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)

Gross and microscopic lesions of Bolivian hemorrhagic fever (BHF) are described in 10 rhesus monkeys that survived from 30 to 78 days after subcutaneous inoculation with a dose of 10(3) plaque-forming units (PFU) of Machupo virus, a dose which produces a severe and generally fatal disease. Six of the monkeys had been given low doses of homologous immune globulin when initial signs of infection appeared. Monkeys exhibited clinical signs in two phases. The initial signs of acute infection which began to appear about 1 week following inoculation included: diarrhea, depression, anorexia, dehydration, and skin rash. The survivors of this early phase of the illness usually showed improvement before relapsing into the second (or chronic) phase, which was characterized clinically by central nervous system disturbances including incoordination, tremors, convulsions, paresis, and muscle atrophy. Microscopic lesions were similar in both immune globulin-treated and untreated animals. These included widespread lymphoreticular infiltrates in the walls and adventitia of blood vessels of the brain, spinal cord, pancreas, intestine, liver kidney, adrenal, parathyroid, heart, and skeletal muscle. Diffuse lymphocytic infiltrates not confined to the vascular or perivascular tissues were present to a variable degree in many of these and other organs. Several monkeys exhibited lymphocytic inflammation of the choroid, meninges, peripheral nerves, and ganglia.
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PMID:Pathology of chronic Bolivian hemorrhagic fever in the rhesus monkey. 18 94

Examined was material taken from five sheep (ewes) and two weaned lambs having naturally contracted Qu rickettsiosis. Described are the clinical symptoms of the disease and the morphologic changes. The diseased animals showed rise in temperature (39.5--40.5 degrees C), loss of appetite, and depression. Some of the weaned lambs manifested slight cough and digestive troubles. Part of the animals showed nervous symptoms--tic movements of the head and limbs. Morphologically, the liver was edematired, of lower compactness, and the spleen was enlarged, the meninges being hyperemic and peppered with pinpointed hemorrhages. Histologically, a strong diffuse activation and proliferation of the liver capillary endothelium was established along with necrobiosis of the liver epithelial cells and a diffuse leukocyte infiltration. Established was also hyperplasia of the reticular cells and the lymph follicles of the spleen and the bronchial lymph nodes. The epithelial cells of the kidney tubules were involved in vacuolar dystrophy, and in the medular section there were fibroblastic proliferations with hyperemia. Inflammatory changes in the brain were also found.
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PMID:[Histopathology of Q rickettsiosis in sheep]. 60 54

Three neonatal calves ranging in age from 4 to 14 days were examined pathologically and bacteriologically. The calves showed depression, anorexia, pyrexia, and difficulty or inability to stand followed by cloudiness of the ocular aqueous humor or cornea. Autopsy revealed congestion, petechiae, and cloudy areas in the meninges. Histologically, the central nervous system (CNS) lesions were prominent and limited to the meninges where fibrinous exudate and infiltrations of neutrophils, macrophages, and lymphocytes were present. There were mild or slight degrees of choroid plexitis and ependymitis. Endophthalmitis was seen as a concurrent lesion in all cases. Fibrinous or fibrinopurulent changes were found in the peritoneum and epicardium as well as in several other organs. Numerous Gram-positive cocci were detected in affected areas of the whole body. Bacteriologically, Streptococcus bovis was isolated from all examined materials consisting of the brain, cerebrospinal fluid, ocular aqueous humor, and several other organs. These results suggest that the lesions were associated with infection of the organism and that the present cases were in the process of septicemia.
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PMID:Clinicopathology of meningoventriculitis due to Streptococcus bovis infection in neonatal calves. 142 May 67

Acute toxicity of cefpirome sulfate (CPR) was examined in 6-week-old mice and rats and immature (5-day-old) rats. The LD50 values of CPR (mg/kg) were as follows: (1) mice: intravenous, 2420 (95% confidence limits, 2122-2758) for males and 2400 (2181-2640) for females; intraperitoneal, 3850 (3407-4351) for males and 4200 (3889-4536) for females; and oral, 16200 (14781-17755) for males and 18500 (17290-19795) for females. (2) 6-week-old rats: intravenous, 1900 (1784-2023) for males and 2080 (1953-2215) for females; intraperitoneal, 6550 (6179-6943) for males and 5800 (5311-6334) for females; subcutaneous, more than 10000 for both sexes; and oral, more than 8000 for both sexes. (3) 5-day-old rats: subcutaneous, between 1750 and 2500 for males and 2080 (1651-2621) for females. Major changes in general health conditions observed in 6-week-old mice and rats were decreased spontaneous activity, lying prone, tremor, respiratory changes (slow or deep respiration, gasping), clonic or clonic-tonic convulsions. In the 6-week-old rats dosed subcutaneously, vocalization, writhing and cutaneous changes at the injection site (dark reddening or blackening, swelling, exfoliation, depilation, induration) were also observed. In the 5-day-old rats dosed subcutaneously, the changes noted were slow respiration, writhing, cyanosis, and dark reddening and swelling of the skin at the injection site. After administration, transient depression of body weight gain or loss of body weight was observed in the mice and rats except the rats dosed orally. These changes disappeared at 7 days after administration at latest, and all surviving animals showed favorable body weight gain thereafter. Necropsies revealed hemorrhage under meninges in the brain in many of the mice and rats which died. Other findings included subcutaneous changes at the injection site in the 6-week-old and 5-day-old rats dosed subcutaneously (dark reddening, retention of dark red fluid, retention of red, white or dark red gelatinous material) and changes in the peritoneal cavity in the 6-week-old rats dosed intraperitoneally (red or dark red spots on the serous membrane, reddening of adipose tissues).
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PMID:[Acute toxicity study of cefpirome sulfate in mice and rats]. 207 98

The oxygen consumption of cerebral arterioles from anesthetized cats was measured using the Cartesian diver microrespirometer following in vitro incubation with 200 micrograms/ml of arachidonate or 50 micrograms/ml of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE). Both agents depressed oxygen consumption severely. This effect was inhibited completely by a combination of superoxide dismutase (SOD) and catalase, indicating that it is mediated by oxygen radicals. Similar depression of oxygen consumption was observed during incubation of the vessels with xanthine oxidase and acetaldehyde as substrate. This enzymic system is known to generate superoxide and hydrogen peroxide. The effect of xanthine oxidase was also partially inhibited by SOD and catalase. The effect of arachidonate was partially inhibited by cyclooxygenase inhibitors. The effect of lipoxygenase inhibitors could not be adequately tested because they depressed oxygen consumption by themselves. Prostaglandins H2 and E2 had no effect on arteriolar oxygen consumption. The results show that arachidonate and 15-HPETE in high concentration depress cerebral arteriolar oxygen consumption via an oxygen radical-mediated mechanism. Furthermore, the radical is generated in the vessel wall and does not require either the brain parenchyma or the formed elements of the blood or the meninges for its production.
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PMID:Reduction in cerebral arteriolar oxygen consumption by arachidonate. 392 Sep 21

The effect of intracisternal inoculation of bacteria on the choroid plexus system, which transports penicillin from cerebrospinal fluid (CSF) to blood, was studied in vitro and in vivo. Meningeal and choroid plexus inflammations as well as CSF pleocytosis were induced in rabbits with intracisternal inoculations of Hemophilus influenzae or Staphylococcus aureus. At various times after bacterial inoculation, the choroid plexuses of the inoculated rabbits were removed and incubated in artificial CSF containing [(14)C]penicillin. The ability of the choroid plexuses to accumulate pencillin in vitro was measured and was found to be depressed as compared with controls. This depression of choroid plexus uptake reversed with resolution of the inflammatory process. In vivo on the day after intracisternal inoculation of Hemophilus influenzae, a decrease in the disappearance of penicillin relative to inulin in the inoculated rabbits (as compared to the controls) was observed when [(14)C]penicillin and [(3)H]inulin were injected intraventricularly and cisternal CSF was sampled 2 h later. This decrease could not be explained by penicillin binding to the CSF exudate. However, the choroid plexus transport system for penicillin was only partially depressed in those inoculated rabbits with bacterially induced inflammation, since in vitro the choroid plexuses could still accumulate penicillin and in vivo CSF penicillin levels could be further increased with probenecid pretreatment. These results suggest that CSF penicillin levels are increased in this model due to three factors: a depression of active efflux of penicillin from the CSF, an increase in permeability to penicillin of inflamed meninges, and, less significantly, by CSF binding of penicillin.
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PMID:Inhibition of penicillin transport from the cerebrospinal fluid after intracisternal inoculation of bacteria. 454 48

Sarcoidosis may involve the central nervous system (CNS) in approximately 5% of cases. Three levels of neurological involvement are possible and include cranial nerve abnormalities, peripheral neuropathies, and lesions of the brain, spinal cord, and meninges. In addition to abnormal neurological findings, psychiatric presentations of CNS sarcoidosis include symptoms of delirium, dementia, depression, personality changes, and psychosis. The diagnosis usually rests on neurological, psychiatry, and cerebrospinal fluid (CSF) abnormalities with a history of sarcoidosis in other organ systems. The CSF, however, may be normal in as many as 30% of cases. The complexities of the illness and the difficulties that may be encountered in making the diagnosis are illustrated with a case of suspected CNS sarcoidosis that presented with delirium and choreoathetosis. The use of steroids as the mainstay of treatment is also discussed.
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PMID:Central nervous system sarcoidosis. 661 71

In a double-blind study, seven Macaca fascicularis monkeys receiving intrathecal (i.t.) morphine in saline, 0.07 mg kg-1, were compared with a control group of four monkeys receiving either lumbar puncture alone (n = 1) or i.t. saline (n = 3). Neither morphine nor saline solutions contained preservatives. Arterial blood gas tensions, respiration, arterial pressure, e.c.g., state of consciousness and motor function were recorded for 24 h. The control group was sacrificed 42 days later and the study group was sacrificed at 6 (n = 2) or 42 days (n = 5) after injection. The central nervous system, meninges, nerve roots and dorsal root ganglia were examined macroscopically and microscopically. Respiratory depression did not occur in either the control or the study groups. There were moderate but statistically significant decreases in systolic and diastolic arterial pressures following i.t. morphine. In both groups, the pathological findings were localized to the cauda equina region and characterized by mononuclear cell infiltration. In neither group was there evidence of demyelination, arachnoiditis or necrosis. Focal endoneurial fibrosis was found in only one animal in the control group following multiple lumbar punctures associated with paraesthesia. The features appeared to correlate with the physical trauma associated with lumbar puncture rather than with the injectate.
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PMID:Acute and chronic effects of intrathecal morphine in monkeys. 689 8

A 6-year-old Doberman bitch was presented for an acute onset of circling, hemiparesis and depression. Clinical examination revealed conjunctivitis, abdominal pain, anaemia, decreased facial sensation, decreased jaw, tongue and pharyngeal tone, decreased conscious proprioception, decreased flexor withdrawal reflexes, and abnormal hemiwalking and hemistanding. Pancytopaenia was evident on haematological evaluation. Bone marrow cytology revealed a bacterial infection. Cerebrospinal fluid analysis was normal. Despite antibiotic treatment, the dog died. On autopsy, widespread multifocal inflammatory lesions were found to be present in the lungs, liver, spleen, meninges, lymph nodes, adrenal glands and kidneys. Listeria monocytogenes was isolated in pure culture from these organs and tissues. Histopathological examination showed numerous gram-positive intracellular rod-shaped bacteria seen in all the above-mentioned organs.
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PMID:Generalised Listeria monocytogenes infection in a dog. 817 88

The effects of neocortical spreading depression (SD) on the expression of immunoreactive c-fos protein were examined within the superficial laminae of trigeminal nucleus caudalis (TNC), a brainstem region processing nociceptive information. KCl was microinjected into the left parietal cortex at 9 min intervals over 1 hr, and SD was detected by a shift in interstitial DC potential within adjacent frontal cortex. The stained cells in lower brainstem and upper cervical spinal cord were counted on both sides after tissues were sectioned (50 microns) and processed for c-fos protein-like immunoreactivity (LI) using a rabbit polyclonal antiserum. C-fos protein-LI was visualized in the ventrolateral TNC, chiefly in laminae I and Ilo and predominantly within spinal segment C1-2 (e.g., -1.5 to -4.5 mm from obex) ipsilaterally. SD significantly increased cell staining within ipsilateral TNC. The ratio of cells in laminae I and Ilo on the left: right sides was 1.32 +/- 0.13 after 1 M KCl, as compared to 1.06 +/- 0.05 in control animals receiving 1 M NaCl instead of KCl microinjections (p < 0.01). The ratio was reduced to an insignificant difference after chronic surgical transection of meningeal afferents and recurrent SD (1.09 +/- 0.11). Pretreatment with intravenous sumatriptan, a 5-HT1-like receptor agonist that selectively blocks meningeal C-fibers and attenuates c-fos protein-LI within TNC after noxious meningeal stimulation, also reduced the ratio to an insignificant difference (1.10 +/- 0.09). Sumatriptan or chronic surgical transection of meningeal afferents, however, did not reduce the ability of KCl microinjections to induce SD. On the other hand, combined hyperoxia and hypercapnia not only reduced the number of evoked SDs from 6.3 +/- 1.0 to 2.5 +/- 1.2 after 0.15 M KCl microinjection, but also significantly (p < 0.01) reduced associated c-fos protein-LI in TNC. These data indicate that multiple neocortical SDs activate cells within TNC. The increase in c-fos protein-LI, observed predominantly ipsilaterally, was probably mediated by SD-induced stimulation of ipsilaterally projecting unmyelinated C-fibers innervating the meninges. If true, this is the first report demonstrating that neurophysiological events within cerebral cortex can activate brainstem regions involved in the processing of nociceptive information via trigeminovascular mechanisms.
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PMID:Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. 838 35


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