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Tumors might grow faster at night: Hormone that keeps us alert also suppresses the spread of cancer

Feb 17, 2016

1981

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Tumors

A recent finding that was published in the journal � Nature Communications by researchers at the Weizmann institute report a surprising finding. It says that during the nighttime, the cancer cells are more active and that they spread quickly during this period. Their findings also suggest that by administering certain therapies in time with the body's day-night cycle may boost their effectiveness. The environment in our body is just right for the cancer to spread while we are asleep � the cancer cells grow while we are unaware and spread their tentacles as quickly as possible.

There was an investigation to understand the relationship between different receptors in the cell � a complex network that is still not fully understood by scientist via which this finding arose. It was seen that the receptors � the protein molecules which are present on the cells' surface or in the cells �take in the biochemical messages which are secreted by the other cells. They then pass them on into the cell's interior. The research team was led by Dr. Mattia Lauriola, who is a postdoctoral fellow in the research group of Prof. Yosef Yarden of the Weizmann Institute’s Biological Regulation Department. He along with Prof. Eytan Domany of the Physics of Complex Systems Department, focussed on two particular receptors. The first one is EGFR which is an epidermal growth factor receptor. It promotes the growth and migration of cells including cancer cells. The second one is characterized by its capability to bind to a steroid hormone called glucocorticoid. This hormone plays an important role in maintaining the body's energy levels during the day. It is also important for the metabolic exchange of materials. Also known as the stress hormone for its level rise in stressful situations and it brings the body to a state of full alert.

The cell receives all sorts of messages all at once with multiple receptors. However, some messages take precedence over others. In the experiment, the researchers found that EGF receptors promote the activity of cell migration, but is suppressed when the GC receptors are bound to their steroid messenger.

It is seen that the levels of the steroid are highest during waking hours and they plummet during sleep. The scientists were curious to know how this would affect the second receptor. When the levels were checked in mice, it was found that there was quite a significant difference. It was concluded that the receptor is much more active during sleep than during waking hours.

The next step in the experiment was to find out how relevant these findings were for cancer – in particular the ones which use the EGF receptors to grow and spread. For this the scientists gave Lapatinib which is a new generation cancer drug to the mouse model. This drug is particularly used to treat breast cancer and is supposed to inhibit EGFR and hence prevent the growth and migration of the cancer cells. The drug was given to mice at different times in the day.

The results showed that there was a significant difference in the sizes of tumor in the difference groups of mice � depending on the time when the drug was administered �during sleep or while awake. The results of the experiment suggest that the levels of the GC steroid have a significant role to play in cancer growth. The scientists have concluded that it could be more effective to administer certain anticancer drugs at night.

Yarden said that what they are proposing is not a new treatment but a new schedule to administer some of the current drugs. It should be increase the effectiveness of the cancer treatment.

References

https://wis-wander.weizmann.ac.il/tumors-might-grow-faster-at-night

https://www.nature.com/ncomms/2014/141003/ncomms6073/metrics/news

Scientists Identify Proteins Crucial To Loss of Hearing

Feb 15, 2016

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Hearing loss is quite a common phenomenon; close to 40 million Americans suffer from it. Till date, there is no known way to reverse the condition as the auditory hair cells, which sense sound and relay that information to the brain do not regenerate. However, in a new study led by the scientists at the University Of Maryland School Of Medicine (UM SOM), the results of which appeared in the latest issue of the journal Nature Communications, something crucial has been discovered. They have found a key clue to how these hair cells develop. The researchers have identified a new role for a particular group of proteins, called RFX transcription factors, in the development and survival of the auditory hair cells.

Ronna P. Hertzano, MD, PhD, Assistant Professor of Otorhinolaryngology-Head & Neck Surgery at the UM SOM and the principal investigator of the study said that this discovery is crucial as it opens up new avenues, not only for understanding the genetics of hearing, but also, eventually for treating deafness. The research was carried out in collaboration with scientists at several institutions, among them Ran Elkon, PhD, an Assistant Professor and computational biologist at the Sackler School of Medicine at Tel Aviv University in Israel.

For the study, mice whose auditory hair cells glow with a green fluorescent protein were used by the researchers as it lets the cells to be identified from other kind of cells. Next generation sequencing was later applied by them � it is a state-of-the-art method to rapidly measure gene expression – to sequence and quantify the thousands of genes that are expressed in hair cells, in comparison with other cells in the ear. The researchers were particularly interested in searching for key regulators of genes for hair cells as they could be key in helping researchers eventually develop techniques to regenerate hair cells. The RFX transcription factors were the key regulator identified by them.

To further their study, the researchers then studied mice that were genetically modified so that two of the RFX transcription factors were lacking in their hair cells. Initially the hair cells in the mice developed normally, but then died quickly, leading to rapid hearing loss. In just three months, the mice were totally deaf.

Hertzano is of the opinion that the genes are likely to work in a similar fashion in humans. She added that it might be possible to use our increased understanding of RFX transcription factor to treat hearing loss, by either protecting hair cells from death or fostering their growth. Next they are on the lookout to identify other genes that have an important role in hair cell function.

This paper appeared in conjunction with another paper published in Nature Communications, by Matthew W. Kelley, PhD, a neuroscientist at the National Institute on Deafness and Other Communication Disorders. Kelley and his team also used mice with fluorescent markers in different cells of the ear followed by next generation sequencing. They didn't go for analyzing groups of cells; on the other hand they performed a comprehensive analysis of the genes that are expressed in the different cells at a single cell resolution. The study is a pioneer in the ear field and can be instrumental in resolving the molecular aspects of the cellular complexity of the inner ear.

Hertzano interest in understanding the genetics of hearing started when she was an MD-PhD student at Tel Aviv University. She has then pursued residency training at the UM SOM Department of Otorhinolaryngology, where she now works as a scientist and a surgeon. Her practice is focused on diseases of the ear and hearing restoration.

Reference Links:

https://medicalxpress.com/news/2015-10-scientists-proteins-crucial-loss.html

https://www.eurekalert.org/pub_releases/2015-10/uoms-sip101315.php

Study says obesity doesn’t protect patients with cardiovascular disease

Feb 14, 2016

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A puzzle had been unsettling demographers Samuel Preston of the University of Pennsylvania and Andrew Stokes of Boston University for quite a while and they set out to demystify it. This phenomenon is referred to as the obesity paradox and the researchers wondered if it would hold up even when approached within different parameters?

The results of their study were published recently in the journal Obesity and according to their findings, the answer is �no'. It was seen that obesity is harmful, not helpful, to someone with cardiovascular disease when accounting for weight history in addition to weight at the time of survey and when adding in smoking as a factor. Preston, a sociology professor in Penn’s School of Arts & Sciences said that there are claims which say that it is a good thing to be obese when you have cardiovascular disease, that if you have fat stores, maybe you’ll live longer. While it is conceivable that there are health advantages, the study show such people are overwhelmed by the disadvantages of being obese, once the two sources of bias are controlled.

The data from more than 30,400 participants from the National Health and Nutrition Examination Survey between 1988 and 2011 was used by Stokes and Preston. The survey is a nationally representative sample considered the gold standard in the United States. Of all the participants considered, 3,388 had cardiovascular disease. Most research of this kind only looked at weight at time of survey. Say like, if a participant who has always weighed 300 pounds lost 100 pounds by the time he weighed in, he would be counted at 200 pounds. So, Stokes and Preston innovated a bit and decided to opt for weight history.

Stokes, who earned both his master’s degree and Ph.D. from Penn and is now an assistant professor in the department of global health at BU, said that it was definitely a new and good idea. If we didn't do that, all the classification would be sort of messed up � it would be akin to classifying a lifelong smoker who quit the day before the survey as a non-smoker even though he would carry the risk of smoking over even after he quit smoking.

With the help of this step, the researchers were able to identify a control group of people who had been normal weight their whole lives, those considered low-risk for disease. Stokes added that adding weight history did have a profound effect on the findings as it eliminated the mortality advantage for those who are overweight or obese. Including the second factor � smoking further contributed to resolving the paradox. Typically, smokers are less likely to be obese, and those who are obese are less likely to smoke. So, the researchers limited their pool to lifelong non-smokers.

The results were quite surprising � by accounting for weight history, the obesity paradox practically disappeared. When smokers were excluded obese equated to significantly higher mortality for those with cardiovascular disease.

Preston said that it is likely that clinicians are somewhat confused and in some cases, it is seen that they do that being overweight or obese is a good thing among people with cardiovascular disease, diabetes and other conditions for which a paradox has been demonstrated. The researchers said these results are significant and could improve disease treatment, as it may help clear confusion of clinicians who resort to the obesity paradox in patient care decisions.

You can live a life free of heart disease risk. To find out how, read this.

Reference Links:

https://www.upenn.edu/pennnews/news/obesity-does-not-protect-patients-with-cardiovascular-disease

https://medicalxpress.com/news/2015-10-obesity-doesnt-patients-cardiovascular-disease.html

How to wake a sleeping cancer cell—and why you might want to

Feb 12, 2016

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Cancer Diagnosis

A new research by Australian scientists published recently in the journal Nature Communications have revealed that cancer cells that lie ‘snoozing’ in the skeleton can be awakened – or left to sleep on – by changes in the bone that surrounds them. This research by researchers at the Garvan Institute of Medical Research is first of its kind and makes uses of state-of-the-art microscopy techniques to watch cancer cells sleep within living bone over a period of months. This study is significant as it suggest ways of exploring new possibilities for treating metastatic cancer in bone.

In many cancers the cancer cells can spread from the original tumour site into bone. Once spread, they settle there and often remain inactive for months or even years. Eventually, when some of these cells wake up, they begin dividing and form secondary cancers in bone dramatically worsening the outcome for cancer patients.

Professor Peter Croucher, the study’s lead investigator and Head of Garvan’s Bone Biology Division said that once a cancer spreads to bone, it becomes quite difficult to treat. Hence, it is important to understand what wakes up the cancer cells from its slumber � is it a change in the environment or it is a signal within the cells.

The research team made use of a groundbreaking technique called intravital two-photon microscopy, the researchers observed what happens to the sleeping cancer cells in the tibia -the main bone in the long part of the leg of a living mouse. They introduced cells from multiple myeloma (a cancer of blood cells that arises in bone) into the mouse, and watched as a small number of the cells lodged in the tibia and drifted into slumber. For detection these cells were marked with a fluorescent dye that was lost rapidly from dividing (wakeful) cells.

Dr. Tri Phan, who co-led the study, remarked that since long bone like a tibia was studied instead of commonly studied skull bones, the researchers could watch the same sleeping cancer cells, in the same bone, in the same mouse, over a long period of time. That is something that hasn’t been tried before. Since, the same set of cells over a prolonged period were studied, it gave vital clues about what reactivates some of them said Prof Croucher. He added that it was observed that the cells that woke up did so at different times. In fact, some cells that woke then went back to sleep again.

The fact that despite coming from the same cancer line the myeloma cells behaves differently led the researchers to the clue that it is a signal from outside the cells that is controlling when they wake. Dr. Michelle McDonald, a bone biologist on the research team, opined in this study, it has been found that bone’s dynamic process of building up and breaking down can send signals to cancer cells to sleep on or to wake. Cells known as ‘osteoblasts’ help build new bone, while ‘osteoclast’ cells break down bone. It has been observed that myeloma cells are usually kept asleep by close association with a layer of osteoblast-like cells, called bone-lining cells, in the endosteum (an internal surface within bone). The bone-lining cells are inactive and provide a quiet environment in which myeloma cells sleep undisturbed.

The myeloma cells can be woken up by activating osteoclasts, which break down bone tissue thereby changing the environment in which the cancer cells sleep. It is a known fact that bone remodeling is an ongoing process happening in all of us – so a myeloma cell could be woken in an essentially random fashion when the local environment of the cancer cells is remodeled by osteoclasts.

Prof Croucher remarked that since it is now understood that the cancer cells are woken by changes in the surrounding bone, two treatment approaches for treating bone metastasis hold promise. The first is that the breakdown of bone by osteoclasts could be inhibited by drugs, so as to keep cancer cells in long-term hibernation. The second is to do the opposite – to wake the sleeping cells by activating osteoclasts and driving the breakdown of bone. Most cancer therapies target active, dividing cells, so it will make the dormant cells more susceptible to therapies � and any residual disease could be eradicated.

Reference Links:

https://www.garvan.org.au/news-events/news/how-to-wake-a-sleeping-cancer-cell-and-why-you-might-want-to

https://medicalxpress.com/news/2015-12-cancer-celland.html

Molecular Brake Stifles Human Lung Cancer

Feb 11, 2016

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A new research published recently in PNAS has revealed that researchers at the Salk Institute have uncovered a molecule whose mutation leads to the aggressive growth of a common and deadly type of lung cancer in humans. �The molecule they have discovered is an enzyme called EphA2 and it typically polices a gene that is responsible for tissue growth. The team of researchers at Salk discovered that when EphA2 is mutated, the cellular systems run hither and thither and quickly develop tumors. The study also suggests that EphA2 could be a new focus for a subset of lung cancer, which affects nonsmokers as well as smokers, and is the leading cause of cancer-related deaths worldwide.

Inder Verma, senior author of the study, professor of genetics and holder of Salk’s Irwin and Joan Jacobs Chair in Exemplary Life Science said that sometimes there are hundreds of mutations in the genes of a patient’s tumors, but it is not known whether they are drivers of the disease or byproducts. Through this research they have found a new way which can aid to identify cancer suppressor genes and understand how they could be targeted for therapies.

It is known that KRAS and p53 are the two gene mutations that are responsible to spur the growth of human tumors. Even though there have been a lot of studies on both these genes, they are quite difficult to target therapeutically. Hence, the research team at Salk decided to look at genes that might police KRAS and p53.

For the study, the team focused on the 4,700 genes in the human genome related to cellular signaling�particularly the ones that can tamp down cell growth and proliferation. The team adapted a genetic screening technique to efficiently test the effect of these thousands of genes on the development of tumor. It was found by the Salk team that in animal models 16 of these cell-signaling genes produced molecules that substantially affected KRAS- and p53-related tumors. Of the 16, the EphA2 enzyme was the one that stood out. EphA2’s significance in lung cancer has not been not clearly understood till date, but the team found that when it was absent, the KRAS-related tumors flourished.

Verma remarked that typically when a mutation occurs in KRAS, a tumor is formed in 300 days. However, in absence of EphA2, the KRAS mutation leads to tumors in just 120 to 150 days. This confirms one thing – EphA2 does have a huge effect on restraining cancer growth when KRAS is mutated. It is seen that mutated KRAS is a common culprit in approximately 10 to 20 percent of all cancers, colon cancer and human lung cancer in particular.

Narayana Yeddula, first author of the paper and a Salk research associate opined that since activating EphA2 led to the suppression of both cell signaling and cell proliferation, this enzyme might serve as a potential drug target in KRAS-dependent lung adenocarcinoma.

The Salk researchers used data from the Cancer Genome Atlas data – a 10-year national project that mapped the genomes of hundreds of patients for over 20 different cancers. The data thus analysed lead to the discovery that genetic alterations of EphA2 were detected in 54 out of 230 patients with adenocarcinoma. It was also found by the team that the loss of EphA2 activated a pathway commonly associated with cancer that promotes tumor growth.

Yifeng Xia, a Salk staff researcher involved in the work remarked about another interesting aspect of the findings. He said that among human lung cancer patients with EphA2 mutations, around 8 percent of patients actually have high EphA2 expression. So, there are cases when EphA2 is not suppressing tumors and is likely to be context-dependent. Hence, for designing new therapeutics there is a need to carefully evaluate the molecule and its functions.

Quit smoking and learn more about lung detoxification here.

References:

https://www.salk.edu/news/pressrelease_details.php?press_id=2129

https://medicalxpress.com/news/2015-11-molecular-stifles-human-lung-cancer.html

Children born in the summer more likely to be healthy adults

Jan 20, 2016

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A new research published recently in the journal Heliyon suggests that women who are born in the summer months are likely to grow up into healthy adults. This study involved almost half a million people in the UK. The authors of the study are of the opinion that more sunlight and hence, higher vitamin D exposure in the second trimester of pregnancy could be one of the likely reason for the outcome. However, more research is needed in this area to substantiate the findings.

As per the study, birth weight and the onset of puberty get affected by the birth month � both these factors have an impact on the overall health of women during their adulthood. The environment in the womb plays a major role in the early life of women � even before birth and can have a significant influence on women's health in later life. This effect is termed as programming and has effects for development throughout childhood and into adulthood.

The researchers from the Medical Research Council (MRC) Epidemiology Unit, University of Cambridge, UK are behind the study and they were keen on finding if birth month had an effect on birth weight, onset of puberty, and adult height. Their study led them to the finding that children who were born during the summer months were slightly heavier at birth, taller as adults and went through puberty slightly later than those born in winter months.

Dr. John Perry, lead author of the study opined that the time when a child is conceived and is born happens largely at random and is irrespective of social class, parent's age or their health. So, looking for patterns with birth month is a powerful study design to identify influences of the environment before birth.

Some previous studies have pointed out to certain effects of the season of birth, like on birth weight and various other health outcomes. Dr. Perry and his team of researchers thought that childhood growth and development, including the timing of puberty, is an important link between early life and later health. That is the reason they decided to study the impact of birth month more closely.

The growth and development data of around 450,000 men and women from the UK Biobank study – a major national health resource that provides data on UK volunteers to shed light on the development of diseases was studied and compared by the researchers. The results of their study indicate that babies born in June, July, and August were heavier at birth and taller as adults. The study also revealed that girls born in the summer started puberty later – an indication of better health in adult life.

Dr. Perry said that it is the first instance when puberty timing has been robustly linked to seasonality. He said that they were surprised, and pleased, to see how similar the patterns were on birth weight and puberty timing. The preliminary result show that birth month definitely has a measurable effect on the development and health. Of course, further study is needed to understand the mechanisms behind this effect.

The factor that can be crucial in deciding the differences between summer babies and winter babies could be a case of how much sunlight the mother gets during pregnancy, as that plays a crucial role in her vitamin D exposure.

Dr. Perry said that the mechanisms that cause these seasonal birth patterns on birth weight, height, and puberty timing is not understood as of now. They need to be before the findings of this study can be translated into health benefits. �The researchers are of the opinion that vitamin D exposure is likely to be of key importance are will study the long-term effects of early life vitamin D on puberty timing and health.

Reference Links:

https://www.medicalnewstoday.com/articles/300882.php

https://www.webmd.com/children/news/20151012/summer-babies-may-be-healthier-adults

Lithium safe, effective for children with bipolar disorder

Jan 19, 2016

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Lithium is a drug that has been used for decades to treat adults with bipolar disease. A new multicenter study of young patients has now revealed that lithium can also be safe and effective for children suffering from the said condition. Bipolar disorder affects approximately 1 percent of teens and is one of the leading causes of disability in adolescence. The disorder usually begins during adolescence or young adulthood.

The research was led by a researcher at the Johns Hopkins Children’s Center. Published recently in Pediatrics, affirms that doctors can now more confidently add lithium to the arsenal of available treatments for this vulnerable population�at least in the short term.

Bipolar disorder is a chronic condition of the brain marked by spontaneous bouts of abnormally high moods and depression. Lithium has been used to treat this condition in adults since ages as it stabilizes mood extremes. But, it has not been seriously tested in young people for safety and effectiveness. So, physicians are in two minds about prescribing it to children and teenagers. Typically, it has been the custom to exclude children and women of childbearing age from many clinical drug trials out of an abundance of caution and ethical concerns. However, in recent years, many have raised concerns that excluding such populations may be detrimental for them, as drugs are either withheld or found to react differently than they do in other groups.

Robert Findling, M.D., M.B.A., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and director of child and adolescent psychiatry at the Johns Hopkins Children’s Center said that even though lithium is like the grandfather of all treatments for bipolar disorder, it has never been rigorously studied in children. He initiated the work when he was working in the capacity of director of child and adolescent psychiatry at Case Western Reserve University School of Medicine.

Often medications used to treat schizophrenia and other such conditions are prescribed to treat bipolar disorder in children. But, Findling said that since, those drugs side effects like – substantial weight gain, etc., many discontinue taking them.

To establish the safety of Lithium use in children, Findling and his colleagues performed a randomized, placebo-controlled prospective study. It involved 81 patients – ranging in age from 7 to 17, diagnosed with bipolar disease – seen at nine academic medical centers across the United States.

53 of these children started a regimen of lithium at a standard dose, which was gradually increased to a maximum tolerated dose over the next eight weeks if mood symptoms weren’t controlled. The remaining 28 patients received placebo. Patients’ symptoms were assessed using a survey called the Young Mania Rating Scale, along with other standard assessment tools for bipolar disorder symptoms and therapies at weekly visits for the first four weeks, and then every other week for the remainder of the study period. Patients were also assessed for any possible side effects, including a weight check.

The results revealed that the patients on lithium experienced far more significant improvement in their symptoms over eight weeks compared with those on the placebo. Also, unlike antipsychotic agents, such as risperidone or olanzapine, lithium treatment was not associated with significant weight gain, and none of the patients experienced serious side effects due to the lithium treatment.

Findling says that their study reveals that lithium is safe and reliable for treating children in the short term. He also added that further analyses are currently in progress to examine the long-term implications of lithium use. The areas, the research team is focusing on include evaluation of any potential side effects, such as weight gain, reduced kidney function or diminished thyroid function. All of these are important considerations, as those with bipolar disorder may need a lifetime of medication and behavioral therapies.

Reference Links:

https://www.hopkinsmedicine.org/news/media/releases/lithium_safe_effective_for_children_with_bipolar_disorder

https://www.medicaldaily.com/bipolar-disorder-children-lithium-proven-safe-effective-short-term-treatment-children-356830

Popular antioxidant seems to spread skin cancer cells in mouse research

Jan 17, 2016

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Antioxidants, like vitamin C and E are known to have anti-cancer benefits, but a new research in mice, the results of which were reported recently in the journal Science Translational Medicine seem to suggest that certain antioxidants can actually increase the risk of metastatic melanoma. Since, it helps in the spread of skin cancer in mice; researchers are worried about its safety in humans.

Martin Bergo, a professor at the University of Gothenburg in Sweden and a senior author of the study said to relieve mucus production in patients with chronic obstructive pulmonary disease (COPD), the antioxidant, N-acetylcysteine is often prescribed. Many people also use it as a dietary supplement to help reduce exercise-related muscle damage, burn fat and prevent fatigue. So, the researchers were shocked when they found that water laced with N-acetylcysteine seemed to accelerate the spread of melanoma. In their study, it was observed that the antioxidant has no effect on the size and the number of tumors, but it did enhance the migration and invasion of these tumors to other parts of the body. Their findings say that N-acetylcysteine was linked to a doubling of the number of lymph-node tumors in mice who drank the laced water, compared to untreated animals.

In some previous research the same research team has reported that some particular antioxidants enhanced lung tumor growth in mice.

The U.S. National Institutes of Health (NIH) says antioxidants are believed to protect healthy cells from damage caused by unstable molecules called “free radicals.” But, this study has shown that antioxidants like N-acetylcysteine protect cancer cells from free radicals that might otherwise slow their growth. There have been other studies which has linked high doses of beta-carotene to increased risk of lung cancer in smokers. NIH has say that high doses of vitamin E can heighten the risk of prostate cancer.

Bergo said if people who are at an increased risk of cancer take nutritional supplements containing antioxidants, it might do them more harm than good. The reason why Bergo's team decided to focus on N-acetylcysteine is because it is a potent antioxidant which quickly dissolves quickly in water making it easier to feed to lab mice.

To further their study, the research team performed follow-up lab tests on human melanoma cells, using N-acetylcysteine and vitamin E. The results were similar – both antioxidants increased the cancer cells' ability to migrate and invade other cells. It is understood that antioxidants’ protective benefits could provide the boost to skin cancer. The researchers also found that a protein that regulates cellular processes was activated in the cells and it was likely involved in the spread of cancer.

Bergo said that for a patient with newly diagnosed lung cancer or melanoma�antioxidants could enhance the progression of the disease. There is no conclusive evidence that support antioxidant supplementation to help cancer patients and hence, it is more sensible to avoid it altogether as it can worsen the disease.

Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society, said that the study results are interesting, but it is not possible to take this information and directly translate it into recommendations for patients. He argued that the results of animal studies don’t necessarily translate into what happens for humans. Clinical trials in people are needed before we can conclude that antioxidants impact the course of cancer treatment.

Lichtenfeld did add that cancer patients should make sure their treatment team knows about all supplements, alternative medications and vitamins they take, so that they get the best advice possible for their particular situation.

Reference Links:

https://medicalxpress.com/news/2015-10-popular-antioxidant-skin-cancer-cells.html

https://www.webmd.com/melanoma-skin-cancer/news/20151007/popular-antioxidant-seems-to-spread-skin-cancer-cells-in-mouse-research

Weaker breaths in kids linked to early pesticide exposure

Jan 15, 2016

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As per a new paper by researchers at the University of California, Berkeley, taking a deep breath might be a bit harder for children exposed to a widely used class of pesticides in agriculture early in life. The findings of the research paper were published recently in the journal Thorax and are the first to link chronic, low-level exposures to organophosphate pesticides�chemicals that target the nervous system to lung health for children.

The study has established a connection between the levels of organophosphate pesticide metabolites in the urine of 279 children living in California’s Salinas Valley with decreased lung function. Each tenfold increase in concentrations of organophosphate metabolites translated into a 159-milliliter decrease in lung function, or about 8 percent less air, on average, when blowing out a candle. The finding has serious implications as the magnitude of this decrease is akin to a child’s secondhand smoke exposure from his or her mother.

Brenda Eskenazi, a professor of epidemiology, maternal and child health and a senior author of the study remarked that breathing problems in agriculture workers who are exposed to these pesticides were known, but these new findings are about children who live in an agricultural area where the organophosphates are being used. She added that this study is the first of its kind to suggest that children exposed to organophosphates have poorer lung function.

The children in this study were part of the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a longitudinal study in which the researchers follow children from the time they are in the womb up to adolescence. As a part of the study urine samples were collected five times throughout the children’s lives, from age 6 months to 5 years, and the levels of organophosphate pesticide metabolites were measured each time. When the children reached 7 years of age, they were given a spirometry test in order to measure the amount of air they could exhale. Other factors that could affect the results were also taken into account � like if mothers smoked, air pollution, presence of mold or pets in the home and proximity to highways.

Rachel Raanan, lead author of the study remarked that the kids in the study with higher pesticide exposure had lower breathing capacity. If the reduced lung function followed them into adulthood, it could leave them at greater risk of developing respiratory problems like COPD (chronic obstructive pulmonary disease).

The pathways for the children’s exposure to pesticides were not examined in the study. However, it was recommended that the farmworkers remove their work clothes and shoes before entering their homes, children be kept away when pesticides is sprayed in nearby fields. Washing fruits and vegetables thoroughly before eating could also be helpful.

Raanan opined that exposure to organophosphate pesticides adds to the growing list of environmental exposures like air pollution, environmental tobacco smoke, etc., each of which is harmful to the developing lungs of children. Since, the use of pesticides is rampant the findings of the study do deserve serious attention. No doubt there are steps taken by health agencies in the U.S. to reduce the use of such pesticides, still more need to be done.

Dr. John Balmes, a UC Berkeley professor of environmental health sciences with a joint appointment at the UC San Francisco School of Medicine, study's co-author and a pulmonary specialist opined that chronic obstructive pulmonary disease is an increasing cause of death around the world.� That is the reason it is important to reduce environmental exposures during childhood that impair breathing capacity and increase the increase the risk for COPD.

Reference Links:

https://news.berkeley.edu/2015/12/03/breathing-capacity-pesticide-exposure/

https://medicalxpress.com/news/2015-12-weaker-kids-linked-early-pesticide.html

Is dopamine to blame for our addictions?

Jan 14, 2016

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Most researchers have a consensus on the key difference between human brains and those of other animals � it is the size and complexity of our cerebral cortex, the brain's outer layer of neural tissue. Most of the research has been focussed on this area as it is believed that cerebral cortex is vital to our unique mental life. However, there are other interesting bits that are identical between humans and animals that are ignored – like tiny group of brain cells that use the chemical dopamine to communicate with other brain cells.

Dopamine, also known as the brain’s “pleasure chemical”, is actually involved in large number physical and mental processes. It is used by a cluster of neurons in the midbrain to transmit messages to other neurons. The dopamine neurons are small in number (~0.0006% of the neurons in the human brain) and found in all mammals and even “simple” animals such as turtles.

In an experiment during the 1950s, researchers discovered that rats seemed to enjoy the stimulation of the nerve bundle that links the dopamine neurons with their targets in the forebrain. On pressing a lever this stimulation was activated; the rats learned to do so and when left unchecked would do so thousands of times in a day. A similar experiment was performed in 1970 on a human patient where a patient learned to press a button to stimulate the dopamine nerve bundle. He pressed the button up 1500 times over the course of a three-hour session and reported experiencing feelings of pleasure during the stimulation. Subsequent studies have revealed that dopamine system can be activated by a wide range of pleasant experiences, like eating, having sex, winning games, listening to music, earning money, getting revenge, etc. it has also been found that addictive drugs, including opiates, alcohol and cocaine also activates the dopamine system and unlike natural ways, these drugs can evoke stronger activation and do not cause satiety.

In simple words, the dopamine system is a pleasure pathway in the brain. It explains why some drugs are so addictive � the activation of the system by drugs is so strong that it makes drugs highly desirable. It must be noted that many mental events occur near the time of a reward, including changes in motivation, arousal, attention, emotion, and learning.

An important aspect of dopamine function is learning. Researchers believe that dopamine neurons change their activity when expectations about reward do not match the reality, signaling a ‘reward prediction error’ that supports learning. The events that result in an increase in dopamine levels are associated with reward, and those that are followed by decreases are linked with disappointment. It is unlikely that we have much awareness of the learning that dopamine activation induces, such as making us attached to things we unknowingly associate with dopamine activation. This lack of awareness might explain why people often make seemingly irrational choices.

The question now is can brain research be used to overcome the effects of dopamine in addiction? While Neuroscientists are actively pursuing the creation of drugs that block the learning induced by dopamine in addiction, there has been very limited success. The reason being – dopamine also has other roles to play – it is difficult to create a drug the blocks the learning without also blocking other functions of dopamine, such as feeling alert, motivated and happy.

Dopamine-induced learning is crucial but it is not the full story behind addiction. However, it does suggest that we should consider whether addiction is something that human reasoning on its own can overcome. Our special cerebral cortex can very well be in control of our actions, but the dopamine system may be its teacher.

Struggling with an addiction? You may want to try this.

Reference Links:

https://medicalxpress.com/news/2015-12-dopamine-blame-addictions.html

https://theconversation.com/explainer-what-is-dopamine-and-is-it-to-blame-for-our-addictions-51268

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