Analysis of the relationship between lifestyle habits and glycosylated hemoglobin control based on data from a Health Management Plan

Ya-Chun Wang,Chi Wang,Ping-Wen Shih,Pei-Ling Tang 대한지역사회영양학회 2020 Nutrition Research and Practice Vol.14 No.3

BACKGROUND/OBJECTIVES: Type 2 Diabetes mellitus (T2DM) is a hereditary disease that is also strongly dependent on environmental factors, lifestyles, and dietary habits. This study explored the relationship between lifestyle habits and glycosylated hemoglobin management in T2DM patients to provide empirical outcomes to improve T2DM management and patient health literacy. SUBJECTS/METHODS: This study enrolled 349 diabetic patients with more than 5 care visits to a Diabetes Mellitus care network under the Health Management Plan led by Taiwan Department of Health (DOH). Based on relevant literature, an Outpatient Record Form of Diabetes Mellitus Care was designed and lipid profile tests were conducted for data collection and analysis. RESULTS: When modeling the data, the results showed that the odds for HbA1c > 7.5% in T2DM patients duration over 10 years was 3.785 (P = 0.002) times that in patients with disease duration of fewer than 3 years. The odds of HbA1c > 7.5% in illiterate patients was 3.128 (P = 0.039) times that in patients with senior high school education or above. The odds of HbA1c > 7.5% in patients with other chronic illness was 2.207 (P = 0.019) times that in participants without chronic illness. Among 5 beneficial lifestyle habits, the odds of HbA1c > 7.5% in patients with 2 or 3 good habits were 3.243 (P = 0.003) and 3.424 (P = 0.001) times that in patients with more than 3 good habits, respectively. CONCLUSION: This empirical outcome shows that maintaining a good lifestyle improves T2DM management and patients" knowledge, motivation, and ability to use health information. Patients with longer disease duration, education, or good lifestyle habits had optimal HbA1c management than those in patients who did not. Thus, effective self-management and precaution in daily life and improved health literacy of diabetic patients are necessary to increase the quality of T2DM care.

Resource Allocation based on Quantized Feedback for TDMA Wireless Mesh Networks

Xu, Lei,Tang, Zhen-Min,Li, Ya-Ping,Yang, Yu-Wang,Lan, Shao-Hua,Lv, Tong-Ming The Institute of Electronics and Information Engin 2013 IEIE Transactions on Smart Processing & Computing Vol.2 No.3

Resource allocation based on quantized feedback plays a critical role in wireless mesh networks with a time division multiple access (TDMA) physical layer. In this study, a resource allocation problem was formulated based on quantized feedback for TDMA wireless mesh networks that minimize the total transmission power. Three steps were taken to solve the optimization problem. In the first step, the codebook of the power, rate and equivalent channel quantization threshold was designed. In the second step, the timeslot allocation criterion was deduced using the primal-dual method. In the third step, a resource allocation scheme was developed based on quantized feedback using the stochastic optimization tool. The simulation results show that the proposed scheme not only reduces the total transmission power, but also has the advantage of quantized feedback.

RON and MET Co-overexpression Are Significant Pathological Characteristics of Poor Survival and Therapeutic Targets of Tyrosine Kinase Inhibitors in Triple-Negative Breast Cancer

Tian-Hao Weng,Min-Ya Yao,Xiang-Ming Xu,Chen-Yu Hu,Shu-Hao Yao,Yi-Zhi Liu,Zhi-Gang Wu,Tao-Ming Tang,Pei-Fen Fu,Ming-Hai Wang,Hang-Ping Yao 대한암학회 2020 Cancer Research and Treatment Vol.52 No.3

Purpose Triple-negative breast cancer (TNBC) is highly malignant and has poor prognosis and a high mortality rate. The lack of effective therapy has spurred our investigation of new targets for treating this malignant cancer. Here, we identified RON (macrophage-stimulating 1 receptor) and MET (MET proto-oncogene, receptor tyrosine kinase) as a prognostic biomarker and therapeutic targets for potential TNBC treatment. Materials and Methods We analyzed RON and MET expression in 187 primary TNBC clinical samples with immunohistochemistry. We validated the targeted therapeutic effects of RON and MET in TNBC using three tyrosine kinase inhibitors (TKIs): BMS-777607, INCB28060, and tivantinib. The preclinical therapeutic efficacy of the TKIs was mainly estimated using a TNBC xenograft model. Results Patients with TNBC had widespread, abnormal expression of RON and MET. There was RON overexpression, MET overexpression, and RON and MET co-overexpression in 63 (33.7%), 63 (33.7%), and 43 cases (23.0%), respectively, which had poor prognosis and short survival. In vivo, the TKI targeting RON ant MET inhibited the activation of the downstream signaling molecules, inhibited TNBC cell migration and proliferation, and increased TNBC cell apoptosis; in the xenograft model, they significantly inhibited tumor growth and shrank tumor volumes. The TKI targeting RON and Met, such as BMS-777607 and tivantinib, yielded stronger anti-tumor effects than INCB28060. Conclusion RON and MET co-overexpression can be significant pathological characteristics in TNBC for poor prognosis. TKIs targeting RON and MET have stronger drug development potential for treating TNBC.

Comprehensive MicroRNAome Analysis of the Relationship Between Alzheimer Disease and Cancer in PSEN Double- Knockout Mice

함수지,김태규,류지원,김용식,Ya-Ping Tang,임혜인 대한배뇨장애요실금학회 2018 International Neurourology Journal Vol.22 No.4

Purpose: Presenilins are functionally important components of γ-secretase, which cleaves a number of transmembrane proteins. Manipulations of PSEN1 and PSEN2 have been separately studied in Alzheimer disease (AD) and cancer because both involve substrates of γ-secretase. However, numerous clinical studies have reported an inverse correlation between AD and cancer. Interestingly, AD is a neurodegenerative disorder, whereas cancer is characterized by the proliferation of malignant cells. However, this inverse correlation in the PSEN double-knockout (PSEN dKO) mouse model of AD has been not elucidated, although doing so would shed light onto the relationship between AD and cancer. Methods: To investigate the inverse relationship of AD and cancer under conditions of PSEN loss, we used the hippocampus of 7-month-old and 18-month-old PSEN dKO mice for a microRNA (miRNA) microarray analysis, and explored the tumorsuppressive or oncogenic role of differentially-expressed miRNAs. Results: The total number of miRNAs that showed changes in expression level was greater at 18 months of age than at 7 months. Most of the putative target genes of the differentially-expressed miRNAs involved Cancer pathways. Conclusions: Based on literature reviews, many of the miRNAs involved in Cancer pathways were found to be known tumorsuppressive miRNAs, and their target genes were known or putative oncogenes. In conclusion, the expression levels of known tumor-suppressive miRNAs increased at 7 and 18 months, in the PSEN dKO mouse model of AD, supporting the negative correlation between AD and cancer.

AZD1480 Can Inhibit the Biological Behavior of Ovarian Cancer SKOV3 Cells in vitro

Sun, Zhao-Ling,Tang, Ya-Juan,Wu, Wei-Guang,Xing, Jun,He, Yan-Fang,Xin, De-Mei,Yu, Yan-Li,Yang, Yang,Han, Ping Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.8

Objective: To study the mechanism of effects of AZD1480 on the SKOV3 ovarian cancer cell line. Methods: The MTT method was used to assess cellular proliferation, flow cytometry for cellular apoptosis, the scratch test to determine migration, transwell chamber assays to detect cellular invasion, plate clone experiments to detect the clone forming ability and Western blotting to determine p-STAT3 protein levels. Results: The proliferation rate, migration ability, invasiveness and the clone forming ability of SKOV3 cells were reduced after treatment with AZD1480, while apoptosis rate and chemotherapeutic susceptibility were increased. After treatment with AZD1480 plus cisplatin, the apoptosis rate increased significantly while the expression level of p-STAT3 protein was decreased. Conclusion: AZD1480 can inhibit the proliferation, invasion, metastasis and clone formation of SKOV3 cells, induce cellulsar apoptosis, increase the chemotherapeutic sensitivity and reduce the expression level of p-STAT3 protein.

Big Data Analysis of Genes Associated With Neuropsychiatric Disorders in an Alzheimer’s Disease Animal Model

Ham, Suji,Kim, Tae K.,Hong, Heeok,Kim, Yong S.,Tang, Ya-Ping,Im, Heh-In Frontiers Media S.A. 2018 Frontiers in neuroscience Vol.12 No.-

<P>Alzheimer’s disease is a neurodegenerative disease characterized by the impairment of cognitive function and loss of memory, affecting millions of individuals worldwide. With the dramatic increase in the prevalence of Alzheimer’s disease, it is expected to impose extensive public health and economic burden. However, this burden is particularly heavy on the caregivers of Alzheimer’s disease patients eliciting neuropsychiatric symptoms that include mood swings, hallucinations, and depression. Interestingly, these neuropsychiatric symptoms are shared across symptoms of bipolar disorder, schizophrenia, and major depression disorder. Despite the similarities in symptomatology, comorbidities of Alzheimer’s disease and these neuropsychiatric disorders have not been studied in the Alzheimer’s disease model. Here, we explore the comprehensive changes in gene expression of genes that are associated with bipolar disorder, schizophrenia, and major depression disorder through the microarray of an Alzheimer’s disease animal model, the forebrain specific PSEN double knockout mouse. To analyze the genes related with these three neuropsychiatric disorders within the scope of our microarray data, we used selected 1207 of a total of 45,037 genes that satisfied our selection criteria. These genes were selected on the basis of 14 Gene Ontology terms significantly relevant with the three disorders which were identified by previous research conducted by the Psychiatric Genomics Consortium. Our study revealed that the forebrain specific deletion of Alzheimer’s disease genes can significantly alter neuropsychiatric disorder associated genes. Most importantly, most of these significantly altered genes were found to be involved with schizophrenia. Taken together, we suggest that the synaptic dysfunction by mutation of Alzheimer’s disease genes can lead to the manifestation of not only memory loss and impairments in cognition, but also neuropsychiatric symptoms.</P>