[Changes in platelet membrane glycoprotein levels in patients with cardiopulmonary resuscitation].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Jun Zhou.
Explore the source record for details and available documents.
OBJECTIVE: To study the correlation between the expression of integrin alpha5beta1 in colorectal carcinomas and the differentiation and metastasis of the tumor cells. METHODS: The expression levels of integrin alpha5beta1 were detected immunohistochemically in 81 pairs of cancerous and non-cancerous tissues of patients with colorectal cancer. RESULTS: The expression of integrin alpha5beta1 was significantly higher in the samples of colorectal carcinomas, than in non-cancerous tissues (P<0.05). Lower expression levels were detected in moderately or well differentiated colorectal carcinomas than in poorly differentiated ones (P<0.05). No significant relation was noted between the expression of integrin alpha5beta1 and lymph node metastasis of the colorectal carcinomas (P>0.05). CONCLUSION: Alpha5beta1 expression is significantly associated with the carcinogenesis and differentiation of colorectal carcinomas, but not with their lymph node metastasis, and the expression level might be used as a valuable pathological indicator for the carcinogenesis and progression of colorectal carcinomas.
OBJECTIVE: To develop a surgical model of acute hepatic failure. METHODS: Hepatectomy was performed in rats according to the method described by Higgins and Anderson. Ninety percent liver resection (removing the left lateral, median, and right lateral lobes) (n=7) and 95% liver resection leaving only half of the caudate lobe (n=13) were performed. Hypoglycemia was corrected by giving 20% glucose in the drinking water, coupled with repeated intraperitoneal injection of 5% glucose adapted to glycemia. While the survival rate, alanine transaminase (ALT) and bilirubin were observed. RESULTS: 95% liver resection decreased survival rates of the rats from 86% (90% liver resection) to 23% (P<0.05), and increased bilirubin levels (4.04+/-2.84 mg/dL vs. 1.25+/-1.85 mg/dL [90% liver resection]). CONCLUSION: 95% liver resection is a good rat model for acute hepatic failure.
OBJECTIVE: To investigate the trends in the change of etiologic types of cardiovascular disease among inpatients in Shanghai area from 1948 to 1999. METHODS: The retrospective estimate was based on the data survey in two major general hospitals of Shanghai. Descriptive statistics were provided for all patients meeting the inclusion criteria. Trend of percentage change was compared using linear regression. Diagnoses were categorized using the International Classification of Diseases, 9th Revision. RESULTS: (1) A total of 37 086 admissions with different etiologic types of heart diseases from 1948 to 1999 was reviewed. The percentage of heart diseases among the inpatients in medical wards was significantly increased during this period, being 9.89%, 15.69%, 20.91%, 23.54% and 24.24% (P < 0.05) for each decade respectively and reaching a peak in 1990s. (2) Patterns of different etiologic types of heart diseases changed markedly from 1948 to 1999. The percentage of coronary heart disease increased from 6.78% in 1940s to 39.19% in 1990s (P < 0.05), cardiac dysrhythmias from 0.63% to 18.84% (P < 0.05), cardiomyopathy from 0.05% to 5.01% (P < 0.05) and endocarditis from 0.02% to 0.69% (P < 0.05). The percentage of rheumatic heart disease decreased from 50.30% to 10.25% (P < 0.05). The percentage of hypertensive heart disease, myocarditis and congenital heart disease remained unchanged. (3) From 1948 to 1999 the overall in-hospital mortality of heart diseases in different decades decreased from 17.91%, 11.51%, 14.07%, 7.35% to 2.39% (P < 0.05). (4) Patients were slightly younger in 1950s (39.7 +/- 5.5) years than those in 1990s (60.1 +/- 12.7) years (P < 0.05). (5) The percentage of male patients increased (ranging from 50.7% in 1940s to 62.4% in 1990s, P < 0.05). CONCLUSIONS: Hospitalization patterns of heart diseases have changed dramatically in the second half of the last century in Shanghai. Coronary heart disease is the most frequent condition requiring hospitalization nowadays and the rates of many age-related heart diseases are increasing and this has been paralleled by a substantial increase of the rates in the community survey. More attention should be paid to these heart diseases in Shanghai and in this century.
OBJECTIVE: To investigate the effect of Guizhi Tang and its active components on the fever induced by EP3 receptor agonist sulprostone in rats. METHOD: The rise in body temperature evoked by a LCV(lateral cerebroventricle)-injection of sulprostone was compared with that of sulprostone induced-fever rats pretreated with Guizgi Tang and its active compounds, cinnamaldehyde, cinnamic acid and total glucosides of paeony. RESULT: Pretreatments with Guizhi Tang and cinnamaldehyde inhibited the rise in body temperature induced by sulprostone, while cinnamic acid tended to augment the fever. The sulprostone-induced fever was blocked by an ip pretreatment of total glucosides of paeony even below the basement. CONCLUSION: Present data suggest that interruption with the down-stream events of EP3 receptor may contribute to the antipyretic action of Guizhi Tang, cinnamaldehyde and the total glucosides of paeony, while cinnamic acid may have no such effect.
Faithful transmission of chromosomes during mitosis is ensured by the spindle assembly checkpoint. This molecular safeguard examines whether prerequisites for chromosome segregation have been satisfied and thereby determines whether to execute or to delay chromosome segregation. Only when all the chromosomes are attached by kinetochore microtubules from two opposite spindle poles and proper tension is placed on the paired kinetochores does anaphase take place, allowing the physical splitting of sister chromatids. Recent studies have provided novel insights into the molecular mechanisms through which the spindle assembly checkpoint is regulated by both the attachment of chromosomes to kinetochore microtubules and the tension exerted on kinetochores.
We have previously discovered the opium alkaloid noscapine as a microtubule interacting agent that binds to tubulin, alters the dynamics of microtubule assembly, and arrests mammalian cells at mitosis (Ye, K., Ke, Y., Keshava, N., Shanks, J., Kapp, J. A., Tekmal, R. R., Petros, J., and Joshi, H. C. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 1601-1606; Ye, K., Zhou, J., Landen, J. W., Bradbury, E. M., and Joshi, H. C. (2001) J. Biol. Chem. 276, 46697-46700; Zhou, J., Panda, D., Landen, J. W., Wilson, L., and Joshi, H. C. (2002) J. Biol. Chem. 277, 17200-17208). Here we show that noscapine does not compete with paclitaxel for tubulin binding and can efficiently inhibit the proliferation of both paclitaxel-sensitive and paclitaxel-resistant human ovarian carcinoma cells (i.e. the parental cell line 1A9 and two derivative cell lines, 1A9PTX10 and 1A9PTX22, which harbor beta-tubulin mutations that impair paclitaxel-tubulin interaction (Giannakakou, P., Sackett, D. L., Kang, Y. K., Zhan, Z., Buters, J. T., Fojo, T., and Poruchynsky, M. S. (1997) J. Biol. Chem. 272, 17118-17125). Strikingly, these cells undergo apoptotic death upon noscapine treatment, accompanied by activation of the c-Jun NH(2)-terminal kinases (JNK). Furthermore, inhibition of JNK activity by treatment with antisense oligonucleotide or transfection with dominant-negative JNK blocks noscapine-induced apoptosis. These findings thus indicate a great potential for noscapine in the treatment of paclitaxel-resistant human cancers. In addition, our results suggest that the JNK pathway plays an essential role in microtubule inhibitor-induced apoptosis.
Optimal NK cell development and activation as well as cytolytic activity involves IL-2R beta signals that also up-regulate expression of the pore-forming effector molecule perforin. Although the Jak/Stat pathway and specifically Stat5 transcription factors are required to promote many of the respective downstream events, the role of additional signaling pathways and transcription factors remains to be clarified. This report investigates the role of NF-kappa B activation for perforin expression by NK cells. It is demonstrated that IL-2-induced up-regulation of perforin in primary NK cells and in a model cell line is blocked by two pharmacological agents known to inhibit NF-kappa B activation. Direct evidence for the activation of the NF-kappa B pathway by IL-2R signals in NK cells involves activation of the IKK alpha kinase, inhibitory protein kappa B alpha degradation, nuclear translocation of p50/p65 complexes, and ultimately, transcriptional activation of the perforin gene via an NF-kappa B binding element in its upstream enhancer. Taken together, these observations strongly suggest that IL-2R signals can activate a pathway leading to NF-kappa B activation in NK cells and that this pathway is involved in the control of perforin expression.
We have previously identified the opium alkaloid noscapine as a microtubule interacting agent that binds stoichiometrically to tubulin and alters its conformation. Here we show that, unlike many other microtubule inhibitors, noscapine does not significantly promote or inhibit microtubule polymerization. Instead, it alters the steady-state dynamics of microtubule assembly, primarily by increasing the amount of time that the microtubules spend in an attenuated (pause) state. Further studies reveal that even at high concentrations, noscapine does not alter the tubulin polymer/monomer ratio in HeLa cells. Cells treated with noscapine arrest at mitosis with nearly normal bipolar spindles. Strikingly, although most of the chromosomes in these cells are aligned at the metaphase plate, the rest remain near the spindle poles, both of which exhibit loss of tension across kinetochore pairs. Furthermore, levels of the spindle checkpoint proteins Mad2, Bub1, and BubR1 decrease by 138-, 3.7-, and 3.9-fold, respectively, at the kinetochore region upon chromosome alignment. Our results thus suggest that an exquisite control of microtubule dynamics is required for kinetochore tension generation and chromosome alignment during mitosis. Our data also support the idea that Mad2 and Bub1/BubR1 respond to kinetochore-microtubule attachment and/or tension to different degrees.
OBJECTIVES: To construct pEGFP-hepatic growth factor (HGF) expression vector, detect its transient expression in transfected human hepatocytes, and to investigate the influence of autocrine HGF expression on the proliferative potential and cytoprotective effects in human hepatocyte. METHODS: Human HGF cDNA was ligated to pEGFP vector. The recombinant plasmid was transfected into human hepatocyte line QZG with liposome. The expression of HGF protein was observed by fluorescence microscopy and immunohistochemistry. Hepatic cells were collected 24, 48, and 72 hours after transfection to detect the number of [(3)H]-TdR uptake in DNA. DNA synthesis was observed by using PCNA stain immunohistochemistry. Acute liver cell damage was induced by carbon tetrachloride. The supernatant of culture 10 days after transfection of pEGFP-HGF was collected to put in the normal culture of hepatic cells. Another sample of supernatant was added with anti-HGF antibody to block the HGF activity as control. Cytoprotective effect was observed by examining the survival rate of hepatocytes and leakage of intracellular alanine transaminase (ALT) and potassium ions. RESULTS: HGF identification of pEGFP-HGF by enzyme digestion showed that HGF fragment had been cloned into BamH I and Sal I sites of pEGFP-N3. Expression of GFP in transfected hepatocytes was observed with fluorescence microscopy. The [(3)H]-TdR uptake became 7 times as much as in the control group 96 hours after transfection. After HGF transfection, survival rate of hepatocytes poisoned by CCl4 significantly increased (83% vs 61%, P < 0.05), and leakage of intracellular alanine transaminase and potassium ions decreased (35.16 U x L-1 vs 65.31 U x L-1, P < 0.01; and 5.59 mmol/L vs 6.02 mmol/L, P < 0.01 respectively). Culture of transfected hepatic cells promoted the proliferation of other non-transfected cells. This effect was blocked by anti-HGF antibody. CONCLUSION: Transfected HGF is expressed in hepatic cells and has the activity of promoting cell division and protecting hepatic cells against poisoning.
Repeated restraint stress (3 h/day for 3 days) causes a chronic down-regulation of body weight in rats. This study determined whether weight loss was influenced by the time of day that rats had access to food or that stress was applied. Groups of male Sprague-Dawley rats were fed a 40% kcal fat diet with food given ad libitum, only during the light phase or only during the dark phase. After 2 weeks of adaptation, rats within each feeding treatment were divided into four groups. One was exposed to repeated restraint at the start of the light phase, another was restrained at the start of the dark phase and the remaining groups were nonstressed controls for restrained rats. Body weight was significantly reduced in ad libitum- and dark-fed restrained rats, compared with nonstressed controls, from Day 2 of restraint, regardless of the time of day that they were stressed. There was no significant effect of restraint on weight change of light-fed rats. Food intake was inhibited by stress in ad libitum- and dark-fed rats, but it was not changed in light-fed rats. Serum corticosterone was increased by restraint in all rats irrespective of feeding schedule. This study demonstrates that stress-induced weight loss only occurs when rats have food available during their normal feeding period (dark phase) and is not determined by increased corticosterone release.
Five novel alkaloids, brachystemidines A-E (1-5), were isolated from the roots of Brachystemma calycinum. Their structures were established by spectral data, especially by 1D and 2D NMR techniques. The crystal structure of brachystemidine D was determined via X-ray diffraction analysis.
Two ring A-rearranged clerodane diterpenes named dunniana acids A (1) and B (2) were isolated from the aerial parts of Clausena dunniana. The structures of 1 and 2 were determined using spectral methods.
The chemical investigation of Cucubalus baccifer L. afforded three new norsesquiterpenoids, cucubalol, cucubalactone and drummondol-11-O-beta-D-glucopyranoside together with two known related compounds, drummondol and 5,7[E]-megastigmadiene-3 beta,4 alpha,9 xi-triol. Their structures were established based on spectral and chemical evidence. No activity was observed in anti-cancer (CDC25), antibacterial (PEPT) and antifungal (YNG) assays.
Several macrolides have been reported to cause QT prolongation and ventricular arrhythmias such as torsades de pointes. To clarify the underlying ionic mechanisms, we examined the effects of six macrolides on the human ether-a-go-go-related gene (HERG)-encoded potassium current stably expressed in human embryonic kidney-293 cells. All six drugs showed a concentration-dependent inhibition of the current with the following IC(50) values: clarithromycin, 32.9 microM; roxithromycin, 36.5 microM; erythromycin, 72.2 microM; josamycin, 102.4 microM; erythromycylamine, 273.9 microM; and oleandomycin, 339.6 microM. A metabolite of erythromycin, des-methyl erythromycin, was also found to inhibit HERG current with an IC(50) of 147.1 microM. These findings imply that the blockade of HERG may be a common feature of macrolides and may contribute to the QT prolongation observed clinically with some of these compounds. Mechanistic studies showed that inhibition of HERG current by clarithromycin did not require activation of the channel and was both voltage- and time-dependent. The blocking time course could be described by a first-order reaction between the drug and the channel. Both binding and unbinding processes appeared to speed up as the membrane was more depolarized, indicating that the drug-channel interaction may be affected by electrostatic responses.
OBJECTIVE: To compare peripheral T lymphocyte apoptosis of chronic bronchitis during an acute episode with that during a stable period. METHODS: Seventeen Chronic Btonchitis patients who presented to the ER with an acute episode were compared with 10 stable Chronic Bronchitis patients seen in the out-patient clinic. Peripheral venous blood was obtained from each patient and T lymphocytes were separated by fluorescent monoclonal antibodies. CD3, CD95 and CD25 were measured by flow cytometry. RESULTS: In the acute episode patients, the total quantity of T lymphocytes with CD3 was (42.63 +/-16.37) and with CD95 (14.15 +/-11.06). In the stable group T lymphocyte CD3 was (64.22 +/-23.90) and CD95 (34.88 +/-8.92) (t=-4.238, P <0.001; t=-8.796, P <0.001). The total quantity of Lymphocyte CD25 did not differ significantly between the two groups (P > 0.05). Total quantity of active T lymphocytes with CD3/CD25 was lower in the acute episode group (6.26 +/-3.94) compared to the stable group (10.52 +/-3143) (t=-1.068, P <0.05). CONCLUSION: T lymphocyte apoptosis increased in Chronic Bronchitis patients who presented with an acute episode. They also experienced a significant disturbance in immune function.
We have previously shown that gamma-tubulin, the third member of the tubulin family that functions in microtubule nucleation, when overexpressed, accumulates throughout the cytoplasm and forms numerous ectopic microtubule nucleation sites in mammalian cells (Shu and Joshi [1995] J. Cell. Biol. 130:1137-1147). We now show that overexpression of gamma-tubulin differentially upregulates the synthesis of alpha- and beta-tubulins in mammalian cells. Surprisingly, despite a dramatic increase in the level of gamma-tubulin protein in transfected cells, there is no obvious alteration in the level of endogenous gamma-tubulin mRNA, suggesting that synthesis of gamma-tubulin might employ a regulatory mechanism other than the autoregulatory pathway shared by alpha- and beta-tubulins. Interestingly, a significant number of mammalian cells transfected with gamma-tubulin fail to form normal bipolar mitotic spindle during mitosis; instead, numerous microtubules occur in the cytoplasm intermingled with the condensed chromosomes. In addition, they reduplicate their DNA after an abnormal mitotic exit. These results thus suggest that the number of microtubule nucleation sites, or even gamma-tubulin itself, might play an important role in the regulation of tubulin synthesis as well as cell cycle progression.
Explore the source record for details and available documents.