Biomedical subjects

J Hou

Publications and source records attributed to J Hou.

At least 91 records · Page 5Linked to original sources

PubMed1999

[Diagnosis and differential diagnosis of primary carcinoma of female peritoneum].

OBJECTIVE: Histogenesis and morphological features of 6 primary carcinomas of female peritoneum were studied. METHODS: H&E staining, histochemical stainings and immunohistochemical stainings were used. RESULTS: Among 6 primary carcinomas there were 4 cases of serous papillary carcinomas, 1 case of endometrioid carcinoma and 1 case of transitional cell carcinoma. CONCLUSION: Primary carcinomas of the female peritoneum were histologically identical to that of the similar epithelial carcinomas arising from the ovaries. The diagnosis was made only when the ovaries are not involved and without no any evidence of similar epithelial carcinoma obtained in the ovaries, uterus or urinary organs. These tumors are considered arising from the secondary Mullerian system. D-PAS and CEA staining are helpful as the accessory criteria for the differential diagnosis between primary carcinoma of the peritoneum and malignant mesothelioma.

Adult↗

PubMed1999

[A preliminary study of loss of heterozygosity on chromosome 1p in primary hepatocellular carcinoma].

OBJECTIVE: Ten (10) loci on chromosome 1p were analyzed to detect LOH in 38 cases of hepatocellular carcinomas (HCC) in order to locate the deletion area and the possible deleted tumor suppressor gene (TSG) in HCC. METHODS: PCR based microsatellite instability analysis were used to detect LOH on chromosome 1p31 and 1p35-p36 in HCC. RESULTS: LOH were detected on chromosome 1p in 84.2% of HCC. High frequency of LOH (> 40%) were occurred at locus D1S186 on 1p31, locus D1S482 on 1p35 and loci D1S243, D1S160, D1S165 and D1S170 on 1p36. CONCLUSION: LOH occurred mostly on chromosome 1p31 and 1p35-p36 in HCC. There may be more than two TSGs which associated with development of HCC on chromosome 1p31 and 1p35-p36.

Adult↗

PubMed1999

[Relationship between expression of estrogen receptor progestrone receptor and the biological characteristics of nasopharyngeal carcinoma].

OBJECTIVE: To Clarity the relationship between the expression of the estrogen receptor (ER), progestogen receptor (PR) and the biological characteristics of nasopharyngeal carcinoma (NPC). METHOD: The immuno-histochemical LSAB method was used to analyse the ER and PR in paraffin section specimen of 71 cases of nasopharyngeal carcinoma. CT scaning and clinic presentation were also put into consideration. RESULT: The expression of ER with (-), (+), (++) and (+++) in 71 cases were: 4(5.63%), 19(26.76%), 27(38.03%) and 21 (26.76%), respectively. The expression of PR with (-), (+) and (++) in 71 cases were: 41(57.75%), 29 (39.44%) and 2(2.82%), respectively. The encroaching of tumor to the tissue of parapharynx, the metastasis rate of lymphonode and clinic stage were related to the expression of ER (P < 0.01). The encroaching of tumor to the tissue of parapharynx, the metastasis rate of lymphonode were also assciated with the expression of PR (P < 0.05). CONCLUSION: NPC is a tumor of hightly expression of ER and PR. The positive intensity of ER and PR were associated with the encroaching extent of NPC, and the metastasis rate of lymphonode. It is significant to detarmine ER and PR of NPC in assessing the biological characterisitics of NPC and predicting the prognosis of NPC. It also suggests that the endocrine therapy can be put into consideration.

Adult↗

PubMed1999

[Determination of nervonic acid in oral tonic by GC].

A method for determination of nervonic acid in oral tonic has been developed by gas chromatography. The samples were derivatized by BF3-CH3OH. Dinonyl phthalate was used as the internal standard. The calibration curve was linear over a range from 0.3 g/L to 3 g/L with a correlation coefficient of 0.9994. The average recovery of the method was 97.04% and the RSD was 0.90%. The method has been successfully applied to quality control of nervonic acid in oral tonic.

Administration, Oral↗

PubMed1999

[The inhibitory effect of selenite and other antioxidants on the complement mediated experimental pulmonary alveolitis].

OBJECTIVE: To test the regulatory effect of selenite and other antioxidants on complement PMN activation feedback mechanism mediated inflammatory response in experimantal pulmonary vasculitis. METHODS: Mouse model of pulmonary Arthus reaction vasculitis developed with BSA sensitization and antigen inhalation was used for tests of inhibitory effect of oral administration of sodium selenite, glycyrrhizin flavonoids and/or vitamin E on the incidence of developing vasculitis, which could reflect the modulation of inflammatory response and tissue injury. RESULTS: A remarkable inhibitory effect of selenite or combined flavonoid and vitamin E on the induction of pulmonary vasculitis were observed as the incidence of vasculitis could drop from 100% of the untreated group down to 25% of the antioxidants treated groups, revealing modulation of inflammatory response. CONCLUSIONS: It indicated a newer insight into mechanism of the inflammatory response could give a novel approach to the modulation of inflammatory response. An adjuvant therapy of selenium and antioxidants to the interventions of inflammatory disorders has been expected.

Animals↗

PubMed1999

[Relationship between complement activation and reactive oxygen species generation in inflammatory response].

OBJECTIVE: To verify the proposed activation feedback mechanism between complement and polymorphonuclear leukocytes(PMN) derived reactive oxygen species(ROS). METHODS: In vitro tests were designed to identify the activation feedback process by alternative activations of complement by inulin or PMNs by 12-O-tetradecanoylphorbol-13-acetate(TPA) in the test medium in consisting serum complement and isolated PMNs, with chemiluminescence technique to determine the production of ROS and complement fixation trial for complement activations. RESULTS: Evidently that activated complement could activate PMNs to release ROS which further activated complement, so the activating feedback cycle was set. CONCLUSIONS: The complement and PMNs-ROS activation feedback cycle mechanism was recognized. It was expected to serve for delineating the regulation of inflammatory response.

Animals↗

PubMed1999

[Dynamic changes of basal core promoter and pre-core mutants of hepatitis B virus in patients with chronic hepatitis B virus infection].

OBJECTIVES: To clarify the association of hepatitis B virus mutants in basal core gene promoter and pre-c region with serum HBeAg state and persistent HBV infection. METHODS: 32 patients, who infected with hepatitis B virus and suffered from several exacerbation during the course of this disease, were followed up for an average of 20.8 months. Using two mis-matched primers to amplify BCP and pre-c gene fragments, in combination with restricted fragment length polymorphism assay, we studied the presence of these two mutants(nt 1762A-->T, 1764G-->A and nt1896G-->A) in 105 serum samples. Direct sequencing was performed on 15 patients' serial samples to identify the efficiency of these rapid and simple methods and other variations in these regions. RESULTS: The presence of these two kinds of mutants increased during the following-up, (62.5% > 46.9%; 31.3% > 12.5%). In most cases, two mutants prevailed and finally displaced the wild type virus; the serology of HBeAg was affected predominantly by the ratio of BCP mutant to wild type. CONCLUSION: BCP and pre-c mutants emerged in the course of chronic infection and were selected positively by the inflammation activity. The serological conditions of HBeAg were changed when the predominant situations of these two mutants were established. The survival of these two mutants implied that mutations in these two regions may contribute to the persistent infection of hepatitis B virus.

Adolescent↗

PubMed1998

Transcriptional regulation of intercellular adhesion molecule-1 in astrocytes involves NF-kappaB and C/EBP isoforms.

ICAM-1 is an inducible cell surface protein that is involved in cell extravasation into inflamed tissues as well as immune responses. ICAM-1 expression is upregulated by proinflammatory cytokines such as TNF-alpha and IL-1beta in numerous cell types including the astrocyte, which functions as an immune effector cell in the central nervous system (CNS). We investigated the mechanism by which the ICAM-1 gene is transcriptionally regulated in astrocytes in response to TNF-alpha and IL-1beta. Human ICAM-1 promoter constructs linked to the reporter gene luciferase were transiently transfected into astrocytes, stimulated with TNF-alpha and IL-1beta, and ICAM-1 promoter activity examined. We determined that binding sites for both NF-kappaB (-186 bp region) and C/EBP (-198 bp region) are involved in TNF-alpha and IL-1beta-mediated ICAM-1 upregulation. Electrophoretic mobility shift assays using antibodies against NF-kappaB and C/EBP isoforms showed that p65 homodimers and p65/p50 heterodimers bind to the NF-kappaB site, and C/EBPdelta homodimers and C/EBPbeta/delta heterodimers bind to the C/EBP site. Transient transfection assays demonstrated that overexpression of p65 could transactivate the promoter activity of ICAM-1 reporter constructs. p50 overexpression had no effect on the basal levels of ICAM-1 transcription, but inhibited, in a dose dependent manner, p65 mediated transcription. Overexpression of C/EBPbeta slightly inhibited basal levels of ICAM-1 promoter activity, however, when C/EBPbeta and p65 were cotransfected, C/EBPbeta completely abolished the transactivating effects of p65. These results demonstrate that cytokine-induced ICAM-1 expression in astrocytes is regulated by interactions between NF-kappaB and C/EBP transcription factors.

Animals↗

PubMed1998

Effect of carotenoids on the respiratory burst of rat peritoneal macrophages.

The effect of four carotenoids (beta-carotene, lutein, bixin and canthaxanthin) on the respiratory burst of rat peritoneal macrophages was investigated. The results obtained showed that carotenoids suppressed the luminol-dependent chemiluminescence generated from PMA-stimulated macrophages at the beginning and after 2 min of the stimulation. Canthaxanthin and bixin had higher suppressive activity than beta-carotene and lutein. The changes in absorption spectra of carotenoids showed that the absorption by carotenoids was diminished during the stimulation of macrophages by PMA and their absorption peaks were either further diminished or blue-shifted after addition of L-arginine to the system, indicating that the carotenoids were consumed and converted to new compounds during the two processes. By using cell-free systems, it was found that carotenoids could scavenge superoxide anion generated by xanthine/xanthine oxidase system. Their ability to scavenge superoxide anion decreased in the order of canthaxanthin > bixin > lutein > beta-carotene. Canthaxanthin also showed the scavenging effect on superoxide anion generated from irradiation of riboflavin. The hydroxyl radical scavenging activity of carotenoids was investigated in the reaction system of Fe2+ and H2O2. There was little difference among their activities. The reaction between carotenoids and nitric oxide led to the decreasing absorption between 400 and 540 nm and the concomitant appearance of the new absorption peaks between 330 and 395 nm. Bleaching of beta-carotene, bixin and canthaxanthin by peroxynitrite resulted in the increasing absorption between 290 and 365 nm and the diminishing absorption between 400 and 500 nm. But the increasing absorption between 280 and 490 nm was observed in bleaching of lutein by peroxynitrite. Carotenoids inhibited thiobarbituric acid-reactive substance (TBARS) formation in AAPH-induced lipid peroxidation of PC liposomes in air. The results suggest that the suppressive effect of carotenoids on the respiratory burst of macrophages may be just a way by which carotenoids in vivo protect host cells and tissues from harmful effects of oxygen metabolites overproduced by macrophages and enhance the generation of specific immune responses.

Animals↗

PubMed1998

Effects of EGb 761 on nitric oxide and oxygen free radicals, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo.

The cardioprotective effects of EGb 761 on the release of nitric oxide (NO), the concentration of serum thiobarbituric acid reaction substance (TBARS), the activity of creatine kinase (CK) and the incidence of ventricular arrhythmias were investigated in myocardial ischemia-reperfusion injury in vivo. Using sodium nitrite (NaNO2) as standard source of nitric oxide (NO), we compared the correlation coefficients of the three measuring methods used currently in the determination of NOFe2+(DETC)2 complex with that of the measuring method suggested in this study. The result showed that measuring the whole height of three splitting signals is the best linear correlation to the concentration of NO comparing with other methods in this system. Using this method, we observed the effects of EGb 761 on NOFe2+(DETC)2 complex in myocardial ischemia-reperfusion injury in vivo. The hearts of the Wistar rats were subjected to 30 min of ischemia and 10 min of reperfusion in vivo. Different doses of EGb 761 (25, 50, 100, 200 mg/kg i.p.), superoxide dismutase (SOD, 10(4) U/kg), l-arginine (50 mg/kg i.p.) and nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine (NNA, 50 mg/kg i.p.) were administered to the ischemia-reperfusion rats. EGb 761 under the dose of 100 mg/kg increased the signal intensity of NOFe2+(DETC)2 complex, while EGb 761 at 200 mg/kg showed an effect of decreasing the signal intensity of NOFe2+(DETC)2 complex. EGb 761 inhibited the formation of TBARS, the release of CK, and mitigated the incidence of ventricular arrhythmias in a dose dependent way. Both l-arginine and SOD increased the signal intensity of NOFe2+(DETC)2 complex and inhibited the formation of TBARS, the leakage of CK and the incidence of ventricular arrhythmia. NNA not only had no protective effects on myocardial injury, but also increased the incidence of reperfusion-induced arrhythmia. In conclusion, EGb 761 has cardiovascular protective effects by means of adjusting the level of NO and inhibiting oxygen free radicals induced lipid peroxidation in myocardial ischemia-reperfusion injury in vivo.

Animals↗

PubMed1998

Apoptosis induced by a chimeric Fas/FLICE receptor: lack of requirement for Fas- or FADD-binding proteins.

Current models for Fas (CD95)-mediated apoptosis suggest that FLICE/caspase-8 is recruited and activated, which results in cell death. However, the role of additional molecules in Fas signaling and FLICE activation is not clear. A chimeric Fas/FLICE (F/F) receptor, containing the extracellular/transmembrane portion of Fas and the caspase region of FLICE, mediated anti-Fas apoptosis. FLICE protease subunits were generated from the F/F precursor. Killing induced by Fas, but not F/F, was blocked by a dominant negative FADD. Apoptosis triggered through Fas and F/F was inhibited by coexpression of CrmA and p35, but not Bcl-xL. F/F bypassed Fas resistance in COS-7 cells and blocking by the death effector domain (DED)-containing viral protein MC159. These results show that: 1) F/F induces cell death, indicating that FLICE activation is sufficient for apoptosis and does not require additional Fas- or FADD-binding proteins; and 2) F/F bypasses proximal defects in Fas signaling that prevent FLICE recruitment or activation.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Expression of active thrombopoietin and identification of its key residues responsible for receptor binding.

In this report expression of the biologically active N-terminal half (amino acids 1-153) of thrombopoietin (TPO153) in Escherichia coli is described and the structure-function relationships in TPO are explored. TPO153 was chosen for expression because of its full biological activity. Since natural TPO153 cDNA expressed poorly, synthetic cDNA was constructed with a unique polymerase chain reaction to enhance the expression. In addition, the 5'-end codons of the synthetic cDNA were altered to maximize the expression. The expressed TPO153 was refolded and then purified to homogeneity. The protein is biologically active, and interestingly, the EC50 of this protein is 8-10-fold smaller in a TPO-dependent cell proliferation assay than that of full-length wild-type TPO. In order to identify the amino acid residues that are involved in the interaction between TPO and its receptor, all charged residues and some of the uncharged residues on the four putative helices of TPO were mutated and biological activities of the mutant proteins were examined. The mutagenesis studies suggest that there are at least two clusters of residues that are vital for TPO to be able to interact with its receptor. These residues are centred respectively around arginine 10 on helix 1 and around lysine 138 on helix IV. The successful expression of the protein in E. coli will greatly facilitate biochemical and crystallographic studies of TPO, and the structure-function relationship studies suggest that TPO has two binding sites which may interact with two individual receptors, resulting in dimerization of the receptors.

Amino Acid Sequence↗

PubMed1998

Osseous hemangiopericytomas of unsuspected intracranial origin.

Two cases of osseous hemangiopericytoma are presented that were initially diagnosed as primary in origin, but later reclassified as metastases, after a history of resection for an intracranial tumor was discovered. An intracranial source should be excluded before an isolated osseous tumor is determined to be a primary hemangiopericytoma.

Aged↗

PubMed1998

Clearance of persistent hepatitis B virus infection in Chinese bone marrow transplant recipients whose donors were anti-hepatitis B core- and anti-hepatitis B surface antibody-positive.

Thirteen hepatitis B surface antigen-positive Chinese patients who received hepatitis B surface antibody-positive marrow (hepatitis B core antibody-positive or -negative: 6 and 7, respectively) via allogeneic bone marrow transplantation (BMT) were studied. After BMT, 4 recipients had serologic clearance of hepatitis B surface antigen from hepatitis B core antibody-positive marrow, but none of the recipients of hepatitis B core antibody-negative marrow had serologic clearance (P=.02). There was no significant difference in the donors' hepatitis B surface antibody titer before BMT for patients with or without serologic clearance of hepatitis B surface antigen (2255.2+/-4244.0 vs. 854.2+/-2306.7 mIU/mL; P=not significant). Adoptive immunity clearance of hepatitis B surface antigen was favored by hepatitis B core antibody positive-donor marrow and was not related to donor pre-BMT hepatitis B surface antibody titer.

Adolescent↗

PubMed1998

Detection of JC virus DNA in human tonsil tissue: evidence for site of initial viral infection.

Progressive multifocal leukoencephalopathy is a demyelinating disease of the human central nervous system that results from lytic infection of oligodendrocytes by the polyomavirus JC (JCV). Originally, JCV was thought to replicate exclusively in human glial cells, specifically oligodendrocytes. However, we have recently shown that JCV can replicate in cells of lymphoid origin such as hematopoietic precursor cells, B lymphocytes, and tonsillar stromal cells. To determine whether tonsils harbor JCV, we tested a total of 54 tonsils, 38 from children and 16 from adult donors. Nested PCRs with primer sets specific for the viral T protein and regulatory regions were used for the detection of JCV DNA. JCV DNA was detected in 21 of 54 tonsil tissues, or 39% (15 of 38 children and 6 of 16 adults) by using regulatory-region primers and in 19 of 54 tonsil tissues, or 35% (13 of 38 children and 6 of 16 adults) by using the T-protein primers. The DNA extracted from children's nondissected tonsil tissue, isolated tonsillar lymphocytes, and isolated stromal cells that demonstrated PCR amplification of the JCV regulatory region underwent cloning and nucleotide sequencing. Of the regulatory-region sequences obtained, nearly all contained tandem repeat arrangements. Clones originating from nondissected tonsil tissue and tonsillar lymphocytes were found to have sequences predominantly of the Mad-1 prototype strain, whereas the majority of clones from the DNA of tonsillar stromal cells had sequences characteristic of the Mad-8br strain of JCV. A few clones demonstrated structures other than tandem repeats but were isolated only from tonsillar lymphocytes. These data provide the first evidence of the JCV genome in tonsil tissue and suggest that tonsils may serve as an initial site of viral infection.

Adolescent↗

PubMed1998

The efficacy of nucleoside analogs against JC virus multiplication in a persistently infected human fetal brain cell line.

The effectiveness of nucleoside analogs in blocking viral multiplication was evaluated using an immortalized human neuroglial cell line capable of sustaining a persistent JCV infection, SVG-JC. Results from in situ DNA hybridization and hemagglutination assays performed on drug treated cultures were used as a measure of viral DNA replication and multiplication, respectively. Of the three drugs tested, Ara-C (cytosine arabinoside), AZT (3'-azido-3'-deoxythymidine), and cidofovir (S)-1-[3-hydroxy-2-(phosphonylmethoxypropyl] cytosine), only Ara-C showed a significant effect in decreasing active JCV replication and multiplication. In vitro data, using different cell types and virus strains have shown that specific drugs can indeed modulate viral infection. However, such modulation has not previously been demonstrated in those cells of the CNS which are specifically targeted by JCV. The SVG-JC cells represent a unique system with which further studies can be conducted on the effects of drugs on brain derived cells that are susceptible to viral infection.

Anti-HIV Agents↗

PubMed1998

[Mechanism of IL-6 secretion in bone marrow cells from multiple myeloma patients].

OBJECTIVE: To explore the mechanism of interleukin-6(IL-6) secretion in bone marrow cells from patients with multiple myeloma(MM). METHODS: Expression of IL-6 in bone marrow mononuclear cells(BMMNC) from MM patients(n = 16) and controls(n = 19) was detected by using double labelled immunofluorescence. RESULTS: In MM group, the positive rates of IL-6 expression were 15.4% +/- 6.5% in BMMNC, 7.9% +/- 2.9% in myeloma cells, and 4.5% +/- 1.2% in stromal cells, while in controls the positive rates were 4.6% +/- 2.3% in BMMNC, 2.6% +/- 1.1% in stromal cells and 0.7% +/- 0.1% in plasma cells, respectively. The positive rates in MM group were all significantly higher than those in controls(P < 0.001). The cytoplasmic IgG+ and vWF+ cells percentages in BMMNC were also significantly higher in MM group than those in controls. CONCLUSION: Elevated IL-6 in MM patients was secreted by both myeloma cells and stromal cells, and the mechanism of both autocrine and paracrine may be involved in pathogeneses of multiple myeloma.

Adult↗

PubMed1998

[Mismatched PCR combined with restriction fragment length polymorphism assay for identification of hot spot for mutation in core promoter sequence of hepatitis B virus in Chinese isolates].

OBJECTIVES: To investigate the prevalence of the core promoter variant in Chinese HBV carriers and to explore the clinical and epidemiological problems of the variant. METHODS: A novel method for detecting the double mutation in core promoter was developed. By using an antisense primer that starts at nt 1765 and bears a mismatch at nt 1767, we introduced an artificially created Bcl I cleavage site if the double mutation was present. The prevalence and clinical significance of mutation in the core promoter were investigated in 114 Chinese individuals infected with HBV. RESULTS: Serum samples from 37 asymptomatic carriers and patients harbored core promoter mutant, some with precore mutation. The prevalence was higher in carriers and patients without HBeAg than those with HBeAg. The results in the PCR-RFLP assay perfectly agreed with the data from direct sequencing. CONCLUSION: The presumed core promoter mutations resulting in decreased HBeAg synthesis might be one of the factors leading to persistence of HBV infection and active liver disease.

Adult↗