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)

Four kochia grazing trials were completed over a period of 3 years. Yearling steers were allowed to graze pure stands of irrigated and fertilized kochia (Kochia scoparia) for periods of 14 to 105 days. A total of 116 steers were given kochia as their sole forage. Twenty control steers were allowed to graze native grass pasture, and 20 steers were allowed to graze both native grass and kochia pastures. Steers grazing only kochia lost weight or gained poorly compared with control steers grazing native grass. Steers that grazed both kochia and native grass had intermediate rates of gain. Signs of toxicosis were observed only in steers grazing kochia alone. Considerable variability in the degree of toxicosis was observed from one year to another. Morbidity in the steers grazing only kochia varied from 0% (Trial 4) to 28% (Trial 1), and mortality varied from 0% (Trials 3 and 4) to 10% (Trial 2). The most common signs observed in clinically affected steers were depression, dehydration, weight loss, muscular weakness, photosensitization, ocular discharge, and crusty muzzle. In all 4 trials, significant elevations in serum glutamic oxaloacetic transaminase (GOT) and serum gamma glutamyl transpeptidase (GGT) were observed in steers grazing kochia. In 3 of the 4 trials, significant elevations in serum bilirubin, serum calcium, and serum protein were also observed in kochia-fed steers. Necropsies were performed on 6 of 9 steers that died or were euthanized. The primary pathologic findings were severe chronic nephrosis (5 steers) and degenerative hepatopathy (5 steers).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kochia (Kochia scoparia) toxicosis in cattle: results of four experimental grazing trials. 271 5

Sporulated oocysts of Eimeria acervulina were administered orally to cage-housed broilers at a dose of 3.5 X 10(5) resulted in mild subclinical coccidiosis. Clostridium perfringens incorporated in feed at a level of 2.5 X 10(8) organisms/g. produced lesions characteristic of necrotic enteritis. Mortality of 8% (7/80) occurred in birds fed a ration inoculated with Cl. perfringens alone. Mortality of 35% (28/80) was observed in birds which received an oral dose of E. acervulina and which were fed simultaneously with a ration containing Cl. perfringens. Birds which were fed an inoculated ration two days after an oral dose of E. acervulina showed 41% (33/80) mortality. Birds which received an inoculated ration for two days before administration of an oral dose of E. acervulina demonstrated 18% mortality (15/80). Birds which were fed an inoculated ration four days after an oral dose of E. acervulina showed 10% mortality. Infection with E. acervulina reduced the pH of intestinal contents with a simultaneous depression in serum protein. A 39% increase in intestinal passage time from 178 to 248 minutes occurred on the fifth day after infection with E. acervulina. These experiments suggest that necrotic enteritis, attributed to proliferation of a toxigenic strain of Cl. perfringens, followed intestinal stasis and minimal lesions induced by mild intestinal coccidiosis.
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PMID:Etiology and pathogenesis of necrotic enteritis. 286 8

UFT, a combination antitumor drug consisting of 1 part Futraful and 4 parts Uracil, was administered preoperatively to 10 patients with gastric cancer, 9 patients with colo-rectal cancer and 1 patient with hepatocellular carcinoma. A pharmacokinetic study was then carried out after oral administration of 600 mg per day of UFT, measuring Uracil, Futraful and 5-FU levels in serum and tumor tissue. Preoperative total doses of UFT for gastric cancer were 3.0-11.4 g, for colo-rectal cancer 3.6-16.8 g and for hepatocellular carcinoma 8.4 g. Side effects, mainly gastrointestinal symptoms, were observed in 3 cases. Abnormalities of liver function test, depression of serum protein and bone marrow damage were observed in 4 cases. 5-FU concentration in the tumor tissue was higher than 0.05 mu/g in 15 of 19 patients (79%). This suggested that 5-FU was maintained in the tumor tissue for a longer period. However, it also suggested that the concentration of Uracil in the tumor tissue corresponded to the total dose of UFT as did the degree of side effects.
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PMID:[Effects of preoperative administration of UFT in gastrointestinal cancer]. 308 Sep 66

A patient with acquired immunodeficiency syndrome (AIDS) who required aggressive nutritional intervention via home parenteral nutrition therapy is described, and nutritional status, etiology and therapeutic management of AIDS-associated malnutrition, role of nutrition support, and factors for consideration in using parenteral nutrition in AIDS patients are discussed. Parenteral nutrition therapy was initiated in a 30-year-old AIDS patient with Kaposi's sarcoma lesions of the gastrointestinal tract because of rapid weight loss, low serum protein levels, and malnutrition. He had previously undergone a small-bowel resection and a jejunojejunostomy, and radiation and antineoplastic-drug therapy was planned. During parenteral nutrition therapy, the patient demonstrated increased physical strength and was able to care for himself during most of the time spent at home or in a long-term-care facility. Aggressive measures, including parenteral nutrition therapy, were discontinued 11 days before the patient's death. Complications of therapy included one episode of sepsis and a tear in the external catheter tubing. Malabsorption and diarrhea mainly caused by gastrointestinal disease, reduced food intake because of oral and esophageal infections, adverse effects from medication, and depression are factors that can contribute to AIDS-associated malnutrition. Also, hypermetabolism resulting from infections and fevers may contribute to malnutrition in AIDS. The extent to which this malnutrition affects the underlying immune dysfunction occurring in the syndrome and the response to other more direct drug therapies in AIDS is not known. Available methods for nutritional intervention are based on clinical experience and anecdotal reports. Because of gastrointestinal disease, an oral diet, supplements, and enteral tube feedings may not meet nutritional goals for an AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parenteral nutrition in the management of gastrointestinal Kaposi's sarcoma in a patient with AIDS. 313 64

Clinical pathological studies were undertaken in 5 calves with experimentally-induced heartwater. The most important findings include a progressive anaemia which may be associated with bone marrow depression and fluctuations in the total and differential white cell count, of which an eosinopenia and a lymphocytosis were the most marked. A severe drop in serum protein, especially in the albumin levels, was observed in all 5 cases. This disease is probably associated with an increased capillary permeability, as the protein content of the pericardial fluid in 1 case that died, approximated that of the serum. The osmolality of the effused fluid was also higher than that of the blood. No significant changes in the serum electrolyte levels occurred, except for total calcium levels which tended to decrease to below normal during the acute stage of the disease. Marked increases in total bilirubin were recorded. This, however, was not associated with liver pathology or haemolysis and may possibly be ascribed to a fasting hyperbilirubinaemia. Darkening of plasma colour was associated with peak rises in total bilirubin. Increases in both blood urea and creatinine levels indicate interference with renal glomerular filtration during the acute stage of the disease.
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PMID:The clinical pathology of heartwater. I. Haematology and blood chemistry. 335 99

Nutritional deficiencies are believed to be instrumental in producing reduced immune responses in a variety of animal species. Malnutrition may result in an increase or a decrease in immune functions, depending upon its degree, and also the timing and severity of the nutritional protein deprivation. Our experimental data suggest that there is a significant impairment of cytotoxic activity against K-562 and of the ability of spleen cells to produce interferon in protein-deprived mice in comparison with control mice. Paradoxically accelerated tumor growth after administration of OK-432 or Lentinan was also noted in protein-deficient tumor-bearing mice. In addition, a clinical randomized study of advanced or recurrent gastric cancer patients treated with MMC and FT(MF) with or without lentinan was performed. We recognized excellent end-point results only in the lentinan-treated patients with normal protein levels, while no effect of this agent was seen in patients with low serum protein levels (below 5.9/dl). Aggressive postoperative chemotherapy for cases with distant lymph node metastasis was performed under active nutritional support without any depression of metabolic and immunological states, resulting in a good 5-year survival rate (36.9%).
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PMID:[Anti-cancer effects of BRMs associated with nutrition in cancer patients]. 338 33

Phenylbutazone (PBZ) toxicosis was induced in 9 ponies to further define the clinical and pathologic changes occurring with this syndrome. Six additional ponies were treated with PBZ and a synthetic prostaglandin E2 to determine the role of prostaglandins in the pathogenesis of PBZ toxicosis. Ponies given only PBZ exhibited CNS depression, anorexia, weight loss, diarrhea, cyanotic mucous membranes, and oral ulcers. Total serum protein concentration gradually decreased during the 10-day treatment period. Marked mucosal atrophy, focal erosions, and ulcers characterized the lesions in the alimentary tract. Ponies given PBZ and prostaglandin E2 remained clinically healthy and did not develop hypoproteinemia or mucosal atrophy. A few erosions were seen, but ulcers were not observed. The results of the present study indicate that mucosal atrophy is a characteristic lesion of PBZ toxicosis. It is also evident that inhibition of prostaglandin synthesis has an important role in the development of this syndrome.
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PMID:Experimentally induced phenylbutazone toxicosis in ponies: description of the syndrome and its prevention with synthetic prostaglandin E2. 386 57

In a series of 13 elderly patients with proven prealbumin-related senile systemic amyloidosis (SSA), depressed serum prealbumin values (110.7 +/- 14.1 micrograms/ml) were found as compared to an age-matched control group (175.1 +/- 20.3 micrograms/ml). As expected, there was a significant correlation between serum prealbumin and serum retinol-binding proteins in both groups of patients. Patients with reactive amyloid protein AA amyloidosis had slightly depressed serum prealbumin concentrations, whereas patients with prealbumin-related familial amyloidosis of Swedish type had prealbumin values within normal limits. Since the serum levels of the acute phase reactants, haptoglobin and amyloid-related serum protein AA, were higher in the group of patients with reactive amyloidosis than in patients with SSA, the depression of the prealbumin levels in SSA is not a result of inflammation. Since SSA is known to contain prealbumin, it is possible that a disturbed prealbumin metabolism in old age results in low prealbumin serum values and deposition of amyloid.
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PMID:Serum prealbumin and retinol-binding protein in the prealbumin-related senile and familial forms of systemic amyloidosis. 403 61

To determine the effect of a combined oral progestin on 5 tests of thyroid function, 21 parous women at least 8 weeks postpartum and with histories of regular menses were studied. A complete physical examination showed all to be normal. The 5 tests performed were radioactive iodine uptake (RAI) at 2 and 24 hours, serum protein-bound iodine (PBI), thyroxine iodine by column, triiodothyronine absorption test, and serum cholesterol. 2 baseline determinations of each test except the RAI were performed on each subject on separate days. Only euthyroid subjects were further tested. Of these 16 were given 10 mg of medroxyprogesterone acetate in combination with .05 mg of ethinyl estradiol cyclically for 20 days. Thyroid function tests were repeated at various intervals from the end of the first week of therapy to over 4 months after starting therapy. Cholesterol and RAI determinations were extremely variable precluding any evidence of drug effect. The other 3 tests showed consistent changes in all patients studied. The serum PBI and thyrozine-iodine by column tests both showed slight elevation within the first week of therapy and further elevation 1 months thereafter. These changes approached hyperthyroidism levels. The triiodothyronine absorption test showed little change in the first week but a definite downward shift thereafter with a maximum depression at 3 months of therapy. This change reached hypothyroidism level. If test were done during the 1 week each month patients were not taking the drug, results were the same. These changes are thought to be due to the estrogen component of the contraceptive drugs. Those physicians depending on these thyroid tests for diagnosis should be aware of these changes in patients taking these drugs.
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PMID:The effect of an oral contraceptive on tests of thyroid function. 417 61

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T(4)) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T(4) disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-(125)I, followed in 5-7 days by (131)I-T(4) intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound (125)I and protein-bound (131)I, and urinary (125)I and (131)I, together with frequent estimates of serum (127)I-T(4) (Murphy-Pattee) and free T(4) (FT(4)), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of (131)I-T(4) during infection included significant decreases in the fractional disappearance rate for T(4) [(k)], and in the clearance and daily disposal of T(4), all of which returned to control values during convalescence. Total serum (127)I-T(4) increased late in the infected period to become greater during convalescence than either before or during infection, while FT(4) did not increase significantly until convalescence. An analysis of serum (131)I-T(4)/(127)I-T(4) and (131)I-T(4)/PB(125)I ratios confirmed these observations. The slope with time of ratios for urinary (125)I/(131)I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum (127)I-T(4) concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine (125)I/(131)I suggests enhanced thyroidal T(4) secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.
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PMID:Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man. 456 63


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