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)

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

The influence of complement system in acute pancreatitis in the rat was examined. Two different experimental procedures were used to induce pancreatitis: distal choledochal ligature and the Pfeffer model as modified by NEVALAINEN. In both procedures an acute pancreatitis developed and complement depression was noted. These results showed that consumption of complement will occur even in pancreatitis induced by other than immunologic models. In a second series the same experimental procedures were used in rats that had been decomplemented by application of cobra venom factor. It was possible to produce an acute pancreatitis of moderate severity.
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PMID:[Significance of the complement system in acute pancreatitis in rats]. 45 45

Comparative assessments of the endocrine and exocrine functions of the pancreas associated with gallstone pancreatitis or alcoholic pancreatitis were performed in a series of 86 patients, 20 with cholelithiasis, 12 with chronic alcoholism, 24 with chronic gallstone pancreatitis and 30 with chronic alcoholic pancreatitis and 32 healthy subjects were served as controls. The patients with cholelithiasis showed exocrine hypersecretion of the pancreas. In the patients with gallstone pancreatitis, all the assessed parameters of exocrine function were depressed. On the other hand, no pancreatic exocrine dysfunction was dispalyed in cases with chronic alcoholism. In the non-calcifying alcoholic pancreatitis, both the volume output and the the maximum concentration and output of bicarbonate were diminished but depression in amylase output was not seen. All these parameters were lowered in patients with calcifying pancreatitis. Elevation of hexosamine concentration in the pancreatic juice was evident in alcoholic pancreatitis as compared with gallstone pancreatitis, being particularly prominent in cases of non-calcifying pancreatitis. Patients with alcoholic pancreatitis were observed to secrete viscous pancreatic juice richer in amylase and hexosamine content, than those in the patients with gallstone pancreatitis. Endocrine dysfunction of the pancreas is more frequent and intense in alcoholic pancreatitis than in gallstone pancreatitis.
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PMID:Comparison of pancreatic dysfunction in chronic alcoholic pancreatitis and chronic gallstone pancreatitis. 97 91

The correlation of endotoxin (ET), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and cellular immune parameters with multiple organ failure and lethal outcome in intraabdominal infections was studied in a group of 18 patients with peritonitis, abscess or pancreatitis. Of these patients, 7 developed respiratory failure and 5 died due to multiple septic organ failure. The peak levels of ET (2.7 +/- 1.3 ng/ml) in the course of the disease were followed by moderate increases of TNF-alpha (mean 147 +/- 41 pg/ml) and IL-6 (170 +/- 61 pg/ml) within 2 days. Analysis of the parameters for the last 12 days prior to death or discharge showed, that the patient group with lethal outcome was characterized by significant lower mean plasma levels of TNF-alpha (less than 75 pg/ml versus greater than 160 pg/ml) and IL-6 (less than 130 pg/ml versus greater than 270 pg/ml), as well as high rates of unstimulated thymidine uptake into peripheral mononuclear blood cells (greater than 44000 cpm/8 x 10(6) PMBC/18 h versus less than 24000 cmp), T-lymphocyte depression (CD3; approximately greater than 40% reduction) with lower T-helper/inducer subset cell numbers (mean CD:CD8 ratio 1.0 +/- 0.55 versus 1.8 +/- 0.2) and lower lectin (PHA) stimulation values (1.9 +/- 1.4 versus 4.1 +/- 1.0). These data demonstrate an anergic immune status with low mediator levels and depressed T-lymphocyte function in patients with poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endotoxin, TNF-alpha, interleukin-6 and parameters of the cellular immune system in patients with intraabdominal sepsis. 150 42

To elucidate the hemodynamic changes in the course of acute pancreatitis in dogs, various parameters were monitored non-invasively and real-timely by the ultrasonic flow probes which had been placed in advance. The dogs were divided into two groups, i.e., control group (CG) and infusion group (IG). In the infusion group, lactated Ringer solution was infused intravenously for 12 hours in order to maintain LAP or CVP at the mean +/- 1 mmHg of its control value before inducing pancreatitis. In the control group, lactated Ringer solution was not infused. Cardiac output (CO) and LV dp/dt abruptly decreased in a few hours and remained low levels in a control group (CG), but not in an infusion group (IG). It shows that the decreased CO was caused by a decrease in preload but not by a depression of contractility. Gastroduodenal arterial flow (GDAF) and GDAF/CO decreased in a few hours and kept low level in CG, but not in IG. Therefore, a decrease in GDAF is mainly caused by an increase in vascular resistance due to an increase in Hematocrit. Superior pancreatico-duodenal venous flow (SPDVF) and SPDVF/CO decreased immediately in both groups, revealing that there is severely depressive outflow from pancreas because of hemorrhage and destruction of pancreatic parenchyma immediately after the onset of pancreatitis. In CG, Total hepatic flow (THF) and Portal vein flow (PVF) gradually decreased in a few hours and kept low levels, but Common hepatic arterial flow (CHAF) did not decrease. This suggests that decrease of THF is due to decrease of PVF. THF/CO increased in CG. PVF/CO decreased in CG, while CHAF/CO increased in both groups. The increased CHAF compensated for the decreased PVF, which may play an important role in protecting the liver.
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PMID:Non invasive analysis of hemodynamic changes in dogs with acute pancreatitis. 172 93

N-(2,2-Diphenylethyl)adenosine (DPEA) has been identified as a potential antipsychotic agent acting via stimulation of adenosine receptors. The projected human therapeutic dose, based on animal studies, is 2-3 mg/kg. DPEA has been tested for potential toxicity in mice, rats, dogs and monkeys. Following single oral doses, median lethal dose values were approximately 10-fold greater in rats than in mice, although similar clinical signs including reduced activity, prostration, and necrosis of the tail were seen in both species. DPEA was well tolerated at daily doses up to 40 mg/kg in rats for 2 weeks. A no observed effect level (NOEL) was not identified in the dog or monkey studies. Reduced activity, dacryorrhea, ptosis, hypothermia, necrosis of the tail, and death occurred in rats given 120 and 160 mg/kg. Pathologic changes consisted of pancreatitis, gastric erosion/ulceration, lymphocyte depletion of the thymus, and pulmonary congestion and hemorrhage at 80 mg/kg or greater. In dogs, sporadic emesis was noted at 12.5 mg/kg and greater, and significant pathologic changes consisted of coronary arteritis associated with myocardial lesions and lymphocyte depletion at 25 and 50 mg/kg, pancreatic acinar necrosis at 50 mg/kg, and renal tubular degeneration at 12.5 mg/kg and greater. Emesis and depression were noted at 25 and 50 mg/kg in monkeys. Renal tubular dilatation and degeneration at 25 and 50 mg/kg were noted in the monkeys. These studies demonstrated that DPEA produced a range of adverse effects in common laboratory animal species.
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PMID:Preclinical toxicity studies of an adenosine agonist, N-(2,2-diphenylethyl) adenosine. 187 77

The effect on endogenous beta-endorphins of a new synthetic protease inhibitor was studied in acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Plasma beta-endorphin concentrations and cardiovascular function were measured. Ten dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 3 mg/kg/h of a new synthetic protease inhibitor, E-3123 (4-(2-succinimidoethylthio)4-geranidinobenzoate methanesuLfonate), in lactate Ringer's solution soon after the induction of pancreatitis. Plasma beta-endorphin concentrations in the control group increased significantly. However, plasma beta-endorphin levels in the protease inhibitor group did not increase as in the control group. The protease inhibitor infusion improved hypotension, myocardial depression, and plasma lactate, suggesting that the inhibitory effect of the protease inhibitor on beta-endorphin release contributed to the improvement.
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PMID:Effect of a new synthetic protease inhibitor on beta-endorphin release during acute pancreatitis in dogs. 187

Acute causes and chronic risk factors for the development of acute renal failure were analyzed in prospective acquired data of 261 patients in a medical ICU. The population was divided into a group requiring dialysis treatment for established renal failure (n = 95) and a collective maintaining mild renal insufficiency (n = 166). Bivariate and linear discriminant analyses revealed that, above all, variables related to bacterial infections (sepsis and administration of antibiotic agents) and pancreatitis contributed to the discrimination, followed by bleeding, volume depletion, and chronic liver disease in the discriminant function. Bivariate analysis also yielded significant results for mechanical ventilation, CNS depression, and surgery. The importance of the nephrotoxic properties of aminoglycosides may be outweighed by their role as an indicator of severe infectious disease. The overall correct classification rate of the discriminant function was 78.5%, which reflects the importance of the predictor variables, but does not allow individual predictions.
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PMID:Impairment of renal function in medical intensive care: predictability of acute renal failure. 218 66

Abdominal eumycotic mycetoma caused by Pseudallescheria boydii was diagnosed in a 3-year-old male Siberian Husky. The dog was examined because of weight loss and signs of depression. Initially, pyrexia was the only clinical finding. Antibiotic and corticosteroid treatment was ineffective. Two weeks later, the dog's appetite had decreased, it had vomited a few times, and the caudal portion of the abdomen was sensitive to palpation. Hematologic and serum biochemical abnormalities consisted of anemia, leukocytosis, hypoglycemia, hypoalbuminemia, hyperglobulinemia, and high alkaline phosphatase activity. One week later, the dog's condition continued to worsen, and testicular swelling was observed. The dog was castrated. Microscopic examination of specimens obtained at surgery revealed pyogranulomatous periorchitis with mycetoma granules. Ketoconazole treatment was initiated and continued until the dog died one month later. Necropsy revealed multifocal duodenal ulcers, with transmural pyogranulomatous enteritis, pancreatitis, and peritonitis. This case is unique because the etiologic agent apparently entered via the intestinal tract rather than by contamination of an external wound.
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PMID:Eumycotic mycetoma caused by Pseudallescheria boydii in a dog. 246 20

The effect of endogenous pituitary and pancreatic beta-endorphins in the physiopathologic factors of acute pancreatitis and the effect of opiate antagonist naloxone in these conditions were studied. Pancreatitis was induced by the injection of 0.5 milligram per kilogram of autologous bile mixed with 10,000 units per kilogram of trypsin into the main duct after ligating the accessory duct. After the induction of acute pancreatitis, plasma beta-endorphin concentrations in systemic and portal blood and cardiovascular function were measured. Ten dogs (control group) were given an intravenous injection of 10 milliliters per kilogram per hour of lactate Ringer's solution one hour before the induction of acute pancreatitis. Six (naloxone group) received an intravenous bolus injection of 2 milligrams per kilogram of naloxone at one hour after the induction of acute pancreatitis and then an intravenous infusion of 2 milligrams per kilogram per hour of naloxone was given under the same conditions as for those in the control group. Beta-endorphin in systemic and portal venous blood in those in the control group increased significantly during the experiments. Beta-endorphin and adrenocorticotropin hormone in systemic venous blood both in the control and naloxone groups increased simultaneously. However, blood pressure, pulse pressure and cardiac output improved quickly after the bolus injection of naloxone and were well maintained during intravenous infusion of naloxone. Also, naloxone improved the survival time from acute pancreatitis and decreased plasma lactate concentrations. Our data show that beta-endorphin, released mainly from the pituitary gland and not from the pancreas, may have an important role in subsequent cardiovascular depression. Also the opiate antagonist naloxone may be effective in the treatment of acute pancreatitis.
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PMID:Plasma beta-endorphin and the effect of naloxone on hemodynamic changes during experimental acute pancreatitis in dogs. 254 May 37


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