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 1:1 mixture of tiletamine hydrochloride and zolazepam hydrochloride was tested on 39 polar bears in and near Churchill, Manitoba, Canada during October 1983. The mean dose for satisfactory immobilization with a single injection was 5.1 mg/kg. Bears showed signs of ataxia from 1-3 min following injection and were usually sitting within 4 min. The mean induction time, taken as the adoption of sternal recumbency, was 5.1 min. Maximum relaxation was usually seen by about 20 min post-injection. The duration of immobilization appeared to be related to the dose of drug received. In bears that received a dose near the mean, recumbency lasted about 2 hr. Cubs of the year recovered more quickly than adults. Preliminary results indicated that the bears did not suffer respiratory depression and were able to thermoregulate while immobilized. Bears could be handled safely while under the effects of the drug and workers could readily evaluate the state of their sedation by their reactions. The drug did not appear to provide good analgesia at the doses tested.
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PMID:Immobilization of polar bears (Ursus maritimus Phipps) with a mixture of tiletamine hydrochloride and zolazepam hydrochloride. 398 43

A 1,4-benzodiazepine, SC-32855, was administered orally once daily at doses of 30, 100, and 300 mg/kg for two weeks to adult Beagle dogs (1/sex/dose). The 300 mg/kg animals were sacrificed in extremis on day three after showing extreme signs of CNS depression. At necropsy, the testes of the 100 mg/kg male weighed considerably less than those of the control. The testicular weights of the 30 and 300 mg/kg animals were comparable to the weight of the control testes. Histopathologic evaluation of the testes of the 100 mg/kg male revealed degenerative and necrotic changes in the seminiferous tubules and cytoplasmic vacuolation in Leydig cells. In the 30 and 300 mg/kg animals, degenerative and necrotic changes were restricted to the seminiferous tubules.
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PMID:Testicular toxicity induced by oral administration of SC-32855, A 1,4-benzodiazepine, in the dog. 612 62

Street opiate addiction produces a significant depression in the absolute number of total T lymphocytes in peripheral blood as measured by the ability of the lymphocytes to rosette sheep red blood cells (SRBC). Associated with the decrease in T cells, there is an increase in the absolute number of null lymphocytes but no significant changes in B lymphocytes or total white blood cell count. The T cell values for 2 different populations of addicts (n = 12 and 32) are 31.8% and 23.1%, whereas the null cell values are 51.1% and 57.6%, respectively. The values for comparable control populations (n = 18 and 10) are: T% = 70.7% and 67.4%, and null % = 9.2% and 14.5%. Self-reported use of marihuana does not significantly alter the distribution of cell populations. A 1- to 3-hr incubation of addicted-derived lymphocytes with 10(-6) to 10(-7) M Naloxone reverses both T cell depression and null cell increase by allowing the null cells to express SRBC receptors. Cyclic AMP and dibutyryl cyclic AMP can also convert the null cells to T cells. The conversion of null to T lymphocytes has additionally been measured by monitoring the increase in PHA-stimulated growth in 72-hr cultures as determined by tritiated thymidine incorporation into DNA. These results support the hypothesis that opiates can alter T lymphocyte number and function in vivo, and that this alteration may produce a significant degeneration in the immune competence of street opiate addicts.
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PMID:Alteration of T and null lymphocyte frequencies in the peripheral blood of human opiate addicts: in vivo evidence for opiate receptor sites on T lymphocytes. 625 68

A 1 4/12 years old boy after having been ill with measles developed gingivostomatitis ulcero-gangrenosa, a disease known as noma in tropical countries. This rare disease usually occurs during severe depression of the immunologic defence like with measles, malnutrition, malignant neoplasmas or chemotherapy, and is caused by a local infection with aerobic and anaerobic bacteria, which usually are part of the normal oral flora. The course of the disease is characterized by an initially edematous swelling of the face followed by ulcerations of the gingiva, progressing as an ulcerophlegmatous inflammation of the oro-facial tissue and finally causing mutilating destruction. Vigorous general and antibiotic treatment has improved the previously poor prognosis.
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PMID:[Noma]. 663 44

A 1-year-old child with severe acetaminophen (APAP) poisoning after ingestion of 10 gm APAP demonstrated central nervous system depression, shock, hypothermia, and metabolic acidosis. There was dramatic improvement during treatment with intravenously administered N-acetylcysteine (NAC) and hemodialysis, and the patient recovered without sequelae. A detailed study of APAP metabolism was carried out during the initial 72 hours after ingestion. APAP-sulfate and APAP-glucuronide accounted for 29% and 33%, respectively, of total drug in urine, whereas cysteine and NAC conjugates accounted for only 12%. The low incidence of severe toxicity in children after overdoses of APAP may be related to greater capacity to metabolize APAP via a nontoxic pathway.
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PMID:Metabolism and pharmacokinetics of acetaminophen in a severely poisoned young child. 673 27

This study examined the effects of selective activation of kappa 1-opioid receptors on excitatory transmission in substantia gelatinosa (SG) using intracellular recordings from SG neurons in transverse slices of the young rat lumbar spinal cord. Monosynaptic and polysynaptic excitatory postsynaptic potentials (EPSPs) were evoked by orthodromic electrical stimulation of A delta or C primary afferent fibers in the dorsal root after blocking inhibitory inputs with bicuculline and strychnine, NMDA receptors with D-2-amino-5-phosphonovaleric acid and mu- and delta-opioid receptors with CTAP and ICI 174,864, respectively. Bath application of dynorphin A1-17 or U-69, 593 caused dual modulation of the peak amplitude of presumed monosynaptic AMPA receptor-mediated EPSPs, decreasing synaptic potentials at nanomolar concentrations in a majority of SG cells examined (dynorphin, 63%; U-69,593, 91%), and increasing EPSPs at micromolar concentrations. Only the inhibitory action of dynorphin A1-17 was consistently and completely blocked by norbinaltorphimine (nor-BNI). Since U-69,593 and nor-BNI are selective for the kappa 1-opioid receptors, the depression of EPSPs is likely to be mediated by the kappa1-opioid receptors. Under conditions of blockade of synaptic transmission with TTX and mu-and delta-opioid receptors, dynorphin A1-17 and U-69,593 hyperpolarize most of SG neurons and decrease their membrane input resistance, the finding suggesting that direct interaction of kappa-agonists with a postsynaptic receptor is likely explanation for the inhibition of EPSPs. However, in some SG cells, the inhibition of EPSPs appears to be of presynaptic origin since dynorphin A1-17 and U-69,593 did depress the EPSPs in the absence of changes in passive membrane properties. Rp-cAMPS, a membrane permeant potent competitive inhibitor of cAMP-activated protein kinase, prevented the depressant effect of dynorphin A 1-17. This finding suggested a possibility that dynorphin A1-17, acting through a decrease in intracellular cyclic AMP levels, can reduce the synaptic responses of SG neurons. These results provide the first electrophysiological demonstration that the activation of kappa 1-opioid receptors inhibits AMPA receptor-mediated primary afferent neurotransmission in the substantia gelatinosa of the young rat spinal cord. This effect may mediate the ability of kappa-receptor agonists to produce antinociception.
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PMID:kappa-opioid receptor agonists modulate excitatory transmission in substantia gelatinosa neurons of the rat spinal cord. 747 39

Drug-induced improvement of depression may be mediated by changes in sleep physiology. The aim of this study was to relate changes in sleep polygraphic variables to clinical state during treatment with citalopram, a highly specific serotonin uptake inhibitor. Sixteen patients took part. The study was single-blind and uncontrolled. A 1-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a 1-week placebo period. For the entire group a significant decrease of rapid eye movement sleep (REMS) and a significant lengthening of REMS latency were observed initially as well as at the end of treatment. No changes in sleep continuity were found, but non-REMS stage 2 (percentage) was significantly increased. On the basis of clinical change, as expressed by the scores of the Hamilton Rating Scale for Depression, at the end of the citalopram treatment the patient group was split in two halves: eight less and eight more improved patients. The groups did not differ with respect to any sleep polygraphic variable.
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PMID:Changes in sleep polygraphic variables and clinical state in depressed patients during treatment with citalopram. 785 86

There are no data concerning the functional or metabolic effects of hypoxia in vivo in smooth muscle. We have therefore used 31P-NMR spectroscopy and intra-uterine pressure measurements to examine simultaneously, in vivo, the effect of ischaemia on uterine metabolites, intracellular pH (pHi) and force. A 1-2 cm portion of uterus from day 1 postpartum anaesthetized rats was exteriorized and an NMR surface coil placed on it. A balloon catheter in the uterine lumen recorded intra-uterine pressure changes from the same area. Reversible occluders were placed around the uterine artery. Occlusion produced a decrease and then abolition of contractions, within 10 min. In four of five animals contraction was abolished within 2 min. Upon reperfusion force was rapidly restored (1 min), in all preparations. The mean level of force was significantly above control (pre-occlusion) 20-30 min after reperfusion. The NMR data showed a significant fall in [ATP] (28%) and [phosphocreatine] (34%) during occlusion. Inorganic phosphate doubled in concentration during this period. Metabolites recovered slowly upon reperfusion, taking 20-30 min to return to pre-occlusion levels. The mean pHi fell from 7.32 to 7.00 upon occlusion and was rapidly reversed upon reperfusion. The changes in pHi closely correlated with the changes in uterine force. Decreases of pHi of a similar magnitude in vitro have previously been shown to abolish contractions; thus it is suggested that during ischaemia in vivo the depression of contraction is caused by the large fall in pHi.
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PMID:An in vivo study of the effects of ischaemia on uterine contraction, intracellular pH and metabolites in the rat. 804 48

A 1-year prospective study of seasonal mood changes was conducted in 250 female Boston area residents, aged 43 to 72, who were participants in a study of vitamin D supplementation. Each woman completed the Profile of Mood States questionnaire at four study visits. There were significant changes over the year in scores for Tension-Anxiety, Depression-Dejection, Anger-Hostility, Fatigue-Inertia, and Confusion-Bewilderment. These scores were all highest or "worst" in the fall and lowest in the spring or summer. Worse mood scores were associated with fewer hours of sleep. Serum thyroxine was positively associated with higher Depression-Dejection scores in August through November and with higher (better) Vigor-Activity scores in February through May. Supplementation with 400 IU of vitamin D did not appear to affect levels or changes in mood scores.
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PMID:Seasonal mood changes in 250 normal women. 814 Jan 83

This study characterizes physiological, histological and behavioral effects of traumatic brain injury (TBI) produced by a controlled pneumatic impactor striking the entire right sensorimotor cortex of the anesthetized rat. Damage to both the fore- and hindlimb sensorimotor areas resulted in a hemiparetic animal which allowed us to use four sensitive behavioral/neurological tests to track the recovery sequelae after injury. Initial experiments measured cardiovascular and respiratory effects after cortical impact which depressed the dura to varying depths. Both 0.5 mm and 1 mm cortical depressions produced a momentary decrease (P < 0.05) in mean arterial blood pressure (MABP) while cortical impacts to depths of 2 mm or 3 mm produced a momentary increase (P < 0.05) in MABP. Normotension was re-established within 30 s after the initial response at all injury levels. Respiratory rate was affected only following 3 mm cortical depressions. A 1 mm cortical depression appeared ideal in terms of minimal cardiorespiratory effects, low mortality and lasting behavioral effects. For behavioral and histologic studies, therefore, additional rats were injured by a 1 mm cortical impact and tested for 8 weeks after TBI using four behavioral tests. Injured rats displayed both fore- and hindlimb deficits up to 56 days while traversing a narrow beam (P < 0.001) and up to 28 days when crossing a pegged beam (P < 0.05). Forelimb deficits evaluated on a wire grid platform were evident for 28 days (P < 0.05). Forepaw preference measured in a non-test setting indicated a bias to use the unaffected forepaw for 35 days (P < 0.05). A biphasic pattern of functional recovery was seen on all tests. A period of rapid functional recovery lasting 7 to 10 days was followed by a slower period of functional recovery lasting many weeks. Possible meanings of this biphasic recovery are discussed as issues of behavioral compensation/adaptation versus true neural recovery. Eight weeks after TBI histological analyses indicated that axonal degeneration was present in the areas adjacent to the ipsilateral cortical injury site. Degenerating fibers also extended across the corpus callosum into the homologous area in the contralateral cortex and were seen in the ipsilateral striatum, somatosensory and motor thalamic nuclei and substantia nigra. Significant axonal degeneration occurred bilaterally around the deep cerebellar nuclei. Degenerating fibers extended into the folia and terminated in the cerebellar granule cell layer. Thus the entire sensorimotor control system appeared to have been affected by a cortical injury.
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PMID:Traumatic brain injury of the forelimb and hindlimb sensorimotor areas in the rat: physiological, histological and behavioral correlates. 888 19


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