Category Archives: Gastroenterology

Genetics of Obesity : Neurotransmitters

2Obesity is the major Public threat.The pattern of Obesity is completely driven by the environmental changes and including the heritability is also strong. The present level of obesity is responsible for over 300,000 deaths per year. Obesity is Genetically interwined with Brain and its mental performance.  Scientists are trying to figure it out on why being are becoming Obese and helping people to stay thinner and healthier. A new Research study showed the link of a change in a DNA in being Obese. This movement in the DRD2 gene, named A1, may cause people to experience less pleasure from food.

The major fact in gaining weight is because of the brain. Researchers foung a higher correlation between higher Body Mass Index and reduced cognitive flexibility visuospatial ability and verbal memory. The Dopamine receptors are the reason for getting Obesity. When someone eats something they like, the brain releases dopamine. This Neurotransmitter meets up with dopamine receptors and the brain then registers that the edibles was a good thing. People with the A1 version of the DRD2 gene have less dopamine receptors. So the research makes a conclusion that people with like these need to eat more to get a difference from their food.the brain

To date, with the help of many doctors around the world, reseacrhers have recruited 6500 patients. They used a number of approaches to find genes involved in weight and have identified 12 different gene disorders that can cause severe obesity in childhood. These genes work in the brain to control the key pathways that are generated by the hormone “Leptin” and are involved in appetite and metabolism (how your body handles the calories you eat). Using a combination of psychometric and functional imaging studies applied to individuals with known genetic lesions in the appetitive pathways, scientists are beginning to gain novel and exciting insights into the interactions between balancing the homeostatic and hedonic feeding.

Hepatobiliary manifestations in inflammatory bowel disease

1Several complications of IBD are related to the liver and the biliary system, which are closely interrelated to with the intestine. The liver which acts as a “processing plant” in the body takes what have been ingested and broken down. It then further sends some of that material to blood cells throughout the body and rest is filtered out and eliminated as waste. The liver also produces bile salts, acids, and cholesterol which are stored in the gallbladder until they are required to help break down digested fat. The primary function of the bile ducts is to transport bile or waste from the liver to the small intestine in the body. The pancreas, which is connected to the same common bile duct as the liver and gallbladder, also transports enzymes to the intestines in turn helping in breaking down of food.

The liver may develop an active inflammation, which usually reduces with appropriate treatment of IBD and this disease involving the liver affects which is about a 5% of people with IBD.

  • The most common symptoms tend to be is low energy and fatigue.
  • The symptoms of more advanced Liver disease include itching, fluid retention, fatigue, jaundice, and a feeling of fullness in the upper abdomen.
  • The blood tests can confirms the presence of liver disease, but sometimes X-ray, an ultrasound, or the liver biopsy mostly makes the definitive diagnosis.

    FATTY LIVER DISEASE (HEPATCI STEATOSIS)
    The foremost liver complication of inflammatory bowel disease is a generally harmless one, influencing people with ulcerative colitis and Crohn’s illness similarly. The condition moreover is connected with other unrelated conditions—including diabetes, pregnancy, and weight. Fatty liver is caused by an abnormality in liver metabolism that results in the accumulation of fat. Because it may be a reasonably minor problem and causes no symptoms, it generally does not require any treatment. It also does not progress to chronic liver disease. In some cases, patients with steatosis are prescribed with steriods.
    PRIMARY SCLEROSING CHOLANGITIS (PSC)
    This condition is a form of severe inflammation and scarring that develops within the bile ducts.  Almost all PSC patients have develops IBD. PSC occurs more frequently in people with ulcerative colitis than in those with Crohn’s disease. The symptoms incorporate nausea, weight loss, jaundice, and itching. Primary Sclerosing Cholangitis usually does not progress with therapeutic treatment for IBD and may ultimately require a liver transplantation for patients. The cause is not known and there’s successful medicine for PSC. To correct the extreme narrowing of the bile ducts, a balloon-tipped tube may be embedded into the duct to enlarge it. Only about some percent of ulcerative colitis patients and 1% of those Crohn’s disease patients develop this condition. On extremely rare events, cancer of the bile ducts (cholangiocarcinoma) may develop. There is also an increased incidence of colonial cancer in IBD patients who have sclerosing cholangitis.
    CHRONIC ACTIVE HEPATITIS
    Hepatitis is a non-specific term for inflammation of the liver and chronic hepatitis also known as long-term hepatitis can be from inflammation of the liver itself related to the IBD, called auto-immune hepatitis. It is treated with the same sorts of medication that ulcerative colitis and Crohn’s infection are treated with to decrease the inflammation. Hepatitis can moreover be from infections like Hepatitis A, B or C disease and ought to be treating the same as in patients without IBD.

A healthy gut : better recovery from spinal cord injury

Our gut microbiota communicates with the central nervous system (CNS) by collaboration with immune cells and discharging metabolites that pass through the blood-brain barrier. Most (~70-80 per cent) immune cells within the body are found inside gut-associated lymphoid tissues. The influence of our gut microbes is far-reaching. From boosting the adequacy of chemotherapy to influencing obesity risk in youth, the gut microbiome is unimaginably important for our body’s overall health. In addition to the more obvious impacts of traumatic spinal line injuries, the researchers say they have auxiliary impacts, counting the loss of bowel control, which can cause disturbance to the gut microbiome.

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Named “dysbiosis,” this disruption happens when “good” bacteria are drained or invade by “bad” bacteria within the gut. Previously, autoimmune illnesses – such as multiple sclerosis and type 1 diabetes – have been connected to dysbiosis, and the researchers say it has been found to play a role in the progression of neurological disorders.

To test their hypothesis, the researchers performed an experiment on mice. They found that mice that were pre-treated with antibiotics to modify their gut microbiomes before spinal cord damage appeared higher levels of spinal aggravation. These mice too recuperated poorly from their injuries. On the flip side, injured mice that were given daily probiotic doses appeared less spinal damage and were able to recapture more hind limb movement. The researchers show that the probiotics contained huge numbers of lactic acid-producing bacteria, which enacted a gut-associated immune cell that can inhibit inflammation. The researchers say these immune cells – called regulatory T cells – could avoid additional damage to the spinal cord after injury. Also, by releasing molecules that advance neuronal development, the probiotic bacteria may really boost spinal cord recuperation.

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One or both of these capacities could clarify how post-injury disturbance of the gut microbiome contributes to the pathology of spinal cord injuries and how probiotics block or turn around these effects. Although the researchers’ discoveries from their mouse study recommend that checking gut changes with probiotics seem to offer assistance to patients who are recovering from spinal cord injuries, the results have not however been affirmed in humans.

Hepatic Complications in Breast Cancer

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Secondary breast cancer within the liver happens when breast cancer cells spread to the liver. It can to be known as liver metastases. When breast cancer spreads to the liver, it can be treated but cannot be cured. Treatment points to control and moderate down the spread of cancer soothe symptoms and give you the best quality of life for as long as possible.

Secondary breast cancer within the liver isn’t the same as cancer that begun within the liver. Hepatic infection related to breast cancer is common and can result from the metastatic spread of the tumor to the liver, or can be caused by systemic treatment with chemotherapeutic or anti-endocrine operators. Metastatic disease to the liver can display clinically and pathologically in various ways. Little is known as to why breast cancer can now and then display as liver-dominant infection or with the liver association as a late event within the disease course. Be that as it may, there are numerous postulations involving metastasis organotropism, which might offer future knowledge. The backbone of treatment for hepatic metastases proceeds to be systemic therapy, but a few locoregional aide therapies exist. In spite of these treatments, liver metastasis from breast cancer is related with a poor prognosis.

Ongoing research of the mechanisms and tropism of liver metastasis from breast cancer will ideally result in moved forward targeted treatments to reduce their frequency and improve results when they arise. Liver metastases may display asymptomatically amid a metastatic screen or may display with upper stomach fullness, a mass, ascites, jaundice or weight loss. Ultrasound or CT check more often than not affirms the diagnosis. Liver work tests are unhinged in 92% of patients at presentation with gamma-glutamyl transferase (GGT) and alkaline phosphatase being the foremost commonly elevated enzymes.

Factors adversely affecting prognosis incorporates jaundice, deranged liver function tests, ascites, discernable hepatomegaly, poor performance status and infection restricted to the liver. The interval between primary presentation and metastatic infection is a vital indicator of survival in bone metastases but may not be vital in liver metastases. The tumor marker CA15-3 is regularly higher in patients who do poorly but is not reported to be an autonomous indicator of survival. Carcino-embryonic antigen (CEA) has not been previously considered in this regard in spite of the fact that it is recognized as useful in checking disease progression.

The influence of infection pattern, both outside the liver and inside the liver has received little consideration. Two studies propose that extra-hepatic disease may impair survival, but there is no information on the prognostic noteworthiness of disease dispersion inside the liver. This study has examined the cases of all patients showing a long time to a single breast unit with metastatic breast cancer involving the liver at the metastatic diagnosis. Survival from the time of metastatic diagnosis was compared with essential disease information, persistent characteristics and design of metastatic disease in an attempt to set up factors anticipating the result. It is hoped that these prognostic factors may be of advantage in fitting treatment to dodge toxicity to patients with only a brief life expectancy for whom palliative support would be most appropriate.