槟榔子中抗血小板聚集及抑制乙酰胆碱酯酶活性的有效成分（英文）

目的：研究槟榔子（Areca catechu）粗提取物中所含的抗血小板聚集及抑制乙酰胆碱酯酶活性的有效成分及其作用机制。方法：使用70%甲醇水溶液对槟榔子进行粗提取。使用生物发光血小板凝集仪在富血小板血浆中测定槟榔子粗提取物的抗血小板聚集作用,使用分光光度计在试管内测定槟榔子粗提取物对乙酰胆碱酯酶活性的抑制作用。检测槟榔子中的多种化合物以测定槟榔子中抗血小板聚集及抑制乙酰胆碱酯酶活性的有效成分。结果：槟榔子粗提取物能够抑制花生四烯酸、二磷酸腺苷、血小板活化因子、肾上腺素及钙离子载体引起的血小板聚集,尤其对二磷酸腺苷及钙离子载体引起的血小板聚集的抑制最为明显;槟榔子粗提取物能够显著抑制乙酰胆碱酯酶的活性。在所检测的槟榔子所含化合物中,只有儿茶素对肾上腺素引起的血小板聚集有显著的抑制作用,而这种抑制作用显著弱于槟榔子粗提取物,提示槟榔子中的其他成分参与了这种抑制作用;鞣酸、没食子酸、薯蓣皂苷元和异去甲槟榔次碱能够抑制乙酰胆碱酯酶的活性,其中鞣酸的抑制作用强于槟榔子粗提取物。结论：槟榔子中含有抗血小板聚集及抑制乙酰胆碱酯酶活性的有效成分,而发挥这些功效的确切成分有待进一步的研究证实。     

Diluted magnetic semiconductor properties in TM doped ZnO nanoparticles

The hydrothermal method was used to create dilute magnetic semiconductor nanoparticles of Zn_1−xCo_xO (x = 0, 0.01, 0.05, 0.09). The effect of cobalt doping on the microstructure, morphological and optical properties of Zn_1−xCo_xO was also studied and the Co doping to host ZnO was confirmed from XRD and EDX analysis. The structural analysis showed that doping of cobalt into ZnO decreased the crystallinity, but the preferred orientation didn''t change. SEM analysis revealed that the cobalt dopant did not have a strong influence on the shape of the synthesized nanoparticles. No defect-related absorption peaks were observed in the UV-Vis spectra. The crystallinity of the doped samples was improved by high growth temperature and long growth time. Ferromagnetic behavior above room temperature was detected in co-doped ZnO nanoparticles. The ferromagnetic behavior increased with increasing Co (up to x = 0.05) doping. The ferromagnetic behavior declined when the Co content was further increased. Related research shows that doped ZnO nanoparticles have better dielectric, electrical conductivity, and magnetic properties than pure ZnO. This high ferromagnetism is usually a response reported for dilute magnetic semiconductors. These semiconductor nanoparticles were further used to designed spintronic based applications.

The enlarged central part M–H loop shows for the Co = 0.09 doped ZnO sample, the ferromagnetic (FM) behavior increased, i.e., a M_r of 0.2412 emu g⁻¹ with a H_c of 85 Oe.     

Quantitative fluorescence imaging analysis for cancer biomarker discovery: application to beta-catenin in archived prostate specimens.

The surprising disparity between the number of protein-encoding genes ( approximately 30,000) in the human genome and the number of proteins ( approximately 300,000) in the human proteome has inspired the development of translational proteomics aimed at protein expression profiling of disease states. Translational proteomics, which offers the promise of early disease detection and individualized therapy, requires new methods for the analysis of clinical specimens. We have developed quantitative fluorescence imaging analysis (QFIA) for accurate, reproducible quantification of proteins in slide-mounted tissues. The method has been validated for the analysis of beta-catenin in archived prostate specimens fixed in formalin. QFIA takes advantage of the linearity of fluorescence antibody signaling for tissue epitope content, a feature validated for beta-catenin in methacarn-fixed prostate specimens analyzed by reverse-phase protein array analysis and QFIA (r = 0.97). QFIA of beta-catenin in formaldehyde-fixed tissues correlated directly with beta-catenin content (r = 0.86). Application of QFIA in a cross-sectional study of biopsies from 42 prostate cancer (PC) cases and 42 matched controls identified beta-catenin as a potential field marker for PC. Receiver operating characteristic plots revealed that beta-catenin expression in the normal-appearing acini of cancerous glands identified 42% (95% confidence intervals, 26-57%) of cancer cases, with 88% (95% confidence intervals, 80-96%) specificity. The marker may contribute to a PC biomarker panel. In conclusion, we report the development and validation of a new method for fluorescence quantification of proteins in archived tissues and its application to archived specimens for an evaluation of beta-catenin expression as a biomarker for PC.     

Multi-chemothermoimmunotherapy for human colon adenocarcinoma in vitro

Effective adjunctive therapies for colorectal carcinoma are clearly needed. We evaluated the cytotoxic responses in vitro of human colon carcinoma cell lines to combined modalities: 5-fluorouracil/leucovorin (5-FU/LV), carboplatin (CP), tumor necrosis factor (TNF) and hyperthermia (HTX). Cytotoxicity was evaluated in a cell proliferation assay using crystal violet staining. 5-FU/LV was administered 2–3 days before TNF and CP, followed 1 h later by HTX. These cell lines were relatively resistant to HTX alone (42°C for 2 h), but were heterogeneous in their responses to various doses of the other single agents. This heterogeneity was also evident for combined modalities: the geneity was also evident for combined modalities: the HCT-15 cell line exhibited significant supra-additivity for selected doses of CP, TNF and 5-FU/LV, which was further enhanced by hyperthermia. In contrast, the HT-29 cell line did not demonstrate a strong pattern for supra-additivity, whereas the DLD-1 cell line had an intermediate response. Thus, our results suggest one approach to develop effective and dose-sparing multimodality therapeutic regimens for colon adenocarcinoma.     

Combined coliform and anaerobic infection of the lacrimal sac

A case is reported of combined coliform and anaerobic bacterial infection of the lacrimal sac, a condition of which there is only one other published case report. In addition, a literature review is presented of the bacteriology of acute dacryocystitis as it applies to this case. Recommendations for the microbiological investigation and management of acute dacryocystitis are made.     

Unusual presentations in myositis ossificans progressiva. A case report

Myositis ossificans progressiva is a rare connective tissue disorder. We present here a case of myositis ossificans progressiva with some unusual presentations and associated congenital skeletal anomalies that are reported very infrequently in the literature. The case report highlights the importance of early diagnosis in a case of rapidly progressive myositis ossificans progressiva.     

Taraxacin, a new guaianolide from Taraxacum wallichii

A new guaianolide, taraxacin (1), and a known sesquiterpene ketolactone (2) have been isolated from an ethyl acetate-soluble part of a methanolic extract of Taraxacum wallichii. The structure of 1 was established using NMR, MS, and X-ray crystallographic methods. The (13)C NMR data of 2 is also being reported for the first time.     

Induction of p21 by p53 following DNA damage inhibits both Cdk4 and Cdk2 activities

DNA damage often activates the p53-p21 pathway and causes G(1)-phase arrest in mammalian cells. Although there is ample evidence that p21 induction by p53 leads to Cdk2 inhibition, it is unclear whether this checkpoint event also leads to Cdk4 inhibition. Diaminocyclohexane(trans-diacetato)(dichloro) platinum(IV) (DAP), a platinum-based coordination complex, is a DNA-damaging agent that is effective against a variety of tumor cells resistant to the parental drug cisplatin. Our previous studies established that treatment of human cancer cells with low effective concentrations of DAP specifically activates the G(1)-phase checkpoint and simultaneously inhibit Cdk4 and Cdk2 activities. Here we demonstrate that DAP treatment of human cancer cells activates the p53-p21 pathway without activating other known mechanisms that inhibit Cdk4 and Cdk2 activities. The induced p21 binds to both the Cdk4/cyclin D and Cdk2/cyclin E complexes and inhibits both of their kinase activities. Conversely, inhibition of p21 induction by cycloheximide or by p21 gene deletion prevents DAP-induced inhibition of Cdk4 and Cdk2 activities. Attenuated p53 expression and p21 induction also eliminates DAP-induced G(1)-phase arrest and inhibition of Cdk4 and Cdk2 activities. Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities.