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Articles by L Han
Total Records ( 8 ) for L Han
  Y Zhou , P Lin , Q Li , L Han , H Zheng , Y Wei , Z Cui , Y Ni and X. Guo

Sputum is the most common sample collected from patients suffering from lower respiratory tract infections and it is crucial for the bacterial identification of these infections. In this study, we enrolled 101 sputum samples from 101 patients with lower respiratory tract infections. Initially, pyrosequencing of the 16S rDNA V3 hypervariable regions of the bacteria contained in the sputum was utilized as a culture-independent approach for microbiota analysis. For comparison, clinical laboratory tests using a culture-dependent automated bacterial identification system for the same cohort of sputum samples were also done. By pyrosequencing, >70,000 DNA fragments were found and classified into 129 bacterial genera after being analyzed by the Ribosomal Database Project (RDP) process. Most sequences belonged to several predominant genera, such as Streptococcus and Staphylococcus, indicating that these genera play an important role in lower respiratory tract infections. In addition, some sequences belonging to potential causative agents, such as Mycoplasma, Haemophilus, and Moraxella, were also found, but these sequences were not found by clinical laboratory tests. For the nine genera detected by both methods, the methods' sensitivities were compared and the results showed that pyrosequencing was more sensitive, except for Klebsiella and Mycobacterium. Significantly, this method revealed much more complicated bacterial communities and it showed a promising ability for the detection of bacteria.

  L Han , Y Wang and S. H. Bryant

This work provides an analysis of across-target bioactivity results in the screening data deposited in PubChem. Two alternative approaches for grouping-related targets are used to examine a compound's across-target bioactivity. This analysis identifies compounds that are selectively active against groups of protein targets that are identical or similar in sequence. This analysis also identifies compounds that are bioactive across unrelated targets. Statistical distributions of compound' across-target selectivity provide a survey to evaluate target specificity of compounds by deriving and analyzing bioactivity profile across a wide range of biological targets for tested small molecules in PubChem. This work enables one to select target specific inhibitors, identify promiscuous compounds and better understand the biological mechanisms of target-small molecule interactions.

  H. C Chang , L Han , R Goswami , E. T Nguyen , D Pelloso , M. J Robertson and M. H. Kaplan

IL-12 activates STAT4, which is a critical regulator of inflammation and T helper type I (Th1) lineage development in murine systems. The requirement for STAT4 in the generation of human Th1 cells has not been examined thoroughly. Compared with control Th1 cultures, expression of the Th1 genes IFN, IL-12Rβ2, and TNF is greatly reduced in Th1 cultures of CD4 T cells isolated from lymphoma patients after autologous stem cell transplantation who have acquired STAT4 deficiency. Moreover, IL-4 and IL-5 production is increased in patient Th1 cultures though there are no defects in the development of Th2 cells. Reconstitution of STAT4 in patient T cells allowed recovery of IFN and IL-12Rβ2 expression, whereas ectopic expression of IL-12Rβ2 did not rescue STAT4 expression, and increased IFN production only to levels intermediate between control and patient samples. These results demonstrate that, as in murine systems, STAT4 is required for optimal human Th1 lineage development.

  Z Han , Z Hong , C Chen , Q Gao , D Luo , Y Fang , Y Cao , T Zhu , X Jiang , Q Ma , W Li , L Han , D Wang , G Xu , S Wang , L Meng , J Zhou and D. Ma

Tumor cells acquire the ability to proliferate uncontrollably, resist apoptosis, sustain angiogenesis and evade immune surveillance. Signal transducer and activator of transcription (STAT) 3 regulates all of these processes in a surprisingly large number of human cancers. Consequently, the STAT3 protein is emerging as an ideal target for cancer therapy. This paper reports the generation of an oncolytic adenovirus (M4), which selectively blocks STAT3 signaling in tumor cells as a novel therapeutic strategy. M4 selectively replicated in tumor cells and expressed high levels of antisense STAT3 complementary DNA during the late phase of the viral infection in a replication-dependent manner. The viral progeny yield of M4 in tumor cells was much higher than that of the parent adenoviral mutants, Ad5/dE1A. M4 effectively silenced STAT3 and its target genes in tumor cells while sparing normal cells and exhibited potent antitumoral efficacy in vitro and in vivo. Systemic administration of M4 significantly inhibited tumor growth in an orthotopic gastric carcinoma mouse model, eliminated abdominal cavity metastases and prolonged survival time. In summary, M4 has low toxicity and great potential as a therapeutic agent for different types of cancers.

  X Wang , W Xie , Y Zhang , P Lin , L Han , P Han , Y Wang , Z Chen , G Ji , M Zheng , N Weisleder , R. P Xiao , H Takeshima , J Ma and H. Cheng

Rationale: Unrepaired cardiomyocyte membrane injury causes irreplaceable cell loss, leading to myocardial fibrosis and eventually heart failure. However, the cellular and molecular mechanisms of cardiac membrane repair are largely unknown. MG53, a newly identified striated muscle-specific protein, is involved in skeletal muscle membrane repair. But the role of MG53 in the heart has not been determined.

Objective: We sought to investigate whether MG53 mediates membrane repair in cardiomyocytes and, if so, the cellular and molecular mechanism underlying MG53-mediated membrane repair in cardiomyocytes. Moreover, we determined possible cardioprotective effect of MG53-mediated membrane repair.

Methods and Results: We demonstrated that MG53 is crucial to the emergency membrane repair response in cardiomyocytes and protects the heart from stress-induced loss of cardiomyocytes. Disruption of the sarcolemmal membrane by mechanical, electric, chemical, or metabolic insults caused rapid and robust translocation of MG53 toward the injury sites. Ablation of MG53 prevented sarcolemmal resealing after infrared laser–induced membrane damage in intact heart, and exacerbated mitochondrial dysfunction and loss of cardiomyocytes during ischemia/reperfusion injury. Unexpectedly, the MG53-mediated cardiac membrane repair was mediated by a cholesterol-dependent mechanism: depletion of membrane cholesterol abolished, and its recovery restored injury-induced membrane translocation of MG53. The redox status of MG53 did not affect initiation of MG53 translocation, whereas MG53 oxidation conferred stability to the membrane repair patch.

Conclusions: Thus, cholesterol-dependent MG53-mediated membrane repair is a vital, heretofore unappreciated cardioprotective mechanism against a multitude of insults and may bear important therapeutic implications.

  M Almeida , L Han , E Ambrogini , S. M Bartell and S. C. Manolagas

Aging or acute loss of estrogens or androgens increases the levels of reactive oxygen species, activates nuclear factor-B (NF-B), and promotes the phosphorylation of p66shc, a redox enzyme that amplifies mitochondrial reactive oxygen species generation and stimulates apoptosis. We report that in mesenchymal progenitor and osteoblastic cell models, H2O2 activated a protein kinase C (PKC)β/p66shc/NF-B signaling cascade and that p66shc was an essential mediator of the stimulating effects of H2O2 on the apoptosis of osteoblastic cells as well as their ability to activate NF-B. 17β-Estradiol (E2) or the nonaromatizable androgen dihydrotestosterone abrogated the effects of H2O2 on p66shc and NF-B activation by attenuating the phosphorylation of the redox-sensitive cytoplasmic kinase PKCβ. Additionally, both E2 and dihydrotestosterone prevented H2O2-induced apoptosis by a mechanism that involved attenuation of p66shc resulting from decreased phosphorylation of PKCβ. Consistent with a kinase-mediated mechanism of sex steroid action, the effects of E2 were reproduced by a polymeric form of estradiol that is not capable of stimulating the nuclear-initiated actions of ER. These results demonstrate that p66shc is an essential mediator of the effects of oxidative stress on osteoblastic cell apoptosis, NF-B activation, and cytokine production. The ability of either estrogen or androgen to attenuate the effects of oxidative stress on osteoblastic cell apoptosis, NF-B activation, and cytokine production results from their common property to suppress PKCβ-induced p66shc phosphorylation via a mechanism that does not require stimulation of the nuclear-initiated actions of sex steroids.

  J Wang , L Zou , S Huang , F Lu , X Lang , L Han , Z Song and Z. Xu

To clarify the role of glutathione S-transferases (GSTs; GSTM1 and GSTT1) status in susceptibility to coronary heart disease (CHD), a meta-analysis of published studies was performed. A total of 19 studies including 8020 cases and 11 501 controls were included in this meta-analysis. In a combined analysis, the relative risks for CHD of the GSTM1 null and GSTT1 null polymorphisms were 1.47 [95% confidence interval (CI): 1.08–2.01] and 1.26 (95% CI: 0.90–1.75), respectively. Three potential sources of heterogeneity including ethnicity, source of control and sample size of study were also assessed. However, no significant association was found in stratified analyses. By pooling data from eight studies (2909 cases and 3745 controls) that considered combinations of GSTT1 and GSTM1 genotypes, a statistically significant increased risk for CHD [odds ratio (OR = 2.38, 95% CI: 1.03–5.48)] was detected for individuals with combined deletion mutations in both genes compared with positive genotypes. Results from the meta-analysis of five studies on GSTs stratified according to smoking status showed an increased risk for individuals with null genotype (OR = 2.21, 95% CI: 1.24–3.92 for GSTM1 and OR = 3.29, 95% CI: 1.49–7.26 for GSTT1) versus non-null genotypes. This meta-analysis suggests that the GSTM1 null genotype may slightly increase the risk of CHD and that interaction between unfavourable GSTs genotypes may exist.

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