War and Ebola: A double nightmare in eastern DR Congo

First came the war, which developed into a brutal, bloody tussle between militias who abused civilians or killed them.

Now Ebola, a name almost as dreaded as death itself, has come.

In the Beni region, in the Democratic Republic of Congo’s eastern province of Kivu, the twin peril has bred fear and despair.

The region is haunted in particular by the Allied Defence Forces (ADF), a Ugandan Islamist rebel group blamed for hundreds of civilian deaths over the past four years.

On August 1, Beni declared an outbreak of Ebola epicentered in Mangina—a small town that had been a relative haven from the fighting—where six members of the same family died of the disease.

“I fled here from Kokola, where the ADF were committing atrocities,” said Pascaline Fitina, a 36-year-old woman, sitting alone, her head in her hands.

“I went to my elder sister, but she has died of Ebola and her husband is being quarantined at the treatment centre. I don’t what to do.”

Pascal Lukula, a 38-year-old farmer with five children, said he was stuck in Mangina, unable to get to other members of his family, because of the encroaching militia.

“We are caught between the hammer and the anvil,” he sighed. “The ADF’s on one side, and Ebola on the other.”

The Congolese health ministry said Wednesday the death toll in the east had reached 42 out of 66 probable and confirmed cases.

The outbreak—the country’s 10th since the disease was discovered in then-Zaire in 1976—was announced just a week after the end of an Ebola flareup in northwestern Equateur province that claimed 33 lives.

Chlorinated water

Ebola causes serious illness including vomiting, diarrhoea and in some cases internal and external bleeding. It is often fatal if untreated.

The disease is caused by a virus that is transmitted to people from wild animals and spreads among humans through close contact with the blood, body fluids, secretions or organs of an infected person.

In Mangina, located 30 kilometres (18 miles) southwest of the city of Beni, suspicion and rumour seem to have spread across the population.

Containers of chlorinated water have been installed in front of all shops and in the markets to provide rudimentary hand protection.

“I wear gloves to protect me from the epidemic,” said Jonas Mumbere, 26, who drives a motorcycle taxi.

“Customers have started to think twice about getting on the motorbike for fear of contamination.”

Elodie Zena, a 28-year-old sex worker, said, “Business has dropped off—customers are afraid. I’ve heard that even the sweat of someone who is infected can contaminate us. I’ve got two children and I don’t how I can feed them.”

Health experts have long fretted about the problems of combating Ebola in the DRC, a vast country that is poor and unstable and shares boundaries with nine countries.

On Tuesday, the World Health Organization (WHO) chief, Tedros Adhanom Ghebreyesus, also warned that conflict had helped create “a conducive environment for the transmission” of Ebola.

Hanna Leskinen of the International Committee of the Red Cross (ICRC) said the grassroots work in combating Ebola lies in locating and treating patients and isolating people who have been in contact with them.

In North Kivu, “people are moving around all the time, fleeing the latest wave of violence,” she said. “It enormously complicates search and followup of infected people.”

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6th Grade Georgia Teacher Donates His Kidney to Save Student's Life: 'There Is No Greater Gift'

A Georgia teacher helped save his student’s life by donating his kidney — after he was inspired by his own son’s experience with kidney failure.

Kaden Koebcke was 2 years old when he was diagnosed with a kidney disease. While he received a kidney from his father, his body rejected the transplant and he’s spent the last 10 years in and out of hospitals, on dialysis and waiting for a kidney donor to save his life, according to Fox 5.

His miracle came in the form of his sixth-grade teacher, William Wilkinson, who taught him technology at the Grace Christian Academy in Powder Springs, Georgia, according to the Atlanta Journal-Constitution.

Kaden, 12, underwent the transplant surgery on Tuesday.

His mother, Cami Koebcke, told the newspaper she was beyond grateful for Wilkinson’s donation.

“There are no words to even begin to describe how this is making me feel for Will to give this amazing gift to my son,” she said. “There is no greater gift.”

Wilkinson revealed to Fox 5 that he was inspired to donate his kidney as he knew what Kaden’s parents were going through.

“My son was actually in kidney failure when he was 2½,” Wilkinson told the outlet. “So, I remember being in that position as a parent wanting someone to help.”

Kaden did not know of his teacher’s decision until just before the surgery, as usually the doner’s identity is kept private, but then Wilkinson stopped by his home at the end of the school year and gave him the news.

“Would you like to know who the donor is?” Wilkinson reportedly asked Cami, who said yes and was consequently shocked by the revelation.

“We almost fell to the floor,” Cami told the outlet.

RELATED: Meet the 2-Year-Old Kansas Boy with Spina Bifida Who Has Stolen the Internet’s Heart!

His family created a Facebook page chronicling Kaden’s journey. On Wednesday, the family shared an update post-surgery, writing, “Kaden and Will are both doing well!”

“Kaden had a great night. He feels pretty good. Thanks to your prayers and our faithful God, his urine output is great! Prayer works!!! He had a plasmaphoresis [sic] treatment this morning and he’s doing well,” the post read.

“Will had a good night as well. He has some discomfort at times but handling it well. He’s already been up 2x to take a walking lap and he sat up in the chair for 2 hours,” the post continued. “Can’t thank you all enough for your prayers. We appreciate you. But it’s not over yet…more recovery to take place so please keep praying!”

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One Reason Why Kidney Transplants Fail

WEDNESDAY, Aug. 15, 2018 — Scottish scientists say they’ve found new clues to why some kidney transplants fail.

It has to do with the amount of “wear and tear” a transplanted kidney has and how that affects its work in the recipient, the new study says.

It was known that the age of the donor could affect how well a transplanted kidney worked, but this is the first time that the “burden of lifestyle and life events” experienced by the donor has been introduced as having an impact, according to the researchers.

They studied kidneys that failed to work after transplant, resulting in either the loss of the kidney or recipients having to go on dialysis until the new kidney started working.

The kidneys had significant changes in key genes and evidence of aging that was consistent with higher levels of “wear and tear,” according to the study authors.

“We now have strong evidence that an organ’s biological age, in combination with physiological stress, plays a major role in … impaired function, occurring. The findings also suggest that these effects are driven by donor characteristics, which may be more of a factor than transplant stress itself,” said researcher Paul Shiels, of the Institute of Cancer Sciences at the University of Glasgow.

“Our findings are important because, not only have we identified the reason why some kidney transplants don’t work when transplanted, we also demonstrate that miles on the biological clock affect the physiological function of organs,” he said in a university news release.

“This isn’t just clinically important, but is also relevant to how we age and how we can maintain good health in old age,” Shiels said.

“By using the signature set of genes from this study to identify less resilient organs before they meet a new recipient immune system, transplant stress could be reduced and outcomes improved,” he concluded.

About 10 to 12 percent of adults worldwide have chronic kidney disease, which can lead to kidney failure and the need for either dialysis or a kidney transplant.

The study was published Aug. 13 in the journal Aging Cell.

More information

The National Kidney Foundation has more on kidney transplants.

Posted: August 2018

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Talazoparib Beneficial in Patients With Advanced Breast Cancer

WEDNESDAY, Aug. 15, 2018 — Single-agent talazoparib provides significant benefit over standard chemotherapy for patients with advanced breast cancer and germline BRCA1/2 mutation, according to a study published online Aug. 15 in the New England Journal of Medicine.

Jennifer K. Litton, M.D., from the University of Texas MD Anderson Cancer Center in Houston, and colleagues conducted a randomized phase 3 trial involving patients with advanced breast cancer and a germline BRCA1/2 mutation. Participants were randomized to receive talazoparib (287 patients) or standard single-agent therapy of the physician’s choice (144 patients).

The researchers found that, compared with the standard therapy group, the talazoparib group had significantly longer median progression-free survival (8.6 versus 5.6 months; hazard ratio for disease progression or death, 0.54; 95 percent confidence interval, 0.41 to 0.71; P < 0.001). For death, the interim median hazard ratio was 0.76 (95 percent confidence interval, 0.55 to 1.06; P = 0.11). The talazoparib group had a higher objective response rate than the standard-therapy group (62.6 versus 27.2 percent; odds ratio, 5.0; 95 percent confidence interval, 2.9 to 8.8; P < 0.001). Overall, 55 and 38 percent of patients who received talazoparib and standard therapy, respectively, had hematologic grade 3 to 4 events. Outcomes reported by patients favored talazoparib, with significant overall improvements and significant delays noted in the time to clinically meaningful deterioration according to the global health status-quality-of-life and breast symptoms scales.

“Talazoparib resulted in a significantly longer progression-free survival than standard-of-care chemotherapy,” the authors write.

The study was funded by the Pfizer company Medivation, which manufactures talazoparib.

Abstract/Full Text

Posted: August 2018

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Reasons for Undergoing Cosmetic Procedures Explored

WEDNESDAY, Aug. 15, 2018 — As well as enhancing physical appearance, patients seek cosmetic procedures for emotional and psychosocial reasons, according to a study published online Aug. 15 in JAMA Dermatology.

Amanda Maisel, from Northwestern University in Chicago, and colleagues conducted a prospective study to estimate the relative importance of factors that motivate patients to seek minimally invasive cosmetic procedures. A total of 511 patients were enrolled and completed a survey instrument.

The researchers found that in addition to motivations pertaining to aesthetic appearance, including the desire for beautiful skin and a youthful, attractive appearance, other motives that were commonly reported were related to physical health, such as preventing worsening of condition or symptoms (53.3 percent), and psychosocial well-being, such as the desire to feel happier and more confident or improve total quality of life (67.2 percent), treat oneself or celebrate (61.3 percent), and look good professionally (54.8 percent). In general, cost- and convenience-related motivations were rated as less important (14.1 percent). Most of the motivations were internally generated and designed to please patients, with patients themselves making the decision to undergo cosmetic procedures. Psychological and emotional motivations were more likely among patients seeking procedures such as body contouring, acne scar treatment, and tattoo removal (86.4, 85.7, and 72.7 percent, respectively).

“This initial prospective, multicenter study comprehensively assessed why patients seek minimally invasive cosmetic procedures,” the authors write. “Common reasons included emotional, psychological, and practical motivations in addition to the desire to enhance physical appearance.”

One author disclosed financial ties to the biotechnology industry.

Abstract/Full Text (subscription or payment may be required)

Posted: August 2018

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Healthy fat cells uncouple obesity from diabetes

About 422 million people around the world, including more than 30 million Americans, have diabetes. Approximately ninety percent of them have type 2 diabetes. People with this condition cannot effectively use insulin, a hormone made by the pancreas that helps the body turn blood sugar (glucose) into energy.

The inability to use insulin, called insulin resistance, results in increasing levels of blood sugar, which, if not controlled, can significantly raise the risk of major health problems such as blindness, kidney failure, heart attacks, stroke and lower limb amputation. In 2015, the World Health Organization estimated that 1.6 million deaths were directly caused by diabetes. Until recently, this type of diabetes was only seen in adults, but it is now also occurring increasingly and more frequently in children.

“Obesity is the most significant risk factor for type 2 diabetes and other metabolic conditions, and affects one in three adults worldwide,” said Dr. Sean Hartig, assistant professor of medicine and of molecular and cellular biology at Baylor College of Medicine. “Although medical consensus recommends making life style changes toward a healthy diet and increased physical activity to both prevent and help control diabetes, this strategy has shown to be difficult to implement and maintain by most people.”

Hartig and his colleagues are exploring alternative ways to control obesity and type 2 diabetes that may involve the use of therapies that would complement the current efforts to educate the public about healthy diets and exercise routines. To achieve this goal, they are studying the cellular and molecular mechanisms involved in fat metabolism using both genetic mouse models and human tissues.

Subcutaneous white fat versus belly fat dictates metabolic health in obesity

Although obesity significantly increases the risk of diabetes, about 30 percent of obese people do not show insulin resistance and do not develop type 2 diabetes or other metabolic conditions, such as fatty liver disease. What leads to obesity while maintaining insulin sensitivity is not well understood; however, scientists know that the condition is associated with the body’s ability to expand the storage of subcutaneous white adipose (fat) tissue.

“Subcutaneous white fat represents 80 percent of all fat tissue in mice and people and it is stored in the hips, arms and legs. When energy intake (food) overwhelms the ability to store calories in subcutaneous white fat, fat ‘spills over’ into organs that are not specialized for storing fat, such as the liver, the pancreas and muscle,” said co-author Natasha Chernis, research technician at Baylor College of Medicine. “People who develop diabetes have more abdominal (belly) fat. Our idea is to find ways to expand subcutaneous white fat depots in obesity, so fat is not stored in places like the abdomen or the liver, where it can cause metabolic problems.”

Another key player in the obesity and diabetes puzzle is the immune system. Obesity leads to developing a low-grade inflammatory response that can interfere with the metabolic functions of subcutaneous white fat tissue. This inflammatory microenvironment likely disturbs this fat tissue’s ability to respond to insulin, contributing in insulin resistance and type 2 diabetes. This is supported by findings that increased levels of pro-inflammatory cytokines, such as interferon-gamma, correlate with insulin resistance, reduced subcutaneous white fat expansion and accumulation of abdominal fat. However, this brings the question, what is different in obese individuals who do not develop insulin resistance and diabetes?

Another piece of the puzzle, miR-30a

“When we started this project six years ago, our goal was to better understand fat metabolism and identify potential ways to help people lose weight,” Hartig said. “We found a microRNA called miR-30a — a small non-coding RNA molecule that regulates gene expression — that could stimulate pathways important for fat metabolism. Originally, we thought that expressing miR-30a would lead to weight loss because it would be driving fat metabolism, but we observed something different. We found miR-30a did not correlate with leanness; instead, it was associated with a form of obesity in which subjects actually maintained insulin sensitivity.”

Hartig and his colleagues discovered that reduced miR-30a expression in fat tissue correlated with insulin resistance in both obese mice and obese humans. Interestingly, overexpressing miR-30a in subcutaneous white fat tissue of obese mice significantly improved insulin sensitivity, reduced levels of blood lipids and decreased buildup of fat in the liver without altering body weight. In addition, the researchers found that miR-30a expression reduced inflammation in subcutaneous white fat tissue.

“We have provided evidence that expression of miR-30a protects fat cells by attenuating inflammation derived from mediators such as interferon gamma and leads to improved insulin sensitivity in obese mice,” Hartig said.

These findings open the possibility of developing therapeutic entry ways for many forms of diabetes, not just diabetes aligned with obesity. For instance, targeting components of the immune system locally within adipose tissue may enable subcutaneous white fat to expand appropriately in lipodystrophies — conditions characterized by abnormal distribution of body fat — where diabetes occurs in patients without obesity.

“We are interested in this idea that we can uncouple obesity from co-morbidities such as heart disease and insulin resistance,” Hartig said. “It has become clear in the past 10 years that obesity doesn’t mean diabetes. We are interested in learning how to manipulate the inflammatory response inside fat tissue of people with insulin resistance or type 2 diabetes so they expand the subcutaneous white fat deposits and become metabolically healthy.”

Read all the details of this study in the journal Diabetes.

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Scientists discover chemical which can kill glioblastoma cells

Aggressive brain tumour cells taken from patients self-destructed after being exposed to a chemical in laboratory tests, researchers have shown.

The study could be the first step in tackling cancers like glioblastoma, which led to Dame Tessa Jowell’s death earlier this year.

The research, led by the University of Leeds, found that the synthetic chemical, named KHS101, was able to cut the energy source of tumour cells from glioblastoma, leading to the death of the cells.

Published in Science Translational Medicine, the research represents an important step forward in tackling this disease, which is one of the deadliest cancers, with a five-year survival rate of less than¬ five per cent.

Over 2,000 people are diagnosed with glioblastoma in the UK every year, and it has recently been discussed in Parliament as a disease which urgently requires improvements in treatment options.

Funded initially by the Medical Research Council, the new study showed promising results which may lead to the development of a therapy to fight brain cancer in years to come.

Dr. Heiko Wurdak, from the University of Leeds who led the international research team, said: “When we started this research we thought KHS101 might slow down the growth of glioblastoma, but we were surprised to find that the tumour cells basically self-destructed when exposed to it.

“This is the first step in a long process, but our findings pave the way for drug developers to start investigating the uses of this chemical, and we hope that one day it will be helping to extend people’s lives in the clinic.”

The study revealed that the chemical was disrupting the mitochondria and metabolism within the tumour cells, and shutting off the energy supply leading to their self-destruction.

To test whether KHS101 could cross the blood brain barrier in mammals, essential for it to be effective in stopping brain cancers, tumour cells were transferred from humans into mice. The blood brain barrier stops most molecules from entering the brain and severely limits treatment options.

The chemical successfully crossed the blood-brain barrier and significantly decreased tumour growth (by around 50 per cent) in mice treated with KHS101 compared with those given a placebo, leading to an increase in survival. Importantly, normal brain cells were unaffected by the chemical.

The team also reviewed how effective KHS101 would be against the different genetic profiles of cells within a tumour, and between tumours in different patients. Genetic variation in tumours has complicated efforts to identify treatments in the past, but the team found that all tested variations of glioblastoma subtype cells responded to the treatment.

Professor Richard Gilbertson, Cancer Research UK’s brain tumour expert who wasn’t involved in the research, said: “Treatment for glioblastoma has remained essentially unchanged for decades, so there is a pressing need for preclinical research like this to identify and characterise potential new drugs.

“While the findings are encouraging, as an experimental chemical, further rigorous testing and refinement of KHS101 is required before trials in people can begin.”

Further research into the properties of KHS101 may lead scientists to discover similar drugs which also disturb the energy sources causing self-destruction of tumour cells, and thus broaden the range of treatment options available in the fight against brain tumours.

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This matrix delivers healing stem cells to injured elderly muscles

A car accident leaves an aging patient with severe muscle injuries that won’t heal. Treatment with muscle stem cells from a donor might restore damaged tissue, but doctors are unable to deliver them effectively. A new method may help change this.

Researchers at the Georgia Institute of Technology engineered a molecular matrix, a hydrogel, to deliver muscle stem cells called muscle satellite cells (MuSCs) directly to injured muscle tissue in patients whose muscles don’t regenerate well. In lab experiments on mice, the hydrogel successfully delivered MuSCs to injured, aged muscle tissue and boosted the healing process while protecting the stem cells from harsh immune reactions.

The method was also successful in mice with a muscle tissue deficiency that emulated Duchene muscular dystrophy, and if research progresses, the new hydrogel therapy could one day save the lives of people suffering from the disease.

Inflammation war zone

Simply injecting additional muscle satellite cells into damaged, inflamed tissue has proven inefficient, in part because the stem cells encounter an immune system on the warpath.

“Any muscle injury is going to attract immune cells. Typically, this would help muscle stem cells repair damage. But in aged or dystrophic muscles, immune cells lead to the release a lot of toxic chemicals like cytokines and free radicals that kill the new stem cells,” said Young Jang, an assistant professor in Georgia Tech’s School of Biological Sciences and one of the study’s principal investigators.

Only between 1 and 20 percent of injected MuSCs make it to damaged tissue, and those that do, arrive there weakened. Also, some tissue damage makes any injection unfeasible, thus the need for new delivery strategies.

“Our new hydrogel protects the stem cells, which multiply and thrive inside the matrix. The gel is applied to injured muscle, and the cells engraft onto the tissues and help them heal,” said Woojin Han, a postdoctoral researcher in Georgia Tech’s School of Mechanical Engineering and the paper’s first author.

Han, Jang and Andres Garcia, the study’s other principal investigator, published their results on August 15, 2018, in the journal Science Advances. The National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health funded the research.

Hydrogel: watery nets

Hydrogels often start out as water-based solutions of molecular components that resemble crosses, and other components that make the ends of the crosses attach to each other. When the components come together, they fuse into molecular nets suspended in water, resulting in a material with the consistency of a gel.

If stem cells or a drug are mixed into the solution, when the net, or matrix, forms, it ensnares the treatment for delivery and protects the payload from death or dissipation in the body. Researchers can easily and reliably synthesize hydrogels and also custom-engineer them by tweaking their components, as the Georgia Tech researchers did in this hydrogel.

“It physically traps the muscle satellite cells in a net, but the cells also grab onto chemical latches we engineered into the net,” Han said.

This hydrogel’s added latches, which bond with proteins protruding from stem cells’ membranes, not only increase the cells’ adhesion to the net but also hinder them from committing suicide. Stem cells tend to kill themselves when they’re detached and free-floating.

The chemical components and the cells are mixed in solution then applied to the injured muscle, where the mixture sets to a matrix-gel patch that glues the stem cells in place. The gel is biocompatible and biodegradable.

“The stem cells keep multiplying and thriving in the gel after it is applied,” Jang said. “Then the hydrogel degrades and leaves behind the cells engrafted onto muscle tissue the way natural stem cells usually would be.”

Stem cell breakdown

In younger, healthier patients, muscle satellite cells are part of the natural healing mechanism.

“Muscle satellite cells are resident stem cells in your skeletal muscles. They live on muscle strands like specks, and they’re key players in making new muscle tissue,” Han said.

“As we age, we lose muscle mass, and the number of satellite cells also decreases. The ones that are left get weaker. It’s a double whammy,” Jang said. “At a very advanced age, a patient stops regenerating muscle altogether.”

“With this system we engineered, we think we can introduce donor cells to enhance the repair mechanism in injured older patients,” Han said. “We also want to get this to work in patients with Duchene muscular dystrophy.”

“Duchene muscular dystrophy is surprisingly frequent,” Jang said. “About 1 in 3,500 boys get it. They eventually get respiratory defects that lead to death, so we hope to be able to use this to rebuild their diaphragm muscles.”

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Does Mountain Dew kill sperm? The truth

Though Mountain Dew does not affect fertility, many other unrelated factors can lower sperm counts and affect male fertility. These include:

  • low testosterone
  • smoking
  • obesity
  • diabetes

Exercising, quitting smoking, and losing weight are some ways to improve fertility. Listed in this article are several other proven methods a person can try to boost their fertility.

Does Mountain Dew affect fertility at all?

Mountain Dew does not affect fertility. It has acquired the reputation of impacting fertility mainly due to caffeine and yellow dye 5:

Does caffeine affect fertility at all?

The Nutrition Journal reviewed 28 studies that looked at different sperm measurements.

The researchers concluded that results were not consistent enough to be conclusive, despite some evidence of negative effects.

Mountain Dew has a higher amount of caffeine in a 12-ounce (oz) serving than some other soft drinks, which has lead to people taking it as proof that Mountain Dew affects fertility.

Comparing 12 oz servings of Mountain Dew and other drinks shows only a small difference in the amount of caffeine in each:

  • Pepsi-Cola: 37.5 milligrams (mg)
  • Coca-Cola Classic: 34.0 mg
  • Diet Coke: 45.6 mg
  • Mellow Yellow: 52.8 mg.
  • Mountain Dew (in various flavors): 55.0 mg.

People should still watch their caffeine intake, although caffeine is unlikely to affect fertility. But it is doubtful that Mountain Dew’s caffeine content would affect fertility when consumed in moderation.

Does yellow dye 5 affect fertility?

Yellow dye 5 is one of the most commonly used food additives.

The chemical name of yellow dye 5 is tartrazine. Tartrazine is what gives Mountain Dew its yellow color. Also, people often cite that tartrazine is a potential allergen as part of the myth.

There are not many current studies on the effects of tartrazine on fertility. One study in rats, although dating back to 1988, was published in Food and Chemical Toxicology and indicated no adverse effects to consuming tartrazine.

The U.S. Food and Drug Administration (FDA) have approved color additives, including tartrazine, for use in both food and drugs.

Tartrazine does pose a risk of allergy to a small portion of the population. People who are allergic to tartrazine may experience side effects from its consumption.

Side effects of tartrazine include:

  • hyperactivity
  • eczema
  • asthma

People who are allergic to tartrazine should avoid its consumption in food and beverages, but not because of any concerns about effects on fertility.

Yellow dye 5, as well as other food dyes, may be contaminated with carcinogens or substances that convert to carcinogens in the body, according to the Center for Science in the Public Interest (CSPI).

Food dyes are among many additives that the CSPI recommend to avoid for a variety of health reasons.

Several proven factors can lower sperm counts and affect male fertility.

According to a review of studies in Biochemistry & Analytical Biochemistry, risk factors for lowering male fertility include:

  • age, which sees testosterone in the blood fall, affecting sperm count from around 30 years of age onward
  • smoking, which can slow sperm down
  • obesity, which affects the number of viable sperm
  • excessive exercise, which may lower sperm count
  • occupational risks, such as regularly working with poisonous chemicals
  • prolonged exposure to heat from a laptop, which can reduce sperm count
  • excessive alcohol consumption
  • scrotal temperature
  • stress levels
  • therapeutic drugs
  • diabetes and raised blood sugars

The same review of studies explored medical causes of male fertility issues, including:

  • varicocele, a condition affecting the testicular veins
  • infections in the male reproductive tract
  • endocrine disorders affecting male hormones
  • disorders that affect male ejaculation
  • genetic and chromosomal defects
  • immunological factors where sperm antibodies form

Changes that can help improve fertility or sperm count include:

  • losing excess weight
  • reducing added and refined sugars in the diet
  • increasing fiber intake from food
  • exercising regularly
  • eating walnuts regularly
  • having a healthful diet rich in nutrients including iron, zinc, and other vitamins and minerals
  • taking folate and antioxidant supplements
  • getting plenty of sleep
  • limiting alcohol consumption
  • reducing soy intake

Takeaway

Mountain Dew does not cause infertility or lower sperm count when consumed in moderation.

Other factors can cause a person to be less fertile, but Mountain Dew does not appear to cause more health effects than other soft drinks.

Mountain Dew is not a healthy drink. People should avoid drinking excessive amounts of any soft drink and sugar-sweetened beverages, including Mountain Dew, so they control their blood sugars and weight, both of which are factors that can affect fertility.

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Stroke: Time not the only factor in emergency care

Neurologist Dr. Camilo R. Gomez pronounced in an editorial published in the Journal of Stroke & Cerebrovascular Diseases in 1993 that “Time is brain!”

“Unquestionably,” he wrote, “the longer therapy is delayed, the lesser the chance that it will be successful.”

In the meantime, however — with the help of new tools — researchers have been taking a closer look at what happens in the brain during and after a stroke, particularly at patterns of blood circulation.

Stroke occurs when the blood supply to a part of the brain stops and cells begin to die due to lack of oxygen and nutrients.

There are two main types of stroke: ischemic and hemorrhagic. Ischemic strokes, which result from clots or blood vessel constrictions, are by far the most common. Hemorrhagic strokes occur when vessels burst.

‘Collateral circulatory competence’

Now, in a new paper published in that same journal, Dr. Gomez — a stroke specialist from Loyola University Medical Center in Maywood, IL — argues that time should not be the only factor to dictate how ischemic stroke is treated.

The effect of time is likely to be different in different cases, depending on what is known as the person’s “collateral circulatory competence.”

When an ischemic stroke occurs, cells in a “core of brain tissue” start to die. However, the cells that surround the core — which is known as the penumbra — can still receive oxygen and nutrients and stay alive if there is good collateral circulation. The more robust the collateral circulation is, the longer the cells live.

In his paper, Dr. Gomez explains how use of a computational model helped identify four types of ischemic stroke that differ by pattern of collateral blood circulation.

He notes that modeling the types allows “forecasting of the fate of the ischemic process over time.”

Time is not the only factor

An optimal pattern “was predictably associated” with a slower injury rate in the affected area and a longer window of opportunity for therapy, for example.

“It is no longer reasonable to believe that the effect of time on the ischemic process represents an absolute paradigm,” argues Dr. Gomez.

He notes that there is increasing evidence of “considerable variability” in the volume of tissue that becomes injured within a given time after the onset of stroke. He also explains that this is “in large part due to the beneficial effect of a robust collateral circulation.”

It’s clearly evident that the effect of time on the ischemic process is relative.”

Dr. Camilo R. Gomez

He concludes that because we can now “readily identify” distinct collateral circulation patterns for different people, it is possible to predict how the aftermath of stroke is likely to affect the brain.

This improves opportunities to analyse the stroke process and select the best treatment.

Acting FAST saves lives

Dr. Gomez’s suggestions affect decisions made in the emergency room, so it is still important to call 911 and get help immediately if you think that someone is having a stroke.

FAST action can save a life. FAST is a simple checklist for helping you decide if someone is having a stroke. It stands for Face, Arms, Speech, Time, as follows:

    • Face: When you ask the person to smile, does one side of their face droop?
    • Arms: When you ask them to raise both arms, does one “drift downward?”
    • Speech: Do they slur their speech when you ask them to “repeat a simple phrase?”
    • Time: If the answer to any of these is “yes,” call 911 straight away.

    In the United States, around 140,000 people die from stroke every year, accounting for some 1 in 20 deaths.

    For 1 out of every 4 of the 795,000 people in the U.S. who have a stroke, it is not their first; and in 87 percent of cases, the stroke is ischemic.

    The total cost of stroke in the U.S. is in the region of $34 billion per year. This includes healthcare, medication, and lost productivity.

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