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Publications and source records attributed to J Su.
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We determined the Zeta sedimentation ratio (ZSR) for 326 normal subjects and 106 inpatients by Chinese-built Zetafuge. The mean ZSR for normal subjces was 52.5 +/- 5.05% and that for inpatients 68.52 +/- 5.54% (P < 0.001). ZSR can be determined by using directly the blood sample with the anticoagulant EDTA-K2; the determination is faster and requires less volume of blood sample; it is not affected by anemia and need not be corrected for age and sex. The results of ZSR are expressed in a new unit, %, not in mm/h. The reference value we established is: < or = 62%. We also discussed the problem of reproducibility, the speed of centrifuge, the height of blood, and compared this method with the westergren method. The agreement between the two methods is 86.6%.
OBJECTIVE: To determine the influence of Sini Decoction (SND) on living quality of patients after percutaneous transluminal coronary angioplasty (PTCA). METHODS: Randomized case-control clinical trail was conducted to evaluate the living quality of 40 post-PTCA patients before and after SND treatment by scoring. RESULTS: The scores in physical symptoms, sense of well-being, depression, satisfaction of life and work capacity of patients after PTCA were improved significantly as compared with before PTCA, P < 0.05-0.01. Scores of patients received SND treatment were higher than those untreated with SND in the first three criteria, P < 0.05, particularly on relieving palpitation and dyspnea. CONCLUSION: SND is helpful to improve the living quality of patients after PTCA.
Grafting hydrogels onto silicone rubber membranes were prepared by radiation technique for medical application. This material is characterized by high purity, hydrophilia, formation of stable hydrogel after water absorption, good biocompatibility, etc. Clinical application was initiated on the basis of animal experiments. The material was used in 47 cases of joint and tendon injuries, in 9 cases of rheumatoid arthritis, and in 4 other cases; totaling 60 cases. All patients were followed up for three and a half years after surgical operation. A general effectiveness of above 86% was noted.
Two flavonoid compounds were isolated from the whole plants of Drosera burmannii Vahl. They were identified as quercetin (I) and hyperoside (II) by means of physicochemical properties and spectral analysis (UV, IR, 1HNMR, 13CNMR and MS).
Mutation of the p53 gene has been reported in hepatocellular carcinoma (HCC) occurring worldwide. The most frequent p53 mutation has been found in HCCs in regions with high hepatitis B virus (HBV) infection and intake of aflatoxin B1 (AFB1). The aim of our study was to examine p53 protein expression in HCCs from a high incidence area of Guangxi, Southern China, where HBV infection and dietary intake of AFB1 are high. Immunohistochemical staining of p53 protein was carried out using a polyclonal rabbit antibody (CM-1). Serial sections were also stained for hepatitis B surface antigen and core antigen. p53 Protein expression was detected in 13 (43.3%) of the 30 HCCs. Expression of p53 was found in 25.0% (1/4) of the < or = 5.0 cm diameter HCCs, in 36.8% (7/19) of the 5.1-10.0 cm diameter HCCs and in 71.4% (5/7) of the >10.0 cm diameter HCCs. Expression of p53 was observed more in moderately and poorly differentiated than in the well differentiated HCCs and more frequently seen in HCCs from younger patients. These data indicate that there is a close association between p53 protein expression and tumor size, histological grade and age of patients. Twenty-seven out of 30 cases (90.0%) were positive for HBV. No significant association between p53 expression and sex. HBV infection, cirrhosis or alpha-fetoprotein has been found.
Recent evidence suggests that AD is associated with the development of cerebral amyloid angiopathy and with significant changes in the blood-brain barrier glucose transporter and basement membrane protein alterations. It is likely that these changes significantly contribute to chronic cerebral hypoperfusion, possibly resulting in progressive neural death in AD. To investigate the etiology of these changes, we have analyzed postmortem tissue sections of frontal cortex of moderately demented AD cases, stained using both single-label and double-label immunocytochemistry to detect vessels and beta-amyloid. The resultant color images are analyzed using HSV (hue-saturation-value) color image analysis, shape analysis, and histogram analysis techniques. These analyses let us segment the tissue images for further statistical analyses.
TIMP-4, a novel human tissue inhibitor of metalloproteinase, was identified and cloned (Greene, J., Wang, M., Raymond, L. A., Liu, Y. E., Rosen, C., and Shi, Y. E. (1996) J. Biol. Chem. 271, 30375-30380). In this report, the production and characterization of recombinant TIMP-4 (rTIMP4p) are described. rTIMP4p, expressed in baculovirus-infected insect cells, was purified to homogeneity by a combination of cation exchange, hydrophobic, and size-exclusion chromatographies. The purified protein migrated as a single 23-kDa band in SDS-polyacrylamide gel electrophoresis and in Western blot using a specific anti-TIMP-4 antibody. Inhibition of matrix metalloproteinase (MMP) activities by rTIMP4p was demonstrated in five MMPs. Enzymatic kinetic studies revealed IC50 values (concentration at 50% inhibition) of 19, 3, 45, 8, and 83 nM for MMP-1, MMP-2, MMP-3, MMP-7, and MMP-9, respectively. Purified rTIMP4p demonstrated a strong inhibitory effect on the invasion of human breast cancer cells across reconstituted basement membranes. Thus, TIMP-4 is a new enzymatic inhibitor in MMP-mediated extracellular matrix degradation and may have therapeutic potential in treating cancer malignant progression.
A novel human tumor growth inhibitor was identified by differential cDNA sequencing. The predicted amino acid sequence of this tumor-suppressing factor has a significant sequence homology to mouse mammary-derived growth inhibitor and thus was named mammary-derived growth inhibitor-related gene (MRG). MRG was found to be expressed in normal and benign human breast tissues but not in breast carcinomas. In situ hybridization analysis demonstrated a stage-specific MRG expression as follows. MRG was barely detectable in breast carcinomas, showed partial and weak expression in benign hyperplasia, but was expressed at a high level in normal breast epithelial cells. To determine if MRG can modulate in vivo growth of human breast cancers, we transfected a full-length MRG cDNA into MDA-MB-231 human breast cancer cells and studied the orthotopic growth of MRG transfectants versus control transfectants in the mammary fat pad of athymic nude mice. Overexpression of MRG in human breast cancer cells significantly suppressed cell proliferation in vitro and tumor growth in an orthotopic nude mouse model. These results suggest that MRG has tumor-suppressing activity, and the loss of MRG expression may be involved in the development and progression of breast cancer.
STRL22 is a human seven transmembrane domain orphan receptor related to known chemokine receptors and expressed in peripheral blood lymphocytes, tumor infiltrating lymphocytes and lymphoid tissues. MIP-3alpha/LARC/Exodus is a CC chemokine that is chemotactic for lymphocytes and that is expressed in activated cells, including monocytes, T cells, endothelial cells, and fibroblasts, and in liver, lung, and some lymphoid tissues. We report here that STRL22-transfected human embryonic kidney 293 cells demonstrated specific binding for MIP-3alpha and that MIP-3alpha, but no other chemokines, produced a calcium flux in the STRL22-transfected cells. We show that MIP-3alpha, unlike other chemokines, produced a calcium flux in freshly-isolated peripheral blood lymphocytes and we show that MIP-3alpha also produced a signal in tumor infiltrating lymphocytes that express STRL22. Since STRL22 is the sixth functional CC chemokine receptor identified, it should be re-named CCR6.
BACKGROUND: X-linked dilated cardiomyopathy (XLCM) has previously been shown to be due to mutations in the dystrophin gene, which is located at Xp21. Mutations in the 5' portion of the gene, including the muscle promoter, exon 1, and the exon 1-intron 1 splice site, have been reported previously. The purpose of this study was to analyze the originally described family with XLCM (and other) for dystrophin mutations. METHODS AND RESULTS: Polymerase chain reaction (PCR) was used to amplify genomic DNA, and reverse-transcriptase PCR amplified cDNA from RNA obtained from heart and lymphoblastoid cell lines. Primers to the muscle promoter, brain promoter, and Purkinje cell promoter were designed, in addition to the exon 1 to exon 14 regions of dystrophin. Single-strand conformation polymorphism analysis was used for mutation detection, and DNA sequencing defined the mutation. Protein modeling was used for amino acid and secondary structure analysis. A missense mutation in exon 9 at nucleotide 1043 was identified that causes an alanine to be substituted for threonine, a highly conserved amino acid, at position 279 (T279A). This mutation results in a change in polarity in the evolutionarily conserved first hinge region (H1) of the protein and substitution of a beta-sheet for alpha-helix in this portion of the protein, destabilizing the protein. CONCLUSIONS: A novel missense mutation in exon 9 of dystrophin causing an abnormality at H1 leads to the cardiospecific phenotype of XLCM.
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A new member of the human cystatin superfamily, called cystatin E, has been found by expressed sequence tag (EST) sequencing in amniotic cell and fetal skin epithelial cell cDNA libraries. The sequence of a full-length amniotic cell cDNA clone contained an open reading frame encoding a putative 28-residue signal peptide and a mature protein of 121 amino acids, including four cysteine residues and motifs of importance for the inhibitory activity of Family 2 cystatins like cystatin C. Recombinant cystatin E was produced in a baculovirus expression system and isolated. An antiserum against the recombinant protein could be used for affinity purification of cystatin E from human urine, as confirmed by N-terminal sequencing. The mature recombinant protein processed by insect cells started at amino acid 4 (cystatin C numbering), and displayed reversible inhibition of papain and cathepsin B (Ki values of 0.39 and 32 nM, respectively), in competition with substrate. Cystatin E is thus a functional cysteine proteinase inhibitor despite relatively low amino acid sequence similarities with human cystatins (26-34% identity with sequences for the Family 2 cystatins C, D, S, SN, and SA; <30% with the Family 1 cystatins, A and B, and domains 2 and 3 of the Family 3 cystatin, kininogen). Unlike other human low Mr cystatins, cystatin E is a glycoprotein, carrying an N-linked carbohydrate chain at position 108. Northern blot analysis revealed that the cystatin E gene is expressed in most human tissues, with the highest mRNA amounts found in uterus and liver. A strikingly high incidence of cystatin E clones in cDNA libraries from fetal skin epithelium and amniotic membrane cells (>0.5% of clones sequenced) indicates a protective role of cystatin E during fetal development.
Several studies have demonstrated that green tea (GT) inhibits various chemically induced cancers in experimental animals. In the present study, effect of GT has been examined on the initiation of aflatoxin B1 (AFB1)-induced hepatocarcinogenesis in the rat. Young male Fischer rats were given AIN-76A diet with or without 0.5% instant GT powder in their drinking water for 2 or 4 weeks. Initiation was examined by hepatic AFB1-DNA binding in vivo, AFB1 metabolism in vitro and by the appearance of AFB1-induced glutathione S-transferase placental form (GST-P)-positive hepatocytes detected by immunohistochemical method. There was no influence of GT feeding on microsome-mediated AFB1 binding to exogenous DNA. However, GT feeding enhanced microsome-mediated formation of non-toxic hydroxylated metabolites of AFB1 by 2-3-fold. Hepatic nuclear AFB1-DNA binding in vivo was significantly inhibited by about 20-30% in animals pretreated with GT: AFB1-induced GST-P positive single hepatocytes were inhibited significantly by 60-70% in rats pretreated with GT. These results suggest that feeding of GT inhibits initiation of AFB1-induced hepatocarcinogenesis in the rat by modulation of AFB1 metabolism, thereby inhibiting AFB1-DNA binding and AFB1-induced GST-P-positive hepatocytes.
UNLABELLED: Postoperative pain is a common reason for the delayed discharge and unanticipated hospital admission of out-patients. In this study, we examined the pattern of pain in ambulatory surgical patients and determined those factors that predict postoperative pain. Ten thousand eight consecutive ambulatory surgical patients were prospectively studied. Preoperative patient characteristics, intraoperative variables, and pain in the postanesthesia care unit (PACU) and the ambulatory surgical unit (ASU) and 24 h postoperatively were documented. The incidence of severe pain was 5.3% in the PACU, 1.7% in the ASU, and 5.3% 24 h postoperatively. In the PACU, younger male adults (36 +/- 13 vs 47 +/- 22 yr), ASA physical status I patients, and patients with a higher body mass index (26 +/- 5 vs 25 +/- 5 kg) had a higher incidence of severe pain. In the group with severe pain, the duration of anesthesia, the duration of stay in the PACU and the ASU, and the time to discharge was longer than in the group without severe pain. In the PACU, orthopedic patients had the highest incidence of pain (16.1%), followed by urologic (13.4%), general surgery (11.5%), and plastic surgery (10.0%) patients. In patients who had general anesthesia, the intraoperative dose of fentanyl was significantly smaller in the group with severe pain than in the group without severe pain when body mass index and duration of anesthesia were taken into consideration. Body mass index, duration of anesthesia, and certain types of surgery were significant predictors of severe pain in the PACU. This knowledge will allow us to identify those patients at risk of severe postoperative pain and manage them prophylactically. IMPLICATIONS: The pattern of pain was examined in 10,008 consecutive ambulatory surgical patients. The incidence of severe pain was 5.3% in the postanesthesia care unit, 1.7% in the ambulatory surgical unit, and 5.3% 24 h postoperatively. Body mass, duration of anesthesia, and certain types of surgery were significant predictors of pain in the postanesthesia care unit. These data will allow us to better predict those patients who need intense prophylactic analgesic therapy.
This study examined in conscious dogs, the coronary and regional myocardial effects of bradykinin (BK) administered by intracoronary route and their modulation by an angiotensin-converting enzyme inhibitor. Eleven dogs were chronically instrumented with a left ventricular (LV) micromanometer, a circumflex coronary catheter, a flow probe, and ultrasonic crystals in the LV posterior wall. In the absence of systemic hemodynamic changes, BK (0.1-10 ng/kg i.c.) produced dose-dependent increases in coronary blood flow velocity (CBFV) and in LV posterior end-diastolic wall thickness (EDWT) but produced no change in LV regional myocardial function as assessed by LV posterior systolic wall thickening. The increases in LV EDWT and CBFV were linearly correlated. The BK B2 antagonist (HOE 140) abolished the effects of BK. Intracoronary enalaprilat (0.75 mg) extended the duration of the effect of BK on CBFV without modification of peak responses and induced a further increase in LV posterior EDWT but no change in LV regional myocardial function. Thus, in conscious dogs, the vasodilator effect of intracoronary BK alone or modulated by enalaprilat is not associated with changes in LV regional myocardial function.
It has been known that anoxic preconditioning (APC) has protective effects not only on cardiomyocyte, but also on vasculature. However, the effects of APC on vascular smooth muscle cells (VSMC) is unknown. On the model of anoxia/reoxygenation (A/R) injury of rabbit VSMC, the effect of APC was observed. It was found that APC could increase the survival rate of VSMC after A/R injury, lower the leakage of lactate dehydrogenase (LDH) and protein from cells, and attenuate peroxidation injury and calcium overload of VSMC. The results also showed that PMA, an activator of protein kinase C (PKC), could mimic, but H7 or polymyxin B (inhibitors of PKC) could abolish the above protective effect of APC. It is suggested that the protective effect of APC on VSMC during A/R injury might be due to the activation of PKC.
This work was done on rat tourniquet shock (ToS) model. It was found that reactivity of isolated perfused aortic ring to noradrenaline decreased, while cGMP content of the aortic tissue increased. These changes could be potentiated by perfusion with L-arginine (NO-precursor). On the other side, when the aortic ring was perfused with L-NNA (NO-synthesis inhibitor) or methylene blue (soluble cGMPase inhibitor), the changes could be attenuated. The effect of these drugs are independent of the presence of vascular endothelium. The results suggest that non-endothelium-derived NO-like relaxing factor may be one of the factors causing low vascular reactivity of the ToS animals.