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Biomedical subjects

W Li

Publications and source records attributed to W Li.

At least 1,279 records · Page 71Linked to original sources
PubMed1992

Role of lymphocytes in silicosis: regulation of secretion of macrophage-derived mitogenic activity for fibroblasts.

We investigated the role of pulmonary lymphocytes in regulating the secretion by alveolar macrophages (AM) of mitogenic activity for lung fibroblasts, in an experimental model of the initial stages of silicotic inflammation and fibrosis. Following intratracheal instillation of silica, pulmonary parenchymal lymphocytes produced a lymphokine(s) that caused modest stimulation of the secretion of mitogenic activity by normal AM. Co-culture of small numbers of lymphocytes from silica-injected animals with AM induced enhanced secretion of fibroblast growth factor activity which was comparable to the maximal response elicited by recombinant interferon-gamma. Lymphocytes from animals given non-fibrogenic titanium dioxide exhibited no such effects. The stimulatory effect of lymphocytes from silica-treated animals in co-culture with macrophages was abrogated when the cells were separated by a microporous membrane. Our findings demonstrate that lymphocytes participating in the response to pulmonary deposition of silica are able to induce the secretion of a growth factor(s) for fibroblasts by pulmonary macrophages, possibly via lymphokines expressed on the cell surface or secreted at sites of cell-to-cell contact.

Animals↗
PubMed1992

[The expression of kainate and GABA receptors in oocytes of Bufo bufo gargarizans].

Oocytes of Bufo bufo gargarizans were used as an expression system for analyzing structure of exogenous membrane protein and their functions. Poly (A)+ mRNA isolated from rat brain was injected into Toad (Bufo bufo gargarizans) oocytes (50 ng/oocyte). Rat brain kainic acid and gamma-aminobutyric acid(GABA) receptors expressed by the injected mRNA were integrated in the oocyte membrane 48 h after the injection at 19 degrees C. Membrane currents induced by kainic acid (5 x 10(-5) mol/L) and GABA (10(-4) mol/L) were 294.0 +/- 6.4 nA (n = 5) and 309.5 +/- 4.9 nA (n = 4) respectively. The kainic acid induced current reached its maximum value at about 10(-3) mol/L. Moreover, it was observed that the 36Cl- influx of the oocytes microinjected with mRNA was one-fold more rapid than the control oocytes. These results indicate that the oocytes of Bufo bufo gargarizans as those of Xenopus laevis can be used to express membrane proteins (receptors & transports) to acquire their proper functions from exogenous mRNA.

Animals↗
PubMed1992

[Research on serotonergic neurons in lateral raphe nucleus of rat with intracellular injection HRP technique].

UNLABELLED: This experiment was carried out on 35 rats with stereotaxic apparatus following a new coordinate which was designed by ourselves. The microelectrode was pushed into the lateral dorsal raphe nucleus (LDR) under direct vision. The neurons with regular rhythm and slow firing rate were searched by intracellular recording, then the singular cell in LDR was filled with HRP by intracellular iontophoresis. RESULTS: 7 HRP labelling neurons with serotoninergic firing characteristics were observed in LDR. The labelling dendrites were found in neighboured structure (periaqueductal gray, laterodorsal tegmental nucleus, dorsal tegmental nucleus, 4th ventricle). This work demonstrated that LDR plays some role in acupuncture analgesia.

Action Potentials↗
PubMed1992

Effectiveness of alpha 2-adrenergic receptor stimulation in reducing the central toxicity following cholinesterase inhibition.

Previous studies in this laboratory have demonstrated that the centrally-acting alpha 2-adrenergic agonist clonidine can offer significant protection against both the acute and chronic toxicity following irreversible cholinesterase inactivation with soman. The purpose of this study was to estimate the contribution of central mechanisms to soman toxicity in a rat model; and to determine the effectiveness of clonidine and a series of related agonists to offer protection against the acute and chronic manifestations of this toxicity. To investigate the central component of soman toxicity, animals were pretreated with the peripherally selective reversible cholinesterase inhibitor pyridostigmine, a standard protective agent. Pyridostigmine pretreatment resulted in significant improvement in survival following soman administration. However, pyridostigmine was not able to inhibit the signs of central soman toxicity, including convulsive behavior. Clonidine and several related drugs produced both a further reduction in lethality and a significant reduction in the central signs of soman toxicity. Signs of delayed toxicity to soman were apparent in rats surviving 48 h after administration as measured in open-field locomotor monitoring. Again, pyridostigmine did not offer protection against such delayed toxicity. When clonidine was included in the regimen, however, significant improvement in performance in this measure was observed. These results are consistent with our earlier findings of significant protection provided by clonidine and related drugs against acute and chronic manifestations of soman toxicity and provide further evidence that 1) central toxicity is an important contributor to soman's actions, and 2) stimulation of central alpha 2-adrenergic receptors limits the expression of this central toxicity.

Adrenergic alpha-Agonists↗
PubMed1992

[Effects of Chinese materia medica in activating blood and stimulating menstrual flow on the endocrine function of ovary-uterus and its mechanisms].

Effects of Salvia miltiorrhiza (SM), Ligusticum chuanxiong (LC) and Artemisia anomale (AA) on the endocrine function of ovary-uterus were studied. In immature Wistar rats, SM increased the level of estradiol (E2) in plasma (131.8 +/- 7.4 pg/ml, P less than 0.01), the weight of uterus (35.3 +/- 4.5 mg, P less than 0.05) and the ovarian PGF2 alpha content (495.0 +/- 41.7 pg/ova., P less than 0.05), but the ovarian PGE2 content was reduced (2198.3 +/- 139.0 pg/ova, P less than 0.01), as compared with that in the control (96.6 +/- 3.2 pg/ml, 23.3 +/- 2.6 mg, 339.0 +/- 30.0 pg/ova, and 3840.8 +/- 480.0 pg/ova. respectively). LC and AA had no influence except that they decrease PGE2 content in ovary (2534.8 +/- 351.3 and 2629.7 +/- 290.7 pg/ova). AA decreased the receptor binding capacity for E2 in uterus (P less than 0.05). SM stimulated the ovulation in immature mice pre-treated with PMSG. LC and AA had no significant effect on ovulation. In pseudopregnant rats (with PMSC-hCG), SM, LC and AA all inhibited the function of corpus luteum, decreased the level of progesterone in plasma (11.1 +/- 2.8, 15.5 +/- 2.5, 19.3 +/- 5.6, respectively, 55.4 +/- 5.4 ng/ml in control, P less than 0.01) and hCG/LH receptor binding capacity of ovary (P less than 0.01). In pseudopregnant animals treated with AA, endogenous PGE2 content of ovary (50.2 +/- 2.7 pg/ml ova.) and the formation of PGE2 form AA in vitro in ovary (1765 +/- 166 pg/mg ova.) were reduced. The PGF2 alpha content in uterus was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Inhibition of growth and metastasis of Lewis lung carcinoma in C57BL mice immunized with PGE2-bovine thyroglobulin conjugate].

C57BL mice were immunized with PGE2 with bovine thyroglobulin (BTG) as protein carrier. One week after immunization, mice were challenged with Lewis carcinoma cells, a tumor with high endogenous production of PGE2. A group of mice orally treated with indomethacin (INDO) was similarly inoculated with the tumor cells for comparison. The results indicated that the PGE2 content in the tumor, as determined by RIA, was very much reduced in both PGE2-immunized and INDO-treated animals. Marked inhibition of tumor growth was observed in PGE2-immunized and in INDO-treated mice, with inhibition rates of 57.4% and 63.1%, respectively. In addition, much less number of lung metastatic foci developed in the two groups of mice as compared to the control (P less than 0.002). BTG had no influence at all on tumor growth and metastatic spread. The results support the view that PGE2 plays an important role in tumor development and metastasis.

Animals↗
PubMed1991

Serum cholesterol concentration and coronary heart disease in population with low cholesterol concentrations.

OBJECTIVE: To examine the relation between serum cholesterol concentration and mortality (from coronary heart disease and from other causes) below the range of cholesterol values generally seen in Western populations. DESIGN: Prospective observational study based on 8-13 years of follow up of subjects in a population with low cholesterol concentrations. SETTING: Urban Shanghai, China. SUBJECTS: 9021 Chinese men and women aged 35-64 at baseline. MAIN OUTCOME MEASURE: Death from coronary heart disease and other causes. RESULTS: The average serum cholesterol concentration was 4.2 mmol/l at baseline examination, and only 43 (7%) of the deaths that occurred during 8-13 years of follow up were attributed to coronary heart disease. There was a strongly positive, and apparently independent, relation between serum cholesterol concentration and death from coronary heart disease (z = 3.47, p less than 0.001), and within the range of usual serum cholesterol concentration studied (3.8-4.7 mmol/l) there was no evidence of any threshold. After appropriate adjustment for the regression dilution bias, a 4 (SD 1)% difference in usual cholesterol concentration was associated with a 21 (SD 6)% (95% confidence interval 9% to 35%) difference in mortality from coronary heart disease. There was no significant relation between serum cholesterol concentration and death from stroke or all types of cancer. The 79 deaths due to liver cancer or other chronic liver disease were inversely related to cholesterol concentration at baseline. CONCLUSION: Blood cholesterol concentration was directly related to mortality from coronary heart disease even in those with what was, by Western standards, a "low" cholesterol concentration. There was no good evidence of an adverse effect of cholesterol on other causes of death.

Cerebrovascular Disorders↗
PubMed1991

Characterization of neuropeptide Y (NPY) receptors in human hippocampus.

We identified a 50 kDa neuropeptide Y (NPY) receptor from human hippocampus by affinity labeling. NPY specific binding and labeling of the receptor were inhibited in parallel by increasing concentrations of unlabeled NPY (IC50 = 0.27 nM and 0.18 nM, respectively). Peptide YY (PYY), but none of the pancreatic polypeptides, was as effective as NPY in displacing [125I]NPY. NPY fragments inhibited binding with the rank order of potency: NPY greater than NPY13-36 greater than NPY20-36 greater than or equal to NPY18-36 greater than NPY1-36 free acid greater than or equal to NPY26-36. These results demonstrate that the human hippocampal NPY receptor is a 50 kDa protein fitting the classification of a Y2 receptor subtype.

Affinity Labels↗
PubMed1991

Expression of interleukin-6 and interleukin-6 receptor in Hodgkin's disease.

Interleukin-6 (IL-6) is a multipotent lymphokine that can mediate differentiation of B cells into Ig-secreting cells, stimulate the growth of plasmacytomas, hybridomas, and T cells, and induce acute-phase proteins in liver cells. It has been suggested that IL-6 is involved in the pathogenesis of several diseases by autocrine or paracrine pathways. To examine whether IL-6 is possibly involved in the pathophysiology of Hodgkin's disease (HD), we analyzed the expression of IL-6 and IL-6 receptor mRNA and protein in cell lines and primary specimens from patients with HD. IL-6-specific transcripts were detected in three of six HD-derived cell lines by Northern blot analysis. In the culture supernatants of four HD-derived cell lines, IL-6 was detected by radioimmunoassay. Biologic activity of IL-6 was confirmed by proliferation of an IL-6-dependent cell line. In situ hybridization experiments showed IL-6-specific transcripts in Hodgkin (H) and Reed-Sternberg (RS) cells in primary tissues of two patients. In addition, mRNAs specific for the IL-6 receptor were detected in five HD-derived cell lines. Immunostaining experiments showed expression of IL-6 receptor molecules on H and RS cells in 8 of 16 cases with HD. Thus, our data suggest that IL-6 might be involved in the pathophysiology of HD.

Antibodies, Monoclonal↗
PubMed1991

Benextramine irreversibly inhibits [125I]neuropeptide Y affinity labeling of the Y2 binding protein in bovine hippocampus.

Affinity labeling of iodinated neuropeptide Y (NPY) to bovine hippocampal binding proteins revealed that benextramine inhibited specific NPY labeling of the 50 kDa NPY binding protein (Y2 binding protein) in a dose-dependent manner (IC50 = 33 microM). Hippocampal membranes, which were pretreated with benextramine and washed, exhibited decreased [125I]NPY labeling of binding proteins in a similar dose-dependent manner. These findings demonstrate that benextramine irreversibly blocks specific NPY binding to the 50 kDa NPY Y2 binding protein.

Affinity Labels↗
PubMed1991

Tyrosine phosphorylation of a common 57-kDa protein in growth factor-stimulated and -transformed cells.

Protein tyrosine phosphorylation was studied in macrophages and fibroblasts to identify putative components of post-receptor mitogenic pathways that might be functionally conserved in different cell types. Nondenaturing conditions were established for the approximately quantitative recovery of anti-phosphotyrosine antibody (alpha PY)-reactive proteins from cells. A common, 57-kDa alpha PY-reactive protein was identified by V8 protease peptide mapping in colony-stimulating factor-1 (CSF-1)- or granulocyte-macrophage colony-stimulating factor (GM-CSF)-stimulated BAC1.2F5 macrophages, in platelet-derived growth factor-stimulated NIH-3T3 cells, and in CSF-1-stimulated NIH-3T3 cells expressing the c-fms/CSF-1 receptor. The 57-kDa protein was phosphorylated on serine and tyrosine and was the only alpha PY-reactive protein band whose phosphorylation was reproducibly increased in GM-CSF-stimulated cells. The effect of the growth factors on the tyrosine phosphorylation of the 57-kDa protein could be mimicked by treatment of the cells with orthovanadate, a phosphotyrosine protein phosphatase inhibitor. In the absence of growth factors, tyrosine phosphorylation of the 57-kDa protein was higher in v-fms or c-fms (F969, S301)-transformed NIH-3T3 cells than in untransformed NIH-3T3 (c-fms) and NIH-3T3 (c-fms, F969) cells. These data indicate that the 57-kDa protein is a common target for growth factor-stimulated tyrosine phosphorylation and potentially important for growth factor mitogenic signaling.

Animals↗
PubMed1991

The structure of a key intermediate in the total synthesis of dendrobine.

(1R*,4R*,5S*,8R*,11S*)-3,11-Dimethyl-5-hydroxy-6-isopropyl-3-azatricy clo[6.2.1.0(4,11)]undec-6-en-2-one, C15H23NO2, Mr = 249.35, monoclinic, P2(1)/c, a = 7.782(2), b = 23.119(4), c = 7.932(2) A, beta = 101.53 (2)degrees, V = 1398.1(5) A3, Z = 4, Dx = 1.184 g cm-3, Mo K alpha, gamma = 0.7107 A, mu = 0.7259 cm-1, F(000) = 544, T = 298 K, R = 0.0464 for 1887 reflections (F0 greater than or equal to 4[sigma (F0)]). The molecules are H-bonded into infinite columns parallel to c involving the hydroxyl group and the carbonyl O atom [O15...O13(x,y,z-1) 2.756(2); H15...O13 1.84(3) A; O-H...O 173(3) degrees]. The bonds from the bridgehead atom of the tricyclic ring to other ring atoms appear to be elongated [av. 1.549(2) A] compared to the other Csp3-Csp3 bonds in the molecule.

Alkaloids↗
PubMed1991

Role of dimerization and modification of the CSF-1 receptor in its activation and internalization during the CSF-1 response.

We have used kinetic and cross-linking approaches to study CSF-1-induced changes in the structure and function of the CSF-1R. Addition of CSF-1 to cells stimulates or stabilizes non-covalent CSF-1R dimerization resulting in activation of the CSF-1R kinase and the tyrosine phosphorylation of the receptor and certain cytoplasmic proteins. The non-covalent dimers become covalently linked via disulfide bonds and/or are subsequently further modified. These modified forms are selectively internalized. Pre-treatment of cells with the alkylating agent, iodoacetic acid (IAA), selectively inhibits covalent dimerization, modification and internalization but enhances protein tyrosine phosphorylation. It is proposed that ligand-induced non-covalent dimerization activates the CSF-1R kinase, whereas the covalent dimerization and subsequent modification lead to kinase inactivation, phosphotyrosine dephosphorylation and internalization of the receptor--ligand complex.

Animals↗
PubMed1991

Primary culture of adult mouse lung fibroblasts in serum-free medium: responses to growth factors.

We report a completely serum-free system for primary culture of fibroblasts from explants of adult mouse lung tissue which permits bioassays for cytokine activity to be performed using unselected populations of cells at low passage number, without interference by serum binding proteins or interacting growth factors. Cultures were established on collagen-coated surfaces in medium MCDB 201 containing albumin, transferrin, epidermal growth factor, lipids, prostaglandin E1, vitamin E, and reducing agents. The cells were morphologically and ultrastructurally typical of fibroblasts in culture and demonstrated expression of vimentin and induction of expression of desmin in culture. Proliferation of the cells was reproducible between different primary cultures and was growth factor dependent. Both cycling and growth-arrested cells exhibited increased DNA synthesis when stimulated with epidermal growth factor, platelet-derived growth factor, or basic fibroblast growth factor, which functioned as complete mitogens, but did not respond to insulin, tumor necrosis factor or interleukin-1 beta. Maximal induction of DNA synthesis by epidermal growth factor required the continued presence of the mitogen in the culture medium. These results cannot be satisfactorily explained by the competence-progression model of responses to mitogenic stimuli but support and extend the findings of other studies using diploid fibroblasts.

Animals↗
PubMed1991

Carboxy-terminal truncations of epidermal growth factor (EGF) receptor affect diverse EGF-induced cellular responses.

The binding of epidermal growth factor (EGF) to its receptor induces tyrosine phosphorylation of phospholipase C gamma (PLC gamma), which appears to be necessary for its activation leading to phosphatidyl inositol (PI) hydrolysis. Moreover, EGF-receptor (EGF-R) activation and autophosphorylation results in binding of PLC gamma to the tyrosine phosphorylated carboxy-terminus of the receptor. To gain further insights into the mechanisms and interactions regulating these processes, we have analyzed transfected NIH-3T3 cells expressing two EGF-R carboxy-terminal deletion mutants (CD63 and CD126) with reduced capacity to stimulate PI hydrolysis, Ca2+ rises, and DNA synthesis. In fact, the CD126 mutant lacking 126 carboxy-terminal amino acids, including four tyrosine autophosphorylation sites, was unable to stimulate PI hydrolysis or Ca2+ rise in response to EGF. Surprisingly, EGF binding to the cell lines expressing CD63 or CD126 mutants was followed by similar stimulation of tyrosine phosphorylation of PLC gamma. Our results suggest that although necessary, tyrosine phosphorylation of PLC gamma may not be sufficient for stimulation and PI hydrolysis. It is clear, however, that the carboxy-terminal region of EGF-R is involved in regulation of interactions with cellular targets and therefore plays a crucial role in postreceptor signaling pathways.

3T3 Cells↗