Biomedical subjects

Jian-Guo Zhang

Publications and source records attributed to Jian-Guo Zhang.

6 recordsLinked to original sources

PubMed2003

Effects of daily activity recorded by pedometer on peak oxygen consumption (VO2peak), ventilatory threshold and leg extension power in 30- to 69-year-old Japanese without exercise habit.

The relationships among walk steps, exercise habits and peak oxygen consumption (VO2peak), ventilatory threshold (VT) and leg extension power (LEP) were examined in 709 apparently healthy Japanese subjects (male 372, female 337) aged 30-69 years. Walk steps were evaluated using a pedometer. VO2peak and VT were assessed by a cycle ergometer test, while LEP was measured with an isokinetic leg extension system (Combi, Anaero Press 3500, Japan). Subjects who participated in exercise three times or more a week demonstrated significantly greater VO2peak and VT when compared with subjects without exercise habits. When a separate analysis was conducted on subjects who exercised fewer than three times per week, we found that the subgroup with the highest number of walk steps showed significantly greater VT in all male subjects and female subjects aged 30-49 years, but a significantly greater VO2peak only in females aged 30-49 years, when compared to the subgroup with the fewest walk steps. These results suggest that although some people exercise less than three times a week, if they are quite active in daily life, such activities might also confer benefits upon their fitness.

Activities of Daily Living↗

PubMed2003

SOCS3 negatively regulates IL-6 signaling in vivo.

Members of the suppressor of cytokine signaling (SOCS) family are potentially key physiological negative regulators of interleukin-6 (IL-6) signaling. To examine whether SOCS3 is involved in regulating this signaling, we have used conditional gene targeting to generate mice lacking Socs3 in the liver or in macrophages. We show that Socs3 deficiency results in prolonged activation of signal transducer and activator of transcription 1 (STAT1) and STAT3 after IL-6 stimulation but normal activation of STAT1 after stimulation with interferon-gamma (IFN-gamma). Conversely, IL-6-induced STAT activation is normal in Socs1-deficient cells, whereas STAT1 activation induced by IFN-gamma is prolonged. Microarray analysis shows that the pattern of gene expression induced by IL-6 in Socs3-deficient livers mimics that induced by IFN-gamma. Our data indicate that SOCS3 and SOCS1 have reciprocal functions in IL-6 and IFN-gamma regulation and imply that SOCS3 has a role in preventing IFN-gamma-like responses in cells stimulated by IL-6.

Animals↗

PubMed2002

Biological evidence that SOCS-2 can act either as an enhancer or suppressor of growth hormone signaling.

Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation of cytokine signaling. The generation of SOCS-2-deficient mice, which grow to one and a half times the size of their wild-type littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit GH action at low concentrations, at higher concentrations it may potentiate signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo, we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not growth-deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual effects on GH signaling in vivo.

Animals↗

PubMed2002

All-optical code-division-multiplexing technique supporting multirate data communications and local-area-network interconnections.

An efficient all-optical code-division-multiplexing (AOCDM) technique is proposed to support multirate data communications and local-area-network (LAN) interconnections with multiple protocols. To achieve this goal, we use a strict optical orthogonal code (OOC) in multirate AOCDM systems to guarantee that both cross- and autocorrelation constraints are minimum (i.e., 1) for incoherent optical processing. In contrast, the use of a conventional OOC may result in correlation constraints of 2, which in turn can degrade system performance. Moreover, implementation issues on AOCDM systems are discussed. These include the design of low-cost optical transmitters and the trade-off among coherence time, spectral width, and pulse width for AOCDM systems. It is shown that multirate AOCDM systems have a high operation flexibility to support data communications and LAN interconnections of both equal and multiple bit rates. For multirate data transmissions, the proposed system can have a better bandwidth efficiency and a lower bit error rate than a system that uses a conventional OOC.

Journal Article↗

PubMed2002

LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival.

Multiple sclerosis (MS) is a disabling inflammatory demyelinating disease of the central nervous system (CNS) that primarily affects young adults. Available therapies can inhibit the inflammatory component of MS but do not suppress progressive clinical disability. An alternative approach would be to inhibit mechanisms that drive the neuropathology of MS, which often includes the death of oligodendrocytes, the cells responsible for myelinating the CNS. Identification of molecular mechanisms that mediate the stress response of oligodendrocytes to optimize their survival would serve this need. This study shows that the neurotrophic cytokine leukemia inhibitory factor (LIF) directly prevents oligodendrocyte death in animal models of MS. We also demonstrate that this therapeutic effect complements endogenous LIF receptor signaling, which already serves to limit oligodendrocyte loss during immune attack. Our results provide a novel approach for the treatment of MS.

Amino Acid Sequence↗

PubMed2002

SOCS-6 binds to insulin receptor substrate 4, and mice lacking the SOCS-6 gene exhibit mild growth retardation.

SOCS-6 is a member of the suppressor of cytokine signaling (SOCS) family of proteins (SOCS-1 to SOCS-7 and CIS) which each contain a central SH2 domain and a carboxyl-terminal SOCS box. SOCS-1, SOCS-2, SOCS-3, and CIS act to negatively regulate cytokine-induced signaling pathways; however, the actions of SOCS-4, SOCS-5, SOCS-6, and SOCS-7 remain less clear. Here we have used both biochemical and genetic approaches to examine the action of SOCS-6. We found that SOCS-6 and SOCS-7 are expressed ubiquitously in murine tissues. Like other SOCS family members, SOCS-6 binds to elongins B and C through its SOCS box, suggesting that it might act as an E3 ubiquitin ligase that targets proteins bound to its SH2 domain for ubiquitination and proteasomal degradation. We investigated the binding specificity of the SOCS-6 and SOCS-7 SH2 domains and found that they preferentially bound to phosphopeptides containing a valine in the phosphotyrosine (pY) +1 position and a hydrophobic residue in the pY +2 and pY +3 positions. In addition, these SH2 domains interacted with a protein complex consisting of insulin receptor substrate 4 (IRS-4), IRS-2, and the p85 regulatory subunit of phosphatidylinositol 3-kinase. To investigate the physiological role of SOCS-6, we generated mice lacking the SOCS-6 gene. SOCS-6(-/-) mice were born in a normal Mendelian ratio, were fertile, developed normally, and did not exhibit defects in hematopoiesis or glucose homeostasis. However, both male and female SOCS-6(-/-) mice weighed approximately 10% less than wild-type littermates.

Animals↗