Biomedical subjects

X He

Publications and source records attributed to X He.

At least 19 recordsLinked to original sources

PubMed1995

Induction of apoptosis of T cells by infecting mice with murine cytomegalovirus.

Cytomegalovirus (CMV) is associated with several lymphocyte dysfunctions, but the precise mechanisms of the dysfunctions are still unclear. To elucidate the mechanisms, a cell cycle-DNA content analysis was performed on splenic T cells of murine CMV (MCMV)-infected BALB/c mice. T cells from mice infected with 3 x 10(3) PFU of MCMV contained a higher percentage of hypodiploid nuclei after 12 or 24 h of culture than those from naive mice. T cells from infected mice also contained a larger amount of fragmented DNA. Taken together, these results suggested that infection with MCMV induced the apoptotic cell death of T cells. This induction of apoptosis accounted for the dysfunction of lymphocytes, at least partially. Flow cytometric analysis showed that T cells as well as B cells from MCMV-infected mice expressed an augmented level of Fas antigen, an apoptosis-associated cell surface molecule, which might be the cause of the apoptosis of cells. T cells from MCMV-infected C57BL/6-lpr/lpr mice with mutations at the lpr/fas locus, however, also showed a substantial level of apoptosis, which was reproducibly lower than that seen in C57BL/6 mice. Therefore, it was suggested that the Fas-mediated pathway contributed to but was not sufficient for the induction of apoptosis and that mechanisms other than the Fas-associated pathway were also involved in the induction of apoptosis.

Animals↗

PubMed1995

Homozygous APC-resistance combined with inherited type I protein S deficiency in a young boy with severe thrombotic disease.

Inherited resistance to activated protein C (APC) is a frequent cause of familial thrombosis. It is associated with a factor V gene point mutation replacing arginine506 in the APC-cleavage site with a glutamine. Thrombotic events are rare during childhood even in patients with homozygous APC-resistance. We now wish to report on a case of severe venous thrombosis, in a 10-year-old boy. He was found to have pronounced APC-resistance due to homozygous factor V gene mutation in combination with inherited type I protein S deficiency. The two traits were independently inherited in the family. The APC-resistance was partially corrected by adding factor V, whereas added protein S was without effect. This is the first reported case of homozygous APC-resistance combined with another inherited prothrombotic disorder. It illustrates how multiple genetic defects may provoke thrombosis at young age and emphasizes the need of complete evaluation of thrombotic patients in order to determine whether multiple risk factors exist.

Adult↗

PubMed1995

[Isolation and identification of a pathogen of grasshoppers].

A pathogen was isolated from natural dead pests of Ceracris kiangsu in Geleshan farm of Chongqin. Its pathogenecity was confirmed by the law of KOCK. It was identified as Pseudomonas pseudoalcaligenes according to its physiological and biochemical properties as well as the G + C content of DNA (63.73mol%). The results of preliminary bioassay show that the pathogen can infect the grasshoppers and Ceracris kiangsu, and also can infect other pests of grassland in a certain extent.

Animals↗

PubMed1995

[Liver-protecting and alanine aminotransferase lowering actions of hongning gantai].

Hongning Gantai has a remarkable counteraction on the elevation of ALT activity of mice and rats induced by chemical damages with CCl4 and D-Gal. It can decrease the BSP-retention. The result of pathologic examination indicates that Hongning Gantai can alleviate liver damages of mice and rats and thus has liver-protecting and ALT-lowering actions.

Alanine Transaminase↗

PubMed1995

[A study on the relationship between in-door air pollution and chronic obstructive pulmonary disease in Xuanwei County].

A cross-sectional study was conducted to explore the relationship between in-door air pollution caused by different fuels for domestic use and chronic obstructive pulmonary disease (COPD) in local population. A total population of 10892 were sampled and analyzed. Results showed in-door air pollution caused by coal-burning was the major risk factor for COPD in Xuanwei County. The risk of residents using soft coal and anthracite to suffer from COPD was 4.36 and 1.55 times, respectively, higher than in those using fire wood.

Air Pollution, Indoor↗

PubMed1995

The expression of acetyl coenzyme A carboxylase is related to megakaryocyte maturation.

We have previously demonstrated that de novo fatty acid synthesis predominantly occurs in later phases of megakaryocyte maturation. Therefore we have investigated the expression of fatty acid synthase (FAS) and acetyl coenzyme A carboxylase (ACC), key enzymes for fatty acid synthesis in megakaryocytes at different phases of maturation. Immature and mature megakaryocytes were isolated. Guinea pig-specific FAS and ACC cDNA probes were prepared by reverse transcriptase reaction-polymerase chain reaction (RT-PCR). The probes were used to assess the expression of mRNA for ACC and FAS by Northern blotting. The hybrids were quantitated by densitometry. Endogenous megakaryocyte ACC was quantitated by virtue of its biotin content by Western blotting with streptavidin and enhanced chemiluminescence (ECL). The ratio of ACC mRNA between mature and immature megakaryocytes was 2.43 +/- 0.86, and the ratio of FAS mRNA was 0.50 +/- 0.13 (mean +/- SD, n = 4). The ratio of endogenous ACC in mature and immature megakaryocytes was 1.96 +/- 0.62 (n = 6). The study showed that the FAS mRNA was expressed in all phases of megakaryocyte maturation. However, both mRNA for ACC and endogenous ACC were demonstrated primarily in mature megakaryocytes. Thus de novo fatty acid synthesis in megakaryocytes may depend on the expression of ACC in mature cells. The expression of ACC occurs during the terminal phases of megakaryocyte maturation and may be a marker of megakaryocyte maturity.

Acetyl-CoA Carboxylase↗

PubMed1994

Generation and characterization of a mouse/human chimeric antibody directed against extracellular matrix protein tenascin.

The murine anti-tenascin monoclonal antibody 81C6, following iodination, has been shown to be an efficient localizing and therapeutic agent in both subcutaneous and intracranial human glioma xenograft models in athymic mice and rats. Similarly, effective monoclonal antibody 81C6 localization has been demonstrated in glioma patients, and Phase I trials with the intact murine IgG2b kappa molecule are currently in progress. In order to maximize the potential for repeated administration by minimizing murine Fc-mediated immunogenicity and reducing Fc-mediated immune effects, we created murine 81C6 variable region/human IgG2 chimeric monoclonal antibodies by the molecular cloning of the variable region genes of mouse 81C6 and their genetic linkage to human constant region exons. The resulting chimeric constructs were introduced into SP2/0 cells, and stable transfectomas were selected by G418 and mycophenolic acid resistance. The resistant clones were screened for anti-tenascin activity on tenascin-coated plates by enzyme-linked immunosorbent assay. The N-terminal amino acid sequence of both heavy and light chains of the purified chimeric 81C6 antibody matched exactly with that of the native mouse 81C6 as well as with that deduced from the nucleotide sequence. The production level of chimeric 81C6 (13.9 mg/ml) from ascites in the highest expressing transfectoma was much higher than that of native mouse 81C6 (2.5 mg/ml). The chimeric antibody showed the same specificity and equivalent affinity for human intact tenascin or tenascin-expressing cells as the native mouse 81C6 antibody. Direct comparison of radioiodinated chimeric and radioiodinated mouse 81C6 biodistribution in subcutaneous and intracranial xenograft-bearing mice showed higher tumor-to-normal tissue ratios for chimeric 81C6 as compared with native mouse 81C6. The improved localizing and clearance characteristics of chimeric 81C6 in xenograft model systems suggests that chimeric 81C6 would be an improved reagent for intracompartmental therapy of tenascin-expressing tumors in the human central nervous system.

Animals↗

PubMed1994

Evidence for cholecystokinin receptor subtype in endocrine pancreas.

Cholecystokinin (CCK) is a gut hormone that regulates pancreatic endocrine functions via CCKA receptors. CCK4 (Trp-Met-Asp-Phe-NH2) has an insulinotropic effect, but is 1000-fold less potent than CCK8. The in vitro potencies and selectivity of newly synthesized CCK4 analogs were investigated. Exchanging various a amino acids, for example Met by Nle and modifying Phe and/or Trp, led to compounds that were much more effective than CCK4 itself and show insulinotropic effects comparable with those of CCK8. Compounds that possess electron withdrawing groups on the C-terminal phenylalanine were especially effective; compounds with electron-donating groups had no effect. In contrast to CCK8 the synthetic CCK4 compounds were selective for the endocrine pancreas: they had no agonistic or antagonistic effect on the contraction of the guinea pig ileum, amylase release from isolated acini, and no major effect on the feeding behavior of mice being supplied with either compound by an implantable AlzetR pump for 8 days. The data indicate that some of the synthetic tetrapeptides exhibit a high affinity for the CCK receptor of the endocrine pancreas and that they are highly selective for this (peripheral) CCKA receptor subtype. The beta-cell CCKA receptors are different from those in exocrine pancreas, smooth muscle, and those for regulating appetite; these peripheral receptor subtypes can be discriminated for the first time.

Amylases↗

PubMed1994

Inhibition of macrophage-induced, antigen-specific T-cell proliferation by poly I:C role of suppressor macrophages.

Poly I:C treatment can inhibit the ability of macrophages (M phi) to induce antigen-specific T-cell proliferation. This study investigated whether this inhibition is the result of suppressor or cytotoxic activity. Pretreatment of M phi with indomethacin in vivo, in vitro or both failed to reverse the inhibition of T-cell proliferation induced by poly I:C-treated, keyhole limpet haemocyanin (KLH)-pulsed M phi, suggesting that prostaglandin production does not mediate the inhibition of T-cell proliferation. The transfer of supernatants from cultures containing poly I:C-treated, KLH-pulsed M phi to cultures containing saline-treated, KLH-pulsed M phi and T cells did not inhibit T-cell proliferation, suggesting that the inhibition of T-cell proliferation by poly I:C is not mediated by the production of soluble suppressor factors. As addition of poly I:C-treated, KLH-pulsed M phi to cultures containing saline-treated, KLH-pulsed M phi did not significantly inhibit KLH-specific T-cell proliferation, the inhibition of T-cell proliferation is also not mediated by direct cell contact or short-range soluble suppressor factors. In addition, poly I:C-treated, KLH-pulsed M phi did not induce cytolysis of syngeneic T cells. These results indicate that cytotoxic or suppressor effector functions of M phi are not involved in the mechanism by which poly I:C inhibits M phi-induced, antigen-specific T-cell proliferation.

Animals↗

PubMed1992

In vivo incorporation of 14C-phenylalanine into ascidian tunichrome.

Ascidia ceratodes exposed to 14C-phenylalanine in the surrounding seawater incorporates the radiolabel into newly biosynthesized tunichrome molecules. Radioactivity can be detected in tunichrome extracted from circulating blood cells within one day following initial exposure to the radiolabel; weak activity (less than or equal to 4 microCi/mol tunichrome = 22 nmol phenylalanine/mol tunichrome) is detected in 1 to 10 days; significantly higher amounts of radiolabel (57 microCi/mol tunichrome = 318 nmol phenylalanine/mol tunichrome) appear 20 days after seawater exposure. Therefore, phenylalanine can function as a precursor in the biosynthesis of tunichrome.

Animals↗

PubMed1992

Twin of I-POU: a two amino acid difference in the I-POU homeodomain distinguishes an activator from an inhibitor of transcription.

I-POU, a POU domain nuclear protein that lacks two conserved basic amino acids of the POU homeodomain is coexpressed in the developing Drosophila nervous system with a second POU domain transcription factor, Cf1-a. I-POU does not bind to DNA but forms a POU domain-mediated, high affinity heterodimer with Cf1-a, inhibiting its ability to bind and activate the dopa decarboxylase gene. The I-POU/Cf1-a dimerization interface encompasses only the N-terminal basic region and helices 1 and 2 of the POU homeodomains with precise amino acid and alpha-helical requirements. twin of I-POU, an alternatively spliced transcript of the I-POU gene, encodes a protein containing the two basic amino acid residues absent in I-POU. Twin of I-POU is incapable of dimerizing with Cf1-a, but can act as a positive transcription factor on targets distinct from those regulated by Cf1-a. These findings suggest that the I-POU genomic locus simultaneously generates both a specific activator and inhibitor of gene transcription, capable of modulating two distinct regulatory programs during neural development.

Amino Acid Sequence↗

PubMed1992

Brain 4: a novel mammalian POU domain transcription factor exhibiting restricted brain-specific expression.

The POU domain gene family of transcription factors share a conserved bipartite DNA binding domain, and exhibit distinct temporal and spatial patterns of expression during development, particularly in the forebrain. A cDNA encoding a new member of the POU-III class of the POU domain gene family, referred to as Brn-4, was isolated from a rat hypothalamic cDNA library. Like other mammalian POU-III genes previously characterized (Brn-1, Brn-2, Tst-1), Brn-4 transcripts are initially widely expressed at all levels of the developing neural tube, but in contrast to other previously described POU-III genes, are subsequently restricted to only a few regions of the adult forebrain, including the supraoptic and paraventricular nuclei of the hypothalamus. Brn-4 was shown to bind to DNA sequences containing the octamer motif and to trans-activate promoters containing this DNA binding motif, based on the actions of a unique N-terminal information. This ontogenic pattern of Brn-4 expression in concert with that of Oct-2 and Pit-1, indicates that certain POU domain genes potentially exert their primary functions widely during early neural development, and in a very limited set of neurons in the mature brain.

Amino Acid Sequence↗

PubMed1992

[RFLPs study of parental origin and mechanism of 3 cases with X chromosome structural abnormality].

In this study, we analysed the parental origin and mechanism of X chromosome abnormalities in 3 cases by using RFLPs on short or long arm of X chromosome as genetic markers. Their karyotypes were 46,X,dup(X)(p21); 46,X,del(X)(p11); 46,X,i(Xq). The results demonstrated that the dup(X)(p21) and the del(X)(p11) were of paternal origin and i(Xq) was of maternal origin. The dup(X)(p21) arose from an unequal sister chromatid exchange. The del(X) (p11) occurred through X chromosome breakage and deletion mechanism. The i(Xq) resulted from X chromosome centromere misdivision in oocyte.

Adolescent↗

PubMed1992

[Study on variation of plasma gamma-aminobutyric acid concentration in rat model of hepatic encephalopathy due to fulminant hepatic failure].

The plasma gamma-aminobutyric acid (GABA) concentration was measured by a radio-receptor assay in rat model of hepatic encephalopathy due to fulminant hepatic failure (FHF) induced by intraperitoneal injection of D-galactosamine (GalN). The results showed that, in FHF group, the plasma GABA increased parallelly with the degree of hepatic encephalopathy after GalN i.p. (r = 0.944, P less than 0.05). In about 48 h, mean plasma GABA concentration was elevated nearly 8-fold. These findings suggest that, in liver failure, elevated plasma GABA concentration may play a role in the pathogenesis of hepatic encephalopathy.

Animals↗

PubMed1992

Nude mouse interim host model for human parathyroid grafts. I. Structure and secretory function.

Human parathyroid (PTG) tissues from cadaver (C-PTG), fetus (F-PTG) and PTG adenoma (A-PTG) were transplanted into the kidney subcapsule of Balb/C nude mice as interim host. The structure and secretory function of the tissues were checked 30, 60, 90, 120, and 150 days after operation. The results showed that PTG tissues from all three donors could retain their structure and secretory function for more than 100 days in the nude mice. The growth and function of PTG tissues from the three donors in nude mice were compared.

Adenoma↗

PubMed1992

[Identification of sex in mouse preimplantation embryos by indirect immunofluorescent assay].

Indirect immunofluorescent assay was used for detecting male-specific H-Y antigen on preimplantation embryos. Our results showed that, embryos examined, 54.1% were H-Y positive (male) and 45.9% were H-Y negative (female). Significant difference was not found between natural sex ratio of kunming strain mouse (male: 52.1%; female: 47.9%) and our results (P greater than 0.05). Moreover, the results sequentially were confirmed by cytogenetic method. 75.50% H-Y positive embryos were male and 82.97% H-Y negative embryos were female respectively (P less than 0.01). Some factors influencing the accurency of sex selection with indirect immunofluorescent assay were also discussed.

Animals↗

PubMed1991

Autoregulation of the immune response in autoimmune disease and cardiac transplantation by photoinactivated autologous lymphocytes.

These studies demonstrate that photochemotherapy can be successfully evaluated in animal models. The therapy mediates specific suppression of immune responses and appears to operate at the level of the effector T cells. Future studies will focus on isolation and characterization of the host response to photochemotherapy. The extention of this form of therapy to conditions mediated by dysfunctional regulation of effector T cells is already in progress in clinical trials of cardiac allograft transplantation and autoimmune disease. The results of these trials will provide more evidence on the role of this form of therapy in autoregulation of the immune response.

Animals↗

PubMed1991

I-POU: a POU-domain protein that inhibits neuron-specific gene activation.

A novel, structurally distinct POU-domain protein has been identified that inhibits activation by another positive POU-domain regulator of neuron-specific transcription units. Two Drosophila POU-domain proteins, I-POU and Cf1-a, are coexpressed in overlapping subsets of neurons during development. Because I-POU lacks two basic residues in the N terminus of its homeodomain, it cannot bind DNA, but it does form a stable heterodimeric complex with Cf1-a, preventing Cf1-a from binding to DNA recognition elements and from transactivating the dopa-decarboxylase gene. The inhibition by I-POU provides a potential strategy by which the activation of genes in development is controlled by a homeodomain-containing protein that does not bind DNA.

Amino Acid Sequence↗