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 aim of the study was to determine the level of total cholesterol and LDL-cholesterol in blood samples taken from 102 patients with recurrent major depression (according to DSM-IV). The analysis was performed during the acute period of major depression in 3 subgroups: with and without suicidal ideation (S+, S-), and after suicidal attempts (AS), and during remission of depressive symptoms. Putative correlations between the level of total cholesterol and severity of depressive symptoms and between total serum cholesterol and LDL-cholesterol and suicidal risk were evaluated. The patients did not suffer from any additional disorders, factors such as specific diet or pharmacotherapy, which could influence the levels of lipids, were absent. The subgroups were identified using clinical evaluation, medical records and Hamilton Depression Rating Scale--HAMD-S as well as a subscale of MMPI-DMS. Biochemical analyses were performed twice in all patients, in the acute period, before pharmacotherapy and after effective pharmacotherapy, in remission. The following parameters were evaluated: total serum cholesterol and LDL-cholesterol, T3, T4, TSH, ALT, AST, proteinogram. In all depressed patients with acute depression symptoms, low levels of total cholesterol and LDL-cholesterol were shown. The level of total cholesterol 160 mg/dl or less and the level of LDL-cholesterol 100 mg/dl or less were observed in persons with suicidal behavior only (S+ and AS). Low total cholesterol and LDL-cholesterol levels in persons in the acute period of major depression provided a useful parameter of suicide risk. A significant statistical correlation between the low level of total cholesterol and suicidal ideation was also found (r = 0.82, p < 0.05) as well as between the low level of serum total cholesterol and severity of depression, as evaluated by HAMD-S (r = 0.27, p < 0.05). During the remission of depressive symptoms, total cholesterol level and LDL-cholesterol increased significantly (p < 0.05) but a significant difference (p < 0.05) between subgroups (S-, S+, AS) were still observed. Low total cholesterol and LDL-cholesterol levels in remission in persons with the diagnosis of recurrent major depression may help to estimate the risk of suicidal behavior in the next depressive disorder. Possibly, low level of serum total cholesterol is a stable feature in some persons with recurrent major depression, probably dependent on their predisposition to autoaggression and presence of depressive disorder.
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PMID:Levels of serum total cholesterol and LDL-cholesterol in patients with major depression in acute period and remission. 1120 67

Cotreatment of rats with a low hepatotoxic dose (30.7 mg/kg, i.p.) of allyl alcohol (AA) and a higher, but nontoxic, dose (150 mg/kg, oral) of caffeine (CF) potentiated the hepatotoxicity of AA. This was verified by significantly higher levels of plasma alanine aminotransferase (ALT) activity and histopathologically greater severity of lesions in the periportal hepatocytes than those due to AA alone. Treatment of rats with 4-methylpyrazole (4-MP) (0.5 mmol/kg, i.p.) (an inhibitor liver alcohol dehydrogenase) for 30 minutes, followed by similar cotreatment with AA and CF, completely prevented the elevation of plasma levels of ALT and histological damage induced by cotreatment with CF and AA 24 hours following their administration. Severe liver damage induced by cotreatment with CF and AA was further, markedly enhanced by phenobarbital pretreatment (80 mg/kg, i.p., 3 days). Thus, extensive necrosis of periportal hepatocytes was noted, as well as edema and accumulation of inflammatory cells in the necrotic foci caused by such pretreatment. The depression of hepatic nonprotein sulfhydryls resulting from CF plus AA was much more severe than that caused by AA or CF alone and appeared as early as 30 minutes after administration. However, much less marked depletion of protein thiols was observed following similar treatments. Significant increase in lipid peroxidation (as measured by melondialdehyde [MDA] formation) was also observed in rat liver but only 24 hours after administration. The production ofMDA in the rat liver was significantly higher after administration of AA plus CF than after administration of AA alone. Pretreatment of rats with phenobarbital further significantly enhanced the formation of 2,4-dinitrophenylhydrazine (DNP)-reactive metabolite(s) (measured as DNP-acrolein adduct equivalents) in rat liver induced by AA (30.7 mg/kg) plus CF (150 mg/kg) within 1 hour following such treatment. Cotreatment with AA and a higher dose of CF resulted in significantly higher excretion of urinary thioethers or mercapturic acids than in rats treated with AA alone. Thus, these data suggest that an increased bioactivation pathway of acrolein involving a P450 mixed-function oxidase system caused by CF may be involved in such potentiating effects of CF on AA-induced hepatotoxicity in rats.
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PMID:Influence of caffeine on allyl alcohol-induced hepatotoxicity in rats. I. In vivo study. 1139 13

A debilitated 9-yr-old female red panda (Ailurus fulgens fulgens) with a recent history of corticosteroid administration displayed anorexia, depression, and diarrhea for 2 days. Blood work revealed a moderate nonregenerative anemia, leukocytosis, hypokalemia, hyperbilirubinemia, and mildly elevated alanine aminotransferase and aspartate aminotransferase. Serology was negative for occult heartworm, Toxoplasma gondii, feline leukemia virus, feline infectious peritonitis, feline immunodeficiency virus, and canine distemper virus. Electron microscopy of the feces demonstrated corona-like virus particles. The panda died 3 days after initial presentation. Histologic findings included multifocal, acute, hepatic necrosis and diffuse, necrotizing colitis. Liver and colon lesions contained intracellular, curved, spore-forming, gram-negative, silver-positive rods morphologically consistent with Clostridium piliforme. This panda most likely contracted Tyzzer's disease subsequent to having a compromised immune system after corticosteroid administration and concurrent disease.
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PMID:Tyzzer's disease in a red panda (Ailurus fulgens fulgens). 1142 5

A 69-year-old male was hospitalized in January 1999 because of visceral leishmaniasis. He had also suffered from anti-hepatitis C virus (HCV)-positive chronic hepatitis for years. All serum hepatitis B virus (HBV) antigens and antibodies were negative except for anti-HBc. The patient was treated with amphotericin B cholesteryl sulfate (2 mg/kg twice a day for 7 days, iv). Fever disappeared on the 3rd day of treatment, the clinical condition improved rapidly and the patient recovered. In May 1999 the patient developed icteric HBsAg-negative acute hepatitis (aspartate aminotransferase 722 U/l; alanine aminotransferase 988 U/l). Anti-HBc IgM was positive and HBV-DNA was detected in serum by PCR. Anti-HAV IgM was negative. A serum sample obtained on presentation and stored at -80 degrees C was retrospectively tested and found positive for HBV-DNA. In July 1999, complete remission of acute hepatitis and seroconversion to anti-HBs was observed. We suppose that a moderate depression of the immune system, probably associated with leishmaniasis, may have enhanced HBV replication in the patient who had an HBsAg-negative 'silent' HBV infection. Restoration of the immune system after successful antiprotozoan therapy might have induced cell-mediated necrosis of the HBV-infected hepatocytes and seroconversion to anti-HBs.
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PMID:Clinical expression of 'silent' hepatitis B virus infection in a patient with visceral leishmaniasis. 1144 Mar 89

Sodium selenate and sodium selenite are used as supplements to poultry and livestock feed to promote growth and prevent selenium deficiency diseases. Both compounds have been found in chemical waste sites. Thirteen-week toxicity studies were conducted by administering the chemicals to groups of male and female F344/N rats and B6C3F1 mice in drinking water. Animals were evaluated for hematology, clinical chemistry, urinalysis (rats only), histopathology, and reproductive system effects. In the studies of sodium selenate, groups of 10 male and 10 female rats and mice received 0, 3.75, 7.5, 15, 30, or 60 ppm sodium selenate for 13 weeks. These concentrations were estimated to deliver 0, 0.1, 0.2, 0.4, 0.6, 1.1 (males), or 0.8 (females) mg selenium/kg body weight for rats and 0, 0.3, 0.5, 0.8, 1.5, or 2.6 mg/kg selenium for mice. All male and female rats exposed to 60 ppm died. The final mean body weights of rats exposed to 30 ppm sodium selenate and of mice exposed to 30 or 60 ppm were 13% to 29% lower than those of the controls. Water consumption by rats and mice exposed to 15 ppm or greater was decreased. Decreases in urine volume and increases in erythrocyte counts, hematocrit, hemoglobin concentrations, alanine aminotransferase activities, urea nitrogen, and urine specific gravity were considered related to dehydration, as indicated by the decreased water consumption and mean body weights in groups showing these differences. Administration of 7.5 ppm sodium selenate or greater was associated with increased incidences of renal papillary degeneration in rats. Dehydration may have been a contributing factor. No lesions related to sodium selenate administration occurred in mice. In the studies of sodium selenite, groups of 10 male and 10 female rats and mice received 0, 2, 4, 8, 16, or 32 ppm sodium selenite for 13 weeks. These concentrations were estimated to deliver 0, 0.08, 0.13, 0.2, 0.4, 0.8 (males), or 0.9 (females) mg/kg selenium for rats and 0, 0.14, 0.3, 0.5, 0.9, or 1.6 mg/kg selenium for mice. Two female rats exposed to 32 ppm died during the study. The final mean body weights of rats and mice exposed to 32 ppm were 17% to 54% lower than those of the controls. Water consumption by exposed rats and mice decreased with increasing exposure concentration. Changes in hematology, clinical chemistry, and urinalysis parameters similar to those observed in rats exposed to sodium selenate were observed in rats exposed to sodium selenite. These effects were also considered related to dehydration, as indicated by the decreased water consumption and mean body weights in exposed groups. Sodium selenite administration was associated with increased incidences of renal papillary regeneration in rats. Dehydration may have been a contributing factor. No lesions related to sodium selenite administration occurred in mice. Based on mortality in rats, body weight depression, and renal lesions, sodium selenate and sodium selenite were more toxic to rats than to mice. These chemicals caused increases in estrous cycle length in rats; sodium selenite also caused an increase in estrous cycle length in mice. Based on mortality, body weight depression, decreased water consumption, and renal papillary lesions, the estimated no-observed-adverse-effect level (NOAEL) in rats was 0.4 mg selenium/kg body weight for sodium selenate and for sodium selenite. Based on body weight depression and decreased water consumption, the estimated NOAEL in mice was 0.8 mg selenium/kg body weight for sodium selenate and 0.9 mg selenium/kg body weight for sodium selenite. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.
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PMID:NTP Toxicity Studies of Sodium Selenate and Sodium Selenite (CAS Nos. 13410-01-0 and 10102-18-8) Administered in Drinking Water to F344/N Rats and B6C3F1 Mice. 1196 37

Forty-six cats with clinical haemobartonellosis were studied; 75 per cent of the cats of known age were two-and-a-half years old or younger, 50 per cent were intact males and 19.5 per cent were castrated males. The predominant signs of the disease were tachypnoea, lethargy, depression, anorexia, infestation with fleas, pale mucous membranes, icterus, emaciation, dehydration, splenomegaly, anaemia, leucocytosis, increased activities of alanine aminotransferase and aspartate aminotransferase, and azotaemia. Thirty-eight per cent of the cats that were tested for feline leukaemia virus (FeLV) antigen were positive, and 22 per cent of those tested for feline immunodeficiency virus (FIV) antibodies were positive. The prevalence of both FeLV and FIV was much higher than in the general Israeli cat population. The cats infected with both Haemobartonella felis and FeLV had a significantly lower body temperature, were more anaemic and the mean cell volume of their erythrocytes was greater than in the cats with haemobartonellosis alone.
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PMID:Retrospective study of 46 cases of feline haemobartonellosis in Israel and their relationships with FeLV and FIV infections. 1216 25

A clinicofunctional analysis of the heart was made in 50 patients suffering from hemorrhagic fever with renal syndrome (HFRS) in the acute period and at the stage of outpatient rehabilitation. Comparison with healthy subjects was made by physical, ECG, echo-CG data, changes in the levels of creatinphosphokinase (MB-fraction) (CPK-MB), asparagine and alanine aminotransferase in the serum. Clinical symptoms of heart pathology, their incidence rate in different periods of the disease, dynamics of ECG deviations, state of heart chambers and left ventricular systolic function are described. The most manifest changes of the studied parameters were observed in acute disease and depended on the disease severity. The detected changes in the end part of the ventricular complex on ECG associated with a relative depression of left ventricular systolic function as well as a rise in the level of CPK-MB indicate affection of the myocardium. Variants of combination and dynamics of the above disorders allowed to single out the most probable syndromes of heart affection in HFRS.
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PMID:[Clinicofunctional characteristics of the heart in hemorrhagic fever with renal syndrome]. 1247 34

Ischemia/reperfusion (I/R) injury remains an important problem in clinical organ transplantation. There is growing evidence that T lymphocytes, and activated CD4+ T cells in particular, play a key role in hepatic I/R injury. This study analyzes the role of signal transducer and activator of transcription 4 (Stat4) and Stat6 signaling in liver I/R injury. Using a partial lobar warm ischemia model, groups of wild-type (WT), T cell-deficient, Stat4-/Stat6-deficient knockout (KO) mice were assessed for the extent/severity of I/R injury. Ninety minutes of warm ischemia followed by 6 hours of reperfusion induced a fulminant liver failure in WT and Stat6 KO mice, as assessed by hepatocellular damage (serum alanine aminotransferase [sALT] levels), neutrophil accumulation (myeloperoxidase [MPO] activity) and histology (Suzuki scores). In contrast, T cell deficiency (nu/nu mice) or disruption of Stat4 signaling (Stat4 KO mice) reduced I/R insult. Unlike adoptive transfer of WT or Stat6-deficient T cells, infusion of Stat4-deficient T cells failed to restore hepatic I/R injury and prevented tumor necrosis factor alpha (TNF-alpha) production in nu/nu mice. Diminished TNF-alpha/Th1-type cytokine messenger RNA (mRNA)/protein elaborations patterns, along with overexpression of heme oxygenase-1 (HO-1)-accompanied hepatic cytoprotection in Stat4 KO recipients. In contrast, HO-1 depression restored hepatic injury in otherwise I/R resistant Stat4 KOs. In conclusion, Stat4 signaling is required for, whereas Stat4 disruption protects against, warm hepatic I/R injury in mice. The cytoprotection rendered by Stat4 disruption remains HO-1-dependent.
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PMID:Stat4 and Stat6 signaling in hepatic ischemia/reperfusion injury in mice: HO-1 dependence of Stat4 disruption-mediated cytoprotection. 1254 Jul 79

This study was aimed to determine whether administration of an inhibitor of caspase-3 protects hepatocellular function in rats with hemorrhagic shock and whether caspases are important pharmacological targets in attenuating liver injury induced by hemorrhagic shock and resuscitation. Male adult rats were subjected to hemorrhagic shock by bleeding to a mean arterial blood pressure of 35-40 mmHg for 1 h and were then resuscitation with 60% shed blood and lactated Ringers solution. A subgroup of animals was injected i.v. with 2 mg/kg caspase inhibitor, Z-DEVD-FMK, prior to blood withdrawal. Fas ligand expression was markedly elevated and caspase-3 activity increased by 3-fold in hemorrhagic untreated rats. The increase in caspase-3 activity was prevented by administration of Z-DEVD-FMK prior to shock and resuscitation. Poly (adenosine diphosphate ribose) polymerase proteolysis was reduced in rats treated with the caspase-3 inhibitor compared with hemorrhagic untreated animals. Plasma aspartate aminotransferase and alanine aminotransferase values showed a significant increase at 6 h of shock in untreated animals (+360% and +515% as compared with sham-operated animals, respectively). Administration of the caspase-3 inhibitor did not prevent the increase in plasma transaminases. The cytosolic concentration of thiobarbituric acid-reactive substances (TBARS) and the oxidized:reduced glutathione ratio increased in the animals with hemorrhagic shock (+94% and +170%, respectively). These parameters were not significantly modified by pretreatment with Z-DEVD-FMK. It appears that caspase inhibition does not attenuate hepatocellular depression and liver injury induced by hemorrhagic shock and resuscitation.
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PMID:Caspase inhibition does not protect against liver damage in hemorrhagic shock. 1255 41

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


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