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 selfmanagement and precaution in daily life and improved health literacy of diabetic patients are necessary to increase the quality of T2DM care.

PURPOSE: Cancer cells develop acquired resistance induced by chemotherapeutic drugs. In this study, we investigated the effects of brief treatment with cytotoxic drugs on the phenotype of breast cancer cells. METHODS: Breast cancer cells MCF7 and BT-474 were briefly treated with paclitaxel or doxorubicin. Clonogenic, migration, and invasion assays were performed on the treated cells. Western blot analysis and RhoA activity assay were also performed. RESULTS: Breast cancer cells when briefly treated with paclitaxel or doxorubicin showed reduced clonogenic ability. Doxorubicin, but not paclitaxel, augmented cell migration and invasion. The invasion-promoting effects of doxorubicin were lost when the two drugs were sequentially used in combination. Myosin light chain (MLC) 2 phosphorylation and RhoA activity were upregulated by doxorubicin and downregulated by paclitaxel. Pretreatment with RhoA inhibitors abolished the migration- and invasion-promoting effects of doxorubicin. CONCLUSION: Doxorubicin activates the RhoA/MLC pathway and enhances breast cancer cell migration and invasion. Therefore, this pathway might be explored as a therapeutic target to suppress anthracycline-enhanced tumor progression.
Blotting, Western ; Breast Neoplasms ; Breast ; Cell Movement ; Doxorubicin ; Myosin Light Chains ; Paclitaxel ; Phenotype ; Phosphorylation ; Up-Regulation

BACKGROUND/OBJECTIVES: Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the in vivo conversion of α-linolenic acid. Many enzymes participating in LCPUFA synthesis are regulated by peroxisome proliferator-activated receptor alpha (PPARα). Therefore, it was hypothesized that the tissue accretion of endogenously synthesized DHA could be modified by PPARα. MATERIALS/METHODS: The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among PPARα homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate (PPARα agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. RESULTS: PPARα ablation reduced the hepatic Acox, Fads1, and Fads2 mRNA levels, as well as the DHA concentration in the liver, but not in the brain cortex. In contrast, PPARα activation increased hepatic Acox, Fads1, Fads2 and Elovl5 mRNA levels, but reduced the DHA concentrations in the liver, retina, and phospholipid of brain cortex, and decreased mRNA and protein levels of the brain-derived neurotrophic factor in brain cortex. CONCLUSIONS: LCPUFA enzyme expression was altered by PPARα. Either PPARα deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance.
Animals ; Brain ; Brain-Derived Neurotrophic Factor ; Clofibrate ; Docosahexaenoic Acids ; Fatty Acid Desaturases ; Liver ; Mice ; Peroxisomes ; PPAR alpha ; Retina ; RNA, Messenger