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81.
One new species of the genus lndocalamus (Bambusoideae) is describedfrom China . It is lndocalamus chishuiensis Y. L. Yang et Hsueh. 相似文献
82.
Activation of autophagy is involved in the protective effect of 17β‐oestradiol on endotoxaemia‐induced multiple organ dysfunction in ovariectomized rats
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Hsin‐Hsueh Shen Pao‐Yun Cheng Yu‐Chen Huang Yu‐Ju Lin Yu‐Yang Huang Kwok‐Keung Lam 《Journal of cellular and molecular medicine》2017,21(12):3705-3717
Oestrogens have been reported to attenuate acute inflammation in sepsis. In this study, the effects of long‐term oestrogen replacement with 17β‐oestradiol (E2) on endotoxaemia‐induced circulatory dysfunction and multiple organ dysfunction syndrome were evaluated in ovariectomized (Ovx) rats. E2 (50 μg/kg, s.c., 3 times/week) was administered for 8 weeks, followed by the induction of endotoxaemia by intravenous infusion of lipopolysaccharides (LPS; 30 mg/kg/4 hrs). Oestrogen deficiency induced by ovariectomy for 9 weeks augmented the LPS‐induced damage, including endotoxic shock, myocardial contractile dysfunction, renal dysfunction and rhabdomyolysis. Cardiac levels of NF‐κB p65, iNOS and oxidized glutathione, free radical production in skeletal muscles, myoglobin deposition in renal tubules, and plasma levels of plasminogen activator inhibitor‐1, TNF‐α, and IL‐6 were more pronounced in the Ovx + LPS group than in the Sham + LPS group. Long‐term treatment of E2 prevented this amplified damage in Ovx rats. Six hours after LPS initiation, activation of the autophagic process, demonstrated by increases in Atg12 and LC3B‐II/LC3B‐I ratios, and induction of haem oxygenase (HO)‐1 and heat‐shock protein (HSP) 70 protein expression in myocardium were increased significantly in the Ovx + E2 + LPS group. These results suggest that activation of autophagy and induction of HO‐1 and HSP70 contribute to the protective effect of long‐term E2 replacement on multiple organ dysfunction syndrome in endotoxaemia. 相似文献
83.
Cloughesy TF Yoshimoto K Nghiemphu P Brown K Dang J Zhu S Hsueh T Chen Y Wang W Youngkin D Liau L Martin N Becker D Bergsneider M Lai A Green R Oglesby T Koleto M Trent J Horvath S Mischel PS Mellinghoff IK Sawyers CL 《PLoS medicine》2008,5(1):e8
Background
There is much discussion in the cancer drug development community about how to incorporate molecular tools into early-stage clinical trials to assess target modulation, measure anti-tumor activity, and enrich the clinical trial population for patients who are more likely to benefit. Small, molecularly focused clinical studies offer the promise of the early definition of optimal biologic dose and patient population.Methods and Findings
Based on preclinical evidence that phosphatase and tensin homolog deleted on Chromosome 10 (PTEN) loss sensitizes tumors to the inhibition of mammalian target of rapamycin (mTOR), we conducted a proof-of-concept Phase I neoadjuvant trial of rapamycin in patients with recurrent glioblastoma, whose tumors lacked expression of the tumor suppressor PTEN. We aimed to assess the safety profile of daily rapamycin in patients with glioma, define the dose of rapamycin required for mTOR inhibition in tumor tissue, and evaluate the antiproliferative activity of rapamycin in PTEN-deficient glioblastoma. Although intratumoral rapamycin concentrations that were sufficient to inhibit mTOR in vitro were achieved in all patients, the magnitude of mTOR inhibition in tumor cells (measured by reduced ribosomal S6 protein phosphorylation) varied substantially. Tumor cell proliferation (measured by Ki-67 staining) was dramatically reduced in seven of 14 patients after 1 wk of rapamycin treatment and was associated with the magnitude of mTOR inhibition (p = 0.0047, Fisher exact test) but not the intratumoral rapamycin concentration. Tumor cells harvested from the Ki-67 nonresponders retained sensitivity to rapamycin ex vivo, indicating that clinical resistance to biochemical mTOR inhibition was not cell-intrinsic. Rapamycin treatment led to Akt activation in seven patients, presumably due to loss of negative feedback, and this activation was associated with shorter time-to-progression during post-surgical maintenance rapamycin therapy (p < 0.05, Logrank test).Conclusions
Rapamycin has anticancer activity in PTEN-deficient glioblastoma and warrants further clinical study alone or in combination with PI3K pathway inhibitors. The short-term treatment endpoints used in this neoadjuvant trial design identified the importance of monitoring target inhibition and negative feedback to guide future clinical development.Trial registration: http://www.ClinicalTrials.gov (#). NCT00047073相似文献84.
Hsu-Feng Lu Jai-Sing Yang Kuang-Chi Lai Shu-Chun Hsu Shu-Ching Hsueh Yuan-Liang Chen Jo-Hua Chiang Chi-Cheng Lu Chyi Lo Mei-Due Yang Jing-Gung Chung 《Neurochemical research》2009,34(8):1491-1497
Curcumin is reported to be a potent inhibitor of the initiation and promotion of many cancer cells. We investigated to examine
whether or not curcumin induce DNA damage in mouse–rat hybrid retina ganglion cell line N18 cells. The Comet assay showed
that incubation of N18 cells with 10, 25 and 30 μM of curcumin led to a longer DNA migration smear (Comet tail). The DNA gel
electrophoresis showed that 20 μM of curcumin for 24 and 48 h treatment induced DNA damage and fragments in N18 cells. The
real time PCR analysis showed that 20 μM of curcumin for 48 h treatment decreased ATM, ATR, BRCA1, 14-3-3σ, DNA-PK and MGMT
mRNA, and ATM and MGMT mRNA expression were inhibited in a time-dependent manner. Our results indicate that curcumin caused
DNA damage and inhibited DNA repair genes which may be the factors for curcumin-inhibited cell growth.
H.-F. Lu and J.-S. Yang are contributed equally to this study. 相似文献
85.
Cheng‐Hong Yang Yu‐Huei Cheng Li‐Yeh Chuang Hsueh‐Wei Chang 《Biotechnology progress》2009,25(3):745-753
To provide feasible primer sets for performing a polymerase chain reaction (PCR) experiment, many primer design methods have been proposed. However, the majority of these methods require a relatively long time to obtain an optimal solution since large quantities of template DNA need to be analyzed. Furthermore, the designed primer sets usually do not provide a specific PCR product size. In recent years, evolutionary computation has been applied to PCR primer design and yielded promising results. In this article, a memetic algorithm (MA) is proposed to solve primer design problems associated with providing a specific product size for PCR experiments. The MA is compared with a genetic algorithm (GA) using an accuracy formula to estimate the quality of the primer design and test the running time. Overall, 50 accession nucleotide sequences were sampled for the comparison of the accuracy of the GA and MA for primer design. Five hundred runs of the GA and MA primer design were performed with PCR product lengths of 150–300 bps and 500–800 bps, and two different methods of calculating Tm for each accession nucleotide sequence were tested. A comparison of the accuracy results for the GA and MA primer design showed that the MA primer design yielded better results than the GA primer design. The results further indicate that the proposed method finds optimal or near‐optimal primer sets and effective PCR products in a dry dock experiment. Related materials are available online at http://bio.kuas.edu.tw/ma‐pd/ . © 2009 American Institute of Chemical Engineers Biotechnol. Prog., 2009 相似文献
86.
Chia-Hsiang Hsueh Wen-Pin Chen Jiunn-Lee Lin Chia-Ti Tsai Yen-Bin Liu Jyh-Ming Juang Hsuan-Ming Tsao Ming-Jai Su Ling-Ping Lai 《Journal of biomedical science》2009,16(1):23
The Brugada syndrome is characterized by ST segment elevation in the right precodial leads V1-V3 on surface ECG accompanied
by episodes of ventricular fibrillation causing syncope or even sudden death. The molecular and cellular mechanisms that lead
to Brugada syndrome are not yet completely understood. However, SCN5A is the most well known responsible gene that causes
Brugada syndrome. Until now, more than a hundred mutations in SCN5A responsible for Brugada syndrome have been described.
Functional studies of some of the mutations have been performed and show that a reduction of human cardiac sodium current
accounts for the pathogenesis of Brugada syndrome. Here we reported three novel SCN5A mutations identified in patients with
Brugada syndrome in Taiwan (p.I848fs, p.R965C, and p.1876insM). Their electrophysiological properties were altered by patch
clamp analysis. The p.I848fs mutant generated no sodium current. The p.R965C and p.1876insM mutants produced channels with
steady state inactivation shifted to a more negative potential (9.4 mV and 8.5 mV respectively), and slower recovery from
inactivation. Besides, the steady state activation of p.1876insM was altered and was shifted to a more positive potential
(7.69 mV). In conclusion, the SCN5A channel defect related to Brugada syndrome might be diverse but all resulted in a decrease
of sodium current. 相似文献
87.
Maria H. Festing Mei Y. Speer Hsueh‐Ying Yang Cecilia M. Giachelli 《Genesis (New York, N.Y. : 2000)》2009,47(12):858-863
Accelerated vascular calcification occurs in several human diseases including diabetes and chronic kidney disease (CKD). In patients with CKD, vascular calcification is highly correlated with elevated serum phosphate levels. In vitro, elevated concentrations of phosphate induced vascular smooth muscle cell matrix mineralization, and the inorganic phosphate transporter‐1 (PiT‐1), was shown to be required. To determine the in vivo role of PiT‐1, mouse conditional and null alleles were generated. Here we show that the conditional allele, PiT‐1flox, which has loxP sites flanking exons 3 and 4, is homozygous viable. Cre‐mediated recombination resulted in a null allele that is homozygous lethal. Examination of early embryonic development revealed that the PiT‐1Δe3,4/Δe3,4 embryos displayed anemia, a defect in yolk sac vasculature, and arrested growth. Thus, conditional and null PiT‐1 mouse alleles have been successfully generated and PiT‐1 has a necessary, nonredundant role in embryonic development. genesis 47:858–863, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
88.
Fibroblast growth factor-10 promotes cardiomyocyte differentiation from embryonic and induced pluripotent stem cells 总被引:1,自引:0,他引:1
Background
The fibroblast growth factor (FGF) family is essential to normal heart development. Yet, its contribution to cardiomyocyte differentiation from stem cells has not been systemically studied. In this study, we examined the mechanisms and characters of cardiomyocyte differentiation from FGF family protein treated embryonic stem (ES) cells and induced pluripotent stem (iPS) cells.Methodology/Principal Findings
We used mouse ES cells stably transfected with a cardiac-specific α-myosin heavy chain (αMHC) promoter-driven enhanced green fluorescent protein (EGFP) and mouse iPS cells to investigate cardiomyocyte differentiation. During cardiomyocyte differentiation from mouse ES cells, FGF-3, -8, -10, -11, -13 and -15 showed an expression pattern similar to the mesodermal marker Brachyury and the cardiovascular progenitor marker Flk-1. Among them, FGF-10 induced cardiomyocyte differentiation in a time- and concentration-dependent manner. FGF-10 neutralizing antibody, small molecule FGF receptor antagonist PD173074 and FGF-10 and FGF receptor-2 short hairpin RNAs inhibited cardiomyocyte differentiation. FGF-10 also increased mouse iPS cell differentiation into cardiomyocyte lineage, and this effect was abolished by FGF-10 neutralizing antibody or PD173074. Following Gene Ontology analysis, microarray data indicated that genes involved in cardiac development were upregulated after FGF-10 treatment. In vivo, intramyocardial co-administration of FGF-10 and ES cells demonstrated that FGF-10 also promoted cardiomyocyte differentiation.Conclusion/Significance
FGF-10 induced cardiomyocyte differentiation from ES cells and iPS cells, which may have potential for translation into clinical applications. 相似文献89.
Njajou OT Blackburn EH Pawlikowska L Mangino M Damcott CM Kwok PY Spector TD Newman AB Harris TB Cummings SR Cawthon RM Shuldiner AR Valdes AM Hsueh WC 《PloS one》2010,5(9):e13048