was considered far for a guppy). The record holder swam around 250 meters a bit over 800 feet.

The male Trinidadian guppy is a colorful fish, even without tattoos. Credit: Emily Kane

Beyond documenting the reproductive benefit of moving, the team also noted other trends in their data. For example, larger males were more likely to move farther than smaller males. And fish that lived longer tended to move more.

Yet, for all the answers this study offers, Fitzpatrick hopes the work helps inspire simple questions, even for folks who dont study ecology or evolution.

I would want people to look outside and wonder when they see an animal, how far from home has that individual moved and why? she said.

Continued here:
Mating, tattoos and leaving home: A tale of growing up guppy - MSUToday

Recommendation and review posted by Bethany Smith

One young producer is taking the goat industry by the horns and giving it a good shake-up as she aims to breed the ultimate crossbred goat.

Emily Watts is a 22-year-old go-getter from South-West Queensland who runs a goat breeding operation on her family properties between Dirranbandi and Bollon.

Ms Watts runs her goat stud alongside her parents, Catherine and Lachlan, who are also the namesakes for her stud, Catlok goats.

The Watts family, who originally ran trade cattle prior to the recent drought, decided to focus on goats as their main operation in 2016 after the lack of rain forced them to look for a more sustainable option.

Catlok focusses on the cross-breeding of Boer bucks and Rangeland does, which the family currently operate across 17,000 ha on their two properties.

"We started just mustering Rangelands for whoever wanted us to muster them and then we bought some in as well, and just kept doing fences internally," Ms Watts said.

"We got to the point where we put a big exclusion fence around both of our places and then we started to introduce the crossing of the Boers to our Rangeland does."

Catlok focus on cross-breeding Boer bucks with their Rangeland does. Photo: Georgia Hoolihan Photography,

Ms Watts said the Rangelands add invaluable traits to the genetics, something which is often overlooked by breeders looking to build weight in their meat animals.

"We definitely don't want to be going full Boer, we want to keep the Rangeland genetic in there," she said.

"I just think the Rangelands, the way they've adapted to the conditions, they've lived here with no help and no support for so long.

"And their fertility is a massive thing, they're re-breed is unbelievable; they'll come in with a weaner on them and then they'll be back in kid, in an uncontrolled environment as well.

"I think also, they have pretty good feet, so when you cross them you're adding the carcase but you're keeping the tough western durability."

However, she also believes that the introduction of a full or first-cross Boer buck to the herd goes a long way in adding meat value, and in a much shorter timeframe.

"The Boers, their growth rates are unreal and their meat, you can just pick them up, they put so much on and it's so much quicker."

"I just think sometimes that running all rangelands is not as profitable, whereas putting the Boers with them has been a lot more profitable and competitive."

Also read: Future bright for goats

Also read: Nuffield scholar's vision for goat industry

Ms Watts went to work on a cattle station in the Northern Territory during her first year out of school, before going to work at a Brahman stud near Cloncurry in Western Queensland.

Working for the stud gave Ms Watts an insight into the professionalism of a breeding operation and spurred her to "have a good crack" with her own goat stud.

"When I was working on the cattle stud, it was great just being introduced to the way a stud works, what they do, how they go about their herd and how they collect data," she said.

"Then when I came home last year I thought, we've got some really good animals and there is interest in people wanting to put, either a full Boer buck or a first-cross buck, into their herd just to make their operation a bit more profitable.

"So I thought well, we need to really make something of this, start distinguishing our best stock and really having a go at the genetics side of things."

This demand for reasonably-priced stud animals is where Catlok has found their niche, using paddock sales as a platform to market goats that thrive in the tough Western-Queensland conditions.

"I really want to keep producing paddock sales, especially for people who have large mobs of Rangelands out west and they want to be able to purchase say, 20 or 40 bucks at a time to cover their mob," Ms Watts said.

"The prices at the moment are just insane and it's pretty hard for them to go to a sale and just spend all that money.

"I think, it's a pretty niche market that I feel we can fill because our animals are born in western conditions and they're not fed to the hilt on grain, they've just adapted to the conditions."

Catlok Goats is a family run operation in South-West Queensland. Photo: Georgia Hoolihan Photography.

Ms Watts will be furthering her education next year at Marcus Oldham College in Geelong, studying a degree in Agribusiness.

The young producer said she hopes to increase her knowledge in order to make her operation as profitable as possible, focusing on genetics and meat quality to achieve best market results.

"We just really want to focus on improving our genetics and start introducing the Myotonic breed, and purchasing genetics from Contender Meat Goats where they imported those genetics from America, their meat goat is very interesting.

"Meat quality and marbling, that really interests me and I hope that we can develop a product for that because there's going to have to be a time where people are putting more money into their genetics, so there needs to be a premium market.

"There's a really big gap in the market there so I'm pretty keen to improve the meat side of things."

It seems nothing will be slowing Ms Watts down as she plans to grow her business and continue making waves in the industry, saying her being a young woman only makes her work harder for success.

"What people have done in the cattle or sheep industry, that's what we want to do with goats," she said.

"We want to become a really good western goat meat stud, and I'm quite passionate about that.

"I think, especially being a younger person and a female, it's a good challenge because the industry can be a little male-dominated I suppose. I'm pretty keen to keep doing it for the long haul."

Want daily news highlights delivered to your inbox? Sign up to the Queensland Country Life newsletter below.

Originally posted here:
Emily Watts takes on goat industry - Queensland Country Life

Recommendation and review posted by Bethany Smith

CEDAR GROVE - One moment the November sky above Cedar Grove Ornithological Research Station was an inert cobalt canvas streakedwitha few white cirrus clouds.

The nextabuff-colored speck soaredover the northern tree line and everything changed.

Danny Erickson of Wauwatosa and Jenn Schneiderman of Madison grabbed binoculars and looked out of the facility's viewing slot toparse out clues onthe fast-approaching mass of feathers, muscle and talons.

"Redtail," saidErickson, CGORS'banding director. "Keep coming, keep coming..."

The raptorsaw a potential meal on the open field below and set its wings indescent.

Seconds later it landed and was captured in a remote-controlled net.

Schneiderman sprinted across the grass to secure the flapping hawk and brought it inside for processing.

"An adult!" Schneiderman said as she presented the bird to the other staff on hand. "And isn't she beautiful?"

Moreover, the bird was exactly the age and speciesresearchers at the station hoped to capture, fit with a high-tech transmitter and release as part of a new Red-Tailed Hawk Project being run by Bryce Robinson of Cornell University.

Cedar Grove Ornithological Research Station got its start as a bird banding site in 1935 under the auspices of the Milwaukee Public Museum with assistance from the Civilian Conservation Corps.

In 1950, Milwaukee natives Dan Berger and HelmutMueller took over and ran it for more than 60 years. It's now runby the CGORS board of directors, volunteers and a few paid staff.

It could well be the mostimportant Wisconsin bird study siteyou've never heard of.

The station has the longest sustained record for observations and trapping of birds of prey in North America.

Since its inception, 45,516 birds, mostly hawks and owls, have been captured, banded and released at the facility.

The work is conducted from Aug. 15 to Nov. 15 each yearin a modest buildingset on31-acres of Department of Natural Resources landnear the Lake Michigan shore in Cedar Grove.

Because of the nature of the work, the property is closed to visitors unless arrangements have been made in advance.

Prevailing westerly winds cause migrating birds of prey to concentrate near Wisconsin's Lake Michigan shoreas they move south.

As such, CGORS is perfectly situated forraptor research studies.

This year the CGORS crew caught, processed and released 788 birds of prey, including 334 saw whet owls, 175 sharp-shinned hawks, 131 red-tailed hawks, 73 merlins, 42 Coopers hawks, 17 peregrine falcons as well as a few each American kestrels, short-eared owls and northern harriers.

The birds are fitted with metal bands and the data areentered in a U.S. Fish and Wildlife Service system. If a band is recovered, mostly when a bird is found dead, or if it's captured at another site, the physical tag can help fill in some blanks about bird movements or life history.

But that technology dates back several centuries.

That's why CGORS decided to work with the Red-tailed Hawk Project, said Suzanne Kaehler, board member and volunteer at the facility.

Attaching a GPS transmitter to a bird allows researchers to obtain locational data around the clock, yielding a far richer and more complete catalog of information.

"Redtails may seem common," Kaehler said. "But we actually don't know that much about them."

The species is native to Wisconsin and, since it can live in a range from urban to rural to naturalhabitats, is doing fairly well.

Indeed, if you see ahawk perched along a highway in the Badger State, odds are it's a redtail.

But is it a resident hawk in its year-round territory? Or a migrating bird taking a rest?

In Wisconsin, it could be either.

The Red-tailed Hawk Projectis working across North Americato study the species, said Robinson, a doctoral candidate at Cornell who is coordinating the research.

The two main pillars of inquiry are evolutionary history andmovement ecology.

"We have many unanswered questions," Robinson said. "Modern technology is, we hope, going to be a big assist in answering them."

As part of the work, researchers are attaching the GPS transmitters to the birds as well as taking blood samples for genetic testing and recording images of the individuals to help with phenotyping.

The solar-poweredtransmitters store locational data and download it whenever in range of a cellular phone tower. The technology allows researchers to constructa nearly 24/7/365 record ofthe birds' movements.

Red-tails are foundfrom Alaska and across northern Canada down to Panama and into the Caribbean.

Literature describes 16 subspecies of redtails, Robinson said.

But due to color types and other variations, it's not clear where to draw manyof the lines.

Among questions the work will attempt to answer: Is the Harlan's redtail found mostly in Alaska actuallya separate species? And is the Krider's redtail, a beautiful, lighter-coloredbird found mostly in the northern plains region, a distinct subspecies or simply a blondervariation of the more common redtails found in the Midwest and East?

About 30 transmitters were attached to redtails in 2020 and another dozen or so are being deployed this year, Robinson said.

Already"full cycle" information over the last year hasrevealed breeding sites in Alaska and northern Canada for some birds that flysouth for thewinter as well as identified other birds in the U.S. that are non-migratory.

It's also helped document behaviors of the species, such as the brooding period when maleredtailsfly widely to hunt and supply food for the females. During this time of "provisioning" by its matethe females stay on or very close to the nest.

Robinson has enlistedresearchers across the continent to participate in the study, including Nick Alioto at Michigan State University, Lucas DeCicco at University of Kansas, Allie Pesano at University of Minnesota Duluth and Hawk Ridge Bird Observatory, Neil Paprockie at University of Idaho, Nicole Richardson, Mark Robbins at University of Kansas Museum of Natural History, Brian Sullivan at Cornell Lab of Ornithology and Jesse Watson at HawkWatch International.

When Kaehler heard about it, she knew CGORS could bean ideal cooperator.

She contacted Robinson and organized the fledgling partnership.

Funding for the four transmitters (about $1,500 each) came fromdonations from Madison Audubon, Jim and Suzanne Otto and Kaehler.

They are the only transmitters attached to redtails in Wisconsin as part of the work.

Robinson visited the Cedar Grove facility in Octoberto conduct training on the transmitters and other aspects of the project.

The goal is to place the tracking deviceson adult redtails so data would help reveal breeding sites and migration information, if appropriate.

That's why although the CGORS crew is excited each time it bandsa raptor, the adult with the rust-colored tail carried into the facility by Schneidermanthat November morning generated a special buzz.

Erickson, the banding director, and Kaehler placed a hood over the bird to calm it.

Then they measured its tail and wing feathers, talons and beak.

It was then weighed (1,088 grams) and a 1 milliliter sample of blood was drawn.

Two snippets of feathers were cut, too, to assist with isotope studies.

The bird was then taken outdoors for a photo session with special attention paid to feather colors.

"Just look at those pantaloons," Schneiderman said, admiring the feathers on the hawk's legs.

Then came time for the GPS transmitter to be attached. The device, about half the size of a deck of playing cards, fit on the bird like a backpack.

A special adaptation has been added to the redtail transmitters this year: the solar panel has been raised about 1/4 inch from the main unit to help it extend above the bird's feathers and improve its access to sunlight for charging.

Once Erickson and Kaehler were convinced the unit's straps were tight enough to hold but loose enough for the hawk to fly and move normally, it was time for release.

Schneiderman carried the bird, now called Rosie, into the woodlot on the south of the property.

She held the hawk at shoulder height and with a slight boost, she let go of its legs.

The redtail didn't miss a beat. Itsoared once more, up and away to the south.

This time though its movements will add to the body of science and perhaps one day even help protect its species.

More information: Cedar Grove Ornithological Research Station is a non-profit, mainly volunteer group dedicated to raptor research. Donations can be made toP.O. Box 156, Glenbeulah, WI 53023 or via PayPal to rptrbander@gmail.com.

You can also donate to theCedar Grove Ornithological Research Station Fund established by the Natural Resources Foundation of Wisconsin. Visit wisconservation.org to learn more.

To learn more about the Red-tailed Hawk Project, visit redtailedhawkproject.org.

THANK YOU: Subscribers' support makes this work possible. Help us share the knowledge by buying a gift subscription.

Excerpt from:
Smith: Hawk study seeks to unlock secrets of redtails - Milwaukee Journal Sentinel

Recommendation and review posted by Bethany Smith

In the summer of 2015, a 7-year-old named Hassan was admitted to the burn unit of the Ruhr University Childrens Hospital in Bochum, Germany, with red, oozing wounds from head to toe.

It wasnt a fire that took his skin. It was a bacterial infection, resulting from an incurable genetic disorder. Called junctional epidermolysis bullosa, the condition deprives the skin of a protein needed to hold its layers together and leads to large, painful lesions. For kids, its often fatal. And indeed, Hassans doctors told his parents, Syrian refugees who had fled to Germany, the young boy was dying.

The doctors tried one last thing to save him. They cut out a tiny, unblistered patch of skin from the childs groin and sent it to the laboratory of Michele de Luca, an Italian stem cell expert who heads the Center for Regenerative Medicine at the University of Modena and Reggio Emilia. De Lucas team used a viral vector to ferry into Hassans skin cells a functional version of the gene LAMB3, which codes for laminin, the protein that anchors the surface of the skin to the layers below.

advertisement

Then the scientists grew the modified cells into sheets big enough for Ruhr University plastic surgeons Tobias Hirsch and Maximilian Kueckelhaus to graft onto Hassans raw, bedridden body, which they did over the course of that October, November, and the following January.

It worked better than the boys doctors could have imagined. In 2017, de Luca, Hirsch, Kueckelhaus, and their colleagues reported that Hassan was doing well, living like a normal boy in his lab-grown skin. At the time though, there was still a big question on all their minds: How long would it last? Would the transgenic stem cells keep replenishing the skin or would they sputter out? Or worse could they trigger a cascade of cancer-causing reactions?

advertisement

Today, the same team is out with an update. Five years and five months after the initial intervention, Hassan is still, for the most part, thriving in fully functional skin that has grown with the now-teenager. He is attending school, and playing sports with his friends and siblings, though he avoids swimming due to blistering in the areas that werent replaced by the lab-grown skin. One of his favorite activities is a pedal-powered go kart. There are no signs his modified stem cells have lost their steam, and no traces of tumors to be found.

The encouraging follow-up data has been instrumental in moving forward a larger clinical trial of the approach, offering hope to the 500,000 epidermolysis bullosa patients worldwide currently living without treatment options.

We were astonished by the speedy recovery, Kueckelhaus, now at University Hospital Muenster, told STAT via email. But experience from skin transplantation in other settings made him and his colleagues wary of the grafts failing as the months and years wore on. Thankfully, wrote Kueckelhaus, those fears never materialized. We are very happy to be able to prove that none of these complications appeared and the genetically modified skin remains 100% stable. The chances are good that he will be able to live a relatively normal life.

Over the last five years, Hassans team of doctors and researchers has put his new skin through a battery of tests checking it for sensitivity to hot and cold, water retention, pigmentation and hemoglobin levels, and if it had developed all the structures youd expect healthy skin to have, including sweat glands and hair follicles. Across the board, the engineered skin appeared normal, without the need for moisturizers or medical ointments. The only flaw they found was that Hassans skin wasnt as sensitive to fine touch, especially in his lower right leg. This mild neuropathy they attributed not to the graft itself, but to how that limb was prepared doctors used a more aggressive technique that might have damaged the nerves there.

The team also used molecular techniques to trace the cells theyd grown in the lab as they divided and expanded over Hassans body. They found that all the different kinds of cells composing the boys new skin were being generated by a small pool of self-renewing stem cells called holoclone-forming cells, carrying the Italian teams genetic correction.

This was quite an insight into the biology of the epidermis, said de Luca. Its an insight he expects will have huge consequences for any efforts to advance similar gene therapies for treating other diseases affecting the skin. You have to have the holoclone-forming cells in your culture if you want to have long-lasting epidermis, he said.

The approach pioneered by de Lucas team will soon be headed for its biggest clinical test yet, after nearly a decade of fits and starts. They expect to begin recruiting for a multi-center Phase 2/3 trial sometime next year.

De Luca first successfully treated a junctional EB patient in 2005. But then a change to European Union laws governing cell and gene therapies forced his team to stop work while they found ways to comply with the new rules. It took years of paperwork, building a manufacturing facility, and spinning out a small biotech company called Holostem to be ready to begin clinical research again. Hassan came along right as they were gearing up for a Phase 1 trial, but data from the boys case, which was granted approval under a compassionate use provision, convinced regulators that the cell grafts could move to larger, more pivotal trials, according to de Luca.

We didnt cure the disease, he told STAT. But the skin has been restored, basically permanently. We did not observe a single blister in five years. The wound healing is normal, the skin is robust. From this point of view, the quality of life is not even comparable to what it was before.

See the original post:
Syrian refugee is thriving five years after last-gasp gene therapy - STAT - STAT

Recommendation and review posted by Bethany Smith

Rockville, Md. (December 8, 2021)Using pulsed laser light under tightly controlled conditions, researchers were able to seein the earlobe skin of anesthetized mice the sequence of cellular events that trigger the beneficial effects of intra-epidermal focal laser-based therapy. The findings are published in a new study in the journal Function. Cells in this layer, called basal keratinocytes, are of the stem cell moiety and absolutely crucial for the continuous renewal of the skin, which occurs throughout the life span. By studying the response of the skin in real time with sophisticated imaging technology, physiologists discovered the sole cell hit by the laser became the epicenter of a wave that spread radially from cell to cell. The wave then rippled in the concentration of ionized calcium (Ca2+) within the affected cells. Ca2+ waves are known to convey messages or instructions that are able to modify cell behavior, including the possibility to modify gene expression.

These results may have significant implications for future device/procedure development, said Fabio Mammano, PhD, study co-researcher from the University of Padova in Italy.They may lead to better dosage and timing of the laser pulses, wavelength optimization and, importantly, selection and/or discovery of drugs that interfere with thesignalingpathways we have identified to further enhance the production of extracellular matrix and collagen, as well as the replacement of scar tissue with fresh epidermal and dermal cellular components.

Read the full article, Calcium signaling in the photodamaged skin: in vivo experiments and mathematical modeling, published ahead of print in Function. Contact APS Media Relations or call 301.634.7314 to schedule an interview with a member of the research team.

Continued here:
Benefits of Pulsed Laser-based Skin Therapy - Newswise

Recommendation and review posted by Bethany Smith

Stem cell therapy, sometimes called regenerative medicine, is one of the most exciting areas of the life sciences sector right now.

Since the pandemic, the sector has emerged into the publics spotlight with new developments in mRNA-based vaccines and therapies.

Nasdaq is the obvious breeding ground for world-class stem cell companies with the likes of Moderna and BioNTech, and lesser known names like Anavex and Enochian.

In Australia, Mesoblast (ASX:MSB) has long been the local poster child for the regenerative medicine industry.

Mesoblast has developed a platform of innovative cellular medicines, but the company has struggled since the FDA rejected its drug in October last year.

Now, other ASX companies like Cynata Therapeutics (ASX:CYP)are making rapid progress to take over the mantle from MSB in this hot field.

Cynata is developing a mesenchymal stem cells (or MSC) technology, which it says has huge therapeutic potential for numerous unmet medical needs.

This includes asthma, heart attack, sepsis, and acute respiratory distress syndrome (ARDS), which all add up to a market opportunity worth $46bn, says the company.

According to CEO Dr Ross Macdonald, who spoke to Stockhead today, MSC is the hottest segment of stem cell therapy at the moment, and has gained a lot of attention recently.

There is a huge interest, and theres been more than 1000 clinical trials conducted around the world using MSC, Dr Macdonald told Stockhead.

He explains that the humans immune system controls many of the bodys functions responsible for repairing tissue after injury or disease, and defending against invading germs like viruses or bacteria.

And just like an orchestral conductor, MSC seems to be playing a central role in that coordination within our immune system.

We now have a firm understanding of how those cells coordinate the bodys responses, and can use that knowledge to enhance those processes that they control, Dr Macdonald explained.

In short, MSC therapies work by expressing a variety of chemokines and cytokines that aid in repair of degraded tissue, restoration of normal tissue metabolism and, most importantly, counteracting inflammation.

And because MSCs play that co-ordination role within the immune system, they can be used to treat different diseases.

However theres one big problem with cell-based therapies, and its not to do with the safety and efficacy.

Its how to manufacture these products on a mass scale, that is the greatest challenge right now, says Dr Macdonald.

Unlike aspirin where it can be synthesised in a chemical lab and produced in bulk, manufacturing a living drug like a cell is a whole lot more complicated.

But that big challenge is the exact area of strength and competitive advantage that Cynata has, Dr Macdonald told Stockhead.

He says Cynata has a technology platform which allows it to manufacture essentially limitless quantities of MSCs, consistently and economically.

Dr Macdonald explains there are two approaches to using cell therapy, the autologous and the allogeneic approach.

The autologous approach is where the patient themselves serves as their own donor.

This is obviously bespoke and inefficient, because the drug can only be manufactured for that one patient, and is obviously not an industrialised process, he said.

But by taking an allogeneic approach, Cynata has the ability to start with a one time donation of cells from one single donor.

Well never have to go back to that human donor ever again, so our process of producing cells has become a very much more typical industrialised process.

The company has a patent for this, with two clinical trials underway and two more under preparation.

A Phase 3 clinical trial for osteoarthritis which is funded by a NHMRC grant has progressed the furthest, while a Phase 2 trial in COVID-19 is ongoing.

Meanwhile a Phase 1 study in GvHD, which was published in prestigious journal Nature Medicine, is probably the closest to commercialisation according to Dr Macdonald.

GvHD is a challenging disease which occurs in patients who have had a bone marrow transplant as part of their chemotherapy treatment for cancer.

Chemo is still very much a sledgehammer therapy where you use very toxic drugs that do kill the cancer cells, but they also kill the surrounding healthy cells that grow hair and bone marrow.

Unfortunately for many patients, the bone marrow transplant reacts against their body and starts to attack all of the tissues in the body, and its ultimately fatal.

Its a horrible death, destroying the lungs, liver, intestines and the skin, Macdonald explains.

Cynatas MSC therapy has been shown to reset that reaction, so the patient can recover from the GvHD, and also recover from their underlying cancer.

With all these clinical trials concurrently under way, Macdonald believes there is a clear significant upside potential for Cynata, particularly given its small market cap of $70m compared to other similar plays like Mesoblast ($1 billion market cap).

Osteopore (ASX:OSX) focuses in bones and specialises in the production of 3D printed bioresorbable implants that are used in surgical procedures to assist with the natural stages of bone healing.

The 3D bio-printer makes a scaffold that mimics bone, with a patented micro-architecture which traps the patients own stem cells.

Orthocell (ASX:OCC) develops collagen medical devices and cellular therapies for the repair and regeneration of human tendons, bone, nerve and cartilage defects.

Its flagship product, the CelGro, is a naturally derived collagen medical device for tissue repair.

Aroa Biosurgery (ASX:ARX) develops FDA-approved medical devices for wounds and tissue repair using its extracellular matrix (ECM) technology, mainly in the United States.

Recent study shows 100% success rates from the use of its Myriad product when patients underwent surgical reconstruction of exposed vital structures such as bone and tendon.

Regeneus (ASX:RGS) Progenza is a cellular therapy targeting pain and inflammation which uses Secretome to improve not only the resident tissue, but the MSCs themselves.

It fills a gap in the current treatment market for osteoarthritis, by providing disease modification and pain relief to address patient symptoms.

Anteris Technologies (ASX:AVR) claims that its Adapt Technology is the first and only bio-scaffold technology that completely re-engineers xenograft tissue into a pure collagen scaffold.

A recent study indicated that Adapt-treated tissue has superior anti-calcification attributes compared with tissues used in competitor valves.

Get the latest Stockhead news delivered free to your inbox.

It's free. Unsubscribe whenever you want.

You might be interested in

Read the rest here:
Mesoblast has long been the one poster child for stem cell therapy. Now Cynata and other ASX stocks have e ... - Stockhead

Recommendation and review posted by Bethany Smith

Inbreeding and wild tigers at risk of extinction

As habitat fragmentation increases worldwide, wild animal populations are shrinking and becoming more isolated, thus facing a heightened risk of inbreeding and extinction. The extent to which the viability of small, isolated populations could be improved by purging deleterious alleles through natural selection is unclear. Anubhab Khan et al. analyzed whole-genome sequences from 57 wild Bengal tigers from either a small, isolated population or large, connected populations in India. The results revealed evidence of partial purging of highly detrimental variants across populations. However, the small, isolated population showed genomic signs of greater inbreeding and a higher overall frequency of deleterious alleles, compared with two large populations. On average, pairs of individuals from the small, isolated population shared approximately 40% of their genomes in tracts at least 1 megabase long, whereas pairs from the large, connected populations shared approximately 1525% of their genomes. Together, the findings suggest that purging may not eliminate all detrimental alleles and inbreeding-associated fitness costs in small, isolated populations. According to the authors, the findings highlight the need for genetic rescue strategies that enhance the fitness of inbred populations by decreasing the frequency of harmful mutations and increasing genetic variation. J.W.

Read online

See more here:
In This Issue - pnas.org

Recommendation and review posted by Bethany Smith

Every year, African lungfish survive to the dry seasons in Africa by creating a cocoon that allows them to live on land for months or even years, until water returns following long periods of heat and drought. This cocoon, in which the lungfish is suspended in a prolonged state of aestivation, or torpor or dormancy, is a great way to prevent water loss, as many others have reported while studying aestivating frogs and other amphibians.

But researchers at The University of New Mexico are trying to find out how these animals survive pathogen and predator attacks when they are in this dormant, vulnerable state. The research could shed light on treating inflammatory diseases and investigating immune systems.

Irene Salinas

A study titled The lungfish cocoon is a living tissue with antimicrobial functions, recently published in Science Advances, was led by Associate Professor of Biology Irene Salinas and her team. The study was led by Ph.D. candidate at the Salinas lab Ryan Heimroth, who graduated in late 2020 and is now a postdoctoral researcher at Emory University. Key contributions were made by postdoctoral researchers in the Salinas lab, Elisa Casadei and Ottavia Benedicenti. Collaborators outside UNM include Chris Amemiya at University of California, Merced, and Pilar Muoz at Universidad de Murcia, Spain.

This study reveals the extraordinary adaptations of the immune system of African lungfish which allow this species to survive the harsh aestivation periods every year. Salinas said this is the most fascinating and fun project she has ever worked on in her entire career as an evolutionary immunologist.

We started this project in 2017 and we knew it was going to be exciting but we never thought that the results were going to be so astounding, she said. When we started this project, we thought the cocoon is formed by mucosal secretions that dry up around the lungfish body, but when we looked closer we realized the cocoon was actually full of cells and the cells were alive. Further experiments revealed that the cocoon is formed and shedding of layer after layer of skin epidermis, thanks to the large numbers of dermal stem cells that lungfish.

We know very little about the immune system of lungfish, Salinas continued, but very old studies from the 1930s gave the researchers some hints. These pioneer studies told them that the lungfish produces unusually large numbers of immune cells called granulocytes. Granulocytes are very important first lines of defense against pathogens and the first cells to migrate to sites of inflammation.

But why do lungfish have so many? Why is that so important? The team looked carefully at how these granulocytes changed when they aestivated lungfish in the laboratory. Granulocytes left their tissue reservoirs, traveled in the blood, and flooded the skin of aestivated animals. This is a hallmark of inflammation, very similar to what happens in the human gut and skin when it is inflamed. Lungfish do it to themselves as soon as they sense that the environment is unfavorable.

So what do these cells do when they get to the skin? Well, they leave the skin and become part of the cocoon, Salinas said. Yes, the cocoon is now not only a layer of mucus that prevents water loss but an immunological shield, full of granulocytes, potent antimicrobial soldiers that can trap and kill pathogens.

Once the researchers saw the granulocytes in the cocoon they were sure the cocoon had immunological functions, Salinas said. Following a series of investigative procedures, they concluded that the cocoon acts as an extracorporeal bacterial trapping device, the lungfish body staying healthy during aestivation, the cocoon fighting bacteria outside the body.

The key to the cocoon antimicrobial function is that granulocytes have fancy magic tricks under their hats, Salinas said. In a process known as extracellular trap formation, granulocyte extrude their DNA along with many antimicrobial compounds that decorate the DNA forming these traps. The lungfish cocoon was full of granulocytes that were caught in the process of making extracellular traps, explaining why bacteria did not penetrate into the aestivating lungfish body.

The team set experiments to answer what happens if a lungfish cocoon cannot make extracellular traps and found that extracellular DNA was essential for lungfish to stay healthy during the aestivation process.

While these findings reveal very fundamental immunological adaptation of a vertebrate animal with extreme biology, they may also illuminate key aspects of maladaptive immune responses that occur during inflammatory diseases at mucosal barriers.

Clearly, lungfish are very good at injuring their skin and sef-inflicting inflammation, Salinas said, yet when water returns, they are able to regenerate their tissues and swim back in the water as if nothing ever happened.

These animals, therefore, may keep many secrets that we could use in the future to treat inflammatory diseases, Salinas said, adding that she also wants to advocate for the investigation of immune systems in non-traditional models, such as the lungfish.

This work was generously supported by the National Science Foundation award #1938816. The team hopes to continue to investigate the immune system of this fascinating animal in the next few years, Salinas noted.

Related article

Image by Gtehal.jpg: Mathaederivative work: Bff - Gtehal.jpg, CC BY 2.5

Link:
UNM research team finds lungfish cocoon is living tissue with antimicrobial functions - UNM Newsroom

Recommendation and review posted by Bethany Smith

Queen's Freddie Mercury once asked, "Who wants to live forever?"

Simon Cowell, Paris Hilton, and a range of other superrich celebs do, apparently.

From Silicon Valley to the X-Factor, thousands of the A-list elite have reportedly signed up to expensive 'cryonics' (aka cryogenics) schemes to have their bodies and brains frozen after they die in the hope of being 'reanimated' deep in the future.

While nobody has successfully died, been frozen, defrosted, and brought back to life just yet, millionaires and billionaires alike are keeping the faith by signing up to expensive 'cryonics' schemes.

These schemes run special ambulances that rush the newly-deceased to super-cold tanks and keep them on ice so that one day, they might live again.

So let's take a look at who's actually planning a dunk into the deep freezer and answer the question: is cryonics even scientifically possible?

Perhaps the most famous cryonics legend is that of Walt Disney.

Since his death in 1966, it's been rumoured that the head of the Mickey Mouse creator was frozen in liquid nitrogen after his death so that scientists could bring him back to life when the technology becomes available in hundreds of years.

Sadly, the 2100s are unlikely to see the famed animator and FBI informant return to the silver screen. Despite running Futurama gags, Disney's family have strongly denied all claims that he was ever frozen.

There is absolutely no truth that my father, Walt Disney, wished to be frozen," Disney's daughter, Diane, said in her biography. "I doubt that my father had ever heard of cryonics.

The rumours were also denied by Dennis Kowalski, the president of the Cryonics Institute. He said: "We have heard of this rumour as well and we can confirm that it is not true."

Indeed, Disney's death certificate says he was cremated, which is the complete opposite of being frozen.

Even 'The X Factor' judges can't resist the lure of eternal life. American Idol head honcho Simon Cowell reportedly told guests at a dinner hosted by former PM Gordon Brown that he had decided to be put on ice.

Cowell reportedly told an audience including Piers Morgan and Amanda Holden in 2009 that: "I have decided to freeze myself when I die. You know, cryonics. You pay a lot of money and you get stuck in a deep freeze once you've been declared dead."

"Medical science is bound to work out a way of bringing us back to life in the next century or so, and I want to be available when they do. I would be doing the nation an invaluable service."

However, Cowell has since gotten cold feet (not literally) about the idea.

On America's Got Talent last year, the cold-blooded music judge told the cameras that he doesn't want to go through with it.

"By the way, I don't want to freeze myself anymore. No one told me you have to chop your head off," he said.

So Simon Cowell and Disney may have pulled out, but there's still growing popularity among the wealthy 1% to undergo the procedure.

Around 2000 people have reportedly signed up to the procedure at one centre of the US-based Cryonics Institute for a price around 150,000.

The Cryonics Institute president, Denis Kowalski, told the Daily Star: "We have billionaires, Hollywood celebs and top surgeons on our books," he said.

"160 bodies are already frozen at our institute, and over 100 pets!"

Britney Spears is reportedly one of the people who have signed up for a 'bus ticket to the future'. Finally free from her conservatorship, she may now be able to perform Toxic when she's 1000 years old.

Paris Hilton is also said to have signed up for the procedure, and wants to be frozen with her dogs Tinkerbell and Cinderella.

If you've got cash to splash, there are cryonic organisations in the US and Russia that could freeze you.

If you pay the 150,000 price tag at the US Cryonics Institute, you'll be picked up by a special ambulance upon your death. All your blood will be removed and replaced with a sort of embalming fluid designed to keep your organs intact.

You'll be dunked in a tank full of liquid nitrogen which needs the occasional top-up.

Once you're frozen, it's just a waiting game until the unspecified date at which science works out how to revive the dead.

Those who sign up for a lifetime membership at the Cryonics Institute can also get their spouse onboard for half price, and underage children go free.

Other cryonics organisations such as Alcor offer membership based models, where you pay a monthly fee of around 41.50 per month on top of a life insurance policy and a fixed price tag.

If you want a cheap deal, Russian cryopreservation company KrioRus will freeze your whole body for 27,000, or you can just get your head done for a bargain at 13,000.

If you can't afford the steep price tag yourself, you can always just freeze your pets. The Cryonics Institute reportedly has more than 110 pets on ice.

For such an expensive service promising major life extension, there is relatively little meat on the bones for most cryonics services.

Due to the fact we don't currently have the technology needed to revive the frozen dead, cryonics is a largely experimental science based on the assumption that the tools for the job will eventually materialise.

On its website, AIcor explains that it is possible to preserve human organs and bodies effectively. "Vitrification" can be used to turn body parts into 'glassy solids' which don't get damaged by ice.

The company also argue that 'molecular nanotechnology' which can restore the damage done by death and the cryonic process will one day be feasible. This technology does not currently exist.

Tesla CEO Elon Musk has speculated previously that cryonics could one day be possible. He told an online 'Ask Me Anything':

"Assuming that the brain is frozen quickly after death, then I think you probably could extract quite a lot of information from it in the future. And you might be able to create something approximating that person."

"I mean there's gonna be a few issues obviously. But the brain is very physical. It's much less mysterious than people think."

However, mainstream scientists are slightly more sceptical. Even if deep-future scientists are able to revive bodies, there's the question of how to restore consciousness and memory to a person who's been dead for possibly hundreds of years.

So while freezing people isn't a challenge, defrosting them is a different story.

See the original post here:
Simon Cowell to Britney Spears: Super-rich freezing their bodies so they can live forever - Daily Star

Recommendation and review posted by Bethany Smith

1. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004;89(6):27452749....

2. Vink JM, Sadrzadeh S, Lambalk CB, Boomsma DI. Heritability of polycystic ovary syndrome in a Dutch twin-family study. J Clin Endocrinol Metab. 2006;91(6):21002104.

3. Dafopoulos K, Venetis C, Pournaras S, Kallitsaris A, Messinis IE. Ovarian control of pituitary sensitivity of luteinizing hormone secretion to gonadotropin-releasing hormone in women with the polycystic ovary syndrome. Fertil Steril. 2009;92(4):13781380.

4. Jakimiuk AJ, Weitsman SR, Navab A, Magoffin DA. Luteinizing hormone receptor, steroidogenesis acute regulatory protein, and steroidogenic enzyme messenger ribonucleic acids are overexpressed in thecal and granulosa cells from polycystic ovaries. J Clin Endocrinol Metab. 2001;86(3):13181323.

5. Dunaif A. Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev. 1997;18(6):774800.

6. Kumar A, Woods KS, Bartolucci AA, Azziz R. Prevalence of adrenal androgen excess in patients with the polycystic ovary syndrome (PCOS). Clin Endocrinol (Oxf). 2005;62(6):644649.

7. Korhonen S, Hippelinen M, Niskanen L, Vanhala M, Saarikoski S. Relationship of the metabolic syndrome and obesity to polycystic ovary syndrome: a controlled, population-based study. Am J Obstet Gynecol. 2001;184(3):289296.

8. DeUgarte CM, Bartolucci AA, Azziz R. Prevalence of insulin resistance in the polycystic ovary syndrome using the homeostasis model assessment. Fertil Steril. 2005;83(5):14541460.

9. Glueck CJ, Papanna R, Wang P, Goldenberg N, Sieve-Smith L. Incidence and treatment of metabolic syndrome in newly referred women with confirmed polycystic ovarian syndrome. Metabolism. 2003;52(7):908915.

10. Celik C, Tasdemir N, Abali R, Bastu E, Yilmaz M. Progression to impaired glucose tolerance or type 2 diabetes mellitus in polycystic ovary syndrome: a controlled follow-up study. Fertil Steril. 2014;101(4):11231128.e1.

11. Karoli R, Fatima J, Chandra A, Gupta U, Islam FU, Singh G. Prevalence of hepatic steatosis in women with polycystic ovary syndrome. J Hum Reprod Sci. 2013;6(1):914.

12. Setji TL, Holland ND, Sanders LL, Pereira KC, Diehl AM, Brown AJ. Nonalcoholic steatohepatitis and nonalcoholic fatty liver disease in young women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2006;91(5):17411747.

13. Vgontzas AN, Legro RS, Bixler EO, Grayev A, Kales A, Chrousos GP. Polycystic ovary syndrome is associated with obstructive sleep apnea and daytime sleepiness: role of insulin resistance. J Clin Endocrinol Metab. 2001;86(2):517520.

14. Phelan N, O'Connor A, Kyaw-Tun T, et al. Lipoprotein subclass patterns in women with polycystic ovary syndrome (PCOS) compared with equally insulin-resistant women without PCOS. J Clin Endocrinol Metab. 2010;95(8):39333939.

15. Wang ET, Cirillo PM, Vittinghoff E, Bibbins-Domingo K, Cohn BA, Cedars MI. Menstrual irregularity and cardiovascular mortality. J Clin Endocrinol Metab. 2011;96(1):E114E118.

16. Schmidt J, Landin-Wilhelmsen K, Brnnstrm M, Dahlgren E. Cardiovascular disease and risk factors in PCOS women of postmenopausal age: a 21-year controlled follow-up study. J Clin Endocrinol Metab. 2011;96(12):37943803.

17. Bhattacharya SM, Jha A. Prevalence and risk of depressive disorders in women with polycystic ovary syndrome (PCOS). Fertil Steril. 2010;94(1):357359.

18. Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ. Emotional distress is a common risk in women with polycystic ovary syndrome: a systematic review and meta-analysis of 28 studies. Hum Reprod Update. 2012;18(6):638651.

19. Legro RS, Arslanian SA, Ehrmann DA, et al.; Endocrine Society. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2013;98(12):45654592.

20. Salley KE, Wickham EP, Cheang KI, Essah PA, Karjane NW, Nestler JE. Glucose intolerance in polycystic ovary syndromea position statement of the Androgen Excess Society. J Clin Endocrinol Metab. 2007;92(12):45464556.

21. ACOG Committee on Practice BulletinsGynecology. ACOG Practice Bulletin No. 108: Polycystic ovary syndrome. Obstet Gynecol. 2009;114(4):936949.

22. Mani H, Davies MJ, Bodicoat DH, et al. Clinical characteristics of polycystic ovary syndrome: investigating differences in white and South Asian women. Clin Endocrinol (Oxf). 2015;83(4):542549.

23. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004;81(1):1925.

24. Woolcock JG, Critchley HO, Munro MG, Broder MS, Fraser IS. Review of the confusion in current and historical terminology and definitions for disturbances of menstrual bleeding. Fertil Steril. 2008;90(6):22692280.

25. Dewailly D, Lujan ME, Carmina E, et al. Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society. Hum Reprod Update. 2014;20(3):334352.

26. Azziz R, Carmina E, Dewailly D, et al.; Task Force on the Phenotype of the Polycystic Ovary Syndrome of The Androgen Excess and PCOS Society. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril. 2009;91(2):456488.

27. Johnstone EB, Rosen MP, Neril R, et al. The polycystic ovary post-Rotterdam: a common, age-dependent finding in ovulatory women without metabolic significance. J Clin Endocrinol Metab. 2010;95(11):49654972.

28. Carmina E, Oberfield SE, Lobo RA. The diagnosis of polycystic ovary syndrome in adolescents. Am J Obstet Gynecol. 2010;203(3):201.e1201.e5.

29. Legro RS, Brzyski RG, Diamond MP, et al.; NICHD Reproductive Medicine Network. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome [published correction appears in N Engl J Med. 2014; 317(15):1465]. N Engl J Med. 2014;371(2):119129.

30. Costello M, Shrestha B, Eden J, Sjoblom P, Johnson N. Insulin-sensitising drugs versus the combined oral contraceptive pill for hirsutism, acne and risk of diabetes, cardiovascular disease, and endometrial cancer in polycystic ovary syndrome. Cochrane Database Syst Rev. 2007;(1):CD005552.

31. Bayer LL, Hillard PJ. Use of levonorgestrel intrauterine system for medical indications in adolescents. J Adolesc Health. 2013;52(4 suppl):S54S58.

32. van Zuuren EJ, Fedorowicz Z, Carter B, Pandis N. Interventions for hirsutism (excluding laser and photoepilation therapy alone). Cochrane Database Syst Rev. 2015;(4):CD010334.

33. Somani N, Turvy D. Hirsutism: an evidence-based treatment update. Am J Clin Dermatol. 2014;15(3):247266.

34. Buzney E, Sheu J, Buzney C, Reynolds RV. Polycystic ovary syndrome: a review for dermatologists: Part II. Treatment. J Am Acad Dermatol. 2014;71(5):859.e1859.e15.

35. Richardson MR. Current perspectives in polycystic ovary syndrome. Am Fam Physician. 2003;68(4):697704.

36. Radosh L. Drug treatments for polycystic ovary syndrome. Am Fam Physician. 2009;79(8):671676.

37. Harrison CL, Lombard CB, Moran LJ, Teede HJ. Exercise therapy in polycystic ovary syndrome: a systematic review. Hum Reprod Update. 2011;17(2):171183.

38. Tang T, Lord JM, Norman RJ, Yasmin E, Balen AH. Insulin-sensitising drugs (metformin, rosiglitazone, pioglitazone, D-chiro-inositol) for women with polycystic ovary syndrome, oligo amenorrhoea and sub-fertility. Cochrane Database Syst Rev. 2012;(5):CD003053.

39. Romualdi D, De Cicco S, Tagliaferri V, Proto C, Lanzone A, Guido M. The metabolic status modulates the effect of metformin on the antimullerian hormone-androgens-insulin interplay in obese women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2011;96(5):E821E824.

40. Moghetti P, Castello R, Negri C, et al. Metformin effects on clinical features, endocrine and metabolic profiles, and insulin sensitivity in polycystic ovary syndrome: a randomized, double-blind, placebo-controlled 6-month trial, followed by open, long-term clinical evaluation. J Clin Endocrinol Metab. 2000;85(1):139146.

41. Dumesic DA, Lobo RA. Cancer risk and PCOS. Steroids. 2013;78(8):782785.

42. Hunter MH, Sterrett JJ. Polycystic ovary syndrome: it's not just infertility. Am Fam Physician. 2000;62(5):10791088.

See the article here:
Diagnosis and Treatment of Polycystic Ovary Syndrome ...

Recommendation and review posted by Bethany Smith

As the name implies, growth hormone deficiency results when the pituitary gland doesn't produce enough growth hormone to stimulate the body to grow. This can result in noticeably short stature in children.

Since growth takes place over many years, and since children grow at different rates, symptoms of growth hormone deficiency may be hard to identify. In addition to noticeably slow growth with normal body proportions, signs may include:

Growth hormone deficiency has no effect on a childs intelligence.

These symptoms may resemble other conditions, so be sure to always consult your child's physician for a diagnosis.

Growth rates vary considerably from child to child. But measured in height, average "normal" growth is often described as:

If your child is less than the third percentile in height for a child of his age, that can be a red flag for growth hormone deficiency.

Damage to the pituitary gland or hypothalamus may be the result of an abnormal formation that occurred before your child was born (congenital) or something that occurred during or after birth (acquired).

Congenital growth hormone deficiency can occur if there are mutations in genes for factors that are important in pituitary gland development, or in receptors and factors (including growth hormone) along the growth hormone pathway; to date, however, the cause of most of these cases is unknown.

Acquired causes of growth hormone deficiency include:

It's also important to remember that growth hormone deficiency is only one of many conditions that may affect your childs growth. Your childs short stature may be caused by other syndromes, and growth failure may be due to decreased nutritional intake, gastrointestinal disorders, diseases that have increased metabolic demand or hypothyroidism.

Some research suggests that there are additional complications from growth hormone deficiency, including:

You and your family are key players in your childs medical care. Its important that you share your observations and ideas with your childs health care provider and that you understand your providers recommendations.

If your child is experiencing symptoms of growth hormone deficiency and youve set up an appointment, you probably already have some ideas and questions on your mind. But at the appointment, it can be easy to forget the questions you wanted to ask. Its often helpful to jot them down ahead of time so that you can leave the appointment feeling like you have the information you need.

If your child is old enough, you may want to suggest that she write down what she wants to ask her health care provider, too.

Some of the questions you may want to ask include:

We view the diagnosis of growth hormone deficiency as an important first step to treatment and, ultimately, to your childs long-term health and continued growth. You can rest assured knowing your child is in capable hands.

Our compassionate staff includes physician specialists who are experienced in the evaluation, diagnosis, and treatment of growth hormone deficiency. And we are uniquely qualified to determine the best course of care for your child. Our child-centric approach ensures that we care for your child as a child, not just another patient.

Because the chain of events involved in growth hormone deficiency is so complex, our researchers are investigating the different events that can cause a child to have short stature. Not all of these individual defects are well understood or easy to detect with a test, making this research vital to treatment strategies.

Our Division of Endocrinologyis one of the world's leading centers dedicated to caring for children and adolescents with acute and chronic endocrine and metabolic disorders. For children who suffer from growth problems, our dedicated team of doctors, nurses, and other caregivers offer hope for a healthier future.

Link:
Growth Hormone Deficiency | Boston Children's Hospital

Recommendation and review posted by Bethany Smith

Information on this web site is provided for informational purposes only. The information is a result of years of practice experience by the author. This information is not intended as a substitute for the advice provided by your physician or other healthcare professional or any information contained on or in any product label or packaging. Do not use the information on this web site for diagnosing or treating a health problem or disease, or prescribing medication or other treatment. Always speak with your physician or other healthcare professional before taking any medication or nutritional, herbal or homeopathic supplement, or using any treatment for a health problem. If you have or suspect that you have a medical problem, contact your health care provider promptly. Do not disregard professional medical advice or delay in seeking professional advice because of something you have read on this web site. Information provided on this web site and the use of any products or services purchased from our web site by you DOES NOT create a doctor-patient relationship between you and any of the physicians affiliated with our web site. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease.

Link:
Home Dr. Sara Gottfried - Sara Gottfried MD

Recommendation and review posted by Bethany Smith