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Articles by B Huang
Total Records ( 5 ) for B Huang
  B Huang , W Qin , B Zhao , Y Shi , C Yao , J Li , H Xiao and Y. Jin
 

MicroRNAs (miRNAs), which are a newly identified class of small single-stranded non-coding RNAs, regulate their target genes via post-transcriptional pathway. It has been proved that miRNAs play important roles in many biological processes. To better understand miRNA function on type 2 diabetes, we used an oligonucleotide microarray to monitor miRNA expression profiles of Goto–Kakizaki (GK) and Wistar rats' skeletal muscle. It was found that seven miRNAs were down-expressed and two miRNAs were over-expressed in the muscle of GK rats. Among them, miR-24 showed the most prominent change. p38 MAPK, which is a direct target of miR-24, also showed expression difference. All the data give a clue that miR-24 might be associated with diabetes through down-regulation of p38 MAPK.

  Q Wang , J Li , J Gu , B Huang , Y Zhao , D Zheng , Y Ding and L. Zeng
 

The green tea constituent, (–)-epigallocatechin-3-gallate (EGCG), has chemopreventive and anticancer effects. This is partially because of the selective ability of EGCG to induce apoptosis and death in cancer cells without affecting normal cells. In the present study, the activity of EGCG against the myeloma cell line, KM3, was examined. Our results demonstrated, for the first time, that the treatment of the KM3 cell line with EGCG inhibits cell proliferation and induces apoptosis, and there is a synergistic effect when EGCG and bortezomib are combined. Further experiments showed that this effect involves the NF-B pathway. EGCG inhibits the expression of the P65 mRNA and P65/pP65 protein, meanwhile it downregulates pIB expression and upregulates IB expression. EGCG also activates caspase-3, -8, cleaved caspase-9, and poly-ADP-ribose polymerase (PARP) and subsequent apoptosis. These findings provided experimental evidence for efficacy of EGCG alone or in combination with bortezomib in multiple myeloma therapy.

  Y Zhang , L Bao , H Zhu , B Huang and H. Zhang
 

Leptospirosis renal disease is one of the common clinical manifestations of leptospirosis, including acute renal failure and tubulointerstitial nephritis. Outer membrane protein A-like protein Loa22 is a lipoprotein from Leptospira interrogans and has been suggested to be a corresponding virulence factor. However, the role of Loa22 in leptospiral nephropathy is not yet understood. In the present study, we constructed a vector and artificially expressed Loa22 in Escherichia coli BL21(DE)pLysS cells. After extensive purification, along with a GST tag protein control, Loa22 protein was used to test the cytotoxicity in cultured rat proximal tubule cells (NRK52E) and examine its effects on the induction of inflammatory responses. Using morphological examination, 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl]-2H-tetrazoium hydrixide absorbance, lactate dehydrogenase assays and an analysis of apoptosis via flow cytometry, it was found that Loa22 protein mediates a direct cytotoxic effect on NRK52E cells in a dose-dependent manner. Using real-time PCR, western blotting and immunofluorescence, it was found that Loa22 protein upregulates the expression of toll-like receptor 2 (TLR2), induces nitric oxide synthase and promotes the production of nitric oxide (NO) and monocyte chemoattractant protein-1 (MCP-1) by NRK52E cells. Additionally, using a TLR2 blocking antibody, it was found that enhanced NO and MCP-1 production by NRK52E cells after Loa22 stimulation requires the activation of TLR2. Collectively, our data suggested that Loa22 is a critical virulence factor of L. interrogans and is involved in the leptospiral nephropathy through mediating direct cytotoxicity and enhancing inflammatory responses.

  M. V Paterno , L. C Schmitt , K. R Ford , M. J Rauh , G. D Myer , B Huang and T. E. Hewett
 

Background: Athletes who return to sport participation after anterior cruciate ligament reconstruction (ACLR) have a higher risk of a second anterior cruciate ligament injury (either reinjury or contralateral injury) compared with non–anterior cruciate ligament–injured athletes.

Hypotheses: Prospective measures of neuromuscular control and postural stability after ACLR will predict relative increased risk for a second anterior cruciate ligament injury.

Study Design: Cohort study (prognosis); Level of evidence, 2.

Methods: Fifty-six athletes underwent a prospective biomechanical screening after ACLR using 3-dimensional motion analysis during a drop vertical jump maneuver and postural stability assessment before return to pivoting and cutting sports. After the initial test session, each subject was followed for 12 months for occurrence of a second anterior cruciate ligament injury. Lower extremity joint kinematics, kinetics, and postural stability were assessed and analyzed. Analysis of variance and logistic regression were used to identify predictors of a second anterior cruciate ligament injury.

Results: Thirteen athletes suffered a subsequent second anterior cruciate ligament injury. Transverse plane hip kinetics and frontal plane knee kinematics during landing, sagittal plane knee moments at landing, and deficits in postural stability predicted a second injury in this population (C statistic = 0.94) with excellent sensitivity (0.92) and specificity (0.88). Specific predictive parameters included an increase in total frontal plane (valgus) movement, greater asymmetry in internal knee extensor moment at initial contact, and a deficit in single-leg postural stability of the involved limb, as measured by the Biodex stability system. Hip rotation moment independently predicted second anterior cruciate ligament injury (C = 0.81) with high sensitivity (0.77) and specificity (0.81).

Conclusion: Altered neuromuscular control of the hip and knee during a dynamic landing task and postural stability deficits after ACLR are predictors of a second anterior cruciate ligament injury after an athlete is released to return to sport.

  B Huang , H Wu , N Hao , F Blombach , J van der Oost , X Li , X. C Zhang and Z. Rao
 

GTPase domains from members of the HflX protein family have their catalytic glutamine residue of the DxxGQ motif substituted by phenylalanine, while they are still able to hydrolyse GTP. This appears to challenge the traditional view of GTP hydrolysis mechanism of Ras-like GTPases. SsGBP from the hyperthermophilic archaeon Sulfolobus solfataricus provided the first crystal structure of the HflX family. Here, we report structure-based mutagenesis analyses on SsGBP. Six-point mutations were individually introduced in the Ras-like GTPase domain including regions of P-loop, switches I and II. Intrinsic GTPase activities and thermal stabilities of these variants together with the wild-type full-length SsGBP and its isolated GTPase domain were analysed. Both functional and structural analyses of G235P and G235S mutants, which showed total and partial loss of the GTP hydrolyzing activity, respectively, support our hypothesis that the role of aligning a nucleophilic water molecule by the Ras Gln60 residue is replaced by the backbone amide group of Gly235 in SsGBP. Together with functional studies of other mutants, we conclude that the classical view of GTP hydrolysis mechanism likely remains the same in the HflX family with a twist in the entity of the nucleophilic alignment.

 
 
 
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