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Biomedical subjects

H Huang

Publications and source records attributed to H Huang.

At least 397 records · Page 22Linked to original sources
PubMed1997

[Pharmacological actions of different species form genus Pyrola].

This paper reporst the pharmacological actions and toxicities of the water extracts from Pyrola calliantha, Pyrola decorta and P. forrestiana. The results show that the actions of P. forrestiana on antiventricular fibrillation, strengthening cardiac musicular contraction and antihypoxia abitity are more stronger, but on antiinflammation and antipyretic, effects of P. decorta and P. calliantha are significantly better than that of P. forrestiana. The effects of the three species on immunization and antisepsis are similar.

Animals↗
PubMed1997

[The regulation effects of Angelica sinensis on the erythrocytic immune function and IL-2 in mice].

The effects of Angelica sinensis solube extract on erythrocytic C3b receptor rosette rate and immune complex rosette rate and activities of interleukine-2 (IL-2) in mice are observed in this article. Angelica sinensis can significantly enhances erythrocytic C3b recepor rosette rate and IL-2 activities. The regulating actions of Angelica sinensis on erythrocytic C3b recepor rosette rate and IL-2 activities may be the direct effects.

Adjuvants, Immunologic↗
PubMed1997

[The effect of antisense human Fas RNA on activation induced apoptosis of T cell].

OBJECTIVE: To explore an approach to the reduction of activation induced apoptosis of T cell so as to maximize the number of CTL and enhance the tumor cytotoxicity. METHODS: CD3-induced Jurkat cell line was used as the activated T cell apoptosis model,and the antisense Fas cDNA was introduced into Jurkat cells with retroviral vector. RESULTS: The expression level of Fas protein in Jurkat cells transducted with the retroviral vector was decreased. Apoptosis was reduced in antisense Fas-transfected Jurkat cells after anti-CD3 or anti-Fas treatment. CONCLUSION: Antisense blocking of Fas expression can partially inhibit Jurkat cell apoptosis induced by anti-CD3 or anti Fas.

Animals↗
PubMed1997

[Detection of hepatitis A virus in environmental samples by coupled reverse transcription and polymerase chain reaction].

A direct reverse transcription coupled with polymerase chain reaction (RT-PCR) was used to detect HAV-seeded sea water, coastal sediment and Arca subcrenata, HAV strain treated by different kind of disinfection, and naturally occurring HAV in Arca subcrenata. The results showed that HAV could be detected in HAV-seeded sea water, coastal sediment and Arca subcrenata. HAV could also be detected in HAV strain disinfected by phenol, suggesting that inactive HAV could also show positive PCR. Only Arca subcrenata collected from Shanghai in 1988 showed positive result by RCR, but negative by immunofluorescence at the same time. This result demonstrated that HAV was not infectious owing to long time storage. The author's method has the advantage of involving fewer manipulations.

China↗
PubMed1997

Umbilical cord blood lead levels in Shanghai, China.

This study was designed to determine the cord blood lead (BPb) levels of babies born in one urban area of Shanghai, and to preliminarily identify the demographic, social environment and prenatal factors which have an effect on the cord BPb concentrations. From August to November 1993, umbilical cord blood samples were obtained from 605 live newborns in the Yangpu Maternal and Child Hospital. 257 samples were excluded from measurement because of clotting. In 348 cord samples, the geometric mean of cord BPb levels was 9.2 micrograms/dl, with a 95% confidence interval of the mean 8.86-9.54 (micrograms/dl). 142 babies (40.8%) had cord BPb levels of 10 micrograms/dl or greater. As a result of this high percentage of newborns with BPb levels equal to or greater than 10 micrograms/dl, we estimate that each year in the Shanghai City about 60,000 newborns are at risk for developing neuropsychological deficiencies caused by maternal lead exposure during pregnancy. To investigate the factors affecting cord blood levels, the subjects with levels greater than the 70th percentile (10.7 micrograms/dl) (n = 104) and less than the 30th percentile (7.4 micrograms/dl) (n = 104) were selected to compare the demographic, environment and prenatal medical history. Increased BPb levels at birth were associated with maternal passive smoking, a family member being occupationally exposed to lead, proximity to major traffic way, household coal combustion, neighborhood coal combustion, low level of maternal occupations, and the increasing occurrence of having the high lead foodstuff pidan (preserved duck egg) during pregnancy. We conclude that prenatal lead exposure has become an important health issue for young children in Shanghai.

Adult↗
PubMed1997

Stem cell factor activates STAT-5 DNA binding in IL-3-derived bone marrow mast cells.

The Kit tyrosine kinase regulates growth and differentiation of many hematopoietic cells through a signal transduction process that remains to be fully elucidated. Kit has been shown to associate with the receptor for erythropoietin (Epo), which is known to activate the signal transducer and activator of transcription, STAT-5. To determine if Kit signal transduction activated latent DNA-binding factors, including STAT-5, we performed electrophoretic mobility shift assays on stem cell factor (SCF)-stimulated mouse bone marrow-derived mast cells (BMMCs). SCF led to the rapid and transient activation of a DNA-binding factor that was identified by supershift analysis as STAT-5. STAT-5 DNA binding was shown to be specific for the oligonucleotide of the correct sequence and was dose-responsive. Epo stimulation of BMMCs led to the activation of a DNA-binding activity that comigrated with the SCF-induced band, but peaked and was maintained at later time points than SCF-induced activation. These data indicate that SCF stimulation of Kit leads to activation of STAT-5 DNA binding with kinetics distinct from Epo-mediated stimulation.

Animals↗
PubMed1997

Myocardial G proteins in murine Chagas' disease.

G protein alpha subunits and their corresponding mRNA levels were determined in hearts obtained from mice infected with Trypanosoma cruzi, the etiologic agent of Chagas' disease. Protein and mRNA levels of the inhibitory G proteins G alpha i2 and G alpha i3 were increased at 21 and 30 days postinfection (PI). After 60 days, the abundance of protein and corresponding mRNA for G alpha i2 and G alpha i3 were no longer significantly different from uninfected mice. Twenty-one days after infection, G alpha s protein levels decreased markedly, but mRNA for the stimulatory protein did not change. Similar to the Gi proteins, by 60 days differences in G alpha s protein between infected and uninfected mice were no longer evident. There was an increase in the magnitude of G beta subunit protein 21 and 30 days PI as compared with uninfected mice. However, 60 days PI the G beta subunit protein decreased to control levels. The close relationship between the infection-associated increase in G alpha i protein and mRNA suggests that control of protein expression is likely to be exerted at the transcription level. In contrast, control of infection-associated decrease in Gs appears to be at the translational level.

Animals↗
PubMed1997

[Clinical observation of cardiac pacemaker in pregnant women].

OBJECTIVE: To study the clinical results in pregnant women with bradycardia implanted with cardiac pacemakers. METHOD: Five pregnant women with bradycardia were retrospectively studied in our hospital from 1980 to 1996. RESULTS: Four of the patients had A-V block, and the other one sinus bradycardia. Classification of cardiac function, showed 1 case of class IV, 3 cases of class III, and 1 case of class II before implantation of cardiac pacemaker. One case had the pacemaker implanted before pregnancy and 4 cases during pregnancy. Cardiac function improved significantly after implantation and pregnancies went uneventfully. Three women had term living birth by cesarean section, and 2 ended by therapeutic abortions safely. CONCLUSION: Bradycardia is a rare and serious complication in pregnancy, especially due to A-V block of III degree. Cardiac pacemaker should be implanted before pregnancy or at early stage of pregnancy in order to maintain adequate heart function. These patients should receive cesarean section.

Adult↗
PubMed1997

[Ultrastructural observation on the uncinate process of chronic sinusitis].

The ultrastructures of the uncinate processes (UP) obtainel from 16 patients with clinical diagnosis of chronic sinusitis were observed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results showed that there were three main surface cell types on the UP: Most of the cilia was leaned, fractured and in disorder; Gaps of the cells increased obviously; Squamous cell metaplasia was seen; The endoplasmic reticulums and mitochondria in cytoplasm were expanded moderatly or seriously. The morphological changes indicated that mucus transportation functions in the anterior ethmoid region and the middle meatus were damaged. It is of great importance in occurrence and development of chronic sinusitis. The demaged nasal mucosa epithlial cells are repairable and reproducible.

Adult↗
PubMed1996

Amino acid-derived phthalimide and saccharin derivatives as inhibitors of human leukocyte elastase, cathepsin G, and proteinase 3.

Amino acid-derived phthalimide and saccharin derivatives have been investigated for their inhibitory activity toward the serine proteinases human leukocyte elastase, cathepsin G, and proteinase 3. The saccharin derivatives were found to be effective time-dependent inhibitors of elastase and proteinase 3 (kobs/[I] values ranged between 180 and 3620 M-1 S-1) and showed weak or no inhibition toward cathepsin G. The corresponding phthalimide derivatives were found to be inactive.

Amino Acid Sequence↗
PubMed1996

Structure and critical residues at the active site of spermidine/spermine-N1-acetyltransferase.

Spermidine/spermine-N1-acetyltransferase (SSAT) is a key enzyme in the degradation of polyamines. Alanine-scanning mutagenesis of all eight arginine residues was used to investigate the arginine residues involved in acetyl-CoA binding. The results indicate that Arg101, Arg142 and Arg143 are important for such binding. The apparent Km values for acetyl-CoA were significantly increased when any one of these residues was replaced by an alanine residue. These mutations also abolished the ability of acetyl-CoA to protect the protein from digestion by trypsin. Co-expression of the inactive R101A (Arg101 --> Ala) mutant and an E152K (Glu152 --> Lys) mutant, previously known to inactivate SSAT, led to restoration of activity, showing that the active enzyme is a dimer with residues contributed by both subunits. The double mutant R101A/E152K acted as a dominant negative when co-expressed with the wild-type SSAT. Transfection of COS-7 cells with a plasmid producing this mutant greatly attenuated the increase in SSAT activity brought about by N1, N12-bis(ethyl)spermine. These results indicate that the double mutant R101A/E152K-SSAT protein can be used to evaluate the importance of SSAT activity in response to exogenous polyamines or polyamine analogues.

Acetyl Coenzyme A↗
PubMed1996

Interactions between ifenprodil and the NR2B subunit of the N-methyl-D-aspartate receptor.

Ifenprodil is an atypical noncompetitive modulator of the N-methyl-D-aspartate (NMDA) receptor (NR) which demonstrates a 140-fold preference for NR2B over NR2A subunits, although the molecular basis for this subunit specificity is unknown. We have made chimeric receptors by fusing the murine forms of NR2A (epsilon 1) and NR2B (epsilon 2) to localize the high affinity determinants of ifenprodil inhibition on the 2B subunit. Binding experiments with 125I-MK-801 implicated the region between amino acids 198 and 356 of NR2B for high affinity ifenprodil interaction. Site-directed mutants at Arg-337 showed that this residue is absolutely required for high affinity ifenprodil inhibition. Polyamines also modulate the NMDA receptor with a preference for NR2B subunits, and the pharmacology of these agents overlaps with ifenprodil. Although the determinants of the polyamine enhancement of iodo-MK-801 binding also localize to the NH2 terminus of NR2B, the point mutants at Arg-337 form receptors that are polyamine-stimulated at wild type levels. In addition, polyamine stimulation depends on the expression of NR1 splice variants, whereas high affinity ifenprodil inhibition is independent of NR1 isoform expression. These studies provide evidence that ifenprodil and polyamines interact at discrete sites on the NR2B subunit.

Alternative Splicing↗
PubMed1996

Arsenite induces apoptosis in Chinese hamster ovary cells by generation of reactive oxygen species.

Arsenic, a human carcinogen, possesses a serious environmental threat but the mechanism of its toxicity remains unclear. Knowledge of how arsenic induces cell death and how cells escape the death path may help to understand arsenic carcinogenesis. We have investigated the nature of sodium arsenite-induced cell death in Chinese hamster ovary K1 cells. Following phosphate-citric acid buffer extraction, apoptotic cells with lower DNA content than the G1 cells were detected by flow cytometry. Immediately after 4 h of 40 microM arsenite treatment, no appreciable fraction of cells with sub-G1 DNA content was detected; however, the sub-G1 cell fraction increased with postarsenite incubation time, and detectable increase started at 8 h of incubation, whereas the intracellular peroxide level as measured by the fluorescent intensity of 2',7'-dichlorofluorescein increased immediately following a 4-h arsenite treatment. Simultaneous treatment with arsenite plus antioxidant (N-acetyl-cysteine, Trolox, and Tempo); copper ion chelator (neocuproine); protein kinase inhibitor (H-7) or protein synthesis inhibitor (cycloheximide) reduced the fraction of sub-G1 cell and internucleosomal DNA degradation. Trolox, neocuproine, or cycloheximide given after arsenite treatment also effectively reduced apoptosis. These results lead to a working hypothesis that arsenite-induced apoptosis in CHO-K1 cells is triggered by the generation of hydrogen peroxide, followed by a copper-mediated Fenton reaction that catalyzes the production of hydroxyl radicals, which selectively activates protein kinase through de novo synthesis of macromolecules.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Hematopoietic stem cells in the mouse embryonic yolk sac.

The yolk sac is the first site of hematopoiesis during mammalian development. The yolk sac is also the first site of blood vessel development. Development of the blood islands in the yolk sac is an integrated process in which these two developmental events, hematopoiesis and vasculogenesis, proceed in concert. This review focuses on mouse yolk sac hematopoietic stem cells (YS-HSC), describing their differentiation in vitro and in vivo. YS-HSC go through a progressive series of changes prior to the initiation of lineage-specific differentiation. Experiments tracing their origins from postulated hemangioblasts, and the subsequent interaction between these stem cells and yolk sac endothelial cells are described. Differences between the extraembryonic YS-HSC and HSC found later within the embryo, perinatally or in adults, are described. YS-HSC have greater reproductive capability than HSC obtained from fetal liver, umbilical cord blood or adult bone marrow; they do not yet express major histocompatibility complex-associated antigens and they are able to reconstitute adult immunocompromised animals even when introduced in small numbers (< 100 cells/mouse). With recent results demonstrating the feasibility of expanding YS-HSC in vitro as well as of introducing new genes into these cells by transfection, the YS-HSC shows promise both as a means of achieving long-term restitution of hematopoiesis across histocompatibility barriers and as a self-renewing vehicle for gene transfer.

Animals↗
PubMed1996

Organization of the mouse cardiac natriuretic peptide locus encoding BNP and ANP.

The genes encoding the mouse atrial natriuretic peptide and B-type natriuretic peptide were previously shown to be physically linked on mouse chromosome 4 (Steinhelper ME, 1993, Structure, expression, and genomic mapping of the mouse natriuretic peptide type-B gene. Circ Res 72: 984-992). In the present study the spatial relationship and orientation of the mouse atrial natriuretic peptide and B-type natriuretic peptide transcription units were identified and a physical map of the mouse cardiac natriuretic peptide locus was obtained. To this end, genomic clones encoding atrial natriuretic peptide and B-type natriuretic peptide were isolated from a mouse genomic library in bacteriophage P1. Three independent clones encoding atrial natriuretic peptide were isolated and two of these also encode B-type natriuretic peptide. Both transcripts were shown to arise from the same DNA strand, with B-type natriuretic peptide encoded approximately 15 kb 5'-of atrial natriuretic peptide based on field inversion gel electrophoresis of fragments amplified with specific oligonucleotides. This finding was confirmed by isolation of subclones comprising the entire locus and by blot hybridization analysis of mouse genomic DNA. The results show that the genes encoding the two natriuretic peptides expressed predominantly in mammalian cardiac myocytes are organized in tandem on mouse chromosome 4. This information provides a physical framework for investigating mechanisms that regulate transcription of the cardiac natriuretic peptide locus.

Animals↗
PubMed1996

A genetic linkage map of the rat derived from recombinant inbred strains.

We have constructed a genetic linkage map in the rat by analyzing the strain distribution patterns of 500 genetic markers in a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown-Norway rat (HXB and BXH recombinant inbred strains). 454 of the markers could be assigned to specific chromosomes, and the amount of genome covered by the mapped markers was estimated to be 1151 centimorgans. By including a variety of morphologic, biochemical, immunogenetic, and molecular markers, the current map integrates and extends existing linkage data and should facilitate rat gene mapping and genetic studies of hypertension and other complex phenotypes of interest in the HXB and BXH recombinant inbred strains.

Animals↗
PubMed1996

Synthesis and evaluation of a polyamine phosphinate and phosphonamidate as transition-state analogue inhibitors of spermidine/spermine-N1-acetyltransferase.

Polyamine analogues such as bis(ethyl)norspermine and N1-ethyl-N11-[(cyclopropyl)methyl]-4,8-diazaundecane (CPENSpm) act as inhibitors of the enzyme spermidine/spermine-N1-acetyltransferase (SSAT) in vitro and possess impressive antitumor activity against a number of cell lines. However, the propensity of these compounds to superinduce SSAT in intact cells limits their usefulness in studies aimed at elucidating the role of SSAT in cellular metabolism. The recently synthesized alkylpolyamine analogue N1-ethyl-N11-[(cycloheptyl)methyl]-4,8-diazaundecane (CHENSpm, 3) is also an effective inhibitor of SSAT and has potent antitumor activity, but does not appear to superinduce SSAT. These findings suggest that it is possible to synthesize polyamine analogues that can be used for selective inhibition of the enzyme in cellular metabolic studies. Along these lines, the phosphate-based transition state analogues 4 and 5 were synthesized and evaluated as inhibitors of isolated SSAT. Phosphonamidate 4 was rapidly hydrolyzed under the assay conditions, and thus did not inhibit the enzyme. However, the phosphinate analogue 5 was an effective inhibitor of purified human SSAT, with a Ki value of 250 microM. The inhibitory activity of 5 was also compared with that of CHENSpm (IC50 = 13 microM), as well as a series of bis-substituted alkylpolyamine analogues. The unsymmetrically substituted polyamine analogue CHENSpm (3) and the phosphinate transition state analogue 5 represent the first functional, nonsuperinducing inhibitors of human SSAT.

Acetyltransferases↗