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Month: May 2023

A new method may help forecast chronic renal illness risk.

A new method may help forecast chronic renal illness risk.

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Heart disease is more likely to strike those with chronic kidney disease (CKD). Researchers created a model to predict cardiovascular risk in CKD patients using proteomics, the study of proteins.

The model was proven to be more reliable than the standard techniques for determining risk. Additionally, scientists found several proteins that might be used in future treatments.

People with chronic kidney disease (CKD) die from cardiovascular disease (CVD) more frequently than any other cause.

Stage 1 of CKD, when there is visible evidence of kidney loss but viable kidney tissue is still present, progresses to stage 5, often known as end-stage renal disease, where dialysis or a kidney transplant is required.

A 2021 study found that stage 4 and stage 5 CKD patients suffer CVD in about half of cases.

The techniques available to medical professionals to assess patients with CKD’s cardiac risk are limited. The Pooled Cohort Equation (PCE), designed by the American College of Cardiology and the American Heart Association in 2013, was created to evaluate cardiovascular risk.

The original version did not, however, account for measurements for chronic kidney disease. Researchers have issued a warning that risk prediction techniques made for the general population may not be as reliable for CKD patients.

A new risk model for cardiovascular disease in CKD patients has been established as a result of an initiative coordinated by scientists at the Perelman School of Medicine at the University of Pennsylvania. According to the researchers, it is more accurate than the methods currently used to assess these people’s cardiac risk.

Protein biomarkers were discovered by researchers.

The extensive study of proteins known as proteomics was used by the researchers to create a model to predict cardiovascular risk. A particular protein may function as a biomarker, a marker for a particular illness in the body.

The Chronic Renal Insufficiency Cohort (CRIC), a prospective study of adults with CKD conducted at seven U.S. clinical centers, and a cohort from Atherosclerosis Risk in Communities (ARIC), a prospective epidemiologic study carried out in four U.S. communities, provided the researchers with nearly 5,000 proteins from 2,667 participants with CKD.

According to Bansal, who was not engaged in the study but cited the model’s and study’s usage of numerous people from various areas throughout the county as one of their advantages

32 proteins were chosen by the researchers to be part of their proteomic risk model using machine learning techniques. These proteins were shown to be the ones that most accurately predicted the risk of cardiovascular disease in CKD patients.

They employed a broad-based approach to identify proteins that may reveal novel biological pathways that increase the risk of cardiovascular disease in individuals with renal illness, focusing on biology and disease mechanisms, according to Bansal.

Research of chronic kidney disease

Cryopreserved plasma samples from the participants chosen for this study from the CRIC were available for proteomic evaluation. The chosen participants had CKD and ranged in age from 21 to 74.

Dialysis patients and participants with end-stage renal disease were excluded. People who at the start of the study self-reported having had coronary heart disease, a myocardial infarction, a stroke, or heart failure were excluded. They were also excluded if they had a documented history of those events.

There were 2,182 participants in the last batch.

Participants in the CRIC were slightly younger, more likely to be men and Black than those in the ARIC. In addition, CRIC participants were less likely to be active smokers and more likely to have a history of diabetes and hypertension.

In comparison to CRIC participants, participants in ARIC had higher total cholesterol levels. There were 459 cardiovascular events throughout a 10-year follow-up period in the CRIC cohort and 173 cardiovascular events in the ARIC cohort.

The risk indicator’s precision

Researchers created a proteomic risk model for incident cardiovascular risk in the participants and used 390 ARIC cohort members, all of whom had CKD, to verify the model.

Researchers also determined the participants’ 2013 PCE. Additionally, they noted the history of hypertension in the participants, as well as their diastolic blood pressure, proteinuria, and estimated glomerular filtration rate (eFGR), a score that represents kidney function.

“They were trying to look at how these biological pathways compare with clinical prediction models, in terms of predicting cardiovascular events,” Bansal said.

The proteomic cardiovascular risk model, according to the researchers, was more accurate in predicting a CKD patient’s risk for having a cardiac event than the PCE and a modified PCE that took into account eFGR scores.

Bansal said, “I believe the study does progress the field.” Over ten years, participants with the highest measure of predicted risk experienced a 60% observed incident cardiovascular event rate.

Nancy Mitchell, RN, a registered nurse with more than 37 years of experience treating patients with chronic renal illness and chronic cardiovascular problems, is optimistic that the study could result in “improving the treatment options for heart disease.”

Researchers may look at how the proteins found in bloodwork relate to cardiac disease and how they may use these discoveries to develop more specialised drugs for the condition, she said.

REFERENCES:

For Renal disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=82

Reduce the Dementia risk by strict blood pressure control.

Reduce the Dementia risk by strict blood pressure control.

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The effects of intensive versus routine hypertension treatment on brain lesions were examined by researchers at the University of Texas Health Science Centre in San Antonio.

The researchers discovered that intensive therapy that maintains blood pressure within normal bounds is associated with a slowed progression of lesions using data from a previous study.

The study results could influence treatment strategies for hypertensive patients to lower the likelihood of lesions that can result in diminished cognitive performance with further research and trials.

Millions of people have hypertension, which can lead to strokes and brain lesions and compromise brain health.

An aggressive blood pressure regimen can slow the growth of white matter lesions in the brain, according to a recent study headed by UT Health San Antonio.

In contrast to patients with systolic blood pressure readings of 140 mm Hg, the researchers compared the MRI scans of individuals who maintained blood pressure levels below 120 mm Hg.

What is considered hypertension?

Millions of Americans suffer from the medical disease known as hypertension, sometimes known as high blood pressure. Nearly half of American adults have hypertension, which the Centres for Disease Control and Prevention claim contributed to more than 670,000 deaths in 2020.

Blood vessel damage and other health issues can result from high blood pressure. Heart attacks and strokes are two conditions brought on by hypertension.

The following blood pressure ranges are described by the American Heart Association:

For individuals, a normal blood pressure reading is defined as an upper number (systolic) less than 120 over a lower number (diastolic) of 80 mm Hg.

  • Blood pressure that is elevated is 120 to 129 over 80 or less.
  • Hypertension in stage 1 is defined as 130-139 above 80-89.
  • 140 over 90 or higher indicates stage 2 hypertension.

When the systolic and/or diastolic values exceed 180 and 120 respectively, a hypertension crisis ensues.

As the cardiologist, Dr. Kershaw Patel points out in the Houston Methodist podcast On Health, “When we talk about high blood pressure, we must realise it affects not just the heart, but also the brain, the kidneys, and other organs in the body.”

Although doctors frequently prescribe prescription drugs to treat high blood pressure, patients can also try to lower or normalise their blood pressure by making changes to their lifestyle.

Dr. Patel stated that lifestyle changes and then drugs are commonly used to manage high blood pressure. And it really comes down to two-thirds lifestyle and one-third medicine. By adjusting a few aspects of our lifestyle, we can significantly lower our blood pressure.

Blood pressure can be normalised by giving up smoking, consuming less alcohol, exercising, eating a low-sodium diet, and eating more fruits and vegetables.

lowering one’s blood pressure to 120

The American Academy of Family Physicians’ (AAFP) standard of care for hypertensive patients is to lower their systolic blood pressure to 140 mm Hg. This goal lowers the risk of cardiovascular death, according to the AAFP.

To assess the effect on white matter lesions (WMLs), the UT Health San Antonio researchers compared the normal treatment target to a more rigorous therapy. The goal of the rigorous treatment program was to lower participants’ systolic blood pressure to under 120 mm Hg.

The researchers examined data from 458 participants using information from the Systolic Blood Pressure Intervention Trial (SPRINT), which tracked participants for 4 years. Participants in the study were “aged 50 years or older with hypertension and without diabetes or a history of stroke,” according to the study’s authors.

At the start and conclusion of their trials, the researchers matched each participant’s treatment to their MRI images. They were searching for WMLs, a type of injury to the brain’s white matter that can result in cognitive impairment.

Treatment that is intensive lessens brain damage

According to the study’s findings, the intensive treatment group’s WML volume progression and fractional anisotropy (FA) declines were slower than those of the conventional treatment group.

The FA result is noteworthy since it represents a “measure of connectivity in the brain.” The right splenium, right tapetum, and left anterior corona radiata are a few of the brain areas that saw slower WML growth.

The study also demonstrates that aggressive blood pressure management may be able to maintain some myelin structure, which, according to the scientists, “ultimately slows the progression of injury patterns associated with dementia.”

According to research author Dr. Tanweer Rashid, who works with the Biggs Institute at UT Health San Antonio, “our study shows that specific areas have greater benefit, representing sensitive regions to track in future trials evaluating small-vessel disease.”

How white matter is impacted by blood pressure?

The study’s findings were discussed by Dr. Arun Manmadhan, a cardiovascular disease expert at Columbia University Irving Medical Centre in New York City.

“White matter lesions are abnormally damaged regions of tissue in the white matter of the brain. According to Dr. Manmadhan, they are frequently brought on by anomalies in the tiny blood arteries that provide oxygen and nutrients to the brain.”

Dr. Manmadhan provided more information on the study’s findings, namely how blood pressure may affect WMLs.

“The current report, which is a SPRINT-MIND substudy, examined the impact of stringent blood pressure management on changes in the brain’s white matter as determined by MRI.”

According to Dr. Manmadhan, the results here point to a potential benefit of tight blood pressure control in slowing the development and progression of white matter lesions, which are linked to a higher risk of dementia and cognitive decline.

Overall, according to Dr. Manmadhan, the study is an asset to the field of hypertension.

This study “adds to the already substantial body of literature that managing blood pressure is very important for not only preventing cardiovascular events but also in maintaining memory and cognition,” the author added.

REFERENCES:

For Dementia disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Japanese Diet May Slow Progression Of Fatty Liver Disease.

Japanese Diet May Slow Progression Of Fatty Liver Disease.

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According to a new study, a Japanese diet can reduce the progression of non-alcoholic fatty liver disease in those who already have the condition.

According to the study, soy products, shellfish, and seaweed have the strongest links to slowed liver fibrosis progression. The Japanese diet encourages eating high-quality foods and consuming less sodium, sugar, and saturated fat.

According to a recent study, persons with non-alcoholic fatty liver disease (NAFLD) may be able to reduce the illness’s progression by adopting a Japanese-style diet.

136 patients with NAFLD were being treated at the Osaka Metropolitan University Hospital in Japan when the study’s authors followed their diet and the development of their illness.

Each person’s diet was evaluated by researchers based on how closely it adhered to the 12-component Japanese Diet Index or mJDI12. High mJDI12 scores were linked to a slowing of the NAFLD-related liver fibrosis development.

There are 12 different foods and dietary groups in the Japanese diet:

  • rice
  • Miso broth
  • pickles
  • soy-based goods
  • yellow and green vegetables
  • fruits
  • seafood
  • mushrooms
  • seaweed
  • emerald tea
  • coffee
  • pork and beef

About the Japanese diet, those who ate more soy, seafood, and seaweed experienced the greatest inhibition of the development of liver fibrosis.

The impact of food on muscle mass was also monitored by the researchers. They discovered that individuals who consumed more soy products did so in addition to having lower rates of fibrosis advancement.

What precisely is non-alcoholic fatty liver disease?

Although it doesn’t directly harm the liver, NAFLD is a condition in which fat deposits there can potentially affect how well the organ functions.

The risk of non-liver malignancies, such as colon cancer, chronic kidney disease, gastric reflux, obstructive sleep apnea, hypothyroidism, periodontitis, polycystic ovarian syndrome, psychiatric issues, and growth hormone issues, is increased in those with NAFLD.

To better understand how the disease progresses, we spoke with Dr. Muhammad Nadeem Aslam, an assistant research scientist in the Department of Pathology at the University of Michigan who was not involved in the study.

Utilizing excessive amounts of fat, especially saturated fat, processed carbohydrates like fructose, glucose, and sucrose. Also, consuming too many calories, causes an imbalance between fat accumulation and breakdown in the liver, with the result being fat buildup in the liver.

Dietitian for heart health Michelle Routhenstein, who was also excluded from the study, stated:

“Foods high in refined sugars, saturated fat, salt, or trans fat can all contribute to fatty liver disease. This is done by causing the body to become more oxidatively stressed and inflammatory.”

While fatty infiltration is typically tolerated, Dr. Aslam added that an excessive buildup of lipids in the liver. This includes triglycerides, free fatty acids, and cholesterol, which can cause cellular stress and the production of reactive oxygen species.

According to Rosenstein, some items that encourage NAFLD include hydrogenated oils, fried foods, drinks, soda, and processed foods.

What makes Japanese cuisine wholesome?

Fresh, unadulterated foods with little refined ingredients, saturated fats, and added sugar make up the majority of the Japanese diet.

Due to their diet’s high soy and fish content, previous studies have shown that those who follow the Japanese diet had a lower risk of cardiovascular disease and stroke.

The largest population of centenarians is found on the island of Okinawa, which is located in southernmost Japan. The extended life expectancy and decreased incidence of obesity among Japanese people may be due to their low-calorie, nutrient-dense diet.

According to studies, Japanese people have the lowest risk of developing age-related illnesses such as diabetes, cancer, arthritis, and Alzheimer’s.

Some advantages of the Japanese diet include the following:

It enhances digestion – Fiber-rich foods that help with digestion include fruits, vegetables, seaweed, soybeans, and soy products. Fruits and vegetables that have been pickled are a wonderful source of probiotics.

It is a nutrient-rich diet – Japanese cuisine naturally contains a lot of minerals, vitamins, and nutrients including omega-3 fats.

Natural low-calorie foods and the Japanese practice of eating until 80 percent full assist prevent overeating. Also, provide the calorie deficit necessary for weight loss, which contributes to maintaining a healthy weight.

The Japanese eating style, in addition to the food, aids in keeping good health. The senses are stimulated when food is consumed from a tiny bowl with numerous different dishes rather than a large plate. They adhere to the “flexible restraint” philosophy, which permits occasional small-portion consumption of snacks and treats.

The following three Japanese foods

The study’s top three foods each have their own advantages, but they also have at least one thing in common: they are low in fat. Dr. Aslam cited soybeans as an example of a plant protein that is high in fiber and low in saturated fat.

Given that soy is a complete protein that contains all necessary amino acids to support the synthesis of muscle proteins, soy is “associated with higher muscle mass,” according to Rosenstein.

“Seafood, especially fish, is a good source of vitamins D and B2 (riboflavin), as well as omega-3 fatty acids. In addition to being a fantastic source of minerals like iron, zinc, iodine, magnesium, and potassium, fish is also high in calcium and phosphorus, according to Dr. Aslam.

According to Routhenstein, seafood may have a suppressive influence on the evolution of fibrosis because of its anti-inflammatory and antioxidant qualities.

Japanese seaweed is a good source of vitamins, minerals, and polyphenols. Dr. Aslam continued, “In addition to vitamins, the majority of edible algae have a special blend of nutrients.

Additional foods that lower NAFLD

The Mediterranean diet is another eating plan with a good reputation for helping those with NAFLD. Lean meats, fruits, vegetables, nuts, legumes, whole grains, and other plant-based foods are highlighted.

According to Routhenstein, green tea is one food in the mJDI12 index that is particularly beneficial for NAFLD because of its antioxidant content.

It “is protective against fatty liver disease because it contains about 200-300 mg of epigallocatechin-3-gallate (EGCG) in one cup,” claimed Routhenstein.

Dr. Aslam noted that coffee beans high in antioxidants are also linked to a generally lower risk for NAFLD.

“Raspberries are rich in insoluble fiber that helps create a short chain fatty acid in the gut called butyrate which studies have shown to be helpful in the reversal and prevention of fatty liver disease,” Routhenstein noted.

Including Japanese food and culture in one’s diet

This study highlights the chance to take charge of your health by including therapeutic foods to help stop the advancement of fatty liver disease, according to Routhenstein.

Dr. Aslam voiced alarm over the fact that so many Americans continue to consume a diet that is “far below dietary guidelines recommendations for healthy dietary patterns.”

“The lack of these nutrient-dense foods in the daily diets can cause diet-related chronic diseases, such as cardiovascular disease, type 2 diabetes, obesity, and fatty liver disease,” claimed Dr. Aslam.

Dr. Aslam praised nutrient-rich diets, which are lower in sodium, sugar, and saturated fat:

“Nutrient-dense foods are those that are prepared with no or little added sugars, saturated fat, and sodium,” said Dr. Aslam. “These foods include vegetables, fruits, whole grains, seafood, eggs, beans, peas, and lentils, unsalted nuts and seeds, fat-free and low-fat dairy products, and lean meats and poultry.”

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?generic=192

Can Alzheimer’s be cured with a new genetic therapy?

Can Alzheimer’s be cured with a new genetic therapy?

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There is presently no cure for Alzheimer’s disease, which is thought to be the root cause of dementia in 32 million individuals worldwide.

The majority of experts think that aberrant amyloid and tau protein buildups in the brain trigger alterations that lead to Alzheimer’s disease.

An experiment using a brand-new gene silencing treatment for Alzheimer’s disease that aims to reduce the body’s level of tau protein was carried out by a multidisciplinary team of researchers.

The most widely accepted explanation regarding the origins of Alzheimer’s disease is that it results from aberrant accumulations of the proteins amyloid and tau, which alter the brain. However, scientists are still unsure of the exact mechanism by which this disease develops.

Alzheimer’s disease, which is believed to afflict 32 million people worldwide, has no known cure, although doctors can treat its symptoms to enhance a patient’s quality of life.

A new gene silencing therapy for Alzheimer’s disease has now being tested by an international team of experts. The treatment turns off the tau protein-coding gene, which reduces the body’s production of the protein.

What impact does tau protein have on Alzheimer’s?

The core cells of the neurological system, called neurons, are where tau is most frequently found. Tau aids in maintaining the tube-like interior shape of nerve cells in a healthy brain.

Microtubules are structures that resemble tubes that aid in maintaining cell shape and guarantee that other proteins and chemicals move around the entire neuron with ease.

The tau protein in an Alzheimer’s patient’s brain separates from the microtubules and instead binds to other tau proteins inside the brain cell. As a result, the microtubules break down and aberrant tau protein accumulations occur.

These tau protein accumulations come together to form “tangles” within the brain cells. As a result, the neurons are unable to communicate with one another.

We spoke with Dr. David Merrill, an adult, and geriatric psychiatrist and the director of the Pacific Brain Health Centre at Providence Saint John’s Health Centre in Santa Monica, California, who was not involved in this study. “We know that tau tangles track with the progression of Alzheimer’s, meaning the worse that Alzheimer’s gets, the more tau tangles there are throughout more and more of the brain,” he said.

And ultimately, he continued, “those lead to neuron dysfunction and death.”

Blocking the gene that codes for tau

In this investigation, scientists developed a medication intended to silence the tau protein-encoding gene. The microtubule-associated protein tau (MAPT) gene is the one in question.

Antisense oligonucleotide BIIB080 is the name of the investigational medication. Small bits of RNA or DNA are used in this type of therapy to prevent a particular RNA from carrying out its intended function. In this instance, those are to act as guidelines for the creation of the tau protein.

Researchers included 46 patients with mild Alzheimer’s disease, with an average age of 66 years, in this phase 1 clinical research. The experiment was held between 2017 and 2020.

Throughout a 13-week treatment period, the trial compared four doses of the experimental medication injected into the nervous system through the spinal canal to a placebo.

Researchers discovered that 24 weeks after therapy, levels of both total tau and phosphorylated tau had decreased by more than 50% in trial participants in the treatment groups that had received the highest dose of the medication.

Over 90% of participants finished the post-treatment period, and 94% of those who received the drug and 75% of those who received a placebo reported mild or moderate side effects. The most frequent side effect of the experimental medication was headaches upon injection.

A ‘plausible’ therapy strategy

Dr. Merrill described this study’s ability to mute the expression of the gene that causes tau tangles in the brains of Alzheimer’s patients as “amazing” when asked about it.

Dr. David Merrill stated that this study “is the first step in demonstrating that this is a safe approach with a plausible biologic mechanism that can then be tested to see if it indeed does what we would expect, which is slow down the progression of Alzheimer’s disease and be a disease-modifying therapy that results in people’s cognition being better for longer.”

Non-participant in this study, Dr. Raphi Wald is a board-certified neuropsychologist at the Marcus Neuroscience Institute, established at Baptist Health South Florida’s Boca Raton Regional Hospital.

According to him, “a great deal of research is currently being conducted on preventing or destroying the abnormal proteins that appear on the brains of people with Alzheimer’s disease.”

“Compared to those without the disease, people with Alzheimer’s tend to have higher levels of the two proteins tau and amyloid in their brains. The majority of Alzheimer’s research has been devoted to preventing these diseases from spreading throughout the brain. This research suggests what might be a useful strategy for doing that,” he said.

The Alzheimer’s Association’s senior director of scientific programs and outreach, Dr. Claire Sexton, commented on this study.

While Alzheimer’s disease anti-amyloid therapies have gotten a lot of attention, the drug development landscape is much bigger, with a variety of targets and approaches being researched, she said. This is a positive report on phase 1 research that targets tau, one of the main indicators of Alzheimer’s disease, using a gene silencing strategy.

What comes next?

Dr. Wald stated that when it comes to the next steps in this research, the most crucial factor with these treatments is how they impact the daily lives of those at risk for or dealing with Alzheimer’s disease.

“Reducing tau is not a guarantee that people will not go on to have worsening cognitive functioning,” he advised. According to Dr. Merrill, the next logical step would be a phase 2 experiment to assess side effect tolerance and safety.

He continued, “And then the actual phase 3 trial would be to really look at treatment efficacy.” “Does memory get better? Does Alzheimer’s patients’ memory deterioration slow down over time? I’d want to see this medication investigated in later-stage clinical trials to determine whether it improves or maintains memory function in Alzheimer’s.

Dr. Sexton emphasized that more research with varied populations will be required to adequately assess the safety, target engagement, and clinical effect in all populations because the study’s subjects were all white.

“However, given the role of tau in not only Alzheimer’s but other dementias — known as tauopathies these results are a significant development and a further cause for optimism in the field,” she continued.

“The therapeutic study aimed against tau is funded by the Alzheimer’s Association Part the Cloud research grant programme, including a project by Dr. Ross Paterson at University College London. According to Dr. Sexton, the subject of his research is a unique substance that is intended to lessen tau formation in Alzheimer’s patients that is associated to dementia.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=31

A blood thinner that doesn’t increase bleeding risk.

A blood thinner that doesn’t increase bleeding risk.

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Anticoagulants are crucial for avoiding harmful blood clots, but they also raise the possibility of severe bleeding. If additional research confirms the potential of a novel molecule, blood thinners may no longer increase the risk of bleeding in the future.

The novel drug deliberately targets just one clotting pathway as opposed to all clotting pathways to prevent thrombosis, allowing clotting to proceed without a risk of bleeding or toxicity.

Blood thinners, often known as anticoagulants, work to dissolve and prevent blood clots, semi-solid blood cell clumps, and other things that might obstruct blood flow. However, anticoagulants sometimes function too effectively, which prevents clotting altogether and causes excessive bleeding from the inside or outside.

In a recent study, scientists from the Universities of British Columbia (UBC) and Michigan introduced a novel substance called MPI 8 that may one day make anticoagulants significantly safer.

At the location of an internal or external wound, blood clots often develop, stop the bleeding, and enable the body to start healing. Internal clots can fill the bloodstream or prevent blood flow to vital organs like the heart, brain, and lungs when they become loose. A heart attack, stroke, or pulmonary embolism may be the outcome.

What are Blood thinners?

Blood clots, which can result in a heart attack or stroke, can be avoided by taking blood thinners by mouth, vein, or skin. If you have heart issues like a valve disease or an erratic heartbeat, you could require them.

Blood clots can obstruct the heart, lungs, or brain from receiving blood. You might need to take blood-thinning medicine to stop this.

It’s critical to follow the directions on the label precisely. The drug won’t be as effective if you don’t take it regularly. Extreme bleeding can result from taking too much.

What blood thinners do?

To prevent blood cells from clumping together in the veins and arteries, several drugs thin the blood. Others work to stop blood clots by lengthening the time it takes for them to form. These are referred to as antiplatelet and anticoagulant medications, respectively.

People who have been given a heart disease diagnosis frequently receive anticoagulant prescriptions from their doctors. The word “coagulate” is a medical phrase that implies “to clot.” By prolonging the time it takes for your blood to clot, these blood thinners prevent blood clots.

Clots are prevented from developing by anticoagulants. Common blood thinners that prevent clotting include:

  • warfarin (Jantoven, Coumadin)
  • Lovenox, enoxaparin
  • heparin

Newer anticoagulants with reduced risk of consequences from bleeding include:

  • Pradaxa’s dabigatran
  • (Eliquis) apixaban
  • Xarelto (rivaroxaban)

Antiplatelet medications, on the other hand, stop blood cells, known as platelets, from congregating and creating clots. These include:

  • aspirin
  • (Plavix) clopidogrel
  • periantine dipyridamole
  • (Ticlid) ticlopidine

What blood thinner is best for you will be decided by your doctor. The dosage you receive will be closely watched, and a prothrombin time (PT) test may occasionally be performed. Your INR, or international normalised ratio, is determined by this blood test.

The INR measures how quickly your blood clots. A person’s medical history determines the optimum INR rate for them. You can stop yourself from bleeding excessively or clotting too quickly by staying within your INR range.

To stop a blood clot from developing, medications that are anticoagulant and antiplatelet are both utilized. To break a blood clot that has already formed, like in the case of deep vein thrombosis (DVT) or pulmonary embolism, for instance, a class of drugs known as thrombolytics may be utilized.

Creating MPI 8 to focus on blood clots

Dr. Jay Kizhakkedathu, the study’s principal author, said: “This is very, very interesting and exciting work.”

Dr. Kizhakkedathu remarked, “You know, we have been doing this for many years, but we finally were able to uncover a molecule which is a blood thinner, but which could help a lot of people.

The chemicals involved in blood coagulation that the researchers concentrated on included polyphosphate. Dr. James Morrissey, one of the study’s co-authors, had previously identified it as a prospective therapeutic target.

Dr. Morrissey said in a news release why the research team decided to focus on polyphosphate, saying it may be “a safer target to go after with an antithrombotic drug because it would just slow down these clotting reactions — even if we take out 100% of the action of the polyphosphate.”

However, it can be challenging to target a single molecule in the blood. According to Dr. Kizhakkedathu, polyphosphate is a negatively charged molecule electrically. It is polyanionic, which means that it has several pockets of negative charge. An anionic molecule, on the other hand, has a single negative charge.

MPI 8 stands for “Macromolecular Polyanion Inhibitor 8.”

“Ionic charges are present throughout our bodies. Nearly every surface in our body is polyanionic, including the surfaces of cells and proteins, according to Dr. Kizhakkedathu. We require highly specialised agents that can bind to polyphosphate, a very precise polyanion.

Because there are so many negatively charged anions in the blood, previous attempts to target polyphosphate with cations, positively charged compounds, were toxic because they bound indiscriminately with so many of them.

According to Dr. Kizhakkedathu, the scientists were able to pinpoint a class of molecules known as the MPIs that possessed “very special properties.” “However, it raises the charge density once it has located its target. It binds very tightly and specifically, he continued.

A breakthrough finding might help future research.

As of now, MPI 8 has been tested on mice by the study’s authors, who discovered that it effectively prevents blood clots without being harmful or increasing the risk of bleeding.

For MPI 8, UBC and the University of Michigan have submitted a patent application with the goal of moving on to studies with larger animals and ultimately humans.

The team’s discovery, according to Dr. Kizhakkedathu, “will a help a lot of people if it gets into the clinical trials and approved.”

REFERENCES:

For Blood thinner medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=47

Scientists use genetic rewiring to increase cells’ lifespan

Scientists use genetic rewiring to increase cells’ lifespan

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Throughout the 20th and 21st centuries, human lifespans have increased, but those increases are slowing down, so researchers are still looking for ways to extend life.

Researchers are now focusing on genetics after examining how healthy meals, hygiene, and medical treatment have all contributed to the gains in lifespan.

By genetically rewiring the circuit that regulates aging, researchers in a recent proof-of-concept study nearly doubled the lifespan of yeast cells. Their research could lead to increased longevity in more advanced organisms, including perhaps even humans.

Can you extend your life? Everyone wants to live long, healthy lives. The National Institutes of Health (NIH) advise us that the best method to lengthen lifespan is to eat a healthy diet, get enough sleep, exercise frequently, have routine checkups with a doctor, and abstain from unhealthy habits like smoking and binge drinking alcohol.

Worms, mice, and even monkeys have lived longer thanks to research being done by scientists to slow down the aging process. Could they, however, do the same for people?

Now, by altering the genetic circuit that regulates aging, a team from the University of California, San Diego, has succeeded in extending the lifespan of a simple organism by about 80%.

The role of synthetic biology in cell ageing

The UC San Diego research team has been investigating the aging process of cells for several years and has found that cells undergo a series of chemical changes as they age, leading to their eventual degeneration and death. But they discovered that not all cells deteriorate in the same way, and this was the subject of their most recent study.

Before making changes to the aging circuits in the single-celled yeast Saccharomyces cerevisiae, they first tested their theories using computer models of cell aging.

They found that there were two ageing processes that the cells went through. For almost half of the cells, ageing was characterised by a loss in the stability of their DNA (nucleolar ageing); for the remaining cells, ageing was characterised by a decline in their mitochondria, the organelles that produce the cell’s energy (mitochondrial ageing).

Increasing lifespan via manipulating gene expression

The expression of two conserved transcriptional regulator molecules, which govern which genes are active in the cell, was altered to control the aging of the cells. Heme activator protein 4 (Hap4) is connected to mitochondrial function, while silent information regulator 2 (Sir2) promotes nucleolar decrease (resulting in DNA instability).

The researchers created a synthetic gene oscillator to rewire this system such that when one of these regulators is expressed and consequently active, it prevents the other from being expressed. They stopped the cells from progressing along either of the two ageing pathways by creating long-lasting oscillations between the two types of cellular degeneration in individual cells. These cells lived longer than usual.

Professor Nan Hao, the study’s principal author, and co-director of the Synthetic Biology Institute at UC San Diego, stated, “Our research serves as a proof-of-concept, demonstrating that, just as mechanical engineers can repair and improve our cars so they last longer, we can also apply the same engineering method to modify and improve our cells so they live longer. The key to this is how we went about doing it: by simulating the natural aging process on computers to inform the engineering of the system and increase longevity.“

Life expectancy nearly quadrupled following genetic rewiring

The scientists forced the yeast cells to alternate between the two ageing pathways on a constant basis by engineering the gene oscillator. By doing this, they prevented the yeast cells from choosing their predetermined course of decline and death and slowed the cells’ ageing process.

The longevity of yeast cells that were artificially rewired and aged under the supervision of the artificial oscillator increased by 82% in comparison to control cells.

And genetic engineering did not appear to hurt them, according to Prof. Hao, told: “The yeast cells survive nicely with a fast growth rate.”

Application that might lengthen life

Theoretically, a similar strategy may be effective in human cells because all cells include gene regulatory circuits that are in charge of numerous physiological processes, including aging.

The goal might not just be to increase the lifespan of more complex species but also to increase the lifespan of particular cells inside those organisms to stave off degenerative diseases.

Prof. Hao issued a warning, noting that it is unknown whether lengthening life might have further effects on cells.

“That is a complex biological query. The length of the cell is not a property that has been selected through evolution, according to our current theory. First, cells must be capable of surviving in an unpredictable, harsh environment that is always changing.

“There is a chance that our long-lived modified cells won’t be as resilient to particular environmental pressures. In other words, extending longevity may lose some common functions, but it is only a theory,” he continued.

Implications for prolonging human healthy life years

There might be a promise for this strategy in people, according to Prof. Hao, “Since both of the two regulators have human equivalents, I think that human cells could benefit from the same approach. In actuality, it will be our next move.”

Aside from the study, Prof. Howard Salis, Principal Investigator at the Salis Lab at Penn State University, concurred:

The risk and morbidity of age-related diseases will decrease if the overall goal of these interventions is to preserve better cell states, according to the study.

Though this study demonstrates that it is possible to turn off the ageing process in a single-celled organism, it is still very early in the development of the technology, and many questions need to be resolved before it can be used on humans.

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Can activity snacking help people with type 1 diabetes?

Can activity snacking help people with type 1 diabetes?

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Light-intensity, 3-minute walks every half-hour can help persons with type 1 diabetes maintain control of their blood sugar levels, according to research.

Sedentary lifestyles are linked to a higher risk of developing major illnesses, and they can make blood sugar management more challenging for those with type 1 diabetes.

While moderate- and high-intensity exercise can help people with type 1 diabetes, it can also cause sudden, dangerous drops in blood sugar levels.

Long stretches of inactivity are thought to be bad for everyone. People with type 1 diabetes should pay particular attention to it because it is linked to the dysregulation of insulin levels. However, for those with type 1 diabetes, excessive activity can result in sharp drops in blood sugar levels.

With safe, brief periods of light-intensity walking, people with type 1 diabetes can maintain blood sugar control, according to a recent study from the University of Sunderland in the UK. This is what the writers refer to as “exercise snacks.”

According to the study, taking a 3-minute walk after every 30 minutes of sedentary activity helped individuals maintain control over their blood sugar levels better than those who were inactive.

The researchers also discovered that the individuals were not at risk for unexpected dips in blood glucose levels due to the brief walking breaks.

A balanced diet vs prolonged periods of sitting

32 persons with type 1 diabetes participated in the trial, which had two sessions spread over two weeks.

Participants in the first exercise sat still for 7 hours. In the second, they took a brief 3-minute stroll after getting up every 30 minutes.

Participants wore a continuous glucose monitor for 48 hours following each treatment. Researchers asked that individuals follow their usual insulin regimens and exercise levels during that time. Additionally, they shared a common breakfast and lunch.

After the brief walks, people maintained an average blood sugar level of 6.9 millimoles per litre (mmol/L), according to the researchers. After the prolonged sitdowns, their blood sugar levels were higher, 8.2 mmol/L.

Blood sugar levels remained within the desired range for 14% longer in participants who consumed exercise “snacks” than in those who did not over the course of 48 hours of monitoring, during, and after the test period.

Walking to stay healthy

Dr. Sumera Ahmed, an assistant professor at Touro University California’s College of Osteopathic Medicine who was not involved in the study, said, “This study is interesting.”

“[I]t is encouraging to know that even frequent, low-intensity, short-duration exercises can aid in extending a person’s time in range who has type 1 diabetes. The prevention of hypoglycemia is more crucial, she said.

Dr. Ahmed further emphasized that people should find it simple to incorporate the study’s little strolls into their regular routines.

She also believed that the activity snacks’ mild effects would make it less likely that they would need to adjust their insulin dosages or carbohydrate intake, as could be necessary with more intense exercise.

Although the study’s seven-hour sessions, which included 14 brief walks, were appropriate for a trial, that is a lot of strolling for a typical day.

Anything more frequent than this may not be realistic or sustainable, according to Dr. Ahmed. “We need further studies to determine if the frequency of light intensity activities beyond the 30 minutes as noted in this study is beneficial,” he added.

Dr. Ana Maria Kausel, an endocrinologist who was also not a part of the study, stated: “I normally advise my patients to take a stroll after meals. Depending on the effort, some studies have indicated that those who walk a block can reduce their blood sugar by 10 mg/dl [7.2 mmol/L] of glucose.

This study shows that low-intensity walks can maintain normal blood sugar levels and are safer than walks of higher intensity.

Exercise and type 1 diabetes: Use caution

Dr. Ahmad noted that the type, intensity, timing, and duration of exercise all affect how persons with type 1 diabetes respond to physical activity in terms of blood glucose levels.

Therefore, she suggested, these people need to eat more carbohydrates or have their insulin doses adjusted before beginning an exercise programme.

Additionally, Dr. Kausel issued a warning: “Type 1 diabetics are especially sensitive to exercise. When engaging in physical activity, they must always exercise caution. All type 1 diabetics should ideally be wearing a continuous glucose monitor when working out.”

Less time spent seated

32 individuals in the study underwent two seven-hour sitting periods spread out over a two-week period.

Participants in one session sat still for the entire seven hours. Every 30 minutes during the other session, they had three-minute breaks from sitting to move around lightly.

Throughout and following each sitting session, participants wore a continuous glucose monitor (CGM) to monitor their blood sugar levels over the course of 48 hours. Everyone had a set breakfast and lunch, and they were instructed to maintain the same dietary regimen, level of physical activity, and insulin dosages throughout the trial.

What occurs in diabetes type 1?

An individual with type 1 diabetes has insufficient insulin production from their pancreas. A hormone called insulin permits glucose, often known as sugar, to enter the body’s cells, where it is used as a source of energy.

Without enough insulin, blood sugar levels rise and may eventually reach dangerous levels. Serious complications from type 1 diabetes, such as eye and foot issues, heart disease, stroke, kidney disease, and nerve damage, can develop if it is not addressed.

There is no known cure for type 1 diabetes, and with time, the pancreas’ capacity to generate insulin continues to deteriorate even more. Pancreatic islet transplantation, which might be able to swap out low-functioning islets with new ones from a healthy donor, is one of the treatments under investigation.

Those who have type 1 diabetes must take many doses of insulin daily and check their blood sugar levels to keep them within acceptable limits.

Hypoglycemia is the everyday main concern. Hypoglycemia symptoms include trembling, shakiness, rapid heartbeat, headaches, nausea, hunger, nervousness or irritability, restless sleep, weakness, and pale complexion.

Losing consciousness and entering a hypoglycemic coma are the worst possible outcomes for people with dangerously low blood sugar levels.

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