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Biomedical subjects

L J Yang

Publications and source records attributed to L J Yang.

At least 37 records · Page 2Linked to original sources

Hepatic injury during ketoconazole therapy in patients with onychomycosis: a controlled cohort study.

To evaluate the incidence, severity, and course of ketoconazole-associated hepatic injury, 211 patients with onychomycosis were randomized by a ratio of 2:1 to receive either ketoconazole (137 patients) or griseofulvin (74 patients). All of them were seronegative for hepatitis B surface antigen (HBsAg) and anti-hepatitis C virus (HCV) and had no biochemical abnormality before therapy. The two groups were comparable in age, sex, and pretherapy liver biochemical tests. Liver biochemical tests were followed up biweekly for 3 months, and then at monthly intervals during the remaining course of therapy. No biochemical abnormality or hepatic injury was found in patients during griseofulvin treatment. Of the patients treated with ketoconazole, 24 (17.5%; 95% confidence interval [CI], 11.1% to 23.9%) showed asymptomatic transaminase elevation. Ketoconazole was discontinued immediately after overt hepatitis developed in another 4 patients (2.9%; 95% CI, 0.1% to 5.7%) who did not succumb to hepatic decompensation. The abnormal biochemical changes in patients with overt hepatitis returned to normal after discontinuing ketoconazole. Elderly patients were more prone to develop overt hepatitis. In patients with asymptomatic liver injury, the abnormal biochemical changes gradually returned to normal despite continuing ketoconazole therapy. The results of this cohort study suggest that ketoconazole-induced overt hepatitis is more common than previously believed and that transient subclinical injury is much more common than overt hepatitis. Therapy with ketoconazole may be continued with caution in the absence of symptoms and/or hyperbilirubinemia, but should be discontinued if overt hepatitis occurs.

Adult↗

Immunohistochemical demonstration of bone morphogenetic protein in odontogenic tumors.

The aim of the present study was to describe the expression and distribution of bone morphogenetic protein (BMP) in odontogenic tumors by immunohistochemistry using monoclonal antibody against bovine BMP (BMPMcAb). Eight types of odontogenic tumors (44 cases), including ameloblastoma (20 cases), cementifying fibroma (8 cases), benign cementoblastoma (5 cases), dentinoma (3 cases), compound odontoma (2 cases), adenomatoid odontogenic tumor (2 cases), calcifying epithelial odontogenic tumor (2 cases) and odontogenic fibroma (2 cases), were studied. The results showed that, according to the immunostaining pattern of BMPMcAb, tumors could be classified into two types: all cementifying fibromas, benign cementoblastomas, dentinomas, odontogenic fibromas, and compound odontomas demonstrated a positive reaction, whereas all ameloblastomas, adenomatoid odontogenic tumors, and calcifying epithelial odontogenic tumors were negative. BMPMcAb-positive odontogenic tumors were those tumors with formation of enamel, dentin, cementum or bone. Therefore, BMP might play an important role in the formation of calcified dental tissues and the development of odontogenic tumors contaning such tissues.

Ameloblastoma↗

Mutational analysis of the potato virus Y 5' untranslated region for alteration in translational enhancement in tobacco protoplasts.

The 185 nucleotide 5' untranslated region (5'UTR) of potato virus Y ordinary strain (PVY-O) showed translation-enhancing activity on the beta-glucuronidase (GUS) gene in tobacco protoplasts. Mutational analysis of the 5'UTR was done to find sequence motifs necessary for the enhancement. Deletions within the 1-130 nucleotide region of 5'UTR stimulated the GUS expression in some cases, while the GUS activity declined with deletions in the 131-185 nucleotide region. The results indicated that the last 55 nucleotides of PVY-O 5'UTR might play the much important role in the translational enhancement in plant cells.

Amino Acid Sequence↗

Detection and isolation of lectin-transfected COS cells based on cell adhesion to immobilized glycosphingolipids.

Two methods are described, one for detection and one for isolation of COS cells transiently expressing vertebrate lectins. The methods are based on specific cell adhesion to polystyrene microwells or magnetic beads adsorbed with glycosphingolipids. In the first method, glycolipids were adsorbed to wells of 96-well polystyrene plates. A suspension of lectin-transfected COS cells was added and the plate was incubated to allow cell adhesion to occur. The plate was then immersed in buffer, inverted (while immersed), and placed in a fluid-filled Plexiglas centrifugation chamber which was sealed to avoid introducing an air-liquid interface. The chamber, with the inverted plate enclosed, was centrifuged to remove nonadherent cells. The plate was then removed from the carrier (while immersed) and righted, and adherent cells were quantitated enzymatically or immunochemically using a 96-well plate reader. COS cells transfected with an expression plasmid carrying the gene for the rat Kupffer cell lectin (fucose and N-acetylgalactosamine specific) adhered specifically to globotetraosylceramide. Glycolipid- and lectin-specific cell adhesion was readily detected even when COS cells were transfected with a plasmid mixture containing 0.5% lectin-carrying plasmid and 99.5% irrelevant plasmid. This sensitivity will facilitate screening of plasmid pools to detect and isolate plasmids expressing mammalian lectin genes. To isolate COS cells transiently expressing lectin, glycosphingolipids were adsorbed to carboxylated magnetic polystyrene microspheres, which were mixed with the lectin-transfected COS cells. Adherent cells were collected on a fixed magnet and plasmid recovered for subsequent amplification.

Adsorption↗

Gangliosides are neuronal ligands for myelin-associated glycoprotein.

Nerve cells depend on specific interactions with glial cells for proper function. Myelinating glial cells are thought to associate with neuronal axons, in part, via the cell-surface adhesion protein, myelin-associated glycoprotein (MAG). MAG is also thought to be a major inhibitor of neurite outgrowth (axon regeneration) in the adult central nervous system. Primary structure and in vitro function place MAG in an immunoglobulin-related family of sialic acid-binding lactins. We report that a limited set of structurally related gangliosides, known to be expressed on myelinated neurons in vivo, are ligands for MAG. When major brain gangliosides were adsorbed as artificial membranes on plastic microwells, only GT1b and GD1a supported cell adhesion of MAG-transfected COS-1 cells. Furthermore, a quantitatively minor ganglioside expressed on cholinergic neurons, GQ1b alpha (also known as Chol-1 alpha-b), was much more potent than GT1b or GD1a in supporting MAG-mediated cell adhesion. Adhesion to either GT1b or GQ1b alpha was abolished by pretreatment of the adsorbed gangliosides with neuraminidase. On the basis of structure-function studies of 19 test glycosphingolipids, an alpha 2,3-N-acetylneuraminic acid residue on the terminal galactose of a gangliotetraose core is necessary for MAG binding, and additional sialic acid residues linked to the other neutral core saccharides [Gal(II) and GalNAc(III)] contribute significantly to binding affinity. MAG-mediated adhesion to gangliosides was blocked by pretreatment of the MAG-transfected COS-1 cells with anti-MAG monoclonal antibody 513, which is known to inhibit oligodendrocyte-neuron binding. These data are consistent with the conclusion that MAG-mediated cell-cell interactions involve MAG-ganglioside recognition and binding.

Animals↗

Distinctive ganglioside patterns revealed by anti-ganglioside antibody binding to differentiating CG-4 oligodendrocytes.

Oligodendrocytes are central nervous system glial cells responsible for myelination of neuronal axons. During brain development oligodendrocyte progenitor cells progress through a series of morphologically and immunohistochemically distinct differentiation steps leading to mature myelin-producing oligodendrocytes. Much of this same differentiation sequence is expressed in vitro by primary oligodendrocyte progenitor cells, and by the clonal progenitor cell line CG-4. We report the use of highly specific monoclonal antibodies against GM1, GD1a, GD1b, GT1b, and GQ1b to determine major brain ganglioside expression and morphological distribution during CG-4 differentiation in vitro. Prominent anti-GD1b antibody stained defined a highly arborized intermediate stage of oligodendrocyte differentiation. In contrast, anti-GT1b antibody bound to discrete patches on the cell bodies of early progenitor cells and more mature oligodendrocytes, and to sites of progenitor arborization. The other anti-ganglioside antibodies tested did not bind above background levels. Cells with anti-GD1b antibody binding and morphology similar to those in differentiating CG-4 cells were detected in rat brain primary cell cultures enriched in oligodendrocyte precursors. The remarkably distinctive ganglioside immunoreactivity on differentiating oligodendrocytes suggests the possibility of a functional role for their surface expression.

Animals↗

[Expression of Bcl-2 gene product in oral lymphoma of mucosa associated lymphoid tissue].

Bcl-2 (B cell leukemia/lymphoma-2), one of apoptosis-suppressing genes, can inhibit apoptosis of both some normal and tumor cells, and is related to the development of some tumors. In present study, the expression of bcl-2 was examined in 26 cases of oral lymphomas of mucosa associated lymphoid tissue (LMALT) using immunohistochemistry. The results showed that 73% of LMALT were positive to bcl-2 antibody. Among three main histological subtypes, the small-cleaved cell type demonstrated highest positive persentage (83%), followed by lymphoplasmacytoid lymphoma (71%) and lymphoplasmacytic lymphoma (51%). In respect to immunological subtypes, bcl-2 was detected in 69% of B cell lymphoma, 75% of T cell lymphoma, and 83% of lymphomas which could not be classified by present immunohistochemistry repectively. The results indicated that the inhibition of apoptosis might not be one of reasons for the development of some LMALT.

Adolescent↗

Clear cell papulosis: report of three cases of a newly recognized disease.

BACKGROUND: Clear cell papulosis is a newly described disease. Since the first report in 1987, no other cases have been reported. OBJECTIVE: Our purpose was to describe three more newly identified cases that further characterize this disease. METHODS: Formalin-fixed and paraffin-embedded biopsy specimens were used for histochemical and immunohistochemical studies. RESULTS: The three patients included two boys and, for the first time, a girl. All three had multiple white papules on the lower part of the abdomen, with or without scattered lesions along the milk lines bilaterally. The main histopathologic finding was the presence of clear cells scattered mainly among the basal cells of the acanthotic epidermis. The clear cells were variably stained by mucicarmine, colloidal iron, alcian blue (pH 2.5), periodic acid-Schiff, the anticytokeratin antibody AE1, carcinoembryonic antigen, epithelial membrane antigen, and gross cystic disease fluid protein-15. CONCLUSION: Clear cell papulosis is a unique clinicopathologic entity. The clear cells were confirmed to be sweat gland secretory cells by their positive immunostaining with gross cystic disease fluid protein-15. The latter was also present in eccrine sweat gland coil cells. However, whether the clear cells were eccrine or apocrine secretory cells could not be determined.

Biopsy↗

Preliminary assessment of the epithelial nuclear-cytoplasmic ratio and nuclear volume density in human palatal lesions.

We have analysed both the nuclear-cytoplasmic (N/C) ratio and nuclear volume densities (VVN) in defined strata from human hard palate lesions with and without malignant potential to determine the prognostic reliability and/or validity of this parameter. Measurements of cellular and nuclear areas of basal and spinous cells from normal (N) and pathological palatal epithelium were made on histological sections using an image analyser. The lesions comprised fibrous hyperplasia (FH), traumatic inflammation (INF), benign hyperkeratosis (HK), squamous cell papilloma (PP), dysplastic epithelium adjacent to invasive carcinoma (CE) and islands of invasive squamous cell carcinoma (CI). In basal cells, no significant differences were detected in comparisons of N/C and VVN between all pathological groups and the N control group. The mean value for CE was lower than that obtained for N. In spinous cells, the only statistically significant comparison was between IF and FH for both N/C and VVN. Both parameters were lower in CE than in N. Of all groups analysed except CI, the CE group is the only one likely to possess an increased malignant potential. The N/C ratio therefore seems to be of no value as a predictor of malignancy in palatal epithelial lesions.

Carcinoma↗

Epidermal growth factor-induced activation and translocation of phospholipase C-gamma 1 to the cytoskeleton in rat hepatocytes.

In this study, we have examined the relationship between epidermal growth factor (EGF)-induced tyrosine phosphorylation of phospholipase C-gamma 1 (PLC-gamma 1) and its translocation from the cytosol to the Triton X-100-insoluble cytoskeleton fraction in rat hepatocytes. The translocation of PLC-gamma 1 was specific for EGF stimulation, because a similar effect was not observed with insulin or vasopressin. EGF caused a transient increase of PLC activity in the cytoskeleton fraction which could be abolished by immunoprecipitating PLC-gamma 1. Tyrosine phosphorylated PLC-gamma 1 was seen only in the cytoskeleton fraction, suggesting that tyrosine phosphorylation is required for PLC-gamma 1 translocation to the cytoskeleton. This process may involve binding of PLC-gamma 1 to actin filaments, since actin was immunoprecipitated together with PLC-gamma 1 in the cytoskeleton after EGF treatment. EGF-induced translocation of PLC-gamma 1 to the cytoskeleton was not inhibited by pertussis toxin, but Gi alpha was translocated in an EGF-dependent manner, suggesting that the interaction of PLC-gamma 1 with its activated Gi-protein is downstream from both PLC-gamma 1 tyrosine phosphorylation and its translocation to the cytoskeleton. Taken together, the present studies indicate that EGF-induced tyrosine phosphorylation of PLC-gamma 1, its association with the cytoskeleton, and its interaction with activated Gi alpha protein are all obligatory for PLC-gamma 1 activation in hepatocytes.

Actins↗

Histogenesis and possible mechanism of chondroid changes in mixed tumour of the skin: immunohistochemical evaluation of bone morphogenetic protein, glycosaminoglycans, keratin, vimentin and neuronal markers.

The distribution of immunoreactivity of bone morphogenetic protein (BMP), the glycosaminoglycans chondroitin 4-sulphate (C4SPG), chondroitin 6-sulphate (C6SPG), dermatan sulphate (DSPG) and keratan sulphate proteoglycans (KSPG), cytokeratin (K8.12), vimentin, glial fibrillary acidic protein (GFAP), actin, desmin, S-100 protein and neuron-specific enolase (NSE) in mixed tumour of the skin was investigated using immunohistochemical methods using monoclonal (MoAb) and polyclonal antibodies (PoAb). A strong BMP immunoreactivity was found characteristically in outer tumour cells of tubuloductal structures and modified myoepithelial cells. Modified myoepithelial cells and chondroidally changed cells showed positive immunoreactivity for C4SPG, C6SPG and DSPG; and KSPG was more pronounced in the modified myoepithelial cells. Vimentin, S-100 protein, GFAP and NSE, but not actin and desmin, were distribute in the outer tumour cells and modified myoepithelial cells in chondroidally changed tissue. Two factors show that chondrogenesis in mixed tumour of the skin is associated with the modified myoepithelial cells through the activity of BMP and biosynthesis of glycosaminoglycans as matrix substance. First, outer or basal tumour cells in mixed tumour of the skin is characterized by the presence of positive immunoreactivity for BMP, KSPG, vimentin, cytokeratin K8.12, S-100 protein, GFAP and NSE, and second, there is a matrix of chondroidally changed tissue containing the reaction products of C4SPG, C6SPG, DSPF and KSPG.

Actins↗

[Distribution of bone morphogenetic protein in human bone and tooth germs: analysis of specificity of monoclonal antibody against bone morphogenetic protein].

A cell strain stably secreting monoclonal antibody against BMP was obtained by hybridoma technique. The monoclonal antibody specifically reacted with the cells of human bone and tooth germs on paraffin embedded tissue sections. Immunohistochemical staining shows that BMP is distributed along collagen fibres in normal bone, also exist in osteoid tissue of new bone, in osteoblasts and in the cells of bone marrow. BMP may be found in human tooth germs such as in predentin, in the cells of outer and inner enamel epithelium, in the cells of dental sac generating alveolar bone. The results demonstrate that generation and growth of human bone and development of tooth germs have relation to BMP. The results at the molecular level prove that some antigenic determinants of human and bovine BMP are the same. BMP function activity inhibition test suggests that this antibody may block the function group of BMP. The ability of the monoclonal antibody to detect antigen and to inhibit generation of new bone makes it potentially useful in purification of BMP and in treating osteosarcoma and other bone tumors.

Animals↗

[Relation between Helicobacter pylori and pathogenesis of chronic atrophic gastritis and the research of its prevention and treatment].

The total detectable rate of Helicobacter pylori (HP) of 485 patients suffering from gastric diseases was 59.6%. The HP in gastric mucosa of chronic atrophic gastritis (CAG) patients was separated from the cell culture in vitro and transferred successively. The mice were perfused with exciccate alum, and the rabbits with aspirin to injure their gastric mucosa, then HP was perfused. Result showed that the change of experimental animals was identical with that of CAG patients by means of bacteriological and pathological examination. It revealed that HP was in agreement with Robert Koch's three principles about pathogenic bacteria. According to the bacterial infectious hypothesis of CAG, 53 Chinese medicinal herbs and prescriptions were investigated with bacteriostatic test. Panax notogenseng and Magnolia officinalis were discovered to be sensitive, Prunus mume and Corydalis yanhusuo were moderate sensitive, and Coptis chinensis and Rheum palmatum highly sensitive to HP. Decoction of Clearing up the Heat and Relieving the Blood Stasis and No.2 recipe of Huowei were used to treat 70 CAG patients with Stomach Heat Syndrome. The effective rate of gastroscopic examination was 85.7%, that of pathological study was 80%. In comparing with the group of Shanjiu Weitai, there was significant difference between the traditional Chinese medicine treated group and Shanjiu Weitai control group, the former being markedly better.

Adolescent↗

[Integrated control of pests injuring Chinese hawthorn Crataegus pinatifida Bge. var. major N.E.Br. by nonpollution techniques].

Field experiments on integrated control of pests injuring Chinese hawthorn by some nonpollution techniques including agricultural biological and physical methods, were carried out in Xinglong County, Hebei Province during 1989-1991. Satisfactory results were obtained. Compared with synthetic pesticides, the new techniques improve the control effect by 30%-60% generally, increase the number of natural enemies by 51.26%-68.51%, and enhance the yield by 47.58%. The test shows that the hawthorns from the field treated by the new techniques are either free of pesticide residual or with a residual 500-1000 times less than the residual standard fixed by FAO/WHO or the state.

Animals↗

Pertussis toxin-sensitive Gi protein involvement in epidermal growth factor-induced activation of phospholipase C-gamma in rat hepatocytes.

Treatment of rat hepatocytes with epidermal growth factor (EGF) produced an enhanced tyrosine phosphorylation of the EGF receptor and phospholipase C-gamma (PLC-gamma) in conjunction with the mobilization of Ca2+. Approximately 30% of the total PLC-gamma was tyrosine-phosphorylated with a maximum being reached after 30 s of incubation with EGF. Pretreatment of the rats with pertussis toxin prior to isolation of the hepatocytes blocked EGF-induced tyrosine phosphorylation of PLC-gamma and Ca2+ mobilization but had no effect on autophosphorylation of the EGF receptor or Ca2+ responses elicited by angiotensin II or phenylephrine. Under these conditions Gi protein alpha subunits were fully ADP-ribosylated. A 41-kDa Gi protein alpha subunit was found to be present in the anti-PLC-gamma immune complex after EGF stimulation as shown by in vitro ADP-ribosylation using [32P]NAD+ and activated pertussis toxin. The kinetics of association between PLC-gamma with Gi alpha protein reached a maximum after 1 min of incubation with EGF. Antibodies specific for the EGF receptor also coimmunoprecipitated a Gi protein alpha subunit. Treatment of hepatocytes with EGF caused first an increase and then a decrease in the amount of Gi protein alpha subunit associated with the EGF receptor. In contrast, studies with cultured rat liver (WB) cells, a cell line in which EGF stimulation of phosphoinositide hydrolysis is not inhibited by pertussis toxin, showed that a stable complex of Gi alpha was not formed with either PLC-gamma or EGF receptor immunoprecipitates. These results indicate that a pertussis toxin-sensitive Gi protein is uniquely involved in the signal transduction pathway mediating EGF-induced activation of PLC-gamma and Ca2+ mobilization in hepatocytes.

Adenosine Diphosphate Ribose↗

Mechanisms of receptor-mediated Ca2+ signaling in rat hepatocytes.

The Ca2+ signal observed in individual fura-2-loaded hepatocytes stimulated with the alpha 1-adrenergic agonist phenylephrine consisted of a variable latency period, a rapid biphasic increase in the cytosolic free Ca2+, followed by a period of maintained elevated cytosolic Ca2+ (plateau phase) that depended on the continued presence of both agonist and external Ca2+. Microinjection of guanosine-5'-O-(3-thiophosphate) elicited a Ca2+ transient with the same basic features. The Ca2+ transient resulting from microinjecting inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) occurred with essentially no latency period and consisted of a rapid spike that decayed back to preinjection levels within 15 s. Microinjection of inositol 1,4,5-trisphosphorothioate (thio-IP3), a nonmetabolizable analog of Ins-1,4,5-P3, elicited a Ca2+ transient that was initially identical to that observed with Ins-1,4,5-P3, except that the cytosolic Ca2+ remained elevated. The maintained thio-IP3-induced Ca2+ increase was dependent on the presence of external Ca2+, suggesting an activation of Ca2+ influx. Reintroduction of external Ca2+ in the presence of 5 microM phenylephrine to Ca(2+)-depleted cells resulted in a 2-fold greater rate of rise in the cytosolic Ca2+ compared to the rate observed upon Ca2+ addition to cells Ca(2+)-depleted by preatement with thapsigargin. The rate of Ca2+ rise upon Ca2+ addition to cells microinjected with thio-IP3 was similar to that observed with phenylephrine. Coinjection of the cells with thio-IP3 plus heparin reduced the rate of Ca2+ rise upon Ca2+ addition to that observed in thapsigargin-treated cells. These data indicate that the mechanism responsible for receptor-mediated stimulation of Ca2+ entry into hepatocytes involves not only capacitative Ca2+ entry but also an additional component mediated directly by Ins-1,4,5-P3.

Animals↗

Atrophie blanche. A clinicopathological study of 27 patients.

Twenty seven patients (8 males and 19 females) with atrophie blanche were observed in the past 7-years. The mean age at onset was 32 years (ranging from 23 years to 57 years) and 19 years (ranging from 11 years to 36 years) for male and female patient, respectively. The mean disease duration was 2.5 years (ranging from 2 months to 16 years) prior to their consultation. Sixty-three percent of them had summer exacerbation. Four patients had essential cryoglobulinemia, one of whom also developed bilateral iliofemoral artery stenosis one year later. Twelve patients also manifested concurrent purpura pigmentosa chronica (PPC)-like lesions. The observation of the natural course and clinical morphology, being divided into white atrophy-predominant and ulcer-predominant type, led to the impression that atrophie blanche and livedo vasculitis are synonyms with the same disease spectrum. Furthermore, white atrophy is not ulcer scars but lesions de novo suggesting dermal vasculopathy. An attempt was made to explain the uniqueness of clinical morphology. First line treatment included local wound care, bed rest and low-dose aspirin plus dipyridamole. Thirteen patients responded to these treatment either at the first attack or the recurrent episodes. Heparin (5000 units subcutaneous injection once daily) was effective for control of intractable painful ulceration in active stage in 70% of the remaining patients.

Adolescent↗