Chromatographic-mass spectrometric analysis of ethanol extract of Maesa perlaria var formosana

Purpose: This study analyzes the chemical composition of ethanol root extracts of Maesa perlaria var. formosana by gas chromatography-mass spectrometry (GC-MS).Methods: The dried root of Maesa perlaria var. formosana was extracted with 95 % ethanol for composition analysis under the following optimum GC-MS conditions: 250 °C inlet temperature, 250 °C MSD detector temperature, and GC oven temperature programmed as follows: initial temperature held at 70 °C for 15 min, then increased at a rate of 2.5 °C/min and held at 170 °C for 15 min; then raised at a rate of 2 °C/min and kept at 180 °C for 20 min; then raised at 2 °C/min and kept at 250 °C for 20 min. Finally, it was raised at 3 °C/min and kept at 280 °C for 15 min.Results: A total of 59 chemical compounds were identified, representing 88.82 % of the composition of the ethanol extracts. The three major components, include 2,4-di-tert-butylphenol (16.76 %), stigmasterol (15.86 %) and campesterol (7.33 %)Conclusion: The results show that a total of 59 components were identified in the ethanol extract of Maesa perlaria var. formosana. The major component, 2,4-Di-tert-butylphenol, exhibits various biological activities.Keywords: Maesa perlaria var. formosana, 2,4-Di-tert-butylphenol, Stigmasterol, Campesterol, Gas chromatography-mass spectrometr

Evolutionary conservation of DNA-contact residues in DNA-binding domains

<p>Abstract</p> <p>Background</p> <p>DNA-binding proteins are of utmost importance to gene regulation. The identification of DNA-binding domains is useful for understanding the regulation mechanisms of DNA-binding proteins. In this study, we proposed a method to determine whether a domain or a protein can has DNA binding capability by considering evolutionary conservation of DNA-binding residues.</p> <p>Results</p> <p>Our method achieves high precision and recall for 66 families of DNA-binding domains, with a false positive rate less than 5% for 250 non-DNA-binding proteins. In addition, experimental results show that our method is able to identify the different DNA-binding behaviors of proteins in the same SCOP family based on the use of evolutionary conservation of DNA-contact residues.</p> <p>Conclusion</p> <p>This study shows the conservation of DNA-contact residues in DNA-binding domains. We conclude that the members in the same subfamily bind DNA specifically and the members in different subfamilies often recognize different DNA targets. Additionally, we observe the co-evolution of DNA-contact residues and interacting DNA base-pairs.</p

Survival analysis of Stage IIA1 and IIA2 cervical cancer patients

AbstractObjectiveThe aim of this study was to assess the benefits of the 2009 International Federation of Gynecology and Obstetrics (FIGO) staging system for survival of patients with Stage IIA1 and IIA2 cervical cancer (Cx Ca).Materials and MethodsA study cohort of 51 patients with Stage IIA Cx Ca was retrospectively collected from the 2004–2009 hospital-based, long-form Cx Ca data registry at Mackay Memorial Hospital (Taipei, Taiwan). The survivorship and overall survival were compared between these two groups (Stages IIA1 and IIA2) using log-rank test.ResultsThirty-six and 15 patients were classified into Stages IIA1 and IIA2, respectively. Stage IIA2 patients were younger than those with Stage IIA1 disease (mean age, 47.4 vs. 55.1 years, p = 0.008), but no significant difference was observed in confirmed pelvic lymph node status (21.4% vs. 38.5%, p = 0.280) between them. Although the 2-year and 5-year overall survival was better among Stage IIA1 patients, there was no significant difference in survival between Stage IIA1 and IIA2 groups (2-year, 90.6% vs. 77.8%; 5-year, 86.3% vs. 51.9%, p = 0.218).ConclusionAlthough there was a trend in survival difference between Stage IIA1 and IIA2 patients, the difference was not statistically significant. The revised FIGO 2009 staging system for Cx Ca defines a group of Stage IIA patients with bulky tumor (Stage IIA2) that are generally younger than Stage IIA1 patients. It is sensible to investigate an alternate or enhanced treatment scheme for Stage IIA2 patients. Ideally, the treatment scheme should prevent unnecessary radical surgery if a patient can be exposed to either chemotherapy or radiotherapy, alone or in combination

Genetic Polymorphism of XRCC1 Arg399Gln Is Associated With Survival in Non–Small-Cell Lung Cancer Patients Treated With Gemcitabine/Platinum

IntroductionElevated DNA-repair capacity has been related to chemoresistance of platinum doublet chemotherapy in non–small-cell lung cancer (NSCLC). We evaluated whether single nucleotide polymorphisms of DN- repair genes excision repair cross-complementing group 1 (ERCC1), ERCC2, x-ray repair cross-complementing group 1 (XRCC1), XRCC3, and RRM1 associate with treatment outcome in NSCLC patients receiving gemcitabine plus platinum as their first-line chemotherapy.MethodsGenotyping for eight polymorphisms in five DNA-repair genes was performed with the GenomeLab nucleotide polymorphismstream Genotyping System in 62 advanced NSCLC patients in a training set and 45 patients in a validation set treated with gemcitabine/platinum.ResultsIn the training set, the wild-type genotype of XRCC1 Arg399Gln (G/G) was associated with decreased median overall survival (OS) (22 months, 95% confidence interval [CI], 10–34 months versus not reached, log-rank test, p = 0.005) than those carrying variant genotypes (G/A+A/A). In addition, there was a statistically significant longer median OS in patients carrying wild-type ERCC2 Asp312Asn genotype (G/G) (51 months, 95% CI, 19–82 months versus 10 months, log-rank test, p < 0.001) than those carrying heterozygous variant genotypes (G/A). In the multivariate Cox model, we found a significant effect of XRCC1 Arg399Gln (G/A+A/A versus G/G, hazard ratio [HR] 0.290; 95%CI, 0.12–0.705, p = 0.006) and ERCC2 Asp312Asn (G/A versus G/G, HR 14.04; 95% CI, 2.253–87.513, p = 0.005) polymorphisms on patients’ OS. In the validation set, only XRCC1 399ConclusionsGenetic polymorphism of XRCC1 Arg399Gln may be a candidate for contributing interindividual difference in the OS of gemcitabine/platinum-treated advanced NSCLC patients

Tmem16F forms a Ca2+-Activated Cation Channel Required for Lipid Scrambling in Platelets during Blood Coagulation

Collapse of membrane lipid asymmetry is a hallmark of blood coagulation. TMEM16F of the TMEM16 family that includes TMEM16A/B Ca(2+)-activated Cl(−) channels (CaCCs) is linked to Scott syndrome with deficient Ca(2+)-dependent lipid scrambling. We generated TMEM16F knockout mice that exhibit bleeding defects and protection in an arterial thrombosis model associated with platelet deficiency in Ca(2+)-dependent phosphatidylserine exposure and procoagulant activity and lack a Ca(2+)-activated cation current in the platelet precursor megakaryocytes. Heterologous expression of TMEM16F generates a small-conductance Ca(2+)-activated nonselective cation (SCAN) current with subpicosiemens single-channel conductance rather than a CaCC. TMEM16F-SCAN channels permeate both monovalent and divalent cations, including Ca(2+), and exhibit synergistic gating by Ca(2+) and voltage. We further pinpointed a residue in the putative pore region important for the cation versus anion selectivity of TMEM16F-SCAN and TMEM16A-CaCC channels. This study thus identifies a Ca(2+)-activated channel permeable to Ca(2+) and critical for Ca(2+)-dependent scramblase activity during blood coagulation