Thrombolytic therapy for acute cerebral vascular occlusion.
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Biomedical subjects
Publications and source records attributed to F Liu.
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An immunocytochemical method using an antibody probe to recognise the epithelial membrane antigen was used to screen smears obtained surgically from bone-marrow in 88 patients with gastric cancer. Tumor cells were detected in the bone-marrow of 58 patients (65.9%). The EMA positive cells in the marrow were not correlated with the location and node status of the stomach. In the stage of TNM I, II, III and IV, the positive rates of micrometastases in the bone marrow were 42.9%, 57.1%, 73.7% and 69.0%, respectively. The results showed that the poorer differentiated lesion, the higher rate of positive cells in the bone marrow. The curative surgery and multimodality treatment after operation could result in remission of positive cells in some patients. The method can detect occult metastases in bone marrow, and may be useful to monitor patients for evidence of response. It can measure the efficacy of adjuvant therapy, and predict prognosis of the patients.
AIM: To study the effect of nicardipine (Nic) on the cytoplasmic free calcium concentration ([Ca2+]i) in thymocytes and on the proliferation of thymus lymphocytes from mice in vitro. METHODS: The [Ca2+]i was measured by loading cells with the fluorescent dye Fura-2. The lymphocyte proliferation was determined by [3H] thymidine incorporation. RESULTS: Nic 1-30 mumol . L-1 elevated [Ca2+]i of resting thymocytes with the percentages of its increase 43%-192% and 12%-148% in the presence and absence of extracellular Ca2+ respectively. Mitogen Con A 5 mg . L-1 also released Ca2+ from intracellular stores. Nic decreased the enhancement of [Ca2+]i induced by Con A. The IC50 (mumol . L-1) was 26.8 (95% limit: 24.8-29.0) and approximated to 10 in the presence and absence of extracellular Ca2+ respectively. Nic 1-30 mumol . L-1 did not stimulate the proliferation of resting lymphocytes from mouse thymuses (P > 0.05), but inhibited the proliferation when the lymphocytes had been stimulated by Con A (P < 0.01). CONCLUSION: Nic elevated [Ca2+]i, which decreased the response of lymphocytes to mitogen.
Expression of P21, P53, P185 proteins, mutations of ras, p53 genes in colorectal adenoma, carcinoma and transitional mucosa were studied using immunohistochemicstry and PCR-RFLP methods. The results showed that the positive rates of P21, P53 and P185 proteins in colorectal adenoma were 53.3%, 27.6% and 13.3% respectively, the expression of P21 and P53 were associated with the malignant potential of adenoma. The positive rates of P21, P53 and P185 proteins in colorectal carcinoma were 72.9%, 37.8% and 47.2% respectively. 9 adenomas and 40 carcinomas contained more than two protein expressions and their co-expression was associated with the malignant potential of adenoma and the prognosis of carcinoma. The mutation rates of ras gene in colorectal adenoma and carcinoma were 26.7% and 41.9% respectively. The ras gene mutation was associated with the malignant potential of adenoma. The mutation rates of p53 gene (codon 248) in adenoma and carcinoma were 3.3% and 14.9% respectively. The prognosis of patients having gene mutation of both ras and p53 were poor. The results suggested that the alterations of ras, p53 and c-erbB-2 genes are involved in the tumorigenesis and development of colorectal carcinoma.
522 cases of benign prostate hyperplasia from 1980 to 1994 were reviewed. Prostate incidental carcinoma (PIC) was identified in 26 cases (4.98%). In order to study the pathomorphological features and to study the causes for missed diagnosis of this entity, the authors observed and analysed the numbers of carcinomatous foci their distribution, classification, staging and differentiation, morphological features and prostate specific antigen (PSA) markers. It was found that 23 cases exhibited a pathological structure of uniform pattern and 3 cases with pluriform pattern. Adenocarcinoma was most common. 17 cases were A1 stage and 9 cases were A2 stage. Isolated multiple foci of invasion and alterations of architecture are important pathological features of these cases. Missed diagnosis of prostate cancer is related to the small amount of biopsy tissue, contrast between benign and malignant prostate epithelial tissue not distinct, scarce nuclear anaplasia, careless microscopic observation, or observer lacks the ability to differentiate between pathologic types and pluriform patterns. Different PSA reactions may be related to tumor differentiation and classification.
OBJECTIVE: To investigate high risk factors of neonatal hyperglycemia. METHODS: According to the gestational age, postnatal age, weight, hypoxia, infection, 336 hospitalized newborns receiving continuous intravenous infusion of glucose controlled by pump were divided into the study and control groups respectively, the incidences of hyperglycemia between two groups were analysed statistically. RESULTS: The results showed that the high risk factors of neonatal hyperglycemia were gestational age ( < 37 week), postnatal age ( < 72h), weight ( < 2 500g), hypoxia and (or) infection. CONCLUSIONS: In neonates with one or more high risk factors of hyperglycemia, strict control of infusion speed; treatment of original diseases and frequent monitoring of blood glucose should be noted.
One satellite DNA family, cloned from Glycine max, was sequenced and chracterized. The unit of the repetitive sequences was 91bp. They concentrated on the arms of chromosomes M2 and M11, and spreaded on whole chromosomes Sm7 and M12. Southern blot analysis with 18 acessions, belonged to subgenus Glycine and subgenus Soj a of genus Glycine, showed that the repetitive sequences were specific to subgenus Soj a. It was subgenus specific repetitive sequence. This result, from another aspact, supported the idea that the three species in subgenus Soj a should be considered as one species.
A gas chromatographic-mass spectrometric method is described for the quantitative analysis of bencynonate in human plasma. Deuterated bencynonate served as the internal standard and selected-ion monitoring of the fragments of bencynonate and internal standard permitted the quantitation of bencynonate down to 25 pg/ml of plasma. The assay is linear for plasma bencynonate concentrations in the range 25 pg/ml-3 ng/ml. At 0.25 ng/ml the recovery and coefficient of variation are 54.3% and 19.1%, respectively. Application of the method to clinical studies gave data for the pharmacokinetics and relative bioavailability of bencynonate in man.
Transforming growth factor-beta (TGF-beta) signals by contacting two distantly related transmembrane serine/threonine kinases called receptors I (T beta R-I) and II (T beta R-II). TGF-beta binds to T beta R-II, which is a constitutively active kinase and this complex recruits T beta R-I, causing its phosphorylation and signal propagation to downstream substrates. The biochemical properties of this interaction were analyzed with reconstituted receptor systems. T beta R-I and T beta R-II baculovirally expressed at high levels in insect cells have the ligand binding properties of receptors expressed in mammalian cells, and form a complex in which T beta R-I phosphorylation is dependent on the kinase activity of T beta R-II. Furthermore, T beta R-I and T beta R-II can form a complex in vitro, and their cytoplasmic domains can specifically interact in a yeast two-hybrid system. In vitro complex formation with catalytically active T beta R-II is necessary and sufficient for T beta R-I phosphorylation, which within this complex does not require the catalytic activity of T beta R-I, thus mimicking T beta R-I phosphorylation in intact cells. In addition, T beta R-I phosphorylated in vitro remains associated with T beta R-II. These results suggest that T beta R-I and T beta R-II have affinity for each other, however, the ligand is required for stable complex formation under physiological conditions. Once formed, this complex is sufficient for T beta R-I phosphorylation by T beta R-II.
A new site of serine phosphorylation (Ser-1035/1037) has been identified in the kinase domain of the insulin receptor. Mutant receptors missing these two serines were expressed in Chinese hamster ovary cells overexpressing protein kinase C alpha. These mutant receptors lacked a phorbol ester-stimulated phosphoserine containing tryptic peptide as demonstrated by both high percentage polyacrylamide/urea gel electrophoresis and two-dimensional tlc. Moreover, a synthetic peptide with the sequence of this tryptic peptide was phosphorylated by isolated protein kinase C alpha and co-migrated with the phosphopeptide from in vivo labeled receptor. These results indicate that serine-1035 and/or 1037 in the kinase domain of the insulin receptor are phosphorylated in response to activation of protein kinase C alpha.
A gas chromatographic method with flame ionization detection (FID) for the quantitative analysis of meperidine and mass spectrometry (MS) for the qualitative analyses of meperidine and its metabolites in urine was established. Meperidine, normeperidine and acetyl normeperidine in urine were extracted with ether. Free and conjugated meperidinic and normeperidinic acids in urine, which are hydrophillic, were hydrolyzed by acid, esterified with methanol and derivatized with acetic anhydride. Meperidine and its four metabolites were identified by GC-MS. Meperidine was measured by GC-FID during 72 h after intramuscular administration of meperidine to an addict.
Transcription of the Acanthamoeba tbp gene is stimulated by a cis-acting promoter element that is bound by an activator protein, TATA-binding protein promoter binding factor (TPBF). Here, we report the complete purification of TPBF and describe its transcription activating and DNA-binding properties. TPBF contains two polypeptides with molecular weights of 51,000 and 50,000, whereas the native molecular weight of TPBF suggests it is dimeric or trimeric in solution. Phosphatase treatment of TPBF converts the 51,000 molecular weight species to the 50,000 molecular weight form, demonstrating that TPBF is phosphorylated. Phosphorylation reduces DNA binding by TPBF, as assessed by electrophoretic mobility shift assays after phosphatase treatment. TPBF makes numerous contacts with the bases and phosphate backbone of its DNA recognition element, and the pattern of these contacts suggests that it is a novel type of DNA-binding protein. TPBF can bind to additional, low affinity sites within the TBP gene promoter, suggesting that, in addition to positive activation of tbp gene expression, TPBF could also inhibit transcription by competing for binding sites for other proteins within the TBP promoter.
Selection of substrates for an RNA enzyme, the catalytic subunit of RNAase P from E. coli, has been carried out by simulation of evolution in vitro in the presence and absence of the protein cofactor of the enzyme. In the presence of the protein, substrates resembling precursor tRNAs, which were readily cleaved by the catalytic RNA, were selected in addition to others, with different sequences and structures (one of which resembled the precursor to 4.5S RNA) that were not readily cleaved by the catalytic RNA alone. The ribonucleoprotein enzyme is more versatile than the RNA enzyme, and our results suggest that it and 4.5S RNA may have evolved after ancestral tRNAs.
Neurotransmitter released from neurons is known to signal to neighbouring neurons and glia. Here we demonstrate an additional signalling pathway in which glutamate is released from astrocytes and causes an NMDA (N-methyl-D-aspartate) receptor-mediated increase in neuronal calcium. Internal calcium was elevated and glutamate release stimulated by application of the neuroligand bradykinin to cultured astrocytes. Elevation of astrocyte internal calcium was also sufficient to induce glutamate release. To determine whether this released glutamate signals to neurons, we studied astrocyte-neuron co-cultures. Bradykinin significantly increased calcium levels in neurons co-cultured with astrocytes, but not in solitary neurons. The glutamate receptor antagonists D-2-amino-5-phosphonopentanoic acid and D-glutamylglycine prevented bradykinin-induced neuronal calcium elevation. When single astrocytes were directly stimulated to increase internal calcium and release glutamate, calcium levels of adjacent neurons were increased; this increase could be blocked by D-glutamylglycine. Thus, astrocytes regulate neuronal calcium levels through the calcium-dependent release of glutamate.
Insulin, in the presence of phorbol esters, was observed to stimulate the tyrosine phosphorylation of a major 80 kDa protein by immunoblotting with anti-phosphotyrosine antibodies in Chinese hamster ovary cells overexpressing the insulin receptor and protein kinase C alpha. The protein was specifically immunoprecipitated by antibodies to protein kinase C and anti-phosphotyrosine antibodies were capable of immunoprecipitating protein kinase C enzymatic activity from these cells. When this tyrosine phosphorylated protein kinase C was treated with a tyrosine-specific phosphatase, a 35% decrease in its enzymatic activity was observed and this inhibition was blocked by inclusion of a tyrosine phosphatase inhibitor, vanadate, in the reaction mixture. These results indicate that under certain conditions insulin can stimulate the tyrosine phosphorylation of protein kinase C and this phosphorylation can affect its enzymatic activity.
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The population of Linxian in China has one of the world's highest rates for esophageal/gastric cardia cancer, as well as documented nutritional deficiencies. To determine whether dietary supplementation with a multi-vitamin multi-mineral preparation could reduce the risk of esophageal cancer and favorably influence precursor lesions, 3,318 individuals age 40-69 with cytologically determined grade 1 or grade 2 esophageal dysplasia were randomly assigned to receive either an active multi-vitamin multi-mineral supplement or a placebo. Pills were distributed at monthly visits and incident cancers or deaths were recorded. At 30 and 72 months subsequent to randomization all living participants without a known incident cancer were asked to undergo repeat cytological examination of their esophagus. Based on these procedures participants were classified as having no dysplasia, dysplasia grade 1, dysplasia grade 2 or near cancer dysplasia. Diagnoses of cancer were based on the cytology findings plus available histologic, radiologic and clinical materials. At the end of the study there was little overall difference in cumulative risk of esophageal cancer between those receiving vitamin/mineral supplementation and those receiving placebo. There was, however, a significant increase in reversion to non-dysplastic cytology among the group receiving the active treatment. The odds of not having any dysplasia at the two post-randomization screens was 1.23 times higher in the active treatment group than in the placebo group. Within each treatment group higher categories of dysplasia were associated with higher rates of cancer.