Effects of estrogen treatment in multiple sclerosis

A study by UCLA researchers reveals the cellular basis for how the hormone estrogen protects against damage to the central nervous system in people with multiple sclerosis (MS). The researchers found that estrogen treatment exerts positive effects on two types of cells during disease -immune cells in the brain and also cells called oligodendrocytes. Complementary actions on these two types provide protection from disease.

Multiple sclerosis is a chronic autoimmune, neurodegenerative disease marked by visual impairment, weakness and sensory loss, as well as cognitive decline. These symptoms emerge when inflammatory immune cells destroy the myelin sheath that surrounds nerve processes called axons. Loss of that protective insulation disrupts electrical communication between nerve cells. The third trimester of pregnancy has been previously shown to reduce relapse rates by approximately 70 percent as compared to before pregnancy, and other studies have shown benefit over the long term due to multiple pregnancies.

An estrogen unique to pregnancy that is made by the fetus and placenta has been proposed by Dr. Rhonda Voskuhl and colleagues to mediate this pregnancy protection in both the MS mouse model as well as in two successfully completed clinical trials of estriol treatment in MS patients. How that happens has remained a critical question. Voskuhl, who led the latest study, reported mouse studies showing that estrogen protected the brain from damage by activating a protein called estrogen receptor beta (ERb). Her new research identifies which cells within the brain are mediating this protective effect.

The researchers first genetically eliminated ERb in either immune cells of the brain or in oligodendrocytes, the cells that make the myelin sheath, as a way of making cells unresponsive to estrogen during the MS like disease in mice. They then treated mice without or with ERb in these cells to ask if disease protection was lost or not. Loss of protection during treatment meant that the treatment was acting on the cell that had the receptor removed. Results showed that the estrogen-like treatment was acting on both immune cells of the brain as well as on oligodendrocytes, together resulting in repair of myelin and less disability.

Drug developers often optimize therapies by targeting only one single cell type. By contrast, this study confirms that this estrogen-like compound can combat MS via complementary effects on two distinct cell types. Voskuhl and other UCLA researchers are in fact now developing a next-generation estrogen-like compound with robust biochemical effects on oligodendrocytes and immune cells in the brain.
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Diabetes leads to retinopathy

Loss of vascular cells in the retina of the eye, loss of barrier function in vessels, edema, and a cascade of inflammatory events lead to blindness. The eye generates a dihydroxy metabolite from polyunsaturated fatty acids that initiates pericyte loss and breakdown of the endothelial barrier function in the eye, the scientists said. This leads to vascular edema and ultimately to a proliferation of new blood vessels and loss of vision.

The small molecule which initiates this process is a diol of a long chain poly unsaturated fatty acid produced by sEH, the researchers said. The enzyme converts an anti-inflammatory epoxy fatty acid into the pro inflammatory and in this case, toxic diol. The research team demonstrated this process and the cellular mechanism involved in diabetic mice and in transgenic mice that over-produce the sEH enzyme.

They were able to block the process by inhibiting the sEH enzyme. The expression of the sEH enzyme also increased with severity of diabetic retinopathy in human patients.The expression of the soluble epoxide hydrolase gene was shown to increase in the retinas of human patients with the severity of the disease with non-proliferative diabetic retinopathy. Diabetic eye disease can affect many parts of the eye, including the retina, macula, lens and the optic nerve.

Diabetic retinopathy is the most common diabetic eye disease and a leading cause of adult blindness. Chronically high blood sugar from diabetes damages the tiny blood vessels in the retina, leading to diabetic retinopathy, according to the National Eye Institute (NEI) of the National Institutes of Health. The blood vessels can leak fluid or hemorrhage and distorting vision. The sEH enzyme generates a toxic metabolite, but when the enzyme is inhibited, eye disease is prevented.

Inhibiting the soluble epoxide hydrolase preserves fatty acid epoxides which reduce the late or proliferative stages of diabetic retinopathy and macular degeneration. Research team used the same soluble epoxide hydrolase inhibitors to block production of a pro inflammatory mediator that initiates the early stages of vascular permeability and inflammation of the retina. They discovered that 19,20-dihydroxydocosapentaenoic acid, a product of soluble epoxide hydrolase (sEH) activity, as a key regulator of pericyte loss and endothelial barrier breakdown has brought to light a previously unknown mechanism of action in the induction of diabetic retinopathy.

 Inhibition of sEH blocks formation of this degenerative lipid metabolite thereby halting disease progression, which is of vital interest for the potential management of this blinding disease.The diol of the fatty acid linoleate produced by the soluble epoxide hydrolase was highly toxic to cells leading to vascular permeability and sepsis. These epoxy fatty acid chemical mediators control blood pressure, fibrosis, immunity, tissue growth, pain and inflammation.
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Lung cancer causes hypertension

Shortness of breath and respiratory distress often increase the suffering of advanced-stage lung cancer patients. These symptoms can be triggered by pulmonary hypertension, the pulmonary hypertension is due to immune and inflammatory processes triggered by cancer cells. Lung cancer has long since taken on the character of an epidemic: the disease is already responsible for more than a quarter of all cancer deaths, and the trend is rising.

One reason for this is that the prognosis is poor: only one-fifth of patients are still alive five years after diagnosis. This is partly due to the fact that lung cancer is often not recognized until it is in an advanced stage. Another problem is that a variety of different lung cancers exist, each of which requires its own therapeutic concept. Doctors have observed that many patients with progressive lung cancer develop shortness of breath and respiratory distress.

The same symptoms also occur in diseases such as pulmonary arterial hypertension. Scientists measured the diameter of the pulmonary artery of many lung cancer patients using computer tomography. They found thickening of the walls of the pulmonary artery in more than half of the patients. This is a clear indication that these patients also suffer from pulmonary hypertension.

To identify the causes, the lung researchers analyzed three different forms of lung cancer in mice. These were tumour types that grow at different rates and can be experimentally induced in the lungs of mice. All three mouse models showed signs of pulmonary hypertension as tumour growth progressed.

Further experiments showed that the immune cells release various chemical messengers, as is generally observed in inflammatory reactions. Conversely, pulmonary hypertension did not occur when the mice in the experiment lacked functioning immune cells. This is an indication that inflammatory processes triggered by lung cancer may be responsible for pulmonary hypertension.
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Fatty liver can damage other organs

Nonalcoholic fatty liver disease  NAFL increases the risk of chronic liver diseases such as liver cirrhosis, liver cancer, type 2 diabetes and cardiovascular diseases. Altered secretion of the fatty liver increases production of glucose, fats, and proteins like hepatokine fetuin-A, which are releases into the bloodstream.

The secreted substances of the fatty liver enter other organs and trigger further reactions. People who had experienced an increased pancreatic fatty degeneration have reduced insulin secretion.

Fatty liver and fatty degeneration of the pancreas triggers increased local immune cell infiltration and inflammation that increase the disease.
However, adipose tissue is not harmful, it can even have protective effects: adipose tissue located around the blood vessels of the kidney has regenerative properties.

The factor that leads to pathological changes is fetuin-A, which is produced by the fatty liver, instead of protecting tissue as before, the adipose tissue brings out inflammatory processes that leads to a restriction of renal function.
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Foods for healthy heart

Lutein is a xantrophyll-  yellow pigments from the carotenoid family, it is present in brightly coloured vegetables and fruit like yellow and red peppers, kale, carrots, broccoli and spinach. It can reduce risk of cardiovascular disease.

Poor diet increases inflammatory processes in the body. Inflammation is a major factor in many types of coronary artery disease, such as myocardial infarction, lutein has ability to protect tissues from oxidative stress and inflammation.

Regular intake of healthy diet can reduce risk of developing cardiovascular heart disease. High blood concentrations of lutein can reduce coronary heart disease, stroke, and metabolic syndrome.

Lutein is absorbed and stored by the cells of the immune system in the blood.
The higher the level of lutein in the blood, the lower the level of inflammation in the body. Lutein treatment lowers the inflammatory activity of the cells.
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Soy can ease painful inflammatory bowel disease symptoms

Eating soy regularly could ease painful inflammatory bowel disease (IBD) symptoms.

Researchers have discovered addition of staple beans to a sufferer's repertoire may improve symptoms of weight loss and an enlarged spleen.

The most common forms of IBD are Ulcerative Colitis (UC) and Crohn's Disease (CD). UC affects the colon and
rectum.

Researchers from Pennsylvania State University induced mice with a condition similar to Ulcerative Colitis UC. They added a soy-protein
concentrate into their diet and removed other protein sources.

 Amy Wopperer, the study author, said: 'Soy-protein concentrate calm markers of colonic inflammation and loss of gut barrier function in the mice with induced IBD.'

The mice were given a soy-protein concentrate of 12 per cent, which was based on the amount humans generally consume. The concentrate also protect human bowel cells.

Omega-3s may serve as therapy for type 1 diabetes

Type 1 diabetes is an auto-immune condition that activates the immune system to destroy pancreas cell. When the cells are destroyed, pancreas cannot produce insulin.

People with type 1 diabetes depend on insulin to replace what the body cannot produce, new research discovered that omega-3 fatty acids can reduce autoimmune responses of the disease.

Omega-3 fatty acids can stop inflammatory process in the body, this process can stop or prevent autoimmune diseases.

Non-obese diabetic mice were used for an experiment, omega-3 was increased in their diet  and were tested every 3 months to detect glucose and insulin tolerance.

The researchers examined the pancreas of the mice for insulitis, they discovered that adding omega-3 to the diet of mice improved glucose metabolism and control blood sugar and insulin for 182 days and prevents autoimmunity.

Causes of frequent urination in women

Urination is the release of urine from the bladder, frequent urination is the need to urinate more than normal.

Cleveland Clinic said the average person should urinate between six to eight times a day.

Some of the causes of frequent urination are: drinking too much water, diabetes, overactive bladder, urinary tract infection, pregnancy, menopause, obesity, weak pelvic floor organs and inflammatory bladder disorder.

Treatment for frequent urination depends on the cause, visit your doctor anytime you experience frequent urination.