Volume 1, Issue 1

Hypertension is the most common cardiovascular condition in clinical practice and a major risk factor for stroke and cardiovascular events. There are more than 270 million hypertension patients in China, and the prevalence of hypertension in the high-latitude cold areas is significantly higher than in the low-latitude warm areas. The unique epidemiological characteristics and risk factors of hypertension in the cold regions of China urge for establishment of the prevention and control system for targeted and more effective management of the condition.

Eukaryotes and microbiota produce H 2 S, using the same substrates and enzymes which constitute the reverse-trans-sulfuration and transsulfuration pathways. The homeostasis of gut microbiota impacts on the structural and functional integrity of gut epithelial barrier. Microbiota also serve as signalling sources to inform the host of the metabolism and functional changes. Microbiota dysbiosis negatively affect human health, contributing to diseases like obesity, diabetes, inflammatory bowel diseases, and asthma. Not by coincidence, these pathological conditions are also closely related to the abnormal metabolism and function of H 2 S signalling.H 2 S serves as a bacterial signal to the host and the host-produced H 2 S impacts on the population and size of microbiota. These bi-directional interactions become especially important for the digestion and utilization of sulfur amino acid in diet. Dietary restriction of sulfur amino acid increases the endogenous production of H 2 S by the host and consequently offers many health benefits. It, on the other hand, decreases the nutritional supply to the microbiota, which could be remedied by the co-application of prebiotics and probiotics. It is strategically sound to target the expression of H 2 S-producing enzymes in different organs to slow aging processes in our body and promote better health.

Because of the overbearing low temperature, cold areas increase the morbidity and mortality of chronic non-communicable diseases (chronic diseases) in exposed populations. With the growth of the aging population and the superposition of lifestyle risk factors, the number of people with chronic diseases in cold areas is climbing, and the family and social burdens are rising. These health-threatening circumstances in the cold areas render the general practitioners to face serious challenges and difficulties in the community management of chronic diseases. This paper summarizes the current situation of chronic disease management in cold areas and explores the relevant management models so as to provide a useful reference for regional health construction, graded diagnosis and treatment, and prevention and control of chronic diseases in China.

Thrombotic diseases are the leading causes of death worldwide, especially in cold climates. Traditional Chinese medicine (TCM)-based therapies have gained increasing popularity worldwide, but also raised some concerns about its efficacy, safety profile and exact mechanisms. TCM has been traditionally used in the management of thrombosis and convincingly proven effective in modifying thrombosis progression, particularly the platelet function, coagulation system and fibrinolytic system. This review article focuses on TCM regulation of thrombosis with brief discussion on the fundamental aspects and relevant background information for better understanding of the subject. In addition to its antithrombotic effects, we will dive insight into the cellular and molecular mechanisms of TCM as pharmacological regulators of platelet aggregation, coagulation, and fibrinolysis. With increasing awareness and understanding of the benefits and potentials of TCM, TCM products will in no doubt gain its broader applications in the treatment of thrombosis and associated disorders, which in turn will deepen our understanding of its pharmacological and molecular mechanisms. Finally, current review provides a perspective view on the future directions to TCM research on thrombosis.

Introduction Bioactive secondary metabolites from the microbes living in frigid, toxic or other extreme environments are emerging as a new medicinal resource. Here, we report the discovery of new antidiabetic and anti-inflammatory compounds with novel structures from endophytic fungi hosted toxic medicinal plant. Methods The endophytic fungus isolated from toxic plants was fermented and extracted. The obtained extracts were purified with preparative HPLC to yield pure compounds. The purified compounds were examined by PTP1b inhibition and NO inhibition assays to evaluate their bioactivities. Results One new tridepsides (Compound 1), one new benzeneacetic acid derivative (Compound 3) and five known compounds (Compounds 2 and 4-7) were isolated from the ethyl acetate extract of Colletotrichum gloeosporioides, an endophytic fungus obtained from a toxic medicinal plant Tylophora ovata. Their structures were determined by spectroscopic data (1D and 2D NMR, HRESIMS) analyses. Compound 2 showed significant inhibitory activity against PTP1b with an IC50 value of 0.84 μM. Compounds 2 and 3 exhibited moderate inhibitory activities against the NO (nitric oxide) release in LPS-induced RAW 264.7 cells at 10 μM with percent inhibition of 39% and 33%, respectively. Conclusion The Compound 2 has potent PTP1b inhibitory effect indicating its antidiabetic potential and thus might be considered a lead compound for antidiabetic drug development.

Acute liver injury (ALI) is characterized by apoptosis, inflammation, and oxidative stress, and pathogenic mechanism of ALI is poorly understood. Apoptosis-stimulating of p53 protein 1 (ASPP1) is involved in environmental responses, tumor growth, and NF- K B activity, which is of critical importance to ALI. However, the role of ASPP1 in ALI remains largely unexplored. The current study aimed to determine the role of ASPP1 in ALI induced by CCl4 and the underlying mechanism. ASPP1 expression was detected in wild type (WT) mice with ALI induced by CCl4. The function of ASPP1 in ALI induced by CCl4 was investigated using conventional knockout ASPP1 mice. ASPP1 expression significantly increased in ALI mice at 24 hours after CCl4 injection. Deletion of ASSP1 ameliorated apoptosis, inflammation, and necrosis in ALI relative to WT mice. In addition, deficiency of ASPP1 improved liver flood flow as well as ALT and AST levels. The levels of phosphorylated p65 and phosphorylated IκBα were lower in ASPP1-/- mice than in WT mice with ALI. These results implicate that deletion of ASPP1 may act via inhibition of the NF-κB pathway and protect mice from ALI, which may be a new potential therapeutic target for the treatment of ALI.