Evaluation Indicators for Priorities of Standardization in Traditional Medicine: using Analytic Hierarchy Process(AHP)

The entire manuscript is available for download as a single PDF file. Higher-resolution images are unavailable. For assistance, please contact [email protected]. Fieldwork Team: Philippe Beaujard (Director of Research, French National Centre for Scientific Research). Technical Team: Dr. Vika Zafrin (Digital Scholarship Librarian, BU Libraries), Eleni Castro (OpenBU and Electronic Theses & Dissertations Librarian, BU Libraries), Dr. Fallou Ngom (Director of the African Studies Center), Dr. Peter Quella (Assistant Director, African Studies Center), Mustapha Hashim Kurfi (PhD Candidate, Department of Political Science), and Zachary Gersten (Research Assistant, African Studies Center). This collection of Malagasy Ajami materials is copied as part of the African Studies Center’s African Ajami Library. This project is partly funded by the BU African Studies Center. We thank Dr. Tim Longman, past Director of the African Studies Center, and the entire African Studies team for their support. For Inquiries: Please contact Professor Fallou Ngom ([email protected]).The material is the fourth part of the second of two texts copied and owned by Jean, a diviner-healer (called ombiasy in Malagasy). Jean belonged to the Anakara Clan and lived in a village called Vatomasina in the Antemoro region (in the valley of the Matatàña River). The original author of the material is unknown. The material was photographed between 1983 and 1990. The material was written on paper school notebooks. While the exact content of material is unknown, it is believed to contain guidance for charms, divination, and healing through prayers, geomancy, and astrology

A Two-Patch Mathematical Model for Temperature-Dependent Dengue Transmission Dynamics

Dengue fever has been a threat to public health not only in tropical regions but non-tropical regions due to recent climate change. Motivated by a recent dengue outbreak in Japan, we develop a two-patch model for dengue transmission associated with temperature-dependent parameters. The two patches represent a park area where mosquitoes prevail and a residential area where people live. Based on climate change scenarios, we investigate the dengue transmission dynamics between the patches. We employ an optimal control method to implement proper control measures in the two-patch model. We find that blockage between two patches for a short-term period is effective in a certain degree for the disease control, but to obtain a significant control effect of the disease, a long-term blockage should be implemented. Moreover, the control strategies such as vector control and transmission control are very effective, if they are implemented right before the summer outbreak. We also investigate the cost-effectiveness of control strategies such as vaccination, vector control and virus transmission control. We find that vector control and virus transmission control are more cost-effective than vaccination in case of Korea

Bile Acid Signal-Induced Phosphorylation of Small Heterodimer Partner by Protein Kinase Cζ is Critical for Epigenomic Regulation of Liver Metabolic Genes

Bile acids (BAs) are recently recognized key signaling molecules that control integrative metabolism and energy expenditure. BAs activate multiple signaling pathways, including those of nuclear receptors, primarily farnesoid X receptor (FXR), membrane BA receptors, and FXR-induced FGF19 to regulate the fed-state metabolism. Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Here we show that protein kinase Cζ (PKCζ) is activated by BA or FGF19 and phosphorylates SHP at Thr-55 and that Thr-55 phosphorylation is critical for the epigenomic coordinator functions of SHP. PKCζ is coimmunopreciptitated with SHP and both are recruited to SHP target genes after bile acid or FGF19 treatment. Activated phosphorylated PKCζ and phosphorylated SHP are predominantly located in the nucleus after FGF19 treatment. Phosphorylation at Thr-55 is required for subsequent methylation at Arg-57, a naturally occurring mutation site in metabolic syndrome patients. Thr-55 phosphorylation increases interaction of SHP with chromatin modifiers and their occupancy at selective BA-responsive genes. This molecular cascade leads to repressive modifications of histones at metabolic target genes, and consequently, decreased BA pools and hepatic triglyceride levels. Remarkably, mutation of Thr-55 attenuates these SHP-mediated epigenomic and metabolic effects. This study identifies PKCζ as a novel key upstream regulator of BA-regulated SHP function, revealing the role of Thr-55 phosphorylation in epigenomic regulation of liver metabolism

Histone Deacetylase Inhibitors Selectively Target Homology Dependent DNA Repair Defective Cells and Elevate Non-Homologous Endjoining Activity

Background: We have previously used the ATAD5-luciferase high-throughput screening assay to identify genotoxic compounds with potential chemotherapeutic capabilities. The successful identification of known genotoxic agents, including the histone deacetylase inhibitor (HDACi) trichostatin A (TSA), confirmed the specificity of the screen since TSA has been widely studied for its ability to cause apoptosis in cancer cells. Because many cancers have acquired mutations in DNA damage checkpoints or repair pathways, we hypothesized that these cancers may be susceptible to treatments that target compensatory pathways. Here, we used a panel of isogenic chicken DT40 B lymphocyte mutant and human cell lines to investigate the ability of TSA to define selective pathways that promote HDACi toxicity. Results: HDACi induced a DNA damage response and reduced viability in all repair deficient DT40 mutants although ATM-nulls were least affected. The most dramatic sensitivity was observed in mutants lacking the homology dependent repair (HDR) factor BLM or the non-homologous end-joining (NHEJ) and HDR factors, KU/RAD54, suggesting an involvement of either HDR or NHEJ in HDACi-induced cell death. To extend these findings, we measured the frequencies of HDR and NHEJ after HDACi treatment and monitored viability in human cell lines comparably deficient in HDR or NHEJ. Although no difference in HDR frequency was observed between HDACi treated and untreated cells, HDR-defective human cell lines were clearly more sensitive than wild type. Unexpectedly, cells treated with HDACis showed a significantly elevated NHEJ frequency. Conclusions: HDACi targeting drugs induced significant increases in NHEJ activity in human cell lines but did not alter HDR frequency. Moreover, HDR is required for cellular resistance to HDACi therapy; therefore, NHEJ does not appear to be a critical axis for HDACi resistance. Rather, HDACi compounds induced DNA damage, most likely double strand breaks (DSBs), and HDR proficiency is correlated with cell survivalclose4

Investigation on Sex Hormone-Disruption Effects of Two Novel Brominated Flame Retardants (DBDPE and BTBPE) in Male Zebrafish (Danio rerio) and Two Human Cell Lines (H295R and MVLN)

Decabromodiphenyl ethane (DBDPE) and 1,2-bis(2,4,6-tribromo-phenoxy) ethane (BTBPE) are novel brominated flame retardants (NBFRs) and have been detected in variety of environment and biota. Although sex endocrine-disrupting potential has been suggested in experimental studies, their adverse effects on sex steroid hormones and underlying mechanisms are largely unclear. The purpose of the present study is to investigate the sex hormone-disrupting effects of two NBFRs using in vivo and in vitro models together. For this, male zebrafish (Danio rerio) along with human adrenocortical carcinoma (H295R) and breast carcinoma (MVLN) cell lines were employed. In male zebrafish, 14-day exposure to DBDPE significantly increased 17β-estradiol (E2) concentrations. Disruption of sex hormone regulation was also suggested after exposure to BTBPE, i.e., the increasing trend of E2 levels, E2/11-ketotestosterone (11-KT) ratio, and estrogen receptor-alpha (erα) and erβ gene expression levels. In H295R cells, an E2/T ratio showed an increasing trend by DBDPE exposure, but transcriptions of major genes in steroidogenesis pathway were not affected. Taken together, our observation implies that two NBFRs could cause the sex hormone disruption potential in male zebrafish and H295R cells but probably not through alteration of steroidogenesis pathway