Biomedical subjects
Publications and source records attributed to Y Dong.
Neocheiropteris palmatopedata is a rare medicinal plant which only distributes in the boundary among Guizhou, Yannan and Sichuan. The paper reports cultivation methods with using rhizome and spores of N. palmatopetata as reproduction materials.
For exploring cellular immunity disturbances in children with acute lower respiratory infection (ALRI) caused by respiratory syncytial virus (RSV) the level of interleukin-2 (IL-2) soluble interleukin-2 receptor (sIL- 2R), the expression rate of interleukin-2 receptor (IL-2R) on T cells and percentage of T lymphocyte subsets were determined in peripheral blood of 25 acute cases. The results showed that compared acute stage of RSV associated ALRI with recovery stage and control group, the level of peripheral blood IL-2 and expression rates of IL-2R decreased but the level of sIL-2R increased. The level of IL-2 had positive correlation with IL-2R and percentage of CD4+ cells, but had negative correlation with sIL-2R and percentage of CD8+ cells. The plasma sIL-2R level had negative correlation with expression rate of IL-2R, but had a positive correlation with clinical severity. These results suggested that human body had a functional disturbance in cellular immunity when infected with RSV.
Gap junction channel forming connexins share a common membrane topology which has four transmembrane spanning segments with the amino- and carboxy termini both located on the cytoplasmic side. Both, mutation and truncation of the carboxyl tail of some connexins have been shown previously to have profound effects on channel function. Truncation of the carboxyl tail of connexin50 (Cx50) and connexin46 (Cx46) occurs naturally during the maturation of fiber cells in the mammalian lens. This system therefore offers the unique opportunity to study not only the cleavage process but also the functional role played by the cleaved domain, in a physiologically relevant context. As a first step, we now report on the cleavage of the 70 kDa ovine isoform of Cx50. The calcium-activated neutral protease calpain (EC 3.4.22.17) was identified as the enzyme which removed a 32 kDa carboxyl portion from the Cx50 molecule in mature lens fiber cells. The amino-terminal 38 kDa portion remained embedded in the plasma membrane and was isolated and visualized as channel structures. The amino-terminal sequence of the cleaved 32 kDa portion matched an interior portion of the published amino acid sequence of the ovine Cx50 isoform. Thus, two closely spaced calpain cleavage sites were identified in the Cx50 molecule which were located carboxy-terminal from the predicted exit of the fourth transmembrane spanning segment by 62 or 72 amino acid residues, respectively. These data provide the basic information required for the future construction of Cx50 mutants to explore the functional consequences of this cleavage.
In 1991-1995 by using the Rieckmann in vitro micro-method, susceptibilities of Plasmodium falciparum to eight antimalarials in the China-Lao PDR and China-Myanmar border areas were tested. The resistant rates of P. falciparum to chloroquinine were 95.0%-100%; IC50 114-240nmol/l. P. falciparum resistant rates to amodiaquine resistance accounted for 83.5%-100%, IC50 52-72nmol/l. All cases were sensitive to quinine, IC50 470-608nmol/l. P. falciparum isolates from the Lao PDR frontier were highly sensitive to artesunate, dihydroartemisinin, and arteether. Resistant rates from other areas were 0-11%. P. falciparum from China-Myanmar and Lao PDR border areas were also sensitive to mefloquine, IC50 68-88nmol/l. A longitudinal survey of the sensitivity of P. falciparum in vivo on the China-Lao PDR border showed that the average defervescent time of falciparum malaria was treated by pyronaridine increased from 32.7 +/- 16.0 hours during 1984-85 to 56.2 +/- 27.4 hours in 1995; the recrudescence rate rose up from 15.2% to 37.5%. The results monitored in vitro showed that all cases assessed in 1988 for response to pyronaridine were sensitive, but 36.4% of cases had emerging resistance, IC50 increased from 13nmol/l to 40 nmol/l. The above results suggested that P. falciparum in these areas has expressed resistance to chloroquine and amodiaquine. However, the parasites are still sensitive to artemisinin, pyronaridine, mefloquine, quinine, but with a declining sensitivities.
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To explore the role of HLA-DRB1 genes in the development of rheumatoid arthritis (RA) and the correlations between HLA-DR alleles and clinical manifestations of patients with RA we studied 86 patients and 106 race matched controls in whom HLA-DR typing was performed by the method of DNA amplification with sequence-specific primers (PCR-SSP). The subtypes of HLA-DR4 were determined by the method of hybridization of PCR products with sequence-specific oligonucletides (PCR-SSO). The absence or presence of HLA-DR4 and its subtypes was evaluated with the clinical and serological characteristics of the patients. Compared with controls, an increased gene frequency of HLA-DR4 (48.8% vs 17.9%, P < 0.001) and a decreased frequency of HLA-DR5 (16.3% vs 27.4%, P = 0.06) were found. The DRB1 * 0405 accounted for 61.9% of DR4+ RA patients and 21.1% of DR+4 controls (P < 0.01). There was no difference between the DR4+ and DR4- patients with respect to age, sex, duration of disease, extra-articular manifestations including secondary Sjogren's syndrome. But rheumatoid factor (RF) was associated with HLA-DR4 (P < 0.05). According to the X-ray stage, the patients of DR4+ were more severe than those of DR4- (P < 0.05). HLA-DR4 and DR4 subtype of DRB1 * 0405 were related to the development of RA in Chinese. HLA-DR4 can be a useful prognostic marker in the patients with RA.
Down-regulation of gelsolin, an actin-binding protein, is frequently found in several types of transformed cells and tumors. The present study demonstrates that gelsolin protein and RNA were absent or markedly reduced in human breast cancer cell lines relative to "normal" mortal human mammary epithelial cells and benign, immortalized cell lines. Moreover, actin filaments were usually attenuated coincident with the reduction in gelsolin. Gelsolin was also missing or greatly decreased in 70% of 30 human sporadic, invasive breast carcinomas examined by immunocytochemistry and in 100% of virally induced mouse and chemically induced rat mammary carcinomas evaluated by Northern analysis. Southern analysis revealed no major mutations in the gelsolin gene of human breast cancer cells. Our results show that partial or total loss of gelsolin expression is common to the majority of breast cancers of diverse etiologies in three animal species and point to gelsolin as a candidate suppressor of breast cancer.
Involvement of p53 gene alterations has been demonstrated in a variety of human neoplasias including urinary bladder carcinomas. N-Butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced urinary bladder carcinogenesis models in rodents have been widely used to study carcinogenic processes in this organ. In the present study, transitional cell carcinomas induced in the urinary bladders of male F344 rats treated with 0.05% BBN for 16 or 32 weeks and then sacrificed at experimental week 32 were analyzed for mutational changes in the p53 and H-ras genes by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis and subsequent DNA sequencing. The total p53 mutation incidences were 3/10 (30%) and 8/12 (66.7%) in rats treated with BBN for 16 weeks followed by 16 weeks' non-treatment, or in rats treated with BBN for 32 weeks, respectively, while the H-ras mutation incidences were 0/10 (0%), and 1/12 (8.3%), respectively. The present results indicate that mutations in the p53 gene might be involved in the process of urinary bladder carcinogenesis by BBN as part of a multistep pathway. However, considering the decreasing tendency in lesions with p53 mutations after stopping BBN administration, a p53 mutation alone would not appear to be sufficient to give a marked selective advantage to mutant cells. No evidence of H-ras mutation involvement was gained even for the late course of rat urinary bladder carcinogenesis.
Viral vector-mediated transfer of chemosensitization genes represents a promising new approach to the treatment of cancer. Previous reports have demonstrated that transfection of the bacterial cytosine deaminase (cd) gene into mammalian cells can sensitize them to the otherwise nontoxic nucleoside, 5-fluorocytosine (5-FC). We now report that a replication-deficient adenovirus vector that transduces the cd gene (Ad.CMV-cd) highly sensitizes 9L gliosarcoma cells to 5-FC, and that gene transduction is associated with a potent bystander effect that is not dependent on direct cell-to-cell contact. Stereotactic injection of Ad.CMV-cd into established rat gliomas, followed by systemic administration of 5-FC in vivo, results in prolongation of survival.
OBJECTIVE: To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease. PATIENTS: Twelve patients with unilateral internal carotid artery occlusive disease (1 with severe stenosis and 11 with occlusion) and no cortical infarction in the chronic stage (mean +/- SD age, 64 +/- 5 years). MAIN OUTCOME MEASURES: Midsagittal corpus callosum area-skull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence Scale-Revised (Digit Span, Arithmetic, Picture Arrangement, Object Assembly, Block Design, and Digit Symbol), and cerebral metabolic rate of oxygen (measured with position emission tomography by using the oxygen 15 steady-state technique). RESULTS: The degree of cognitive impairment varied but was strongly correlated with the severity of callosal atrophy (r = 0.92, P < .001). Patients with callosal atrophy and cognitive decline also showed decreased oxygen consumption in the bilateral cerebral cortices. Stepwise regression analysis revealed that the severity of white matter lesions, especially in the centrum semiovale, and that of cortical atrophy in the hemisphere with arterial disease were 2 important factors for callosal atrophy. CONCLUSIONS: Callosal atrophy is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease without cortical infarction. Callosal atrophy might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cognitive impairment with widespread cortical hypometabolism in carotid artery occlusive disease without large cortical lesions.
Cytosine arabinoside (ara-C) is a cytidine analog that incorporates into replicating DNA and induces lethal DNA strand breaks. Although ara-C is a potent antitumor agent for hematologic malignancies, it has only minimal activity against most solid tumors. The rate-limiting step in intracellular ara-C activation is phosphorylation of the prodrug by deoxycytidine kinase (dCK). The present results demonstrate that both retroviral and adenoviral vector-mediated transduction of the dCK cDNA results in marked sensitization of glioma cells lines to the cytotoxic effects of ara-C in vitro. We also demonstrate that ara-C treatment of established intradermal and intracerebral gliomas transduced with dCK results in significant antitumor effects in vivo. These data suggest that viral vector transduction of the dCK gene followed by treatment with ara-C represents a new chemosensitization strategy for cancer gene therapy.
The levels of p53 protein were detected by immunocytochemistry in 197 endoscopic biopsy specimens of esophagus. Nuclear p53 protein was present in 2.9% of normal mucosa, 6.7% of inflammatory mucosa, 38.8% of mild dysplasia, 52.0% of moderate or severe dysplasia, 61.1% of carcinomas in situ, 62.5% of invasive carcinomas. Moreover, we examined 14 cases of esophageal carcinoma with extensive dysplasia near the carcinoma and found high levels of p53 protein in both dysplasias and carcinomas in 8 cases. In one case, carcinoma presented high level of p53 protein while the adjacent dysplasia did not. In another case, the result was just the opposite. Negativity for p53 immunostaining was found in 4 cases. These data indicated that p53 protein accumulation occurred before tumor invasion in the multistage esophageal carcinogenesis. The timing and the frequency of p53 protein accumulation made p53 gene an attractive marker for the early diagnosis an the evaluation of chemopreventive agents.
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RPSP, a refined polysaccharide peptide fraction isolated by fast performance liquid chromatography (FPLC) from the crude powder of total peptide-bound polysaccharides of cultivated Coriolus versicolor Cov-1 dose-dependently inhibited the proliferation of a human hepatoma cell line (HEPG2). The effective dose causing 50% inhibition following 3-day exposure to RPSP was 243 +/- 36 micrograms/ml for HEPG2. However, little or no inhibitory effects were detected in normal human foetal hepatocytes. On the other hand, in the pretreatment group, in which RPSP was administered i.p. for two weeks before sarcoma 180 inoculation in nude mice, the incidence of tumor growth was less (2 out of 5 mice) than that of the control group (all 5 mice). The tumor size of the control group was about 3-5 times bigger than that of the pretreatment group. In tumor-bearing nude mice, 5 days after sarcoma 180 inoculation, i.v. administration of RPSP significantly suppressed the growth of tumor mass. The inhibition rate was 93.6% on day 13. Furthermore, administration of RPSP did not cause any pathological lesions in vital organs of rabbits such as heart, liver, spleen, lung and kidney. In conclusion, these results indicate that RPSP acts by directly suppressing tumor cell growth in vitro and the prevention of in vivo growth of tumor mass is probably mediated also via its immunomodulating effects.
Cyclophosphamide is an inactive prodrug which is converted by hepatic cytochrome P450 2B1 to cytotoxic metabolites which produce interstrand DNA cross-linking in a cell cycle-independent fashion. The limited ability of these metabolites to cross the blood-brain barrier contributes to the poor activity of cyclophosphamide against brain tumors. In this study we demonstrate that replication deficient retroviral and adenoviral vector-mediated gene transfer of cytochrome P450 2B1 into 9L glioma cells significantly increases the sensitivity of these tumor cells to cyclophosphamide in vitro, and prolongs the survival of animals bearing intracerebral 9L tumors treated with cyclophosphamide in vivo. Attempts to improve the effectiveness of retrovirally mediated transduction of the P450 2B1 gene by increasing the concentration of cyclophosphamide delivered to the tumors using intracarotid and intratumoral injections did not prolong animal survival, although survival was increased when a second treatment with P450-expressing retroviral vectors and cyclophosphamide was administered. These results suggest that in situ transduction of tumor cells with the P450 2B1 gene using retroviral and adenoviral vectors increases their sensitivity to cyclophosphamide and may have a potential role in the therapy of malignant gliomas.
In this paper, the sense and antisense mammalian expression vectors of T24-ras activated oncogene were introduced into cultured NIH3T3 cells in sense-->antisense and antisense-->sense orders. The transfected cells were selected by drug selection. The morphology change, Southern hybridization, frequency of soft agar colonies and the detection of P21 amount were investigated. The results showed that the sense recombinant could cause the malignant transformation of NIH3T3 cells while the antisense recombinant could inhibit this kind of transformation. Furthermore, the inhibitory effect varied according to the different transfected orders.
We demonstrated previously that the hammerhead ribozyme designed by us against the activated oncogene T24-ras cleaved the target mRNA specifically and efficiently in vitro. To study its properties in vivo, we cloned the DNA fragment encoding the ribozyme into the eukaryotic expression vector pSMG and transfected it into the T24-ras gene transformed NIH3T3 cell lines. The intracellular cleavage of T24-ras mRNA was evaluated on either the cytological level or the molecular level. The malignant cells expressing ribozyme were partially reversed in morphology as evidenced by slower growth speed, partial recovery of contact-inhibition, reduced frequency of colony forming in soft agar and close-to-normal behaviour in agglutination teat. The primer extension experiment verified that the ribozyme had efficiently cleaved the transcripts of T24-ras gene at the target site in vivo.