Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1258 38

Male and female F-344 rats and B6C3F1 mice (10/sex/group) were exposed to N,N-dimethylformamide (DMF) by whole body inhalation exposure at 0, 50, 100, 200, 400, or 800 ppm, 6 h/day, 5 days/week, for 13 weeks. A concentration-dependent depression in body weight occurred in rats of both sexes at 400 (6-11%) and 800 ppm (20-22%). In contrast, all weight changes in both sexes of mice were within 10% of controls. No rats died, while 5 mice died from nonexposure-related causes. Relative liver weights were significantly increased at all DMF concentrations in both sexes and both species. Activities of serum sorbitol dehydrogenase (SDH) were statistically increased in male and female rats (200 to 800 ppm) on study days 4, 24, and 91 (13 weeks). Activities of alanine aminotransferase (ALT) and isocitrate dehydrogenase (ICD) were statistically increased in both sexes of rats exposed to 800 ppm DMF at all time points. Cholesterol (CHOL) levels were statistically increased in male and female rats (50-800 ppm) at all sampling time points. Levels of total bile acids (TBA) were statistically increased in both sexes of rats (400-800 ppm) on days 24 and 91. Centrilobular hepatocellular necrosis (minimal to moderate) was seen in rats of both sexes exposed at 400 and 800 ppm, with the lesions more severe in females. Centrilobular hepatocellular hypertrophy (minimal to mild) was found in all groups of DMF-exposed male mice, and in female mice exposed at 100-800 ppm. For male and female rats the no-observed-adverse-effect concentration (NOAEC) for microscopic liver injury was 200 ppm. The NOAEC was 50 ppm for female mice, but an NOAEC based upon the absence of microscopic liver injury was not determined in male mice.
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PMID:Thirteen-week inhalation toxicity of N,N-dimethylformamide in F344/N rats and B6C3F1 mice. 1265 34

Catechol-O-methyltransferase (COMT) enzyme is a widely distributed enzyme that catalyses O-methylation of catecholamines and other compounds having a catechol structure. Because there has been some concern about the consequences of a low COMT activity in the development of oestrogen-dependent cancers and because one of the COMT inhibitors, tolcapone, has caused serious liver injuries in Parkinsonian patients, the histopathology and clinical chemistry of Comt-gene-disrupted mice were studied at the age of 12 months. Owing to the high COMT activities in liver and kidney and the role of COMT in the metabolism of catechol oestrogens, special emphasis was given to the histology of the liver, kidney and oestrogen-dependent organs such as mammary glands and uterus. The mice of both heterozygous and homozygous genotypes appear to be physically healthy and fertile. Diurnal motility rhythm and behaviour in measuring anxiety and depression were equal in all genotypes. At the age of 12 months, the body weight of homozygous mice was 7-9% lower than that of the other groups. This was reflected in histology as a diminished incidence of vacuolation of liver cells (fatty change). Macroscopic pathology and histopathology revealed no abnormal findings in any COMT genotype. The values of some clinical chemistry parameters, such as alkaline phosphatase, alanine aminotransferase, urea, glucose, calcium and proteins, were at a higher level in homozygous animals compared with the wild-type mice. However, all the values remained within the normal physiological range, and the differences in enzyme levels between genotypes were not reflected as histopathological findings in the relevant organs. No changes in haematological parameters or plasma catecholamine concentrations were noted but plasma 3,4-dihydroxyphenylethylene glycol levels were high in COMT null mice. The results suggest that the full or 50% lack of Comt gene as such is not associated with any toxic consequences.
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PMID:Tissue histopathology, clinical chemistry and behaviour of adult Comt-gene-disrupted mice. 1288 3

A study was conducted to evaluate the effects of ochratoxin A (OA) on Escherichia coli-challenged broiler chickens. Day-old broiler chicks were separated into two groups of 92 chicks each, with one group fed a control mash diet, and the other fed a mash diet containing 2 ppm OA. On day 14, each group was further separated into two groups, with one group inoculated with E. coli O78 (1 x 10(7) colony-forming units/0.5 ml), whereas the other group was not inoculated with E. coli. After E. coli inoculation on day 14, four birds from each group were euthanatized at 1, 2, 3, 5, 7, 10, 14, and 21 days postinoculation. Escherichia coli infection caused dullness, depression, huddling, and diarrhea. Mortality was 14.3% in chicks infected with E. coli but fed no OA. Mortality increased to 35.7% in chicks fed OA and infected with E. coli. Decreased body weight and reduced feed intake were observed in chicks fed OA, and the effects were more pronounced in chicks fed OA and infected with E. coli. Increased serum levels of aspartate aminotransferase, alanine aminotransferase, uric acid, and creatinine and decreased levels of total proteins, albumin, globulins, calcium, and phosphorus were observed in OA-fed birds. Escherichia coli infection did not cause significant alteration in any of the serum biochemical parameters. The presence of OA in poultry rations increased mortality and the severity of an E. coli infection.
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PMID:Effect of ochratoxin A on Escherichia coli-challenged broiler chicks. 1288 1

Nineteen dogs from Greece with chronic ehrlichiosis were studied. The dogs exhibited bicytopenia or pancytopenia, bone marrow hypoplasia, seroreactivity to Ehrlichia canis (E. canis) antigens, and had no history of drug or radiation exposure. Anorexia, depression, severe bleeding tendencies, hypoalbuminemia, and increased serum alanine aminotransferase activity were also hallmarks of the disease. All these animals eventually died, irrespective of the treatment applied. Some dogs were also serologically positive for Rickettsia conorii, Leishmania infantum (L. infantum), and Bartonella vinsonii subspp. berkhoffii. Polymerase chain reaction testing of bone marrow samples revealed E. canis, Anaplasma phagocytophilia, Anaplasma platys, and L. infantum in some dogs. Concurrent infections did not appear to substantially influence the clinical course and final outcome of the chronic canine ehrlichiosis.
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PMID:Chronic canine ehrlichiosis (Ehrlichia canis): a retrospective study of 19 natural cases. 1513 Oct 97

We examined the role of nitric oxide (NO) produced by an inducible isoform of NO synthase (iNOS) using N[6]-(iminoethyl)-lysine (L-NIL), a selective iNOS inhibitor, in the rat model of lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) and investigated changes in organ function, plasma levels of NOX (metabolites of NO) and endothelin. We induced experimental DIC by the sustained infusion of 30 mg kg(-1) LPS for 4 h via the tail vein. We then investigated the effect of L-NIL (6 mg kg(-1), from - 0.5 to 4 h) on LPS-induced DIC. Blood was withdrawn at 4 and 8 h, and all four groups (LPS with or without L-NIL at 4 and 8 h) consisted of eight rats. Three of the animals in the 8-h LPS group died, and we examined blood samples from five rats in this group. None of the other rats died. The LPS-induced elevation of creatinine, alanine aminotransferase, glomerular fibrin deposition and plasminogen activator inhibitor was significantly suppressed by L-NIL coadministration, although L-NIL did not affect the platelet count, fibrinogen concentration or the level of thrombin-antithrombin complex. Moreover, plasma levels of the D-dimer that reflect the lysis of cross-linked fibrin were significantly increased by L-NIL coadministration in the LPS-induced DIC model. Plasma levels of NOX and endothelin were obviously increased by LPS infusion. However, both levels were significantly suppressed in the LPS + L-NIL group, when compared with the LPS group. Although mean arterial pressure (MAP) was significantly decreased between 2 and 8 h compared with the control in the LPS group, this depression was significantly attenuated in the LPS + L-NIL group. Our results suggest that NO induced by iNOS contributes to hypotension (depressed MAP), the progression of hepatic and renal dysfunction, microthrombus deposition and elevated endothelin levels in the rat model of LPS-induced DIC.
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PMID:Selective inducible nitric oxide synthase inhibition attenuates organ dysfunction and elevated endothelin levels in LPS-induced DIC model rats. 1586 3

1. A study was conducted to evaluate the effects of ochratoxin A (OA) on broiler chicks challenged with Salmonella gallinarum. 2. One hundred and seventy-six 1-d-old broiler chicks were divided into two groups of 88 chicks each, with one group fed on a control mash diet and the other given a mash diet containing 2 ppm OA. On d 14, each group was further subdivided into two groups with one group infected with S. gallinarum and the other uninfected. 3. Following S. gallinarum inoculation on d 14, 4 birds from each group were killed at 1, 2, 3, 5, 7, 10, 14 and 21 d post inoculation. 4. S. gallinarum infection caused dullness, depression, weakness, increased thirst, droopy wings, ruffled feathers and greenish-yellow diarrhoea. S. gallinarum infection in the absence of OA caused 11.5% mortality which increased to 28.8% in the presence of OA. 5. Decreased body weight and reduced feed intake were observed in chicks fed on the diet containing OA. S. gallinarum infection also reduced the body weights of chicks, with the effects being more marked in chicks receiving OA. The OA diet led to increased serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, uric acid and creatinine, and decreased levels of total proteins, albumin, globulins, calcium and phosphorus. S. gallinarum infection did not cause significant alteration in any of the serum biochemical parameters. 6. Mortality and the severity of S. gallinarum infection in broiler chicks were increased by the presence of OA in the diet.
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PMID:Effect of ochratoxin A on broiler chicks challenged with Salmonella gallinarum. 1626 1

Monthly variations in serum chemistry of the American lobster, Homarus americanus Milne-Edwards, were investigated at one location in Long Island Sound (LIS). Comparisons between three locations within and outside LIS were also made for a single time point. Most serum analytes displayed significant fluctuation over the study period and between locations. Temporal patterns could be classified as: low in cool months/high in warm months, i.e. Na, Cl, Na:K ratio, Ca, albumin:globulin ratio, percentage Fe saturation; high in cool months/low in warm months, i.e. pH, K, urea, total protein, albumin, globulin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipaemia; June spike, i.e. glucose, cholesterol, creatine kinase, iron, transferrin iron-binding capacity; other less obvious fluctuations, i.e. Mg, PO4; and no apparent fluctuation, i.e. HCO3, alkaline phosphatase. The proportion of samples correctly classified into month of collection by a subset of 13 analytes using discriminant analysis improved as the months progressed from May (0.75) to October (>0.95). Discriminant analysis also resolved 96.5% of samples by location. The significant depression of serum calcium at the eastern LIS site correlates with excretory calcinosis, a calcium storage disease described from lobsters at this site, but contrasts with a seasonal elevation in serum calcium recorded in the temporal component of the study. Serum proteins, the electrolytes Ca and K and the enzymes ALT and AST proved to have the strongest spatio-temporal patterns of variation. Serum chemistry is a useful research tool for lobster populations, but the dearth of information on the homology of analyte functions in this species with those in vertebrate species makes interpretation of the results challenging. Late summer/autumn water conditions appear to cause stress for lobsters in LIS.
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PMID:Spatio-temporal variation in serum chemistry of the lobster, Homarus americanus Milne-Edwards. 1630 28

Inadvertent ingestion of thiafentanil oxalate by a captive adult female mountain lion (Puma concolor) caused a prolonged clinical syndrome that included sedation and depression, muscle tension, and myopathy that was incompletely antagonized by naltrexone HCl. A serum chemistry profile revealed markedly elevated creatinine phosphokinase (CK; 490,450 IU/l), alanine aminotransferase (ALT; 1,896 IU/l), and aspartate aminotransferase (AST; 4,321 IU/l) 2 days after onset. The affected animal's condition gradually improved over the next 15 days in response to supportive therapy that included diazepam (5 mg as needed), Normasol R (3 l/day), dexamethasone (tapering dose starting at 1 mg/kg), and ketoprofen (1 mg/kg). She eventually recovered completely. Based on these observations, carcasses of animals immobilized with thiafentanil should be marked and disposed of properly to preclude opportunities for secondary exposure and potential intoxication in scavenging species. In addition, caution is advised when using thiafentanil in animals that could be preyed upon before full metabolism of the drug.
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PMID:Suspected secondary thiafentanil intoxication in a captive mountain lion (Puma concolor). 1645 79

A 74-year-old man with depressive symptoms was admitted to a psychiatric hospital due to insomnia, loss of appetite, exhaustion, and agitation. Medical treatment was initiated at a daily dose of 20 mg paroxetine and 1.2 mg alprazolam. On the 10th day of paroxetine and alprazolam treatment, the patient exhibited marked psychomotor retardation, disorientation, and severe muscle rigidity with tremors. The patient had a fever (38.2 degrees C), fluctuating blood pressure (between 165/90 and 130/70 mg mm Hg), and severe extrapyramidal symptoms. Laboratory tests showed an elevation of creatine phosphokinase (2218 IU/L), aspartate aminotransferase (134 IU/L), alanine aminotransferase (78 IU/L), and BUN (27.9 mg/ml) levels. The patient received bromocriptine and diazepam to treat his symptoms. 7 days later, the fever disappeared and the patient's serum CPK levels were normalized (175 IU/L). This patient presented with symptoms of neuroleptic malignant syndrome (NMS), thus demonstrating that NMS-like symptoms can occur after combined paroxetine and alprazolam treatment. The adverse drug reaction score obtained by the Naranjo algorithm was 6 in our case, indicating a probable relationship between the patient's NMS-like adverse symptoms and the combined treatment used in this case. The involvement of physiologic and environmental aspects specific to this patient was suspected. Several risk factors for NMS should be noted in elderly depressive patients whose symptoms often include dehydration, agitation, malnutrition, and exhaustion. Careful therapeutic intervention is necessary in cases involving elderly patients who suffer from depression.
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PMID:Possible neuroleptic malignant syndrome related to concomitant treatment with paroxetine and alprazolam. 1672 68


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