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)

Salt poisoning has been described under various circumstances in adult cattle. Presenting clinical signs in 6 Holstein beef cattle with such poisoning were primarily dysfunction of the central nervous system and included ataxia, opisthotonus, nystagmus, depression, muscle twitching and intermittent convulsions, as well as abdominal pain and polydipsia. Diarrhea occurred in 2, and blindness in 3/6 cattle. Hypernatremia (161.8 - 178.8 mmol/L) and hyperosmolality (331.81 - 366.18 mOsm/L) were present in all animals. To treat the affected cattle, access to fresh water was restricted, vascular volume was expanded with isotonic saline and then hypotonic fluid (5% Dextrose solution) i.v. and dexamethasone im was administered. Although biochemical parameters returned to normal reference ranges, 3/6 affected animals remained blind.
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PMID:Salt poisoning in beef cattle. 1508 Feb 19

Glioblastoma multiforme is the most malignant astrocytic neoplasm and the most common brain neoplasm of humans. Spontaneous neoplasms of the brain are rare in nonhuman primates. This report describes three glioblastomas in adult captive-reared baboons. The animals exhibited a range of clinical signs, including depression, weight loss, weakness, and blindness. All three neoplasms were located in the cerebrum, with extension into the pons in one case. Histologically, the tumors were similar and were characterized by cellular pleomorphism, multinucleated cells, areas of necrosis, microvascular proliferation (glomeruloid bodies), and palisading of neoplastic cells around blood vessels and areas of necrosis. Two baboons exhibited gemistocytic differentiation, and in one baboon, the neoplastic cells were predominantly spindle shaped with a fascicular growth pattern. Immunohistochemical staining for glial fibrillary acidic protein, vimentin, and S-100 protein was positive, whereas immunostaining for synaptophysin and chromogranin A was negative. Positive staining for the cell proliferation marker Ki67 ranged from 8.2% to 13.9%. Terminal deoxynucleotidyl transferase mediated dVTPnick end labeling (TUNEL) staining ranged from 1.8% to 5.7%. These baboon glioblastomas share many features with those of humans.
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PMID:Glioblastoma multiforme in three baboons (Papio spp). 1523 46

The aim of this study is to examine the influence of depression on headache onset following laboratory stress and on psychophysiological variables associated with tension-type headaches (TTHs). Diagnostic interviews identified three groups: headache prone and depressed (HP/D, N = 13); headache prone not depressed (HP/ND, N = 22); and healthy controls (HC, N = 13). Ss completed a laboratory stress task. Blind evaluations of pericranial muscle tenderness (PMT) and pressure pain thresholds (PPT) were obtained immediately before, immediately after and 24 h post-task. Ss also recorded headaches (HA) before, during, immediately post-task and for 24 h post-task. HP/D Ss were more likely than HP/ND Ss or HC Ss to report a headache during and immediately following the stress task (P < 0.05). HP/D Ss exhibited higher PMT than HP/ND Ss or HC Ss before and following the stress task (P < 0.05). HP/D Ss exhibited lower finger PPT at all assessments and lower temporalis PPT at two of three assessments than HC Ss (P < 0.05) but did not significantly differ from HP/ND Ss at most assessments. Depression increased vulnerability to TTH following laboratory stress and was associated with elevated PMT. In individuals with frequent headaches, depression may aggravate existing central sensitization increasing vulnerability to TTHs.
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PMID:Depression increases onset of tension-type headache following laboratory stress. 1536 65

Visual impairment among the elderly is a major health problem. With advancing age, the normal function of eye tissues decreases and there is an increased incidence of ocular pathology. Demographic studies have shown that age is the best predictor of blindness and visual impairment. The most common causes of age related visual impairment in the elderly are presbyopia, cataracts, age related macular degeneration, primary open angle glaucoma and diabetic retinopathy. Untreated visual impairment leads to physical handicap, increased incidence of fall, depression, social isolation and dependency. Active screening for visual loss in the elderly should be part of the health examination. The elderly should be encouraged to come for formal 1-2 yearly eye assessment for early detection of visual impairment and to treat all associated problems in order to prevent permanent visual loss.
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PMID:Age related visual impairment in the elderly. 1577 99

Changes in emotional and social behaviour are considered to be amongst the most common and debilitating consequences of traumatic brain injury (TBI). Little is known of the effects of TBI on alexithymia, which refers to impairment in aspects of understanding emotions. In the current study TBI patients (N=28) were compared with demographically matched healthy controls (N=31) on the Toronto Alexithymia Scale-20 (TAS-20), a measure that taps three distinct characteristics of the alexithymia concept; difficulty in identifying emotions, difficulty in describing emotions and externally oriented thinking. Patients and controls also completed measures of anxiety, depression, quality of life, and measures of fluency to assess executive function. Patients showed greater levels of alexithymia, in terms of difficulty identifying emotions and reduced introspection. Difficulty in identifying emotions was associated with poorer quality of life, even when depression and anxiety were controlled. Difficulty in identifying emotions was also uniquely associated with executive function deficits. Thus, although studies typically focus on aspects of cognitive change following head injury, these results lend support to Becerra et al.'s (Becerra, R., Amos, A., & Jongenelis, S. (2002). Organic alexithymia: a study of acquired emotional blindness. Brain Injury, 16, 633-645.) notion of an 'organic alexithymia', and suggest that more attention should be focused upon assessment of emotional change post-head injury.
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PMID:Cognitive and psychosocial correlates of alexithymia following traumatic brain injury. 1589 16

Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90 mg F/kg). A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity. Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe. Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.
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PMID:Superphosphate poisoning of sheep: the role of fluoride. 1603 Aug 46

Methanol remains to be a major public and environmental health hazard. Formic acid is the toxic metabolite responsible for the metabolic acidosis observed in methanol poisoning in humans, in non-human primates and in folate-depleted rodents. Cytochrome oxidase inhibition by formate leads to lactic acid accumulation, which contributes significantly to metabolic acidosis. Toxic effects in human beings are characterized by formic acidemia, metabolic acidosis, ocular toxicity, nervous system depression, blindness, coma and death. Elimination of formate is one of the principles of management in methanol poisoning. Hemodialysis facility is not readily available in all the places, in developing countries like India. Formate dehydrogenase (EC 1.2.1.2) acts directly over formate and converts formate into CO(2) in the presence of NAD. Effect of single intravenous bolus infusion of formate dehydrogenase, obtained from Candida boidinii; in methanol-intoxicated folate deficient rat model was evaluated. Folate depletion induced by methotrexate (MTX) treatment. Carbicarb (Carb) (equimolar solution of sodium carbonate and sodium bicarbonate) was used to treat metabolic acidosis. Experimental design consists of seven groups, namely Saline control, methanol control, MTX control, Enzyme control, MTX-methanol control, MTX-methanol-Carb and MTX-methanol-Carb-Enz group. Male wistar rats treated with MTX (0.3mg/kg) for a week, were injected (i.p.) with methanol (4 gm/kg), 12h latter, Carbicarb solution was infused, following this enzyme was infused (i.v.) in bolus. Blood samples were collected every 15 min for an hour from the cannulated left jugular vein and blood methanol, formate were estimated, respectively, with HPLC and fluorimetric assay. Blood pH, blood gases pO(2), pCO(2) and bicarbonate were monitored with blood gas analyzer in order to evaluate acid base status of the animal. Results obtained show that there is significant elimination of formate within 15 min. It may be concluded that single bolus infusion of formate dehydrogenase facilitates fast removal of formate, a highly toxic metabolite in methanol poisoning.
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PMID:Therapeutic response to single intravenous bolus administration of formate dehydrogenase in methanol-intoxicated rats. 1618 30

Motion-induced blindness (MIB) occurs when target stimuli are presented together with a moving distractor pattern. Most observers experience the targets disappearing and reappearing repeatedly for periods of up to several seconds. MIB can be viewed as a striking marker for the organization of cognitive functioning. In the present study, MIB rates and durations were assessed in 34 schizophrenia-spectrum disorder patients and matched controls. The results showed that positive symptoms and excitement enhanced MIB, whereas depression and negative symptoms attenuated the illusion. MIB was more frequently found in normal subjects. The results remained consistent after adjusting for reaction time and error rates. Hence, MIB may provide a valid and reliable measure of cognitive organization in schizophrenia.
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PMID:Reduced perception of the motion-induced blindness illusion in schizophrenia. 1624 90

A 9-week-old miniature mule foal presented to the Veterinary Medical Teaching Hospital for acute blindness, ataxia, and depression following an overdose of an over-the-counter ivermectin-based de-worming medication. Ophthalmic examination and electrodiagnostic evaluation eliminated outer retinal abnormalities as the primary cause of the bilateral blindness, implicating instead a central neurologic effect of the drug. With symptomatic and supportive care, the foal recovered fully and regained its vision.
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PMID:Suspected ivermectin toxicosis in a miniature mule foal causing blindness. 1640 42

This review describes a group of diseases known as the transmissible spongiform encephalopathies (TSEs), which affect animals and humans. Examination of affected brain tissue suggests that these diseases are caused by the acquisition and deposition of prion protein (PrP). Creutzfeldt-Jakob disease (CJD) is the most important form of TSE in humans with at least four different varieties of the disease. Variant CJD (vCJD), a new form of the disease found in the UK, has several features that differ from the classical forms including early age of onset, longer duration of disease, psychiatric presentation (for example, depression) and extensive florid plaque development in the brain. About 10 per cent of patients with CJD exhibit visual symptoms at disease presentation and approximately 50 per cent during the course of the disease. The most commonly reported visual symptoms include diplopia, supranuclear palsies, complex visual disturbances, homonymous visual field defects, hallucinations and cortical blindness. Saccadic and smooth pursuit movements appear to be more rarely affected. The agent causing vCJD accumulates in lymphoid tissue such as the spleen and tonsils. The cornea has lymphoid tissue in the form of corneal dendritic cells that are important in the regulation of the immune response in the anterior segment of the eye. The presence of these cells in the cornea has raised the possibility of transmission between patients via optical devices that contact the eye. Although such transmission is theoretically possible it remains highly improbable.
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PMID:Creutzfeldt-Jakob disease and vision. 1643 Apr 33


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