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Biomedical subjects

H Jiang

Publications and source records attributed to H Jiang.

At least 307 records · Page 17Linked to original sources
PubMed1999

[Pharyngoscopic observation during sleep in patients with obstructive sleep apnea syndrome].

OBJECTIVE: To analyse collapse sites of pharynx and their anatomical causes during sleep in patients with obstructive sleep apnea syndrome(OSAS), and compared with the results of Muller's maneuver. METHODS: The pharynges in 43 sleeping patients with OSAS were examined endoscopically. The area changes at each segment(velo-, oro- and hypopharynges) were calculated during the episodes of apnea. A site having greater than 75% narrowing of airway lumen was defined as a narrowing or obstructive site. RESULTS: 1. All patients had obstruction at velopharynx during asleep. Airway collapses at multiple sites in 79% of cases(28% at velo- and oropharynx; 21% at velo- and hypopharynges; and 30% at velo-, oro- and hypopharynges). 2. At each segment the anatomical factors causing obstruction were variable among patients. The common abnormalities were posterior displacement of soft palate or uvula, enlarged tonsil, thicken or posterior displacement of tongue base, collapse of pharyngeal wall, redundant mucosa or lateral bands of pharynx etc. 3. The positivity of pharyngeal obstruction was higher in this study as compared with of Muller's maneuver the latter was taken place while the patient was awaken. Comparison of the positive rate of the narrowing sites determined between sleep observation and Muller's maneuver in same patients: at velopharynx(100% vs 91%), at oropharynx (58% vs 42%) and at hyperpharynx (51% vs 28%). CONCLUSION: Multiple obstructions in the pharynx are common. Examination of the pharynx during asleep may be more accurate then while the patient was awaken.

Female↗
PubMed1999

Experimental study on preservation of rat fatty liver.

OBJECTIVE: To investigate the effects of cold preservation on rat fatty liver. METHODS: We observed the changes of portal perfusion pressure, endothelin-1, enzymes release in the effluent and mortality of sinusoid lining cell after 0h, 6h, or 12h preservation respectively and a subsequent 30 min reperfusion in rat fatty liver groups and control groups by using isolated perfused rat liver model. And we compared fatty liver groups with control groups by these indices. RESULTS: There was no obvious difference between mildly fatty liver group and control group after long time (12h) preservation, between moderately fatty liver group and control group after short time (6h) preservation, between severely fatty liver group and control group without preservation (0h), while preservation reperfusion injury was more severe in moderately fatty liver group than in control group after long time (12h) preservation and in severely fatty liver group than in control group after short time (6h) preservation. CONCLUSIONS: The authors suggested that a mildly fatty liver donor could be used in the same way as nonfatty liver and a moderately fatty liver donor could be used depending on the time of preservation and the balance of the emergent needs of recipient and donor organ supply, while severely fatty liver donor should be discarded without hesitation.

Animals↗
PubMed1999

[Flow injection analysis of 3,4-dihydroxybenzoic acid with inhibited chemiluminescent detection].

It was found that 3,4-dihydroxybenzoic acid (protocatechuric acid) inhibited chemiluminescence of luminol-H2O2 reaction catalyzed by Co2+. On this basis, a flow injection method has been developed for the determination of protocatechuric acid. The method is simple, convenient and sensitive with detection limit of 2.7 x 10(-7) mol/L and is effective to determine protocatechuric acid in the range of 1 x 10(-6)-1 x 10(-5) mol/L. The variation coefficient of eleven determinations for 8 x 10(-6) mol/L protocatechuric acid is 2.3%.

English Abstract↗
PubMed1998

Translocation efficiency, susceptibility to proteasomal degradation, and lipid responsiveness of apolipoprotein B are determined by the presence of beta sheet domains.

Apolipoprotein (apo) B100 is an atypical secretory protein in that its translocation across the endoplasmic reticulum membrane is inefficient, resulting in the partial translocation and exposure of apoB100 on the cytoplasmic surface of the endoplasmic reticulum. Cytosolic exposure leads to the association of nascent apoB with heat shock protein 70 and to its predisposition to ubiquitination and proteasomal degradation. The basis for the inefficient translocation of apoB100 remains unclear and controversial. To test the hypothesis that beta sheet domains present in apoB100 contribute to its inefficient translocation, we created human apoB chimeric constructs apoB13,16 and apoB13,13,16, which contain amino-terminal alpha globular domains but no beta sheet domains, and apoB13,16,beta, which has an amphipathic beta sheet domain of apoB100 inserted into apoB13,16. These constructs, along with carboxyl-terminal truncations of apoB100, apoB34 and apoB42, were used to transfect HepG2 and Chinese hamster ovary cells. In contrast to the lack of effect of proteinase K on apoB13,16 and apoB13,13,16, the levels of apoB34, apoB42, and apoB13,16,beta were decreased by 70-85% after proteinase K-induced proteolysis in both HepG2 and Chinese hamster ovary cells. Either oleic acid or proteasomal inhibitors (N-acetyl-leucinyl-leucinyl-norleucinal and lactacystin) significantly increased the cell levels of apoB13,16,beta, apoB34, apoB42, and full-length apoB100 but had no effect on the cell levels of apoB13,16 and apoB13,13,16. When HepG2 cells were incubated with a microsomal triglyceride transfer protein inhibitor, the cellular levels of apoB13,16,beta, apoB34, and apoB42 were decreased by 70-80%, whereas the levels of apoB13,16 and apoB13,13,16 were unaffected. The effects of microsomal triglyceride transfer protein inhibition were reversed by lactacystin. Our results clearly demonstrate that the translocation efficiency, susceptibility to proteasomal degradation, and lipid responsiveness of apoB were determined by the presence of a lipid binding beta sheet domain. It is possible that beta sheet domains may at least transiently facilitate the interaction of apoB with the lipid bilayer surrounding the translocation channel.

Apolipoprotein B-100↗
PubMed1998

Phospholipase cbeta4 is specifically involved in climbing fiber synapse elimination in the developing cerebellum.

Elimination of excess climbing fiber (CF)-Purkinje cell synapses during cerebellar development involves a signaling pathway that includes type 1 metabotropic glutamate receptor, Galphaq, and the gamma isoform of protein kinase C. To identify phospholipase C (PLC) isoforms involved in this process, we generated mice deficient in PLCbeta4, one of two major isoforms expressed in Purkinje cells. PLCbeta4 mutant mice are viable but exhibit locomotor ataxia. Their cerebellar histology, parallel fiber synapse formation, and basic electrophysiology appear normal. However, developmental elimination of multiple CF innervation clearly is impaired in the rostral portion of the cerebellar vermis, in which PLCbeta4 mRNA is predominantly expressed. By contrast, CF synapse elimination is normal in the caudal cerebellum, in which low levels of PLCbeta4 mRNA but reciprocally high levels of PLCbeta3 mRNA are found. These results indicate that PLCbeta4 transduces signals that are required for CF synapse elimination in the rostral cerebellum.

Animals↗
PubMed1998

The role of ubiquitin conjugation in glucose-induced proteolysis of Saccharomyces maltose permease.

In Saccharomyces, the addition of glucose induces a rapid degradation of maltose permease that is dependent on endocytosis and vacuolar proteolysis (Medintz, I., Jiang, H., Han, E. K., Cui, W., and Michels, C. A. (1996) J. Bacteriol. 178, 2245-2254). Here we report on the role of ubiquitin conjugation in this process. Deletion of DOA4, which causes decreased levels of available ubiquitin, severely decreases the rate of glucose-induced proteolysis, and this is suppressed by the overproduction of ubiquitin. Overexpression of ubiquitin in an endocytosis-deficient end3-ts strain results in the glucose-stimulated accumulation of a larger molecular weight species of maltose permease, which we demonstrate is a ubiquitin-modified form of the protein by utilizing two ubiquitin alleles with different molecular weights. The size of this ubiquitinated species of maltose permease is consistent with monoubiquitination. A promoter mutation that reduces expression of RSP5/NPI1, a postulated ubiquitin-protein ligase, dramatically reduces the rate of glucose-induced proteolysis of maltose permease. The role of various ubiquitin-conjugating enzymes was investigated using strains carrying mutant alleles ubc1Delta ubc4Delta, ubc4Delta ubc5Delta, cdc34-ts2/ubc3, and ubc9-ts. Loss of these functions was not shown to effect glucose-induced proteolysis of maltose permease, but loss of Ubc1, -4, and -5 was found to inhibit maltose permease expression at the post-transcriptional level.

Endocytosis↗
PubMed1998

Changes in serum melatonin levels in response to pinealectomy in the chicken and its correlation with development of scoliosis.

STUDY DESIGN: Normal, sham, and groups of chickens subjected to pinealectomy from which serum melatonin levels were measured and correlated with scoliosis development in a period of 5 weeks. OBJECTIVES: To measure serum melatonin levels in chickens subjected to pinealectomy and control chickens and correlate findings with development of scoliosis. SUMMARY OF BACKGROUND DATA: In a previous study by others, scoliosis developed in 100% of chickens subjected to pinealectomy, and serum melatonin levels were found to be reduced. Previous results in a study by the authors showed scoliosis developing in only approximately 55% of chickens that underwent pinealectomy. METHODS: Young chickens were subjected to pinealectomy. Control groups consisted of sham operation and normal groups. Radiographs and blood samples were taken at weekly intervals to monitor scoliosis development and measure serum melatonin levels using radioimmunoassay techniques. RESULTS: Scoliosis developed in only 52% of chickens that underwent pinealectomy, but all had low levels of serum melatonin and no circadian rhythm. The chickens in the two control groups maintained normal serum melatonin levels and rhythms. CONCLUSIONS: Pinealectomy in young chickens reduces serum melatonin levels and eliminates the melatonin circadian rhythm. It can also produce scoliosis, but low levels of serum melatonin are a poor predictor of development of scoliosis.

Animals↗
PubMed1998

Rapid cytochrome c release, activation of caspases 3, 6, 7 and 8 followed by Bap31 cleavage in HeLa cells treated with photodynamic therapy.

Photodynamic therapy (PDT) is a clinical approach that utilizes light-activated drugs for the treatment of a variety of pathologic conditions. The initiating events of PDT-induced apoptosis are poorly defined. It has been shown for other proapoptotic stimuli that the integral endoplasmic reticulum protein Bap31 is cleaved by caspases 1 and 8, but not by caspase-3. Further, a 20 kDa Bap31 cleavage fragment is generated which can induce apoptosis. In the current report, we sought to determine whether Bap31 cleavage and generation of p20 is an early event in PDT-induced apoptosis. The mitochondrial release of cytochrome c, involvement of caspases 1, 2, 3, 4, 6, 7, 8, and 10 and the status of several known caspase substrates, including Bap31, were evaluated in PDT-treated HeLa cells. Cytochrome c appeared in the cytosol immediately following light activation of the photosensitizer benzoporphyrin derivative monoacid ring A. Activation of caspases 3, 6, 7, and 8 was evident within 1-2 h post PDT. Processing of caspases 1, 2, 4, and 10 was not observed. Cleavage of Bap31 was observed at 2-3 h post PDT. The caspase-3 inhibitor DEVD-fmk blocked caspase-8 and Bap31 cleavage suggesting that caspase-8 and Bap31 processing occur downstream of caspase-3 activation in PDT-induced apoptosis. These results demonstrate that release of mitochondrial cytochrome c into the cytoplasm is a primary event following PDT, preceding caspase activation and cleavage of Bap31. To our knowledge, this is the first example of a chemotherapeutic agent inducing caspase-8 activation and demonstrates that caspase-8 activation can occur after cytochrome c release.

Amino Acid Chloromethyl Ketones↗
PubMed1998

Promiscuous coupling of receptors to Gq class alpha subunits and effector proteins in pancreatic and submandibular gland cells.

Mice with deficiencies in one or more Gq class alpha subunit genes were used to examine the role of the alpha subunit in regulating Ca2+ signaling in pancreatic and submandibular gland cells. Western blot analysis showed that these cells express three of the four Gq class subunits, Galphaq, Galpha11, and Galpha14 but not Galpha15. Surprisingly, all parameters of Ca2+ signaling were identical in cells from wild type and four lines of mutant mice: 1) Galpha11-/-, 2) Galpha11-/-/Galpha14-/-, 3) Galpha14-/-/Galpha15-/-, and 4) Galphaq-/-/Galpha15-/-. These parameters included the Kapp for several Gq class coupled receptors, induction of [Ca2+]i oscillations by weak stimulation, and a biphasic [Ca2+]i response by strong stimulation. Furthermore, Ca2+ release from internal stores and Ca2+ entry were not affected in cells from any of the mutant mice. We conclude that Galphaq, Galpha11, and Galpha14 promiscuously couple several receptors (m3 muscarinic, bombesin, cholecystokinin, and alpha1 adrenergic) to effector proteins that activate both Ca2+ release from internal stores and Ca2+ entry.

Animals↗
PubMed1998

Pro-phenol oxidase activating proteinase from an insect, Manduca sexta: a bacteria-inducible protein similar to Drosophila easter.

Activation of pro-phenol oxidase (proPO) in insects and crustaceans is important in defense against wounding and infection. The proPO zymogen is activated by a specific proteolytic cleavage. PO oxidizes phenolic compounds to produce quinones, which may help to kill pathogens and can also be used for synthesis of melanin to seal wounds and encapsulate parasites. We have isolated from the tobacco hornworm, Manduca sexta, a serine proteinase that activates proPO, and have cloned its cDNA. The isolated proPO activating proteinase (PAP) hydrolyzed artificial substrates but required other protein factors for proPO activation, suggesting that proPO-activating enzyme may exist as a protein complex, one component of which is PAP. PAP (44 kDa) is composed of two disulfide-linked polypeptide chains (31 kDa and 13 kDa). A cDNA for PAP was isolated from a hemocyte library, by using a PCR-generated probe based on the amino-terminal amino acid sequence of the 31-kDa catalytic domain. PAP belongs to a family of arthropod serine proteinases containing a carboxyl-terminal proteinase domain and an amino-terminal "clip" domain. The member of this family most similar in sequence to PAP is the product of the easter gene from Drosophila melanogaster. PAP mRNA was present at a low level in larval hemocytes and fat body, but became much more abundant in fat body after insects were injected with Escherichia coli. Sequence data and 3H-diisopropyl fluorphosphate labeling results suggest that the same PAP exists in hemolymph and cuticle.

Amino Acid Sequence↗
PubMed1998

Benzo[a]pyrene diol epoxide and bleomycin sensitivity and susceptibility to cancer of upper aerodigestive tract.

BACKGROUND: Tobacco smoking is an established risk factor for cancers of the upper aerodigestive tract, and measurement of chromosomal aberrations, i.e., chromatid breaks, induced in lymphocytes in vitro by bleomycin has been shown to be a predictor of risk for these cancers. In a case-control study, we recruited case subjects who were previously treated with surgery and/or radiotherapy for stage I or stage II squamous cell carcinoma of the head and neck to test the hypothesis that lymphocytic chromatid breaks induced by benzo[a]pyrene diol epoxide (BPDE), a tobacco mutagen, may also be associated with risk of developing cancers of the upper aerodigestive tract. METHODS: Case subjects were matched to control subjects on the basis of age, sex, ethnicity, and smoking status. Primary lymphocytes from 67 case subjects and 81 control subjects were treated with 2 microM BPDE for 24 hours, and the frequency of induced chromatid breaks was determined. All statistical tests were two-sided. RESULTS: Lymphocytes from case subjects compared with lymphocytes from control subjects showed significantly more breaks per cell induced by BPDE (mean+/-standard deviation, 0.77+/-0.38 versus 0.49+/-0.25; P<.001). Lymphocytes from 64.2% of case subjects were sensitive to BPDE (using a cutoff value of > or =0.60 break per cell). Subjects in the highest quartile of chromatid breaks had an approximately 20-fold increased risk of cancer compared with those in the lowest quartile after adjustment for age, sex, ethnicity, and smoking status. The association between BPDE sensitivity and cancer risk was higher in former smokers than in current smokers and higher in younger patients than in older patients. Subjects with sensitivity to both BPDE and bleomycin were at a 19.2-fold increased risk of cancer compared with those who were not sensitive to either agent. CONCLUSIONS: Mutagen sensitivity assays may aid in identifying individuals at risk of cancer, and use of parallel assays with two mutagens may improve risk predictability.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1998

First analysis of mortality and occupational radiation exposure based on the National Dose Registry of Canada.

A cohort mortality study of occupational radiation exposure was conducted using the records of the National Dose Registry of Canada. The cohort consisted of 206,620 individuals monitored for radiation exposure between 1951 and 1983 with mortality follow-up through December 31, 1987. A total of 5,426 deaths were identified by computerized record linkage with the Canadian Mortality Data Base. The standardized mortality ratio for all causes of death was 0.61 for both sexes combined. However, trends of increasing mortality with cumulative exposure to whole body radiation were noted for all causes of death in both males and females. In males, cancer mortality appeared to increase with cumulative exposure to radiation, without any clear relation to specific cancers. Unexplained trends of increasing mortality due to cardiovascular diseases (males and females) and accidents (males only) were also noted. The excess relative risk for both sexes, estimated to be 3.0% per 10 mSv (90% confidence interval 1.1-4.8) for all cancers combined, is within the range of risk estimates previously reported in the literature.

Adolescent↗
PubMed1998

A parallel study of in vitro sensitivity to benzo[a]pyrene diol epoxide and bleomycin in lung carcinoma cases and controls.

BACKGROUND: Because only a fraction of smokers develop neoplastic lesions, host factors may affect their susceptibility to the carcinogenic effects of tobacco smoke. Benzo[a]pyrene diol epoxide (BPDE) is the metabolic product of benzo[a]pyrene (B[a]P), a constituent of tobacco smoke. Therefore, BPDE sensitivity may shed some light on smoking-related carcinogenesis. METHODS: First, differential BPDE sensitivity was tested in five lymphoblastoid cell lines. Then sensitivity to BPDE and bleomycin (an excellent lung carcinoma risk predictor) was tested in parallel in the lymphocytes of 57 lung carcinoma cases and 82 controls. RESULTS: The optimal BPDE treatment duration was 24 hours. The xeroderma pigmentosum cell line was the most sensitive, followed by head and neck cancer, ataxia telangiectasia, and normal cells. The mean breaks per cell for cases and controls were 0.78 and 0.46, respectively (P < 0.0001). BPDE sensitivity was significantly associated with lung carcinoma, with an odds ratio (OR) of 7.26, compared with an OR of 4.56 for bleomycin sensitivity. There was also a dose-response correlation between the quartiles of BPDE-induced breaks and lung carcinoma risk, with ORs of 2.39, 3.12, and 15.03. It is noteworthy that individuals who were sensitive to both BPDE and bleomycin had a significantly increased OR of 38.36. CONCLUSIONS: BPDE sensitivity may be a biologic marker to identify individuals who are susceptible to the carcinogenic effects of tobacco smoke. BPDE and bleomycin sensitivity might represent different repair or sensitivity pathways; however, when these assays are used in parallel, they might refine our ability to identify high risk individuals.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1998

Nerve growth factor treatment prevents the increase in superoxide produced by epidermal growth factor in PC12 cells.

Stimulation of pheochromocytoma (PC12) cells with the mitogen epidermal growth factor (EGF) produced a rapid and robust accumulation of intracellular reactive oxygen species (ROS), an accumulation which, in other systems, has been shown to be essential for mitogenesis. Brief pretreatment of the cells with nerve growth factor (NGF) suppressed the EGF-mediated ROS increase. EGF failed to produce elevations in ROS in a PC12 variant stably expressing a dominant-negative p21(ras) construct (PC12-N17) or in cells pretreated with the MEK inhibitor PD098059. NGF failed to suppress the increase in ROS in the PC12 variant nnr5, which lacks p140(trk) receptors. The suppression of the increase in ROS by NGF was restored in nnr5 cells stably expressing p140(trk) (nnr5-trk), but NGF failed to prevent the increase in ROS in nnr cells expressing mutant p140(trk) receptors that lack binding sites for Shc and phospholipase Cgamma. Among several inhibitors of superoxide-generating enzymes, only the lipoxygenase inhibitor, nordihydroguaiaretic acid reduced EGF-mediated ROS accumulation. The inhibitory action of NGF on ROS production was mimicked by the nitric oxide donor, sodium nitroprusside, and was blocked by an inhibitor of nitric-oxide synthetase, L-nitroarginine methyl ester. These results suggest a novel mechanism for the rapid interruption of mitogenic signaling by the neurotrophin NGF.

Animals↗
PubMed1998

Mutual education between hematopoietic cells and bone marrow stromal cells through direct cell-to-cell contact: factors that determine the growth of bone marrow stroma-dependent leukemic (HB-1) cells.

A stroma-dependent cell line (HB-1) was established from myelogenous leukemic cells of CBA/N mouse. Characterization of the cells showed that HB-1 proliferated on hematopoietic supportive stromal cells (MS-10), but did not survive or proliferate on hematopoietic nonsupportive cells (MS-K). Direct contact between HB-1 and MS-10 appears to be necessary for HB-1 to proliferate on MS-10. We found that interleukin-1alpha (IL-1alpha) produced by MS-10 plays a major role in the survival and proliferation of HB-1. IL-11 did not support the proliferation of HB-1 cells by itself, but enhanced the proliferation of HB-1 cells in the presence of IL-1alpha. The expression of IL-1alpha and IL-11 was induced in MS-10 by the direct contact with HB-1 cells, and the expression of IL-1 receptor type I (IL-1RI) and interleukin-11 receptor (IL-11R) was induced in HB-1 cells by the attachment of the cells to MS-10. These findings show the existence of two-way interactions between HB-1 and MS-10.

Acute Disease↗
PubMed1998

T cell vaccination induces T cell receptor Vbeta-specific Qa-1-restricted regulatory CD8(+) T cells.

Vaccination of mice with activated autoantigen-reactive CD4(+) T cells (T cell vaccination, TCV) has been shown to induce protection from the subsequent induction of a variety of experimental autoimmune diseases, including experimental allergic encephalomyelitis (EAE). Although the mechanisms involved in TCV-mediated protection are not completely known, there is some evidence that TCV induces CD8(+) regulatory T cells that are specific for pathogenic CD4(+) T cells. Previously, we demonstrated that, after superantigen administration in vivo, CD8(+) T cells emerge that preferentially lyse and regulate activated autologous CD4(+) T cells in a T cell receptor (TCR) Vbeta-specific manner. This TCR Vbeta-specific regulation is not observed in beta2-microglobulin-deficient mice and is inhibited, in vitro, by antibody to Qa-1. We now show that similar Vbeta8-specific Qa-1-restricted CD8(+) T cells are also induced by TCV with activated CD4(+) Vbeta8(+) T cells. These CD8(+) T cells specifically lyse murine or human transfectants coexpressing Qa-1 and murine TCR Vbeta8. Further, CD8(+) T cell hybridoma clones generated from B10.PL mice vaccinated with a myelin basic protein-specific CD4(+)Vbeta8(+) T cell clone specifically recognize other CD4(+) T cells and T cell tumors that express Vbeta8 and the syngeneic Qa-1(a) but not the allogeneic Qa-1(b) molecule. Thus, Vbeta-specific Qa-1-restricted CD8(+) T cells are induced by activated CD4(+) T cells. We suggest that these CD8(+) T cells may function to specifically regulate activated CD4(+) T cells during immune responses.

Animals↗