New Drug for Treatment of Myocardial Infarction Now in Cuba

Havana, Jul 25 (Prensa Latina) A medication for the treatment of acute myocardial infarction, developed by the Center for Genetic Engineering and Biotechnology (CIGB), will be available in Cuba next year, the Granma newspaper announced today.

The product, called CIGB-500, is made up of six amino acids and will help to extend the quality and duration of life of people with this disease, considered one of the most serious conditions of ischemic heart disease, the statement points out.

It also expands the cellular mechanisms of cytoprotection during hepatic or cardiac ischemia and the episodes of reperfusion which occur when significant times are used during surgery, Jose Brito, CIGB's director of national promotion and distribution, explained to the newspaper.

The biotechnological compound completed its preclinical and developmental stage. In 2008, a clinical study phase I on healthy volunteers was completed, and phase II on affected patients began in November 2013, Brito added.

After the studies carried out, it was concluded that CIGB-500 is not incompatible with the most commonly used drugs approved for the treatment of this condition, said Yunia Delgado, a specialist of the Communication Group of the center.

With the development of this synthetic peptide, it is expected to satisfy national demand and join the National Health and Export System, Delgado continued.

According to the report Biomedical Projects of the CIGB Business Portfolio, this project is the first medication applied for the treatment of this disease.

Also, the text adds, it will reduce the extent of the infarction, protect the body's epithelial organs from damage caused by ischemia-reperfusion events, treat liver damage and control and reduce the progression of hepatic fibrosis.

According to the Public Health Statistical Directory, severe myocardial infarction is the third cause of death from heart disease in Cuba, responsible for 7,177 deaths in 2017.

Cardiac reperfusion is a medical procedure which may save a person's life after a heart attack.

Toothpaste Can Cause Diabetes, Study Says

Washington, Jul 24 (Prensa Latina) The titanium dioxide present in toothpaste favors the appearance of diabetes type two, according to research by the University of Texas, United States.

To demonstrate that statement, the authors analyzed small samples of pancreas tissue from 11 volunteers, says an article in the journal Chemical Research in Toxicology.

As a result, eight of them suffered from diabetes type two and titanium dioxide (E171) was found in their parts. No trace of the chemical was found in the remaining three people.

The authors announced they expect to repeat the experiment in a larger group of people.

E171 is widely used in cosmetics and food industries for its ability to provide a whitish color to products.

Diabetes type two is a metabolic disorder characterized by high blood sugar levels. Its classic symptoms are excessive thirst, frequent urination and constant hunger.

New health calculator can help predict heart disease risk, estimate heart age

A new online health calculator can help people determine their risk of heart disease, as well as their heart age, accounting for sociodemographic factors such as ethnicity, sense of belonging and education, as well as health status and lifestyle behaviours. The process to build and validate the tool is published in CMAJ (Canadian Medical Association Journal).

Cardiovascular disease is the leading cause of death in Canada, although risks of death from heart disease are modifiable with lifestyle changes. Most people are unaware of their cardiovascular risk until they experience a cardiac event, which may be fatal.

"What sets this cardiovascular risk calculator apart is that it looks at healthy living, and it is better calibrated to the Canadian population," says Dr. Doug Manuel, lead author, senior scientist at The Ottawa Hospital and a senior core scientist at the Institute for Clinical Evaluative Sciences (ICES).

Using a "big data" approach, researchers used routinely collected data on 104 219 Ontario residents from the Canadian Community Health Surveys (2001 to 2007) linked to ICES data on hospitalizations and deaths to develop and validate the Cardiovascular Disease Population Risk Tool (CVDPoRT).

The calculator allows individuals to accurately predict their risk of hospitalization or death from cardiovascular disease within the next five years. For example, if their risk is five percent, it means that five in 100 people like them will experience a serious cardiovascular event in the next five years. The calculator also provides heart age, an easy-to-understand measure of heart health.

Unlike other risk prediction tools, the Cardiovascular Disease Population Risk Tool considers many factors, such as sociodemographic status, environmental influences like air pollution, health behaviours ranging from smoking status to alcohol intake to physical activity, health conditions and more. The list includes:

  • Age
  • Smoking status and lifetime exposure
  • Alcohol consumption
  • Diet
  • Physical activity
  • Stress
  • Sense of belonging
  • Ethnicity
  • Immigration status
  • Education
  • Socioeconomic status of the neighbourhood
  • Diabetes
  • High blood pressure

"A lot of people are interested in healthy living, but often we don't have that discussion in the doctor's office," says Dr. Manuel, who is also a professor at the University of Ottawa. "Doctors will check your blood pressure and cholesterol levels, but they don't necessarily ask about lifestyle factors that could put you at risk of a heart attack and stroke. We hope this tool can help people -- and their care team -- with better information about healthy living and options for reducing their risk of heart attack and stroke."

In addition to personal use, policy-makers can use the tool to calculate risk profiles for different populations. Currently set up for use in Canada, it can be adapted for any of the 100 countries around the world that collect health survey data.

Protecting tropical forest carbon stocks may not prevent large-scale species loss

Tropical forests are rich in carbon and biodiversity. As the world seeks to curb human-induced climate change, will protecting the carbon of tropical forests also ensure the survival of their species?

A study published today in the leading journal Nature Climate Change suggests the answer to this question is far from straightforward.

Investments designed to prevent massive carbon losses from the world's tropical forests are likely to be least effective for biodiversity in the most ecologically valuable forests, according to research by an international team, led by scientists from Lancaster University's Environment Centre (UK) and The Brazilian Agricultural Research Corporation (EMBRAPA).

Alarmingly, in these forests, up to 77% of species that would have been protected through biodiversity conservation were not protected through measures focused solely on protecting carbon stocks.

"Securing tropical forest carbon should remain a central conservation objective," said Dr. Gareth Lennox, co-lead author of the study and a Senior Research Associate at Lancaster University. "Not only will this slow climate change but it also has the potential to safeguard the unique and irreplaceable wildlife that inhabits these ecosystems. However, to ensure that those species survive, biodiversity needs to be treated as a priority -- alongside carbon -- of conservation efforts."

The global importance of tropical forests

Tropical forests store more than a third of the world's land carbon. When released to the atmosphere by humans, through forest disturbances -- such as logging and fires -- and deforestation, this carbon exacerbates global warming.

Protecting tropical forest carbon is therefore a key aim of international initiatives to blunt climate change and has attracted tens of billions of dollars of financing.

Tropical forests are also the world's most biodiverse ecosystems, harbouring more than two-thirds of Earth's land species, but the implications for biodiversity of investments focused only on protecting carbon stocks have until now remained unclear.

The relationship between carbon and biodiversity

The international team, comprised of scientists from Brazil, Europe and Australia, spent 18 months measuring the carbon content and species richness of plants, birds and dung beetles in 234 tropical forests in the Brazilian Amazon.

In a scientific first, they assessed carbon and biodiversity levels in forests spanning the range of human impacts, from those minimally disturbed to those recovering after complete clearance of vegetation.

Using these unprecedented data, the team found that more carbon meant more biodiversity in severely damaged forests, as anticipated. Contrary to expectations, however, where human impacts were less intense, increasing amounts of carbon did not come with more species.

Co-lead author Dr. Joice Ferreira from EMBRAPA outlined the significance of these findings: "The changing relationship between carbon and biodiversity across forests that have suffered different kinds of human disturbances explain our findings. As cleared and highly disturbed sites recover from the effects of agricultural use and severe wildfires, biodiversity also recovers. However, this linkage between carbon and biodiversity breaks down mid-recovery. The result: Forests with the greatest carbon content do not necessarily house the most species, meaning carbon-focused conservation can miss large swathes of tropical forest biodiversity."

Focusing on both biodiversity and carbon

Alongside these more alarming findings, the study offered hope for aligning carbon and biodiversity conservation efforts. "Although trade-offs are inevitable, conflicts between carbon and biodiversity can be reduced by more integrated planning," said Dr. Toby Gardner, Senior Research Fellow at the Stockholm Environment Institute and study co-author. "By considering carbon and biodiversity together, we found, for example, that the number of large tree species that can be protected can be increased by up to 15% relative to a carbon-only approach for just a 1% reduction in carbon coverage."

While promising remote sensing tools are being developed to measure forest carbon, increasing biodiversity protection through carbon investments is only possible with extensive field monitoring. Yet, in Brazil, progress in this area is sorely lacking. Joice Ferreira described the situation, "As a megadiverse country, Brazil needs additional, integrated mechanisms to guarantee comprehensive monitoring of its biodiversity. Unfortunately, with government actions reducing scientific capacity and environmental protection, we are witnessing the exact opposite."

Ultimately, curbing climate change requires the safeguarding of biodiversity. Co-author Professor Jos Barlow from Lancaster University explained why, "Biodiversity and climate change are inextricably linked in tropical forests. A warming climate and changing rainfall patterns will lead to the extinction of many tropical species, while it is within tropical biodiversity itself that forest carbon resides. Species-poor forests will eventually become carbon-poor. Therefore, tackling the climate crisis requires that both tropical forest carbon and tropical forest species are protected together."

The 'Big Bang' of Alzheimer's: Scientists ID genesis of disease

Scientists have discovered a "Big Bang" of Alzheimer's disease -- the precise point at which a healthy protein becomes toxic but has not yet formed deadly tangles in the brain.

A study from UT Southwestern's O'Donnell Brain Institute provides novel insight into the shape-shifting nature of a tau molecule just before it begins sticking to itself to form larger aggregates. The revelation offers a new strategy to detect the devastating disease before it takes hold and has spawned an effort to develop treatments that stabilize tau proteins before they shift shape.

"We think of this as the Big Bang of tau pathology. This is a way of peering to the very beginning of the disease process."

Dr. Mark Diamond, Director for UT Southwestern's Center for Alzheimer's and Neurodegenerative Diseases "This is perhaps the biggest finding we have made to date, though it will likely be some time before any benefits materialize in the clinic. This changes much of how we think about the problem," said Dr. Marc Diamond, Director for UT Southwestern's Center for Alzheimer's and Neurodegenerative Diseases and a leading dementia expert credited with determining that tau acts like a prion -- an infectious protein that can self-replicate.

The study published in eLife contradicts the previous belief that an isolated tau protein has no distinct shape and is only harmful after it begins to assemble with other tau proteins to form the distinct tangles seen in the brains of Alzheimer's patients.

Scientists made the discovery after extracting tau proteins from human brains and isolating them as single molecules. They found that the harmful form of tau exposes a part of itself that is normally folded inside. This exposed portion causes it to stick to other tau proteins, enabling the formation of tangles that kill neurons.

"We think of this as the Big Bang of tau pathology," said Dr. Diamond, referring to the prevailing scientific theory about the formation of the universe. "This is a way of peering to the very beginning of the disease process. It moves us backward to a very discreet point where we see the appearance of the first molecular change that leads to neurodegeneration in Alzheimer's. This work relied on a close collaboration with my colleague, Dr. Lukasz Joachimiak."

Despite billions of dollars spent on clinical trials through the decades, Alzheimer's disease remains one of the most devastating and baffling diseases in the world, affecting more than 5 million Americans alone.

Dr. Diamond is hopeful the scientific field has turned a corner, noting that identifying the genesis of the disease provides scientists a vital target in diagnosing the condition at its earliest stage, before the symptoms of memory loss and cognitive decline become apparent.

His team's next steps are to develop a simple clinical test that examines a patient's blood or spinal fluid to detect the first biological signs of the abnormal tau protein. But just as important, Dr. Diamond said, efforts are underway to develop a treatment that would make the diagnosis actionable.

He cites a compelling reason for cautious optimism: Tafamidis, a recently approved drug, stabilizes a different shape-shifting protein called transthyretin that causes deadly protein accumulation in the heart, similar to how tau overwhelms the brain.

"The hunt is on to build on this finding and make a treatment that blocks the neurodegeneration process where it begins," Dr. Diamond said. "If it works, the incidence of Alzheimer's disease could be substantially reduced. That would be amazing."

Dr. Diamond's lab, at the forefront of many notable findings relating to tau, previously determined that tau acts like a prion -- an infectious protein that can spread like a virus through the brain. The lab has determined that tau protein in the human brain can form many distinct strains, or self-replicating structures, and developed methods to reproduce them in the laboratory. He said his newest research indicates that a single pathological form of tau protein may have multiple possible shapes, each associated with a different form of dementia.

Dr. Diamond, who holds the Distinguished Chair in Basic Brain Injury and Repair, is founding Director of the Center for Alzheimer's and Neurodegenerative Diseases, and Professor of Neurology & Neurotherapeutics with the Peter O'Donnell Jr. Brain Institute at UT Southwestern. He collaborated on the study with co-corresponding author Dr. Joachimiak, an Assistant Professor in the Center for Alzheimer's and Neurodegenerative Diseases and an Effie Marie Cain Scholar in Medical Research.

The research was supported with funding from the Rainwater Charitable Foundation, the National Institutes of Health, and the Effie Marie Cain Endowed Scholarship.

Musical surgery: Flutist plays Bach & Mozart as doctors cut out her brain tumor

Surgery to remove a brain tumor is terrifying at best, but one patient decided to make the process a little more bearable, by playing the flute during the operation, providing surgeons with a recital in the most unusual of places.

Sofia Pinaeva, 28, underwent the surgery at University Hospital in Graz, Austria. She opted to stay awake for the surgery; if asleep, the patient runs a higher risk of losing brain function in the procedure.

But staying awake is one thing. Playing the flute while surgeons slice into your brain is another.

“From the outside, that's rather unusual,” 28-year-old Pinaeva said, while laughing, as reported by Kurier. However, the music teacher said there was “no question” about whether she would perform during the operation.

 

FILE PHOTO © Sam Edwards

“Bach, Mozart, I played everything that came to mind,” she said.

While it seems crazy, her surgeons would have had to make sure that Pinaeva’s mind was active and cognizant in another way, had she not chosen to play the flute.

“We are looking for tasks and functions that are easy to answer during the operation,” psychologist Karla Zaar said. “That would be different for every patient. Some have to describe pictures in a whole sentence, for example: 'This is a tree.'” The clinic has also had patients who identified dinosaurs from photos or who completed mathematical equations during such procedures.

Pinaeva is now recovering from her operation, which removed about half of the tumor – more than would have been possible were she to have slept during the surgery. She is doing well, and even arranged a garden party with friends just days after the surgery.

“I have a brain tumor,” she said. “Some people react as if I'm already dead. But it goes on. It is important to me to show that this diagnosis is not a death sentence.”

  • Published in World

Fountain of youth? Scientists pinpoint gene related to aging

There may have been a major scientific breakthrough in understanding aging, as scientists have identified a gene that plays a key role in kick-starting the process that makes cells start turning "old."

Researchers from the University of Buffalo in New York have discovered that one particular gene, CD36, triggers the beginning of the phenomenon of senescence. After it is activated, cells stop dividing and start to wither.

Senescence is a natural occurrence in the life cycle of every cell. It has long been the focus of medical research, because senescent cells are thought to contribute to a range of ailments, from heart disease and cataracts to arthritis.

 
© Getty

The new study, published in the journal Molecular Omics, found that CD36 was particularly active in older, senescent cells. The scientists were also able to cause young, healthy cells to quickly act as if they were old by increasing their CD36 activity.

“What we found was very surprising,” one of the researchers, Ekin Atilla-Gokcumen, explained. “Senescence is a very complex process, and we didn’t expect that altering expression of one gene could spark it, or cause the same effect in surrounding cells.”

The researchers did not set out to investigate CD36. Rather, they wanted to catalogue all genes related to the aging of cells. They were particularly interested in the lipid-related genes that are involved in this process, because previous studies have shown that lipids play an important role in cellular aging.

CD36 quickly emerged as a gene of interest because it repeatedly popped up in different tests designed to capture the factors that cause cell aging.

READ MORE: Vain, self-centred & successful: ‘Mental toughness’ drives narcissists to success, study finds

While the discovery is exciting, the gene’s exact role in the aging process remains shrouded in mystery. Scientists know that CD36 guides the body in building a protein that sits on the surface of cells, but what exactly the protein does is still being studied. The researchers say the gene represents an exciting topic for deeper research into how cells age.

“Our research identifies CD36 as a candidate for further study. Senescence is a fundamental aspect of being a cell, but there is still a lot that we don’t know about it,” said Omer Gokcumen, one of the paper’s authors. “Senescence seems to have implications for old age and cancer, so understanding it is very important.”

Marriage may protect against heart disease/stroke and associated risk of death

Marriage may protect against the development of heart disease/stroke as well as influencing who is more likely to die of it, suggests a pooled analysis of the available data, published online in the journal Heart.

The findings prompt the researchers to suggest that marital status should be included as a risk factor for heart disease/stroke and likely survival in its own right.

Most (80%) cardiovascular disease can be attributed to well known risk factors: age; sex; high blood pressure; high cholesterol; smoking; and diabetes. But it's not clear what influences the remaining 20 per cent.

The findings of previous research on the impact of marital status have been somewhat mixed, so in a bid to clarify the issues, the authors trawled research databases for relevant published studies.

They drew on 34 out of a total of 225, all of which had been published between 1963 and 2015, and involved more than 2 million people aged between 42 and 77 from Europe, Scandinavia, North America, the Middle East, and Asia.

Pooled analysis of the data revealed that, compared with people who were married, those who weren't (never married, divorced, widowed) were at heightened risk of developing cardiovascular disease (42%) and coronary artery heart disease (16%).

Not being married was also associated with a heightened risk of dying from both coronary heart disease (42%) and stroke (55%).

When the data were broken down further, the analysis showed that divorce was associated with a 35 per cent higher risk of developing heart disease for both men and women, while widowers of both sexes were 16 per cent more likely to have a stroke.

While there was no difference in the risk of death following a stroke between the married and the unmarried, this was not the case after a heart attack, the risk of which was significantly higher (42%) among those who had never married.

The authors caution that the methods used and adjustments made for potentially influential factors varied considerably across all the studies, which may have affected the results of their analysis.

Similarly, there was no information on same sex partnerships or the quality of marriage, and the potential role of living with someone, as opposed to being married to them, was not explored.

But this is the largest study to date, with the age and ethnicity of the participants strengthening the wider applicability of the findings, the authors point out.

And there are various theories as to why marriage may be protective. These include earlier recognition of, and response to, health problems; better adherence to medication; better financial security; enhanced wellbeing; and better friendship networks.

"Future research should focus around whether marital status is a surrogate marker for other adverse health behaviour or cardiovascular risk profiles that underlies our reported findings or whether marital status should be considered as a risk factor by itself," the authors conclude.

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