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Biomedical subjects

J G Zhang

Publications and source records attributed to J G Zhang.

At least 19 recordsLinked to original sources
PubMed2006

Fermentation quality and nutritive value of a total mixed ration silage containing coffee grounds at ten or twenty percent of dry matter.

Six wethers were used in a replicated 3 x 3 Latin square to study the fermentation quality and nutritive value of total mixed ration (TMR) silages that included wet coffee grounds (WCG). The TMR were prepared using a commercial compound feed, timothy hay, alfalfa hay, dried beet pulp, and a vitamin-mineral supplement in a ratio of 36.5:30:20:12:1.5, respectively, on a DM basis, with timothy hay and alfalfa hay being replaced by WCG at 0, 10, or 20%. All TMR silages, irrespective of WCG addition, were well preserved, with a low pH and ammonia-N content and a high lactic acid content. Intakes by wethers of TMR silages containing 0 and 10% WCG were 96.6 and 94.8 g/kg of BW(0.75), and did not differ (P > 0.05). Intake of TMR silage containing 20% WCG was 76.8 g/kg of BW(0.75), which was equal to 80% of that of the TMR silage with no WCG (quadratic: P < 0.01). Increasing concentrations of WCG in the rations decreased the digestibility of DM, CP, ADF, NDF, and energy, and increased that of ether extract (P < 0.05). The TDN and DE contents of the TMR silages with 0 and 10% WCG were similar, but the TMR silage with 20% WCG was lower (P < 0.05). With progressive increases in WCG concentrations, N intake did not differ, but fecal and urinary N increased linearly (P < 0.001), and retained N decreased linearly (P < 0.001). This study demonstrated that the proportion of WCG to be incorporated into TMR silages should not exceed 10% of the DM.

Ammonia↗
PubMed2005

The role of preoperative pulmonary function tests in the surgical treatment of scoliosis.

STUDY DESIGN: A retrospective study on the correlation between preoperative pulmonary function tests, preoperative pulmonary symptoms, and postoperative pulmonary complications. OBJECTIVE: To evaluate the incidence of immediate postoperative pulmonary complications and their correlation to pulmonary function tests, preoperative pulmonary symptoms, and surgical approaches. SUMMARY OF BACKGROUND DATA: The pulmonary function of patients with scoliosis is likely to be abnormal, whereas surgical procedures may lead to further deterioration and postoperative pulmonary complications. Evaluation of the pulmonary symptoms and pulmonary function before surgery is helpful to predict and avoid postoperative pulmonary complications by selecting the appropriate surgical approach. METHODS: This study reviewed 298 scoliosis patients (107 male, 191 female) who underwent anterior and/or posterior operation. The mean age of the patients was 16.4 years (range 6-62 years). The average coronal Cobb angle was 73.26 degrees (range 45-141 degrees). Preoperative pulmonary function tests of 115 cases were normal, whereas the other 183 cases were abnormal. Seventeen cases had preoperative pulmonary symptoms and 3 of them had normal preoperative pulmonary function tests. Seventy-nine cases received transthoracic surgery, and 19 cases had postoperative pulmonary complications, including postoperative ventilation support in 6 cases, atelectasis in 4 cases, hydrothorax in 2 cases, pneumothorax in 3 cases, pneumonia in 3 cases, and hypoxemia in 1 case. Of these 19 patients, 12 patients received anterior transthoracic procedure. When the patients with abnormal pulmonary function tests were divided into 3 groups: 1) 60% < or = forced vital capacity ratio < 80%; 2) 40% < or = forced vital capacity ratio < 60%; and 3) forced vital capacity ratio < 40%, the incidence of postoperative pulmonary complications were 2.72% (3 out of 110), 7.40% (4 out of 54) and 31.60% (6 out of 19), respectively. RESULTS: There was significant correlation between abnormal preoperative pulmonary function tests and preoperative pulmonary symptoms (P = 0.0086). No significant correlation was found between preoperative pulmonary symptoms and postoperative pulmonary complications (P = 0.5164). There was a trend that the postoperative complications increased with the deterioration of pulmonary function. The correlation between postoperative pulmonary complications and the surgical approach was statistically significant (P = 0.0000); the incidence of postoperative pulmonary complication of transthoracic procedure was 18 times as that of posterior approach. No significant difference was noted regarding ages, preoperative coronal Cobb angles, and preoperative pulmonary function between these 2 groups. There was no significant correlation between preoperative pulmonary symptoms and postoperative complications. CONCLUSIONS: The incidence of postoperative pulmonary complications increased with the deterioration of pulmonary function tests. The posterior procedure had a very low incidence of postoperative pulmonary complications, but a transthoracic procedure increased the complications significantly. Preoperative pulmonary symptoms usually predicted abnormal results of pulmonary function tests but had no correlation with postoperative pulmonary complication.

Adolescent↗
PubMed2002

Ten-year follow-up study of lower thoracic hemivertebrae treated by convex fusion and concave distraction.

STUDY DESIGN: A retrospective review of patient records with recent clinical and radiologic assessment was conducted. OBJECTIVE: To evaluate the long-term results of fully segmented hemivertebrae treated by convex fusion combined with instrumented concave subcutaneous distraction. SUMMARY OF BACKGROUND DATA: Convex fusion has been described for the treatment of hemivertebrae in children, whereas distraction without fusion has been shown to enhance spinal growth. No long-term follow-up studies have combined these two methods. METHODS: Between 1986 and 1994, six consecutive patients (5 males and 1 female) with hemivertebrae located at T11 or T12 underwent convex anterior and posterior fusion as well as concave subcutaneous distraction without fusion. RESULTS: The mean age at surgery was 3.4 years. The mean follow-up period was 10.8 years (range, 8-14 years). There was a mean improvement of 41% in the coronal deformity, from a mean angle of 49 degrees before surgery to 29 degrees at the latest follow-up assessment. In four of the cases, this correction was achieved immediately after surgery and did not significantly change despite repeated distraction. The kyphosis improved in three cases, remained unchanged in one case, and deteriorated in two cases. In these two cases, an adjacent wedge vertebra contributed to the kyphotic deformity. CONCLUSIONS: Although growth-mediated correction was seen in only two cases, this procedure could be recommended for children with severe deformities and decompensation in the lower thoracic spine. It is safer than hemivertebra excision, with less risk of spinal cord injury. The concave distraction produces immediate improvement in the coronal balance, such that there is no need to wait for uncertain growth-mediated correction in patients who undergo convex fusion only.

Child, Preschool↗
PubMed2001

Vitamin E succinate protects hepatocytes against the toxic effect of reactive oxygen species generated at mitochondrial complexes I and III by alkylating agents.

The mechanism of alpha-tocopheryl succinate (TS) cytoprotection against mitochondria-derived oxidative stress was investigated. Incubation of isolated rat hepatocytes with ethyl methanesulfonate (EMS), a mitochondrial alkylating toxicant caused mitochondrial dysfunction and necrotic cell death that was dependent on the production of reactive oxygen species (ROS) and lipid peroxidation. Mitochondria isolated from these cells showed a 3-fold increase in lipid hydroperoxides and a selective depletion of alpha-tocopherol (T), which preceded cell death. The pretreatment of hepatocytes with TS dramatically enriched cells and mitochondria with alpha-tocopherol and provided these membranes with complete protection against EMS-induced oxidative damage. TS pretreatment suppressed EMS-induced cellular ROS production, generated from mitochondrial complex I and III sites. In addition, the treatment with either rotenone (ROT, a complex I inhibitor) or antimycin A (AA, a complex III inhibitor) potentiated EMS-induced lipid peroxidation and necrotic cell death which were again completely prevented by TS treatment. Surprisingly, TS did not protect hepatocytes against thenoyltrifluoroacetone (TTFA), a complex II inhibitor-induced enhancement of EMS-induced toxic oxidative damage. We conclude that the inhibition of mitochondrial ROS production and lipid peroxidation by T released from TS, are the critical events responsible for TS-mediated cytoprotection against toxic oxidative stress derived from both mitochondrial complexes I and III. Our findings suggest that TS treatment may prove useful in combating diseases associated with mitochondrial-derived oxidative stress.

Animals↗
PubMed2001

The SOCS box of suppressor of cytokine signaling-1 is important for inhibition of cytokine action in vivo.

Suppressor of Cytokine Signaling-1 (SOCS-1) is an essential physiological inhibitor of IFN-gamma signaling. Mice lacking this gene die in the early postnatal period from a disease characterized by hyperresponsiveness to endogenous IFN-gamma. The SOCS box is a C-terminal domain shared with over 30 other proteins that links SOCS proteins to an E3 ubiquitin ligase activity and the proteasome, but whether it contributes to inhibition of cytokine signaling is currently disputed. We have deleted only the SOCS box of the SOCS-1 gene in mice and show that such mice have an increased responsiveness to IFN-gamma and slowly develop a fatal inflammatory disease. These results demonstrate that deletion of the SOCS box leads to a partial loss of function of SOCS-1.

Animals↗
PubMed2001

Mitochondrial electron transport inhibitors cause lipid peroxidation-dependent and -independent cell death: protective role of antioxidants.

Mitochondrial electron transport inhibitors induced two distinct pathways for acute cell death: lipid peroxidation-dependent and -independent in isolated rat hepatocytes. The toxic effects of mitochondrial complex I and II inhibitors, rotenone (ROT) and thenoyltrifluoroacetone (TTFA), respectively, were dependent on oxidative stress and lipid peroxidation, while cell death induced by inhibitors of complexes III and IV, antimycin A (AA) and cyanide (CN), respectively, was caused by MMP collapse and loss of cellular ATP. Accordingly, cellular and mitochondrial antioxidant depletion or supplementation, in general, resulted in a dramatic potentiation or prevention, respectively, of toxic injury induced by complex I and II inhibitors, with little or no effect on complex III and IV inhibitor-induced toxicity. ROT-induced oxidative stress was prevented by the addition of d-alpha-tocopheryl succinate (TS) but surprisingly TS did not afford hepatocytes protection against TTFA-induced oxidative damage. TS treatment prevented ROT-induced mitochondrial lipid hydroperoxide formation but had no effect on the loss of mitochondrial GSH or cellular ATP, suggesting a mitochondrial lipid peroxidation-mediated mechanism for ROT-induced acute cell death. In contrast, only fructose treatment provided excellent cytoprotection against AA- and CN-induced toxicity. Our findings indicate that complex III and IV inhibitors cause a rapid and severe depletion of cellular ATP content resulting in acute cell death that is dependent on cellular energy impairment but not lipid peroxidation. In contrast, inhibitors of mitochondrial complex I or II moderately deplete cellular ATP levels and thus cause acute cell death via a lipid peroxidation pathway.

Adenosine Triphosphate↗
PubMed2001

Enhanced antioxidant and cytoprotective abilities of vitamin E succinate is associated with a rapid uptake advantage in rat hepatocytes and mitochondria.

Numerous in vitro studies attest to the enhanced ability of vitamin E succinate (TS), as compared with conventional vitamin E compounds such as unesterified d-alpha-tocopherol (T) and d-alpha-tocopheryl acetate (TA), to protect hepatocytes from toxic oxidative stress. In the present study we tested the hypothesis that this unique protective ability is related to an enhanced cellular accumulation of TS. The results of this study indicate, using both in vitro and in vivo model systems, that acute TS administration results in a rapid increase in T and TS content and antioxidant protection of hepatocytes and mitochondria. In contrast, conventional vitamin E compounds such as T and TA lack these same protective properties. We suggest that TS acts as a unique delivery system for T, rapidly accumulating in cellular and mitochondrial membranes and gradually releasing active T to prevent membrane oxidative damage. We propose that TS administration may prove useful for the prevention and treatment of oxidative stress-mediated diseases, especially those of mitochondrial origin.

Animals↗
PubMed2001

SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice.

Prolactin is essential for proliferation and differentiation of the developing mammary gland. We have explored a role for Suppressor of Cytokine Signaling 1 (SOCS1) as a modulator of the prolactin response using mice deficient in SOCS1, which were rescued from neonatal death by deletion of the Interferon gamma (IFN gamma) gene. SOCS1(-/-)/IFN gamma(-/-) mice exhibited accelerated lobuloalveolar development in the mammary gland during late pregnancy and precocious lactation. Significantly, the lactogenic defect in prolactin receptor heterozygous females could be rescued by deletion of a single SOCS1 allele. These findings establish a role for SOCS1 as a negative regulator of prolactin signaling and suggest that SOCS1 is required for the prevention of lactation prior to parturition.

Alleles↗
PubMed2001

Suppressor of cytokine signaling-1 attenuates the duration of interferon gamma signal transduction in vitro and in vivo.

Suppressor of cytokine signaling-1 (SOCS-1) is a cytokine-inducible intracellular protein that functions to negatively regulate cytokine signal transduction pathways. Studies in vitro have shown that constitutive overexpression of SOCS-1 inhibits signaling in response to a range of cytokines, including interferons (IFN). Mice lacking SOCS-1 die from a complex disease characterized by liver degeneration and massive inflammation. Whereas there is clear evidence of increased IFNgamma signaling in SOCS-1(-/-) mice, it is unclear to what extent this is due to increased IFNgamma levels or to increased IFNgamma sensitivity. Here we have used SOCS-1(-/-) IFNgamma(-/-) mice, which remain healthy and produce no endogenous IFNgamma, to demonstrate that in vitro and in vivo hepatocytes lacking SOCS-1 exhibit a prolonged response to IFNgamma and that this correlates with a dramatically increased sensitivity to the toxic effects of IFNgamma in vivo. Thus, SOCS-1 is required for the timely attenuation of IFNgamma signaling in vivo.

Animals↗
PubMed2001

Endoplasmic reticulum stress prolongs GH-induced Janus kinase (JAK2)/signal transducer and activator of transcription (STAT5) signaling pathway.

The desensitization of the GH-induced Janus kinase 2 (JAK2) and signal transducer and activator of transcription 5 (STAT5) signaling pathway plays a crucial role in GH regulation of hepatic genes. Previous studies have demonstrated that the inactivation of the GH-induced JAK2/STAT5 pathway is regulated by protein translation and suppressors of cytokine signaling (SOCS). In this study we sought to explore the relationships between endoplasmic reticulum stress, GH-induced JAK2/STAT5 activity and SOCS expression. 1,2-bis(o-Aminophenoxy)ethane-N,N,N,N-tetraacetic acid (acetoxymethyl)ester (BAPTA-AM), used to provoke endoplasmic reticulum stress, caused a drastic inhibition of protein translation that correlated with the phosphorylation of the eukaryotic translation initiation factor 2alpha. Both GH and BAPTA-AM caused a rapid induction of the transcription factor C/EBP homology protein (CHOP) and an additive effect was observed with combined treatment, which suggests a regulatory role of GH on endoplasmic reticulum stress. Endoplasmic reticulum stress did not interfere with the rapid GH activation of STAT5 DNA binding activity. However, BAPTA-AM prolonged the DNA binding activity of STAT5 without affecting STAT5 or JAK2 protein levels. GH-induced phosphorylation of JAK2 and STAT5 DNA binding activity were prolonged in the presence of BAPTA-AM, suggesting that endoplasmic reticulum stress prevents the inactivation of STAT5 DNA binding activity by modulating the rate of JAK2/STAT5 dephosphorylation. Like BAPTA-AM, the endoplasmic reticulum stressors dithiothreitol and A23187 also prolonged the GH-induced STAT5 DNA binding activity. We were not able to correlate BAPTA-AM effects to the GH-dependent expression of SOCS proteins or SOCS mRNA, suggesting that endoplasmic reticulum stress modulates the rate of JAK2/STAT5 dephosphorylation through mechanisms other than inhibition of SOCS expression. This study indicates that cellular stress may modulate transcription through the JAK/STAT pathway.

Animals↗
PubMed2000

Competition and coexistence in spatially subdivided habitats.

While non-spatial models predict that like species cannot stably coexist, empirical studies suggest that similar species have similar distributions due to shared habitat requirements. A model is developed to discuss competition and coexistence in subdivided but locally stable habitats. The model predicts that in some cases it is possible for one species to exclude the other species from a geographic region, while in other cases two competing species can stably coexist. The equilibrium level and the fraction of doubly occupied patches, if there is coexistence, are determined by the strength of competition on colonization and exclusion in such a system. Also, it is possible for two ecologically identical species to stably coexist, and two asymmetrically competing species can coexist when there is a trade-off between local competition ability and invasion ability. When rescue effects are considered, the stable region at internal equilibrium point would be reduced, but the fraction of doubly occupied patches would be enlarged.

Animals↗
PubMed2000

Glutathione depletion and the production of reactive oxygen species in isolated hepatocyte suspensions.

Diethyl maleate (DEM) (5 mM) and ethyl methanesulfonate (EMS) (35 mM) treatments rapidly depleted cellular reduced glutathione (GSH) below detectable levels (1 nmol/10(6) cells), and induced lipid peroxidation and necrotic cell death in freshly isolated rat hepatocytes. In hepatocytes incubated with 2.5 mM DEM and 10 mM EMS, however, the complete depletion of cellular GSH observed was not sufficient to induce lipid peroxidation or cell death. Instead, DEM- and EMS-induced lipid peroxidation and cell death were dependent on increased reactive oxygen species (ROS) production as measured by increases in dichlorofluorescein fluorescence. The addition of antioxidants (vitamin E succinate and deferoxamine) prevented lipid peroxidation and cell death, suggesting that lipid peroxidation is involved in the sequence of events leading to necrotic cell death induced by DEM and EMS. To investigate the subcellular site of ROS generation, the cytochrome P450 inhibitor, SKF525A, was found to reduce EMS-induced lipid peroxidation but did not protect against the loss of cell viability, suggesting a mitochondrial origin for the toxic lipid peroxidation event. In agreement with this conclusion, mitochondrial electron transport inhibitors (rotenone, thenoyltrifluoroacetone and antimycin A) increased EMS-induced lipid peroxidation and cell death, while the mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone, blocked EMS- and DEM-mediated ROS production and lipid peroxidation. Furthermore, EMS treatment resulted in the significant loss of mitochondrial alpha-tocopherol shortly after its addition, and this loss preceded losses in cellular alpha-tocopherol levels. Treatment of hepatocytes with cyclosporin A, a mitochondrial permeability transition inhibitor, oxypurinol, a xanthine oxidase inhibitor, or BAPTA-AM, a calcium chelator, provided no protection against EMS-induced cell death or lipid peroxidation. Our results indicate that DEM and EMS induce cell death by a similar mechanism, which is dependent on the induction of ROS production and lipid peroxidation, and mitochondria are the major source for this toxic ROS generation. Cellular GSH depletion in itself does not appear to be responsible for the large increases in ROS production and lipid peroxidation observed.

Alkylating Agents↗
PubMed2000

Suppressor of cytokine signaling-3 preferentially binds to the SHP-2-binding site on the shared cytokine receptor subunit gp130.

Suppressor of cytokine signaling-3 (SOCS-3) is one member of a family of intracellular inhibitors of signaling pathways initiated by cytokines that use, among others, the common receptor subunit gp130. The SH2 domain of SOCS-3 has been shown to be essential for this inhibitory activity, and we have used a quantitative binding analysis of SOCS-3 to synthetic phosphopeptides to map the potential sites of interaction of SOCS-3 with different components of the gp130 signaling pathway. The only high-affinity ligand found corresponded to the region of gp130 centered around phosphotyrosine-757 (pY757), previously shown to be a docking site for the tyrosine phosphatase SHP-2. By contrast, phosphopeptides corresponding to other regions within gp130, Janus kinase, or signal transducer and activator of transcription proteins bound to SOCS-3 with weak or undetectable affinity. The significance of pY757 in gp130 as a biologically relevant SOCS-3 docking site was investigated by using transfected 293T fibroblasts. Although SOCS-3 inhibited signaling in cells transfected with a chimeric receptor containing the wild-type gp130 intracellular domain, inhibition was considerably impaired for a receptor carrying a Y-->F point mutation at residue 757. Taken together, these data suggest that the mechanism by which SOCS-3 inhibits the gp130 signaling pathway depends on recruitment to the phosphorylated gp130 receptor, and that some of the negative regulatory roles previously attributed to the phosphatase SHP-2 might in fact be caused by the action of SOCS-3.

Amino Acid Sequence↗
PubMed2000

Distribution of gamma satellite DNA on the human X and Y chromosomes suggests that it is not required for mitotic centromere function.

The bulk of the DNA found at human centromeres is composed of tandemly arranged repeats, the most abundant of which is alpha satellite. Other human centromeric repetitive families have been identified, one of the more recent being gamma satellite. To date, gamma satellite DNAs have been reported at the centromeres of human chromosomes 8 and X. Here, we show that gamma-X satellite DNA is not interspersed with the major DZX1 alpha-X block, but rather is organised as a single array of approximately 40-50 kb on the short-arm side of the alpha satellite domain. This repeat array is absent on two mitotically stable Xq isochromosomes. Furthermore, a related repeat DNA has been identified on the human Y chromosome. Fluorescence in situ hybridisation has localised this satellite DNA to the long arm side of the major DYZ3 alpha-Y domain, outside the region previously defined as that required for mitotic centromere function. Together, these data suggest that while blocks of highly related gamma satellite DNAs are present in the pericentromeric regions of both human sex chromosomes, this repeated DNA is not required for mitotic centromere function.

Animals↗