Archive for the ‘Gene Therapy Research’ Category

Jilly Bean x OG Shatter Review
Today we #39;re taking a look at some shatter that was given to me by Gabe from RateMyWeed after he went out to Denver, CO for the first Extract Artists Cup hosted by Top Shelf Extracts. While I don #39;t believe this is the 1st Place "Oh Jilly Gee" made by Ryan Skipton of TSE, it is comprised of the same genetics that achieved that 1st place flavor. Only problem is I got to it after a few weeks and some travel, so there is a cloudy spot nucleating in the center, but besides that it #39;s top notch. Thanks again Gabe and all the Artists involved with the Cup!

By: oilhashgrassandglass

Originally posted here:
Jilly Bean x OG Shatter Review - Video

How Can Cancer Patients Preserve Their Fertility?
Patients newly diagnosed with cancer may be exploring options for preserving their fertility. Dr. Stephen Lincoln of Genetics IVF Institute, explains egg freezing and sperm freezing for fertility preservation in cancer patients.

By: fertilityauthority

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How Can Cancer Patients Preserve Their Fertility? - Video

Webinar on WHS for Genetic Counselors
Beyond the Textbooks for Wolf-Hirschhorn Syndrome: Lessons for Prenatal and Pediatric Genetic Counselors Co-hosted by NSGC #39;s Prenatal Counseling Ultrasound Anomalies and Pediatric Clinical Genetics Special Interest Groups (December 11, 2012)

By: 4psupportgroup

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Webinar on WHS for Genetic Counselors - Video

Leprosy Could Help Heal Us? (Brainstorm Ep125)
Shirts and Stuff http://www.zazzle.com Follow us on Twitter twitter.com Like us on Facebook http://www.facebook.com Medical News tinyurl.com Material Science News tinyurl.com Genetics News tinyurl.com Hosted by http://www.youtube.com Contributors http://www.facebook.com - Raychelle and Monica http://www.facebook.com

By: qdragon1337

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Leprosy Could Help Heal Us? (Brainstorm Ep125) - Video

Morning Cardio Tabata Training with Sponsored Athlete Kimberly Ho
Hey Everyone! Tabata training today for morning cardio with Baby Cory. Get ACTIVE!!! Products used: Advanced Genetics "F-10" (Fat burner) and "GP3". http://www.advancedgenetics.ca Seen wearing Public Myth "Zip Leggings", "Freedom Tank" and "Cami Bra", as well as Muscles By Meyers sweater. http http://www.musclesbymeyers.com

By: Kim Ho

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Morning Cardio Tabata Training with Sponsored Athlete Kimberly Ho - Video

WFTB success genetics or mindset ?
a brief look at what really makes some one successful in sports is it genetics or something more ???

By: VJFitness

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WFTB success genetics or mindset ? - Video

AVON night skincare routine
Cleanser, Resurfacing, Absolute Even Genetics Night Cream

By: avonrep1

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AVON night skincare routine - Video

AMES, Iowa, Jan. 30, 2013 /PRNewswire/ --NewLink Genetics Corporation (NLNK), a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics, today announced the pricing of an underwritten public offering of 4,000,000 shares of its common stock at a price to the public of $11.40 per share, which was the previous day's closing price. The net proceeds to NewLink from this offering are expected to be approximately $42.5 million, after deducting underwriting discounts and commissions and other estimated offering expenses payable by NewLink. The offering is expected to close on or about February 4, 2013, subject to customary closing conditions. NewLink anticipates using the net proceeds from the offering for general corporate purposes, including clinical trial, preclinical and other research and development expenses, capital expenditures, working capital and general and administrative expenses.

Jefferies & Company, Inc. and Stifel Nicolaus Weisel are acting as joint book-running managers in the offering and Baird, Canaccord Genuity Inc. and Cantor Fitzgerald & Co. are acting as co-managers. NewLink has granted the underwriters a 30-day option to purchase up to an aggregate of 600,000 additional shares of common stock.

The securities described above are being offered by the Company pursuant to a shelf registration statement previously filed with, and declared effective by, the Securities and Exchange Commission (the "SEC"). A preliminary prospectus supplement and accompanying prospectus relating to the offering have been filed with the SEC and are available on the SEC's website at http://www.sec.gov. Copies of the final prospectus supplement and the accompanying prospectus relating to this offering, when available, may be obtained from Jefferies & Company, Inc., Attention: Equity Syndicate Prospectus Department, 520 Madison Avenue, 12th Floor, New York, NY 10022, or by telephone at 877-547-6340, or by email at Prospectus_Department@Jefferies.com, or from Stifel, Nicolaus & Company, Incorporated, Attention: Syndicate, One Montgomery Street, Suite 3700, San Francisco, California 94104, or by calling (415) 364-2500.

This press release shall not constitute an offer to sell or the solicitation of an offer to buy, nor shall there be any sale of, these securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or jurisdiction.

About NewLink Genetics CorporationNewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small-molecule immunotherapy product candidates intended to treat a wide range of oncology indications.

Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements of NewLink that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this press release are forward-looking statements, within the meaning of The Private Securities Litigation Reform Act of 1995. The words "anticipate," "expect," "intend," "may," "will," "could," "should," or the negative of these terms or other similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These forward-looking statements include, among others, statements about the Company's expectations with respect to its proposed offering, including its intention to offer and sell shares, the closing of the offering and the Company's intended use of proceeds from the offering. Such statements are based on the Company's expectations as of the date of this press release and are subject to certain risks and uncertainties that could cause actual results to differ materially, including but not limited to the risks and uncertainties associated with market conditions and the satisfaction of customary closing conditions related to the proposed offering, as well as those risks discussed in NewLink's Annual Report on Form 10-K for the year ended December 31, 2011, in its Quarterly Report on Form 10-Q for the quarterly period ended September 30, 2012, and in its other filings with the Securities and Exchange Commission. The forward-looking statements in this press release represent NewLink's views as of the date of this press release. NewLink anticipates that subsequent events and developments will cause its views to change. However, while it may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. You should, therefore, not rely on these forward-looking statements as representing NewLink's views as of any date subsequent to the date of this press release.

Contact: Gordon Link Chief Financial Officer 515-598-2925 glink@linkp.com

Originally posted here:
NewLink Genetics Corporation Announces Pricing of Public Offering of Common Stock

The rats completely recovered from a stroke within two weeks with stem cell therapy (Wiki Commons)

Stem cell therapy administered shortly after a stroke could significantly increase the sufferer's chance of a complete recovery.

When administered to rats within 30 minutes of suffering a stroke, the rodents made a full recovery within two weeks, a study showed.

The research, published in BioMed Central's open access journalStem Cell Research & Therapy, found that stem cells from the bone marrow of fat can improve the recovery of rats following a stroke.

Researchers at La Paz University Hospital found that treatment improved the amount of brain and nerve repair, as well as the animal's ability to complete tasks.

Rats were treated intravenously with stem cells half an hour after a stroke. In humans, such rapid response is known to dramatically improve the outcome of victims.

The researchers found improvements in the stem cell group within 24 hours of the treatment, compared to the control group.

The FAST response advertising campaign has aimed to increase awareness of symptoms. Facial and arm weakness and speech problems suggest it is time to call emergency services.

Human trials

A delay in treatment can result in death or long-term disabilities. A stroke occurs when the blood supply to part of the brain is cut off.

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Stem Cell Therapy Helps Stroke Victims Recover in Two Weeks

LONDON (ShareCast) - ReNeuron Group received the green light to complete the final stages of first phase safety testing of its ReN001 stem cell therapy for disabled stroke patients in Scotland, the company announced Tuesday.

The ReN001 stem cell therapy was being administered in ascending doses to a total of 12 stroke patients who have been left disabled by an ischaemic stroke, the most common form of the condition.

ReNeuron is now set to proceed with dosing the last three patients after getting clearance from the Data Safety Monitoring Board which reviewed the study.

The first of the three patients was treated with ReN001 and discharged from hospital. The remaining two are scheduled to be treated this March.

Last year, interim data from the first five patients treated in the study were presented by the Glasgow clinical team. Sustained reductions in neurological impairment and spasticity were observed in all patients compared with their stable pre-treatment baseline performance.

Further and longer term data from the study are expected to be presented in scientific conference later this year.

The company has submitted an application to the UK regulatory authority to commence a multi-site phase two clinical trial to examine the efficacy of ReN001 in patients disabled by an ischaemic stroke. Preparations are underway to begin the trial mid-year.

RD

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ReNeuron Group edges further in stem cell therapy research for stroke patients

Video 1 - The Fight To Be Healthy
geneticagereversal.nsproducts.com Turning back the hands of time. Gene research has uncovered ways to genetically turn back on "youthful" genes with LifePak Nano.

By: David Allison

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Video 1 - The Fight To Be Healthy - Video

-- CHOP Researchers' New Single-Platform Tool Streamlines Diagnoses of Complicated Multisystem Disorders--

PHILADELPHIA, Jan. 29, 2013 /PRNewswire-USNewswire/ --More powerful gene-sequencing tools have increasingly been uncovering disease secrets in DNA within the cell nucleus. Now a research team is expanding those rapid next-generation sequencing tests to analyze a separate source of DNAwithin the genes inside mitochondria, cellular power plants that, when abnormal, contribute to complex, multisystem diseases.

The study team, headed by a specialist in mitochondrial medicine at The Children's Hospital of Philadelphia (CHOP), adapted next-generation sequencing to simultaneously analyze the whole exome (all the protein-coding DNA) of nuclear genes and the mitochondrial genome. "A first step in developing treatments for a disease is to understand its precise cause," said Marni J. Falk, M.D., the director and attending physician in the Mitochondrial-Genetic Disease Clinic at Children's Hospital. "We have developed a one-step, off-the-shelf tool that analyzes both nuclear and mitochondrial DNA to help evaluate the genetic cause of suspected mitochondrial disease."

Falk and colleagues describe their customized, comprehensive test, which they call the "1:1000 Mito-Plus Whole-Exome" kit, in the journal Discovery Medicine, published Dec. 26, 2012. Her co-corresponding author, biostatistician Xiaowu Gai, Ph.D., now of the Loyola University Stritch School of Medicine, collaborated on developing the test while at Children's Hospital.

While each mitochondrial disease is very rare in the population, hundreds of causes of mitochondrial diseases are known. Some originate in mutations in DNA specific to the mitochondria, tiny structures located outside the cell nucleus, while many other mitochondrial diseases are based in nuclear DNA genes that affect mitochondrial function. The role of mitochondria in human disease has been recognized only since the 1980s, based on pioneering research by Douglas C. Wallace, Ph.D., now at Children's Hospital, and a co-author of the current study.

Many mitochondrial diseases remain poorly understood. One complicating factor is heteroplasmya mixture of mutated and normal mitochondrial genomes within the same cells or tissues. In contrast to conventional gene sequencing, which can detect only heteroplasmic mutations that reach levels of at least 30 to 50 percent, the customized kit has the sensitivity to detect mitochondrial genome mutations present at levels as low as 8 percent. To achieve their results, the study team adapted an existing whole-exome sequencing kit from Agilent Technologies, expanding it to encompass the mitochondrial genome.

The availability of the new kit, said Falk, if used for either clinical or research purposes, may shorten the "diagnostic odyssey" experienced by many patients and families seeking the cause of debilitating and puzzling symptoms. "Many families travel from one specialist to another for years, searching for the cause of their rare disease," she says. Specific treatments are not always available, but identifying their disease cause may be the first step toward discovering treatments.

A second recent study by Falk and colleagues reviews progress in diagnosing mitochondrial disease, through their experience at a single center over a rapidly changing three-year period before whole-exome sequencing was generally available. The retrospective review in Neurotherapeutics, published Dec. 27, 2012, covers 152 child and adult patients evaluated at CHOP's Mitochondrial-Genetics Diagnostic Clinic from 2008 to 2011.

"Before 2005, very few individuals could receive definitive molecular diagnoses for mitochondrial diseases, because of limitations in both knowledge and technology," said Falk. "Since that time, the clinical ability to sequence whole mitochondrial DNA genomes has significantly improved the diagnosis of many mitochondrial disorders."

During the study period covered in the review article, the clinic at CHOP confirmed definite mitochondrial disease in 16 percent of patients and excluded primary mitochondrial disease in 9 percent. While many diagnostic challenges clearly remain, Falk says the advent of massively parallel nuclear exome sequencing is revealing increasingly more of the genes in nuclear DNA that affect mitochondrial function, and the precise genetic disorder in a given patient, even if it is novel or uncommon. She added that molecular genetics is yielding a more nuanced understanding of the cellular pathways underlying symptoms in many mitochondrial disorders. "Those pathways offer potential new targets for treating these disorders," said Falk.

Continue reading here:
Scientists Create One-Step Gene Test for Mitochondrial Diseases

Jan. 28, 2013 Because half of all instances of hearing loss are linked to genetic mutations, advanced gene research is an invaluable tool for uncovering causes of deafness -- and one of the biggest hopes for the development of new therapies. Now Prof. Karen Avraham of the Sackler Faculty of Medicine at Tel Aviv University has discovered a significant mutation in a LINC family protein -- part of the cells of the inner ear -- that could lead to new treatments for hearing disorders.

Her team of researchers, including Dr. Henning Horn and Profs. Colin Stewart and Brian Burke of the Institute of Medical Biology at A*STAR in Singapore, discovered that the mutation causes chaos in a cell's anatomy. The cell nucleus, which contains our entire DNA, moves to the top of the cell rather than being anchored to the bottom, its normal place. Though this has little impact on the functioning of most of the body's cells, it's devastating for the cells responsible for hearing, explains Prof. Avraham. "The position of the nucleus is important for receiving the electrical signals that determine proper hearing," she explains. "Without the ability to receive these signals correctly, the entire cascade of hearing fails."

This discovery, recently reported in the Journal of Clinical Investigation, may be a starting point for the development of new therapies. In the meantime, the research could lead towards work on a drug that is able to mimic the mutated protein's anchoring function, and restore hearing in some cases, she suggests.

From human to lab to mouse

Prof. Avraham originally uncovered the genetic mutation while attempting to explain the cause of deafness in two families of Iraqi Jewish descent. For generations, members of these families had been suffering from hearing loss, but the medical cause remained a mystery. Using deep genetic sequencing, a technology used to sequence the entire human genome, she discovered that the hearing impaired members of both families had a mutated version of the protein Nesprin4, a part of the LINC group of proteins that links the cell's nucleus to the inner wall of the cell.

In the lab, Prof. Avraham recreated this phenomenon by engineering the mutation in single cells. With the mutation in place, Nesprin4 was not found in the area around the cell nucleus, as in healthy cells, but was spread throughout the entire cell. Investigating further, she studied lab mice that were engineered to be completely devoid of the protein.

Created in Singapore, the mice were originally engineered to study the biology of LINC proteins. The fact that they were deaf came as a complete surprise to researchers. Without this protein serving as an anchor, the cell nucleus is not located in the correct position within inner ear cells, but seems to float throughout. This causes the cells' other components to reorient as well, ultimately harming the polarity of the cells and hindering electrical signals. It's a mutation that took a heavy toll on the cells' ability to transfer sound signals, explains Prof. Avraham, rendering the mice deaf.

Given the similarity between mouse and human inner ear cells, researchers predict that the same phenomenon is occurring in human patients with a mutation in the Nesprin4 gene.

Looking for a wider impact

Prof. Avraham says that she and her collaborators are the first to reveal this mutation as a cause of deafness. "Now that we have reported it, scientists around the world can test for mutations in this gene," she notes. The mutation could indeed be a more common genetic cause of deafness in a number of populations. And because Nesprin4 belongs to a family of proteins that have been linked to other diseases, such as muscular coordination and degeneration disorders, this could prove a ripe area for further research.

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Discovering the missing 'LINC' to deafness

New Delhi, Jan 28 (IANS) In a scientific breakthrough that promises improved grain yields, greater drought tolerance and disease resistance, a global research team, including Indian scientists, has completed sequencing of chickpea (black gram).

"The project team had 49 scientists from 23 organisations in 10 countries, including Indian Council for Agriculture Research (ICAR)," an official from the agriculture ministry said.

The research was the result of years of genome analysis by the International Chickpea Genome Sequencing Consortium led by the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT).

The global research partnership succeeded in identifying 28,269 genes of chickpea.

"Re-sequencing of additional 90 chickpea types provided millions of genetic markers. This has great potential in developing drought tolerant and disease resistant varieties of this important pulse crop," the official said.

Nature Biotechnology, the highest ranked journal in the area of biotechnology, has featured the research in its latest issue on Jan 27.

Chickpea or gram is the second largest pulse crop in the world, grown in about 11.5 million hectares.

While India is the largest producer (also importer and consumer) of chickpea, it is grown in a number of African countries including Ethiopia, Tanzania and Kenya.

Chickpea is also an important component of the pulse industry in Australia, Canada and USA.

Excerpt from:
Decoded chickpea gene could help multiply yield

Jan. 29, 2013 Women with harmful mutations in the BRCA gene, which put them at higher risk of developing breast and ovarian cancer, tend to undergo menopause significantly sooner than other women, allowing them an even briefer reproductive window and possibly a higher risk of infertility, according to a study led by researchers at UC San Francisco.

Moreover, the study showed that carriers of the mutation who are heavy smokers enter menopause at an even earlier age than non-smoking women with the mutation.

While the authors note that further research is needed, given the size and demographics of the study, women with the abnormal gene mutation should consider earlier childbearing, and their doctors should encourage them to initiate fertility counseling along with other medical treatments, the scientists said.

The study will be published online in Cancer on January 29, 2013.

This is the first controlled study to explore the association between BRCA1 and BRCA 2 and the age at onset of menopause, the authors said.

"Our findings show that mutation of these genes has been linked to early menopause, which may lead to a higher incidence of infertility,'' said senior author Mitchell Rosen, MD, director of the UCSF Fertility Preservation Center and associate professor in the UCSF Department of Obstetrics, Gynecology and Reproductive Sciences. "This can add to the significant psychological implications of being a BRCA1/2 carrier, and will likely have an impact on reproductive decision-making,'' Rosen said.

Mutations in either of the genes BRCA 1 or BRCA 2 can produce a hereditary, lifetime risk of developing breast cancer and ovarian cancer. Some women decide to reduce their risk by undergoing prophylactic surgery to remove at-risk tissue, including their breasts and ovaries. The abnormal genes are the most identified inherited cause of breast cancer -- carriers are five times more likely to develop breast cancer than those without the mutations, according to the National Cancer Institute.

The new study was designed to determine whether women with the BRCA1 or BRCA2 mutation have an earlier onset of menopause compared with unaffected women.

The researchers looked at nearly 400 female carriers of mutations in the BRCA gene in northern California and compared their onset of menopause to that of 765 women in the same geographic area without the mutation. Most of the women in the study were white because almost all of the BRCA1/2 carriers within the UCSF cancer risk registry are white.

The scientists found that women with the harmful mutation experienced menopause at a significantly younger age -- 50 years -- compared to age 53 for the other midlife women.

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Early menopause may occur in women with BRCA gene

Jan. 29, 2013 Chemotherapy is one of the most common treatments for cancer patients. However, many patients suffer from serious side-effects and a large proportion does not respond to the treatment. Researchers from the Biotech Research and Innovation Centre (BRIC) and Center for Healthy Aging, University of Copenhagen, now show that the gene FBH1 helps turn up the effect of chemotherapy.

The results were recently published in the journal Nature Communications.

"Our results show that the gene FBH1 is crucial in order for some chemotherapeutics to become active in the body and kill the cancer cells. If we can find a feasible method to increase the activity of the gene, we can use our cells' own resources to improve cancer treatment, says associate professor Claus Srensen who has lead the team of researchers behind the results.

Own gene helps chemotherapy fight cancer

The researchers have used a method called RNA interference to study whether some of the genes in our DNA are important for cancer cells to react to certain chemotherapeutics.

"By using the method to remove single genes from cancer cells and then exposing the cells to chemotherapy, we found that FBH1 is important for the effect of the chemotherapy. Actually, the presence of the gene was an absolutely requirement in order to effectively kill the cancer cells with the type of chemotherapeutics we have studied, says postdoc Kasper Fugger who has led the experimental part of the investigation.

Chemotherapy act by exposing cancer cells to a kind of extreme stress when they divide. The result is detrimental damage to the cells' DNA that cannot be repaired, causing the cells to die. The new results show that it is in fact FBH1 that contributes to the formation of DNA damage when treating with chemotherapy and this knowledge can be used to optimize cancer therapy.

Selection of patients for chemotherapy

In the last decade it has become clear that targeted treatment to individual cancer patients is crucial for an effective treatment with least possible side-effects. By assessing the presence of FBH1 in a tumour the doctors can get an indication of whether the patient will benefit from chemotherapy.

"Our results could help indicate that patients with low or no FBH1 in the cancer cells will not benefit from certain types of chemotherapy, but should be administered another type of treatment. So by using the genetic fingerprint of a tumour doctors can adjust the treatment to individual patients, says Claus Srensen.

Continued here:
Gene found that turns up effect of chemotherapy

Public release date: 29-Jan-2013 [ | E-mail | Share ]

Contact: Dana Mortensen Mortensen@email.chop.edu 267-426-6092 Children's Hospital of Philadelphia

More powerful gene-sequencing tools have increasingly been uncovering disease secrets in DNA within the cell nucleus. Now a research team is expanding those rapid next-generation sequencing tests to analyze a separate source of DNAwithin the genes inside mitochondria, cellular power plants that, when abnormal, contribute to complex, multisystem diseases.

The study team, headed by a specialist in mitochondrial medicine at The Children's Hospital of Philadelphia (CHOP), adapted next-generation sequencing to simultaneously analyze the whole exome (all the protein-coding DNA) of nuclear genes and the mitochondrial genome. "A first step in developing treatments for a disease is to understand its precise cause," said Marni J. Falk, M.D., the director and attending physician in the Mitochondrial-Genetic Disease Clinic at Children's Hospital. "We have developed a one-step, off-the-shelf tool that analyzes both nuclear and mitochondrial DNA to help evaluate the genetic cause of suspected mitochondrial disease."

Falk and colleagues describe their customized, comprehensive test, which they call the "1:1000 Mito-Plus Whole-Exome" kit, in the journal Discovery Medicine, published Dec. 26, 2012. Her co-corresponding author, biostatistician Xiaowu Gai, Ph.D., now of the Loyola University Stritch School of Medicine, collaborated on developing the test while at Children's Hospital.

While each mitochondrial disease is very rare in the population, hundreds of causes of mitochondrial diseases are known. Some originate in mutations in DNA specific to the mitochondria, tiny structures located outside the cell nucleus, while many other mitochondrial diseases are based in nuclear DNA genes that affect mitochondrial function. The role of mitochondria in human disease has been recognized only since the 1980s, based on pioneering research by Douglas C. Wallace, Ph.D., now at Children's Hospital, and a co-author of the current study.

Many mitochondrial diseases remain poorly understood. One complicating factor is heteroplasmya mixture of mutated and normal mitochondrial genomes within the same cells or tissues. In contrast to conventional gene sequencing, which can detect only heteroplasmic mutations that reach levels of at least 30 to 50 percent, the customized kit has the sensitivity to detect mitochondrial genome mutations present at levels as low as 8 percent. To achieve their results, the study team adapted an existing whole-exome sequencing kit from Agilent Technologies, expanding it to encompass the mitochondrial genome.

The availability of the new kit, said Falk, if used for either clinical or research purposes, may shorten the "diagnostic odyssey" experienced by many patients and families seeking the cause of debilitating and puzzling symptoms. "Many families travel from one specialist to another for years, searching for the cause of their rare disease," she says. Specific treatments are not always available, but identifying their disease cause may be the first step toward discovering treatments.

A second recent study by Falk and colleagues reviews progress in diagnosing mitochondrial disease, through their experience at a single center over a rapidly changing three-year period before whole-exome sequencing was generally available. The retrospective review in Neurotherapeutics, published Dec. 27, 2012, covers 152 child and adult patients evaluated at CHOP's Mitochondrial-Genetics Diagnostic Clinic from 2008 to 2011.

"Before 2005, very few individuals could receive definitive molecular diagnoses for mitochondrial diseases, because of limitations in both knowledge and technology," said Falk. "Since that time, the clinical ability to sequence whole mitochondrial DNA genomes has significantly improved the diagnosis of many mitochondrial disorders."

See the original post:
Scientists create 1-step gene test for mitochondrial diseases

Public release date: 29-Jan-2013 [ | E-mail | Share ]

Contact: Associate professor Claus Srensen claus.storgaard@bric.ku.dk 45-31-61-98-48 University of Copenhagen

Chemotherapy is one of the most common treatments for cancer patients. However, many patients suffer from serious side-effects and a large proportion does not respond to the treatment. Researchers from the Biotech Research and Innovation Centre (BRIC) and Center for Healthy Aging, University of Copenhagen, now show that the gene FBH1 helps turn up the effect of chemotherapy.

"Our results show that the gene FBH1 is crucial in order for some chemotherapeutics to become active in the body and kill the cancer cells. If we can find a feasible method to increase the activity of the gene, we can use our cells' own resources to improve cancer treatment, says associate professor Claus Srensen who has lead the team of researchers behind the results.

Own gene helps chemotherapy fight cancer

The researchers have used a method called RNA interference to study whether some of the genes in our DNA are important for cancer cells to react to certain chemotherapeutics. "By using the method to remove single genes from cancer cells and then exposing the cells to chemotherapy, we found that FBH1 is important for the effect of the chemotherapy. Actually, the presence of the gene was an absolutely requirement in order to effectively kill the cancer cells with the type of chemotherapeutics we have studied, says postdoc Kasper Fugger who has led the experimental part of the investigation.

Chemotherapy act by exposing cancer cells to a kind of extreme stress when they divide. The result is detrimental damage to the cells' DNA that cannot be repaired, causing the cells to die. The new results show that it is in fact FBH1 that contributes to the formation of DNA damage when treating with chemotherapy and this knowledge can be used to optimize cancer therapy.

Selection of patients for chemotherapy

In the last decade it has become clear that targeted treatment to individual cancer patients is crucial for an effective treatment with least possible side-effects. By assessing the presence of FBH1 in a tumour the doctors can get an indication of whether the patient will benefit from chemotherapy.

"Our results could help indicate that patients with low or no FBH1 in the cancer cells will not benefit from certain types of chemotherapy, but should be administered another type of treatment. So by using the genetic fingerprint of a tumour doctors can adjust the treatment to individual patients, says Claus Srensen.

See the rest here:
Researchers find gene that turns up effect of chemotherapy

NEW YORK (Reuters Health) - Women carrying BRCA mutations tied to breast and ovarian cancer may hit menopause a few years earlier than other women, according to a new study.

Doctors already discuss with those women whether they want immediate surgery to remove their ovaries and breasts, or if they want to start a family first and hold off on ovary removal.

"Now they have an additional issue to deal with," said Dr. Mitchell Rosen, who worked on the new study at the University of California, San Francisco Medical Center.

An estimated one in 600 U.S. women carries the BRCA1 or BRCA2 gene mutation.

Those mutations greatly increase the risk of breast and ovarian cancer. According to the National Cancer Institute, a woman's chance of getting breast cancer at some point in her life increases from 12 to 60 percent with a BRCA mutation, and ovarian cancer from 1.4 percent to between 15 and 40 percent.

What has been less well studied is whether those mutations also affect a woman's egg stores and her chance of getting pregnant.

For the new study, the researchers surveyed 382 California women who carried the BRCA1 or BRCA2 mutation and another 765 women who weren't known carriers. The study team focused specifically on women who went through menopause naturally - and not those who had their ovaries removed before menopause.

Women with the genetic mutations said they'd stopped getting their periods at age 50, on average, compared to age 53 for other women. The youngest natural menopause, at age 46, came for women with a BRCA mutation who were also heavy smokers, Rosen and his colleagues reported Tuesday in the journal Cancer.

Their study only included white women, so it's unknown whether the findings apply to other racial and ethnic groups. It's also not clear whether mutation carriers had any trouble conceiving - although it's more likely, the researchers said.

"The earlier you go into menopause, the more likely you are to not be able to have kids," Rosen told Reuters Health.

Continue reading here:
Cancer gene mutation linked to earlier menopause

Types of CSSR recombination
For more information, log on to- shomusbiology.weebly.com Download the study materials here- shomusbiology.weebly.com Site-specific recombination, also known as conservative site-specific recombination, is a type of genetic recombination in which DNA strand exchange takes place between segments possessing only a limited degree of sequence homology.[1][2][3] Site-specific recombinases (SSRs)perform rearrangements of DNA segments by recognizing and binding to short DNA sequences (sites), at which they cleave the DNA backbone, exchange the two DNA helices involved and rejoin the DNA strands. While in some site-specific recombination systems just a recombinase enzyme and the recombination sites is enough to perform all these reactions, in other systems a number of accessory proteins and/or accessory sites are also needed. Multiple genome modification strategies, among these Recombinase-mediated cassette exchange (RMCE), an advanced approach for the targeted introduction of transcription units into predetermined genomic loci, rely on the capacities of SSRs. Site-specific recombination systems are highly specific, fast and efficient, even when faced with complex eukaryotic genomes.[4] They are employed in a variety of cellular processes, including bacterial genome replication, differentiation and pathogenesis, and movement of mobile genetic elements (Nash 1996). For the same reasons, they present a potential basis for the development of genetic engineering tools.[5 ...

By: Suman Bhattacharjee

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Types of CSSR recombination - Video

MENLO PARK, Calif., Jan. 29, 2013 (GLOBE NEWSWIRE) -- Pacific Biosciences of California, Inc., (PACB), provider of the PacBio(R)RS High Resolution Genetic Analyzer, today recognized TSMC, the world's largest and premier dedicated semiconductor foundry as its 'Supplier of the Year' for 2012. TSMC is on the leading edge of semiconductor wafer processing and has been a trusted collaborator of Pacific Biosciences, manufacturing the key component of its proprietary SMRT(R) Cells for DNA sequencing on the PacBio RS system.

"TSMC was selected as a premier supplier of Pacific Biosciences because of their extensive engineering experience, technological insight and exceptional level of service," said Michael Hunkapiller, Ph.D., President and Chief Executive Officer of Pacific Biosciences. "In 2012, their joint engineering efforts along with their commercial flexibility resulted in significant performance and yield improvements of our SMRT Cells. With TSMC's continued support, we have just launched the SMRT Cell V3, which provides equivalent sequencing performance with less library input required."

The Supplier of the Year award program recognizes suppliers partnering with Pacific Biosciences for continuously evolving its core technologies while promoting efficiency and creating value.

About Pacific Biosciences

Pacific Biosciences of California, Inc. (PACB) offers the PacBio(R)RS High Resolution Genetic Analyzer to help scientists solve genetically complex problems. Based on its novel Single Molecule, Real-Time (SMRT(R)) technology, the company's products enable: targeted sequencing to more comprehensively characterize genetic variations; de novo genome assembly to more fully identify, annotate and decipher genomic structures; and DNA base modification identification to help characterize epigenetic regulation and DNA damage. By providing access to information that was previously inaccessible, Pacific Biosciences enables scientists to increase their understanding of biological systems.

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Pacific Biosciences Names TSMC Supplier of the Year

Public release date: 28-Jan-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, January 28, 2013The U.S. Department of Agriculture (USDA) invests nearly $10 million a year to support about 250 nanoscale science and engineering projects that could lead to revolutionary advances in agriculture and food systems. Examples of current projects in development are presented in a Special Research Section published in Industrial Biotechnology, a peer-reviewed journal from Mary Ann Liebert Inc., publishers. The articles are available on the Industrial Biotechnology website.

In their introductory article, "Overview: Nanoscale Science and Engineering for Agriculture and Food Systems," Co-Guest Editors Norman Scott, PhD, Professor, Cornell University (Ithaca, NY) and Hongda Chen, PhD, National Program Leader, National Institute of Food and Agriculture, USDA (Washington, DC), describe the promising early advances nanotechnology is enabling all along the food supply chain, from production through consumption, and especially in the area of food safety.

This special issue of IB includes the review article "Bioactivity and Biomodification of Ag, ZnO, and CuO Nanoparticles with Relevance to Plant Performance in Agriculture" by Anne Anderson and coauthors, Utah State University, Logan, in which they discuss the environmental factors that affect the biological activity and potential agricultural utility of nanoparticle. In the original research article "Effect of Silver Nanoparticles on Soil Denitrification Kinetics" Allison Rick VandeVoort and Yuji Arai, Clemson University (South Carolina), describe the effects of three different silver nanoparticles on native bacteria-mediated soil denitrification.

The short communication "Soft Lithography-Based Fabrication of Biopolymer Microparticles for Nutrient Microencapsulation" by Natalia Higuita-Castro, et al., The Ohio State University and Abbott Nutrition Products Division, Columbus, OH, describes a high-throughput microfabrication method to encapsulate nutrients that can enhance food nutritional value and appearance. Dan Luo and colleagues, Cornell University, Ithaca, NY, present a promising microfluidic-based scale-up method for cell-free protein production in the methods article "Cell-Free Protein Expression from DNA-Based Hydrogel (P-Gel) Droplets for Scale-Up Production."

"The rapid expansion in nanoscale science and technology in our community with new insights and methods in biomolecular and cellular processing will spur industrial biotechnology innovation in a number of important sectors," says Larry Walker, PhD, Co-Editor-in-Chief and Professor, Biological & Environmental Engineering, Cornell University, Ithaca, NY.

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About the Journal

Industrial Biotechnology, led by Co-Editors-in-Chief Larry Walker, PhD, and Glenn Nedwin, PhD, MBA, is an authoritative journal focused on biobased industrial and environmental products and processes, published bimonthly in print and online. The Journal reports on the science, business, and policy developments of the emerging global bioeconomy, including biobased production of energy and fuels, chemicals, materials, and consumer goods. The articles published include critically reviewed original research in all related sciences (biology, biochemistry, chemical and process engineering, agriculture), in addition to expert commentary on current policy, funding, markets, business, legal issues, and science trends. Industrial Biotechnology offers the premier forum bridging basic research and R&D with later-stage commercialization for sustainable biobased industrial and environmental applications.

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Innovative uses of nanotechnology in food and agriculture

PHILADELPHIA Benjamin F. Voight, PhD, assistant professor of Pharmacology and Genetics at the Perelman School of Medicine at the University of Pennsylvania, has received an award for over $100,000 from the W.W. Smith Charitable Trust to study the complex patterns of genetic inheritance and environmental factors that underlie cardiovascular disease specifically in type-2 diabetics.

I am extremely honored to receive support from the W.W. Smith Charitable Trust, says Voight. As a newly minted investigator, support at this level is highly valuable in helping me to establish my independent research career. It is also a huge intellectual boost to receive support from such an important organization with strong ties to Philadelphia.

Heart disease is substantially elevated in patients with type-2 diabetes, yet the biological and genetic basis for this elevated risk is not well understood.

My research aims to fill this apparent gap in knowledge by applying statistical approaches in human genetics and computational biology to characterize the genetic risk of heart disease in patients with type-2 diabetes, says Voight. We will be looking for novel disease mechanisms and biological pathways contributing to this elevated risk. A better understanding of processes contributing to this predisposition is an important step in clinical management of both diseases, as well as a useful strategy to identify biological targets for therapeutic intervention.

The most interesting component of the project is the idea that approaches in human genetics are particularly well situated to identify unknown biological processes contributing to disease. Systematic and unbiased studies in human populations have the potential to alter clinical practices for the better, as well as help focus therapeutic innovations on biological systems directly relevant to humans, explains Voight.

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Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.

The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 fiscal year.

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2011, Penn Medicine provided $854 million to benefit our community.

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Penn Researcher Receives W.W. Smith Charitable Trust Award to Study Cardiovascular Disease and Diabetes

Every cancer patient could soon have a genetic profile made of their tumour so they can be treated with new smart drugs that can dramatically improve their survival.

Scientists at the Institute of Cancer Research believe the technique will prove so effective that it will turn cancer into a chronic disease that people live with, rather than die from.

Work at the institute's new Tumour Profiling Unit will begin this year to analyse patients' cancer cells for changes to their DNA. These mutations allow the tumour to grow out of control and even develop resistance to chemotherapy.

By identifying key genetic changes, researchers hope to target specific drugs at individual patients.

Breast cancer patients are already beginning to benefit from such personalised medicine. The drug Herceptin is highly effective - but only in women who have tumours positive for a protein called HER2.

Other cancer patients are now set to benefit.

Professor Alan Ashworth, from the institute, said: "None of this is science fiction.

"One would think in five or 10 years this will be absolutely routine practice for every cancer patient, and that's what we're aiming to bring about."

Tumour profiling has been made possible by the rapid advances in DNA analysis.

A decade ago it took several years and millions of pounds to analyse the genetic blueprint inside cells; now it can be done in days for 1,000.

Continue reading here:
Genetic Map Gives Hope On Cancer Treatment

Copy number control in plasmids
For more information, log on to- shomusbiology.weebly.com Download the study materials here- shomusbiology.weebly.com Plasmids used in genetic engineering are called vectors. Plasmids serve as important tools in genetics and biotechnology labs, where they are commonly used to multiply (make many copies of) or express particular genes.[4] Many plasmids are commercially available for such uses. The gene to be replicated is inserted into copies of a plasmid containing genes that make cells resistant to particular antibiotics and a multiple cloning site (MCS, or polylinker), which is a short region containing several commonly used restriction sites allowing the easy insertion of DNA fragments at this location. Next, the plasmids are inserted into bacteria by a process called transformation. Then, the bacteria are exposed to the particular antibiotics. Only bacteria that take up copies of the plasmid survive, since the plasmid makes them resistant. In particular, the protecting genes are expressed (used to make a protein) and the expressed protein breaks down the antibiotics. In this way, the antibiotics act as a filter to select only the modified bacteria. Now these bacteria can be grown in large amounts, harvested, and lysed (often using the alkaline lysis method) to isolate the plasmid of interest. Another major use of plasmids is to make large amounts of proteins. In this case, researchers grow bacteria containing a plasmid harboring the gene of interest. Just as the ...

By: Suman Bhattacharjee

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Copy number control in plasmids - Video