Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course of 24 patients with insulin-requiring diabetes mellitus who had received total parenteral nutrition (TPN) was retrospectively analyzed. Routine nutritional assessment disclosed significant depression of anthropometric indices and secretory protein levels in patients with chronic renal failure complicating juvenile onset diabetes mellitus (JODM). Biochemical complications including hypo- or hyperglycemia were significantly more frequent (p less than 0.001) in JODM than in maturity-onset diabetes and found to a lesser degree in patients with renal failure. The catheter infection rate was substantially higher (17%) than usually encountered in TPN therapy. Positive nitrogen balance was achieved in the majority of patients with an average 84% and 92% of estimated protein and caloric requirements being provided. Close monitoring and a protocol of infusion plus supplemental subcutaneous regular insulin was useful in providing adequate TPN safely to these high-risk patients.
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PMID:Total parenteral nutrition in patients with insulin-requiring diabetes mellitus. 308 5

This study tested the hypothesis that the increased glucose requirement of lactation had effects that were independent of the suckling-dependent inhibition of postpartum endocrine function in beef cows. Mature Hereford cows were either suckled ad libitum and infused with saline iv (n = 9) from d 2 through 4 (d 0 = jugular catherization on d 32 +/- 3 postpartum); were nonsuckled and infused with saline from d 2 through 4 (n = 10); or were nonsuckled and infused with phlorizin (3 g/d) from d 2 through 4 (n = 10). Nonsuckled cows infused with phlorizin had lower (P less than .05) plasma concentrations of glucose and amino acid nitrogen (AAN) on d 2 compared with pre-infusion levels (d 1), but their metabolic profile returned to levels similar to the suckled cows by d 3 and 4. Nonsuckled cows infused with saline had elevated glucose and insulin and lower AAN and free fatty acids (FFA) on d 3 and 4 compared with pre-weaning (d 1) levels (P less than .05). Nonsuckled cows infused with phlorizin did not show this weaning-induced elevation in glucose and insulin. The number of luteinizing hormone (LH) pulses was not affected by treatment. However, in contrast to the large LH pulses observed in the nonsuckled cows infused with saline, both the suckled cows and the nonsuckled cows treated with phlorizin had more small and fewer large amplitude pulses (P less than .01). Treatment did not affect serum concentrations of follicle stimulating hormone, gonadotropin release in response to gonadotropin releasing hormone (25 micrograms) or the number of cows ovulating by 55 d after calving. We conclude that the increased glucose clearance caused by phlorizin infusion or lactation results in depression of LH pulse amplitude in suckled postpartum beef cows.
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PMID:Hypoglycemia alters pulsatile luteinizing hormone secretion in the postpartum beef cow. 310 70

Ischemic stroke is a major disabling disease. There are 500,000 new cases in U.S. every year, and the middle cerebral artery (MCA) is the artery most often occluded. In this paper recent results of experimental MCA occlusion are reviewed, with special emphasis on those factors contributing to irreversible damage. Occlusion of MCA in the rat causes a pronounced decline of flow in the neostriatum to less than 10% of normal. The area of low flow is surrounded by a zone 0.2-0.5 mm wide, across which blood flow increases steeply. Beyond this zone, changes in flow are more gradual, and perfusion is reduced to about 1/3 of normal in the adjacent ipsilateral cortex. The MCA occlusion leads to a sharply demarcated infarct and to scattered neuronal injury in the adjacent cortical tissue. It is suggested that the ischemic core is identical with the tissue infarct, i.e. that it is the initial pattern of blood flow which determines the volume and topography of infarction. Waves of spreading depression are detected in the cortical low perfusion area during the first hours of MCA occlusion, and glucose consumption is increased, presumably due to an increased demand for ionic transport. In hyperglycemic animals, the number of spreading depressions is reduced as is the glucose consumption. The repeated waves of spreading depression in combination with partial energy depletion may induce selective neuronal injury in the peri-infarct zone, a suggestion which finds support in the fact that hyperglycemia ameliorates neuronal injury around the infarction.
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PMID:Mechanisms of brain damage in focal cerebral ischemia. 328 72

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

The widespread presence of fingernail polish remover in the home makes the product a common source of ingestion, as evidenced by recent poison center data. Its principal component, acetone, is present in relatively high concentration. The syndrome of acetone intoxication presents as generalized central nervous system/respiratory depression, hyperglycemia, and ketosis. Despite its ubiquitous presence and high potential for severe intoxication, no reports are found describing the toxicity and supportive care following its ingestion by children. The authors present a 30-month-old patient with severe acetone intoxication secondary to fingernail polish remover ingestion. Also noted is the need to include acetone ingestion in the differential diagnosis of apparent diabetic ketoacidosis.
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PMID:Acute acetone intoxication in a pediatric patient. 336 29

The effect of two mutant genes for obesity (ob/ob) and diabetes (db/db) on the accumulation rate of radiolabeled estradiol was examined in female C57BL/KsJ mice. Mutant mice were match-paired with normal (+/?) animals at 16 weeks of age. All ob/ob and db/db mice exhibited overt obesity and hyperglycemia relative to normals. The distribution and uptake of the radiolabeled estradiol was subsequently examined in specified CNS and peripheral tissues. In all cases, the db/db and ob/ob mutant conditions resulted in a depressed cellular accumulation of radiolabeled estradiol in both CNS and peripheral tissues relative to normal mice. The ob/ob mutation resulted in a more severe depression of tissue estradiol uptake than did the db/db mutation. These studies indicate that the abnormal metabolic and hormonal states induced by the mutations, and not the mere presence of the genomic mutation itself, probably accounts for the depressed cellular affinity for gonadal steroids in these murine models.
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PMID:Obese (ob/ob) and diabetes (db/db) mutations: two factors modulating brain and peripheral tissue accumulation of estradiol in C57BL/KsJ mice. 365 29

More than 3600 white men, from 30 to 79 years old and without a history of myocardial infarction, underwent submaximal treadmill exercise tolerance tests as part of their baseline evaluation for the Lipid Research Clinics Mortality Follow-up Study. The exercise test was conducted according to a common protocol and coded centrally; depression of the ST segment by at least 1 mm (visual coding) and/or 10 microV-sec (ST integral, computer coding) signified a positive test. Concurrent measurements of age, blood pressure, history of cigarette smoking, and plasma levels of lipids, lipoproteins, and glucose, as well as other coronary risk factors, were obtained. Cumulative mortality from cardiovascular disease was 11.9% (22/185) over 8.1 years mean follow-up among men with a positive exercise test vs 1.2% (36/2993) over 8.6 years mean follow-up among men with a negative test. Three-quarters (43) of these deaths were due to coronary heart disease. The relative risk for cardiovascular mortality associated with a positive exercise test was 9.3 before and 4.6 after age adjustment. Cardiovascular mortality rates were especially elevated (relative risk 15.6 before and 5.1 after age adjustment) among the 82 men whose exercise tests were adjusted "strongly" positive based on degree and timing of the ischemic electrocardiographic response. A positive exercise test was also moderately associated with noncardiovascular mortality; the relative risk for all-cause mortality was 7.2 before and 3.4 after age adjustment. The relative risk for cardiovascular mortality associated with a positive exercise test was not appreciably altered by covariance adjustment for known coronary risk factors other than age. A positive exercise test was a stronger predictor of cardiovascular death than were high plasma levels of low-density lipoprotein cholesterol, low plasma levels of high-density lipoprotein cholesterol, smoking, hyperglycemia, or hypertension. Its impact on risk of cardiovascular death was equivalent to that of a 17.4 year increment in age.
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PMID:Predictive value of the exercise tolerance test for mortality in North American men: the Lipid Research Clinics Mortality Follow-up Study. 373 17

Anesthesia, surgical trauma, heparinization, priming volume composition, and temperature control of the heart-lung machine individually affect carbohydrate, protein, or lipid metabolism during cardiac operations. The impact of some of these factors on glucose and insulin regulation was assessed before, during, and after normothermic cardiopulmonary bypass in nondiabetic patients with use of a servo-controlled insulin delivery system. With a glucose-free prime, cardiopulmonary bypass induced a slight hyperglycemia but no endogenous insulin response, suggesting a partial inhibition of insulin secretion. Nonetheless, insulin release could be stimulated by exogenous glucagon. A glucose load in the priming fluid led to marked and persistent hyperglycemia without commensurate insulin release. Elevated stress hormone levels, a concomitant reduction of insulin release and insulin action, and a depression of peripheral glucose utilization, as demonstrated by glucose clamp experiments, contributed to these perturbations of glucose and insulin metabolism. Although the metabolic alterations observed are not critical in routine cardiac operations, they may become clinically significant in postoperative states with unusual persistence of stress conditions.
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PMID:Alterations of insulin and glucose metabolism during cardiopulmonary bypass under normothermia. 388 Aug 48

Ten clinically healthy cats were allotted into 2 groups. Group A was given the low (60 ml), and group B was given the high (120 ml) recommended dose of a commercial hypertonic sodium phosphate enema. Enema retention was enforced. All cats developed clinical and/or laboratory abnormalities, with group B cats being more severely affected. Clinical signs that occurred rapidly included depression, ataxia, vomition, bloody diarrhea, mucous membrane pallor, and stupor; tetany was not seen. One cat in group B died. Laboratory abnormalities included hypernatremia, hyperphosphatemia, hypocalcemia, hyperglycemia, calculated hyperosmolality, and metabolic acidosis with high anion gap probably due to hyperlacticacidemia. There were no significant gross or microscopic lesions associated with enema administration. Therefore, the use of hypertonic sodium phosphate enema at recommended doses is potentially dangerous to cats.
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PMID:Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. 401 52

The influence of plasma free fatty acid (FFA) concentration on the secretion of human growth hormone (HGH) was investigated. (a) FFA depression was produced by means of a nicotinic acid (NA) infusion for either 1 or 5 hr in the presence of glucose-induced hyperglycemia. Controls received only saline. (b) FFA depression was also produced by a 90 min NA infusion and then rapid FFA elevation by a lipid-plus-heparin (lipid) infusion. This procedure was compared with a similar NA infusion not followed by lipid. (c) FFA elevation was produced either by a lipid or by a norepinephrine (NE) infusion and then HGH secretion was stimulated by insulin-induced hypoglycemia. Each subject in this group received both the lipid and the NE infusion on seperate days as well as two control tests (insulin alone and NE alone). Depression of FFA resulted in an increase of HGH with a lag period of approximately 2 hr. Maximal HGH rise after 1 hr NA infusion was 7.7+/-1.9 ng/ml and with 5 hr NA infusion 14.3+/-3.6 ng/ml (both significantly higher than during saline infusion, P < 0.025 and < 0.005 respectively) and occurred despite continuous hyperglycemia. Lipid infusion just before the expected HGH increase prevented the HGH response to FFA depression. HGH rise during insulin hypoglycemia (32.2+/-6.5 ng/ml) was significantly inhibited by prior FFA elevation whether achieved by lipid infusion (maximum HGH rise 11.4+/-1.6 ng/ml) or by NE infusion (maximum HGH rise 19.0+/-6.2 ng/ml). The results are suggestive of a negative feedback loop between plasma FFA and HGH secretion, of importance for subacute rather than acute changes in the plasma FFA concentration. FFA lack itself seems to be the signal for HGH release despite the lag period between FFA decrease and HGH increase. Glucose and FFA can at least not fully replace each other in their respective influence on HGH release.
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PMID:Studies on the relationship between plasma free fatty acids and growth hormone secretion in man. 463 23


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