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Biomedical subjects

S Yang

Publications and source records attributed to S Yang.

At least 541 records · Page 30Linked to original sources
PubMed1994

Contents of trace elements in the hair of aplastic anemia patients and their treatment based on an overall analysis of symptoms and signs.

The content of 12 trace elements in the hair of 20 aplastic anemia patients was determined and compared with that of normal subjects as control. The results showed that patients with deficiency of yin had a significant decrease in lithium, calcium, strontium, and chromium, those with deficiency of yang had a distinct decrease in zinc magnesium barium, strontium, calcium, and lithium, and those with deficiency of both yin and yang had a general decrease in all the 12 trace elements. Changes in trace element content in hair may serve as a guide to opening up new vistas in the treatment of aplastic anemia on the basis of an overall analysis of symptoms and signs.

Adolescent↗
PubMed1994

[Application of multilocus enzyme electrophoresis in studies of taxonomy and population genetics of S. typhi in Xinjiang].

Multilocus enzyme electrophoresis (MEE) was employed to study the genotype taxon and population genetics of 154 isolates of S. typhi from Xinjiang in recent 11 years. Seven kinds of enzymes were examined and determined. One hundred and fifty-four strains of S. typhi were classified into 69 electroretic types (ETs) and 10 clones (CLa-CLj). Among those 154 strains 80 epidemic isolates belonged to 21 ETs and 3 clones (CLe, f, j). ET17, 20, 21, 24, 26, 27 were the main ETs (61.30%), and CLf was the dominant clone (95.00%). Seventy-four non-epidemic isolates belonged to 48 ETs and 9 clones (CLa, b, c, d, f, g, h, i, j), no obvious dominant ET was found in them, and the main clone CLh accounted for 43.30%. It demonstrated that both outbreak and sporadic epidemics could be caused by many strains of ETs and clones, but the distribution of the former ETs was more concentrated and the preponderance of clones was more obvious. The analyses on structure of population genetics indicated that all of 7 enzymes were polymorphic. Genetic diversity among the enzyme loci was quite high, with an average of 0.35 per locus (H). The average number of alleles per locus (h) was 6.14. There was no significant difference in h or H between the isolates of different sources (P > 0.05). It was clear that S. typhi of different sources in Xinjiang were originated from the same population. The results also showed that there was a dominant allele in every enzyme locus. Natural selection was the main role in the evolution of S. typhi.

Alleles↗
PubMed1994

Patent gut infections in immunosuppressed adult C57BL/6N mice following intraperitoneal injection of Cryptosporidium parvum oocysts.

Two experiments were conducted to determine if intraperitoneal (i.p.) and/or subcutaneous (s.c.) injection of Cryptosporidium parvum oocysts could produce patent gut infections in dexamethasone (DEX) or dexamethasone phosphate (DEXp)-immunosuppressed adult female C57BL/6N mice. The results from experiment 1 were suggestive but did not unequivocally demonstrate that i.p. injection of oocysts could produce patent gut infections in these mice. In experiment 2, all mice were individually caged, immunosuppressed with DEXp (groups 1 and 2) or DEX (groups 3 and 4), and administered C. parvum oocysts either by orogastric intubation (groups 1 and 3), i.p. (group 2), or s.c. (group 4). All but 1 mouse in groups 1 and 3 began shedding oocysts in their feces on day 3 post-infection (PI). Mice in these 2 groups continued to shed oocysts until they were killed on day 17 PI. Mice administered oocysts s.c. did not shed oocysts. In group 2, 1 mouse died, 1 failed to shed oocysts, and 1 began shedding oocysts on day 3 PI. The remaining 5 mice started shedding oocysts on either days 8, 10, or 14 PI and continued to shed oocysts until they were killed. We conclude that immunosuppressed adult C57BL/6N mice administered oocysts i.p. can develop patent gut infections with C. parvum.

Animals↗
PubMed1993

1 alpha, 25-Dihydroxyvitamin D3 and 19-nor-1 alpha, 25-dihydroxyvitamin D2 suppress immunoglobulin production and thymic lymphocyte proliferation in vivo.

BALB/CANNHSD female mice were intraperitoneally (i.p.) injected with 1,25-dihydroxyvitamin D-3 (1,25-(OH)2D3) (20 ng/day) or 19-nor-1,25-(OH)2D2 (100 ng/day) for 7 days and then given the same dose every other day thereafter until day 17 for measuring cell-mediated immunity and on day 33 for observing immunoglobulin production. To observe Ig production, the mice were immunized with an injection of hemocyanin (150 microgram/0.1 ml, i.p.) on day 8. On the day 7, 15 and 20 after immunization, the IgG1, and on day 17 and 20, the IgG3 levels in 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2 groups were significantly lower than in the control group. To measure cell-mediated immunity, mice were sensitized with dinitrofluorobenzene (DNFB) on the shaved abdominal skin. The number of thymic lymphocytes and their stimulation index were significantly reduced by 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2. These results demonstrate that 1,25-(OH)2D3 and 19-nor-1,25-(OH)2D2 can suppress immunoglobulin production and thymic lymphocyte proliferation in vivo. 19-Nor-1,25-(OH)2D2 at doses of 100 ng/day was less effective than 1,25-(OH)2D3 at doses of 20 ng/day.

25-Hydroxyvitamin D 2↗
PubMed1993

Surfactant protein A-binding proteins. Characterization and structures.

An alveolar cell membrane protein acts as a surfactant protein A (SP-A) receptor; it binds SP-A and regulates surfactant secretion. We identified such alveolar cell membrane SP-A-binding proteins using anti-idiotype antibodies directed against the surfactant protein binding region of anti-surfactant antibodies. These monoclonal anti-idiotype antibodies, A2C and A2R, also recognize an alveolar cell membrane protein of approximately 30 kDa. A pulmonary protein of approximately 30 kDa binds SP-A. Unique cDNAs encoding this protein were identified in human (4.1-kilobase) and porcine (1.8-kilobase) lung expression libraries. Coding regions of these cDNAs cross-hybridize with each other under stringent conditions. Both cDNAs encode similar approximately 32-kDa proteins that bind SP-A. The human and porcine SP-A recognition (SPAR) proteins resemble each other, as well as other cell membrane receptors. Their projected structures are consistent with cell membrane receptors. Recombinant human and porcine SPAR proteins bind SP-A as well as the two anti-idiotype antibodies just as do native lung proteins of approximately 30 kDa. SPAR transcripts are expressed primarily in lung. The cellular distribution of these transcripts, as determined by in situ hybridization, is similar to that of SPAR protein, as determined by immunohistochemistry; both are found in cells consistent with type II pneumocytes. SPAR-producing cells resemble the alveolar cells expressing SP-B and SP-C transcripts in appearance, location, and distribution. Therefore, cDNAs for pulmonary SP-A-binding proteins from two disparate species have been isolated and sequenced, and the recombinant proteins they encode bind the same ligand. Further structural, functional, and genetic studies of these proteins may help explain how pulmonary surfactant secretion is regulated.

Amino Acid Sequence↗
PubMed1993

Major role of antigen-presenting cells in the response of rat encephalitogenic T cells to myelin basic proteins.

The encephalitogenic potential of a segment of myelin basic protein in experimental autoimmune encephalomyelitis is not always mirrored by the ability of the peptide to mediate in vitro activation of encephalitogenic T cells. Recent studies from our laboratory have demonstrated that the responsiveness of Ag-specific T cells in experimental autoimmune encephalomyelitis is determined not exclusively by Ag but also by the nature of the APC. By varying APC during the in vitro selection of T cells, we could generate distinct sets of rat encephalitogenic T cells, as evidenced by the diversity of TCR usage. Here we establish the importance of APC in the activation of rat encephalitogenic T cells by myelin basic protein peptides. Peptides 69-84-Gly and (P80)68-86, which lacked stimulatory activity toward many encephalitogenic T cells in our proliferation assay when standard APC were used, become strongly stimulatory in the presence of less commonly used APC, i.e., an Ia+ T cell clone (LOA) or an Ia-inducible rat glial cell clone (F10). Nonstimulatory APC failed to activate encephalitogenic T cells even when major cytokines were added, suggesting that these cytokines are not among the factors limiting the activating potential of the APC. Thus, whether or not an immunocompetent T cell can be activated by a given Ag in an autoimmune response may be determined by the properties of APC. This finding has implications for current research efforts to identify pathogenic self proteins.

Amino Acid Sequence↗
PubMed1993

Vitamin D deficiency suppresses cell-mediated immunity in vivo.

Severe vitamin D deficiency has been produced in mice as evidenced by severe hypocalcemia and an absence of 25-hydroxyvitamin D in blood. Vitamin D deficiency was accompanied by a slight decrease in body weight and food consumption. Vitamin D-deficient and vitamin D-sufficient mice were sensitized with dinitrofluorobenzene (DNFB). Sensitivity to DNFB was determined by treatment of one ear with DNFB. The ratio of thickness of the treated ear to that of nontreated ear was used as an index of cell-mediated immune reaction. The incorporation of [3H]thymidine into the DNA of the ear was also used as an index of cell-mediated immunity as was the response of thymus lymphocytes to concanavalin A. Vitamin D deficiency markedly decreased the ear thickness ratio and the [3H]thymidine incorporation ratio in DNFB-sensitized mice. Similarly, the incorporation of [3H]thymidine into the DNA of concanavalin A-treated thymus lymphocytes from DNFB-sensitive mice was significantly reduced in vitamin D deficiency. These results show that in vivo vitamin D deficiency impairs cell-mediated immunity. The provision of a vitamin D-sufficient diet for 8 weeks corrected the impaired response of the immune system, while vitamin D administration for 3 weeks did not.

Animals↗
PubMed1993

Biochemical characterization of a protein inhibitor for DNA ligase I from human cells. Regulation/replication/repair/recombination.

An inhibitor for DNA ligase I has recently been purified from human cells. This inhibitor of 55-75 kDa forms a reversible complex with DNA ligase I, but has no effect on DNA ligase II and T4 DNA ligase, suggesting that it may play a regulatory role for DNA replication and repair. This report shows that the inhibitor was sensitive to heating at 52 degrees C and to trypsin treatment, indicating that it is a heat-labile protein. The inhibitor affected the ligation of double- and single-strand breaks in natural and synthetic DNA, but had no effect on the formation of the ligase-AMP complex and on the subsequent reaction following the formation of the AMP-DNA complex. These data indicate that the major mechanism of action for the inhibitor is the blocking of the second step of the reaction, in which the AMP moiety is transferred from the ligase-AMP to DNA. The site of interaction for the enzyme is therefore localized in a domain associated with the DNA binding or the AMP-transferring function.

Adenosine Monophosphate↗