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)

As part of an overall assessment of immunological function, several aspects of cellular immunity and circulating lymphocyte subpopulations were evaluated in a group of 10 patients with idiopathic autoimmunhemolytic anemia (AIHA). The absolute numbers of circulating T and B cells were reduced in the patient group compared to normals. A shift from "corticosteroid-sensitive" to "corticosteroid-resistent" and activated cells in the cytogram of clustered Fe-(III)-hydroxide-glucane saccharose labeled T lymphocytes was apparent. In vitro studies of cellular reactivity, as evaluated by PHA, ConA, PWM, antigens and allogeneic cell induced proliferation showed a blend of general or selective depression and sometimes a normal or increased activity with no definite correlation with both the number of circulating T cells and the extent of the hemolytic activity by the disease. The possible significance of the findings is discussed.
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PMID:Functional and surface characterisitics of lymphocytes from patients with warm-antibody type autoimmunhemolytic anemia (AIHA). 30 50

3-alpha-Hydroxy-5-beta-pregnan-20-one [pregnanolone (PA)] and 3-beta-hydroxy-5-pregnen-20-one 3-sulfate [pregnenolone sulfate (PS)] are steroids that have been shown in biochemical studies to be active at the GABA-benzodiazepine-chloride receptor complex, Pa as a "barbiturate-like" agonist and PS as a "picrotoxin-like" antagonist. Since other compounds that are active at this site interact with the effects of pentobarbital and ethanol, the behavioral effects of these steroids alone and in combination with pentobarbital and ethanol were tested. Pa blocks the convulsions caused by pentylenetetrazole (PTZ) and increases motor activity when given alone in low doses. In combination with either pentobarbital or ethanol, it enhances the depression in motor activity, hypothermia, and hypnosis. In contrast, PS has no effect on PTZ convulsions and depresses motor activity by itself. With pentobarbital, PS enhances the depression in motor activity but has no effect on hypothermia or hypnosis. With ethanol, PS enhances the hypothermia but does not affect motor activity or hypnosis. Therefore, Pa and PS show different but not opposite effects in interacting with compounds active at the GABA-benzodiazepine-chloride receptor complex.
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PMID:Interaction of pregnanolone and pregnenolone sulfate with ethanol and pentobarbital. 151 42

The concentration of norepinephrine in the hippocampus of rats anesthetized with halothane (Wyeth-Ayerst, Philadelphia, Pa) is found to be markedly increased, presumably due to the stress of handling and administering the anesthetic. This increased norepinephrine concentration persists for about 50 minutes but is obliterated when the anesthetized rat is concussed. This 50-minute period corresponds to the time it takes for a rat (or human), comatose for 1-2 seconds following concussion, to regain normal memory. No changes in 3,4-dihydroxybenzene-acetic acid (DOPAC), 3-(3,4-dihydroxyphenyl) alanine (L-DOPA), and 3,4-dihydroxybenzylamine (DHBA) were noted. 5-Hydroxy indole acetic acid (HIAA) showed a depression at 5 minutes and again at 30 minutes, changes that were consistent but not considered statistically significant.
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PMID:Changes in hippocampal monoamine concentration following halothane anesthesia and concussion. 154 72

Trimethyltin (TMT) is an alkyltin that targets neurons of the limbic system. A gene probe (i.e., mRNA) for myelin basic protein (MBP), a major component of central nervous system myelin, was used to monitor this toxic neuropathy in Sprague-Dawley rats. Animals were administered a single intraperitoneal injection of TMT-hydroxide at a neuropathic (8.0 mg/kg/body wt) or nonneuropathic (0.8 mg/kg/body wt) dose and sampled at 1, 3, or 7 days postexposure to correlate the progression of hippocampal neuropathology with probe (i.e., MBP-mRNA) levels. Microscopic examination of the brain showed only moderate but progressive damage over the 7-day postexposure period in animals treated with the neuropathic dose. Neuronal loss was first observed in the dendate gyrus and CA4 at 1 day postexposure, and progressed to the CA3c sector at 3 and 7 days postexposure. Elsewhere in the brain, minimal involvement of the entorhinal cortex neurons occurred 3 days postexposure and intensified by 7 days. No histological damage was seen at the nonneuropathic (0.8 mg/kg) dose. For gene probe analysis, the brain was divided into anterior and posterior halves. In rats treated with the neuropathic dose of TMT, the anterior brain showed progressive depressions of MBP-mRNA levels over the 1-, 3-, and 7-day postexposure period that correlated with increasing hippocampal neuropathology. The posterior brain showed no significant changes in MBP-mRNA levels with respect to that of controls over the same time period. At the nonneuropathic dose (0.8 mg/kg) a significant depression of MBP-mRNA levels occurred in the anterior brain at 7 days postexposure in the absence of overt histological damage.
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PMID:Myelin basic protein-mRNA used to monitor trimethyltin neurotoxicity in rats. 170 32

With the use of a micropolarographic system, the effects of a series of isopropyl alcohol concentrations on oxygen uptake by the corneal epithelium of the rabbit were measured in vivo. Based on an exposure period of 10 sec, followed by a saline rinse, concentrations of greater than 31% were found to cause an abrupt and severe decline in oxygen uptake, with oxygen flux responses associated with 44% and greater being indistinguishable 60 min later from those of an epithelially denuded cornea. Initial flux variations, e.g. a mild depression at 24% and a mild elevation at just under 31%, were still evident 1 h following exposure. A slope model for estimating that concentration, the aerobic reduction dosage, which would reduce the oxygen flux activity of the epithelium to half, called here the ARD50, was found for this exposure time to be 37%. That estimate is in very close agreement with measured responses. A susceptibility ratio (SR), for comparing the relative toxicities of different agents based on the quotient of their ARD50 values, was calculated here for sodium hydroxide and isopropyl alcohol, and found to be 50:1.
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PMID:Aerobic responses of the cornea to isopropyl alcohol, measured in vivo. 361 54

To determine the ability of mineral supplements to elevate depressed milk fat percent, we placed 42 Holstein cows in early to midlactation in seven blocks and assigned each to one of six treatments: control (25% corn silage and alfalfa haylage, 75% concentrate, mostly corn, dry matter); control plus magnesium oxide ground to pass a .425-mm sieve; control plus prilled magnesium oxide sieved to between 1.70 and .425 mm; control plus sodium bicarbonate; control plus reactive powdered magnesium oxide to pass a 45 microns sieve; and control plus powdered magnesium hydroxide. Sodium bicarbonate was 1% of diet as fed, magnesium oxide .5%, magnesium hydroxide .7% later reduced to .5%. Cows were fed control ration for 3 wk to induce milk fat depression, then were changed to treatment rations for 5 wk. Five cows (unblocked) were continued on each dietary treatment for a digestibility study after the feeding trial. All mineral supplements produced greater milk fat percent and yield of milk fat per day than control and all magnesium treatments produced greater milk fat percent than sodium bicarbonate. Magnesium oxide passing a .425-mm sieve produced the greatest increase of milk fat percent. Milk production was most for sodium bicarbonate treatment. Supplementation with magnesium increased ruminal magnesium concentration by factors of 1.26 to 3.75. Blood serum, urine, and fecal magnesium concentrations and fecal pH were more for cows fed magnesium than those fed sodium bicarbonate treatments. Kidney filtration ratios of element to creatinine increased for magnesium when diets were supplemented with magnesium and increased for phosphorus and sodium when diets were supplemented with sodium bicarbonate.
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PMID:Response of milking cows fed a high concentrate, low roughage diet plus sodium bicarbonate, magnesium oxide, or magnesium hydroxide. 609 3

The effects of delta 9-tetrahydrocannabinol (delta 9-THC), two of its metabolites, 8 beta-hydroxy-delta 9-THC and 11-hydroxy-delta 9-THC, and cannabidiol were comparatively studied by means of an iron-induced cortical focal epilepsy in conscious rats with chronically implanted electrodes. delta 9-Tetrahydrocannabinol produced depression of the spontaneously firing epileptic focus, excitatory behavior, generalized after-discharge-like bursts of epileptiform polyspikes and frank convulsions. The pharmacological profiles of the two metabolites differed from that of the parent compound: 11-Hydroxy-delta 9-THC did not precipitate convulsions, but it did elicit all the other effects of delta 9-THC; the 8 beta-hydroxy derivative, on the other hand, exerted only two delta 9-THC-like effects; that is, it evoked polyspike bursts and convulsions. In contrast, cannabidiol, even in large doses (100 mg/kg) was devoid of all the effects of delta 9-THC. Furthermore, pretreatment with cannabidiol markedly altered the responses to delta 9-THC in the following ways: focal depression was partially blocked, polyspike activity was enhanced and convulsions abolished. Phenytoin pretreatment elicited similar effects, but it failed to block the delta 9-THC-induced convulsions. In general, the cannabinoids exhibit a wide spectrum of CNS effects ranging from focal depression to convulsions; specifically, however, the pharmacological profile of each agent can differ markedly; for example, the convulsant properties of delta 9-THC are not a universal characteristic of this class of drugs.
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PMID:Central excitatory properties of delta 9-tetrahydrocannabinol and its metabolites in iron-induced epileptic rats. 627 53

To examine the role of vitamin D in human phosphate absorption, we studied patients with chronic renal disease on hemodialysis, before and after correction of vitamin D deficiency. Thirty-centimeter segments of jejunum were perfused with test solutions containing varying concentrations of phosphate; phosphate absorption rate and electrical potential difference were measured. The data reveal that dialysis patients have depressed phosphate absorption, but the degree of this depression is modest, compared to the extent of their depressed calcium absorption. Therapy with 1,25-(OH)2D3 for 1 wk restored phosphate absorption rate to near normal. With or without 1,25-(OH)2D3 therapy, phosphate absorption was not influenced by calcium in the perfused test solutions. Examination of kinetic data suggests that the vitamin D deficiency of chronic renal failure causes a reduction by half in the rate of active phosphate absorption. By contrast, our data suggest that vitamin D deficiency does not alter passive phosphate absorption. By aspirating jejunal contents after ingestion of different foods, with and without aluminum hydroxide, the physiologic luminal phosphate concentration was found to vary between 0.7 and 12.2 mM. At the lower end of this range, phosphate absorption would be mediated entirely by active transport; at the higher phosphate concentrations, phosphate absorption would be mainly mediated by passive transport.
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PMID:Absorption of phosphate in the jejunum of patients with chronic renal failure before and after correction of vitamin D deficiency. 668 2

In vivo effects of actively produced or passively administered isologous anti-idiotypic antisera (aId) on the benzylpenicilloyl- (BPO) specific IgE and IgG formation in BALB/c mice have been studied. Isologous anti-BPO aId were raised in BALB/c mice by immunization with purified anti-BPO antibodies isolated from ascites induced with BPO-bovine gamma-globulin in the same mouse strain. Mice producing isologous anti-BPO aId exhibited long-term suppression of BPO-specific IgE and IgG antibody responses induced by BPO-ovalbumin (BPO-OVA) in aluminum hydroxide. Simultaneously, they produced increased amounts of anti-BPO aId after each challenge with the BPO-OVA antigens. Passive administration of isologous anti-BPO aId into syngeneic mice previously sensitized with BPO-OVA caused depression of BPO-specific IgE antibody levels for 2 to 3 weeks. When anti-BPO IgE had again reached its previous level, passively administered aId had decreased to the level of untreated mice. Passive administration of anti-BPO aId also depressed the primary anti-BPO IgE formation for 2 to 3 weeks. In all these experiments the IgE antibody formation against the carrier proteins used for BPO-antigens was not affected. These results show that IgE and IgG antibodies share major idiotypic determinants and that IgE production is accessible to regulation by aId.
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PMID:Suppression of the benzylpenicilloyl- (BPO) specific IgE formation with isologous anti-idiotypic antibodies in BALB/c mice. 738 Dec 1

4-Hydroxy-4-phenylcaproamide (HPhCA), at high doses or rates of IV injection depressed the ventral root reflexes elicited by nerve or dorsal root stimulation. The D (direct) and I (synaptic) ventral root waves and the antidromic (A) dorsal root wave evoked by intraspinal stimulation were also depressed. Similar effects were produced when HPhCA was applied topically on the cord dorsum. At 80 mg/kg and 8 mg/kg/min, the spinal reflexes and the I wave were facilitated for 4 to 6 h, but the D and A waves were depressed. Intracellular recordings from motoneurons showed that HPhCA injection produced: hyperpolarization that lasted several hours, short lasting (< 20 min) facilitation of both EPSPs and IPSPs as well as spike-like potentials (SLPs) that were triggered by EPSPs even though the neuron was hyperpolarized. SLPs may reach the threshold for full spikes. Our results suggest that the spinal depression results from hyperpolarization of motoneurons and the initial facilitation appears to be presynaptic. The late facilitation may be produced by SLPs. HPhCA does not appear to mimic the actions of GABA in primary afferents fibers and motoneurons.
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PMID:Efficacy of a putative GABA analog on synaptic transmission in the cat spinal cord. 827 30


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