Can cancer drugs help overcome antibiotic resistance?

Can cancer drugs help overcome antibiotic resistance? In a new study published in the Cell journal Chemistry and Biology, Dr. Gerry Wright and colleagues have systematically screened drugs called protein kinase inhibitors and found several candidate compounds that can prevent antibiotic resistance.

With the increased (and almost ubiquitous) use of antibiotics -- from taking antibiotics unnecessarily to fight a virus to the overuse in antibacterial handsoaps -- resistance to we are rapidly running out of effective antibiotics. In an attempt to identify potential new drugs to prevent or overcome such resistance, Dr. Wright’s group tested 80 protein kinase inhibitors, many of which were developed as anti-cancer agents.

So, what’s the connection? Protein kinases are molecules in the cell that respond rapidly to external stimuli. For example, an increase in growth-promoting hormones in the body leads to the activation of protein kinases and results in rapid changes in the cell that leads to growth and proliferation. Protein kinases act as the middle-man that handles the exchange from the outside environment to the response of the cell. Most of the time this is a good thing. It allows for regrowth of skin after wounding and allows for the turnover of the cells in our body to create new ones. Prolonged over-activation of these kinases, however, can be detrimental and is commonly found in cancer cells. New drugs that prevent the activation of these protein kinases (aka protein kinase inhibitors) are being developed to help fight cancers and prevent such growth and proliferation. It turns out that many of these same protein kinases may also be inappropriately activated and therefore contribute to the development of antibiotic resistance. This study sheds some light into new ways to overcome antibiotic resistance.

http://www.cell.com/chemistry-biology/abstract/S1074-5521(11)00411-X

Have a question or comment? Send me an email -- jck@n3scicom.com


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New vaccines for breast cancer and ebola being developed

Two articles published in this week’s Early Edition of the Proceedings of the National Academies of Science (PNAS) explore the efficacy of new vaccines -- one against the deadly Ebola virus and the second targeting breast cancer tumors. In addition to the reported efficacy of each vaccine, what is interesting about these two papers is that in both cases, the addition of a specific type of adjuvant (an adjuvant is an agent that by itself does little, but when it is given along with a vaccine or drug will improve the efficacy of that drug by inducing a stronger immune response) dramatically improved the responses to the vaccine and produced a therapeutic response. In both studies, the administration of the vaccine alone without the adjuvant did little to induce a response.

Both groups used a protein called the Toll-like receptor (TLR) agonist as the adjuvant of choice. The Ebola vaccine was given with a TLR3 agonist called poly I, poly C or poly I:C, while the breast cancer vaccine was given along with a TLR2 agonist called PamCys. Although use of TLR agonists as cancer vaccine agonists is not a new idea, it is intriguing to see two non-overlapping fields use similar agents to help augment the immune responses and to eliminate a virus or tumor cell. It would seem that TLR adjuvants are very powerful agents to help induce the proper immune response and fight off viral and tumor invasion. Use of similar agents is very disparate diseases bodes well for usefulness of these TLR agonists in therapeutic settings.

Have a question or comment? Send me an email -- jck@n3scicom.com

Lakshminarayanan, V et. al. PNAS 2011 Dec 14
http://www.pnas.org/content/early/2011/12/13/1115166109.long

Phoolcharoen, W. et. al. PNAS 2011 Dec 5
http://www.pnas.org/content/early/2011/11/29/1117715108.long

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Bacteria can influence weight

Yet another study has linked the profile of bacteria found in your colon (called the microbiome) to obesity and weight gain. This paper, published in Nature Reviews Endocrinology (7:639-646), reviewed the latest studies to investigate the contribution of bacteria to nutrient metabolism and obesity. Their review has demonstrated that numerous studies have begun to understand the influence of the profile of bacteria in the control of overall weight. Together, all of these studies suggest that the microbiome may be a critical player in metabolism and can influence weight gain or loss.

Awareness of symptoms/risk factors for colorectal cancer is low

A new study by Dr. Emily Power and colleagues, published in the journal BMC Cancer , indicates that awareness of the symptoms or risk factors for colorectal cancer is low.

Participants were asked to recall the symptoms of colorectal cancer (changes in normal bowel habit, rectal bleeding, blood in the stool, lump in the abdomen, or unexplained extreme tiredness) and risk factors for colorectal cancer (family history, high consumption of red/processed meat, increased body fat/obesity, or alcohol consumption).

Overall, respondents were able to recall just 1 symptom and 1 risk factor. Women faired better than men in ability to recall symptoms, while men outperformed women in the recall of risk factors. Older participants were more aware of symptoms and risk factors than young participants. While this study was conducted among participants only in the UK, this paper highlights the critical need for increased education of the symptoms and risk factors associated with colorectal cancer.

Clear here to read the paper.

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Lung cancer rates decline in the US!

The Center for Disease Control and Prevention (CDC) just released the results of a study assessing smoking rates and the incidence of lung cancer in the US. While the incidence of lung cancer has been steadily declining in men over the past few years, in women, a decrease in incidence was evident for the first time. This decline in lung cancer correlated with a decrease in smoking rates in both men and women, indicating a link between smoking and lung cancer.

According to the CDC, smoking costs $193 billion, $96 billion in health related costs and an additional $97 billion in productivity loss due to illness and premature death.

For more information and access to the report, visit the CDC Vital Signs Adult Smoking web page. (or click here).


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Funding NIH grants

A group called the Traditional Values Coalition has just released an action alert asking their members/followers to contact their Congressmen. They want people to demand that Congress freeze funding of what they refer to as "bizarre" and "questionable" NIH research projects. It is unclear what constitutes a "bizarre" or "questionable" project or who will be the one to make such a decision, however, according to this group this type of work should be halted. This is a clear attempt to just push their agenda.

All NIH research projects are peer-reviewed. This means that the experts in the field have donated their time to review and critically assess each grant. In fact, each grant is read and critiqued by at least three researchers within a panel. After the initial review, these professionals then get together to debate the merits and limitations of each grant to decide which proposals are so exceptional that they are worthy of funding. Through this rigorous process only the best proposals are funded.

With the economy in such a weak state and funding for research at an all time low, competitiveness for grants has increased significantly. Therefore, only a small fraction of these meritorious projects are actually receiving money. Indeed, estimates are that less than 10% of all grants submitted per cycle are actually funded.

Why should those outside the field, those who are not experts on these topics, be able to stop these research projects? Please, leave the decisions about what science should be funded to the experts who are best able to judge the projects.

A new cancer vaccine

It has been a relatively long standing theory that an effective cancer vaccine can and will be created. Such a vaccine would infect and replicate only in cancer cells and would leave normal cells unscathed. A new publication in the journal Nature (477:99-102 at nature.com) demonstrates that researchers have conducted the first clinical trial demonstrating efficacy of just such a cancer vaccine.

Using vaccinia virus, the virus used to develop the small pox vaccine, Dr. Breitbach and colleagues engineered a virus that can seek out and infect cells that express the protein EGFR, a protein that is commonly elevated in cancers. In fact, the vaccinia virus can only live and replicate in cells with EGFR overexpression. Their data show that this engineered virus can be injected intravenously and can selectively infected cancer cells (but not normal cells). When the virus finds and infects these cancer cells, it can effectively kill them. Importantly, by using this vaccinia virus technique, researchers were able to produce high enough levels of vaccine to eliminate a significant amount of the tumor. This is a big step forward towards the development a new therapy in patients.

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HDAC4 regulates fasting/feeding states

Many studies have shown that the control of lipid (fat) stores during fasting and feeding states is largely dependent on SIRT1 and FoxO activity. This latest study investigates the role of these proteins in obesity and adds another level of regulation to the mix.

Using a drosophila model, Wang et. al. (Cell 145:596-606) provide evidence that the serine/threonine salt-inducible kinase (SIK) 3 controls lipid storage or lipolysis in a HDAC4/FoxO dependent manner. During feeding, insulin activates SIK3 (its mammalian homolog is SIK2), phosphorylates HDAC4, which prevents its activation and subsequent movement to the nuclear compartment. This inhibits the deacetylation and activation of FoxO and ultimately increases lipid storage. Under fasting conditions, SIK3 activity is inhibited, HDAC4 remains in an active, dephosphorylated state where it can easily translocate to the nucleus. In the nucleus, HDAC4 deacetylates and activates FoxO to increase lipolysis as a mechanism to provide energy to the starving organism. When the organism re-feeds, FoxO is acetylated via the action of p300 and CBP and HDAC4 is re-phosphorylated. Therefore, HDAC4 activity is a critical regulator of fasting or feeding states.

This pathway is not limited to drosophila. Using a mouse hepatocyte cell line, Wang et. al. confirm their findings in mammals, suggesting a universality of this mechanism.

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Nicotine suppresses appetite by activation of neurons of the arcuate nucleus

Many people use smoking as a mechanism to suppresses appetite and control their body weight. Nicotine in cigarettes is the culprit, affecting peripheral energy expenditures, but also affecting the central nervous system to regulate feeding. Mineur et. al.(Science 332:1330-1332) have now uncovered some the of the molecular steps involved in nicotine-induced anorexia. In mouse models, nicotine binds to the nicotinic acetylcholine receptor (nAChR) in the arcuate nucleus (ARC) region of the brain. Here it activates the pro-opiomelanocortin (POMC) neurons that begin to fire more frequently. This stimulates downstream melanocortin 4 receptors, ultimately releasing melanocortin, a known inhibitor of feeding behavior. The hope is that this work can lead to the development of new therapy to treat obesity and other metabolic syndromes.

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A new protein that controls obesity

Obesity is on the rise. Our diets aren’t healthy (or low in calories) and we are increasingly sedentary. Many scientists are researching how to control obesity and how to prevent obesity-related diseases including diabetes, cardiovascular disease and cancers. A new study by Zhang et al (Journal of Biological Chemistry 286:28396 August 12, 2011) identifies another player in the regulation of body mass and obesity. This protein, beta-arrestin 1, appears to regulate the expression of genes involved in metabolism and in inflammation. Since both are linked to many obesity-related diseases, these investigators investigated its role in obesity. Elimination of the gene increases body mass and metabolic dysregulation in mice fed a high fat diet. Conversely, overexpression of beta-arrestin 1 reversed these effects and restored normal weight, even in the presence of excess calories. While this is far from a magic pill to control weight and obesity, it does provide insight into how the body regulates weight and its metabolism.

Access to the internet is changing what we remember

A new study in Science Magazine by Drs. Sparrow, Liu, and Wegner (vol 333: 776, Aug 2011), demonstrates that we are using the internet as an external memory source to provide access to all the information we want to retain. All we have to do is remember how we found it.

Their data show that if we know we can just search for info again, we remember the website where we found the answer. Likewise, if we download the data, we recall the folder where it is stored. In either case, we are not as likely to remember the data itself. However, if we think the information is erased, our own recall of the information is pretty accurate. This study indicates that we are increasingly relying on having constant access as an external memory source (the internet). We just have to remember how we got there to find it!

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A new player in tumor metastasis

Primary tumors metastasize to distant locations through a process called endothelial to mesenchymal transition (EMT). Tumor cells have to move from the primary location, enter the bloodstream, travel to the distant site, enter that tissue and begin to grow in the new environment. In order to accomplish this, tumor cells alter the genes that are expressed. Breast tumor cells, for example, are epithelial cells that have begun to grow uncontrollably. As these cells emerge from the breast and enter into the bloodstream, many genes that define the tumor as a epithelial cell are switched off and genes that allow for movement (mesechymal genes) are turned on. Therefore, due to changes in the gene expression, primary breast tumors emerge from the breast, enter the bloodstream, and migrate to the lung where metastatic disease occurs. Scientists can detect the profiles of genes that change when tumors become metastatic, but how this switch occurs still remains unclear.

In a recent article in Oncogene (2011, 30:3440-3453) Dr. Xiang and colleagues at the University of Louisville, the University of Alabama, and the Louisville Veterans Administration Medical Center have provided new insight into how these genes are activated or inhibited. Their study shows that a gene regulator, called miR-155, acts as a switch that prevents breast tumor cells from migrating from the breast into the blood. Surprisingly, they also found that miR-155 can promote the formation of lung metastases if the tumor cells have already entered the bloodstream. While miR-155 appears to decrease the expression of genes involved in EMT and movement from the primary site, if tumor cells do manage to migrate, miR-155 can help promote their migration and growth in the lung. This is a bit of a double edged sword. These data do suggest that activation of miR-155 when breast tumor cells are confined only within the breast could be effective to prevent metastasis, however if the breast cells have already left the breast location, then activation of miR-155 will promote metastasis.

Skin cells produce their own cortisol

The ability of our skin to maintain and repair its integrity is crucial to our survival. Upon wounding, an inflammatory response is initiated, followed by wound healing and regrowth of the skin layers, or skin epithelium. This inflammatory response is mediated by proteins including the cytokine interleukin-1 (IL-1) that occurs in the skin at the site of injury. IL-1 stimulates the production of glucocorticoids (cortisol) that are tasked to ward off any infiltrating foreign agents prior to initiation of wound repair.

Cortisol is a glucocorticoid steroid hormone that is released in when the immune response is in full swing. Until now, it has been thought that the adrenals were the only site of cortisol production. In this recent paper, Dr. S. Vukelic and colleagues (Journal of Biological Chemistry 286: 10265-10274, March 25, 2011) clearly demonstrate both in cell based (in vitro) and in animal based (in vivo) models that corticol synthesis occurs within the epithelium itself. This is the first evidence that local production of cortisol by specialized skin cells termed kertinocytes can control the local inflammatory response. Indeed, Vukelic et. al. demonstrate that keratinocytes contain the proper enzymes for corticol conversion from cholesterol precursors including CYP11B1, the cytochrome P450 gene necessary for the final conversion step to cortisol. The production of cortisol in keratintocytes is equivalent to that produced by the adrenals. Production peaks at 48 hours after injury and is followed by wound repair and skin regrowth.

This paper is significant because it suggests that local production of glucocorticoids may have clinical significance by influencing the rate of repair after injury.

CD40 co-activation increases patient survival in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDA) is a lethal disease. Only a small number of patients qualify for surgery and among those, few survive longer than 5 years. Current standard of care is chemotherapy (gemcitabine treatment), however this treatment, unfortunately, has limited efficacy.

New evidence reported in Science Magazine (Science 331:1612-1616, March 25, 2011) shows that preventing the activation of white blood cells or leukocytes, which are in high concentration in the tissues surrounding the pancreatic tumor, may improve the overall survival rate of patients. Dr. GL Beatty and colleagues are studying in mice how blocking a protein on the leukocytes, called CD40, can prevent the suppression of the immune system. This would allow for the patient’s own immune cells (macrophages) to attack the tumor to destroy it. In their mouse models, the combination of gemcitabine + anti-CD40 treatment helps promote survival cancer ridden mice. These data show promise for developing new therapeutic approaches to treat pancreatic ductal carcinoma.

New mutations found in Head and Neck cancer

Efforts are underway to identify the mutations in tumor cells that may give rise to cancer. Analysis of mutations in tumors from patients with head and neck squamous cell carcinoma (HNSCC) identified some familiar players (TP53, CDKN2A, PTEN, PIK3CA, HRAS ) along with some new faces (NOTCH, IRF6, TP63, CASP8, EZH2).

HNSCC is the 6th most common non-skin cancer. Risk factors that contribute to the development of HNSCC include tobacco, alcohol, and human papilloma virus infection. By comparing the sequence of genes (via a process called exon sequencing) in the tumors of patients with HNSCC with the sequence in normal, non-cancerous cells in their blood, Nicolas Stransky and colleagues have identified new mutations that were not previously known to be altered in HNSCC. These findings, published in Science Express on July 28, 2011 (DOI 10.1126/science.1208130) www.sciencemag.org, offer new insight into the regulation of HNSCC. Further, this data offers potential new targets to attack to prevent continued tumor growth.

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US judge decides in favor of federally funded stem cell research

The US District Court judge ruled today that NIH is allowed to fund research on cell lines derived from human embryos as long as it does not fund the creation of the lines. This means that federal funding can be used for research using the existing embryonic cell lines.

To read the summary of the decision, click here.

Are taller women at higher risk for cancer?

The average height of men in the US is 5 ft 9 1/5 inches. Women in the US, on average, are a commanding 5 ft 4 inches, according to the National Health Statistics published by the CDC (Oct 2008). Being tall may have its advantages like reaching the upper cabinets or having an advantage in catching a rebound, but a recent study in Lancet Oncology revealed a downside to tallness.

According to the study by Dr. Jane Green, et. al., tall women are at higher risk for developing cancer. Analysis of data from the Million Women Study, a study of women’s health conducted in middle age women from the UK between 1996 and 2001, revealed that the risk of developing any cancer type increased along with height in women. When they looked at individual cancers, tall women had increased risk for developing colon, rectal, melanoma, breast, endometrial, ovarian, kidney, CNS, non-Hodgkin lymphoma, and leukemia cancers. This link appears to be independent of other potentially influencing factors including smoking or socioeconomic status.

Improving body image may help with weight loss

Want to lose weight? Incorporating sessions to improve body image may improve the amount lost, according to a study published today in the International Journal of Behavioral Nutrition and Physical Activity. Their results demonstrated a significant improvement in overall weight loss amounts when body image was addressed (-7.3% vs -1.7%).


BioMed Central: www.biomedcentral.com
Intl Journal of Behavioral Nutrition and Physical Activity: http://www.ukdistribute.com/links/1310722818976-Body%20image%20change%20and%20improved%20eating%20self_regulation.pdf


Obesity is a growing public health problem in the US and around the world. Current estimates indicate 25-33% of the US population is obese (defined as a body mass index > 25). With increasing lack of physical activity, these numbers are predicted to rise over the coming years. Obesity is linked to many diseases including diabetes, cardiovascular and cancer. Health care costs rise with increased obesity rates. It is not easy to lose weight, but the health and financial benefit of doing, on a personal and societal level, so far exceeds the potential risks.

Over the years, many approaches to weight loss have been published. Some are healthy options that can lead to sustained weight management. Others are fad diets that are both ineffective and unhealthy. This study addressed whether body image could be a significant factor in determining overall outcome of weight management programs. By comparing a program that incorporated sessions on body image with the same program that included general sessions about health, Carraca et. al. demonstrated a significant increase in overall weight loss when body image sessions were included (-7.3% with sessions vs -1.7% without). Body image improved and the preoccupation with societal influence on body image decreased.

There is no magic pill or fad diet that will work. It comes down to effort, desire, and commitment to increased physical activity and a healthy lifestyle. Including methods to improve body image seem to be a key component to add to the mix that may lead to successful and maintained weight loss.

Potential new biomarker for neurofibromatosis identified

Published today in BMC Medicine, scientists have found a new biomarker, MIA, for neurofibromatosis, a disease that affects 1 in 3000. Although many cases are benign cafe au lait spots, some cases can result in malignant peripheral nerve sheath tumors. Identification of a marker in the blood will help diagnosis.

This study, published by (Kolanczyk et. al.), has found that expression of a protein, called melanoma-inhibitory activity/cd-rap or MIA, can be readily detected in the blood. MIA expression is correlated with tumor burden, so the more tumors present, the higher the MIA content in the serum. This could result in a non-invasive test to detect NF1 tumors, especially for those with subcutaneous and internal tumors that are difficult to otherwise detect.

Kolanczyk et. al. BMC Medicine
http://www.biomedcentral.com/

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RNA binding protein influences chemotherapy resistance

Genes and their level of expression is important in cells. It is what gives a particular cell its unique qualities. Different levels of different genes are expressed in cells in the liver compared with those in the lung, for example. In cancer, the amount of gene expression is frequently altered, resulting in either increased concentrations (overexpression) or not quite enough (underexpression). Such alterations could lead to aberrant growth or even to resistance to current cancer chemotherapy.

Increasing evidence has been accumulating that implicate an RNA binding protein, called HuR, in the development of chemotherapeutic resistance. Several papers in the past few years have shown that increased amounts of HuR, along with where the protein in located in the cell, can dramatically alter how a cancer cell responds to therapy. In pancreatic cancer cells, increased HuR levels in the cytoplasm of the cell significantly aids in the response to gemcitabine, the current chemotherapy for pancreatic cancer. In breast cancer, and now in glioma cells, increased HuR levels increases the resistance to currently used chemotherapy including tamoxifen, etoposide, cisplatin and topotecan.

While this data is still in the preclinical stages, and much more needs to be done before it can be used in the clinic, it still offers new insights into how resistance develops in cancer. RNA binding proteins are not particularly well studied compared with other proteins and microRNAs. It is exciting to see a slow and steady progression in this field.

Natalia Filippova et. al.
Molecular Cancer Research 9:648-659

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A significant percentage of internet addicts suffer from depression

Internet addiction is a problem for 4% of US college students, according to a recent paper by Christakis et. al., published in the BMC Medicine, June 22, 2011. Unlike previous studies that had problematic participant selection biases that inflated the percentage of those addicted to the internet, this study selected 18 - 20 year old undergraduate students from a broader audience at large public US universities.

Using facebook to select and survey these students, Christakis et. al. demonstrate that 4% of students had internet addiction and a significant proportion admitted to longer daily use of the internet than they had intended. This percentage was lower than previous reports, however it is possibly a better representation of the general population. Interestingly, they also found that 12% of participants also suffered moderate to severe depression, suggesting an overlap in these ailments. Statistical analysis of their data revealed that depressed people are 24% more likely to also have internet addiction. As internet usage continues to increase, it will be critically important to address issues of depression and loss of physical connectivity with other people.

Dimitri Christakis et. al.
BMC Medicine 2011, 9:77

http://www.biomedcentral.com/1741-7015/9/77

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deFEATing cancer

In the quest to understand how cancer develops and is spread, scientists have been searching for the gene, genes, or signaling pathways whose inappropriate expression or mutation results in disease. In a paper published in the new open access journal from Nature, Scientific Reports, Takahashi et. al. have identified a potential initiator of cancer.

They found that a protein called CGI-01 was overexpressed in many cancerous tissues, but faintly expressed, if at all, in normal tissues. This protein, which they renamed FEAT for Faintly Expressed in normal tissues, Aberrant overexpression in Tumors, appears to be turned on in early stages of pre-cancerous lesions or cancer itself. When expressed, FEAT protein inhibits cell death mechanisms, or apoptosis, leading to increased and uncontrolled cell growth. Mice expressing heaps of FEAT protein spontaneously develop either hepatocellular carcinoma (HCC), a form of liver cancer, or lymphoma, a blood cancer. More in depth analysis investigating how FEAT actually promotes cancer revealed that FEAT overexpression results in activation of cell signaling cascades, both tyrosine kinase and hedgehog signaling pathways, that have previously been implicated in cancer promotion. May this be a way to detect early stages of cancer development? If this data holds true, it could be a promising detection tool.

Atsushi Takahashi et al, Scientific Reports 1: 15.
http://www.nature.com/srep/index.html

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Gossip, Gossip, Gossip - how negative gossip influences us

Let's face it -- we gossip. Positive, neutral or negative gossip about people is spread. More often by some people than by others, but nonetheless, it exists. We even gossip about people we don't know. It turns out that our brains more readily remember unfamiliar faces when they are associated with negative gossip when compared with neutral or positive gossip. In this recent study in Science Magazine (Science 332: 1446-1448 June 17, 2011), authors, Anderson et. al., show that negative gossip actually results in longer visual focus on that face. This increases our ability to recall and remember that face.

Normally, when an emotionless and unfamiliar face is shown to us, the focus of our eyes switches back and forth between each eye. We don't perceive this switching because approximately equal amounts of time are divided between each eye and we are looking at one image. Scientists tested if this eye dominance was altered at all if the faces shown were associated with different forms of gossip. They hypothesized that gossip may increase the amount of time focused on a particular image, leading to increased memory and recall.

By showing an facial image to one eye and a separate (non-facial) to the other eye -- they used a house image -- scientists found that the dominance of the images that is seen switches back and forth between the eyes. However, when a face is associated with negative information, or gossip, more time is spent looking at that image than the non-facial image. This is not true for positive or neutral-associated faces. Does this mean that we learn better from negative information? Perhaps. But, what it does indicate is that our brains do not retain or focus on faces that associate with neutral, or non, information as readily as those that are associated with negative gossip.

Our immune systems can detect if bacteria is viable or not

Immune cells are able to recognize whether a bacteria is viable or not. This new evidence is remarkable, but why does this matter? Vaccines used to ward off disease come in two main varieties, live-attenuated (viable) or killed (dead) forms. Use of viable vaccines produces a more robust immune response. Until now, the underlying reason why has remained unknown. Sander et. al. (Nature 474: 385-389, June 10, 2011) demonstrate that an underlying reason for this is that the immune system can differentiate between viable and non-viable agents.

The presence (and detection) of prokaryotic mRNA signals to the immune system that the invading bacteria is viable and, therefore, potentially infectious. As a result, a strong immune response is initiated. It is not just presence of prokaryotic mRNA, however, but specifically, the immune cells recognize a lack of the 3’ -polyA tail on this mRNA. This means that killed virus that can retain the prokaryotic mRNA (i.e. killing with paraformaldehyde retains the mRNA) or is vaccines that are augmented with prokaryotic mRNA can produce an enhanced immune response. This could have a significant impact on vaccine design and development.

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Nicotine suppresses appetite by activation of specific neurons

Many people use smoking as a mechanism to suppresses appetite and control their body weight. Nicotine in cigarettes is the culprit, affecting peripheral energy expenditures, but also affecting the central nervous system to regulate feeding. Mineur et. al. (Science 332: 1330-1332, June 10, 2011) have now uncovered some the of the molecular steps involved in nicotine-suppressed appetite control. In mouse models, nicotine binds to its receptor (the nicotinic acetylcholine receptor or nAChR) in a specific region of the brain called the arcuate nucleus (ARC). Here nicotine activates the pro-opiomelanocortin (POMC) neurons that begin to fire more frequently. This increased neuron stimulation produces more melanocortin that is known to decrease the urge to eat. The hope is that this work can lead to the development of new therapy to treat obesity and other metabolic syndromes.

miRNAs strike again!

The ever-increasing number of articles documenting how miRNAs are key players in gene regulation, where overexpression or underexpression of a myriad of miRNAs results in disease states, continues to rise. Clearly, gene regulation is complex and control of transcription or translation is a key determinate in the development of disease. MicroRNAs are proving to be critical mediators of disease states and could potentially be therapeutic targets. Combined with other forms of regulation (epigenetic, transcriptional regulation, post-transcriptional modifications, and so on...) it will be possible to understand how cells specially fine-tune gene expression to maximize performance and prevent disease. Once a complete picture -- involving miRNAs, proteins, RNA, DNA, epigenetic mediators -- is fully realized, then real targeted therapy can be designed. But first, we must understand how each component works. Every new paper documenting how miRNAs control genes and disease is another step to understanding how to successfully target diseases with pharmacologic agents.

You've earned your science degree, so now what?

Talking with friends and colleagues over the years about their (and my own) efforts to navigate a science career, has led to a list of things to think about what to do when heading on from your student or postdoc life. I hope it is helpful. It is by no means exhaustive, just a list of things that have consistently come up over the years for me and for my friends.

So, here are a few things to think about as you wade through those murky waters!

You’ve earned a Ph.D. and maybe even completed (or are in the process of completing) a postdoc. Now what?

If you are interested in academics, it is a rewarding career. It provides tremendous freedom and flexibility. You are essentially an owner of a small business. Therefore you are in control of all of it -- hiring, firing, management, marketing, generating money, billing, advertising, and everything/anything else you can think about.

Not everyone is interested in staying in academics. This is perfectly acceptable (in some ways more than fine!). Not all scientists like the lifestyle or want to live grant to grant. Academics is changing. Dramatically changing. To add to the lack of grant funding upheaval, there aren’t enough positions available. If you were like me or countless other Ph.D.’s looking at what to do with their careers, you were advised to “look into industry”.

So, what can you do with your extensive, specific, scientific training? As one PI told me once; with a Ph.D. you successfully train yourself out of practically every job.

1. Start early to plan your next move.

I didn’t really do this too extensively and really wish I had. It is important to get the skills and training you need while you are still in graduate school or in your postdoc position. Most of the research you will do to figure out your next step will be up to you.

If you are interested in an academic career, this applies to you as well. You need to make sure you have the right background and training to get a faculty position. You will need publications and (most likely) grants. You need to show that you are productive and fundable. Money is the name of the game, so be sure you can show you know how to get it. Be sure to have a mentor who will help make this happen. If this person is not the person you are working for, you need to find someone who will fill this role for you. It is essential. You will need someone to advocate on your behalf to help you get the faculty position. Without this person, you will not succeed in moving into a tenure-track job (if tenure-track will still exist).

If you want to leave the bench, you also need to start planning early. Since most people will not understand what you are doing or why you aren’t staying in academics, you cannot rely on too many people for help. That being said, your future is your own and you need to take very good care of its planning. Think about what your skills and strengths are to see what type of career is good for you. There are many advice columns and websites that can help you start looking for a career.

When you figure out what field you may be interested in pursuing, start networking. Say, for example, you are interested in science policy. Your training will not provide anything that will help you get this type of job, so you need to rectify this issue. If you have access to classes in policy, that’s a good place to start. You might also try to volunteer in your school government relations department. You might try to volunteer for a national organization. The point is that you need to establish your background in policy beyond just saying you are have an interest in policy. Volunteering or taking classes will help you meet people who work in these fields. They can advise you much better on what you need to do or who you need to meet.

Remember it is YOUR career. Don’t let anyone distract you from your goal. If you are in a situation that is not good for you, think seriously about whether or not it is beneficial for you to stay. Leaving a postdoc before you had planned (or even after you just started) to be in another lab that is a better fit for you may not be a bad plan. It will be uncomfortable for you to leave, but it would be worse to sabotage your career because you don’t want to have the conversation.

2. Be prepared for the outcome.

If you leave a position unexpectedly or approach your PI to say that this opportunity may not be right for you, be aware that you may be asked to leave. In the end, it will probably be a good move since you were looking to leave anyway, but just be aware of this possibility.

3. Network, network, network

You need to meet as many people as possible -- and I mean outside the lab and other researchers you hang around with normally. This takes effort and time, but will pay off in the end. Go to meetings and networking events outside of academic settings. There are networking events for professionals that take place all the time. Most networking organizations will allow you to attend a few meetings without joining up, so you can test drive it to see if it is the right fit for your needs.

Remember you are networking for professional reasons, not out making new friends. When you go to these, you need to have something to offer someone. You can’t just ask for help without lending a hand or help in some fashion.

Also, have your elevator speech ready. You will need to say what you want to accomplish or what you do in 10-30 seconds (the time it takes to ride up in an elevator). If you talk too long, no one will listen.

4. First impressions mean everything.

You will never have a second chance to make a first impression. You’ve heard this one before, but it’s true. Be ready and do your homework! If you don’t have your pitch together or don’t know what path you want to go on, that’s ok (it takes time to work it out) but be ready to answer questions intelligently and succinctly.

Also, if you don’t care about what you are doing or want to do, why should anyone else?


5. Keep an open mind

Since things don’t always work out according to plan, keep an open mind. Educating yourself is never a wasted cause. If you don’t pursue a specific career path, learning about it and meeting people involved in the field will not be useless. You don’t know when or how you’ll use the information.

6. Show up

Show up every day. Even if you decide to work from home, do something career related every day. Someone once said that 90% of life is just showing up. It’s true. By going to networking events and meeting new people, or going to seminar, or being sure to make it to class, showing up means a lot. People will remember you, even if they don’t know your name or what you do. If you are there, it counts. It helps to get yourself noticed, but that is another story for another time.

7. Bring something to the table

Never show up empty handed. It’s good advice for parties and its good advice for job/career hunting. You want a specific job, come up with ways that you can improve the company through working in that position. For example, you want to be the involved in scientific business development for a non-profit. What are some ways you could increase their business? Are there new avenues that have not yet been explored? Even if you don’t use these ideas or they don’t work out, you have provided your future employer with some insight into how you think (and that you are thinking). If they have thought of the idea, then great! You obviously are thinking up some good ideas.

8. Follow through

If you say you will provide something, then do so. If you tell someone you will let them know by a specific date, then do it. This is along the lines of showing up, it’s also good manners and it will help others remember who you are. If you establish yourself as the person who finishes the job when you say you will, it will create a lasting positive impression. Conversely, if you never provide what you say you will, when you say you will, this will make a very bad impression. Nothing spreads faster than bad news about someone.

9. Follow the directions

If you are asked to provide a research plan along with your cv, then do so. If you don’t you probably won’t be considered. Why should you make someone who you want to impress work at finding out about you? Make it easier for them (and let them know you can follow simple directions) by providing the information they want to see.


10. Feed forward

Help others out. If you take advice or help from someone, be sure to turn around and help someone else. They will appreciate it just as much as you did. It’s a good way to say thank you.




There is so much potential if you remain bench-side or go off into the world of industry. Be creative about your career, but also be thoughtful. Designing a new path can combine interesting fields that have not traditionally been combined before. You won’t lose anything by exploring new options -- you might even find something you really enjoy doing!


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New CDC guidelines

The Centers for Disease Control issued the latest report in a series addressing environmental and policy factors to improve nutrition, increase physical activity and reduce obesity. This current report, the Children’s Food Environment State Indicator Report, 2011, proposes guidelines that states can implement to help improve child health. These recommendations include:


reducing amount of television viewing time

reducing the intake of sugary beverages

removing televisions from children’s bedrooms

reducing the availability of sugary, low nutrition snacks from schools and institutions

provide water as the primary beverage at day care facilities

increase access to supermarkets and health food stores

For access to the full report, visit http://www.cdc.gov/media/releases/2011/p0426_foodforchildren.html



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Potential new markers detecting heart attacks

Scientists have found that changes in expression of small RNA molecules, termed microRNAs, may be a novel way to detect acute myocardial infarction (AMI) or heart attack. Two microRNAs, miR208 and miR499, in particular were shown to be significantly increased in the blood plasma from AMI or viral myocarditis patients.

Currently, AMI can be detected by increased expression of cardiac troponin, a marker of heart damage. Scientists reported in the journal Circulation: Cardiovascular genetics (3:499-506, 2010 MF Corsten, et.al.) that miR208 and miR499 levels were correlated with those of troponin. Interestingly, expression was elevated in patients with AMI, regardless of race, sex, weight, kidney function or blood pressure levels.

Taken together this suggests that miRNA detection may be a useful new detection method for AMI. Since the process used to detect miRNAs, called realtime PCR, is very sensitive and fast, detection of miRNA208 and miR499 to diagnose AMI may be feasible in a clinic.


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Trial of HIV drug stopped

The clinical trial testing the efficacy of the oral HIV antiretroviral drug, Truvada, was terminated in South Africa yesterday. External analysis by the Independent Data Monitoring Committee determined there was no detectable decrease in HIV transmission rate between those receiving Truvada and those who did not.

This study, conducted by the Family Health International, a Durham, NC based group, tested the efficacy of daily administration of an oral formulation of Truvada in women. Testing included 2,000 women. Expectations were that a daily pill form of Truvada would be effective. Previous clinical trials of Truvada as a vaginal gel formulation resulted in a dramatic 40% decrease in transmission rates. Scientists are investigating whether this disappointing result was a consequence of the mode of drug administration or due to non-adherence/non-compliance with the daily dosing of the pills.

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Philadelphia Science Festival

Saturday kicked off the two week Philadelphia Science Festival. It is two weeks filled with activities for everyone, including seminars, debates, and a carnival.

Interested in science? Have kids who like science? Check it out!

The festival runs for 2 weeks starting April 16. More information is available at
www.philasciencefestival.org

Gut bacteria may increase risk of cardiovascular disease

It is increasingly evident that the gut microflora is critically important for digestion, immunity, and proper weight maintenance. Changes to the bacterial content of the GI tract can lead to onset of obesity and various diseases due to changed immune function. In their latest paper in Nature, Wang et. al. show that gut microflora is an important regulator of cardiovascular disease as well. They identified small molecules in the plasma that are predictive of increased risk for cardiovascular disease (CVD). Of all the potential compounds found in the plasma, one in particular was associated with CVD. This was TMAO (trimethylamine N-oxide), a metabolite of choline. A diet rich in fat contains high levels of phosphatidyl choline (PC). In the small intestine, this PC is converted to choline. The bacterial microflora that resides in the intestine digests this choline turning it into trimethylamine (TMA). TMA is a gas that is absorbed through the intestinal tract and converted in the liver to TMAO. Interestingly, their data show that increased TMAO is correlated with increased risk for cardiovascular disease, peripheral artery disease (PAD), coronary artery disease (CAD), history of myocardial infarction and atherosclerosis. Further, when the bacterial content was altered with antibiotic treatment, TMAO levels decreased, as did the risk for CVD and other diseases. Taken together, these data suggest that development of a healthy bacterial microflora could dramatically impact the risk for many cardiovascular diseases.


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Insights into tobacco smoking addiction

Tobacco smoking leads to 90% of all lung cancer cases and contributes to other lung and heart diseases. As shown in a recent publication in Nature, scientists at the Scripps Institute may have a new method for combatting smoking addiction. Their research shows that a specific subunit of the nicotine receptor, the α5 subunit of the acetylcholine receptor, sends inhibitory signals at high doses of nicotine in the brain to prevent continued smoking (or intake of nicotine). When functioning normally, activation of this receptor operates to avoid the negative effects of high nicotine levels. Activating this subunit could be a new way to stop smoking.


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IL-15 implicated in celiac and inflammatory bowel disease

In diseases including celiacs and inflammatory bowel disease, the inflammatory cells in the intestinal mucosa mount an immune response to antigens in the ingested food. In a recent study in Nature, DePaolo and colleagues have found a new enemy in those suffering from these diseases. The cytokine, IL-15, an activator of the immune response, is elevated in patients. This leads to an increase in T lymphocyte development, specifically Th1 cell development, and an produces an inflammatory response leading to the digestive complications found in celiacs and inflammatory bowel disease. These findings also suggest that anti-IL15 therapy may be an effective way to prevent these diseases or restore systems back to normal.


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Diamond Nanoparticles to treat cancer

Attaching tiny diamond chips, just slivers of carbon really, to nanoparticles helps to shrink lung tumor cells in animal models, according to recent research by Ho et. al. in the latest Science Translational Medicine. Scientists created small nanoparticles with attached diamond specks and the chemotherapeutic agent, doxorubicin (dox) and injected them into mice with lung cancer. These nanoparticles zoomed in on their target, the cancerous tumor, without causing any auxiliary toxicity that is seen when dox is just injected directly into mice. Therefore, higher doses of dox could be given without having liver toxicity or other side effects.


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Very bad fad diet

The New York Times published an article this week about a new fad diet. It’s appalling. Apparently, a cosmetic surgeon and an orthodontist are prescribing human chorionic gonadotropin (hCG) -- a pregnancy hormone that is given to help aid women in becoming pregnant -- to women who want to lose weight. The claim is that hCG along with a 500 calorie per day diet will result in a pound per day weight loss. First, giving hCG as a weight-loss aid is an off-label prescription, meaning that there is no scientific data indicating that it is safe or effective as a weight loss aid. The limited data that does exist shows that it is no more effective than sugar pills. Second, a 500 calorie diet is unsustainable. Those who follow a calorie restricted diet (including some monks and others) consume at least 1000 to 1200 calories per day. Anyone who restricts themselves to 500 calories a day of course is going to lose weight, but that is incredible unhealthy (because you are not eating) and will cause irreparable damage if continued long term, if you don’t die first. It is inconceivable that these physicians are advocating this diet and the NYT is promoting it. How can any self-respecting physician tell their patients who trust them to not eat and to inject an substance with unknown side effects into them to lost weight? There is no magic bullet or key diet that will result in weight loss. There are proven ways to lose weight. Many scientific studies have shown, repeatedly, that the key to weight loss is to exercise and to eat a healthy, well balanced diet, one that doesn’t restrict you to eating a pea and cracker per day

Panel to review bioethics rules

New evidence of a clinical trial conducted in the 1940s containing blatant ethical abuses has prompted President Obama to establish a panel to investigate clinical trial ethical rules.

Based on new revelations of a study conducted in Guatemala in the 1940s, the Presidential Commission for the Study of Bioethical Issues has convened a panel to investigate the ethical rules for clinical trials. Apparently, between 1946-1948 in a US-funded study, Guatemalan prisoners and soldiers were exposed to syphilis and gonorrhea in order to study how to treat the disease. At that time, indications were that penicillin was a successful treatment for disease. Unfortunately, some wanted to test other treatment options, so they infected prisoners, soldiers and others with syphilis or gonorrhea and tested other therapies. No data was published from this study and it isn’t clear if other therapies were developed. The scientists did receive institutional approval to conduct the study but it does not appear that individuals knew they were being infected and tested.

Ethical policies regarding use of human subjects have changed dramatically since the 1940s. Today, no experimentation on humans can occur without the expressed informed consent of the patient involved. An international panel, with advisors from 10 countries, will review these policies and ensure the safety of human subjects.


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Fungus fights malaria!

Scientists at the University of Maryland and the Johns Hopkins University have been testing different antimicrobial or peptide blockers that prevents the transmission of the parasitic infection from mosquito to human. What appears to be most effective in animal models is a combination of the antimicrobial with peptide blockers and an antibody. While fungi have been used successfully in the past to fight malaria, the inoculation of the mosquito had to occur within a short timeframe of parasite infection, or the treatment was rendered useless. Using these new engineered fungus, the need to inoculate the mosquitoes shortly after parasitic infection appears to be eliminated. This study has just been published in Science magazine (vol 331:1074).

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Inhibition of CSR regrows hair!

Baldness is a common aliment that many people would rather reverse or avoid completely. Stress and other life events can impact hair follicle growth and lead to a form of baldness. This suggests that stress hormones, including corticosteroids, are major contributors to the problem. Indeed, in mouse models, inhibition of corticosteroid releasing hormone (CSR), adrenocortropic hormone or glucocorticoids can impair hair follicle growth. A recent article in PLoS One by Wang et al has shown by inhibiting two forms of the corticosteroid releasing hormone (CSR1 and CSR2) together, but not either one alone, synergized to regrow hair in mice. In this paper, administration of a CSR1/CSR2 inhibitor, astressin-B, for only 5 days produced dramatic hair regrowth on the heads and back of balding mice. The hair that regrew did so quickly (within a matter of weeks) and lasted for at least 4 months -- a long time in a mouse lifespan.

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Potential new method to treat antibiotic resistant bacteria

Antibiotic resistant bacteria infections are on the rise. Numbers of MRSA (methicillin-resistant Staphylococcus aureus) cases are skyrocketing and ways to treat them are limited. By using the proteins expressed in the bacteria itself, scientists have found a new way to eliminate such bacterial infections.

When bacteria infect human cells, the bacteria hijacks the human DNA in the cell to allow for successful propagation. This is done by controlling the human RNA and protein levels in the cell and turning on or off the genes to promote the bacteria’s survival.

Most current methods to treat bacterial infections either focus on blocking proteins on the human cell that control entry of the bacteria into the cell or by not allowing bacteria from taking control of the human DNA/RNA machinery. A new approach turns the attention to the bacterial proteins themselves and have shown that by blocking the bacterial genes, infected cells can be effectively eliminated from the body.

This new technique uses a small molecule inhibitor (RNPA-1000) to block the action of a bacterial RNAse enzyme that normally causes the human RNA to be degraded. By blocking this RNAse, the human RNA remains and continues to accumulate in the cell. As the cell becomes completely filled with so much RNA, cell death pathways are triggered and the cell dies.

Although the RNAse inhibitor (RNPA-1000) does work, it won’t be used in the clinic because of some toxicity to normal uninfected cells. RNPA-1000 is, however, being used as a model to design new drugs that work in similar ways.

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Plos Pathogens 7: 1-13, 2011

Anti-cocaine vaccines show promise against addiction

Studies demonstrated that conjugation of cocaine analogs to adenoviral protein particles resulted in the successful induction of an immune response that was able to successfully sequester the cocaine in the bloodstream, preventing it from affecting the brain. Similar approaches are underway to develop anti-nicotine and anti-alcohol vaccines.

Several groups are investigating whether such technology will be successful at treating other addictions including nicotine, heroin, and alcohol. The underlying theory is that adenoviral particles that are no longer infectious will be able to elicit an immune response and that by attaching nicotine, cocaine or other addictive drug to these particles will create a specific antibody response. Initial studies show that a significant and specific response is achievable (Hicks et al, Molecular Therapeutics 2011; Polosa et al, Trends in Pharmacological Sciences 2011). Clinical trials to test some of these vaccines are currently underway.

Genome papers published 10 years ago

Happy Anniversary! It was 10 years ago this month that the first complete human genome sequence was published in Science and Nature Magazines. Discussion and planning of the project had started in1986 when the National Academies of Science gathered a group of experts to discuss the feasibility and advisability of undertaking such an enormous task. They produced a report in 1988 advising that plans should proceed ahead. It would involve private and public partnerships that would have to develop new technology to do the job. Estimates were that it would take over 10 years and cost $3billion US. Expectations were that sequencing the human genome would revolutionize modern medicine.

In reality the human genome project was finished ahead of schedule and below budget. A truly remarkable feat! It launched the field of medical genetics and personalized medicine. The idea that medicines will be tailored to your specific genome is remarkable. While some have questioned why more clinical applications like personalized medicine haven’t been developed, many advances linking genomic differences and clinical treatment have emerged. Drugs such as gleevac (chronic myeloid leukemia), warfarin (anti-clotting), mercaptopurine (immune suppression), interferon (hepatitis C), herceptin (breast cancer) and tamoxifen (breast cancer) among others that are administered based on presence of specific genomic sequences or expression of particular proteins have been developed as a consequence of this project. Many more are in development or will be developed as research continues.

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More data on Hormone Replacement Therapy

Hormone replacement therapy (HRT) has been controversial in recent years. First thought to be helpful to avoid symptoms of menopause and to reduce the development of cardiac disease in post-menopausal women, clinical trials were halted in 2002 because of significant increases to the development of breast cancer and to no apparent benefit to reducing cardiac disease. While estrogen treatment alone, compared with estrogen + progesterone combinations, is better (reduced risk for developing breast cancer and lowers risk of cardiovascular disease and stroke), further studies have tried to determine if timing of administration offered any effect. Turns out that it does, although it’s not necessarily glowing news. Researchers in Britain just published findings in the Journal of the National Cancer Institute (2011, volume 103:296-305) indicating that taking HRT at the time or shortly after onset of menopause significantly increases the risk of developing breast cancer compared with those who took a greater than 5 year break before starting HRT therapy. Data in this paper also validates previous studies by the Women’s Health Initiative. Both groups have now shown that the risk of developing breast cancer increased coordinately with an increase in body mass index, however the risk associated with HRT did not further increase with BMI and therefore obesity does not influence the elevated risk associated with HRT. Additionally, although risk of breast cancer increases with prolonged HRT exposure, these risk levels decrease back to levels of those who have never taken HRT within 2- 3 years.

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writing increases test scores

Everyone has experienced at some point in their life that anxious feeling just before taking an important test. For some, this type of high anxiety can decrease performance leading to lower test scores. Some good news on how to circumvent this has just emerged in a new paper published this week in Science Magazine (vol 331:211-213). Knowing that long-term journal keeping or writing is a therapeutic approach to alleviate depression in some patients, Drs. Gerardo Ramirez and Sian Beilock hypothesized that writing about the fears of the upcoming test just prior to taking the test may help alleviate some anxiety and increase test scores. The researchers tested high school and college students by having them write about their fears about the test 10 minutes prior to test taking and found that this exercise did indeed increase test scores. The writing, they found, had to be about the anxieties they were feeling (termed expressive writing) and that writing about just any topic didn’t produce the same results. This meant that a mere distraction from the test wasn’t enough to reduce anxiety and increase scores, but that discussing the anxiety was important. Overall, this study suggests that a simple writing exercise just prior to an important test may help to increase test scores.

Music and our brains

An interesting paper was just published in Nature Neuroscience recently (online January 9, 2011). Dr. Valorie Salimpoor and her colleagues demonstrated for the first time that music enjoyment results from the release of the pleasure-seeking neurotransmitter dopamine deep within the ancient parts of our brain, the limbic system. Using imaging techniques, PET and functional MRI or fMRI, and linking this data to when people feel the most enjoyment from their music of choice, they show that dopamine is released in the caudate and the nucleus accumbens regions in our brains. Interestingly, the dopamine levels increased both in anticipation of the enjoyment as well as at peak enjoyment levels, although dopamine levels rose at a greater rate during peak enjoyment in the nucleus accumbens while decreased during the peak in the caudate regions. What this means is yet to be deciphered completely.

Why does this matter? Previous reports have implicated dopamine in pleasure from music in the past, however none have done so directly. Also, this clearly shows that these regions within the limbic system are used for more than just survival. An ancient part of our brain is wired to enjoy the less tangible things like music. It helps to explain why music is so important and is such a part of our daily lives. It’s everywhere and it’s used to evoke emotions and to sell us stuff all the time!