I read a recent article which examined the neuromodulators and neurotransmitter systems involved with reinforcing properties of food. Essentially, when you eat, your brain releases a whole slew of chemicals (dopamine, opioids, serotonin). The article found a good amount of evidence to suggest that dopamine (DA) may be the neurotransmitter that most strongly links the genetic and environmental factors which contribute to obesity. Most of this evidence pointed to previous studies involving rats that demonstrated DA D2 receptor antagonists can enhance meal size and duration of feeding.

Trying to find the role of DA in addiction was a bit more difficult of an undertaking. Animal studies have shown that cocaine, the most reinforcing of abused drugs, blocks the dopamine transporters, which leads to compulsive drug administration. DA D2 receptor levels have been shown to mediate reinforcing responses to drugs of abuse. Those with lower DA D2 receptor levels have demonstrated more feelings of pleasantness and euphoria when dosed with a stimulant drug, methylphenidate. However, this only links people with lower DA D2 receptor levels to having a higher inclination to liking drugs rather than having a higher likelihood to become addicted. That being said, there have also been studies demonstrating higher levels of addiction in individuals with reduced DA D2 receptors, reflecting a “Reward Deficiency Syndrome” that is less sensitive to reward stimuli. Essentially, those with lower dopamine receptor levels are less fulfilled by activities that induce the release of dopamine.

This idea about “Reward Deficiency Syndrome” seems to link almost seamlessly to overeating as having a lower sensitivity to reward stimuli would make people more vulnerable to food intake as a way to compensate for this perceived deficit. This raises interesting possibilities in the treatment of obesity as one possible treatment might involve improving DA function. This type of creativity used to find parallels between seemingly disparate activities (obesity and drug abuse) is not only a fascinating to think about, but also bears amazing practical implications.

By-line:

Mariana Ashley is a freelance writer who particularly enjoys writing about online colleges. She loves receiving reader feedback, which can be directed to mariana.ashley031 @gmail.com.

Recently, scientists at Massachusetts’ premiere research institution, Massachusetts Institute of Technology (MIT), have discovered evidence that points to a specific gene they believe controls the spread of the mutated cells in an aggressive kind of cancer called small cell lung cancer.

To uncover this evidence, the researchers used a newly developed method called whole-genome profiling.  The process of whole-genome profiling is like taking a genetic fingerprint of multiple subjects, and then comparing the results to highlight similarities, differences, and aberrations.

In the lab, scientists were able to follow the progression of the cancer from start to finish in mice.  Humans diagnosed with small cell lung cancer typically die within five years of being diagnosed.  The cancer spreads so quickly, in fact, that researchers are unable to study it, because people are very frequently diagnosed late in the disease’s progression.

With the mice, however, who were developed without two important tumor-suppressing genes, they could track the cancer’s metastasis and from there — using whole-genome profiling — isolate chromosomes that had been deleted or duplicated.  In the case of small cell lung cancer, a few short strands of genetic code had been replicated in the mice, specifically a piece of chromosome 4, including a gene known as Nuclear Factor I/B, or NFIB.

While MIT scientists are uncertain of NFIB’s precise role, they do know that it does play a part in the generation of lung cells.  Furthermore, when their findings were compared with some from another important cancer research facility, the Dana-Farber Cancer Institute, they discovered that NFIB is also duplicated in human small cell lung tumors.

Current knowledge of NFIB suggests that it codes for a transcription factor — it controls the expression of other genes — so MIT scientists now are beginning to search for the other genes associated with NFIB.

Developments like this are pivotal as scientists seek the elusive cure for cancer.  This new information about overexpressed NFIB in small cell lung cancer, for example, will probably drive new pharmaceutical campaigns that will attempt to target and slow or stop the mutation in humans, thus at least halting the progression of one very aggressive kind of cancer.

Byline:

This is a guest post by Jane Smith from background check. She is a Houston based freelance writer and blogger. Questions and comments can be sent to: janesmth161 @ gmail.com

What is PCR?

PCR is a technology based machine that is used in the field of biotechnology. PCR is used for the amplification of DNA- producing accurate copies of single-stranded sequence. It is used to amplify a sample of DNA when there isn’t enough to analyze (sample of DNA from a crime scene, archeological samples).

Functionality and Importance of PCR

It is a very important and helpful tool in the field of molecular biology, genetics, forensic, evolution, paternity testing and mutation. During the working of PCR a reaction takes place commonly known as PCR reaction. Reaction requires several components to function i.e., template DNA, oligonucleotide primers, deoxynucleotide triphosphates (dNTPs), magnesium chloride, key ingredient, DNA polymerase and taq polymerase that is obtained from the thermostable bacterium Thermus aquaticus most commonly used to drive the replication process. Primer is also a very important component of the reaction. Primers are short sequences of nucleotides designed to bind either side of the region of interest on the DNA molecule to be analyzed. Fragment of a DNA is double stranded.

Steps of PCR

PCR reaction consists of three main steps that are denaturation, annealing and extension.

1. Denaturation: One to several minutes at 94-96 C° during which the DNA denatured into single strands.
2. Annealing: At 50-65 C ° during which the primers hybridize or “anneal” (by way of hydrogen bonds) to their complementary sequences on either side of the target sequence.
3. Extention : For fragments up to 3 kb primer extension is normally carried out  at 72 C ° during which the polymerase binds and extends a complementary DNA strand from each primer and add approximately 60 bases per second at 72C°.

During the whole process PCR machine works like a copying machine. Each cycle result in a doubling of the starting template material. In a standard 30-cycle reaction a single template molecule can produce over 250 million copies.

Applications and General Use of PCR:

• Method of identifying a gene of interest, or to test for disease.
• PCR detect and identify bacteria and viruses causing infections such as tuberculosis, HIV, and many others.
• Once primer’s designed for the DNA of a specific organism, using PCR to detect the presence or absence of a pathogen in a patient’s blood or tissues simple experiment.
• Used in genetic testing to determine whether patients carry a genetic mutation that could be passed on to their children (e.g. the mutation)
• Used to detect evolutionary relationships on ancient samples.
• Genes from various related organisms amplified, sequenced and then analyzed for similarities/differences.
• If two organisms have very similar genetic sequences, they are most likely closely related.

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The prostate is a doughnut-shaped composite organ apart of the male reproductive system which is located under the bladder, and in front of the bowel.  The prostate stores and secretes an alkaline fluid consisting of semen (20%-30%), spermatazoa, and seminal vesicle fluid.  Spermatazoa expelled in prostatic fluid have better motility, longer survival and better protection over DNA than that expelled with seminal vesicular fluid.

According to the Prostate Cancer Foundation, prostate cancer is the most common cancer in America not relative to the skin, with breast cancer (also relative to high estrogen) effecting women in almost equal numbers.

Estrogen

Prior to the 21st century, estrogen was considered a carcinogen.  Both recent and older studies have evidence against estrogen as a contributor to inflammation, disease, and cancer.  Certain researchers and endocrinologists, such as Ray Peat, Ph.D. agree with pre-21st century assessment, as Peat states the following,

“In good health, an animal’s systems are designed so that certain tissues will be intensely but briefly stimulated by estrogen. This stimulation by estrogen doesn’t produce the normal amount of carbon dioxide, so the tissue experiences oxygen deprivation, leading to swelling and cell division. (Along with the reduced carbon dioxide production, there is increased lipid peroxidation). Any similar stimulation, whether it’s produced by soot, or suffocation, or irradiation, will produce the broad range of estrogen’s effects, beginning with inflammation but ending with atrophy or cancer if it is too prolonged.”

Evidence: link between prostate cancer and estrogen

In the Journal of Cellular Biochemistry (Volume 102, Issue 4), Giuseppe Carruba produced an article entitled “Estrogen and prostate cancer: An eclipsed truth in an androgen-dominated scenario” (pages 899-911, 1 November 2007)  In the abstract, he explains that prostate cancer in humans is generally considered a paradigm of androgen-dependent tumor, but that estrogen’s role in the prostate is equally as important.  He explains the same accumulation of steroid derivatives with distinct biological activities occurs similarly in hydroxylated estrogens in the human breast.  He goes on to state that there is long-term evidence that administration of estrogens and androgens combined create prostate cancer in rats.  He concludes that estrogen plays a critical role in prostate cancer, and should be more considered than androgens alone.

Causes of raised estrogen

Radiation, birth control, stress, gut inflammation/irritation, unsaturated oils and hypothyroidism all commonly contribute to high amounts of the hormone estrogen.  Obviously in males, they should not worry about a contraceptive pill.  However, the diet of Americans is extremely high in unsaturated oils (popular in almost all restaurants, fast food chains, and processed foods), as well as additives and allergens which contribute to digestive disruption.  It’s commonly advocated to strenuously exercise (a form of stress), and reduce levels of salt (reducing progesterone production).  Elevated estrogen in either gender is possible, and with the evidence of it’s impact on prostate cancer, it seems best to avoid it, and hope for further research.

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The authors of the study modeled depression on mice to investigate susceptibility to depression symptoms such as anhedonia, anxiety and loss of interest. Mice were exposed to mild stress over a period of six weeks and were then tested for symptoms of depression against a control group that was not exposed to stress using standard tests for mouse depression models. Notable differences were observed within the experimental, stressed group. Only some of the stressed mice exhibited symptoms of depression, while others showed little or no change in behavior. The depressive symptoms were reversed by the administration of a trycyclic antidepressant.

To examine the differences between the stress-susceptible and stress-resilient mice the authors of the study looked at mRNA expression of neurotrophic factors in different regions of the brain. The most notable differences were observed in the expression of glial cell-derived neurotrophic factor (Gdnf) in the striatum. Chronic stress was shown to reduce Gdnf expression in the stress-susceptible mice, but not in the stress-resilient mice. This difference was traced to the epigenetic status of the Gdnf promoter. In stress-susceptible mice the promoter of Gdnf was shown to be bound by significantly fewer acetylated histones. The authors of the study show that the main difference between these two groups of mice is the level of expression of certain histone deacetylases. The susceptibility to depression exhibited by some of the mice can be explained by an increase in histone deacetylase expression in reaction to chronic stress. The other mice did not exhibit such increase and, therefore, did not develop depressive symptoms.

This study is a major step toward elucidating the molecular basis for variability in depression susceptibility. The causes of epigenetic differences at the Gdnf promoter remain unknown but can most likely be attributed to various environmental and genetic factors. The epigenetic basis of this variability also points to new pharmocological targets for antidepressants. While drugs currently used to treat depression fall into the categories of tricyclics and seratonin reuptake inhibitors, histone deacetylase inhibitors could also prove to be effective.

By-line:
This guest post is contributed by Barbara Jolie, who writes for online classes. She welcomes your comments at her email Id: barbara.jolie876@gmail.com.

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Proc Natl Acad Sci U S A. 2011 Apr 11. [Epub ahead of print]

Loss of lysine-specific demethylase 1 nonautonomously causes stem cell tumors in the Drosophila ovary.

Eliazer S, Shalaby NA, Buszczak M.

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148.
Abstract

Specialized microenvironments called niches keep stem cells in an undifferentiated and self-renewing state. Dedicated stromal cells form niches by producing a variety of factors that act directly on stem cells. The size and signaling output of niches must be finely tuned to ensure proper tissue homeostasis. Although advances have been made in identifying factors that promote niche cell fate, the mechanisms that restrict niche cell formation during development and limit niche signaling output in adults remain poorly understood. Here, we show that the histone lysine-specific demethylase 1 (Lsd1) regulates the size of the germline stem cell (GSC) niche in Drosophila ovaries. GSC maintenance depends on bone morphogenetic protein (BMP) signals produced by a small cluster of cap cells located at the anterior tip of the germarium. Lsd1 null mutant ovaries carry small germline tumors containing an expanded number of GSC-like cells with round fusomes that display ectopic BMP signal responsiveness away from the normal niche. Clonal analysis and cell type-specific rescue experiments demonstrate that Lsd1 functions within the escort cells (ECs) that reside immediately adjacent to cap cells and prevents them from ectopically producing niche-specific signals. Temporally restricted gene knockdown experiments suggest that Lsd1 functions both during development, to specify EC fate, and in adulthood, to prevent ECs from forming ectopic niches independent of changes in cell fate. Further analysis shows that Lsd1 functions to repress decapentaplegic (dpp) expression in adult germaria. The role of Lsd1 in regulating niche-specific signals may have important implications for understanding how disruption of its mammalian homolog contributes to cancer and metastasis.

PMID: 21482791 [PubMed - as supplied by publisher]

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It is interesting to see another related research about ecdysone and GSC control (link).

EMBO J. 2011 Mar 18. [Epub ahead of print]

Ecdysteroids affect Drosophila ovarian stem cell niche formation and early germline differentiation.

König A, Yatsenko AS, Weiss M, Shcherbata HR.

Max Planck Research Group of Gene Expression and Signaling, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.
Abstract

Previously, it has been shown that in Drosophila steroid hormones are required for progression of oogenesis during late stages of egg maturation. Here, we show that ecdysteroids regulate progression through the early steps of germ cell lineage. Upon ecdysone signalling deficit germline stem cell progeny delay to switch on a differentiation programme. This differentiation impediment is associated with reduced TGF-β signalling in the germline and increased levels of cell adhesion complexes and cytoskeletal proteins in somatic escort cells. A co-activator of the ecdysone receptor, Taiman is the spatially restricted regulator of the ecdysone signalling pathway in soma. Additionally, when ecdysone signalling is perturbed during the process of somatic stem cell niche establishment enlarged functional niches able to host additional stem cells are formed.

PMID: 21423150 [PubMed - as supplied by publisher]

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Researchers at the St. Jude Children’s Research Hospital in Memphis have found that breastfeeding helps women who have survived cancer in childhood, and decreases their risk of obesity and weak bones, conditions which are typically associated with cancer survivors. People who have been affected by cancer early in their lives and who beat the disease are known to be prone to health problems later in life – known as “late effects”, these conditions weaken survivors and affect their ability to lead a normal and healthy life, even though they are free of the cancer.

In women who have survived childhood cancer, there are three late effects that are commonly observed – bone mineral density deficits which lead to brittle bones and the development of early osteoporosis, metabolic syndrome which generally leads to increased BMI, obesity (survivors of lymphocytic leukemia and those who have had bone marrow transplantations are at a high risk for obesity), diabetes and cardiovascular disease, and the risk of developing cancer (most commonly breast cancer). Cancer survivors who breastfeed their children have shown that they are at the least risk for all three late effects. In addition to this, they can improve the quality of their health by adhering to the right diet, following a regular exercise routine, avoiding smoking, and engaging in safe sexual behavior.

Survival rates for childhood cancers are improving by the day – according to Cancer Research UK, for every 10 children diagnosed with cancer, as many as 8 beat the disease and survive for five years or more, a higher number when compared with the 3 out of 10 that survived in the late 1960s. These numbers can be boosted by encouraging women who have survived cancer to breastfeed their children.

Studies in cancer biology have also allowed us to realize that children who have survived cancer may have their growth hormones affected by the radiation and chemotherapy, and as a result, may be unable to lactate as young mothers. They should be provided with the right support to be able to breastfeed, whenever it is possible for them to do so. Breastfeeding also reduces the risk of breast cancer which women cancer survivors are easily prone to.

Thanks to the advances in cancer biology and health science programs, we can improve the quality of life for cancer survivors, and minimize their future cancer risks as well.

—-
This guest post is contributed by Tina Marconi, she writes on the topic of online vet tech programs .  She welcomes your comments at her email id: tinamarconi85[@]gmail[.]com.

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Physicians Group Management (PGM) is such one of medical billing companies with solutions for medical practice, providing medical billing and practice management services to physicians and healthcare facilities. They can provide a range of services and products to fully cover the entire medical practice workflow.

In particular, the EMR systems they offer are powerful, yet easy-to-use platforms in practice management. The emr software programs used by physicians are the popular Amazing Charts.

You can visit their website to learn more about their PGM products and services.

Cell, Volume 143, Issue 6, 978-990, 10 December 2010
Copyright © 2010 Elsevier Inc. All rights reserved.
10.1016/j.cell.2010.11.022

Authors
Laixin Xia, Shunji Jia, Shoujun Huang, Hailong Wang, Yuanxiang Zhu, Yanjun Mu, Lijuan Kan, Wenjing Zheng, Di Wu, Xiaoming Li, Qinmiao Sun, Anming Meng, Dahua Chensend emailSee Affiliations

Highlights

• CB differentiation involves antagonism of BMP signaling through regulation of Tkv
• Fu regulates CB differentiation by antagonizing BMP signal via interaction with Tkv
• Fu acts in concert with Smurf to terminate BMP signal by ubiquitinating Tkv in CBs
• Fu has a conserved role in antagonizing BMP/TGFβ signals from fly to vertebrate

Summary

In the Drosophila ovary, germline stem cells (GSCs) are maintained primarily by bone morphogenetic protein (BMP) ligands produced by the stromal cells of the niche. This signaling represses GSC differentiation by blocking the transcription of the differentiation factor Bam. Remarkably, bam transcription begins only one cell diameter away from the GSC in the daughter cystoblasts (CBs). How this steep gradient of response to BMP signaling is formed has been unclear. Here, we show that Fused (Fu), a serine/threonine kinase that regulates Hedgehog, functions in concert with the E3 ligase Smurf to regulate ubiquitination and proteolysis of the BMP receptor Thickveins in CBs. This regulation generates a steep gradient of BMP activity between GSCs and CBs, allowing for bam expression on CBs and concomitant differentiation. We observed similar roles for Fu during embryonic development in zebrafish and in human cell culture, implying broad conservation of this mechanism.

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