Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genetically obese mice (C57BL/6J-ob/ob), fed ad libitum, demonstrated a precipitous increase in the spontaneous death rate after 50 weeks. The first signs of morbidity were a ruffled hair coat and a progressive motor ataxia. Necropsy revealed that obese mice had pale and fatty livers, urolithiasis and grossly distended bladders. Microscopically, the hepatocellular changes observed in all aged obese mice included: a loss of orientation of hepatocytes, an enormous variability in the size of both hepatocytes and their nuclei, and an extensive deposition of both large and small lipid droplets, confirmed by an increase content of triacylglycerols. A subacute-to-chronic, multifocal, necrotizing hepatitis was also present. Kidneys from aged obese mice contained hypertrophied glomeruli and increased PAS-stained material. Tubular dilation with compaction of the tubular cells was also seen. There were no significant alterations in the microanatomy or mineralization of femurs from obese mice, yet there was a significant increase in plasma alkaline phosphatase activity. In obese mice at 62-63 weeks of age, hyperglycemia was present even in spite of hyperinsulinemia. Pituitary immunoreactive ACTH and its molar ratio to pituitary immunoreactive beta-endorphin were also increased in obese mice at this age. Even though the etiology of the decreased lifespan of genetically obese mice remains uncertain, the possibility is discussed that an overall defect in the central nervous system may be involved.
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PMID:Hormonal, metabolic and morphologic studies of aged C57BL/6J obese mice. 673 67

Numerous studies in recent years had proved pathogenetic correlation of the intestinal ecological community, not only with diseases of the gastrointestinal tract but also with diseases such as atherosclerosis and hypertension, urolithiasis and pyelonephritis, gallstones and hepatitis. In its role in maintaining homeostasis an intestinal microflora isn't inferior to any other vital organs. All this allowed to distinguish it as an independent body. Recently, as one of the most important factors for the development of dyslipidemia scientists consider breaking the functional state of the liver, as well as changes in blood lipid spectrum and disturbance of cholesterol metabolism begins at the level of the hepatocyte. However, in 2001, Carneiro de Moura proposed a theory of violation of the microbial community in the colon as one of the ways to lipid metabolism. By reducing the detoxification function of intestinal microflora associated with Microecological disorders of various origins, the first "hit" is to the host liver--is on one side. On the other--the vast majority of microorganisms are characterized by a pronounced ability of bile acids deconjugation, and therefore the increased reproduction in the ileum of bacteria (especially anaerobic, with enhanced activity against deconjugation activity to related bile acids) and the formation of toxic endogenous bile salts, acids are important prerequisites for the occurrence of violations of all functions of the liver, including the activities of Kupffer cells and the whole system of mononuclear macrophages. In this regard, the formation and progression of dyslipidemia, regardless of the target organ must be closely linked with the digestive tract by micro. Schematically it can be represented as follows: violation of microecology intestine --> accumulation of endotoxin in the gut --> entry of endotoxins in portal vein to the liver --> RES of liver cell damage --> strengthening the pathological effects of toxicants other (non-microbial) origin --> dysfunction of hepatocytes --> dislipoproteidemiya.
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PMID:[Intestinal dysbiosis and atherogenic dyslipidemia]. 2049 50

In a large population of animals, it is normal to have some die each day from causes not related to disease, which is often referred to as natural causes. In poultry production, this phenomenon is commonly referred to as daily mortality. In egg-producing chickens, many of the natural causes of death are associated with making an egg. The causes of normal mortality in commercial egg-laying chicken flocks have been described very little to date. A commercial chicken egg farm, housing approximately two million single-comb white leghorn chickens (Gallus gallus domesticus) in 16 egg-producing flocks, was visited on a monthly basis to monitor bird health, body conditioning, skeletal integrity, and causes of daily mortality in an attempt to provide early detection of health abnormalities. A representative sample of daily mortality from each flock was necropsied to determine the cause of death. Reported herein is a summary of visits for a period of 38 mo from June 2011 to July 2014. The top 15 causes of normal mortality, in rank order of prevalence, were determined to be the following: egg yolk peritonitis, hypocalcemia, gout, self-induced molt, salpingitis, caught by spur, intussusception or volvulus (twisted intestine), cannibalism (pick out), tracheal plug, septicemia, fatty liver syndrome, internal layer, layer hepatitis, persecution, and prolapsed vent. Other causes noted were hyperthermia (during summer), trauma, coccidiosis, ovarian neoplasia, being egg bound, urolithiasis, peritonitis (not egg yolk induced), leg fracture, caught in the structure, tumor (other than ovarian origin), wing fracture, exsanguination, and cardiomyopathy.
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PMID:Causes of Normal Mortality in Commercial Egg-Laying Chickens. 2895 10