Thyroid disease as a risk factor for cerebrovascular disease.

BACKGROUND: Thyroid disease is the medical condition impairing function of the thyroid. Among this disorder category, hyperthyroidism is that the thyroid gland produces excessive amounts of thyroid hormones whereas hypothyroidism is that the thyroid gland does not produce enough thyroid hormone. Various studies have supported the comorbid association between thyroid disease and cardiovascular disorder. However, there is insufficient evidence to prove the relationship between cerebrovascular disease (CVD) and thyroid disease. METHODS: In this study, we tried to verify that thyroid disease increases the risk of CVD development employing a population-based database, National Health Insurance Research Database of Taiwan. A total of 16,808 hyperthyroidism cases and 5793 hypothyroidism patients with corresponding control subjects were studied, respectively. Hazard ratio (HR) by the Cox regression was used to quantify risk of CVD in different groups of subjects, that is, case patients versus matched controls. Further stratification studies for risk factors of CVD were performed to evaluate the comorbid association between CVD and hyperthyroidism/hypothyroidism. RESULTS: Evaluation results have shown that hyperthyroidism increased 38% of the hazard of developing follow-up CVD (adjusted HR, 1.38) whereas hypothyroidism increased even higher the risk (adjusted HR, 1.89). Further stratification studies for risk factors of CVD suggested that the comorbid association between hypothyroidism and CVD was comparable to those influences from cardiac risk factors, such as diabetes mellitus, hyperlipidemia, hypertension, or renal failure and so forth. CONCLUSIONS: Thyroid disease may predispose to onset of CVD. Advanced analysis is required to investigate the pathologic mechanism underlying the association between CVD and thyroid disease.

Identification of cucurbitacins and assembly of a draft genome for Aquilaria agallocha.

BACKGROUND: Agarwood is derived from Aquilaria trees, the trade of which has come under strict control with a listing in Appendix II of the Convention on International Trade in Endangered Species of Wild Fauna and Flora. Many secondary metabolites of agarwood are known to have medicinal value to humans, including compounds that have been shown to elicit sedative effects and exhibit anti-cancer properties. However, little is known about the genome, transcriptome, and the biosynthetic pathways responsible for producing such secondary metabolites in agarwood. RESULTS: In this study, we present a draft genome and a putative pathway for cucurbitacin E and I, compounds with known medicinal value, from in vitro Aquilaria agallocha agarwood. DNA and RNA data are utilized to annotate many genes and protein functions in the draft genome. The expression changes for cucurbitacin E and I are shown to be consistent with known responses of A. agallocha to biotic stress and a set of homologous genes in Arabidopsis thaliana related to cucurbitacin bio-synthesis is presented and validated through qRT-PCR. CONCLUSIONS: This study is the first attempt to identify cucurbitacin E and I from in vitro agarwood and the first draft genome for any species of Aquilaria. The results of this study will aid in future investigations of secondary metabolite pathways in Aquilaria and other non-model medicinal plants.