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Biomedical subjects

J Lin

Publications and source records attributed to J Lin.

At least 469 records · Page 26Linked to original sources
PubMed1997

Studies on efficacy of praziquantel and mebendazole-medicated salt in treatment of Echinochasmus fujianensis infection.

The therapeutic effect of praziquantel and mebendazole-medicated salt has been studied in 109 cases with Echinochasmus fujianensis infection. These cases were randomly divided into four groups: 2 groups with a single dose of praziquantel 5 mg/kg or 2.5 mg/kg; and other 2 groups with mebendazole 800mg or 400 mg in 10d table salt. Four weeks after treatment, the egg negative conversion rates were 100%, 92.3%, 85.2% and 71.4% respectively, the egg reduction rates were 84.8-100%, and side-effects were mild. The symptoms caused by infection such as abdominal pain, diarrhea, distension and anorexia were obviously relieved. These data indicated that praziquantel is the drug of choice in the treatment of Echinochasmus fujianensis. The dosage is only 2.5 mg/kg, and its egg negative conversion rate and reduction rate reach 92.3% and 95.4%, respectively. For convenience, the dosage can be made according to their age. Children under 12 take half a tablet (100 mg), and one tablet (200 mg) for those over 12. This dosage is approximately equal to 2.5-5.0 mg/kg. Although the efficacy of mebendazole is lower than praziquantel, its egg negative conversion rate also reaches 71.4-85%. Mebendazole-medicated salt can be used for treating Echinochasmus fujianensis infection as the presence of co-infection with nematodes.

Adolescent↗
PubMed1997

Research on the mechanism of endothelin inflammatory effects on human mesangial cells.

OBJECTIVE: To investigate the mechanism of endothelin (ET) inflammatory effects on human mesangial cells (HMC). METHODS: The following experiments were performed on cultured HMC after ET-1 stimulation: (1) the expression of tumor necrosis factor-alpha (TNF alpha), interleukin-1 beta (IL-1 beta), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelin-1 (ET-1) itself messenger ribonucleic acid (mRNA) was determined by Northern Blot analysis; (2) the TNF alpha concentration was tested with radioimmunoassay; the IL-1 activity was assayed by the enhancement of thymocyte proliferation in response to mitogen; the surface expression of ICAM-1 and VCAM-1 was measured with cell enzyme linked immunoadsorbent assay (ELISA) analysis. RESULTS: ET-1 (10(-7) mol/L) induced the following changes on HMC: (1) up-regulation of the expression of TNF alpha mRNA and protein; (2) up-regulation of the expression of ICAM-1 and VCAM-1 mRNA and protein; (3) up-regulation of the expression of ET-1 itself mRNA. However, the expression of IL-1 mRNA and protein was not changed. CONCLUSIONS: ET-1 can stimulate HMC to produce TNF alpha, ICAM-1 and VCAM-1, and thereby induce inflammatory effects. ET-1 can also stimulate HMC to up-regulate the expression of ET-1 itself, so as to amplify inflammatory effects. So, ET-1 is actually an inflammatory mediator and may play an important role in the pathogenesis of glomerulonephritis.

Cells, Cultured↗
PubMed1997

[Clinical evaluation on laparoscopic diagnosis of pelvic endometriosis by heat-colour test with endocoagulation].

OBJECTIVE: To assess the value of heat-colour test (HCT) with endocoagulation under laparoscopy as a new method for diagnosis of pelvic endometriosis (EM). METHODS: Laparoscopic visible examination (LVE), lesion biopsy and HCT with endocoagulation were employed for diagnosis of EM in 83 cases of infertility. Brown-black colour changes of peritoneal tissue after endocoagulation with controlled heating (100 C) indicate EM implants (HCT positive). RESULTS: LVE indicated that 35 cases had peritoneal lesions typical of EM in appearance. HCT was positive in all cases of visible EM lesions. 48 cases showed no visible peritoneal lesions by LVE, but nonpigmented peritoneal EM lesions were detected by HCT in 20 of the 48 cases. A variety of gross appearances of nonpigmented EM lesions were found in our study including: peritoneal hyperemia (70.9%), circular peritoneal defects (12.7%), semitransparant glandular excrescences (10.9%), white opacification of the peritoneum (10.9%) and normal appearance (5.4%). 25 biopsies were taken from nonpigmented peritoneal lesions in 13 cases. Histology examinations revealed the presence of EM in 64.0% of them. CONCLUSIONS: HCT is a reliable, sensitive and accurate method for diagnosis of EM. It can overcome multiple factors for missing diagnosis of EM by LVE and biopsy. The clinical significance of HCT is its ability to detect nonpigmented endometriotic lesions, to differentiate the causes of pelvic adhesions, therefore to increase accuracy of FIGO EM staging under laparoscopy.

Endometriosis↗
PubMed1997

[Infective factors of adult secretory otitis media].

There were histories of the upper expiratory tract infection in 49 out of 86 cases in adult secretory otitis media (SOM). Among them, thirty two cases were administrated antibiotics a week ago when the effusions were collected. The patient's Eustachian tubes in twenty nine cases were clinically ventilated. The endotoxins were positive in 39 out of 86 specimen tested with limulus assay, among these specimen, bacteria were cultured from 11 specimen. The data exibited that the appearance of the SOM is related to the existence of the infective factors in the middle ear cavity. The upper expiratory tract infection before the onset of the middle ear effusions is one of the important causes inducing the disease. The lower rate of bacteria culture than that of endotoxins is related with the administration of antibiotics before the onset of the disease. The administration of antibiotics in the treatment of the middle ear effusions will help to elimilate bacteria in the cavity of the middle ear effusions, improve the ventilating function of the Eustachian tube and make the effusions turn to disappearance.

Adolescent↗
PubMed1996

Blockade of multiple costimulatory receptors induces hyporesponsiveness: inhibition of CD2 plus CD28 pathways.

T-lymphocyte activation requires engagement of the T cell receptor with antigen-major histocompatibility complex, and simultaneous ligation of costimulatory pathways via the lymphocyte receptors CD2 and CD28/ CTLA4. Anti-CD2 monoclonal antibody (mAb) blocks the interaction of the antigen-presenting cell receptor CD48 with its ligand CD2, whereas CTLA4Ig binds with high affinity to the antigen-presenting cell ligands B7-1 and B7-2, blocking their interaction with CD28/CTLA4. We tested the immunosuppressive effects of simultaneously blocking both costimulatory pathways. Using donor C57BL/6J (H2b) hearts transplanted to CBA/J (H2k) recipients, anti-CD2 mAb plus CTLA4Ig administered at the time of transplantation prolonged cardiac allograft mean survival time to >120 days compared with untreated controls (12.2+/-0.5 days, P<0.01), anti-CD2 mAb alone (24.8+/-1.0 days, P<0.01), or CTLA4Ig alone (55.0+/-2.0 days, P<0.01). Retransplantation of these recipients with donor-specific and third-party grafts demonstrated that hyporesponsiveness and tolerance were achieved. In vitro stimulation of lymphocytes from tolerant recipients with donor-specific alloantigen resulted in normal cytotoxic T lymphocyte and mixed lymphocyte reaction responses, showing that clonal deletion or anergy did not occur, but that graft adaptation or suppression likely helped to maintain long-term graft survival. In vitro combinations of anti-CD2 mAb and CTLA4Ig suppressed the generation of allogeneic cytotoxic T lymphocytes (58%) and the mixed lymphocyte reaction (36%); CTLA4Ig was more effective in this regard and the two agents were not synergistic. Anti-CD2 mAb and CTLA4Ig suppressed mitogen-driven proliferation in differential fashions, suggesting that they affected independent signaling pathways. Anti-CD2 mAb and CTLA4Ig also inhibited interleukin (IL)-2, IL-4, and IL-2 receptor (CD25). These data indicate that anti-CD2 mAb plus CTLA4Ig induces hyporesponsiveness and tolerance. The mechanism is likely related to the initial disruption of independent pathways of T-lymphocyte activation leading to antigen-specific long-term graft survival.

Abatacept↗
PubMed1996

Nonpeptidal P2 ligands for HIV protease inhibitors: structure-based design, synthesis, and biological evaluation.

Design and synthesis of nonpeptidal bis-tetrahydrofuran ligands based upon the X-ray crystal structure of the HIV-1 protease-inhibitor complex 1 led to replacement of two amide bonds and a 10 pi-aromatic system of Ro 31-8959 class of HIV protease inhibitors. Detailed structure-activity studies have now established that the position of ring oxygens, ring size, and stereochemistry are all crucial to potency. Of particular interest, compound 49 with (3S,3aS,6aS)-bis-Thf is the most potent inhibitor (IC50 value 1.8 +/- 0.2 nM; CIC95 value 46 +/- 4 nM) in this series. The X-ray structure of protein-inhibitor complex 49 has provided insight into the ligand-binding site interactions. As it turned out, both oxygens in the bis-Thf ligands are involved in hydrogen-bonding interactions with Asp 29 and Asp 30 NH present in the S2 subsite of HIV-1 protease. Stereoselective routes have been developed to obtain these novel ligands in optically pure form.

Amino Acid Sequence↗
PubMed1996

Calcineurin mediates calcium-induced potentiation of adenylyl cyclase activity in dispersed chief cells from guinea pig stomach. Further evidence for cross-talk between signal transduction pathways that regulate pepsinogen secretion.

In cholera toxin-treated gastric chief cells, incubation with a cholinergic agonist (carbamylcholine), a regulatory peptide (cholecystokinin), or a calcium ionophore (A23187) causes a dose- and time-dependent potentiation of cAMP levels. Because this augmented response is calcium/calmodulin-dependent, we hypothesized that it was mediated by calcineurin (protein phosphatase 2B). To test this hypothesis, we examined the actions of calcineurin inhibitors on secretagogue-induced potentiation of cAMP levels in guinea pig chief cells. Preincubation of cells with 0.1 microM FK-506 completely prevented carbachol-induced augmentation of cAMP levels and pepsinogen secretion from cholera toxin-treated cells. Cyclosporin-A, another calcineurin inhibitor, also prevented the augmented cAMP response. FK-506 and cyclosporin inhibited augmentation of cAMP levels following treatment with cholecystokinin(26-33) and A23187, but not the smaller increase in cAMP following treatment with a phorbol ester that activates protein kinase C. Hence, the actions of calcineurin inhibitors were limited to secretagogues that increase cellular calcium. Rapamycin, an agent that competes with FK-506 for the immunophilin, FK binding protein 12, does not inhibit calcineurin. In the present study, preincubation with rapamycin did not prevent carbachol-induced augmentation of cAMP levels in cholera toxin-treated chief cells. However, a molar excess of rapamycin reversed the inhibitory actions of FK-506. These experiments provide further evidence that the actions of FK-506 on cholera toxin-treated gastric chief cells are caused by its inhibitory actions on calcineurin. FK-506 also inhibited potentiation of cAMP levels when carbachol was added to cells that were preincubated with forskolin, an agent that directly activates adenylyl cyclase. We conclude that, in gastric chief cells, calcineurin mediates cross-talk between the calcium/calmodulin and adenylyl cyclase signaling pathways.

Adenylyl Cyclases↗
PubMed1996

Actions and expression of RAB-GDP dissociation inhibitor in dispersed chief cells from guinea pig stomach.

Rab proteins are a family of ras-like proteins that are involved in intracellular membrane trafficking. Rab-GDP dissociation inhibitor prevents dissociation of GDP from Rab proteins and extracts Rab proteins from cell membranes in vitro. In the present study, we examined the effects of recombinant rab-GDI on Rab proteins in gastric chief cells. Rab-GDI extracted GTP-binding proteins, including Rab3 and Rab5, from chief cell membranes in a dose-dependent manner. Maximal concentrations of rab-GDI (> or = 50 micrograms/ml) removed approx. 40% of membrane-associated Rab3. Moreover, preincubation of permeabilized chief cells with rab-GDI resulted in a 35% decrease in GTP gamma S(100 microM)-induced pepsinogen secretion, suggesting that membrane-associated Rab proteins are involved in the final stages of secretion. Immunostaining of chief cell cytosolic and membrane fractions with GDI-specific antisera revealed bands at 56 and 48 kDa, respectively, indicating that chief cells express two isoforms of rab-GDI. In gastric chief cells, regulation of Rab proteins by rab-GDI plays an important role in mediating exocytosis.

Animals↗
PubMed1996

Surface-epitope masking and expression cloning identifies the human prostate carcinoma tumor antigen gene PCTA-1 a member of the galectin gene family.

The selective production of monoclonal antibodies (mAbs) reacting with defined cell surface-expressed molecules is now readily accomplished with an immunological subtraction approach, surface-epitope masking (SEM). Using SEM, prostate carcinoma (Pro 1.5) mAbs have been developed that react with tumor-associated antigens expressed on human prostate cancer cell lines and patient-derived carcinomas. Screening a human LNCaP prostate cancer cDNA expression library with the Pro 1.5 mAb identifies a gene, prostate carcinoma tumor antigen-1 (PCTA-1). PCTA-1 encodes a secreted protein of approximately 35 kDa that shares approximately 40% sequence homology with the N-amino terminal region of members of the S-type galactose-binding lectin (galectin) gene family. Specific galectins are found on the surface of human and marine neoplastic cells and have been implicated in tumorigenesis and metastasis. Primer pairs within the 3' untranslated region of PCTA-1 and reverse transcription-PCR demonstrate selective expression of PCTA-1 by prostate carcinomas versus normal prostate and benign prostatic hypertrophy. These findings document the use of the SEM procedure for generating mAbs reacting with tumor-associated antigens expressed on human prostate cancers. The SEM-derived mAbs have been used for expression cloning the gene encoding this human tumor antigen. The approaches described in this paper, SEM combined with expression cloning, should prove of wide utility for developing immunological reagents specific for and identifying genes relevant to human cancer.

Amino Acid Sequence↗
PubMed1996

cDNA sequence analysis and expression of cardiotoxin V and a new cardiotoxin VII from Naja naja atra (Taiwan cobra).

The cDNAs encoding cardiotoxin V and a new cardiotoxin VII were constructed from the cellular RNA isolated from the venom glands of Naja naja atra by reverse transcription-polymerase chain reaction. Although 95% nucleotide sequence homology was observed with the two cardiotoxins, there were nine amino-acid substitutions between cardiotoxin V and cardiotoxin VII. The cardiotoxins were subcloned into the expression vector pET 20b(+) and transformed into BL21(DE3) E. coli strain. The expressed protein was isolated from the inclusion bodies of E. coli, and purified by reverse-phase high-performance liquid chromatography. The purified recombinant cardiotoxin showed immunoreactivity with anti-cardiotoxin III antibodies as revealed by immunoblot analysis.

Amino Acid Sequence↗
PubMed1996

The role of Glu 57 in the mechanism of the Escherichia coli MutT enzyme by mutagenesis and heteronuclear NMR.

The role of the conserved residue Glu-57 in the mechanism of the MutT enzyme from Escherichia coli was investigated by mutagenesis and heteronuclear NMR methods. The enzymatic activity of the E57Q mutant is at least 10(5)-fold lower than that of the wild type enzyme. The solution structure of the E57Q mutant, based on comparisons of 1H-15N NOESY HSQC spectra and 1H-15N HSQC spectra to those of the wild type enzyme, differs in a region near Glu-57. The dissociation constants (KD) of the E-Mg2+ and E-Mn2+ complexes increased 3.3- and 3.6-fold, respectively, in the E57Q mutant, while the KD of E-dGTP is unaltered from that of the wild type enzyme. The enhanced paramagnetic effect of enzyme-bound Mn2+ on 1/T1 of water protons is halved in the E57Q mutant indicating an altered metal-binding site. 1H-15N HSQC titrations of E57Q with MnCl2 show selective attenuation of the side chain NH signals of Gln-57 and the backbone NH signals of Gly-37, Gly-38, Lys-39, Glu-53, Glu-56, Gln-57, and Glu-98, indicating proximity of bound Nm2+ to these residues. The same resonances of the wild type and the E57Q mutant enzymes are attenuated by Mn2+, but significantly smaller paramagnetic effects (relative to the largest effect on Lys-39) are found on Gly-37, Gly-38, Val-58, and Glu-98 of the mutant, indicating an altered position of the bound divalent cation. Thus Glu-57 is probably a ligand to the enzyme-bound metal, and the profound loss of catalytic activity in the E57Q mutant results from structural and electronic changes at the site of the enzyme-bound divalent cation. 1H-15N HSQC titrations of the wild type enzyme with MgCl2 show changes in chemical shifts of 15N and NH resonances in regions closely overlapping those induced by the E57Q mutation itself, suggesting that the loss of the negative charge at Glu-57, either by mutation or by neutralization with Mg2+, induces a similar effect. In the E57Q mutant, the slow exchange of the side chain NH2 protons of Gln-57 and NOE's from the NH2 protons of Gln-57 to the beta and gamma protons of Glu-98 suggests hydrogen bonding of Gln-57 to Glu-98 in the free enzyme. 1H-15N HSQC titrations of both the wild type and mutant enzymes with dGTP show changes in 15N and NH chemicals shifts of residues in a cleft formed by beta-strands A, C, and D on one side and loop I, the end of loop IV, and the beginning of helix II on the other side, suggesting this cleft to be the nucleotide binding site. These changes in chemical shift were smaller or absent in titrations of the wild type or mutant enzymes with AMPCPP or Mg2+-AMPCPP, in accord with the strong preference of the MutT enzyme for guanine over adenine nucleotide substrates.

Amino Acid Sequence↗
PubMed1996

The cotranslational integration of membrane proteins into the phospholipid bilayer is a multistep process.

During the cotranslational integration of a nascent protein into the endoplasmic reticulum membrane, the transmembrane (TM) sequence moves out of an aqueous pore formed by Sec61alpha, TRAM, and other proteins and into the nonpolar lipid bilayer. Photocross-linking reveals that this movement involves the sequential passage of the TM domain through three different proteinaceous environments: one adjacent to Sec61alpha and TRAM and two adjacent to TRAM that place different restrictions on TM domain movement. In addition, the TM sequence is not allowed to diffuse into the bilayer from the final TRAM-proximal site until translation terminates. Cotranslational integration is therefore linked to translation and occurs via an ordered multistep pathway at an endoplasmic reticulum site that is multilayered both structurally and functionally.

Cross-Linking Reagents↗