Body constitutions of traditional Chinese medicine caused a significant effect on irritable bowel syndrome.

BACKGROUND: According to the theory of traditional Chinese medicine (TCM), all types of body constitutions, except for the Gentleness (ie, the control group in our study), have disease susceptibility and affect the disease development process. This study attempted to investigate the relationship between TCM body constitutions and irritable bowel syndrome (IBS). METHODS: This cross-sectional study was based on Taiwan Biobank (TWB) and collected clinical data from 13 941 subjects aged 30 to 70. The results of the study showed that subjects with Yang-deficiency (N = 3161 subjects, odds ratio [OR] = 2.654, 95% CI = 1.740-3.910), Ying-deficiency (N = 3331 subjects, OR = 1.096, 95% CI = 0.627-1.782) or Stasis (N = 2335 subjects, OR = 1.680, 95% CI = 0.654-3.520) were more likely to have IBS. RESULTS: If the subjects with two or more TCM body constitutions: Yang-deficiency + Ying-deficiency (OR = 3.948, 95% CI = 2.742-5.560), Yang-deficiency + Stasis (OR = 2.312, 95% CI = 1.170-4.112), Ying-deficiency + Stasis (OR = 1.851, 95% CI = 0.828-3.567), or Yang-deficiency + Ying-deficiency + Stasis (OR = 3.826, 95% CI = 2.954-4.932) were also prone to IBS. CONCLUSION: These results confirmed the high correlation between TCM body constitutions and IBS. Because the current treatment for IBS is not entirely satisfactory, integrated traditional Chinese and Western medicine might provide patients with an alternative treatment option to alleviate IBS.

Enhanced Risk of Osteoporotic Fracture in Patients with Sarcopenia: A National Population-Based Study in Taiwan.

Sarcopenia is a progressive and generalized skeletal muscle disorder associated with poor health outcomes in older adults. However, its association with the risk of fracture risk is yet to be clarified. Therefore, this study aimed to assess the incidence and consequence of osteoporosis-related fractures among patients with sarcopenia in Taiwan. A retrospective, population-based study on 616 patients with sarcopenia, aged >40 years, and 1232 individuals without sarcopenia was conducted to evaluate claims data from Taiwan's National Health Insurance Research Database collected in the period January 2000−December 2013. The incidence rate of osteoporosis-related fracture was 18.13 and 14.61 per 1000 person years in the patients with sarcopenia and comparison cohort, respectively. Patients with sarcopenia had a greater osteoporotic fracture risk (adjusted hazard ratio [HR] 2.11; 95% confidence interval [CI] 1.47−3.04) after correcting for possible confounding. Additionally, females showed statistically significant correlations of sarcopenia with osteoporosis-related fracture risk (HR 1.53; CI 0.83−2.8 for males and HR 2.40, CI 1.51−3.81 for females). During this retrospective study on the fracture risk in Taiwan, an adverse impact of sarcopenia was observed, which substantiates the need to work toward sarcopenia prevention and interventions to reverse fracture susceptibility in patients with sarcopenia.

Arabidopsis glutamate receptor GLR3.7 is involved in abscisic acid response.

The ionotropic glutamate receptor (iGluR) plays an important role in neuronal signaling in animal cells. There are at least 20 glutamate receptor-like (GLR) genes in Arabidopsis thaliana. These genes are involved in seed germination, root growth, wounding response, stomata closure, etc. A recent study showed that Arabidopsis clade III glutamate receptor GLR3.7 is involved in salt stress response. We tested whether GLR3.7 is involved in abscisic acid (ABA) response. In the present study, we found that the expression of GLR3.7 was reduced by ABA treatment. Under ABA-treated condition, GLR3.7 overexpression lines exhibited significantly higher seed germination rate at 60, 72 and 84 h under ABA-treated condition. A point mutation in 14-3-3 binding site of GLR3.7 in GLR3.7-S860A overexpression lines exhibited higher seed germination inhibition under ABA-treated conditions. Our results support that GLR3.7 is involved in ABA response in Arabidopsis. In addition, Ser-860 of GLR3.7 appears to be important in ABA response.

Late-onset epilepsy and subsequent increased risk of dementia.

Inflammation is considered as a key pathogenesis factor of dementia and epilepsy. However, epilepsy's association with dementia, particularly its role in the development of dementia, remains unclear. To evaluate the association between epilepsy and the risk of dementia, in Taiwan, we have now conducted a retrospective cohort study comprising 675 individuals (age, ≥50 years) with epilepsy and 2,025 matched control subjects without epilepsy. In order to match individuals diagnosed with epilepsy with those with no diagnosis of epilepsy (comparison cohort), we utilized exact matching at a ratio of 1:3. Compared with those in the comparison cohort, individuals in the epilepsy cohort had a significantly increased risk of developing dementia (adjusted hazard ratio = 2.87, p < 0.001). A similar result has been observed after stratifying for sex (adjusted hazard ratio in males = 2.95, p < 0.001; adjusted hazard ratio in females = 2.66, p < 0.001). To conclude, based on these data, epileptic individuals ≥50 years were at a greater risk of developing dementia than people who do not have epilepsy, which indicates that a diagnosis of epilepsy presents a greater risk for the development of dementia.

Prodigiosin-induced cytotoxicity involves RAD51 down-regulation through the JNK and p38 MAPK pathways in human breast carcinoma cell lines.

RAD51 is essential for homologous recombination (HR)-mediated repair of DNA double-strand breaks (DSBs) in mammalian cells. RAD51 is an attractive target for anticancer drugs, given high RAD51 levels are frequently observed in many human tumors and associated with increased resistance to DSBs-inducing chemotherapeutics. Prodigiosin is a bacterial tripyrrole pigment with potent anticancer activity and also provokes DSBs. We hereby aimed to elucidate the role of RAD51 in prodigiosin-induced cytotoxicity. Prodigiosin was found to down-regulate RAD51 in multiple human breast carcinoma cell lines irrespective of p53 status. Mechanistically, prodigiosin lowered RAD51 mRNA expression, whereas blockade of proteasome-mediated degradation failed to restore RAD51 levels following prodigiosin treatment. In addition, prodigiosin triggered phosphorylation of JNK and p38 MAPK, while pharmacological inhibition of JNK or p38 MAPK attenuated prodigiosin-mediated inhibition of RAD51 mRNA expression. Lastly, cells with enforced RAD51 expression showed increased resistance to prodigiosin-induced cytotoxicity as well as inhibition of colony formation. Collectively, we conclude that RAD51 down-regulation represents one of the modes of prodigiosin's cytotoxic action, ostensibly by augmenting the genotoxic effect of prodigiosin through suppression of RAD51-mediated HR repair. Our findings further implicate the use of prodigiosin to potentiate the cytotoxicity of DSB-inducing chemotherapeutics through RAD51 down-regulation.