Gene/Protein Disease Symptom Drug Enzyme Compound
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 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gene encoding the rat mitochondrial benzodiazepine receptor (MBR) was cloned and characterized. Hybridization of a previously cloned cDNA for MBR to genomic Southern blots indicated that the gene was probably present at one copy per haploid genome. Rapid amplification of cDNA ends with rat adrenal RNA was used to obtain 47 nt of additional sequence upstream from our previously cloned MBR cDNA proving to be a crucial step in cloning the first exon of this gene. The MBR gene is comprised of four exons spanning approx. 10 kb. The first intron, contained within a 8-kb stretch of this gene, is located within the 5'-untranslated sequence, whereas the remaining two introns are much shorter (641 and 854 bp) and interrupt the coding sequence. The third intron contains sequences homologous to rodent B1 repetitive elements and a novel sequence closely resembling part of a repetitive element belonging to the Alu family in humans. The transcription start point was mapped by S1 nuclease protection assays suggesting that the first exon is just 56 bp in length. The sequence upstream from this region contains three GC boxes but lacks other known consensus recognition sites for sequence-specific transcription factors.
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PMID:Structure of the rat gene encoding the mitochondrial benzodiazepine receptor. 133 14

Labelling of peripheral blood Lymphocytes surface antigens was carried out using the method of colloidal gold, enhanced with silver staining. Instead of PBS the minimal essential medium (MEM) according the Eagle, pH 7.2, was used rinsing of isolated lymphocytes. Visibility of positive reactions on lymphocytes at application of both mentioned media was the same. Positive reaction at demonstration of p24 BLV on cells acquired the from of black cap while the IgG expression was observed in the from of diffuse dispersion of colloidal gold on cells. Differences between the application of individual media were observed in the shape of peripheral lymphocytes in smears. Utilization of Eagle's MEM resulted in more uniform shapes and optically smooth surfaces when viewed under a light microscope.
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PMID:Immunogold silver staining method for light microscopic detection of peripheral blood lymphocyte surface antigens with monoclonal antibodies. 133 22

An experimental model of hepatitis E was established in Rhesus Monkeys. Four animals were inoculated with stool suspensions that obtained from patients with hepatitis E. Two animals injected with PBS were taken as negative controls. After 4-6 weeks the ALT of the four animals infected HEV raised 3-4 times and the live biopsy showed acidophilic degeneration of hepatocytes and coagulative liver cell necrosis. Acidophilic bodies were frequently observed. Foci of lytic single-cell necrosis were also observed. Degenerative and microinflammatory changes in liver parenchyma in zones 1-2 of liver lobules were accompanied by inconspicuous infiltrations in portal tracts. 27-34 nm virus-like particles were recovered from the stools of infection animals by IEM.
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PMID:[Experimental infection with hepatitis E virus in rhesus monkeys]. 133 1

The Hedley method for DNA ploidy analysis on paraffin-embedded tissue allows retrospective studies of large numbers of common and rare tumors for which treatment, progression, and outcome are known. However, the technique is cumbersome and has many variables, only some of which can be controlled at the time of laboratory analysis. We performed DNA ploidy analyses on two blocks from two islet cell tumors and on five blocks from two colon carcinomas. Sections of 50-microns thickness were deparaffinized in xylene, rehydrated in graded alcohols and in distilled water, and disaggregated with various enzymatic treatments: 0.05% pepsin (30 and 90 min), 0.5% pepsin (30 and 90 min), 0.05% protease (60 min), and 0.1% protease (60 min). The cell suspensions obtained were filtered, washed in PBS, and visually evaluated in a hemocytometer. Nuclei were treated with RNAse (0.1%) and stained with 50 micrograms/ml propidium iodide. Results were evaluated with the following criteria: (a) recovery of DNA aneuploid and/or G2M cells (cell-cycle analysis and visual evaluation); (b) coefficient of variation of the major peak (DNA diploid or DNA aneuploid depending on the case); (c) amount of debris (background events and visual evaluation); (d) mean channel for the G0G1 peak; (e) event rate; and (f) G2M/G0G1 ratio. The best results were observed with 0.05% protease when there was tissue necrosis and hence cell fragility, with 0.1% protease when there was significant tissue fibrosis, and with 0.05% pepsin (90 min) when there were intact cellular specimens without fibrous entrapment. The original procedure using 0.5% pepsin for 30 min produced less cell recovery, and histogram quality similar to or worse than these modifications in all cases studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzymatic treatments on paraffin blocks for DNA flow cytometry. 134 22

A monoclonal antibody to the rat nerve growth factor (NGF) receptor, 192 IgG, accumulates bilaterally and specifically in cholinergic basal forebrain (CBF) cells following intraventricular injection. An immunotoxin composed of 192 IgG linked to saporin (192 IgG-saporin) has been shown to destroy cholinergic neurons in the basal forebrain. We sought to determine if intraventricular 192 IgG-saporin affected choline acetyltransferase (ChAT) enzyme activity in the CBF terminal projection fields. ChAT assays from 192 IgG-saporin-treated animals showed significant time-dependent decreases in ChAT activity in the neocortex, olfactory bulb and hippocampus, compared to PBS- or OKT1-saporin-injected controls. ChAT and tyrosine hydroxylase activity in the striatum was always unchanged by 192 IgG-saporin. ChAT immunohistochemistry was confirmative of major cell loss in the CBF, while other cholinergic nuclei appeared unremarkable. The data provide further evidence of the selectivity of 192 IgG-saporin in abolishing cholinergic, NGF receptor-positive CNS neurons.
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PMID:Specificity of 192 IgG-saporin for NGF receptor-positive cholinergic basal forebrain neurons in the rat. 135 6

The neuroprotective characteristics of the functional antagonist of metabotropic stimulated phosphoinositide hydrolysis, 2-amino-3-phosphonoproprionate (D,L-AP3), were examined alone and in combination with the non-competitive N-methyl-D-aspartate (NMDA) antagonist, MK-801, against ibotenate induced brain injury. Postnatal day (PND) 7 rats received unilateral stereotaxic intrastriatal injections of 10 nmol ibotenate and treated with either D,L-AP3 (600 nmol i.c.), MK-801 (1 mg/kg i.p.) or both. The severity of brain injury was assessed on PND 12 by comparison of the weights of injected and contralateral cerebral hemispheres. Ibotenate induced injury was partially reduced by treatment with MK-801 (34.0 +/- 4.4% protection, P < 0.05 vs. PBS treated, independent t-test) but not D,L-AP3. However, combined treatment with both MK-801 and D,L-AP3 produced marked synergistic neuroprotection (83.5 +/- 7.6% protection, P < 0.001 vs. PBS treated, independent t-test). The data suggest that metabotropic stimulated phosphoinositide hydrolysis contributes to excitotoxic neuronal injury in the presence of concurrent ionotropic receptor activation.
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PMID:Neuroprotective synergism of 2-amino-3-phosphonoproprionate (D,L-AP3) and MK-801 against ibotenate induced brain injury. 136 Dec 25

Adult Swiss webster mice were injected with 3 x 10(6) colony-forming units (cfu) of group G or 2.5 x 10(6) cfu of group A streptococci at intradermal injection sites on the right and left paralumbar areas of the back. The mice were sacrificed at intervals between 4 hours and 14 days post-injection (p.i.) and full thickness biopsies of skin 10 mm in diameter encompassing the sites of injection were taken. One tissue specimen was homogenized in PBS and plated to determine the number of cfu, while another was used for histopathological studies. The number of viable group A and group G streptococci in the tissue increased to 3 x 10(9) cfu by 96 hours p.i.: after 192 hours p.i. the group A cells had declined to 2.7 x 10(6) cfu compared to 1.1 x 10(8) cfu for group G cells. No streptococci of either group were detected at 336 hours (14 days p.i.). Gross edematous lesions induced by either streptococcus group were evident on all animals at 24 hours (p.i.). Group G streptococci lesions were larger and persisted longer than lesions induced by group A. Histological examination consistently revealed more inflammation and necrosis in tissue sections from mice injected with group G streptococci.
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PMID:Comparison of skin changes induced on mice by either group A type 12 or group G streptococci. 136 27

Our studies of alpha-thrombin as a growth factor have led to the development of a synthetic peptide (p508) that in vitro competes with thrombin for binding to high affinity receptors, and enhances mitogenic activity. To determine if this peptide could be used to accelerate wound closure in vivo, full thickness 6 mm dermal biopsy wounds on the dorsal skin of anesthetized rats were treated with p508 peptide, thrombin or PBS as control. At day 7, the p508 treated wound areas were 20% to 50% smaller than either thrombin or PBS treated wound sites. This suggests that p508 enhances aspects of wound healing, and avoids the normal in vivo regulatory mechanisms of intact thrombin.
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PMID:A synthetic peptide representing the thrombin receptor-binding domain enhances wound closure in vivo. 136 52

Donor-specific blood transfusion prolongs the survival of fully allogeneic ACI (RT1a) renal allografts in PVG (RT1c) recipients from 7-10 days to greater than 100 days. We have observed significant differences in the alloantibody (Ab1) responses to ACI renal allografts in control and DSBT-treated PVG recipients: DSBT is associated with decreased IgG and IgM alloantibody circulating in serum, deposited in the allograft, and produced in culture by splenocytes. In the present studies the effects of DSBT on alloantibody production and renal allograft survival were extended to examine other recipient strains: F344 (RT1lv1), BN (RT1n), W/F (RT1u) and LEW (RT1l). Animals of each recipient strain were injected i.v. with 0.5 ml of ACI blood alone or followed by a renal allograft. Studies on the kinetics of IgM and IgG alloantibody responses were performed by flow cytometry on lymphocytes from donor ACI, PVG, and PVG.R1 (RT1.Aa class I MHC antigen on PVG background) rats. In F344 and PVG rats, DSBT from ACI rats elicited a transient IgM response that peaked at day 7 and was not followed by a switch to IgG. In control PBS transfused F344 recipients, an ACI renal allograft stimulated both IgM and IgG alloantibody production. DSBT pretreatment significantly decreased circulating IgG alloantibody following ACI renal transplantation and prolonged graft survival in F344 recipients. In DSBT-treated F344 recipients that rejected ACI renal allografts acutely, small amounts of IgG (5-12 mode channel shift) were detected in sera harvested 7 days after transplantation, whereas almost no IgG was detected in the sera from DSBT treated F344 rats that accepted their renal allografts indefinitely. In contrast, DSBT alone from ACI to BN, W/F, or LEW strains elicited a transient IgM response that peaked at day 7 and was followed by a strong IgG response that peaked on days 10-14 and remained high through day 21. DSBT failed to prolong ACI renal allograft survival in any of these strains (survival less than 11 days in control and DSBT rats). The alloantibody response to DSBT in all five recipient strains examined was directed primarily to RT1.Aa class I MHC antigens, as determined by binding studies on lymphocytes from ACI, PVG and PVG.R1 rats and alloantibody blocking studies using biotinylated rat monoclonal antibodies to distinct epitopes of the RT1.Aa antigen. The relative magnitude of blocking of R2/10P and R2/15S binding by sera from BN, W/F, and LEW rats was: control allograft recipients greater than DSBT pretreated allograft recipients greater than DSBT alone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:IgG alloantibody responses to donor-specific blood transfusion in different rat strain combinations as a predictor of renal allograft survival. 137 Jul 37

The conditioned corral preference paradigm was used to assess reinforcing effects of substance P (SP) and its N- and C-terminal fragments injected unilaterally into the region of the nucleus basalis magnocellularis (NBM) in rats. Behavioral testing was carried out in a circular open field, consisting of 4 quadrants equally preferred by the animals prior to conditioning. A single conditioning trial was performed. Rats received one microinjection (0.5 microliter) of SP (0.74 pmol), of the N-terminal fragment SP (1-7) and the C-terminal fragment analog DiMe-C7 (each at doses of 0.074, 0.74, and 74 pmol), or vehicle (phosphate-buffered saline; PBS). After injection the rats were placed into the open field with the four quadrants being separated by Plexiglas barriers (closed corral). During the test for conditioned corral preference, when provided a choice between the four quadrants, only those rats injected with SP and the equimolar dose of DiMe-C7 (0.74 pmol) spent more time in the treatment corral, indicative of a positively reinforcing action. None of the other doses of DiMe-C7 and of SP(1-7) influenced the preference behavior. For rats injected with 0.74 pmol SP, SP (1-7), and DiMe-C7, a behavioral analysis was performed for the 15 min conditioning trial. SP and DiMe-C7 reduced rearing and grooming behavior, whereas DiMe-C7 and SP(1-7) increased locomotor activity. However, the acute behavioral effects of SP and its fragments were not correlated with the subsequent place preference behavior during the test trial. The results are discussed in the framework of a structure/activity relationship for the positively reinforcing properties of SP in the region of the NBM. Furthermore, neuropathological implications of the present data are considered, since the homologous nucleus basalis of Meynert in man is known to degenerate in Alzheimer's disease, which is characterized behaviorally by a progressive deterioration in associative functioning.
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PMID:Positively reinforcing effects of the neurokinin substance P in the basal forebrain: mediation by its C-terminal sequence. 137 Sep 40


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