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  • Leptin “Replacement Therapy” Study in Obese Women Begins | Newswire
    these factors could explain the classic scenario Why can two healthy people eat the same foods and be physically active while at the same time one of them will lose weight and the other will gain weight Adding leptin to the body when the hormone amount drops may prevent slowed metabolism and result in an increased rate of weight loss Dr Zolotov works in the Laboratory of Molecular Genetics at Rockefeller University headed by Marilyn M Simpson Professor and Howard Hughes Medical Institute Investigator Jeffrey Friedman Dr Friedman discovered leptin so named for the Greek word leptos or thin and the human gene that is responsible for it in 1994 He studies the hormone along with the neurobiological and other hormonal processes that regulate body weight Obesity is usually defined as having a body mass index of 30 or greater or at least 30 percent above one s ideal weight Body mass index is a measurement that gauges a person s weight in relation to their height to determine total body fat Recent federal estimates indicate that 55 percent of American adults or 97 million are either overweight or obese Obesity is a growing problem every year in the United States Health risks such as increased propensity to heart disease diabetes and high blood pressure are associated with being overweight The new study lasts approximately 20 weeks During the first nine weeks volunteers must stay at the Rockefeller University Hospital but may be approved to go to school or work by study investigators Participants will be placed on a free supervised low calorie diet for the entire duration of the study They will also be provided with either leptin or a placebo drug treatment while dieting Study participants will also meet with a hospital social worker to reinforce the importance

    Original URL path: http://newswire.rockefeller.edu/2001/05/08/leptin-replacement-therapy-study-in-obese-women-begins/ (2016-02-13)
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  • Sagit Zolotov | Newswire
    weight regulating hormone leptin will be given to obese women in a new study at The Rockefeller University Hospital in New York City to test the effects of the treatment on weight loss More Tags Obesity Sagit Zolotov Search for Categories Science News Awards and Honors Campus News Grants Gifts Topics Video Archive 2015 2014 2013 2012 2011 more About Contact Follow rockefelleruniv Like The Rockefeller University RU Footer The

    Original URL path: http://newswire.rockefeller.edu/tag/sagit-zolotov/ (2016-02-13)
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  • Resistance to Leptin Contributes to Obesity | Newswire
    blood pressure stroke sleep apnea gallstones some cancers and forms of arthritis according to the National Institute of Diabetes and Digestive and Kidney Diseases NIDDK part of the federal government s National Institutes of Health NIDDK supported the research along with the Robert J Jr and Helen C Kleberg Foundation In the new study Friedman and his coinvestigators from Columbia University St Luke s Roosevelt Hospital Center University of Melbourne and the Howard Florey Institute of Experimental Physiology and Medicine found that three strains of obese mice all with normally high levels of leptin are overweight because they have varying degrees of insensitivity to the protein The team examined the effect of leptin given during a 30 day period as infusions either into the fat tissue under the skin or directly into the fluid that bathes the brain and spinal column This innovative technique called ICV infusion was developed by coauthor Dr Derek A Denton of the Howard Florey Institute in Melbourne Australia Normal weight lean mice receiving leptin by either method lost significant weight and fat with low doses delivered via ICV infusion having the same effects as high doses given as subcutaneous infusions into the fat tissue For example during ICV infusion at a constant rate of 8 nanograms ng per hour lean mice lost 15 percent of their body weight yet this dose had no effect when given to other lean mice by the subcutaneous injection The difference between the increased potency of leptin in lean mice receiving the protein via ICV infusion and those receiving subcutaneous injections shows that the central nervous system in particular the hypothalamus is an important site of leptin action says Friedman Indeed chronic ICV infusions of very low doses of leptin replicate the weight reducing effects of much higher doses of leptin given by injection The basis for this apparent difference is not clear but may suggest that the transport of leptin across the blood brain barrier which allows leptin to enter the brain from the body s blood stream may be an important step in the body s processing of leptin s signal Specifically in normal lean mice injecting leptin subcutaneously at an infusion rate of 200 ng per hour for example led to an increase in blood levels from 5 to 7 ng milliliter and resulted in a 5 percent reduction in weight A doubling of leptin levels led to a 9 percent reduction in weight while a five fold increase in leptin levels yielded a 15 percent weight loss Other lean mice receiving leptin through ICV infusion rapidly lost fat reaching their lowest weight by the eighth day of treatment and maintained it for the remainder of the 30 day infusion period The mice reduced their food intake to its lowest level a drop of more than 50 percent by the third day but their food intake crept back to original levels by the eighth day After the 30 days of ICV the researchers replaced the cerebrospinal fluid

    Original URL path: http://newswire.rockefeller.edu/1997/08/04/resistance-to-leptin-contributes-to-obesity/ (2016-02-13)
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  • Collaboration finds kidney disease tied to DNA damage | Newswire
    disease last year when he came across the FAN1 mutation His lab found that FAN1 was mutated in 9 out of the 10 families with karyomegalic interstitial nephritis Smogorzewska head of the Laboratory of Genome Maintenance at Rockefeller joined Hildebrandt in a collaboration to draw out the details of this possible genetic cause Our lab is very interested in this gene and others that are involved in DNA damage and we have the tools to study them so we were eager to join Hildebrandt s lab in understanding how these patients cells behaved Smogorzewska says The relationship between FAN1 and kidney disease was an exciting and surprising finding for Smogorzewska she first identified FAN1 as a postdoc at Harvard Medical School But she wasn t looking at the kidney she was studying Fanconi anemia a genetic disease that interferes with a cell s ability to repair DNA damage leading to cancer bone marrow failure and other health problems DNA damage by itself is an everyday occurrence for cells as many as 1 million so called lesions can exist in the DNA of each cell each day If the person is healthy the cells identify and repair the damage For others the damage goes unchecked leading to a dangerous environment in the body that has been implicated in several disorders including Fanconi anemia as well as cancer and premature aging After identifying FAN1 Smogorzewska found that it helps repair DNA damage similar to genes implicated in Fanconi anemia But a study of the genomes of patients with the disease revealed that none of them had a mutation in FAN1 Smogorzewska went on to identify other genes that had a causal relationship with Fanconi anemia but uncovering the functions of FAN1 remained a focus of her research In the present study Smogorzewska s lab used its FAN1 expertise to investigate whether there was a causal relationship between the gene mutation and kidney disease One test took cells from the patients and exposed them to mitomycin C a drug often used in chemotherapy Mitomycin C causes crosslinking in DNA which is where both strands of the double helix become bonded together in such a way that they can t separate rendering them unable to replicate and create new cells FAN1 is known to repair this DNA damage and when the lab looked at the patients cells in the presence of the drug they saw significant damage meaning FAN1 wasn t working properly When the corrected version of the FAN1 gene was placed back in these cells their ability to repair the crosslinking damage was restored This is our proof that we ve likely identified the right gene the ability of the FAN1 protein to restore the cells function Additionally if you find multiple families with the same phenotype and the same gene being mutated it s a really good indication that you have the right gene says Smogorzewska Though they may have found the gene there is still much to learn about the

    Original URL path: http://newswire.rockefeller.edu/2012/08/08/collaboration-finds-kidney-disease-tied-to-dna-damage/ (2016-02-13)
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  • DNA damage | Newswire
    two dozen other institutions found that patients who had a specific kind of kidney disease called karyomegalic interstitial nephritis were likely to also have a mutation on FAN1 a gene that is involved in fixing DNA damage More Tags Agata Smogorzewska crosslink DNA damage kidney disease Search for Categories Science News Awards and Honors Campus News Grants Gifts Topics Video Archive 2015 2014 2013 2012 2011 more About Contact Follow

    Original URL path: http://newswire.rockefeller.edu/tag/dna-damage/ (2016-02-13)
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  • Researchers identify DNA damage repair gene in Fanconi anemia pathway | Newswire
    a disorder that leads to bone marrow failure and leukemia among other cancers as well as many developmental abnormalities Seeking other proteins that may play a part in the disease Smogorzewska and colleagues developed a test to screen thousands of genes for those that might be involved in repairing DNA damage Using a vast library of small hairpin RNAs which can silence genes by preventing their transcripts from being translated into proteins the team eliminated each of more than 32 000 human proteins from cells in the test tube The researchers bombarded the defective cells with a molecule that causes crosslinks to test whether the missing protein impaired the cells ability to survive after the damage These tests winnowed the list to 2 000 genes Then we had to narrow it down Smogorzewska says So we did additional assays looked at the domain architecture of candidate proteins and found one that is particularly interesting A gene which they dubbed FAN1 had two properties that suggested it could be important to DNA repair One region of the gene coded for what s called a nuclease an enzyme that cuts nucleic acids the stuff that makes up DNA It also had a UBZ domain which usually binds proteins that are embellished by ubiquitin a very common modification found during DNA damage response generally that is essential during crosslink repair The team wanted to confirm FAN1 s role in DNA damage response so they tagged the gene with a fluorescent protein and studied what happened when they damaged DNA both by using a laser to cut the DNA and a molecule that induced inter strand crosslinks FAN1 glommed onto sites of the DNA damage The researchers found that when they induced a mutation in the UBZ domain of the gene it was rendered

    Original URL path: http://newswire.rockefeller.edu/2010/07/20/researchers-identify-dna-damage-repair-gene-in-fanconi-anemia-pathway/ (2016-02-13)
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  • FAN1 | Newswire
    involved in guarding against a particularly dangerous peril called the inter strand crosslink when two strands of DNA become stuck together and can t be unzipped for their proper replication or transcription A mutation in the gene that produces this protein may lead to the deadly cancer causing disorder known as Fanconi anemia and may be involved in breast cancer as well the experiments show More Tags Agata Smogorzewska FAN1

    Original URL path: http://newswire.rockefeller.edu/tag/fan1/ (2016-02-13)
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  • Two proteins act as molecular tailors in DNA repair | Newswire
    Our cells encounter on average 10 inter strand crosslinks a day says Agata Smogorzewska head of the Laboratory of Genome Maintenance at Rockefeller University We suspected that these two proteins directly participated in the repair process Until now we knew that they localized to the sites of damage but we had no idea what they were doing there This work breaks that barrier The two proteins called FANCI and FANCD2 are part of the Fanconi anemia pathway which repairs inter strand crosslinks If any one of the 13 proteins in this pathway is damaged the result is Fanconi anemia a blood disorder that leads to bone marrow failure and leukemia among other cancers as well as many physiological defects In 2007 when Smogorzewska discovered FANCI it was shown that the protein formed a complex with FANCD2 which is then chemically altered through a process called ubiquitylation The chemically altered complex is then recruited to the site of the crosslink where it joins forces with other repair molecules Beyond these details the researchers knew that repair involves snipping out and replacing the damaged DNA but didn t know if FANCI and FANCD2 play a role in this molecular tailoring Using a specialized cell system of frog egg extracts the researchers found that the two proteins are essential in the excision and insertion steps providing powerful evidence that Fanconi anemia is a bona fide DNA repair disorder explains Smogorzewska The finding also explains why cells taken from Fanconi anemia patients die when exposed to inter strand crosslink inducing agents such as chemotherapy drugs The beauty of this work is that we now have a system that enables us to explore the behavior of other key proteins in Fanconi anemia and form a picture of how they all work together says Smogorzewska This

    Original URL path: http://newswire.rockefeller.edu/2009/11/12/two-proteins-act-as-molecular-tailors-in-dna-repair/ (2016-02-13)
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