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Biomedical subjects

Z Xie

Publications and source records attributed to Z Xie.

At least 127 records · Page 7Linked to original sources

Pleiotropic alterations in lipid metabolism in yeast sac1 mutants: relationship to "bypass Sec14p" and inositol auxotrophy.

SacIp dysfunction results in bypass of the requirement for phosphatidylinositol transfer protein (Sec14p) function in yeast Golgi processes. This effect is accompanied by alterations in inositol phospholipid metabolism and inositol auxotrophy. Elucidation of how sac1 mutants effect "bypass Sec14p" will provide insights into Sec14p function in vivo. We now report that, in addition to a dramatic accumulation of phosphatidylinositol-4-phosphate, sac1 mutants also exhibit a specific acceleration of phosphatidylcholine biosynthesis via the CDP-choline pathway. This phosphatidylcholine metabolic phenotype is sensitive to the two physiological challenges that abolish bypass Sec14p in sac1 strains; i.e. phospholipase D inactivation and expression of bacterial diacylglycerol (DAG) kinase. Moreover, we demonstrate that accumulation of phosphatidylinositol-4-phosphate in sac1 mutants is insufficient to effect bypass Sec14p. These data support a model in which phospholipase D activity contributes to generation of DAG that, in turn, effects bypass Sec14p. A significant fate for this DAG is consumption by the CDP-choline pathway. Finally, we determine that CDP-choline pathway activity contributes to the inositol auxotrophy of sac1 strains in a novel manner that does not involve obvious defects in transcriptional expression of the INO1 gene.

Bacterial Proteins↗

Salicylic acid induces rapid inhibition of mitochondrial electron transport and oxidative phosphorylation in tobacco cells

Salicylic acid (SA) is known to induce alternative pathway respiration by activating expression of the alternative oxidase gene. In the present study we report a rapid mode of action by SA on plant mitochondrial functions. SA at concentrations as low as 20 &mgr;M induced inhibition of both ATP synthesis and respiratory O2 uptake within minutes of incubation in tobacco (Nicotiana tabacum) cell cultures. Biologically active SA analogs capable of inducing pathogenesis-related genes and enhanced resistance also caused rapid inhibition of ATP synthesis and respiratory O2 uptake, whereas biologically inactive analogs did not. Inhibition of ATP synthesis and respiratory O2 uptake by SA was insensitive to the protein synthesis inhibitor cycloheximide, but was substantially reduced by the antioxidant N-acetylcysteine, suggesting a possible role for reactive oxygen species in the inhibition of mitochondrial functions. With exogenous NADH as the respiratory substrate, mitochondria isolated from SA-treated tobacco cell cultures were found to have normal capacities for both ATP synthesis and respiratory O2 uptake; direct incubation of isolated mitochondria with SA had no significant effect on these mitochondrial functions. These results indicate that (a) the respiration capacities of isolated mitochondria do not correspond to the in vivo respiration activities in SA-treated cell cultures and (b) the SA-induced inhibition of respiration in tobacco cell cultures may involve other components that are not present in isolated mitochondria. Given the recently demonstrated roles of mitochondria in plant disease resistance and animal apoptosis, this rapid inhibition by SA of mitochondrial functions may play a role in SA-mediated biological processes, including plant defense responses.

Journal Article↗

Norepinephrine-stimulated MAP kinase activity enhances cytokine-induced NO production by rat cardiac myocytes.

The effect of norepinephrine (NE) on cytokine-stimulated nitric oxide (NO) production by cardiac myocytes has not been previously reported. NE alone caused no significant increase in NO-2 levels over vehicle. Addition of NE to interleukin-1beta (IL-1beta) significantly increased inducible NO synthase (iNOS) mRNA expression, iNOS protein, and NO-2 production vs. IL-1beta alone. Addition of the alpha-adrenergic blocker prazosin or the beta-adrenergic blocker propranolol partially reduced the NE-mediated increase in iNOS mRNA expression and NO-2 production. Addition of prazosin and propranolol together completely abolished the NE-induced increase in iNOS mRNA expression and NO-2 production. NE significantly enhanced mitogen-activated protein (MAP) kinase activity that was reduced by prazosin, propranolol, and PD-98059, a selective MAP kinase kinase inhibitor. Addition of PD-98059 reduced the NE-mediated increase in iNOS mRNA expression and NO-2 production. We report for the first time that NE enhances IL-1beta-stimulated NO production by activation of alpha- and beta-adrenergic receptors through a novel MAP kinase mechanism.

Adrenergic alpha-Agonists↗

TNF-alpha enhances cardiac myocyte NO production through MAP kinase-mediated NF-kappaB activation.

We have previously reported that interleukin-1beta (IL-1beta) alone induced nitric oxide (NO) production by neonatal rat cardiac myocytes (CM). The effects of tumor necrosis factor-alpha (TNF-alpha) on inducible NO synthase (iNOS) were not characterized. Unlike IL-1beta, TNF-alpha alone failed to enhance NO production in CM. However, the addition of TNF-alpha to IL-1beta significantly enhanced iNOS mRNA expression, iNOS protein synthesis, and NO production (NO(-)(2)). TNF-alpha enhancement of IL-1beta-induced NO(-)(2) production was blocked by PD-98059, a selective mitogen-activated protein (MAP) kinase kinase inhibitor, but not calphostin C (Cal C), a protein kinase C inhibitor. TNF-alpha-enhanced MAP kinase activity was associated with an increase in IL-1beta-stimulated NF-kappaB activity. PD-98059, but not Cal C, inhibited both TNF-alpha-enhanced MAP kinase and NF-kappaB activities. Thus TNF-alpha enhancement of IL-1beta-induced NO production is associated with MAP kinase-mediated activation of NF-kappaB.

Animals↗

Improvement in the capillarity of the left ventricular wall of stroke-prone spontaneously hypertensive rats following angiotensin II receptor blockade.

The effect of the angiotensin II type 1 receptor blockade, candesartan cilexetil (TCV116), on the capillarity of the innermost region of the left ventricular subendocardium were studied in stroke-prone spontaneously hypertensive rats (SHRSP). The rats were fed for 32 days on chow that contained TCV116, the average dose being 0.96 mg/kg/day. Compared with values from control SHRSP, the systolic blood pressure, left ventricular weight and cross-sectional area of cardiomyocytes decreased. A significant increase in the total capillary density was coupled with a decrease of capillary domain areas in all capillary portions. The proportion of venular capillary portions, which was low in control SHRSP, increased significantly, suggesting neoangiogenesis of capillaries. The results indicate that AT1-receptor blockade caused regression of the hypertrophied cardiomyocytes and improved capillarity of the left ventricular wall.

Angiotensin Receptor Antagonists↗

Kinetics of thermal inactivation of penaeus penicillatus acid phosphatase

The kinetics of thermal inactivation of Penaeus penicillatus acid phosphatase have been studied using a kinetic method related to the substrate reaction during irreversible inhibition of the enzyme activity as previously described by Tsou (Adv. Enzymol. Relat. Areas Mol. Biol. (1988) 61, 381-436). The kinetics of thermal inactivation of the enzyme show that the reaction is irreversible. The microscopic rate constants were determined for thermal inactivation of free enzyme and the enzyme--substrate complex. The results show that the presence of substrate has a significant protective effect against thermal inactivation of the enzyme.

Journal Article↗

Apoptosis. Molecules and mechanisms.

This review of the molecules and pathways involved in programmed cell death (apoptosis) discriminates triggers of apoptosis (e.g. chemotherapy, radiation, Fas ligation), modulators of apoptosis (e.g. Bcl-2 family members, Bcl-2 interacting proteins, Apafs, IAPs, and Fas/FasL modulators including FLICE and FLIPs), effectors (caspases 1-13) and cleavage substrates (e.g. PARP). Special consideration is given to the structure-function relationship of Bcl-2 family members and to their post-transcriptional modification. Brief references are made to the role of apoptotic pathway in leukemias and lymphomas and to strategies of modulating apoptotic pathways.

Animals↗

[The endocytic routes of exogenous antigen in murine dendritic cells and macrophages].

OBJECTIVE: To compare the endocytic routes of exogenous antigen in murine dendritic cells (DC) and macrophages. METHODS: Murine bone marrow-derived DC and peritoneal macrophages were pulsed with HRP-5 nm colloidal gold for 10 minutes and chased for 0-120 minutes in culture medium. Intracellular distribution of 5 nm colloidal gold was explored by means of cellular enzymatic-chemistry of acidic phosphatase and MHC II cellular immunochemistry under electron microscope. RESULTS: After 10 minutes pulse with HRP-5 nm colloidal gold and then 30 minutes of chase, most of HRP-5 nm colloidal gold internalized by DC entered into MHC II positive MIICs, but a little entered into acidic phosphatase-positive lysosomes. In contrast to DC, most of lysosomes of macrophages were accessed by HRP-5 nm colloidal gold, and a small portion of HRP-5 nm colloidal gold entered into MIICs. After 60 minutes of chase, 5 nm colloidal gold could hardly be seen within macrophages, whereas most of 5 nm colloidal gold retained in DC. CONCLUSION: The endocytic route of exogenous antigen in DC apparently differs from that in macrophages. Most of antigens taken by macrophages enter into lysosomes within 30 minutes. In the case of DC, most of internalized antigens enter into MIICs, which may be related to their unique antigen-presenting function. In addition, macrophages seem to have more powerful capacity of scavenging exogenous antigen than DC.

Animals↗

[Evaluation of CT in the diagnosis of esthesioneuroblastoma].

OBJECTIVE: To assess the role of CT in the diagnosis, staging and post-treatment follow-up of esthesioneuroblastoma. METHODS: Thirteen cases of pathologically comfirmed esthesioneuroblastoma were analysed retrospectively. RESULTS: On preoperative check up, according to Kadish staging, no case was in stage A, 4 cases were in stage B, 7 in stage C. Tumor scans showed soft tissue density. In 3 cases, calcification was found inside of the tumor. In the 4 cases on scan and enhanced CT, the tumors were heterogeneously enhanced in 3. On enhanced CT, the tumor density was obviously higher than that of the surrounding soft tissue in 6 cases. Postoperative follow-up CT revealed tumor recurrence within 3 months to 2 years in 4 cases. Tumor invasion involved nasal cavity and ethmoid sinus(13 cases), maxillary sinus (12 cases), sphenoid sinus(10 cases), frontal sinus (2 cases), orbit (7 cases). Intracranial invasion occurred in 3 cases, and lymph node metastases in 4 cases. CONCLUSION: CT is valuable in pre-operative staging and monitoring recurrence of esthesioneuroblastoma. Although esthesioneuroblastoma has characteristic CT features on enhancement and multiple invasions to neighboring structures, reliable diagnosis is dependent on pathological confirmation.

Adolescent↗

[Liver metastasis in colorectal cancer and tumor angiogenesis].

OBJECTIVE: To investigate the association between tumor angiogenetic activity and metastatic potential of colorectal cancer (CRC) retrospectively. METHODS: The microvessel density (MVD) and the level of vascular endothelial growth factor (VEGF) expression were examined immunohistochemically from 61 specimens obtained by surgical resection of CRC. RESULTS: MVD was (27.0 +/- 8.4) and the expression of VEGF was (59.75 +/- 12.36)%. Both were significantly higher in the group of liver metastasis, and in the group of lymph node metastasis (P < 0.01, P < 0.05). Survival analysis indicated a significant difference between increasing MVD group and the control group (P < 0.01). CONCLUSIONS: VEGF-mediated angiogenesis plays an important role in liver metastasis of CRC, and MVD appears to be a new prognostic factor for the prediction of outcome in patients with CRC.

Colorectal Neoplasms↗

[Study on cytotoxicity to leukemia cell and enhancement of immunologic functions of jiexinkang].

Cytotoxicity to leukemia cell and enhancement of immunologic functions of jiexinkang (JXK, traditional Chinese medicine) were observed in 34 cases of leukemia in vitro. The results showed that the leukemia cytotoxicity in the group of vincristine combined with JXK was significantly higher than that in vincristine alone. It was also found among all the observed cases that 20 refractory or recurred patients resistant to vincristine showed an obvious intention of the anti-toxicity efficiency when JXK was added. Jiexinkang alone had anti-leukemia cell effect, too. We explored JXK effects on immunologic functions in mice, and found that IFNr and NK activities of normal and experimental model mice were significantly higher than those of control group(P < 0.01). The results indicate that JXK has an effect of anti-leukemia cell and may improve the cell-immunologic functions.

Adjuvants, Immunologic↗

[Protective effects of ischemic preconditioning on ischemia reperfusion injuries of kidney: experimental studies].

We studied the serum levels of SOD and creatinine(Cr) of venous blood and changes in renal tissue structures under electromicroscope in the ischemia referfusion(I/R), the ischemic preconditioning(PC1, PC2, PC3), and the control groups in rabbits. The results were that the serum levels of SOD and Cr in the I/R group were obviously higher than that in the PC and control groups after one-hour ischemia and one-hour reperfusion(P < 0.001). There were no significant difference in Cr levels between the PC2 and control groups; there were significant degenerate and necrotic changes under the electromicroscope in renal tissues in the I/R group, but there were no significant change in the PC and control groups. The results suggest that PC plays a role in protecting the kidney from injury induced by ischemia and reperfusion.

Animals↗

[Electrocardiographic T-wave amplitude of normal population and its correlation with age, sex and race].

OBJECTIVE: To establish a normal electrocardiographic T wave amplitude standard in Chinese population according to age and sex. METHODS: The electrocardiographic T wave amplitudes in 4,322 persons among normal population; aged from birth to eighty-five years old divided into 11 age-groups, were analyzed. The 97.5th percentile(P97.5) and 2.5th percentile(P2.5) were considered as the upper and the lower limit of normal T wave amplitudes and T/R ratio. Wilcoxon rank sum test was used to determine whether the normal electrocardiographic T wave amplitude and the T/R ratio were different in P97.5 value versus mean + 1.96 s value, in men versus women, and in Chinese versus Americans. The linear correlation analysis was used to examine the association between normal T amplitude and age as well as between T/R ratio and age. RESULTS: The normal T wave amplitudes and T/R ratio in all leads were greater in P97.5 value than in mean + 1.96 s value and were greater in men than in women. The normal T wave amplitudes of adults were greater in Chinese than in Americans except V1 lead in which the amplitudes were greater in Americans than in Chinese. There was moderate or marked correlation of normal T wave amplitude and T/R ratio with age in most of the leads. CONCLUSION: There are marked differences of age, sex and race in normal electrocardiographic T wave amplitudes.

Adolescent↗

Association of N- and C-terminal domains of phospholipase D is required for catalytic activity.

Rat brain phospholipase D1 (rPLD1) belongs to a superfamily defined by the highly conserved catalytic motif (H(X)K(X)4D, denoted HKD. RPLD1 contains two HKD domains, located in the N- and C-terminal regions. Deletion mutants of rPLD1 that contained only an N- or C-terminal HKD domain exhibited no catalytic activity when expressed in COS 7 cells. However, when N-terminal fragments containing one of the HKD domains were cotransfected with a C-terminal fragment containing the other HKD domain, PLD activity was restored. Furthermore, immunoprecipitation assays showed that the N- and C-terminal halves of rPLD1 were physically associated when expressed in COS 7 cells. In addition, deletion of 168 amino acids from the N terminus of rPLD1 significantly enhanced basal PLD activity while inhibiting the response to phorbol ester. Likewise, the coexpression of this truncated N-terminal half with the C-terminal half resulted in increased PLD activity. In summary, this study provides direct evidence that the enzymatic activity of rPLD1 requires the presence of the HKD domains in both the N- and C-terminal regions of the molecule. More importantly, the two halves of rPLD1 can associate, and this may be essential to bring the two HKD domains together to form an active catalytic center. These findings provide new insights into the catalytic mechanism of enzymes of the PLD superfamily.

Animals↗