Biomedical subjects
Publications and source records attributed to Y Shi.
The experiment has shown that the aqueous extract and alcohol extract of Radix et Rhizoma Rhei can markedly inhibit the production of LPO in mice liver in vitro, and the aqueous extract also restrains the LPO increase in mice liver-caused by adriamycin or D-galactose.
Effects of Ca2+ channel blockers (nicardipin and nifedipin) and Ca2+ ionophore A23187 on the basal secretion and on the secretion stimulated by GRH or inhibited by SMS, a SRIF analogne of GH were investigated in monolayer cell cultures of 23 cases of human pituitary GH-secreting adenomas. The roles of GRH and SMS in 45Ca influx were investigated also. The GH secretion of most GH adenomas was depended on Ca2+, but the abnormality in different link of GH secretion mediated by Ca2+ was observed. The defects of receptor and post-receptor including Ca2+ channel and Ca(2+)-GH secretion couple regulated by GRH and SRIF were found in 66.7% and 55.6% of GH adenomas respectively. These abnormalities may contribute to GH hypersecretion in GH adenomas.
OBJECTIVE: This paper is the summary of "National Symposium on the Value of Immunodiagnostic Assays in Schistosomiasis by Treatment Effects Assessment" which was directed by the Expert Advisory Committee for Schistosomiasis of the Ministry of Public Health. This symposium was held to evaluate the diagnostic effects of the new system of detection in the sensitivity and specificity by treatment assessment. MATERIALS AND METHODS: Twelve laboratories with 14 assay systems participated in this collaborative study, in which, 450 sera were detected by double blind trial using a classical antibody detection with ELISA as a control. RESULTS: The results showed that 6 test systems were superior or close to the classical antibody detection, especially in evaluating the value of treatment effects. CONCLUSIONS: It is unanimously recognized that much progress has been made in the research of immunodiagnosis of schistosomiasis in China, but many problems remain to be solved and worth further studying.
OBJECTIVE: To investigate the status of DNA methylation in gastric carcinogenesis. METHODS: We analysed methylation pattern of c-myc, c-Ha-ras oncogenes by southern blot hybridization. DNA from cancerous, paracancerous and non-cancerous area of surgically resected samples in 21 cases of advanced gastric cancer were digested with MspI/HpaII and hybridized with the two genomic 32P labelled probes. In addition, the level of total genomic DNA methylation was measured by incubating DNA with 3H-S-Adenosylmethionine (3H-SAM) in the presence of a methylase which methylates all the cytosine residues that are in the double CpG (cytosine-guanine). RESULTS: The results indicated that both c-myc and c-Ha-ras oncogene fragments containing CCGG sequence were hypomethylated in DNA samples from cancerous (10/21 and 5/10) and paracancerous (13/21 and 4/10) areas. Moreover, the level of total genomic DNA methylation in cancerous tissue was significantly lower than that in non-cancerous and paracancerous mucosa tissues (P < 0.05). The results from two methods are incompletely alike. CONCLUSION: These results supported a strong correlation between DNA hypomethylation and gastric carcinogenesis, particularly methylated pattern of c-myc and c-Ha-ras oncogenes fragments containing CCGG sequence was abnormal in gastric mucosa tissue from gastric cancerous and paracancerous areas.
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180 cases of vascular malformation in brain (BVM) including 156 cases of brain biopsy and 24 autopsy cases were examined with routine pathological methods. The attempt of this study is to realize the pathological change and incidnce of each type and to find out the main cause of hemorrhage in BVM. According the morphological characteristics, 180 cases of BVM were classified into five types. They are: arteriovenous type 159 cases, venous type 3 cases, cavernous type 6 cases, capillary telangiectasis 1 case, and mixed type 11 cases. Hemorrhage was the most common clinical manifestation and main cause of death in BVM. The mechanism of hemorrhage may be due to either hemodynamic disturbance in local area or changes of the blood vessel wall. Besides these, there are five cases of BVM accompanied with brain tumor. They may be two independent diseases occurred in the same person. No relationship was found between the occurrence of these 2 entities.
PURPOSE: To observe the immunological changes in epiretinal membranes from the patients with proliferative vitreoretinopathy (PVR). METHODS: Twelve samples of epiretinal membranes obtained during vitreous surgeries for PVR were examined by direct and indirect immunofluorescein histochemistry. RESULTS: The cellular membranes in 8 cases were composed of retinal pigment epithelial cells, fibroblast-like cells, macrophages and collagen. Positive stainings of IgG, C3+ collagen type III and macrophage-marker Ki-M7 (CD68) was seen in the membranes. CONCLUSION: The results indicate that humoral immune components and macrophages may play an important role in the development of epiretinal membrane formation.
To study the role of Ca2+ in the pathogenesis of pituitary growth hormone secreting adenomas, the function of Ca2+ in 23 cases of human pituitary GH-secreting adenoma was investigated in monolayer cell culture. It was found that Ca2+ channel blockers nicardipin and nifedipin inhibited basal and growth hormone releasing hormone (GRH)-stimulated GH secretion in 87.5% and 100.0% of the GH adenomas, respectively, demonstrating that in most human pituitary GH adenomas, the basal and GRH regulated GH secretion is Ca2+ dependent. The GRH and sometostatin (SRIF) agonist octreotide regulated the processes of GH secretion via Ca2+ had defects in different steps including receptor, postreceptor Ca2+ channel and Ca(2+)-GH secreting coupling in 6(66.6%) and 5(55.5%) cases of 9 GH adenomas respectively. Among them, the defects in GRH receptor and SRIF regulated Ca2+ channel are the main causes of the dysfunction of GH adenomas. These defects may be related to GH hypersecretion in GH adenomas. Our data provides advance evidences for intrinsic defects of GH adenomas.
The present study demonstrats that immunoreactive GH mRNA is expressed at low level in normal human peripheral blood lymphocytes by RT-PCR amplification and hybridization. Northern blot analysis of total RNA from lymphocytes with a pituitary hGH cDNA probe revealed a faint transcript migrating almost coincident with pituitary hGH menssenger RNA. Reverse transcription-polymerase chain reaction from total RNA of lymphocytes by using hGH specific primers generated a predicted 702 base pair band with almost the same size as pituitary and also hybridized with pituitary hGH cDNA probe specifically in Southern blot analysis, which indicates a low level expression of GH-like mRNA in human peripheral blood lymphocytes.
Pharmacological regulation of the peritoneal stomata was studied by using traditional Chinese medicine and a medical image processing system attached to SEM. The results showed that the numbers, diameters and distributive density of the peritoneal stomata were significantly increased (P < 0.05) in the groups of white atractylodes rhizome and the pilose asiabell root. However, the effect of astraglus root was not obvious in comparison with the controls (P > 0.05). This was for the first time to show the regulation of the peritoneal stomata by using traditional Chinese medicines. According to the mechanism of the peritoneal stomata and ascites drainage, white atractylodes rhizome and pilose asiabell root may exert an important action on ascites treatment.
The expression of P16 protein was examined in 45 cases of non-Hodgkin's lymphoma (NHL), 4 cases of reactive hyperplasia of lymph node (RHLN) and 6 cases of normal spleen with immunohistochemical staining. Positive reaction of P16 protein was observed in some lymphocytes of RHLN and splenic nodule and around splenic sinus. The positive rate of P16 protein expression in NHL was 37.8% (17/45). The positive rates of P16 protein expression for the low intermadiate- and high-grade malignancy groups were 66.7% (10/15), 37.5% (6/16) and 7.1% (1/14) respectively. There was a significant difference between the low malignancy NHL and the high malignancy NHL (P < 0.005) in expression rate of P16 protein. It suggests that P16 protein expression may be one of the important parameters in estimating the prognosis of patients with NHL.
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A novel cellular protein, Abl-interactor-1 (Abi-1), which specifically interacts with the carboxy-terminal region of Abl oncoproteins, has been identified in a mouse leukemia cell line. The protein exhibits sequence similarity to homeotic genes, contains several polyproline stretches, and includes a src homology 3 (SH3) domain at its very carboxyl terminus that is required for binding to Abl proteins. The abi-1 gene has been mapped to mouse chromosome 2 and is genetically closely linked to the c-abl locus. The gene is widely expressed in the mouse, with highest levels of mRNA found in the bone marrow, spleen, brain, and testes. The Abi-1 protein coimmunoprecipitates with v-Abl and serves as a substrate for kinase activity. When overexpressed in NIH-3T3 cells, abi-1 potently suppresses the transforming activity of Abelson leukemia virus expressing the full-length p160v-abl kinase but does not affect the transforming activity of viruses expressing a truncated p90v-abl or v-src kinases. We suggest that the Abi-1 protein may serve as a regulator of Abl function in transformation or in signal transduction.
Brief (1-2 h) exposure of Clone 9 cells to inhibitors of oxidative phosphorylation such as azide is known to markedly increase glucose uptake. Clone 9 cells express GLUT1 but not GLUT2, -3, and -4, and the azide effect was not accompanied by any increase in cellular or plasma membrane GLUT1 level. To identify the molecular event underlying this apparent increase in GLUT1 intrinsic activity, we studied the acute effects of azide on the substrate binding activity of GLUT1 in Clone 9 cells by measuring glucose-sensitive cytochalasin B binding. The glucose-displaceable, cytochalasin B binding activity was barely detectable in membranes isolated from Clone 9 cells under control conditions but was readily detectable after a 60-min incubation of cells in the presence of 5 mM azide showing a 3-fold increase in binding capacity with no change in binding affinity. Furthermore, the cytochalasin B binding activity of purified human erythrocyte GLUT1 reconstituted in liposomes was significantly reduced in the presence of cytosol derived from azide-treated Clone 9 cells but not in the presence of cytosol from control cells; this effect was heat-labile and abolished by the presence of the peptide corresponding to the GLUT1 COOH-terminal sequence. These results suggest that a cytosolic protein in Clone 9 cells binds to GLUT1 at its COOH-terminal domain and inhibits its substrate binding and that azide-induced metabolic alteration releases GLUT1 from this inhibitory interaction. Studying the binding of cytosolic proteins derived from 35S-labeled Clone 9 cells to glutathione S-transferase fusion protein containing glucose transporter COOH-terminal sequences, we identified 28- and 70-kDa proteins that bind specifically to the cytoplasmic domain of GLUT1 and GLUT4 in vitro. We also found a 32P-labeled, 85-kDa protein that binds to GLUT4 but not to GLUT1 and only in cytosol derived from azide-treated cells. The roles, if any, of these glucose transporter-binding proteins in the azide-sensitive modulation of GLUT1 substrate binding activity in Clone 9 cells are yet to be determined.
Activation of T lymphocytes can result in a functional immune response, anergy or apoptosis. Functional T cell activation requires the interaction of the TCR with Ag presented by MHC molecules on APC concurrent with appropriate interactions between cell surface accessory molecules. Interestingly, the level of CD28 expression is regulated during T cell development as well as during T cell activation and proliferation, suggesting that CD28 could play a role in determining the outcome of activation of TCR during T cell ontogeny. We identify, herein, a novel function of murine CD28 in the regulation of activation-induced apoptosis in thymocytes. In vivo, or combined in vivo and in vitro treatment with mAbs to CD28 prevents apoptosis of CD4+CD8+ thymocytes induced by Abs to the TCR complex. Prolonged administration of anti-CD28 Abs increased the number of both CD4+CD8- and CD4-CD8+ T cells in the thymus, while the number of CD4+CD8+ T cells is relatively unchanged. Furthermore, this treatment leads to a dramatic enlargement of peripheral lymphoid organs characterized primarily by the expansion of B cells. The number of CD4+CD8- T cells in the spleen of anti-CD28-treated mice is also moderately increased, while the number of CD4-CD8+ cells is relatively unchanged.
BACKGROUND: The authors previously found p53 mutations in 24% of malignant thyroid tumors, representing a wide stating spectrum. Overexpression of MDM2, most often due to gene amplification, has been suggested to be an additional mechanism for abrogation of the p53 function. In the current study, MDM2 gene expression and amplification were examined in a randomly selected subset of these tumors to explore the possibility that wild-type p53 may be inactivated by complexing with MDM2 in specimens without p53 mutations. METHODS: MDM2 gene expression and amplification were studied by Northern and Southern blot analysis, respectively. Twenty-two thyroid tumors were included: 16 papillary carcinomas, 1 follicular carcinoma, 3 anaplastic carcinomas, and 2 multinodular goiters (adenomatous goiters). RESULTS: A two- to threefold increase in MDM2 expression in 4 of 20 thyroid carcinomas was found. It was noteworthy that all of these four samples harbored p53 mutations. The association between increased MDM2 expression and p53 mutation was statistically significant (P < 0.005). No evidence of MDM2 gene amplification or rearrangement accounting for such an increase in MDM2 expression was found. CONCLUSIONS: Genetic and/or environmental factors contributing to random p53 mutations also may cause increased MDM2 expression. Given the moderate increase in MDM2 expression without associated genetic alterations such as gene amplification and rearrangement, MDM2 may not play any significant role in the development and progression of thyroid carcinoma.
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