Prediction of water solubility and toxicity of substituted indoles to photobacterium Phosphoreum using molecular connectivity indices and quantum chemical parameters.
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Indoles↗
Biomedical subjects
A Zhang
Publications and source records attributed to A Zhang.
Vasorelaxant effects of purified green tea epicatechin derivatives in rat mesenteric artery.
The effects of four epicatechin derivatives, (-) epicatechin, (-) epicatechin gallate, (-) epigallocatechin and (-) epigallocatechin gallate, isolated from jasmine green tea, on the contractions were studied in mesenteric arteries isolated from male Sprague-Dawley rats. All four derivatives (30-500 microM) non-competitively reduced the contractile response to phenylephrine in a concentration-dependent manner with epigallocatechin gallate being the most potent. The relaxant effects of epicatechin derivatives were unaffected by the ATP-sensitive K+ channel blocker glibenclamide (3 microM) or the Ca2+-activated K+ channel blocker charybdotoxin (100 nM). Four epicatechin derivatives also reduced the sustained contractions induced by phenylephrine (1 microM) and endothelin I (5 nM) in normal Krebs solution, whilst they did not relax the phorbol 12-myristate 13-acetate (TPA, 2 microM)-contracted arteries in the absence of extracellular Ca2+. In arteries contracted with 60 mM K+, each of epicatechins caused a relaxation. However, epicatechin derivatives did not affect the transient contraction induced by 100 microM caffeine in Ca2+-free solution. The present results suggest that epicatechin derivatives from green tea leaves relaxed rat mesenteric arteries probably by inhibiting Ca2+ influx. The protein kinase C-dependent contractile pathway and intracellular Ca2+ release may not be involved.
Animals↗
Endothelium-dependent relaxation to hydrogen peroxide in canine basilar artery: a potential new cerebral dilator mechanism.
In prostglandin F2alpha(PGF2alpha)-precontracted isolated canine basilar arterial rings, hydrogen peroxide (H2O2) produced endothelium-dependent relaxations at concentrations of from 4.4 x 10(-7) - approximately 4.4 x 10(-5) M. Removal of extracellular Ca2+ ([Ca2+]0) attenuated the relaxant effects of H2O2. Complete inhibition of H2O2 relaxant action was obtained after buffering intracellular Ca2+ ([Ca2+]i), in the endothelial cells, with 10 microM 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM). The H2O2-induced relaxations could be abolished completely by 1200 u/ml catalase and was suppressed significantly by 0.5 microM atropine, 150 microM NG-monomethyl-arginine (L-NMMA), 50 microM NG-nitro-L-arginine methyl ester (L-NAME), 1 microM Fe2+, or 5 microM methylene blue. These inhibitory effects of L-NMMA, L-NAME, or atropine could be reversed partly by 50 microM L-arginine. The Fe2+ inhibition of H2O2-stimulated relaxation was reduced significantly by either 1 mM deferoxamine (a Fe2+ chelator) or 100 microM dimethyl sulfoxide (DMSO, a *OH scavenger). Such relaxant effects of H2O2 were enhanced, significantly, by an acetylcholinesterase antagonist, neostigmine. A variety of pharmacological antagonists (of diverse vasodilator agents) could not inhibit the relaxant action of H2O2. Our observations suggest that at suitable pathophysiological concentrations, H2O2 could induce release of an endothelium-derived relaxing factor (EDRF), probably nitric oxide (NO), from endothelial cells of the canine cerebral artery. The H2O2 relaxant effects are clearly Ca2+-dependent, require formation of cyclic guanosine monophosphate (cGMP), and may be associated with release of endogenous acetylcholine (ACh).
Acetylcholine↗
Alcohol-induced vascular damage of brain is ameliorated by administration of magnesium.
Ethanol ingestion can cause irreversible neuronal and vascular damage in the brain and stroke-like events. Using an intact in vivo rat brain (pial) model, TV image-intensification, cultured cerebral vascular muscle cells, digital-image analysis, and a novel Mg2+ ion-selective electrode to measure extracellular ionized Mg2+, studies were designed to determine whether: 1) perivascular or systemic administration (i.v. or intra-arterial) of magnesium aspartate HCI (MgA) exert vasodilator effects on arterioles (65-130 microm o.d.) and venules (60-135 microm); 2) nonvasodilator doses of MgA could modify vascular spasms induced by BaCl2 and ethanol; 3) nonvasodilator doses of MgA could ameliorate or prevent the cerebral vascular damage induced by high doses of ethanol; and 4) ethanol depletes cerebral vascular muscle of intracellular Mg ions ([Mg2+]i). Perivascular application of MgA (0.01-100 micromol) produced dose-dependent vasodilatation of cerebral arterioles and venules; arterioles yielded greater vasodilator responses compared to venules. Nonvasodilator doses of Mg (1.0, 4.0 micromol/min), administered i.v. or intra-arterially, into a branch of the internal carotid artery, prevented: 1) the spasmogenic actions of ethanol and Ba2+; and 2) the vasculotoxic actions (rupture of postcapillary venules and focal hemorrhages) of ethanol. In addition, ethanol depleted cerebral vascular muscle cells of [Mg2+]i; blood levels of ionized Mg2+ rose after IP ethanol. Despite the fact that systemic infusion of low nonvasodilator doses did not result in dilatation of the pial arterioles and venules, plasma total and ionized Mg rose 18-230%, depending upon dose of MgA and time of plasma sampling. These data support the idea that Mg2+ can act as a local vasodilator on brain microvessels and possess antispasmodic properties on brain arterioles and venules. In addition, our results indicate that Mg may possess some unique cerebral vascular protective properties against the vasculotoxic effects of ethanol. Lastly, these findings suggest ethanol-induced cerebrovasospasm and vascular damage appear to be associated with a rapid loss of [Mg2+]i from cerebral vascular muscle cells.
Animals↗
Magnesium deficiency exacerbates brain injury and stroke mortality induced by alcohol: a 31P-NMR in vivo study.
Mimicking in rats the reduced level of dietary magnesium (Mg) intake, seen in present-day Western World populations, short-term (4 weeks) restriction of Mg intake (30-35% normal) resulted in a 40% loss in brain intracellular free Mg2+ ions ([Mg2+]i) and significant rises in brain intracellular pH (pHi) and phosphocreatine ([PCr]) but no change in [ATP] or [Pi] as measured by 31P-NMR spectroscopy. Such Mg-deficient animals (serum Mg fell 65%), when given ED40 stroke doses of ethanol, demonstrated a 100% stroke mortality. These findings indicate that: 1) moderate, short-term Mg deficiency makes the brain vulnerable to hypoxic-lethal stroke insults induced by alcohol administration, and 2) brain [Mg2+]i appears to play an important role in finely regulating brain pHi and [PCr].
Animals↗
Analysis of mechanisms and frequency of CDKN2A/B gene loss during progression of RAS-transformed rat embryo fibroblast clones.
Rat embryo fibroblasts (REFs) are inefficiently transformed by RAS-oncogenes. Induction of p16INK4A expression by RAS has been suggested to contribute to this resistance. Glucocorticoid hormones, (DEX), enhance REF transformation by RAS and facilitates the isolation of transformed and immortal cell lines. We show that DEX induced cell proliferation is paralleled by a decrease in Cdkn2a gene transcripts, suggesting a mechanism for hormone promotion. The mechanisms of progression into hormone independent cell lines were examined. Twenty-two of 30 clones which reached a population size of approximately 10(6) cells could be established as cell lines. All lines studied showed homozygous deletions of the Cdkn2 loci (Cdkn2a and Cdkn2b) on RNO5. LOH was found for all RNO5 genetic markers examined in 7 of 19 cell lines, suggesting non-disjunction events. In the remaining 12 cell lines, both copies of Cdkn2 appeared to be lost by deletions/rearrangements, some of which could by demonstrated by karyotype analysis. We conclude that (i) clonal expansion of RAS-transfected REF by DEX is paralleled by down-regulation of Cdkn2a expression; (ii) homozygous deletion of Cdkn2 were estimated to occur at a frequency of 2 x 10(-8)/cell/generation or higher, and (iii) deletion/rearrangements and nondisjunction appear to be the main mechanisms leading to deletion of Cdkn2.
Animals↗
Trimethylamine N-oxide as a probable source of urinary dimethylamine in man; a statistical approach.
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Adult↗
[Detection and enrichment of fetal cells in maternal circulation for prenatal diagnosis of fetal sex].
OBJECTIVE: To study fetal cells from maternal peripheral blood for prenatal diagnosis of fetal sex. METHODS: Samples of peripheral blood in 64 women of 8-40 gestational weeks were collected to enrich the fetal nucleated red blood cells by density gradient centrifugation. DNA was extracted from each samples of enriched fetal cell for PCR amplification of Y chromosome specific DNA to determine fetal sex. RESULTS: Fetal nucleated red cells were found in 25 out of 64 maternal samples (39.06%). Y chromosome 149 bp was found in 28 cases of the 33 mothers given birth to male babies. One Y specific DNA sequence was detected in 31 women had female babies. The sensitivity was 84.85% and specificity 96.77%. The overall agreement of the diagnosis was 90.63%. CONCLUSION: Density gradient centrifugation can enrich fetal nucleated red blood cells from maternal peripheral blood. Fetal sex can be determined by PCR amplification of Y chromosome specific DNA with these fetal cells.
Blood Circulation↗
[Study on inhibition and prevention of tumor and antioxidative effects of lithium carbonate in tumor bearing mice].
Two Kinds of tumor-bearing mice (hepatoma H22 and sarcoma S180) were administered with lithium carbonate (Li2CO3) for 17 or 10 days (advanced and simultaneous administration), in order to observe the effects of prevention and treatment of Li2CO3 on malignant tumor, as well as the relationship between Li2CO3 and lipid peroxidation in tumor-bearing mice. Meanwhile, we compared the toxic and side effects of cyclophosphamide (CP) with that of Li2CO3. The results showed that Li2CO3 had no significant toxic or side effects with the suggested doses. In the tests of inhibition and prevention of tumor, Li2CO3 could significantly inhibit the grouth of the two kinds of tumor, and increase the activity of superoxide dismutage (SOD) and decrease the contents of Malonyldialdehyde (MDA). In addition, Li2CO3 had no effect on the white blood cells (WBC) and decreased the micronucleus frequency (MNF) in bone marrow polychromatic erythrocytes (PCE), while CP had definite effect of decreasing the WBC and increasing the MNF in the tumor-bearing mice.
Animals↗
[Study on invasibility and multiplication of Toxoplasma strains with different virulence toward Vero-cells].
AIM: To investigate the pathogenic mechanisms of Toxoplasma strains with different virulence. METHODS: Tachyzoites from 3 strains, Viz. RH, B36 and Fukaya strains, were challenged to in vitro cultivated Vero-cells. Systematic examinations on the earliest invasion time, the invasion rate and intracellular multiplication were performed under different cultivation conditions. RESULTS: The tachyzoites of all the 3 strains invaded the host cells within a short period after inoculation. Invasion rates were all increased along with the prolonged duration of infection. The intracellular multiplication was found to be most active in RH strain, moderate in B36, and comparatively slow in Fukaya strains. Using purified tachyzoites freed from host debris and proteins and adding sufficient FCS in the medium may facilitate the invasion and subsequent multiplication of the parasite. CONCLUSION: Strain differences in pathogenicity to the host may be correlated to the genetically predetermined multiplication capabilities of the parasites after being invaded to the host cell, and that environmental factors may give certain impact on the invasibility of the parasite.
Animals↗
[Correlation between the dose and the anti-Toxoplasma effect of activated mouse macrophages induced by IFN-gamma and the synergism between IFN-gamma and TNF-alpha].
AIM: To find out the dose dependence of the anti-Toxoplasma effect induced by IFN-gamma and to determine the possible synergistic activity between TNF-alpha and IFN-gamma. METHODS: The in vitro effect of cultivated mouse peritoneal macrophages activated by IFN-gamma alone or IFN-gamma combined with different doses of TNF-alpha on the intracellular tachyzoites of RH strains and the nitric oxide (NO) level in the culture medium supernatant were simultaneously determined. RESULTS: With the increase in the dose of IFN-gamma, the anti-Toxoplasma effect was augmented and the NO level was enhanced. At 24 hours after tachyzoite invasion, a significant reversed correlation was demonstrated between the NO level and the number of intracellular parasites. CONCLUSION: The anti-Toxoplasma effect of macrophages activated by IFN-gamma appears to be dose-dependent and TNF-alpha acts synergitically with IFN-gamma in the activation of macrophages. The production of reactive NO could be an important effector in the IFN-gamma primed anti-Toxoplasma action.
Animals↗
[The ultraviolet spectra of alpha,alpha'-dioxoketene cyclic S,S-acetals(N,N-acetals)].
In this paper, the ultraviolet spectra of alpha,alpha'-dioxoketene cyclic S,S-acetals (N,N-acetals) have been studied and their changing characters with the change of chemical structure have been indicated.
English Abstract↗
The detection of simian virus 40 in human tumors by polymerase chain reaction.
Simian virus (SV) 40 is a deoxyribonucleic acid (DNA) virus that induces mesotheliomas, ependymomas, bone tumors, and lymphomas in hamsters. In recent years SV40 sequences have been detected in approximately 60% of mesotheliomas and ependymomas, in 33% of bone tumors and sarcomas, and in 13% of lymphomas. Because the amount of human specimens available for molecular studies is usually minimal, the method most commonly used to demonstrate SV40 in human specimens is the polymerase chain reaction (PCR). PCR is a highly sensitive and useful technique. In the PCR reaction, different sets of primers are used for targeting different regions of DNA. The regions of the SV40 genome targeted by PCR include the large T-antigen, the small t-antigen, the origin of replication, and viral protein-1 capsid protein. The use of these different sets of primers to test human tumor specimens for SV40 produce a different percentage of positive results. This is because these experiments revealed that some primers are more specific than others which may also detect sequences belonging to other DNA papovaviruses. Therefore, the combined use of different sets of primers is recommended when it is important to distinguish SV40 from other related papovaviruses such as BK and JC, which can also be occasionally present in human cells. Furthermore, these experiments demonstrated that polymerase chain reaction analyses for simian virus 40 can be performed better and easier when using deoxyribonucleic acid extracted from fresh and/or frozen tissue. Deoxyribonucleic acid from paraffin embedded specimens should not be used routinely for simian virus 40 testing because of the high risk of obtaining false negative results. However, these paraffin derived deoxyribonucleic acids can be used reliably in molecular laboratories specialized in these type of analyses. This paper describes the methods that we have developed to test simian virus 40 in human specimens.
Base Sequence↗
Exposure of piglet coronary arterial muscle cells to low concentrations of Mg2+ found in blood of ischemic heart disease patients result in rapid elevation of cytosolic Ca2+: relevance to sudden infant death syndrome.
Exposure of cultured piglet primary neonatal coronary arterial smooth muscle cells to concentrations of ionized Mg2+ ([Mg2+]o (i.e., 0.48, 0.3, 0.15 mM) found in blood of patients presenting with ischemic heart disease and in hypoxic neonates resulted in concentration-dependent elevation in intracellular free Ca2+ ions ([Ca2+]i; the lower the [Mg2+]o, the higher the [Ca2+]i rise. The lowest concentration of [Mg2+]o tested, i.e., 0.15 mM, resulted in a clear rounding-up (i.e., contraction) of many of the coronary smooth muscle cells; reintroduction of normal 1.2 mM [Mg2+]o failed to restore either normal [Ca2+]i or cell shape.
Animals↗
Short-term reduction in dietary intake of magnesium causes deficits in brain intracellular free Mg2+ and [H+]i but not high-energy phosphates as observed by in vivo 31P-NMR.
31P-NMR spectroscopic studies were performed in vivo on brains of rats fed 30-35% normal dietary Mg intake for 6 weeks. Within 2 weeks of the moderately restricted Mg diet serum Mg fell 50%, and brain intracellular free [Mg2+]i fell 15%; within 3 weeks of restricted diet, brain [Mg2+]i fell 40% and remained at this level for the additional 3 weeks. Intracellular pH (pH[i]) progressively rose in a reciprocal manner for 4 weeks. At no interval of time did brain phosphocreatine (PCr), [ATP], or inorganic phosphate change despite the fall in brain [Mg2+]i, brain pH(i) and serum Mg. The Mg-deficiency-induced cytosolic loss of protons (resulting in an alkaline cytosol) could be a compensatory mechanism to stabilize [PCr], [ATP] and [ADP] levels via creatine kinase, thus maintaining cytosolic phosphorylation potential. The rise in pH(i) associated with Mg-deficiency would also account for increased cerebral vascular muscle contractility under these conditions. Lastly, these studies indicate that brain [Mg2+]i may change without a concomitant change in cell [ATP], and that brain [Mg2+]i may be a useful marker for total body Mg2+ status.
Adenine Nucleotides↗
A small, stable RNA induced by oxidative stress: role as a pleiotropic regulator and antimutator.
Exposure of E. coli to hydrogen peroxide induces the transcription of a small RNA denoted oxyS. The oxyS RNA is stable, abundant, and does not encode a protein. oxyS activates and represses the expression of numerous genes in E. coli, and eight targets, including genes encoding the transcriptional regulators FhlA and sigma(S), were identified. oxyS expression also leads to a reduction in spontaneous and chemically-induced mutagenesis. Our results suggest that the oxyS RNA acts as a regulator that integrates adaptation to hydrogen peroxide with other cellular stress responses and helps to protect cells against oxidative damage.
Acclimatization↗
Low levels of serum ionized magnesium are found in patients early after stroke which result in rapid elevation in cytosolic free calcium and spasm in cerebral vascular muscle cells.
Ninety-eight patients admitted to the emergency rooms of three urban hospitals with a diagnosis of either ischemic stroke or hemorrhagic stroke exhibited early and significant deficits in serum ionized Mg2+ (IMg2+), but not total Mg, as measured with a unique Mg2+-sensitive ion-selective electrode. Twenty-five percent of these stroke patients exhibited >65% reductions in the mean serum IMg2+ found in normal healthy human volunteers or patients admitted for minor bruises, cuts or deep lacerations. The stroke patients also demonstrated significant elevation in the serum ionized Ca2+ (ICa2+)/IMg2+ ratio, a sign of increased vascular tone and cerebrovasospasm. Exposure of primary cultured canine cerebral vascular smooth muscle cells to the low concentrations of IMg2+ found in the stroke patients, e.g. 0.30-0.48 mM, resulted in rapid and marked elevations in cytosolic free calcium ions ([Ca2+]i) as measured with the fluorescent probe, fura-2, and digital image analysis. Coincident with the rise in [Ca2+]i, many of the cerebral vascular cells went into spasm. Reintroduction of normal extracellular Mg2+ ion concentrations failed to either lower the [Ca2+]i overload or reverse the rounding-up of the cerebral vascular cells. These results suggest that changes in Mg2+ metabolism play important roles in stroke syndromes and in the etiology of cerebrovasospasm associated with cerebral hemorrhage.
Adult↗
Elevation of extracellular magnesium rapidly raises intracellular free Mg2+ in human aortic endothelial cells: is extracellular Mg2+ a regulatory cation?
Extracellular magnesium ions [Mg2+]o are known to regulate functions of endothelial cells, but whether [Mg2+]o can alter intracellular free ionized magnesium [Mg2+]i in these cells remains unknown. The present studies, using digital imaging microscopy and the Mg2+ fluorescent probe, mag-fura-2, determined effects of elevation of [Mg2+]o on [Mg2+]i in cultured human aortic endothelial cells. With normal Mg2+(1.2 mM)-containing incubation media, [Mg2+]i was 0.51+/-0.04 mM with a heterogeneous distribution. The ratio of [Mg2+]i/[Mg2+]o was 0.52+/-0.07. Elevation of [Mg2+]o up to 4.8 mM increased [Mg2+]i to 0.80+/-0.07 mM in 2-10 min and lowered the ratio of [Mg2+]i/[Mg2+]o to 0.16+/-0.02. Irrespective of the observed increments of [Mg2+]i, a subcellular heterogeneous distribution of [Mg2+]i was always evident in all cells tested. Our results suggest that [Mg2+]o can regulate [Mg2+]i more rapidly than heretofore believed, supporting the hypothesis that extracellular Mg2+ can exert regulatory effects on endothelial cell functions and probably act as extracellular regulatory cations
Cells, Cultured↗