Category: Health

{Activation of D2 neurons could discourage alcoholics from wanting another drink}

By activating particular neurons, we may be able to influence alcohol drinking behavior, according to new findings published by researchers at the Texas A&M Health Science Center College of Medicine in the journal Biological Psychiatry.

The group’s prior research showed that alcohol consumption alters the physical structure and function of neurons, called medium spiny neurons, in the dorsomedial striatum. Essentially, they found that activation of one type of neuron, called D1, determines whether one drink leads to two. Now, they’ve discovered the ones that tell us to stop.

These neurons can be thought of like a tree, with many branches, and many small protrusions, or spines, coming off of them. Each neuron has one of two types of dopamine receptors–D1 or D2–and so can be thought of as either D1 or D2 neurons. D1 neurons are informally called part of a “go” pathway in the brain, while D2 neurons are in the “no-go” pathway. In other words, when D2 neurons are activated, they discourage action–telling you to wait, to stop, to do nothing.

“At least from the addiction point of view, D2 neurons are good,” said Jun Wang, MD, PhD, the corresponding author on the paper and assistant professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M College of Medicine. “When they are activated, they inhibit drinking behavior, and therefore activating them is important for preventing problem drinking behavior.”

The trouble is, even in individuals without alcoholism, D2 neurons tend to become deactivated when we drink too much. This deactivation means there is nothing telling us to stop drinking, so we drink more, in a self-perpetuating cycle.

The researchers found that in animal models, repeated cycles of excessive alcohol intake, followed by abstaining from alcohol, actually changed the strength of these neuronal connections, making D2 signals less powerful–which results in essentially training the individual to seek alcohol. “Think of the binge drinking behavior of so many young adults,” Wang said. “Essentially they are probably doing the same thing that we’ve shown leads to inhibition of these so-called ‘good’ neurons and contributes to greater alcohol consumption.”

These findings provide insight into another mechanism underlying the complicated disease we call alcoholism. “Our current and previous research are essentially two sides of the same coin,” Wang said. “D1 and D2 medium spiny neurons have essentially opposing roles in alcohol consumption.”

By manipulating the activity of these neurons, the researchers were actually able to change the alcohol-drinking behavior of the animal models who had been “trained” to seek alcohol. By activating D2 neurons, they were able to decrease alcohol consumption, and the more the D2 neurons were activated, the greater the effect is likely to be.

The research was supported in part by a grant from the National Institute on Alcohol Abuse and Alcoholism (NIAAA).

Although Wang cautions that we are still a long way from testing this in humans, in theory, if we could someday use drugs or electrical stimulation or some other method of activating the D2 neurons–these so-called “no-go” neurons–then we might be able to prevent alcoholics from wanting another drink. “That’s the ultimate goal,” Wang said. “I hope these findings will eventually be able to be used for treatment for alcohol addiction.”

{Scientists have identified for the first time the ‘cell of origin’ — in other words, the first cell from which the cancer grows — in basal cell carcinoma, the most common form of skin cancer, and followed the chain of events that lead to the growth of these invasive tumors.}

Our skin is kept healthy by a constant turnover, with dying skin cells being shed and replaced by new cells. The process is maintained by ‘progenitor’ cells — the progeny of stem cells — that divide and ‘differentiate’ into fully-functional skin cells to replenish dying skin. These cells are in turn supported by a smaller population of ‘stem cells’, which remain silent, ready to become active and repair skin when it becomes damaged.

However, when this process goes awry, cancers can arise: damaged DNA or the activation of particular genes known as ‘oncogenes’ can trigger a cascade of activity that can lead ultimately to unchecked proliferation, the hallmark of a cancer. In some cases, these tumours may be benign, but in others, they can spread throughout the body — or ‘metastasise’ — where they can cause organ failure.

Until now, there has been intense interest in the scientific field about which types of cell — stem cell, progenitor cell or both — can give rise to tumours, and how those cells become transformed in the process of tumour initiation and growth. Now, in a study published in Nature, researchers led by Professor Cédric Blanpain at the Université Libre de Bruxelles, Belgium, and Professor Ben Simons at the University of Cambridge, have demonstrated in mice how skin stem and progenitor cells respond to the activation of an oncogene. Their studies have shown that, while progenitor cells can give rise to benign lesions, only stem cells have the capacity to develop into deadly invasive tumours.

The researchers used a transgenic mouse model — a mouse whose genes had been altered to allow the activation of an oncogene in individual stem and progenitor cells. The oncogene was coupled with a fluorescent marker so that cells in which the oncogene was active could be easily identified, and as these cells proliferate, their ‘daughter’ cells could also be tracked. These related, fluorescent cells are known as ‘clones’.

By analysing the number of fluorescently-labelled cells per clone using mathematical modelling, the team was able to show that only clones derived from mutant stem cells were able to overcome a mechanism known as ‘apoptosis’, or programmed cell death, and continue to divide and proliferate unchecked, developing into a form of skin cancer known as basal cell carcinoma. In contrast, the growth of clones derived from progenitor cells becomes checked by increasing levels of apoptosis, leading to the formation of benign lesions.

“It’s incredibly rare to identify a cancer cell of origin and until now no one has been able to track what happens on an individual level to these cells as they mutate and proliferate,” says Professor Blanpain. “We now know that stem cells are the culprits: when an oncogene in a stem cell becomes active, it triggers a chain reaction of cell division and proliferation that overcomes the cell’s safety mechanisms.”

“While this has solved a long-standing scientific argument about which cell types can lead to invasive skin tumours, it is far more than just a piece of esoteric knowledge,” adds Professor Simons. “It suggests to us that targeting the pathways used in regulating cell fate decisions — how stem cells choose between cell proliferation and differentiation — could be a more effective way of halting tumours in their tracks and lead to potential new therapies.”

{Statistics from Rwanda Biomedical Center (RBC) indicate that obesity is gradually increasing among Rwandans which is creating fear of consequences that may arise from it if no immediate measures are devised. }

During the one week reserved for testing non-communicable diseases held last month, 35 of 2600 people from Kigali city had abnormal weight, 12% had hypertension while 1% was detected with much sugar in blood.

The Integrated Household Living Conditions Survey (EICV) carried in 2014/2015 indicates that 22% of Rwandan population is obese.

Talking to IGIHE the head of non-communicable diseases department at RBC, Dr Francois Uwinkindi has cited poor diet, consuming much sugar and oily foods among the causes of such obesity.

“Today people eat eating poorly.The processed foods contain much sugar and oil. We nowadays spend most of the time sitting without doing sports. Most people no longer walk but, rather, use cars which increase obesity among Rwandans.”

He explained that only few people are aware of choosing a balanced diet that does not leave them prone to obesity risks.

{{Breeds other diseases }}

Dr Uwinkindi says obesity can cause other non-communicable diseases including diabetes, hypertension, heart attack and can increase the risk of breast cancer, intestine cancer and neck cancer among others.

{{Regular sports }}

Apart from advice to consume organic fresh food, Dr Uwinkindi says Rwandans should organize regular physical exercises other than waiting for specific hours designated by the government.

“At least 30 minutes of daily sports can reduce risks of obesity-related diseases, “he said.

Information from the World Health Organization indicates that 2,800,000 of world population die of obesity while 35.8 million people have obesity related diseases, reducing life expectancy.

{Findings also disprove addition of stronger immunologic agent yields a better vaccine}

In the study, researchers worked with a species of Old World monkeys, rhesus macaques to reproduce the trial results of RV144, the only HIV vaccine that has been tested and shown to reduce the rate of HIV acquisition in a phase III clinical trial.

A new scientific study conducted by a team of leading AIDS scientists reveal results that lead the way to the development of an effective human vaccine against human immunodeficiency virus (HIV). In the study published in Nature Medicine, researchers worked with a species of Old World monkeys, rhesus macaques to reproduce the trial results of RV144, the only HIV vaccine that has been tested and shown to reduce the rate of HIV acquisition in a phase III clinical trial.

Researchers were interested in not only recapitulating the findings from the RV144 trial, but also determining if replacing the alum adjuvant–a substance commonly found in non-living vaccines known to induce antibody-mediated immunity–with a different adjuvant, MF59 would decrease simian immunodeficiency virus (SIV) acquisition at an increased rate and yield a more efficacious vaccine. Although MF59 is known to help stimulate the human body’s immune response, the idea that it could lead to greater vaccine efficacy is a popular working theory shared by scientists worldwide.

Rafick-Pierre Sekaly, PhD, the Richard J. Fasenmyer Professor of Immunopathogensis, is a pioneering AIDS researcher, co-director of the CFAR Proteomics and Systems Biology Core, a professor of pathology at Case Western Reserve University School of Medicine. He helped to lead this study which simulated potential HIV infection by rectally challenging the macaques with SIV, the primate form of HIV. Simulation in macaques has been a critical step in progressing HIV research, since the virus does not replicate well in most other model organisms.

With this simulation complete, researchers were able to successfully reproduce the RV144 trial results in macaques, ultimately finding that the RV144 vaccine combined with the alum adjuvant reduced the risk of acquisition by 44 percent, which is within the range of the 31 percent efficacy previously measured in humans. However, researchers were surprised to learn that changing the adjuvant to MF59 did not result in a significantly better vaccine, but instead rendered the altered vaccine unable to prevent SIV acquisition at a greater rate and triggered an adaptive immune response only at the site of infection, thereby disproving the commonly believed hypothesis. Importantly, researchers were able to uncover more about the alum group’s mode of action in the RV144 vaccine which, to-date, is not fully understood. Researchers discovered a unique association between an intercellular pathway known as Ras-Raf-MEK-ERK (RAS) and the efficacy of RV144. Ten of twelve genes associated with the RAS pathway were expresses within the vaccine and have been shown to trigger several subsets of innate and adaptive responses that, in turn, are associated with a decreased risk of SIV acquisition in the alum-vaccine group. Whether RAS activation is an important hallmark of HIV-vaccine efficacy in humans is an area for further study.

According to Dr. Sekaly, “These fascinating clinical results effectively dispel our previous belief that the RV144 vaccine could possibly become more effective with the MF59 adjuvant. Instead, we found that the modified vaccine actually triggered the recruitment of innate cells in the site of infection. Through this research, we were able to confirm the efficacy of the current RV144 vaccine in preventing infection by HIV/SIV in macaques, creating an even clearer pathway to the near-term development of this vaccine for human use.”

Based on the pre-vaccination RNA expression of the macaque, Dr. Sekaly and his team were also able to accurately predict whether or not the animal was going to respond to the RV144 vaccine in alum, correctly forecasting the response in two thirds of the macaques tested. These findings have tremendous implications for the use of personalized medicine in vaccinology, an exciting exploration of genomics that is already underway in the scientific community.

“We have seen that pre-selecting subjects that will benefit from a therapy based on their predicted response or risk of disease is an excellent way to improve potential outcomes,” said Dr. Sekaly. “These study results strongly support the notion that personalized and predictive vaccinology will soon become a reality, including in HIV–a disease area for which this type of precision medicine is desperately needed but has not yet been extensively studied.”

{The process by which a mother’s diet during pregnancy can permanently affect her offspring’s attributes, such as weight, could be strongly influenced by genetic variation in an unexpected part of the genome, according to research.The discovery could shed light on why many human genetic studies have previously not been able to fully explain how certain diseases, such as type 2 diabetes and obesity, are inherited.}

The study, published in Science and co-authored by University of Cambridge and King’s College London, shows that the genetic variation of ribosomal DNA (rDNA) could be driving how the environment within the womb determines an offspring’s attributes. rDNA is the genetic material that forms ribosomes — the protein building machines within the cell.

Lead researcher Professor Vardhman Rakyan from QMUL said: “The fact that genetic variation of ribosomal DNA seems to play such a major role suggests that many human genetics studies could be missing a key part of the puzzle. These studies only looked at a single copy part of individuals’ genomes and never at ribosomal DNA.

“This could be the reason why we’ve only so far been able to explain a small fraction of the heritability of many health conditions, which makes a lot of sense in the context of metabolic diseases, such as type 2 diabetes.”

The environmental factors that play a role alongside genetic factors in determining a person’s attributes are also present in the in-utero environment. When offspring are in the womb, what their mothers experience environmentally (for example, diet, stress, smoking), influences the attributes of offspring when they are adults. This ‘developmental programming’ is understood to be a large contributor to the obesity epidemic seen today.

A major contributor to this process is ‘epigenetics’. This describes naturally-occurring modifications to genes that control how they are expressed. One such modification involves tagging DNA with chemical compounds called methyl groups. These epigenetic markers determine which genes are expressed or not expressed. Liver cells and kidney cells are genetically identical apart from their epigenetic marks. It has been proposed that in response to a poor in-utero environment, an offspring’s epigenetic profile will change.

The team compared the offspring of pregnant mice when given a low protein diet (8 per cent protein) and a normal diet (20 per cent protein). After they were weaned, all offspring were given a normal diet, and the team then looked at the difference in the offspring’s DNA methylation, from mothers exposed to low protein and those that were not.

Professor Rakyan said: “Initially, we found nothing, so that was a big surprise, but then we looked at the data in a different way. We looked at the ribosomal DNA data and found huge epigenetic differences.

“When cells are stressed, for example when nutrient levels are low, they alter protein production as a survival strategy. In our low protein mice mothers, we saw that their offspring had methylated rDNA. This slowed the expression of their rDNA, which could be influencing the function of ribosomes, and resulted in smaller offspring — as much as 25 per cent lighter.”

These epigenetic effects occur in a critical developmental window while the offspring is in-utero but is a permanent effect that remains into adulthood. A mother’s low protein diet while pregnant is therefore likely to have more severe consequence on the offspring’s epigenetic state and weight than an offspring’s own diet after it has been weaned.

Professor Rakyan added: “Looking beyond the epigenetic markers, when we looked at the basic genetic sequence of the rDNA, we found an even bigger surprise. Even though all the mice in the study were bred to be genetically identical, we found that the rDNA between the individual mice was not genetically identical, and that even within an individual mouse, different copies of rDNA were genetically distinct. So there is huge variation in rDNA which is also playing a big role in determining the attributes of offspring.”

In any given genome, there are many copies of rDNA, and Professor Rakyan and colleagues found that not all copies of the rDNA were responding epigenetically. In offspring from mothers who were fed on low protein diets, it was only one form of rDNA — the ‘A-variant’ — that appeared to undergo methylation and affect weight.

This means that the epigenetic response of a given mouse is determined by the genetic variation of the rDNA — those who have more A-variant rDNA end up being smaller.

Heritability (how much the risk of a disease is explained by genetic factors) of type 2 diabetes has been estimated to be between 25 and 80 per cent in different studies. However, only about 20 per cent of the heritability of type 2 diabetes has been explained by genome studies of people with the disease.The major role that genetic variation of rDNA appears to have and the fact that rDNA analysis would not have been included in these studies could explain some of this missing heritability.

The findings also complement other studies that have found that mice that are put on high fat diets have offspring who show increased rDNA methylation.This suggests that methylation is a general stress response and may also explain the rise in obesity that is happening across the world.

{When a man has a healthy rod, it without doubt leads to him being happy. Most relationships today have failed due to the man’s inability to perform under the sheets due to his manhood being unhealthy.}

Every man should understand his equipment needs to be well taken care of and if you take care of your rod properly, it won’t disappoint you when it’s time to hit the sheets with your woman.

I have got 4 ways to do take good care of your manhood.

{{1. Reduce alcohol intake }}

To increase the health of your rod and perform excellently in bed, you should reduce your alcohol intake. Alcohol reduces cell function and also nerve response. So too much alcohol consumption isn’t good for you.

{{2. Drink lots of water }}

Water helps flush out impurities in the body. It also helps the body get rid of oxidants and toxins that damage cells and reduce efficiency and function. Drinking lots of water helps keep your kidney and male reproductive system functioning properly and this leads to a good health for your rod.

{{3. Eat healthy}}

You have got to eat healthy if you want your rod to perform properly. Less of junks and more of balanced diet is what every man needs to ensure he is healthy down there. Eating right helps your body function properly which also reflects on your organ.

{{4. Regular exercise }}

Regular exercise will improve blood circulation and your organ would benefit from it. Exercises that stimulate and activate the thighs and groin should be considered, eg squats. This would help strengthen the legs and invigorate the tissues and cells in this region and increase your cardio vascular capacity.

Have a healthy sex life with these tips.

{There are certain signs that reveal something might be wrong with you as a woman down there and it’s really important you don’t ignore these signs.}

Here are 5 health conditions you should never ignore

{{1. Bleeding after sex }}

If you bleed after sex, it’s important you see a doctor immediately. Bleeding after sex could be a sign of benign growth. Bleeding after sex could also signal cervical cancer.

{{2. Painful sex }}

If you experience pain in your lower abdomen or pelvis during sex, this could signal fibroids or endometriosis. It’s important you see your doctor if you experience this. Sex can also be painful due to a condition known as vaginismus.

{{3. Itch }}

Thrush is the most common cause of itching. Thrush can be easily treated by using antifungals such as Canesten but it’s advisable you see a doctor to be sure it’s thrush because there are other conditions that can cause your vagina to itch. Using scented products on your vagina and douching can cause your vagina to itch.

{{4. Smell }}

A fishy smell in the vagina is most likely due to bacterial vaginosis and it’s important you have yourself checked. Taking yoghurt helps maintain the good bacteria in the vagina, thereby decreasing the occurrence of bacterial vaginosis.

{{5. Abnormal discharge }}

Vaginal discharge is normal in women from puberty to menopause and the quantity of the discharge varies from woman to woman and throughout the monthly cycle. But there are instances when the discharge is abnormal. If the colour or amount of your discharge changes, it’s important you visit a doctor. A chalky white discharge could signal thrush while a frothy yellow or green discharge could signal a sexually transmitted infection known as trichomonaisis.

{Most people start their day with a hot bath but they are missing out on the benefits of having a cold shower.}

Here are 5 benefits of having a cold shower

{{1. I’s goof for the skin }}

If you love your skin, you should consider having a cold shower because hot water is bad news for your skin. Hot water removes the water-retentive fatty substances in the skin. This makes your skin dry and cracked.

{{2. Heat affects your sperm count }}

If you want to maintain a healthy sperm count, it’s advisable you ditch hot tubs and baths. It’s been found that spending more than 30 minutes in water with temperature 40 degree Celsius and above may lower your sperm count.

{{3. Makes you alert }}

Having a cold shower in the morning increases alertness. Having a cold shower in the morning has been found to increase oxygen intake thereby releasing a rush of blood through the body.

{{4. Improves circulation }}

Having a cold shower has been found to improve circulation. The improved blood circulation gotten from having a cold shower is believed to help lower blood pressure, clear blocked arteries and improve immunity.

{{5. Helps relieve muscle soreness }}

According to a 2009 study, cold water bath helps relieve sore muscles.This is the reason you see athletes take ice baths after training as it helps them reduce muscle soreness.