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To explore the need for faculty development among Chinese medical educators. Leaders at each medical school in China were asked to complete a 123-item survey to identify interest in various topics and barriers and perceived benefits of participating in faculty development programs. Interest levels were high for all topics. Experience with Hospital Management and Research positively correlated with interest in learning more (p less than 0.001). Ninety-two percent believe that international experiences are very or extremely important to medical educators' career advancement. Chinese medical education faculty members have a strong interest in faculty development programs.

Pediatric asthma seriously endangers the well-being and health of children worldwide. Baicalin (BA) protects against diverse disorders, including asthma. Therefore, this study explored the mechanism of BA in pediatric asthma. The ovalbumin (OVA)-induced asthmatic mouse model was established to evaluate BA efficacy from aspects of oxidative stress, inflammation, blood cells in bronchoalveolar lavage fluid (BALF) and collagen deposition. Differentially expressed microRNAs (miRs) in BA-treated mice were analyzed. Effects of BA on PDGF-BB-induced smooth muscle cells (SMCs) were assessed. miR downstream mRNA and the related pathway were predicted and verified, and their effects on asthmatic mice were evaluated. BA effectively reversed OVA-induced oxidative stress and inflammation, as well as decreased the number of total cells, eosinophils and neutrophils in BALF, and collagen deposition. miR-103 was significantly upregulated after BA treatment. BA inhibited the abnormal proliferation of PDGF-BB-induced SMCs, which was prevented by miR-103 knockdown. miR-103 targeted TLR4 and regulated the extent of NF-κB phosphorylation. In vivo, miR-103 inhibition weakened the alleviating effects of BA on asthma, which was then reversed after silencing of TLR4. We highlighted that BA has the potency to halt the pediatric asthma progression via miR-103 upregulation and the TLR4/NF-κB axis inhibition. [ABSTRACT FROM AUTHOR]

Rice blast resistance ( R ) genes-mediated resistance response depends on various resistance-related genes involved in incompatible interactions. In this work, the expression profiles of innate rice immunity related genes were examined in the mediated resistance response of true/field resistance genes. Three sets of rice near-isogenic lines (NILs) were used: the resistant NILs carrying true resistance genes in the genetic background of the susceptible cultivar Nipponbare (NB), NB-Pib, NB-Pizt, NB-Pik and NB-Pita2; NILs bearing field resistance genes pi21 in the susceptible cultivar Aichiasahi (AA) AA-pi21, Kahei (KHR). The marker gene OsWRKY45 of salicylic acid (SA) signalling was upregulated in all tested cultivars. And, JAmyb (marker gene of jasmonic acid signalling) showed higher upregulation in the resistance lines with nucleotide-binding sites and leucine-rich repeat (NBS-LRR) R genes Pib , Pizt , Pik , Pita2 and Pikahei than in NB and KHS. SalT of abscisic acid (ABA) signalling may be involved in the R/Avr interaction, including Pizt , Pik , pi21 and Pikahei . However, SalT was shown to negatively regulate Pib/AvrPib interaction. OsPR1b and PBZ1 were differentially expressed and strongly activated at a later stage by 48 h post-inoculation. Interestingly, there was evidence that OsPR1b and PBZ1 played an important role in the pi21- mediated response. It was shown that OsRAR1 could be upregulated in the true resistance line NB-Pita2 and the field resistance line KHR, while OsSGT1 and OsHSP90 could be upregulated in all tested lines. The involvement of these genes illustrated the complexity of the downstream signalling pathways in the mediated resistance response of true/field resistance genes.

Objective: To define roles of B7-1 co-stimulation factor expressed in human malignant cell lines in mediating anti-tumor T cell immune responses., Methods: Examining human leucocyte antigen (HLA) and B7 expressions on 8 human blood malignancies cell lines by flow cytometry. Transfecting B7-1 gene to B7-1 negative (B7(-)) Raji and B7(-) Jurkat cell lines by liposome, and comparing the potencies of blood malignant cell lines in the induction of T cell activation by examination of T cell cytokine mRNAs before and after transfection using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR)., Results: High level of HLA I and II molecules were expressed in most human blood malignant cell lines examined, and the co-stimulatory factor B7-2 was also highly expressed. In contrast, another member of B7 family: B7-1 was either not expressed or very limitedly expressed in most of these hematopoietic malignant cell lines. Most importantly, transfection of B7-1 gene to B7(-). Raji and B7(-). Jurkat cell lines made these cell lines better antigen presenting cells for stimulation of anti-tumor T cell activation, which was demonstrated by up regulation of expression of T cell cytokines IL-2, IL-4 and INF-gamma mRNAs after incubation of these tumor cells with T cells for 24 h., Conclusions: B7 co-stimulation plays an important role in anti-tumor immunity. Transfection of B7-1 gene to the human hematopoietic malignant cell lines that are deficient in the B7-1 expression empowers their antigen presentation potency for activation of anti-tumor T cells. Our results suggested that repairing the deficiency of B7-1 co-stimulatory pathway in tumor cells might be a novel immunotherapeutic approach for human hematopoietic malignancies.

For the purpose of thrombocytopenia gene therapy, recombinant RevTet-On and pRevTRE/TPO retrovirus were packaged and transfected to NIH3T3 after selected with G418 and hygromycin, the two inserting recombinant retrovirus cell strain RevTet-On3T3/TPO were established. TPO expression was controlled and regulated by doxycydine (Dox). After using Dox to control the expression of TPO in RevTet-On3T3/TPO cells, the result showed that when Dox is added to the RevTet-On3T3/TPO cells, cell populations expressed TPO highly in the presence of 2 mg/L of Dox, and lowly in the absence of Dox. By using the RevTet-On gene expression system (the retrovirus vector RevTet-On regulation system to control the expression gene by Dox), it could modulate the expression of multiple genes by tetracyline and its derivatives. This system maybe provides a safe and efficacient way for the thrombocy to penia gene therapy.

To study the significance of calcium in the apoptosis of HL-60 cells induced by VP-16, the technology of flow cytometry, confocal laser scanning microscopy and Western blot were used. The results showed that VP-16 could induced the apoptosis of HL-60 cells and transient increase of intracellular calcium concentration; EGTA [ethylene glycol-bis(2-aminoethyl)-N,N,N',N'-tetraacetic acid], that could combine the extracellular calcium, did not prevent the apoptosis of HL-60 cells. BAPTA-AM [1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxy-methyl) ester], however, a chelating agent of intracellular calcium ions, could prevent apoptosis and the release of cytochrome C from HL-60 cells. It was concluded that the calcium plays an important role in apoptosis and the release of cytochrome C.

A new apoptosis-related gene TFAR19 was recently cloned. A primary functional analysis indicates its role in the apoptotic process of TF-1 cells. To clarify TFAR19 was involved in which apoptotic pathway, the changes in TFAR19 expression were observed during the apoptotic processes of Jurkat cells induced with various methods: serum deprivation, VP-16 treatment and Fas McAb activation. Then TFAR19 expression in Jurkat cells was detected with flow cytometry and Western blot, and TFAR19 mRNA with RT-PCR. Our results showed that expression of TFAR19 in Jurkat cells was increased at 12 hours after serum deprivation, 2 hours after VP-16 treatment and 2 hours after Fas McAb activation, respectively. These observations suggested that TFAR19 was involved in the apoptotic process of Jurkat cells induced with serum deprivation, DNA destruction and death receptor activation. It might take effect in the early apoptotic process. TFAR19 is a participant of the "final common pathway" in the apoptotic pathway.

To control thrombopoietin (TPO) expression by doxycycline in CHO cells, Tet-On gene expression system was used. Recombinant plasmid pTRE-TPO was successfully constructed. pTRE-TPO and pTK-Hyg were cotransfected into CHO-Tet-On cells. Cells resistant to hygromycin were cloned, high expression and low background clone was selected, and named as CHO-Tet-On-TPO. There was no significant TPO expression in the absence of doxycycline, the TPO level in the cell culture supernatant was 0.1 micro g/L. After exposure to 2 mg/L doxycycline, TPO expression was greatly increased, the TPO level in the cell culture supernatant reached 10.8 micro g/L. Tet-On gene expression system is a ready access to the tight-regulated and high-level gene expression system. It is likely to provide a safe and regulatable way for TPO gene therapy.