Autoimmune kidney disease

Monash researchers have solved a mystery, revealing how certain immune cells work together to instigate autoimmune kidney disease.The study, led by Professor Michael Hickey and Professor Richard Kitching from Monash University's Centre for Inflammatory Diseases. In glomerulonephritis, an immune disease of the kidney, rogue immune cells damage the kidney via a misdirected inflammatory attack.

Special cells called monocytes continuously patrol the glomeruli by crawling within its blood vessels. Monocytes are very good at 'picking up and removing rubbish' and being on the lookout for signs of infection and tissue injury. However in autoimmunity, some immune cells in the circulation are highly reactive to molecules picked up in the kidney.

Patrolling monocytes can display these molecules to the reactive immune cells in the bloodstream, resulting in the rogue cells remaining in the kidney and turning on an unnecessary and damaging inflammatory attack. This autoimmune damage to the kidney can severely impact on the normal function of the kidney, if left untreated.

 This damage occurs while the cells are moving around in the kidney blood vessels. This process, known as intravascular antigen recognition, has never been described before for the key helper T cells that direct and control the immune response.
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Gene may protect against heart disease

Scientists have identified a gene that may play a protective role in preventing heart disease. Their research revealed that the gene, called MeXis, acts within key cells inside clogged arteries to help remove excess cholesterol from blood vessels.

UCLA-led study in mice found that MeXis controls the expression of a protein that pumps cholesterol out of cells in the artery wall. MeXis is an example of a "selfish" gene, one that is presumed to have no function because it does not make a protein product.

However, recent studies have suggested that these so-called "unhelpful" genes can actually perform important biological functions without making proteins and instead producing a special class of molecules called long non-coding RNAs, or lncRNAs.

lncRNAs are important for the inner workings of cells involved in the development of heart disease," said Dr. Peter Tontonoz, senior author of the study. Considering many genes like MeXis have completely unknown functions, the study suggests that further exploring how other long non-coding RNAs act will lead to exciting insights into both normal physiology and disease.

In the study, researchers found that mice lacking MeXis had almost twice as many blockages in their blood vessels compared to mice with normal MeXis levels. In addition, boosting MeXis levels made cells more effective at removing excess cholesterol.
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Reversing insulin resistance

Researchers at Vanderbilt University have discovered how insulin crosses the capillary endothelium to exit blood vessels and stimulate skeletal muscle cells-a major finding that may lead to new ways to reverse insulin resistance, a hallmark of type 2 diabetes. This was made possible by the development of a novel microscopy technique which allowed measurement of insulin movement across the endothelial wall of skeletal muscle capillaries in the mouse.

One of insulin's key functions is to stimulate glucose uptake by muscle, where it is stored or used as fuel. To stimulate glucose uptake insulin must cross the endothelial barrier into muscle tissue. Impaired delivery of insulin into tissue is a key feature of insulin resistance and type 2 diabetes.

Using a quantitative intravital fluorescence microscopy technique they developed combined mathematical modeling, the researchers showed that insulin moves across the endothelium by fluid-phase transport. Such movement is not dependent on the presence of endothelial insulin receptors or limited by saturation of endothelial transport processes, as had been hypothesized previously.

Better understanding of the variables controlling insulin movement across the endothelial wall could lead to improved strategies for reversing insulin resistance, including development of small molecules that enhance insulin delivery or novel insulin analogs that can access muscle more easily. The fluorescence microscopy technique developed for these studies can be applied to other drugs and hormones to study molecular access to a range of tissues.
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Roles of Mesp1 gene

Researchers at the Université libre de Bruxelles and University of Cambridge identified the role of key gene Mesp1 in the earliest step of cardiovascular lineage segregation. This discovery may help to better understand congenital heart defects. The heart is the first organ that forms during development and contains four regions (ventricles and atria), which contain cells that perform specialized functions: the beating cardiomyocytes ensure the pumping activity, vascular cells represent the inner lining and blood vessels, and the pacemaker cells regulate the heartbeat.

Unless the progenitor cells are specified at the correct time, migrate to the correct location, and differentiate into the correct cell types, severe malformations of the heart occur. In human patients, these are recognized as congenital heart diseases, which represent the most common cause of severe birth defects in newborn babies. Previous studies had shown that a diverse range of heart progenitor cells arises from different pools of cells expressing the Mesp1 gene. However, it remained unclear how the various progenitors can be distinguished at the molecular level, and what molecular mechanisms promote specification into a particular heart region or cardiac lineage.

Researchers led by Pr. Cédric Blanpain, Laboratory of Stem Cells and Cancer, Université libre de Bruxelles, Belgium, and Pr. Berthold Göttgens, the University of Cambridge, identified the role of Mesp1 in the earliest step of cardiovascular lineage segregation by single cell molecular profiling and lineage tracking. Fabienne Lescroart and colleagues isolated Mesp1 expressing cells at different stages of embryonic development and performed single cell transcriptomic analysis of these early cardiac progenitors to identify the molecular features associated with regional and cell type identity of cardiac progenitors.

They demonstrated that the different populations of cardiac progenitors are molecularly distinct. To determine the role of the transcription factor Mesp1 in regulating the cardiovascular differentiation program and the heterogeneity of early cardiovascular progenitors, they also performed single cell molecular profiling of these early progenitors in a Mesp1 deficient context. These experiments showed that Mesp1 is required for the exit from the pluripotent state and the induction of the cardiovascular gene expression program.

Bioinformatic analysis identified, among these early Mesp1 progenitors, distinct populations of cells corresponding to progenitors committed to different cell lineages and regions of the heart, identifying the molecular features associated with early lineage restriction and regional segregation of the heart. While progenitor cells are not yet differentiated, this new analysis shows that cardiovascular progenitors are already "primed" or pre-specified to give rise to cardiac muscle cells or vascular cells. The researchers found that these different populations are also born at different time points and are located at specific locations at this early stage of development.

The researchers have identified the earliest branching point between the cardiac and vascular lineages, and shown that Notch1 marks the early progenitor committed to the vascular lineage during early embryonic development. Understanding the molecular features associated with early cardiovascular lineage commitment and heart regions will be important to design new strategies to instruct cardiovascular progenitors to adopt cardiac or vascular identity from different heart regions that can be used for cellular therapy of cardiac diseases.
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High salt diet hobbles the brain

A new study has shown that mice fed with a very high-salt diet experienced declined blood flow to their brain, the integrity of blood vessels in the brain suffered, and performance on tests of cognitive function plummeted.

Researchers found that those effects were not as long has been widely believed, a natural consequence of high blood pressure. Instead, they appeared to be the result of signals sent from the gut to the brain by the immune system.

The study, conducted by researchers at Weill Cornell Medicine in New York. The research sheds light on a subject of keen interest to scientists exploring the links between what we eat and how well we think, and the mediating role that the immune system plays in that communication.

This suggests that even before a chronic high-salt diet nudges blood pressure up and compromises the health of tiny blood vessels in the brain, the oversalted gut is independently sending messages that lay the groundwork for corrosion throughout the vital network.

In the small intestines of mice, the authors of the new research found that a very high-salt diet prompted an immune response that boosted circulating levels of an inflammatory substance called interleukin-17. These high levels of IL-17 set off a cascade of chemical responses inside the delicate inner linings of the brain's blood vessels.

The result in mice fed with the high-salt diet: blood supply to two regions crucial for learning and memory-the cortex and hippocampus slowed markedly. And mental performance slid. Compared to mice fed a diet lower in salt, the maze-running skills of the mice who consumed high-salt levels faltered, and they failed to respond normally to whisker stimulation, or a new object in their cage.

In mice, that evidence of cognitive impairment was apparent even in the absence of high blood pressure. The immune system's role in sending signals between brain and gut is also seen in diseases like multiple sclerosis, rheumatoid arthritis, psoriasis and inflammatory bowel disease-all disorders that are linked to poor functioning of the brain's blood vessels.
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Lumify for treating eye redness

Ocular redness is a common condition that can be caused by inflammation of almost any part of the eye. With frequent use, non-selective redness relieving eye drops that constrict blood vessels in the eye can result in users developing a tolerance or loss of effectiveness, as well as rebound redness.

 In contrast, low-dose brimonidine, the active ingredient in Lumify, selectively constricts veins in the eye, increasing the availability of oxygen to surrounding tissue, thereby reducing the potential risk of these side effects.

Patients with eye redness and irritation can experience negative social connotations, which may impact daily life, having a drop that reduces redness without the side effects of rebound hyperemia or tachyphylaxis, which may lead to overuse and potential corneal toxicity, Lumify is adequate and accurate for treating the condition without side effects.
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Link between obesity and diabetes

Researchers have identified a major mechanism by which obesity causes type 2 diabetes, which is a common complication of being overweight. In obesity, insulin released into the blood by the pancreas is unable to pass through the cells that form the inner lining of blood vessels.

As a result, insulin is not delivered to the muscles, where it usually stimulates most of the body's glucose to be metabolized. Blood glucose levels rise, leading to diabetes and its related cardiovascular, kidney and vision problems.

 A major problem in obesity is the delivery of circulating insulin to the muscle, this problem involves immunoglobulins, which are the proteins that make up circulating antibodies. The researchers found that obese mice have an unexpected chemical change in their immunoglobulins.

The abnormal immunoglobulins then act on cells lining blood vessels to inhibit an enzyme needed to transfer insulin from the bloodstream into the muscle. Type 2 diabetes patients have the same chemical change, and if immunoglobulins from a type 2 diabetic individual is given to a mouse, the mouse will becomes diabetic.
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Regeneration of blood vessels

A new study led by researchers identifies a signaling pathway that is essential for angiogenesis, the growth of new blood vessels from pre-existing vessels. The finding may improve current strategies to improve blood flow in ischemic tissue, such as that found in atherosclerosis and peripheral vascular disease associated with diabetes.

The research shows that the formation of fully functional blood vessels requires activation of protein kinase Akt by a protein called R-Ras, and this mechanism is necessary for the formation of the hallow structure, or lumen, of a blood vessel.This showed the biological process needed to increase blood flow in ischemic tissues.

Research team used a combination of 3D cell culture and living tissue to show that vascular endothelial growth factor VEGF promotes vascularization, but the vessel structures formed are chaotic, unstable and non-functional. Functional vessels need to have a lumen; a pipe-like opening that allows oxygenated blood and nutrients to travel through the body and VEGF alone cannot fully support the formation of such a vessel structure.

 VEGF activates Akt to induce endothelial cells to sprout. Then, R-Ras activates Akt to induce lumen formation. The second step involving Akt activation by R-Ras stabilizes the microtubule cytoskeleton in endothelial cells, creating a steady architecture that promotes lumen formation. VEGF and R-Ras activation of Akt signaling are complementary to each other, both are necessary to generate fully functional blood vessels to repair ischemic tissue.  
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How the skin controlled blood pressure

Skin plays a surprising role in regulating blood pressure and heart rate, Skin is the largest organ, covering two square metres in humans - helps regulate blood pressure and heart rate in response to changes in the amount of oxygen available in the environment.

High blood pressure is associated with cardiovascular disease, such as heart attack and stroke. For the vast majority of cases of high blood pressure, there is no known cause. It is often associated with reduced flow of blood through small blood vessels in the skin and other parts of the body, a symptom which can get progressively worse if the hypertension is not treated.

Previous research has shown that when a tissue is starved of oxygen - as can happen in areas of high altitude, or in response to pollution, smoking or obesity, for example - blood flow to that tissue will increase. In such situations, this increase in blood flow is controlled in part by the 'HIF' family of proteins.

To investigate what role the skin plays in the flow of blood through small vessels, a team of researchers exposed mice to low-oxygen conditions. These mice had been genetically modified so that they are unable to produce certain HIF proteins in the skin.

The study was set up to understand the feedback loop between the skin and the cardiovascular system. By working with mice. Researchers were able to manipulate key genes involved in this loop. They discovered that in mice lacking one of two proteins in the skin HIF-1α or HIF-2α, the response to low levels of oxygen changed compared to normal mice and that this affected their heart rate, blood pressure, skin temperature and general levels of activity.

Mice lacking specific proteins controlled by the HIFs also responded in a similar way.
In addition, the response of normal, healthy mice to oxygen starvation was more complex than expected. In the first ten minutes, blood pressure and heart rate rise, and this is followed by a period of 36 hours where blood pressure and heart rate decrease below normal levels. 48 hours after exposure to low levels of oxygen and blood pressure the heart rate levels had returned to normal.

Loss of the HIF proteins or other proteins involved in the response to oxygen starvation in the skin, was discovered to change when this process starts and how long it takes. Skin's response to low levels of oxygen may have substantial effects on how the heart pumps blood around the body.
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E-cigarette can cause lung diseases

E-cigarettes lead to as many lung diseases as tobacco products,
researchers compared saliva samples from tobacco smokers, e-cigarette smokers and nonsmokers. They found that e-cigarette smokers were likely to develop dangerous proteins associated with lung diseases such as COPD and cystic fibrosis and that the devices are not better for people than regular cigarettes.

E-cigarettes might not be the ideal alternative smokers addicted to tobacco are looking for. Previous research has proven that e-cigarettes can cause lifelong damage to the heart, one puff of an e-cigarette is all it takes to increase the risk of having a heart attack. E-cigarette smokers have elevated levels of neutrophil-extracellular-trap NET related proteins in their airways. NET proteins fight off pathogens, but increased levels of them can lead to inflammatory lung illnesses.

E-cigarettes are as dangerous as smoking - just ONE puff could be all it takes to increase the risk of a heart attack. E-cigarettes do inflict life-long damage on nonsmokers' hearts that is similar to tobacco cigarettes. Replacing tobacco products with e-cigarettes is dangerous, some of the flavoring agents and other products used in e-cigarettes are toxic.

The proteins are associated with COPD and cystic fibrosis, both of which make it hard for patients to breathe. E-cigarette smokers also have increased NET levels outside of their lungs, according to the study. This can cause cell death in tissues that line organs and blood vessels. E-cigarette smokers have an increased risk of suffering from bronchitis, asthma, bronchiectasis and wheezing. E-cigarettes is as bad as tobacco cigarettes
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Genes and environment can increase the risk of congenital heart defects

Infants of mothers with diabetes have increased risk of congenital heart defects. Such developmental defects are likely caused by a combination of genetic and environmental factors. The molecular mechanisms by which maternal diabetes disrupts normal heart development in genetically susceptible individuals remain unclear.

The Cardiovascular Research describe a gene-environment interaction resulting in congenital heart defects in both mouse and fly model systems. Interaction between two genes, Endothelial Nitric Oxide Synthase and Notch1, would result in more severe types of congenital heart defects in animal models. Diabetes is known to be associated with decreased nitric oxide levels in blood vessels.

Maternal diabetes, in combination with a mutation in Notch1, would result in a higher risk of congenital heart disease.
Researchers showed that maternal hyperglycemia reduces the chromatin accessibility of the Endothelial Nitric Oxide Synthase gene, resulting in decreased nitric oxide production.

This loss of nitric oxide is associated with an increase in expression of Jarid2, a known repressor of the Notch1 gene. This directly inhibited Notch1 expression to levels below a critical threshold necessary for normal heart development. This study lends support to a gene-environment interaction model where maternal hyperglycemia raises the risk of congenital heart defects by reducing Notch1 expression.

The results reveal the epigenetic machinery by which maternal hyperglycemia disrupts the Nitric Oxide and Notch1 signaling pathways, leading to congenital heart defects. Infants that are exposed to hyperglycemia develop a congenital heart defect, which supports the idea that there are genetically susceptible individuals.
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Ascorbic acid for treating vitamin C deficiency

Ascorbic acid - vitamin C occurs naturally in foods such as citrus fruit, tomatoes, potatoes, and leafy vegetables. Vitamin C is important for bones and connective tissues, muscles, and blood vessels.

Vitamin C also helps the body absorb iron, which is needed for red blood cell production. Ascorbic acid is used to treat and prevent vitamin C deficiency.
Smoking can make ascorbic acid less effective.

Dose needs may be different during pregnancy or while you are breast-feeding a baby. Do not use ascorbic acid without your doctor's advice in either case.

Drink plenty of liquids while you are taking ascorbic acid. The chewable tablet must be chewed before you swallow it. Ascorbic acid gum may be chewed as long as desired and then thrown away.

Do not crush, chew, or break an extended-release tablet. Swallow it whole. Measure liquid medicine with a special dose-measuring spoon or medicine cup. If you do not have a dose-measuring device, ask your pharmacist for one.

Keep the orally disintegrating tablet in the package until you are ready to take it. Use dry hands to remove the tablet and place it in your mouth. Do not swallow the tablet whole. Allow it to dissolve in your mouth without chewing. Swallow several times as the tablet dissolves.

Store ascorbic acid at room temperature away from moisture and heat. Do not stop using ascorbic acid suddenly after long-term use at high doses, or you could have "conditional" vitamin C deficiency.

Symptoms include bleeding gums, feeling very tired, and red or blue pinpoint spots around your hair follicles. Follow your doctor's instructions about tapering your dose. Conditional vitamin C deficiency can be difficult to correct without medical supervision.

Stop using ascorbic acid and call your doctor at once if you have: joint pain, weakness or tired feeling, weight loss, stomach pain; chills, fever, increased urge to urinate, painful or difficult urination; or severe pain in your side or lower back, blood in your urine.
Common side effects may include:
heartburn, nausea, diarrhea and stomach cramps.
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Breast cancer cells recycle ammonia waste as fuel

According to the latest research, breast cancer cells recycle ammonia, a waste byproduct of cell metabolism, and use it as a source of nitrogen to fuel tumor growth. The presence of ammonia accelerates proliferation of cultured breast cancer cells, while suppressing ammonia metabolism can stunt tumor growth in mice.

This showed the biological role of ammonia in cancer and may inform the design of new therapeutic strategies to slow tumor growth. Ammonia is toxic for breast cancer cells, it could be used to feed tumors by serving as a source for the building blocks that tumors need to grow.

Cancer cells consume nutrients voraciously and generate excess metabolic waste. One such byproduct, ammonia, is normally transported in blood vessels to the liver, where it is converted into less toxic substances and excreted from the body as urea.Tumors have few blood vessels, and as a result, ammonia accumulates in the tumor's local environment at concentrations that would be toxic for many cells.

When glutamine is broken down during cell metabolism, ammonia containing nitrogen is released as a byproduct.
Tracing the fate of this marked ammonia, the researchers examined different cellular metabolites in breast cancer cells and in human tumors transplanted into mice. They found cancer cells recycled ammonia with high efficiency, incorporating it into numerous components-primarily the amino acid glutamate, a fundamental building block for proteins, as well as its derivatives.

Higher concentrations of ammonia appeared to accelerate the growth of lab-grown breast cancer cells. Ammonia exposed cells doubled up seven hours faster than cells grown without ammonia. In 3-D cultures-a technique that allows cells to divide in all directions as they do inside the body, ammonia exposure increased the number of cells and surface area of cell clusters by up to 50 percent compared with cells grown without ammonia.

Ammonia also accelerated tumor growth and proliferation in mice with transplanted human breast cancer. When the team blocked the activity of glutamate dehydrogenase GDH-an enzyme that specifically assimilates ammonia to carry out its function, tumor growth slowed significantly compared to tumors with intact GDH activity. Repressing ammonia metabolism stunts tumor growth in mice.
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Tissues nanotransfection device

Researchers have developed a new technology called Tissue Nanotransfection TNT, it can generate any cell type for treatment within the patient's body. This technology can be used to repair injured tissue or restore function of aging tissue like organs, blood vessels and nerve cells.

Researchers reprogram skin cells to become vascular cells in injured legs that lacked blood flow. Within one week, active blood vessels appeared in the injured leg, the leg was healed at the second week.

The technology also reprogram skin cells in the live body into nerve cells that were injected into brain-injured mice to help them recover from stroke.
The device delivers new DNA or RNA into living skin cells to change their function.

This technology can convert skin cells into elements of any organ with a touch. It takes less than a second and is non-invasive. The chip does not stay permanently in the body after use and the technology keeps the cells in the body under immune surveillance.

TNT technology has two major components: nanotechnology-based chip designed to deliver cargo to adult cells in the live body and the design of specific biological cargo for cell conversion.

 This cargo converts an adult cell from one type to another. TNT doesn't require any laboratory-based procedures and may be implemented at the point of care.
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Facts about glioblastoma

Glioblastoma GBM is the most aggressive tumor that can form in the brain. Glioblastomas are tumors that developed from astrocytes- supportive tissue of the brain.

Glioblastomas are found in the cerebral hemispheres of the brain, but can be found anywhere in the brain or spinal cord. It can cause brain bleeding, which may have been related to the clot.

These tumors are cancerous because the cells reproduce quickly and they are supported by a large network of blood vessels.

There two types of glioblastoma
Primary - The tumors are common and very aggressive.
Secondary - These tumors have slower growth rate and very aggressive.

Common symptoms are - headache, nausea, vomiting, and drowsiness. Depending on the location of the tumor, patients can develop different symptoms like weakness on one side of the body, memory and speech difficulties, and visual changes.

The exact cause of glioblastoma is not known. It can be difficult to treat because the tumors contain so many different types of cells. Some cells may respond very well to certain therapies, while others may not be improve.

However, because of the way it spreads, it is impossible to remove every microscopic growth from the brain. Therefore, it will continue to grow.

Radiation and chemotherapy may be used to slow the growth of tumors that cannot be removed with surgery.
Patients have a ten percent chance of surviving five years after their diagnosis.
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New drug for sickle cell disease

Sickle cell disease is an inherited blood disorder in which the red blood cells are abnormally shaped. This restricts the flow in blood vessels and limits oxygen delivery to the body’s tissues, causing to severe pain and organ damage.

The U.S. Food and Drug Administration has approved Endari (L- glutamine oral powder) for patients five years and above  with sickle cell disease to reduce severe complications associated with the blood disorder.

The average life expectancy for sickle cell patients is 40 to 60 years. Common side effects of Endari are constipation, nausea, headache, abdominal pain, cough and pain in the extremities
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Low blood flow in the brain may be a sign of dementia

High blood pressure and decreased blood flow in the brain may cause the build-up of dangerous amyloid plaque in the brain. Having problems with the blood vessels in the brain may affect thinking, cognition and memory.

Brain's blood vessels work like a plumbing system that distributes oxygen to every parts of brain cells and remove waste materials from the cells.

The brain relaxes its vessels to maintain constant blood flow as it adjusts for changes in blood pressure, but the brain vessels in Alzheimer's patients prevent blood flow and allow amyloid to get to the brain cells.

Alzheimer's patients have lower blood flow in their brains than the people without the disease. They experience cognitive decline and memory loss that leads to dementia.

Taking blood pressure lowering drugs can reduce the effects on memories of affected people because the drugs can cross the blood-brain barrier and prevents the toxins from getting to the brain.
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Thrombectomy can prevents stroke complications

Inadequate blood supply to the brain can cause stroke or when blood vessel within the brain ruptures, causing brain tissue to die.

 A stroke is a medical emergency, it requires immediate treatment. During a stroke, the brain does not receive enough oxygen and nutrients, which can leads to death of brain cells.

A thrombectomy is a surgical procedure used to remove a blood clot -thrombus from the brain. The thrombus obstructs blood flow and may cause tissue death.

Thrombectomy is effective in patients with blood clots up to 24 hours after a stroke. Stroke can occur when brain blood vessel bursts.

Thrombectomy is safer than clot-busting drugs because it has no side effects.

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Fetus DNA and risk of pre-eclampsia in pregnancy

Pre-eclampsia affects many pregnancies and is suspected when a woman have high blood pressure. It can cause fits, stroke and liver problems.

Researchers studied the genetic make-up of babies born from pre-eclamptic pregnancies and compared their DNA with healthy babies.

Improper formation of placenta is associated with pre-eclampsia. The baby's genes that produces the placenta was examined to see if their is a link between the baby's DNA and pre-eclampsia.

There were some features in a baby's DNA that can increase the risk of pre-eclampsia. Baby's DNA comes from its parent's genes, DNA changes linked with pre-eclampsia are common in people carrying this sequence in their DNA so the inherited changes increase the risk.

Researchers discovered that DNA variations close to the gene that makes a protein called sFlt-1 with significant differences between the babies born from pre-eclamptic pregnancies and normal babies.

At high levels sFlt-1 released from the placenta into the mother's bloodstream can cause damage to her blood vessels, causing high blood pressure, kidneys, liver and brain damage. A baby carrying these genetic variants increases the risk of pre-eclamptic pregnancy.

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Effects of diabetes on vital organs

 The raised blood sugar levels that result from diabetes can cause a wide range of serious health issues. When people have diabetes, the body either does not make enough insulin or cannot use what it has effectively. As a result, the amount of sugar in the blood becomes higher than normal.

 Blood sugar is the main power source for the human body. It comes from the food people eat. The hormone insulin convert glucose into fuel. Diabetes may
cause complications in the circulatory system, which can lead to heart attack and stroke.

Diabetes can damage large blood vessels, causing macrovascular disease.
It can also damage small blood vessels, causing what is called microvascular disease. Microvascular disease can
cause eye, kidney, and nerve problems.

Excess blood sugar decreases the elasticity of blood vessels and causes them to narrow, impeding blood flow.
When people have diabetes, they can develop nerve damage because the blood vessels can not supply enough oxygen.

Nerve damage usually happens some 25 years or more after diagnosis. The most common form is peripheral neuropathy which causes pain and numbness in toes, feet, legs, and arms.

Over time, high blood sugar levels damage blood vessels in the kidneys. This damage prevents the kidneys from filtering waste out of the blood.
According to the National Institute of Diabetes and Digestive and Kidney Diseases, diabetes is one of the major
causes of kidney disease.

Diabetes is the most frequently identified cause of gastroparesis. This is a condition that causes the stomach to slow the movement of food into the small intestine.

A person with gastroparesis may experience symptoms such as nausea, abdominal pain, and acid reflux.
Gastroparesis may cause: nausea, vomiting, acid reflux, bloating, abdomen pain and weight loss

Diabetes can interfere with the body's ability to send and implement responses to sexual stimuli. It can cause erectile dysfunction in men. If you have
diabetes, you can manage it by monitoring your glucose level and working closely with your health providers.

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