The development of efficient and reliable ways to make precise, targeted changes to the genome of living cells is a long-standing goal for biomedical researchers. Recently, a new tool based on a bacterial CRISPR-associated protein-9 nuclease (Cas9) from Streptococcus pyogenes has generated considerable excitement (1). This follows several attempts over the years to manipulate gene function, including homologous recombination (2) and RNA interference (RNAi) (3). RNAi, in particular, became a laboratory staple enabling inexpensive and high-throughput interrogation of gene function (4, 5), but it is hampered by providing only temporary inhibition of gene function and unpredictable off-target effects (6). Other recent approaches to targeted genome modification zinc-finger nucleases [ZFNs, (7)] and transcription-activator like effector nucleases [TALENs (8)] enable researchers to generate permanent mutations by introducing doublestranded breaks to activate repair pathways. These approaches are costly and time-consuming to engineer, limiting their widespread use, particularly for large scale, high-throughput studies.

The functions of CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) and CRISPR-associated (Cas) genes are essential in adaptive immunity in select bacteria and archaea, enabling the organisms to respond to and eliminate invading genetic material. These repeats were initially discovered in the 1980s in E. coli (9), but their function wasnt confirmed until 2007 by Barrangou and colleagues, who demonstrated that S. thermophilus can acquire resistance against a bacteriophage by integrating a genome fragment of an infectious virus into its CRISPR locus (10).

Three types of CRISPR mechanisms have been identified, of which type II is the most studied. In this case, invading DNA from viruses or plasmids is cut into small fragments and incorporated into a CRISPR locus amidst a series of short repeats (around 20 bps). The loci are transcribed, and transcripts are then processed to generate small RNAs (crRNA CRISPR RNA), which are used to guide effector endonucleases that target invading DNA based on sequence complementarity (Figure 1) (11).

One Cas protein, Cas9 (also known as Csn1), has been shown, through knockdown and rescue experiments to be a key player in certain CRISPR mechanisms (specifically type II CRISPR systems). The type II CRISPR mechanism is unique compared to other CRISPR systems, as only one Cas protein (Cas9) is required for gene silencing (12). In type II systems, Cas9 participates in the processing of crRNAs (12), and is responsible for the destruction of the target DNA (11). Cas9s function in both of these steps relies on the presence of two nuclease domains, a RuvC-like nuclease domain located at the amino terminus and a HNH-like nuclease domain that resides in the mid-region of the protein (13).

To achieve site-specific DNA recognition and cleavage, Cas9 must be complexed with both a crRNA and a separate trans-activating crRNA (tracrRNA or trRNA), that is partially complementary to the crRNA (11). The tracrRNA is required for crRNA maturation from a primary transcript encoding multiple pre-crRNAs. This occurs in the presence of RNase III and Cas9 (12).

During the destruction of target DNA, the HNH and RuvC-like nuclease domains cut both DNA strands, generating double-stranded breaks (DSBs) at sites defined by a 20-nucleotide target sequence within an associated crRNA transcript (11, 14). The HNH domain cleaves the complementary strand, while the RuvC domain cleaves the noncomplementary strand.

The double-stranded endonuclease activity of Cas9 also requires that a short conserved sequence, (25 nts) known as protospacer-associated motif (PAM), follows immediately 3- of the crRNA complementary sequence (15). In fact, even fully complementary sequences are ignored by Cas9-RNA in the absence of a PAM sequence (16).

The simplicity of the type II CRISPR nuclease, with only three required components (Cas9 along with the crRNA and trRNA) makes this system amenable to adaptation for genome editing. This potential was realized in 2012 by the Doudna and Charpentier labs (11). Based on the type II CRISPR system described previously, the authors developed a simplified two-component system by combining trRNA and crRNA into a single synthetic single guide RNA (sgRNA). sgRNAprogrammed Cas9 was shown to be as effective as Cas9 programmed with separate trRNA and crRNA in guiding targeted gene alterations (Figure 2A).

To date, three different variants of the Cas9 nuclease have been adopted in genome-editing protocols. The first is wild-type Cas9, which can site-specifically cleave double-stranded DNA, resulting in the activation of the doublestrand break (DSB) repair machinery. DSBs can be repaired by the cellular Non-Homologous End Joining (NHEJ) pathway (17), resulting in insertions and/or deletions (indels) which disrupt the targeted locus. Alternatively, if a donor template with homology to the targeted locus is supplied, the DSB may be repaired by the homology-directed repair (HDR) pathway allowing for precise replacement mutations to be made (Figure 2A) (17, 18).

Cong and colleagues (1) took the Cas9 system a step further towards increased precision by developing a mutant form, known as Cas9D10A, with only nickase activity. This means it cleaves only one DNA strand, and does not activate NHEJ. Instead, when provided with a homologous repair template, DNA repairs are conducted via the high-fidelity HDR pathway only, resulting in reduced indel mutations (1, 11, 19). Cas9D10A is even more appealing in terms of target specificity when loci are targeted by paired Cas9 complexes designed to generate adjacent DNA nicks (20) (see further details about paired nickases in Figure 2B).

The third variant is a nuclease-deficient Cas9 (dCas9, Figure 2C) (21). Mutations H840A in the HNH domain and D10A in the RuvC domain inactivate cleavage activity, but do not prevent DNA binding (11, 22). Therefore, this variant can be used to sequence-specifically target any region of the genome without cleavage. Instead, by fusing with various effector domains, dCas9 can be used either as a gene silencing or activation tool (21, 2326). Furthermore, it can be used as a visualization tool. For instance, Chen and colleagues used dCas9 fused to Enhanced Green Fluorescent Protein (EGFP) to visualize repetitive DNA sequences with a single sgRNA or nonrepetitive loci using multiple sgRNAs (27).

Targeting efficiency, or the percentage of desired mutation achieved, is one of the most important parameters by which to assess a genome-editing tool. The targeting efficiency of Cas9 compares favorably with more established methods, such as TALENs or ZFNs (8). For example, in human cells, custom-designed ZFNs and TALENs could only achieve efficiencies ranging from 1% to 50% (2931). In contrast, the Cas9 system has been reported to have efficiencies up to >70% in zebrafish (32) and plants (33), and ranging from 25% in induced pluripotent stem cells (34). In addition, Zhou and colleagues were able to improve genome targeting up to 78% in one-cell mouse embryos, and achieved effective germline transmission through the use of dual sgRNAs to simultaneously target an individual gene (35).

A widely used method to identify mutations is the T7 Endonuclease I mutation detection assay (36, 37) (Figure 3). This assay detects heteroduplex DNA that results from the annealing of a DNA strand, including desired mutations, with a wildtype DNA strand (37).

Another important parameter is the incidence of off-target mutations. Such mutations are likely to appear in sites that have differences of only a few nucleotides compared to the original sequence, as long as they are adjacent to a PAM sequence. This occurs as Cas9 can tolerate up to 5 base mismatches within the protospacer region (36) or a single base difference in the PAM sequence (38). Off-target mutations are generally more difficult to detect, requiring whole-genome sequencing to rule them out completely.

Recent improvements to the CRISPR system for reducing off-target mutations have been made through the use of truncated gRNA (truncated within the crRNA-derived sequence) or by adding two extra guanine (G) nucleotides to the 5 end (28, 37). Another way researchers have attempted to minimize off-target effects is with the use of paired nickases (20). This strategy uses D10A Cas9 and two sgRNAs complementary to the adjacent area on opposite strands of the target site (Figure 2B). While this induces DSBs in the target DNA, it is expected to create only single nicks in off-target locations and, therefore, result in minimal off-target mutations.

By leveraging computation to reduce off-target mutations, several groups have developed webbased tools to facilitate the identification of potential CRISPR target sites and assess their potential for off-target cleavage. Examples include the CRISPR Design Tool (38) and the ZiFiT Targeter, Version 4.2 (39, 40).

Following its initial demonstration in 2012 (9), the CRISPR/Cas9 system has been widely adopted. This has already been successfully used to target important genes in many cell lines and organisms, including human (34), bacteria (41), zebrafish (32), C. elegans (42), plants (34), Xenopus tropicalis (43), yeast (44), Drosophila (45), monkeys (46), rabbits (47), pigs (42), rats (48) and mice (49). Several groups have now taken advantage of this method to introduce single point mutations (deletions or insertions) in a particular target gene, via a single gRNA (14, 21, 29). Using a pair of gRNA-directed Cas9 nucleases instead, it is also possible to induce large deletions or genomic rearrangements, such as inversions or translocations (50). A recent exciting development is the use of the dCas9 version of the CRISPR/Cas9 system to target protein domains for transcriptional regulation (26, 51, 52), epigenetic modification (25), and microscopic visualization of specific genome loci (27).

The CRISPR/Cas9 system requires only the redesign of the crRNA to change target specificity. This contrasts with other genome editing tools, including zinc finger and TALENs, where redesign of the protein-DNA interface is required. Furthermore, CRISPR/Cas9 enables rapid genome-wide interrogation of gene function by generating large gRNA libraries (51, 53) for genomic screening.

The rapid progress in developing Cas9 into a set of tools for cell and molecular biology research has been remarkable, likely due to the simplicity, high efficiency and versatility of the system. Of the designer nuclease systems currently available for precision genome engineering, the CRISPR/Cas system is by far the most user friendly. It is now also clear that Cas9s potential reaches beyond DNA cleavage, and its usefulness for genome locus-specific recruitment of proteins will likely only be limited by our imagination.

From NEB expressions Issue I, 2014 Article by Alex Reis, Ph.D., Bitesize Bio Breton Hornblower, Ph.D., Brett Robb, Ph.D.and George Tzertzinis, Ph.D., New England Biolabs, Inc.

Read the original post:

CRISPR/Cas9 and Targeted Genome Editing: A New Era in ...

Recommendation and review posted by simmons

I

nventing a nonsurgical way to zap away fat is probably not the first thing that comes to mind when one thinks about the revolutionary genome-editing technique CRISPR, but maybe it should be.

A Boston dermatologist credited with developing the novelapproach to fat loss is now the owner of aprized internet domain: crispr.com.

Though perhaps not as lucrative as the technology itself, thedomain could have been advantageousforCRISPR-focusedcompanies Editas Medicine, CRISPR Therapeutics, Intellia that might have seen a clever branding opportunity. Butuntil recently, crispr.com had languished in the electronic ether for a decade, under the control of a cybersquatting computer engineer.

advertisement

According tothe Internet Corporation for Assigned Names and Numbers (ICANN), the nonprofit organization that coordinates domain names, however, CRISPR.comis now owned by Dr. Dieter Manstein.

The German-born dermatologist, who is affiliated with Massachusetts General Hospital, is best known for inventing Coolsculpting, a controlled cooling way to remove body fat, and although he also does serious research on melanoma,he does not seem to be into genome-editing for, say, acne prevention.

University of California appeals CRISPR patent setback

Manstein did not reply to interview requests, but internet records show he is a prolific buyer of domain names, with 776 registered to his Gmail account. They include some related to his profession laserskintreatments.net, lasertattoo.org, bodysculpting.com, and germanskincare.com, for example and some not, such as iwantmyson.com.

No public records indicate what Manstein paid for crispr.com, but some domain names similar to crispr.com are currentlygoing for up to five figures.An auction for crisprcas9.co (Cas9 is the enzyme used in the most common CRISPR system) starts at $2,000, with bids due May 8, while genecrispr.com and genomecrispr.com were both asking a shade under $40,000.

Experts doubt the domain name purchased by Manstein commanded anything close to this years priciest so far. 01.com, for instance, would have set you back $1,820,000, while Refi.com sold for $500,000 and Physician.com for $179,000.

Nikolay Kolev was the previous owner of CRISPR.com. Kolev, who on Twitter describes himself as a father, husband, software developer, Orthodox Christian, and Bulgarian in California, wasnt prescient when he registered crispr.com in March 2006.

Rather, he credited the domains existence to the photo-sharing site Flickr, which was popular when he first registered CRISPR.com in 2006.

I registered (or won it on an auction, I cant recall) as a Flickr-like version of crisper, he told STAT via Twitter. Yes, Flickr was cool at the time.

Like many domain name owners, Kolev didnt build a website. He did not answer questions about whether he was approached by any of the biotech companies, and none of the likely suspectsreplied to questions from STAT as to whether they ever sought to purchase it.

Domain-name brokers, however, noticed that a transaction for crispr.com was in escrow as of March 31, meaning a buyer had deposited payment with a third party and was waiting for Kolev to transfer ownership. As of this month, according to ICANN, the new owner is Manstein.

Sharon Begley can be reached at sharon.begley@statnews.com Follow Sharon on Twitter @sxbegle

Trending

Science march on Washington, billed as historic, plagued by

Science march on Washington, billed as historic, plagued by organizational turmoil

A virus, fished out of a lake, may have

A virus, fished out of a lake, may have saved a mans life and advanced

Behind the photo: How heroin took over an Ohio

Behind the photo: How heroin took over an Ohio town

Recommended

Chan, Zuckerberg boost open-access biology with grant to Cold

Chan, Zuckerberg boost open-access biology with grant to Cold Spring Harbor

The Broad Institute is testing the limits of what

The Broad Institute is testing the limits of what nonprofit means

Prize fund for new antibiotics could mean true innovation

Prize fund for new antibiotics could mean true innovation

Go here to see the original:

CRISPR.com was for sale, and you won't guess who bought it - STAT

Recommendation and review posted by simmons

Even since Alexander Fleming stumbled across penicillinthe first antibiotic drugscientists knew our fight with evolution was on.

Most antibiotics work by blocking biological processes that allow bacteria to thrive and multiply. With prolonged, low-dosage use, however, antibiotics become a source of pressure that forces bacteria to evolveand because these microorganisms are extremely adept at swapping and sharing bits of their DNA, when one member becomes resistant, so does most of its population.

Even more terrifying is this: because the same family of antibiotics generally act on the same biological pathways, when bacteria generate a mutation that resists one type of drug, it often renders that entire family of drugs useless.

The arms race with increasing high rates of antibiotic resistance has forced scientists to think outside the box. Although still a work in progress, teams of scientists are now working on a truly creative strategy: a pill carrying the genome-editing power tool CRISPR that instructs harmful bacteria to shred their own genes to bits.

In essence, scientists are returning CRISPR to its roots. While best known as a handy way to manipulate DNA in mice and humans, CRISPR is actually a part of the bacterias immune defense system.

Just like our immune systems can turn against ourselves, scientists are now hoping to give harmful bacteria a destructive autoimmune disease.

When optimized, a CRISPR pill could have the ability to precisely target single strains of harmful bacteria, while leaving other typesincluding beneficial bacteria in the gutintact.

First, the bad news: were rapidly losing our war on microbugs, and if things dont change were heading full throttle into an antibiotic apocalypse.

Part of the bacterias survival prowess comes from their ability to rapidly multiply. Under the right conditionsa damp, nutrition-packed human cell, for examplethe common gut bug E. Coli multiplies exponentially, doubling every thirty minutes. This gives their DNA plenty of chances to mutate and for the species to adapt.

Whats more, bacteria arent stingy about sharing their DNA. Antibiotic-resistant genes are often carried on snippets of genetic material that floats around in the bacterias innards. Microbugs can literally extend a tube out to their neighbors to inject these genetic pieces, thus sharing their resistant genes far and wide.

In what is likely the most chilling demonstration of antibacterial resistance in action, you can now watch a strain of bacteria become impervious to increasingly higher doses of an antibioticup to 1,000 times higherin just 11 days.

Obviously, heaping larger and larger doses of drugs on already weak patients isnt the solution. What we need isnt stronger drugs, but smarter drugs.

Most of our current antibiotics work in one of few ways: interfering with the bacterias DNA repair system, stopping the bacterias ability to reproduce, or weakening the bacterias cell wallsomething our cells dont haveuntil it explodes.

The downside of antibiotics is they are a sledgehammer that depletes and destroys the gut microbial community, says Dr. Jan Peter van Pijkeren at the University of Madison-Wisconsin, who is working on CRISPR-based antibiotics. You want to instead use a scalpel in order to specifically eradicate the microbe of interest.

The new CRISPR pill eschews all traditional ideas, instead relying on the bacterias mortal enemy: a type of virus called bacteriophages (or, more endearingly, phages).

Like all viruses, phages cant reproduce on their own. Instead, they constantly invade bacteria and inject viral genomes into the hosts, hoping to co-opt bacterial machinery to make armies of phage replicas.

This onslaught of foreign genetic material has spurred bacteria into developing a sophisticated defense system. When bacteria detect viral DNA, they store bits and pieces of it into their own genome to form a genetic sequence that we call CRISPRa molecular memory of the phage, so to speak.

When the bacteria detect a matching viral DNA sequence, they activate CRISPR and, together with a pair of protein scissors called Cas-9, the system destroys the viral DNA. Voila, invasion blocked.

Scientists have found that the CRISPR system doesnt cut the bacterias own DNA under normal circumstances; when it does, the result is lethal.

This spurred an ingenious idea: scientists could use phages to inject custom Trojan horses that trick the bacteria into cutting its own genes.

The idea of CRISPR-based approaches is to enact sequence-specific antimicrobial activity, placing selective pressure against genes that are bad rather than conserved bacterial targets, explains Dr. Timothy Lu at MIT.

Previously, Lus team successfully manufactured phages that carry DNA similar to antibiotic-resistant genes. Because the phage DNA was misdeemed a foreign invader, it spurred the bacterias CRISPR system into action, snipping away at its own genome and committing suicide.

Bacteria cells without the resistant gene didnt sound their alarm bells, and in turn were spared and ended up dominating the population.

Similarly, van Pijkeren is working on a CRISPR pill that contains a phage harboring bits of genomic DNA of Clostridium difficile.

C. diff is an infection that is notoriously difficult to treat, causing long-term gastrointestinal distress in nearly half a million Americans in a single year, resulting in at least 15,000 deaths. The current best treatmentwhen antibiotics failis a fecal transplant from healthy donors, but the method is still considered experimental, and long-term effects are unclear (there is, of course, also the ick factor).

Because phages are readily chewed up in our stomach acid, van Pijkeren is working on packaging them up into Lactobacillus bacteriaa common probiotic often present in yogurt.

As an initial proof-of-concept step, the team has successfully engineered Lactobacillus bacteria to produce phages that target themselves. The next step, van Pijekeren explains, is to use these probiotics as motherships that travel the gut, dispensing phages along the way to infect any nearby C. diff, and tricking them into hacking up their own DNA.

Toexploit these microbes to deliver therapeutics is very appealing because we know humans have been safely consuming them for thousands of years, says van Pijkeren.

Promises aside, scientists already see several snags that might prevent the CRISPR pill from unleashing its full power.

Part of it is the delivery vehiclethe phage. Phages are rather particular about the types of bacteria they invade, and matching courier to target will require additional research.

Scientists also worry that if not all targeted bacteria are killed or if the process isnt fast enough, some resilient members may evade the attack. Bacteria are also known to develop resistance to phage invasionwhich means that if the treatment continues, selection pressure will push the population towards resistance.

But phages arent the only way to deliver CRISPR pills, and scientists are hopeful.

The way I view it is not that we will be able to make an evolution-proof therapy, but that the genetic engineering tools will become more robust so that as evolution happens, we can rapidly develop countermeasures, says Lu.

Banner Image Credit: Shutterstock

More:

CRISPR Pill May Be Key in Fight Against Antibiotic Resistance - Singularity Hub

Recommendation and review posted by simmons

News and research before you hear about it on CNBC and others. Claim your 2-week free trial to StreetInsider Premium here.

Intellia Therapeutics, Inc. (NASDAQ: NTLA) and CRISPR Therapeutics AG (NASDAQ: CRSP), two leading genome editing companies focused on the development of potentially curative therapies, announced that the United States Patent and Trademarks Office (USPTO) is expected to issue a CRISPR/Cas9 genome editing patent to Vilnius University (Vilnius). Intellia and CRISPR are nonexclusive sublicensees for a defined field of human therapeutic, prophylactic, and palliative uses (including companion diagnostics), excluding anti-fungal and anti-microbial applications.

The Vilnius patent claims are directed to CRISPR/Cas9 complexes assembled in vitro and used for site-specific modification of target DNA sequences. CRISPR/Cas9 complexes, referred to as CRISPR ribonucleoproteins or RNPs, are contemplated for use in a number of ex vivo applications in which cells, such as blood cells, may be corrected or edited outside of the body before being returned to a patient as a potential therapeutic. The patent is expected to issue on May 2, 2017 as U.S. Patent No. 9,637,739.

This new patent, together with the companies respective rights to foundational CRISPR/Cas9 intellectual property co-owned by The Regents of the University of California, University of Vienna and Dr. Emmanuelle Charpentier, provide CRISPR and Intellia with complementary rights to inventions claimed by the earliest developers in the discovery and application of CRISPR/Cas9 technology.

Intellia has a non-exclusive, royalty-free, worldwide sublicense to the Vilnius intellectual property through a 2014 license agreement with Caribou Biosciences, Inc., under which Intellia has an exclusive, worldwide sublicense to certain of Caribous developed or in-licensed CRISPR/Cas9 technology intellectual property for a defined field of human therapeutic, prophylactic, and palliative uses (including companion diagnostics), excluding anti-fungal and anti-microbial applications. Caribou has certain rights to Vilnius Universitys intellectual property through a cross-license agreement with the DuPont Company.

CRISPR acquired rights to this patent as a result of a cross-option and license agreement with Intellia which was completed in connection with the global agreement on foundational intellectual property for CRISPR/Cas9 gene editing that both companies jointly announced with the co-owners and licensors, as well as another licensee, on December 16, 2016. Under the cross-option and license agreement, CRISPR has a royalty-free worldwide sublicense to Intellias rights to the Vilnius intellectual property.

Link:

Intellia (NTLA), CRISPR Therapeutics (CRSP) Receive U.S. Patent for CRISPR/Cas9 Ribonucleoprotein Complexes - StreetInsider.com

Recommendation and review posted by sam

transOMIC technologies now offers the pCLIP-dual vector system for combinatorial knockouts, where one vector expresses two gRNAs, each targeting a separate gene.

The transEDIT-dualCRISPR system was developed in collaboration with Dr. Greg Hannon ofCold Spring Harbor LaboratoryandCancer Research UKand Dr. Simon Knott ofCedars-Sinai, using a new algorithm that creates novel and superior gRNA sequences targeting the human genome.

"Our transEDIT-dualCRISPR products give researchers a superior set of genome-editing tools. These tools speed up the pace of our understanding of complex biological pathways, which helps to rapidly identify key therapeutic targets," said Blake Simmons, CEO of transOMIC technologies. "We expect the transEDIT-dualCRISPR arrayed library and our new combinatorial gene knockout kits to take our customers' research further, faster."

More information about the transEDIT-dualCRISPR arrayed library and combinatorial knockout kits can be found athttp://www.transomic.com/Products/transEdit/transEDIT-dual-CRISPR/Product-Overview.aspx

About transOMIC:Since 2012, transOMIC has been providing the international scientific community with research products that help unravel genetic complexity and give insight into gene function, ultimately providing biological understanding of disease and possibilities for therapeutics.We have an extensive offering of gene-based products to enable research scientists to perform genome editing, gene knockdown, and gene over-expression studies. Our leading-edge products are developed through ongoing collaborations with academic thought leaders.

CONTACT: Blake Simmons, 1-256-327-9513, blake@transomic.com

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/transomic-technologies-launches-transedit-dual-crispr-combinatorial-gene-knockout-kits-300446303.html

SOURCE transOMIC technologies

http://www.transomic.com

Excerpt from:

transOMIC technologies Launches transEDIT-dual CRISPR ... - PR Newswire (press release)

Recommendation and review posted by sam

DUBLIN--(BUSINESS WIRE)--Research and Markets has announced the addition of the "Global Crispr Market Forecast 2017-2025" report to their offering.

Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) is fragments of prokaryotic DNA containing short redundancies of base sequences.

The Global CRISPR market by application generated revenue of $361 Million in 2016 and is anticipated to contribute $5966 Million by 2025, growing at a CAGR of 36.79% during the forecasted period of 2017-2025. The global CRISPR market is segmented on the basis of geographical analysis, product and end-user.

Increasing demand in drug discovery, late pregnancies leading to birth disorders, synthetic genes leading the way; aging genetic disorders and investment in path breaking research technology are the drivers for CRISPR Market. Drug discovery technology market plays a dominant role in boosting the CRISPR market. Genome editing has been revolutionized with the discovery of the CRISPR-CAS9 system from streptococcus pyogenes.

The possible misuse of CRISPR gene editing tool, slow growth and lack of healthcare budgets in developing countries are some of the restraints for CRISPR Market. CRISPR is linked with various applications such as Genome editing, genetic engineering etc. These applications are considered controversial due to the ethical concerns.

The global CRISPR Market covers the regions of North America, Europe and Asia Pacific. North America is the leading and has the biggest CRISPR Market; it is also anticipated that it will dominate the global cell therapy market. Europe CRISPR market is estimated to grow during the forecast period. Asia Pacific is a dominating region for CRISPR market with its applications like agriculture and animal breeding.

The major market players for CRISPR market are Editas Medicine, Crispr Therapeutics Ag, Horizon Discovery Plc., Sigma-Aldrich, Genscript, Transposagen Biopharmaceuticals, Thermo Fisher Scientific, Caribou Biosciences, Inc., and Precision Biosciences among others.

Market Determinants

Drivers

Restraints

Opportunities

Challenges

Key Topics Covered:

1. Research Scope

2. Research Methodology

3. Executive Summary

4. Market Overview

5. Analytical Overview

6. Market Determinants

7. Market Segmentation

8. Geographical Analysis

9. Company Profiling

For more information about this report visit http://www.researchandmarkets.com/research/63hp4q/global_crispr

Go here to read the rest:

Global CRISPR Market Forecast 2017-2025 - Research and Markets ... - Business Wire (press release)

Recommendation and review posted by simmons

Technology Networks

Quick, Sensitive Diagnostic Tests with CRISPR | Technology Networks Technology Networks Technology Networks is an internationally recognised publisher that provides access to the latest scientific news, products, research, videos and posters. and more »

Read the original:

Quick, Sensitive Diagnostic Tests with CRISPR | Technology Networks - Technology Networks

Recommendation and review posted by sam

LSIPR and law firm HGF held a webinar yesterday focusing on CRISPR and how to navigate the IP landscape.

The two presenters from HGF, Dr Claire Irvine and Catherine Coombes, covered multiple angles on this groundbreaking technology, including the science behind it and the named inventors for the technology.

The panellists also spoke in detail about licensingin European countries, among other issues.

In the US, a CRISPR patent dispute is continuing with an appeal from the University of California (UC), Berkeley in a case against the Broad Institute of Harvard and MITs patents concerning the technology.

The Patent Trial and Appeal Board ruled in February that the Broads patents concerning CRISPR do not interfere with patent claims filed by UC.

The case was referred to in the presentation as potentially being the biggest patentability mess ever.

To watch the webinar, click here. The full presentation is also available on demand.

See the rest here:

CRISPR webinar: HGF discusses IP landscape - Life Sciences Intellectual Property Review (subscription)

Recommendation and review posted by sam

Can a childhood cancer doctor like me have insights about that other end of medicine older adults with dementia? A baby acutely ill with leukemia seems like the polar opposite of a woman with Alzheimer's disease (AD), with her slow, insidious deterioration. Yet each can be progressive and fatal. I've cared for both, in different ways.

As a husband and caregiver, confronting my wife's Alzheimer's disease, I am appalled by the lack of effective therapy for her. As a clinical investigator, I'm appalled by what I see as a lack of direction in clinical dementia research, a lack of structure and a lack of ambitious leadership.

"Every Minute Counts," the PBS TV documentary that aired recently, showed the heart-rending personal devastation of Alzheimer's disease and dementia, and the enormous cost of care for those affected. It ended with a plea for more funding and research. But after decades of research and billions already spent, why aren't we further?

Alzheimer's is now the sixth leading cause of death in the U.S.; it was only 13th two decades ago. Many AD experts acknowledge the lack of progress. Last year, two researchers even wrote that seeking an AD cure is a notion "many believe unrealistic," and that advocating for curative therapy "verges on the promotion of false hope."

Since my wife was diagnosed, just one new drug really a combination of two older drugs has been approved for Alzheimer's. As a cancer doctor, I've watched more than 70 cancer treatments get approved during those same five years.

Even the Alzheimer's Association plainly states "there is no cure for Alzheimer's." Not so plainly stated is that we don't know what causes it, how it happens or how to prevent it.

Of course, we don't really know what causes childhood leukemia either, how it happens or how to prevent it, even with our current sophisticated molecular descriptions and theories. But the survival rate for the most common childhood leukemia has gone from less than 10 percent in the 1960s to over 90 percent now, with incremental progress every five years. Most kids are cured with combination chemotherapy that was developed decades ago, before molecular testing.

Most AD funding goes for molecular or non-therapeutic research, at the expense of clinical work. Sickle cell anemia was called the first "molecular disease" over 60 years ago; we still don't have a cure, even though just this year we might have a gene therapy for it. In AD, the molecular genetics seems more complicated. AD patients have waited years for any therapy, much less one from "precision medicine." Is this the right strategy?

It's not all bad news. Last year, three commercial drug trials announced results, and they showed glimmers of hope. Two were reported as failures by the media, but company press releases (TauRx, Lilly) reported modest positive effects. The third drug, from Biogen, seemed better at slowing the decline in some patients, but it evidently did not stop the disease.

AIDS therapy, like cancer, is an area of medicine that seemed hopeless at first. The leadership of Dr. William Paul, an "AIDS Czar," is credited with accelerating clinical progress in that condition. Still incurable, nevertheless AIDS patients' lives are now extended from months to years.

Nothing has really changed for Alzheimer's patients over the past five years. Brilliant scientists are working, but in the usual atmosphere of creative academic chaos. There are a few AD clinical trial groups, much like cancer trials groups, but the comparison of their activity is stark. In the state of Washington, where I live, there are over 600 cancer studies recruiting patients; in AD there are about a dozen such studies.

Much foundational AD work still needs to be done at the bedside, in overall strategy, trial coordination, informed consents, vigorous subject recruitment and consensus development, so appointing an accountable, identifiable, directive clinical research leader seems like an important way to accelerate progress.

Dr. Ron Louie is a clinical professor of pediatrics at the University of Washington, Seattle; his email is ronlouie@u.washington.edu.

Visit link:
Alzheimer's clinical research lacks leadership - Baltimore Sun

Recommendation and review posted by simmons

CRISPR technology is a simple yet powerful tool for editing genomes. It allows researchers to easily alter DNA sequences and modify gene function. Its many potential applications include correcting genetic defects, treating and preventing the spread of diseases and improving crops. However, its promise also raises ethical concerns.

In popular usage, "CRISPR" (pronounced "crisper") is shorthand for "CRISPR-Cas9." CRISPRs are specialized stretches of DNA. The protein Cas9 (or "CRISPR-associated") is an enzyme that acts like a pair of molecular scissors, capable of cutting strands of DNA.

CRISPR technology was adapted from the natural defense mechanisms of bacteria and archaea (the domain of single-celled microorganisms). These organisms use CRISPR-derived RNA and various Cas proteins, including Cas9, to foil attacks by viruses and other foreign bodies. They do so primarily by chopping up and destroying the DNA of a foreign invader. When these components are transferred into other, more complex, organisms, it allows for the manipulation of genes, or "editing."

CRISPRs:"CRISPR" stands for "clusters of regularly interspaced short palindromic repeats." It is a specialized region of DNA with two distinct characteristics: the presence of nucleotide repeats and spacers. Repeated sequences of nucleotides the building blocks of DNA are distributed throughout a CRISPR region. Spacers are bits of DNA that are interspersed among these repeated sequences.

In the case of bacteria, the spacers are taken from viruses that previously attacked the organism. They serve as a bank of memories, which enables bacteria to recognize the viruses and fight off future attacks.

This was first demonstrated experimentally by Rodolphe Barrangou and a team of researchers at Danisco, a food ingredients company. In a2007 paperpublished in the journal Science, the researchers usedStreptococcus thermophilusbacteria, which are commonly found in yogurt and other dairy cultures, as their model. They observed that after a virus attack, new spacers were incorporated into the CRISPR region. Moreover, the DNA sequence of these spacers was identical to parts of the virusgenome. They also manipulated the spacers by taking them out or putting in new viral DNA sequences. In this way, they were able to alter the bacteria's resistance to an attack by a specific virus. Thus, the researchers confirmed that CRISPRs play a role in regulating bacterial immunity.

CRISPR RNA (crRNA):Once a spacer is incorporated and the virus attacks again, a portion of the CRISPR istranscribedand processed intoCRISPR RNA, or "crRNA." The nucleotide sequence of the CRISPR acts as a template to produce a complementary sequence of single-stranded RNA.Each crRNA consists of a nucleotide repeatand a spacer portion, according to a 2014 review by Jennifer Doudna and Emmanuelle Charpentier, published in the journal Science.

Cas9:The Cas9 protein is an enzyme that cuts foreign DNA.

The protein typically binds to two RNA molecules: crRNA and another called tracrRNA (or "trans-activating crRNA"). The two then guide Cas9 to the target site where it will make its cut. This expanse of DNA is complementary to a 20-nucleotide stretch of the crRNA.

Using two separate regions, or "domains" on its structure, Cas9 cuts both strands of the DNA double helix, making what is known as a "double-stranded break," according to the 2014 Science article.

There is a built-in safety mechanism, which ensures that Cas9 doesn't just cut anywhere in a genome. Short DNA sequences known as PAMs ("protospacer adjacent motifs") serve as tags and sit adjacent to the target DNA sequence. If the Cas9 complex doesn't see a PAM next to its target DNA sequence, it won't cut. This is one possible reason thatCas9 doesn't ever attack the CRISPRregion in bacteria, according to a 2014 review published in Nature Biotechnology.

The genomes of various organisms encode a series of messages and instructions within their DNA sequences. Genome editing involves changing those sequences, thereby changing the messages. This can be done by inserting a cut or break in the DNA and tricking a cell's natural DNA repair mechanisms into introducing the changes one wants. CRISPR-Cas9 provides a means to do so.

In 2012, two pivotal research papers were published in the journalsScienceandPNAS, which helped transform bacterial CRISPR-Cas9 into a simple, programmable genome-editing tool.

The studies, conducted by separate groups, concluded that Cas9 could be directed to cut any region of DNA. This could be done by simply changing the nucleotide sequence of crRNA, which binds to a complementary DNA target. In the 2012 Science article, Martin Jinek and colleagues further simplified the system by fusing crRNA and tracrRNA to create a single "guide RNA." Thus, genome editing requires only two components: a guide RNA and the Cas9 protein.

"Operationally, you design a stretch of 20 [nucleotide] base pairs that match a gene that you want to edit," saidGeorge Church, Robert Winthrop Professor of Genetics at Harvard Medical School. An RNA molecule complementary to those 20 base pairs is constructed. Church emphasized the importance of making sure that the nucleotide sequence is found only in the target gene and nowhere else in the genome. "Then the RNA plus the protein [Cas9] will cut like a pair of scissors the DNA at that site, and ideally nowhere else," he explained.

Once the DNA is cut, the cell's natural repair mechanisms kick in and work to introduce mutations or other changes to the genome. There are two ways this can happen. According to theHuntington's Outreach Project at Stanford (University), one repair method involves gluing the two cuts back together. This method, known as "non-homologous end joining," tends to introduce errors. Nucleotides are accidentally inserted or deleted, resulting inmutations, which could disrupt a gene. In the second method, the break is fixed by filling in the gap with a sequence of nucleotides. In order to do so, the cell uses a short strand of DNA as a template. Scientists can supply the DNA template of their choosing, thereby writing-in any gene they want, or correcting a mutation.

CRISPR-Cas9 has become popular in recent years. Church notes that the technology is easy to use and is about four times more efficient than the previous best genome-editing tool (calledTALENS).

In 2013, the first reports of using CRISPR-Cas9 to edit human cells in an experimental setting were published by researchers from the laboratories ofChurchandFeng Zhangof the Broad Institute of the Massachusetts Institute of Technology and Harvard. Studies using in vitro(laboratory) and animal models of human disease have demonstrated that the technology can be effective in correcting genetic defects. Examples of such diseases includecystic fibrosis, cataracts and Fanconi anemia, according to a 2016 review article published in the journal Nature Biotechnology. These studies pave the way for therapeutic applications in humans.

CRISPR technology has also been applied in the food and agricultural industries to engineer probiotic cultures and to vaccinate industrial cultures (for yogurt, for example) against viruses. It is also being used in crops to improve yield, drought tolerance and nutritional properties.

One other potential application is to create gene drives. These are genetic systems, which increase the chances of a particular trait passing on from parent to offspring. Eventually, over the course of generations, the trait spreads through entire populations, according to theWyss Institute. Gene drives can aid in controlling the spread of diseases such as malaria by enhancing sterility among the disease vector femaleAnopheles gambiaemosquitoes according to the 2016 Nature Biotechnology article. In addition, gene drives could also be usedto eradicate invasive species and reverse pesticide and herbicide resistance,according to a 2014 article by Kenneth Oye and colleagues, published in the journal Science.

However, CRISPR-Cas9 is not without its drawbacks.

"I think the biggest limitation of CRISPR is it is not a hundred percent efficient," Church told Live Science. Moreover, the genome-editing efficiencies can vary. According to the 2014 Science article by Doudna and Charpentier, in a study conducted in rice, gene editing occurred in nearly 50 percent of the cells that received the Cas9-RNA complex. Whereas, other analyses have shown that depending on the target, editing efficiencies can reach as high as 80 percent or more.

There is also the phenomenon of "off-target effects," where DNA is cut at sites other than the intended target. This can lead to the introduction of unintended mutations. Furthermore, Church noted that even when the system cuts on target, there is a chance of not getting a precise edit. He called this "genome vandalism."

The many potential applications of CRISPR technology raise questions about the ethical merits and consequences of tampering with genomes.

In the 2014 Science article, Oye and colleagues point to the potential ecological impact of using gene drives. An introduced trait could spread beyond the target population to other organisms through crossbreeding. Gene drives could also reduce the genetic diversity of the target population.

Making genetic modifications to human embryos and reproductive cells such as sperm and eggs is known as germline editing. Since changes to these cells can be passed on to subsequent generations, using CRISPR technology to make germline edits has raised a number of ethical concerns.

Variable efficacy, off-target effects and imprecise edits all pose safety risks. In addition, there is much that is still unknown to the scientific community. In a 2015 article published in Science, David Baltimore and a group of scientists, ethicists and legal experts note thatgermline editing raises the possibility of unintended consequences for future generations"because there are limits to our knowledge of human genetics, gene-environment interactions, and the pathways of disease (including the interplay between one disease and other conditions or diseases in the same patient)."

Other ethical concerns are more nuanced. Should we make changes that could fundamentally affect future generations without having their consent? What if the use of germline editing veers from being a therapeutic tool to an enhancement tool for various human characteristics?

To address these concerns, the National Academies of Sciences, Engineering and Medicine put together acomprehensive report with guidelines and recommendationsfor genome editing.

Although the National Academies urge caution in pursuing germline editing, they emphasize "caution does not mean prohibition." They recommend that germline editing be done only on genes that lead to serious diseases and only when there are no other reasonable treatment alternatives. Among other criteria, they stress the need to have data on the health risks and benefits and the need for continuous oversight during clinical trials. They also recommend following up on families for multiple generations.

Additional resources

Broad Institute: A timeline of pivotal work on CRISPR

More here:

What Is CRISPR? - livescience.com

Recommendation and review posted by sam

Researchers at the Wellcome Trust Sanger Institute and their colleagues at the University of British Columbia have developed a novel method for studying how the bacterium Chlamydia trachomatis interacts with the human immune system. Theyused a combination of gene-editing and stem cell technologies to make the model that helped lead to the discovery of two genes from our immune system, interferon regulatory factor 5 (IRF5) and interleukin-10 receptor subunit alpha (IL-10RA), as key players in fighting a Chlamydia infection.

The results, reported inNature Communications ("Exploiting Induced Pluripotent Stem Cell-Derived Macrophages to Unravel Host factor Influencing Chlamydia trachomatis Pathogenesis"), identify novel drug targets for the sexually transmitted disease.

In this study, scientists created macrophages from human induced pluripotent stem cells to study Chlamydia infection. Macrophages have a crucial role in killing Chlamydia to limit the infection. The macrophages produced responded to the disease in a similar way to those taken from human blood, meaning they are more human-like than those produced by previous methods.

This new model will enable scientists to study how Chlamydia interacts with the human immune system to avoid antibiotics and spread, according toAmy Yeung, Ph.D., first author from the Wellcome Trust Sanger Institute.

"Chlamydia is tricky to study because it can permeate and hide in macrophages where it is difficult to reach with antibiotics. Inside the macrophage, one or two Chlamydia cells can replicate into hundreds in just a day or two, before bursting out to spread the infection," she said. "This new system will allow us to understand how Chlamydia can survive and replicate in human macrophages and could have major implications for the development of new drugs."

The new model has advantages over previous methods that used macrophages either derived from mice, which differ from humans in their immune response, or immortalized human macrophage cell lines, which are genetically different from normal macrophages, she added.

In the study, scientists used CRISPR/Cas9 to genetically edit the human induced pluripotent stem cells, and then see the effects of the genetic manipulation on the resulting macrophages' ability to fight infection.

Robert Hancock, Ph.D., lead author from the University of British Columbia and associate faculty member at the Wellcome Trust Sanger Institute, noted that, "We can knock out specific genes in stem cells and look at how the gene editing influences the resulting macrophages and their interaction with Chlamydia. We're effectively sieving through the genome to find key players and can now easily see genes that weren't previously thought to be involved in fighting the infection."

The team discovered two macrophage genes in particular that were key to limiting Chlamydia infectionIRF5 and IL-10RA. When these genes were switched off, the macrophages were more susceptible to Chlamydia infection. The results suggest these genes could be drug targets for new chlamydia treatments.

"This system can be extended to study other pathogens and advance our understanding of the interactions between human hosts and infections," explainedGordon Dougan, Ph.D., senior author from the Wellcome Trust Sanger Institute. "Weare starting to unravel the role our genetics play in battling infections, such as Chlamydia, and these results could go toward designing more effective treatments in the future."

See the rest here:

CRISPR and Stem Cells Identify Novel Chlamydia Drug Targets - Genetic Engineering & Biotechnology News

Recommendation and review posted by Bethany Smith

Cross-Species Transplantation

One application benefiting from CRISPR/Cas9 technology is xenotransplantation, or cross-species transplantation. It offers the prospect of an unlimited supply of organs and cells, and it could resolve the critical shortage of human tissues.

For ethical and compatibility reasons, xenotransplantation shifted away from nonhuman primates as a potential source of donor tissues. Instead, the discipline began to focus on porcine organs. Nonetheless, in 1997, pig-to-human transplants were banned worldwide due to concerns about the transmission to humans of porcine endogenous retroviruses (PERVs), which are integrated into the genome of all pigs.

According to George Church, Ph.D., professor of genetics, Harvard Medical School, work was undertaken in his laboratory on PK15 porcine kidney epithelial cells to determine if PERVs could be eradicated. It was crucial to avoid disrupting the envelope gene and the terminal regulatory elements, as both of these could be important during normal pig fetal growth. In addition, a highly conserved target in the viral polymerase gene was desired for the guide RNA (gRNA) to bind.

First, the copy number of PK15 PERV was determined to be 62. Then, when CRISPR/Cas9 was used along with two gRNAs, one which did the bulk of the work, all 62 copies of the PERV pol gene were disrupted, demonstrating the possibility that PERVs could be inactivated for potential clinical pig-to-human xenotransplantation. The repeats were well separated, and not clustered, which could have meant higher toxicity.

After two weeks of cell culture, about 8% of clones were 100% altered, and no rearrangements were found. Although a few off-target effects and point mutations were expected, they were deemed unlikely to have an impact on pig fetal development. As with conventional breeding, PERV-free clones were empirically selected as they were the healthiest.

In addition to disrupting dozens of endogenous viral elements, Dr. Churchs group altered dozens of genes involved in immune and blood-clotting functions to increase human compatibility. Some of the changes were so extensive that more powerful DNA recombination tools, and not CRISPR, were utilized.

This work may benefit eGenesis, a Cambridge biotech focused on leveraging CRISPR technology to deliver safe and effective human transplantable cells, tissues, and organs. eGenesis was cofounded by Dr. Church and Luhan Yang, Ph.D., in early 2015 and is based on their research.

Continued here:

More Tooth, More Tail in CRISPR Operations | GEN - Genetic Engineering & Biotechnology News (press release)

Recommendation and review posted by sam

The ability to quickly and cheaply detect minute amounts of specific nucleic acid (DNA and RNA) sequences could bring significant public health benefits. For example, it could be used to detect viral or bacterial infections in a population during outbreaks. Other possible uses include finding antibiotic-resistance genes in bacteria or tumor mutations in the body. Current methods for detecting nucleic acids involve trade-offs in sensitivity, specificity, simplicity, cost, and speed.

Drs. James J. Collins and Feng Zhang of the Broad Institute of MIT and Harvard developed a new approach by adapting the CRISPR system, which bacteria use to defend themselves from other microbes. CRISPR enzymes use short guide RNAs to identify specific target sequences to cleave. Zhangs group previously discovered that one CRISPR enzyme, called Cas13a, has an interesting collateral effect. After being activated by its target RNA sequence, Cas13a goes on to indiscriminately slice other non-targeted RNA nearby.

The researchers took advantage of this property to design a CRISPR-based nucleic acid detection platform. To detect when a target sequence was present, they added reporter RNA designed to emit a signal when cut. Whenever Cas13a was activated, it would go on to cut the reporter RNA and emit a signal. The study was funded in part by NIHs National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of Mental Health (NIMH). The team described their approach online in Science on April 13, 2017.

The scientists first tested Cas13a enzymes from different bacteria to identify which had the best RNA-guided cutting activity. As amounts of DNA and RNA in samples can be minute, the researchers applied a technique called recombinase polymerase amplification, which can amplify nucleic acids without special equipment. Another enzyme could also be added to the reaction to convert DNA to RNA for Cas13a detection.

The team called this system SHERLOCK. Tests showed that SHERLOCK could detect RNA or DNA molecules at minute levels called attomolar levels. Established nucleic acid detection approaches can be similarly sensitive, but SHERLOCK gave more consistent results.

The researchers demonstrated several potential uses. SHERLOCK was able to detect specific strains of Zika and Dengue virus. It could detect Zika virus in serum, urine, and saliva from patients. It could distinguish pathogenic strains of bacteria. It could distinguish single base differences in DNA extracted from human saliva. Finally, it could detect cancer mutations among DNA fragments at levels like that found in patient blood.

Notably, SHERLOCK yielded comparable results when its components were freeze-dried, reconstituted, and tested on glass fiber paper. The scientists calculated that a paper test could be designed and created in a matter of days for as little as $0.61 per test. These qualities highlight the potential of this system for diagnostic field applications.

We can now effectively and readily make sensors for any nucleic acid, which is incredibly powerful when you think of diagnostics and research applications, Collins says. The scientific possibilities get very exciting very quickly.

This article has been republished frommaterialsprovided byNIH. Note: material may have been edited for length and content. For further information, please contact the cited source.

Read more:

Quick, Sensitive Diagnostic Tests with CRISPR - Technology Networks

Recommendation and review posted by Bethany Smith

DENVER--(BUSINESS WIRE)--

World licensing leader MPEG LA, LLC today invited holders of CRISPR-Cas9 patents to participate in the creation of a global CRISPR-Cas9 Joint Licensing Platform that will make their groundbreaking technologies widely accessible.

Pooling the foundational CRISPR patent rights under a single nonexclusive, cost-effective, transparent license will allow the market to focus on the creation of new products and therapies that accelerate and expand CRISPRs deployment, said Larry Horn, MPEG LA President and CEO. Just as MPEG LAs pioneering efforts to manage licensing overhead and mitigate litigation risk helped assure the success of digital video in the consumer electronics industry, the CRISPR-Cas9 Joint Licensing Platform can do the same for healthcare and other biotechnology industries but with an impact far more profound.

At the same time, both foundational and other patent owners would be rewarded for their inventions from their fair share of reasonable royalties from the pool and incentivized to develop more, added Kristin Neuman, Executive Director, Biotechnology Licensing at MPEG LA. As a voluntary market-based business solution that balances access with incentive, an independently managed pool offers the best hope for addressing market and public interests in a way that will unleash CRISPRs full potential for the benefit of humanity.

MPEG LA welcomes CRISPR-Cas9 patent holders who would like to participate in this ground floor opportunity to create a Joint Licensing Platform to visit http://www.mpegla.com/main/pid/CRISPR/default.aspx for more information, including terms and procedures governing patent submissions and eligibility. At least one eligible patent is necessary to participate in the license development process, and eligibility will be determined by MPEG LA at no cost to submitters. Interested parties are asked to make their initial patent submissions by June 30, 2017. Although submissions will continue to be accepted in order to assure that the joint license includes as much relevant intellectual property as possible for the benefit of the market, those who submit patents by that date and are found eligible will be invited to attend an initial meeting with other eligible patent rights holders to explore the potential for joint terms on which the CRISPR-Cas9 Joint Licensing Platform may be offered. Except for confidentiality, participation is without obligation or commitment, including attendance at future meetings, until such time as an eligible patent holder may decide to join the Joint Licensing Platform.

MPEG LA, LLC

MPEG LA is the worlds leading provider of one-stop licenses for standards and other technology platforms. Starting in the 1990s, it pioneered the modern-day patent pool helping to produce the most widely used standards in consumer electronics history. MPEG LA has operated licensing programs for a variety of technologies consisting of more than 14,000 patents in 84 countries with some 230 patent holders and more than 6,000 licensees. By assisting users with implementation of their technology choices, MPEG LA offers licensing solutions that provide access to fundamental intellectual property, freedom to operate, reduced litigation risk and predictability in the business planning process. In turn, this enables inventors, research institutions and other technology owners to monetize and speed market adoption of their assets to a worldwide market while substantially reducing the cost of licensing. In addition to consumer electronics, MPEG LA is developing advanced Li-Ion battery and other gene editing patent pools and has conceived licensing ventures for molecular diagnostics and oligonucleotide therapeutics. For more information, go to http://www.mpegla.com.

View source version on businesswire.com: http://www.businesswire.com/news/home/20170425005584/en/

View post:

MPEG LA Invites CRISPR-Cas9 Patents to be Pooled in a One-Stop License - Yahoo Finance

Recommendation and review posted by simmons

Source: American Association of Swine VeterinariansAs resistance to antibiotics grows in the United States, researchers are looking for new ways to fight germs like Clostridium difficile, a bacterium that can cause fatal infections in hospitals and nursing homes.

One way to do that: a CRISPR pill that instructs harmful bacteria to self-destruct. CRISPR is the powerful gene-editing technology already being explored as a way to precisely edit human genes to cure diseases. But the technologys versatility is such that its being studied for a huge range of other uses. Just last week scientists in Boston showed they could craft CRISPR into cheap, simple diagnostic tests.

Now scientists want to turn it into ultra-precise antimicrobial treatments to specifically kill your bacteria of choice, says food scientist Jan-Peter Van Pijkeren of the University of Wisconsin-Madison.

While not a household name, Clostridium difficile tops the U.S. Centers for Disease Control and Preventions list of urgent drug-resistant threats. A 2015 study by the agency found that the bug caused nearly half a million infections in Americans, including 15,000 deaths.

CRISPR was actually discovered in bacteria. In fact, the system is an immune defense bacteria use to fend off invading viruses called bacteriophage.

The way it works is that bacteria store memories of viral DNA in their own genomes as clustered regularly interspaced short palindromic repeats or CRISPRs. They use this memory, plus a DNA-slicing enzyme known as a Cas to recognize and chop up the genes of invading bacteriophage.

Van Pijkerens idea is to use bacteriophage to send a false message to C. difficile, one that instead causes the bacteria to make lethal cuts to its own DNA.

To do it, Van Pijkeren lab is developing bacteriophage capable of carrying a customized CRISPR message. On their own, the bacteriophage would quickly get broken down by stomach acid. So to get the viruses into a person, Van Pijkeren plans to add them to a cocktail of innocuous bacteria, or probiotic, that a person could swallow as a pill or a liquid.

Van Pijkeren compares the probiotic to a mothership. As the probiotic bacteria pass through a persons intestinal tract, the bacteriophage would burst forth and infect any nearby C. difficile, causing them to hack up their own DNA.

Van Pijkeren says the probiotic is still in early stages of development and hasnt been tested in animals. However, researchers have previously shown that using bacteriophages to trigger CRISPR can efficiently kill skin bacteria and might also help combat Shigella sonnei, a diarrheal infection common in the developing world.

A few companies, including Eligo Bioscience in Paris and Locus Biosciences, a spinout from North Carolina State University, have started to pursue CRISPR-based antibiotics commercially.

The appeal of using CRISPR is that such drugs would be very specific theoretically, they would kill a single species of germ while leaving beneficial bacteria intact. Broad-spectrum antibiotics, by contrast, kill off large swaths of both good and bad bacteria. In fact, the overuse and abuse of conventional antibiotics is what leads to resistance in the first place.

As long as we house patients together in a hospital or in a nursing home and we give a lot of them antibiotics were going to have a problem with C. difficile, says Herbert DuPont, director of the Center for Infectious Diseases at the University of Texas.

Thats why alternatives like the one Van Pijkerens is developing are greatly needed. However, Peter Fineran, a microbiologist at the University of Otago in New Zealand, says there is still quite a long way to go before this replaces our current antibiotics.

He says one challenge in deploying the approach against more types of bacteria will be finding suitable bacteriophage. Thats because each type tends to infect only specific bacteria. Fineran predicts CRISPR will become a complementary tool in the arsenal against the rise in antibiotic resistant and pathogenic bacteria.

Continued here:

'CRISPR pill' instructs harmful bacteria to self-destruct - National Hog Farmer

Recommendation and review posted by simmons

A new highly sensitive diagnostic system for diseases has been adapted from CRISPR.

Named SHERLOCK (Specific High-sensitivity Enzymatic Reporter UnLOCKing), the diagnostic systemcould detect miniscule amounts of RNA or DNA from samples and offer rapid, accurate results without the need for sophisticated lab equipment.

'This tool offers the sensitivity that could detect an extremely small amount of cancer DNA in a patient's blood sample, for example, which would help researchers understand how cancer mutates over time,' said Professor James Collins at MIT and Harvard University, who co-led the team behind the system. 'For public health, it could help researchers monitor the frequency of antibiotic-resistant bacteria in a population. The scientific possibilities get very exciting very quickly.'

The team led by Professor Collins and Professor Feng Zhang at MIT and Harvard University combined novel methods with established techniques to amplify genetic material in a sample, find a target sequence and then create a visible result.

The system uses an enzyme called Cas13a which targets RNA, and which was discovered by Professor Zhang of MIT and colleagues last year. By attaching a sequence tag, Cas13a can be guided to find and cut a specific RNA target. Once it has done this it will randomly cut any nearby pieces of 'collateral' RNA, regardless of their sequence.

The system adds so-called fluorescent reporter RNA to the samples, which emits a fluorescent signal only when cut. So if Cas13a finds its target sequence, its subsequent cutting of the reporter RNA produces a fluorescence which can be easily detected without the use of sophisticated equipment.

The precision of the enzyme is such that even a difference ofone base-pair- such as between the genetic codes of the African and American strains of Zika - will affect whether or not activation occurs. It is also able to detect concentrations as low as two molecules in a quintillion.

The system can be run in a standard test tube or on glass fibre paper, and requires no high-tech lab equipment or temperatures higher than body heat. The authors say the molecules for the test can be designed and made for as little as US $0.61.

'One thing that's especially powerful about SHERLOCK is its ability to start testing without a lot of complicated and time-consuming upstream experimental work,' said Professor Pardis Sabeti of Harvard University, a co-author of the paper. 'This ability to take raw samples and immediately start processing could transform the diagnosis of Zika and a boundless number of other infectious diseases.'

Dr Alexander McAdam, a medical microbiologist at Boston Children's Hospital who was not involved in the project, said to STAT: 'They've developed a promising method of detecting extremely low concentrations of [genetic material], but the key word is "promising".It's going to be a long walk from hopeful to clinically useful, and there is a lot to do to demonstrate practicality.'

The study was published in Science.

Excerpt from:

Highly sensitive CRISPR diagnostic tool created - BioNews

Recommendation and review posted by Bethany Smith

[vc_row][vc_column width=1/2][vc_column_text]The Clean Start Weight Loss program is a long-term weight loss solution that keeps the weight off. What makes this program unique is that no other program will:[/vc_column_text][vc_column_text]Reset you appetite, allowing you to eat less

Reset your metabolism to a normal range

Create a new normal weight

Reduce cravings[/vc_column_text][/vc_column][vc_column width=1/2][vc_column_text]Does the Clean Start Weight Loss Program Work?

To date over 60,000 people have participated in this protocol, so you are joining an established, safe, and very effective weight loss program.[/vc_column_text][vc_single_image image=7933 img_size=full alignment=center onclick=custom_link img_link_target=_blank title=Comprehensive Weight Loss Support Included link=http://cleanstartweightloss.com/the-program/][/vc_column][vc_column][/vc_column][vc_column][/vc_column][/vc_row][vc_row][vc_column][vc_column_text]

The results I have seen are amazing. The first 43 day session I lost a total of 49 pounds went on a vacation to Hawaii for two weeks and with maintenance I was able to not gain a pound.

Wally | Patient Clean Start Weight Loss

[/vc_column_text][/vc_column][/vc_row]

See the original post:
Clean Start Weight Loss

Recommendation and review posted by Bethany Smith

At least 20 million Americans, 80 percent of them women, suffer from low levels of thyroid hormones, which can have major consequences. The thyroid gland regulates metabolism, heart, muscle and brain functions. An old, but rarely-used therapy may be a making a comeback among patients looking for a natural solution.

Cheryl Williams, 61, has a lot of energy these days for walking the dog and practicing yoga, but for years she had none and doctors had no idea why.

She said, "They'll say 'oh, everything looks great. All your levels are just great.' I'm going, 'well how come I need a wheelchair to get out of here?'"

Jane Sadler, M.D., a family physician at Baylor Scott and White Medical Center did tests which showed that Cheryl has a thyroid deficiency, hypothyroidism.

"Their body is going to run into problems with heart failure, osteoporosis, low heart rate," said Dr. Sadler.

Hypothyroidism is often treated with synthetic human thyroid hormone, but that didn't improve Cheryl's energy level so Dr. Sadler tried a seldom used remedy: pig thyroid extract. Doctors rarely prescribe the pig hormone because unlike the synthetic hormone, the concentration can vary. But it worked for Cheryl.

"It's rewarding, but I will emphasize that I have to monitor Cheryl's levels of thyroid much more closely than I would somebody on a synthetic thyroid hormone replacement," Dr. Sadler said.

"When I think back now, it's like wow, I can do these things without it being such a challenge and struggle," Cheryl said.

The American Thyroid Association said the number of Americans with thyroid deficiency could be as high as 60 million, with 60 percent undiagnosed. A simple blood test to measure TSH, thyroid stimulating hormone- will provide the answer.

Excerpt from:
New "old" remedy for thyroid disease - WTAJ

Recommendation and review posted by simmons

Testosterone, widely and misleadingly understood to be the male hormone, may provide relief to women experiencing the symptoms of menopause, according to a Shelby Township-based physician and many other experts.

Dr. Charles Mok recently published the book Testosterone: Strong Enough for a Man, Made for a Woman, which educates readers about the benefits of natural hormone replacement therapy.

Mok released the book, his first, in March. It costs $25.99 and is available on Amazon.

The evidence for testosterone therapy is overwhelming, and we want to get the message to doctors and, importantly, to their patients, Mok said.

Advertisement

Men produce 10 times more testosterone than women, but in their early reproductive years women have 10 times more testosterone than estrogen coursing through their bodies.

Many experts believe that its the loss of testosterone, and not estrogen, that causes women in midlife to tend to gain weight, feel fatigue and lose mental focus, bone density and muscle tone as well as their libido. Mood swings, anxiety and hot flashes are other common symptoms.

Testosterone therapy, delivered in the form of a tiny pellet the size of a grain of rice that is inserted underneath the skin, is believed to keep women healthier and relieve many of the above symptoms.

Clinical research shows that testosterone reduces the risk of breast cancer by 50 percent to 75 percent, and natural estrogen cuts the risk of heart attacks by more than 70 percent if used long term, Mok said.

Additionally, theyll have better control of their weight, better energy, better sex, better moods and better hair and skin, Mok said.

Therapy isnt typically covered by health insurance. Treatment in his office is usually about $140 a month, Mok said.

In the book, Mok also explores the history of hormone replacement therapy in the 1940s through the 2002 Womens Health Initiative, which suggested women taking a combination of synthetic estrogen and progesterone had an increased risk of heart disease and breast cancer.

Unfortunately, that led many women away from getting help, Mok said.

Mok, an emergency room doctor, became interested in preventative care after recognizing that some of his patients conditions could have been avoided. Now, hes in the process of finalizing a hormone therapy book geared for men.

The rest is here:
Doctor says testosterone therapy can provide relief for women - The Macomb Daily

Recommendation and review posted by sam

SAN DIEGO, April 25, 2017 /PRNewswire/ GenomeDx Biosciences today announced the publication of interim results from an ongoing prospective clinical study of the impact of the Decipher Prostate Cancer Classifier Post-Op test (Decipher test) on physician and patient decision making after prostate surgery. The interim results showed that knowledge of Decipher test results was associated with a change in both physician and patient treatment decisions, as well as improved decision effectiveness for men with prostate cancer considering adjuvant radiation therapy (ART) or salvage radiation therapy (SRT) after radical prostatectomy (RP). The article, titled "Decipher Test Impacts Decision-Making among Patients Considering Adjuvant and Salvage Treatment following Radical Prostatectomy: Interim Results from the Multicenter Prospective PRO-IMPACT Study," was published online this month ahead of print in the journal Cancer.

Approximately 50% of patients will have one or more adverse tumor pathology features after prostate cancer surgery and will be at increased risk of recurrence, metastasis and death. In these men, a multi-modal treatment is often followed by combining surgery with radiation, and either with or without hormone therapy. While known to improve health outcomes, multi-modal therapy poses potential significant harm to the patient's quality of life, including impeding sexual and urinary functional recovery. The Decipher test provides a genomic assessment of the aggressiveness of the patient's tumor, and is used by physicians to determine the need for and timing of additional therapy after surgery.

"Making additional treatment decisions for men with adverse pathology after surgery is difficult. Prior to the development of genomic assessment for prostate cancer patients, there was a lot of uncertainty around which patients might benefit from postoperative radiation and when to begin treatment," said John Gore. M.D., M.S., Associate Professor of Urology at the University of Washington and Seattle Cancer Care Alliance. "This study demonstrates that Decipher is important to guiding the shared decisions physicians and patients need to make after surgery and provides more confidence in those decisions. We have now completed the trial and look forward to the final study analyses to determine whether the treatment recommendations led to actual treatment decisions and how the use of Decipher has impacted patients' health-related quality of life."

The study included a total of 265 patients who enrolled at 19 community and academic practice settings. At baseline, prior to receipt of Decipher test results, physicians recommended primarily a 'wait-and-see' approach for most patients, irrespective of established clinical risk factors. With knowledge of Decipher test results, 96% and 74% of men with low genomic risk in the adjuvant and salvage arms, respectively, as indicated by Decipher test results, were recommended to observation. Among men whose Decipher test results showed a high genomic risk of metastasis, 37% and 69% of men in the ART and SRT arms, respectively, were recommended to receive intensification to multi-modal therapy. The study also indicated that decision quality was improved for patients considering post-surgery radiation therapy when exposed to Decipher test results, and that the fear of prostate cancer recurrence in the adjuvant and salvage arms decreased among low-risk patients.

"The clinical utility of Decipher seen in this interim analysis demonstrates that knowledge of Decipher test results can influence treatment recommendations and improve decision quality among men with prostate cancer," said Doug Dolginow, M.D., chief executive officer of GenomeDx. "As men in our society are living longer than ever before, determining the appropriate treatment of prostate cancer, which may save or extend life, is important. We believe incorporating Decipher into clinical practice will allow for better stratification of risk, improve decision-making and allow patients to be more confident with the difficult choices they may have to make."

About Decipher GRID and Decipher Prostate and Bladder Cancer Classifier Tests

GenomeDx's Decipher Genomics Resource Information Database (GRID) contains genomic profiles of thousands of tumors from patients with urological cancers, and is believed by GenomeDx to be the largest shared genomic expression database in urologic cancer as well as one of the world's largest global RNA expression databases using cloud-based analytics. GRID is a platform for interactive research collaboration, and may enable more rapid discovery, development, commercialization and adoption of new genomic solutions for key clinical questions in cancer treatment.

Derived from GRID, GenomeDx's Decipher Prostate and Bladder Cancer Classifier tests are commercially available genomic tests that provide a genomic assessment of tumor aggressiveness for individual patients. Decipher Biopsy is indicated for men with localized prostate cancer at diagnosis, Decipher Post-Op is indicated for men after prostate removal surgery and Decipher Bladder is indicated for patients being considered for neoadjuvant chemotherapy prior to radical cystectomy. The Decipher tests are used by physicians to stratify patients into more accurate risk groups than determined by traditional diagnostic tools and to better determine which patients may be more likely to benefit from additional treatment. Each tumor analyzed with a Decipher test adds new data points to the GRID database, which is compiled into a Decipher GRID Profile that may reveal additional biological characteristics of the tumor for ongoing research purposes. Going beyond risk stratification, Decipher and GRID makes accessible genetic information for researchers to potentially better predict responses to therapy and more precisely guide treatment.

More information is available at http://www.deciphertest.com and http://www.deciphergrid.com

About GenomeDx Biosciences

GenomeDx has reimagined the use of genomics as a platform for mass collaboration to improve treatment and outcomes of people with cancer. GenomeDx has built Decipher GRID, a large and fast-growing genomics database in urologic cancer that provides a foundation for open and interactive research collaboration and knowledge creation. Using Decipher GRID and machine learning to analyze vast amounts of genomic data, GenomeDx develops and commercializes proprietary clinical tests that are intended to provide more accurate and useful diagnostic information than traditional diagnostic tools or existing genomic tests. GenomeDx's Decipher Biopsy, Decipher Post-Op and Decipher Bladder are commercially available prostate cancer genomic tests that provide an assessment of tumor aggressiveness based on a patient's unique genomic profile. GenomeDx is headquartered in Vancouver, British Columbia and operates a clinical laboratory in San Diego, California.

Learn more at http://www.GenomeDx.com

SOURCE GenomeDx Biosciences

Original post:
GenomeDx's Decipher Post-Op Demonstrates Positive Impact on Physician, Patient Treatment Decisions in Multicenter ... - Broadway World

Recommendation and review posted by Bethany Smith

Free Community Health Awareness Presentation This Friday Pagosa Daily Post ... custom cleanse programs, Digestive wellness colon therapies, hormone balancing therapy, nutrient testing, women's wellness, thermography, Chiropractic, wellness workshops and retreats, medical massage, weight loss clinic, Neurotherapy, IV therapies ...

More:
Free Community Health Awareness Presentation This Friday - Pagosa Daily Post

Recommendation and review posted by simmons

Donald Trump vilified immigrants during his presidential campaign and has continued to do so since being sworn into office, signing executive orders that target undocumented immigrants, among other measures. As federal immigration officials emboldened by Trump's executive orders seek out and detain undocumented immigrants, their communities are experiencing an increase in fear that can impact their health.

"We noticed that there's a lot of mental health needs and specific health problems that people face when they're undocumented," says Wendy Mironov, a registered nurse with Salud Sin Papeles (Health Without Papers). The grassroots group has been around for two years and focuses on improving the health of and access to health care for undocumented immigrants, families, and communities by educating undocumented immigrants on their rights.

Often undocumented persons don't seek medical care or apply for financial assistance at hospitals or clinics because they're afraid their personal information will be shared with immigration officials or the police. Trying to navigate insurance and hospital bureaucracies without having a valid form of identification or fluency in English also can be a challenge.

Salud Sin Papeles advises people who attend its workshops never to use false identification to get health care but to avoid sharing their immigration status with their health-care provider if possible, or if it's not, to ask them to not record their status on their medical chart. The group also gives undocumented people strategies they can use to negotiate payment plans with hospitals and recommends going to a clinic or medical facility that offers free or low-cost care.

An estimated 307,000 undocumented immigrants lived in Cook County as of 2014, according to a report commissioned by the Illinois Coalition for Immigrant and Refugee Rights. Many can turn to the Cook County Health and Hospitals Systems when sick without fear of being turned over to ICE.

"We do not ask patients about their immigration status," says Monifa Thomas, a CCHHS spokesperson in an e-mailed statement.

Another resource Salud Sin Papeles recommends for undocumented patients is Carelink, a financial assistance program established to help Cook County residents who are uninsured or underinsured relieve their financial responsibility for their health-care services.

"The stress of being undocumented has a huge health-care impact in terms of access to health care and in terms of stress on the body," Mironov says.

Rosa Aramburo came to the United States from northern Mexico 15 years ago. She's now 27 and, thanks to the Deferred Action for Childhood Arrivals (DACA), a medical student at Loyola University Chicago's Stritch School of Medicine. Before DACA, she was uninsured.

"My mom started feeling ill. We went to a health fair and they told us her blood sugar was high, so they told her to go to a doctor to confirm if she had diabetes and get it treated," she says. "But we didn't have insurance, so my mom said she felt fine and we didn't go."

Eventually she convinced her mother to go to a free clinic, which recommended Aramburo take her mother to a hospital for treatment. Her mother was still resistant, but once there they learned she qualified for an affordable emergency care plan, Aramburo says. At the hospital she was diagnosed with diabetic ketoacidosis, which can lead to the impairment of the heart, muscles, and nerves as well as brain swelling, according to the Mayo Clinic.

"The doctor told us she could have died had we had waited another day," says Aramburo.

That experience inspired her to make time when she's not in school to volunteer with Community Health, an organization that offer free health-care services in Chicago's West Town and Englewood neighborhoods.

"They help Polish and Hispanic immigrants. I want to help people like me, like my parents," Aramburo says. "They come from another country and they're kind of lost, just like I was."

And while she has some protections under DACA, she fears for her undocumented parents because they have nothing preventing immigration officials from deporting them.

"I don't think people who support these [immigration] policies have ever faced the fear that you'll never be able to see someone you love ever again," she says.

This constant state of fear can have far-reaching medical implications, and not just for the undocumented community.

"There was a really interesting study about the impact of the raid in Postville, Iowa, eight years ago," says Salud Sin Papeles' Mironov. "Nine months after this raid the birth weight of all children born to Latina mothers, regardless of immigration status, decreased dramatically. So that raid had such a huge health-care impact on the entire state."

The study, published by the University of Michigan's School of Public Health and Institute of Social Research team earlier this year, found that in the 37 weeks after the raid Latino babies born had a 24 percent greater risk of lower birth weight than babies born the previous year. (Low birth weight is associated with increasing a baby's chance of dying or having long-term health and academic problems.)

The study concluded that psychosocial stressors, like the Postville raid, cause pregnant mothers to shift stress hormone balances in ways that affect a developing fetus.

"I think we're just starting to learn the medical impact that being undocumented can have on someone," Mironov says. "It's this huge health-care issue in terms of both access and how it affects the body."

Read the original:
Deportation fears can lead to higher risk of illness in undocumented populations - Chicago Reader

Recommendation and review posted by sam

There comes a time in every woman's life (for argument's sake, let's say it's around 48) that she can no longer ignore the elephant in the room. Andso during a recent visit to a women's health clinic I finally broached the menopause talk.

When I mentioned hormone replacement therapy (HRT, the medical replacement of a woman's oestrogen and progesterone and, sometimes, testosterone) the nurse's eyebrows almost took flight.

"HRT can really help manage the symptoms of menopause and it's safe," she added a little too quickly.

She went on to tell me that few women my age enquired about HRT. She suspected that they simply didn't trust it.

This didn't come as a complete surprise. I'd recently read that since the early 2000s, the number of women taking HRT had fallen by more than 60 per cent. This downward trend was reflected in women I know: of the 10 menopausal and post-menopausal women I spoke with for this article, only two had chosen HRT.

Several told me that their symptoms weren't severe or long-lasting enough to warrant intervention, others had looked at alternative medicine, but a few were still, some years down the track, suffering from anxietyand those interminable hot flashes and night sweats.

The reasons they dismissed HRT were simple they believed it dangerous and perhaps, even, deadly. Now this was a serious indictment for a treatment once billed as the cure-all of menopausal symptoms, as well as osteoporosis and heart disease, so the question had to be asked why?

To get some perspective we need to go back to 2002 when the Women's Health Initiative (WHI) released its longitudinal study, conducted to address health issues causing disease and early deaths in post-menopausal women. While ambivalent about cardiovascular benefits, the study concluded that taking HRT significantly increased the chance of breast cancer.

Few words carry more emotional weight for women than breast cancer (something the media were quick to pick up on), so it was little surprise that women abandoned HRT en masse.But unknown to many (including, it has to be said, many in the medical profession), the report, which was prematurely terminated, was riddled with inconsistencies.

Writing in Science Daily last month, International Menopause Society scientist and one of WHI's principal investigators Professor R. D. Langerwrote: "The incendiary reports indicated that the study was stopped because HRT caused breast cancer and heart attacks, when in reality there was no statistically significant harm for either breast cancer or heart attacks."

Endocrinologist and medical director of WA's Keogh Institute for Medical Professor Bronwyn Stuckey tells me that another problem with the 2002 report was that the results were said to apply to women of all ages, a finding rectified by a subsequent WHI 2007 report which acknowledged "that there was an age at which it's safe to start [HRT] and an age at which you probably should have second thoughts about starting".

The 2007 WHI report righted a series of wrongs, says Stuckey. It revealed that an early uptake of HRT increased protection against cardiovascular disease and led to a drop in type 2 diabetes, but most surprisingly and significantly it showed that there was less breast cancer among menopausal women solely on oestrogen than those on the placebo.

"It also showed that women who stopped taking HRT after five years had the same incidence of breast cancer as women who'd never taken it," says Stuckey.

Surely there was enough here to alleviate the fears of a significant number of women, so why wasn't this better known? Stuckey has her theories.

"It comes down to GPs being scared of it because they've grown up in the WHI era and it's a big problem," she says. "There's also something else at play, too. When you turn 50, the government invites you to have a mammogram, but it would be much more appropriate if women were invited to have their cholesterol checked, because heart disease is a much bigger killer of menopausal women than breast cancer is."

So there it was. This to me seemed the bigger scandal here. The fact that we weren't being given the proper information went beyond sheer negligence and moved into a far less grey area of potentially failing to save lives.

With the current consensus being that the earlier a menopausal woman starts on HRT the better, I know which road I'll be taking. Basically, like any working mother I've got enough worries to lose sleep over, but I'll not allow menopause to be one of them.

Jen Vuk is a freelance writer.

Read the original post:
Menopause is surrounded by unhealthy misinformation - The Sydney Morning Herald

Recommendation and review posted by Bethany Smith

Sarasota, FL (SBWIRE) 04/25/2017 Zion Market Research, the market research group announced the analysis report titled Male Hypogonadism Market: Global Industry Analysis, Size, Share, Growth, Trends, and Forecasts 20162024

Global Male Hypogonadism Market: Overview

Male hypogonadism is a medical condition, wherein the testes fail to generate enough testosterone which leads to incomplete development or delayed puberty. The condition is related to the development of breast tissues, impaired development of muscle mass, lack of deepening of the voice, and impaired body hair growth.

Global Male Hypogonadism Market: Segmentation

The male hypogonadism market is globally segmented into therapy, drug delivery, and type. On the basis of therapy, the market is segregated into testosterone replacement therapy and gonadotropin-releasing hormones therapy. The gonadotropin-releasing hormones therapy is further sub-divided into luteinizing hormone (LH), human chorionic gonadotropin (hCG), follicle-stimulating hormone (FSH), and gonadotropin-releasing hormone (GnRH). Based on the drug delivery, the market is categorized into injectables, topical gels, transdermal patches, and others. Depending on the type, the market is divided into Kallmann syndrome, Klinefelters syndrome, pituitary disorders, and others.

Request Free Sample Report @ https://www.zionmarketresearch.com/sample/male-hypogonadism-market

Global Male Hypogonadism Market: Growth Factors

The key factor that is driving the male hypogonadism market includes increasing cases of testosterone deficiency among men, increasing awareness among people about hypogonadism treatment owing to awareness drives that are organized by several governments across the world, and increasing infertility rates. The high risk of hypogonadism among the aged population with obesity and diabetes and escalating cases of chronic disorders among the geriatrics are further boosting the markets growth. On the other hand, factors such as high side effects of testosterone products challenge the growth of the market. The market players are focusing on research and development activities to introduce newer products with less or negligible side effects and better results. Technological advancements are anticipated to extend new opportunities to the markets growth.

Global Male Hypogonadism Market: Regional Analysis

The male hypogonadism market can be segmented into regions such as North America, Asia-Pacific, Europe, Latin America, and the Middle East and Africa. North America dominates the market owing to the increase in the number of individuals that are suffering from the primary and secondary conditions of hypogonadism, and the rising awareness among the people about treatment. Other factors that contribute to this growth are the presence of unconventional health care infrastructure and growing popularity of the technologically advanced products which will offer new opportunities to the top market players in this market. The region is strongly followed by Europe. Asia-Pacific region is expected to offer productive opportunities to this market owing to the modernization of the healthcare infrastructure in the developing economies of India and China and the growing awareness about the treatment for the condition. In Asia Pacific, there is a rise in the number of people that suffer from hypogonadism and infertility rates coupled with the rise in the geriatric population base having obesity and diabetes are triggering the growth of the market.

Global Male Hypogonadism Market: Competitive Players

Some of the key market players that are involved in the male hypogonadism market include Astrazeneca Plc., Merck & Co. Inc., Laboratories Genevrier, Allergan Plc., Endo International Plc., Ferring, AbbVie Inc., Eli Lilly and Company Ltd., Finox Biotech, Teva Pharmaceutical Industries Ltd., Bayer AG, and IBSA Institut Biochimque.

Request Report TOC (Table of Contents) @ https://www.zionmarketresearch.com/toc/male-hypogonadism-market

Global Male Hypogonadism Market: Regional Segment Analysis

North America U.S. Europe UK France Germany Asia Pacific China Japan India Latin America Brazil The Middle East and Africa

What Reports Provides

Full in-depth analysis of the parent market Important changes in market dynamics Segmentation details of the market Former, on-going, and projected market analysis in terms of volume and value Assessment of niche industry developments Market share analysis Key strategies of major players Emerging segments and regional markets Testimonials to companies in order to fortify their foothold in the market.

Browse detail report @ https://www.zionmarketresearch.com/report/male-hypogonadism-market

More here:
Global Male Hypogonadism Market, 20162024: Type. Size, Share, Trends & Forecast Report - MilTech

Recommendation and review posted by simmons

A research team at the University of Minnesota found a way to heal broken hearts.

Researchers used a 3D printer to create protein patches that mimic heart tissue to treat post-heart attack scars. The research is in collaboration with the University of Wisconsin-Madison and the University of Alabama-Birmingham.

Brenda Ogle, a University biomedical engineering professor and lead researcher for the project, said she and her team have investigated proteins that surround cells in the body for 15 years. The team has been studying how the proteins also called the extracellular matrix influence stem cell behavior.

For many years, weve been trying to develop optimum formulation that can support stem cells in new cardiac [cell] types, Ogle said, adding that theyve focused on cardiac cell types to figure out a way to strengthen them after the muscle cells are damaged and die during a heart attack. Its one of the cell types in the body that cant be recovered.

The team successfully treated mice with the patches and is now planning to test the method on larger animals.

Molly Kupfer, a doctoral student who is part of Ogles team, said a heart attack occurs when there is a blockage in a primary blood vessel that delivers oxygen and nutrients to the heart.

When that happens, you have cell death in the area of the heart that doesnt receive the appropriate oxygen and nutrients, Kupfer said. Those cells that die arent able to recover."

Typically, after a heart attack, the blood clot in the heart is removed at a hospital, and if the heart has not been damaged too badly, doctors monitor the heart long-term, prescribe medicine and regularly check for signs of heart failure, Ogle said.

What you get instead after a heart attack is scar tissue forming, and that scar tissue ultimately fails, Ogle said.

Associate Professor Brenda Ogle places a 3D printed biopatch on a mouse heart in Nils Hasselmo Hall on Tuesday, April 25, 2017. Her research team induces heart attacks in mice, which causes a dead area of cardiac cells. The patch is placed in this dead zone and mimics the cells of the native heart that aren't able to be replenished on their own. "A defining moment was when the [mouse] heart started to beat, and we realized human heart pacing could be possible too," Ogle said.

Kupfer said she worked with Paul Campagnola and his lab at the University of Wisconsin to print the patches; the cells were prepared at the University of Minnesota.

Campagnola, a biomedical engineering professor, said he initially developed the underlying printing technology in 2000.

"The idea of the patch is it could actually behave like native cardiac tissue and assist the function of the heart, Kupfer said, adding that the method used to print the patches results in extremely high resolution structures.

Ogle said before applying the patch to the animal hearts theyre currently testing on, they take a scan of the scarred tissue and create a digital template for the 3D-printer to follow and print the proteins in the same pattern.

Campagnola said the patch provides a stable space for cells to grow and be implanted in damaged areas.

Cardiac cells are also added to the patch when it covers a damaged area. Ogle said it not only provides a support structure, but transplants healthy cells that will eventually become integrated into the heart, stabling it structurally and functionally.

A huge aha moment was when [the cardiac cells] started to beat on this patch synchronously and spontaneously, she said. When that happened, we realized that this could be a viable therapy for the heart, a way to replace those lost muscle cells.

Through the research group at the University of Alabama, Ogle said a study was conducted where the patch was tested on dead or dying tissue in mice hearts and the group saw improvement in the mice after four weeks.

The project was funded through a series of grants from the National Institutes of Health, the National Science Foundation with support from the University, she said.

The group has since received larger funds from the NIH to run a study using the patch on larger animals within the next year.

Ogle said it would take about 10 years until the patch can be used on human patients in a clinical setting.

View original post here:
UMN research team fixes broken hearts with 3D-printed tissue patch - Minnesota Daily

Recommendation and review posted by simmons