Fifth Affiliated Hospital of Xinjiang Medical University

With the development of proteomics and epigenetics, a large number of RNA-binding proteins (RBPs) have been discovered in recent years, and the interaction between long non-coding RNAs (lncRNAs) and RBPs has also received increasing attention. It is extremely important to conduct in-depth research on the lncRNA-RBP interaction network, especially in the context of its role in the occurrence and development of cancer. Increasing evidence has demonstrated that lncRNA-RBP interactions play a vital role in cancer progression; therefore, targeting these interactions could provide new insights for cancer drug discovery. In this review, we discussed how lncRNAs can interact with RBPs to regulate their localization, modification, stability, and activity and discussed the effects of RBPs on the stability, transport, transcription, and localization of lncRNAs. Moreover, we explored the regulation and influence of these interactions on lncRNAs, RBPs, and downstream pathways that are related to cancer development, such as N6-methyladenosine (m6A) modification of lncRNAs. In addition, we discussed how the lncRNA-RBP interaction network regulates cancer cell phenotypes, such as proliferation, apoptosis, metastasis, drug resistance, immunity, tumor environment, and metabolism. Furthermore, we summarized the therapeutic strategies that target the lncRNA-RBP interaction network. Although these treatments are still in the experimental stage and various theories and processes are still being studied, we believe that these strategies may provide new ideas for cancer treatment.

Abstract Flexible electronics have emerged as an exciting research area in recent years, serving as ideal interfaces bridging biological systems and conventional electronic devices. Flexible electronics can not only collect physiological signals for human health monitoring but also enrich our daily life with multifunctional smart materials and devices. Conductive hydrogels (CHs) have become promising candidates for the fabrication of flexible electronics owing to their biocompatibility, adjustable mechanical flexibility, good conductivity, and multiple stimuli‐responsive properties. To achieve on‐demand mechanical properties such as stretchability, compressibility, and elasticity, the rational design of polymer networks via modulating chemical and physical intermolecular interactions is required. Moreover, the type of conductive components (eg, electron‐conductive materials, ions) and the incorporation method also play an important role in the conductivity of CHs. Electron‐CHs usually possess excellent conductivity, while ion‐CHs are generally transparent and can generate ion gradients within the hydrogel matrices. This mini review focuses on the recent advances in the design of CHs, introducing various design strategies for electron‐CHs and ion‐CHs employed in flexible electronics and highlighting their versatile applications such as biosensors, batteries, supercapacitors, nanogenerators, actuators, touch panels, and displays. image

With significant advances in the research and application of nerve conduits, they have been used to repair peripheral nerve injury for several decades. Nerve conduits range from biological tubes to synthetic tubes, and from nondegradable tubes to biodegradable tubes. Researchers have explored hollow tubes, tubes filled with scaffolds containing neurotrophic factors, and those seeded with Schwann cells or stem cells. The therapeutic effect of nerve conduits is improving with increasing choice of conduit material, new construction of conduits, and the inclusion of neurotrophic factors and support cells in the conduits. Improvements in functional outcomes are expected when these are optimized for use in clinical practice.

Abstract Muscle atrophy and functional decline (sarcopenia) are common manifestations of frailty and are critical contributors to morbidity and mortality in older people 1 . Deciphering the molecular mechanisms underlying sarcopenia has major implications for understanding human ageing 2 . Yet, progress has been slow, partly due to the difficulties of characterizing skeletal muscle niche heterogeneity (whereby myofibres are the most abundant) and obtaining well-characterized human samples 3,4 . Here we generate a single-cell/single-nucleus transcriptomic and chromatin accessibility map of human limb skeletal muscles encompassing over 387,000 cells/nuclei from individuals aged 15 to 99 years with distinct fitness and frailty levels. We describe how cell populations change during ageing, including the emergence of new populations in older people, and the cell-specific and multicellular network features (at the transcriptomic and epigenetic levels) associated with these changes. On the basis of cross-comparison with genetic data, we also identify key elements of chromatin architecture that mark susceptibility to sarcopenia. Our study provides a basis for identifying targets in the skeletal muscle that are amenable to medical, pharmacological and lifestyle interventions in late life.

Cardiac aging is evident by a reduction in function which subsequently contributes to heart failure. The metabolic microenvironment has been identified as a hallmark of malignancy, but recent studies have shed light on its role in cardiovascular diseases (CVDs). Various metabolic pathways in cardiomyocytes and noncardiomyocytes determine cellular senescence in the aging heart. Metabolic alteration is a common process throughout cardiac degeneration. Importantly, the involvement of cellular senescence in cardiac injuries, including heart failure and myocardial ischemia and infarction, has been reported. However, metabolic complexity among human aging hearts hinders the development of strategies that targets metabolic susceptibility. Advances over the past decade have linked cellular senescence and function with their metabolic reprogramming pathway in cardiac aging, including autophagy, oxidative stress, epigenetic modifications, chronic inflammation, and myocyte systolic phenotype regulation. In addition, metabolic status is involved in crucial aspects of myocardial biology, from fibrosis to hypertrophy and chronic inflammation. However, further elucidation of the metabolism involvement in cardiac degeneration is still needed. Thus, deciphering the mechanisms underlying how metabolic reprogramming impacts cardiac aging is thought to contribute to the novel interventions to protect or even restore cardiac function in aging hearts. Here, we summarize emerging concepts about metabolic landscapes of cardiac aging, with specific focuses on why metabolic profile alters during cardiac degeneration and how we could utilize the current knowledge to improve the management of cardiac aging.

Abstract MicroRNAs have emerged as important post-transcriptional regulators of gene expression and are involved in diverse diseases and cellular process. Decreased expression of miR-181a has been observed in the patients with coronary artery disease, but its function and mechanism in atherogenesis is not clear. This study was designed to determine the roles of miR-181a-5p, as well as its passenger strand, miR-181a-3p, in vascular inflammation and atherogenesis. We found that the levels of both miR-181a-5p and miR-181a-3p are decreased in the aorta plaque and plasma of apoE −/− mice in response to hyperlipidemia and in the plasma of patients with coronary artery disease. Rescue of miR-181a-5p and miR-181a-3p significantly retards atherosclerotic plaque formation in apoE −/− mice. MiR-181a-5p and miR-181a-3p have no effect on lipid metabolism but decrease proinflammatory gene expression and the infiltration of macrophage, leukocyte and T cell into the lesions. In addition, gain-of-function and loss-of-function experiments show that miR-181a-5p and miR-181a-3p inhibit adhesion molecule expression in HUVECs and monocytes-endothelial cell interaction. MiR-181a-5p and miR-181a-3p cooperatively receded endothelium inflammation compared with single miRNA strand. Mechanistically, miR-181a-5p and miR-181a-3p prevent endothelial cell activation through blockade of NF-κB signaling pathway by targeting TAB2 and NEMO, respectively. In conclusion, these findings suggest that miR-181a-5p and miR-181a-3p are both antiatherogenic miRNAs. MiR-181a-5p and miR-181a-3p mimetics retard atherosclerosis progression through blocking NF-κB activation and vascular inflammation by targeting TAB2 and NEMO, respectively. Therefore, restoration of miR-181a-5p and miR-181a-3p may represent a novel therapeutic approach to manage atherosclerosis.

Adverse cardiac remodeling after myocardial infarction (MI) is associated with extremely high mortality rates worldwide. Although optimized medical therapy, Preservation of lusitropic and inotropic function and protection against adverse remodeling in ventricular structure remain relatively frequent. This study demonstrated that Andrographolide (Andr) significantly ameliorated adverse cardiac remodeling induced by myocardial infarction and improves contractile function in mice with LAD ligation compared with the control group. Briefly, Andr markedly attenuated cardiac fibrosis and relieved inflammation after myocardial infarction. Specifically, Andr significantly blocked oxidative stress and the nuclear translocation of p-P65 following myocardial infarction. At the mechanistic level, antioxidant effect of Andr was achieved through strengthening antioxidative stress capacity and attributed to the activation of Nrf2/HO-1 Signaling. Consistently, H9C2 administrated with Andr showed a decreased oxidative stress caused by hypoxia precondition, but treatment with specific Nrf2 inhibitor (ML385) or the silence of Nrf2 blunted the activation of Nrf2/HO-1 Signaling and removed the protective effects of Andr in vitro. Thus, we suggest that Andr alleviates adverse cardiac remodeling following myocardial infarction through enhancing Nrf2 signaling pathway.

Coacervation plays a critical role in numerous biological activities such as constructing biological tissues and achieving robust wet adhesion of marine sessile organisms, which conventionally occurs when oppositely charged polyelectrolytes are mixed in aqueous solutions driven by electrostatic attraction. Here, a novel type of adhesive coacervate is reported, driven by hydrogen-bonding interactions, readily formed by mixing silicotungstic acid and nonionic polyethylene glycol in water, providing a new approach for developing coacervates from nonionic systems. The as-prepared coacervate is easily paintable underwater, show strong wet adhesion to diverse substrates, and has been successfully applied as a hemostatic agent to treat organ injuries without displaying hemolytic activity, while with inherent antimicrobial properties thus avoiding inflammations and infections due to microorganism accumulation. This work demonstrates that coacervation can occur in salt-free environments via non-electrostatic interactions, providing a new platform for engineering multifunctional coacervate materials as tissue glues, wound dressings and membrane-free cell systems.

BACKGROUND AND AIM: The aim of this study was to investigate whether the platelet-to-lymphocyte ratio (PLR) is an independent predictor of all-cause mortality and cardiovascular (CV) events in patients with acute coronary syndrome (ACS). METHODS: PubMed, Embase, and the Cochrane Library were searched for relevant cohort studies regarding the association between PLR and outcomes of patients with ACS. Either a random- or a fixed-effect model was used for pooling data. RESULTS: Eight studies involving 6627 patients with ACS were included. The cut-off PLR value for defining risk groups was 150, and patients were assigned to the low (≤ 150) or high (> 150) PLR groups. The pooled relative risk (RR) values of in-hospital and long-term mortality were 2.15 (95% CI [confidence interval] 1.73-2.67; p < 0.00001) and 2.27 (95% CI 1.35-3.80; p = 0.002), respectively, comparing the high and the low PLR groups. Compared with the low PLR group, the high PLR group had a significantly increased risk of in-hospital (RR 1.95; 95% CI 1.30-2.91; p = 0.001) and long-term (RR 1.50; 95% CI 1.08-2.09; p = 0.01) major adverse CV events. CONCLUSIONS: Elevated PLR was found to be a predictor of all-cause mortality and CV events.

Gut microbiota (GM) metabolites can modulate the physiology of the host brain through the gut-brain axis. We wished to discover connections between the GM, neurotransmitters, and brain function using direct and indirect methods. A diet with increased amounts of sugar and fat (high-sugar and high-fat (HSHF) diet) was employed to disturb the host GM. Then, we monitored the effect on pathology, neurotransmitter metabolism, transcription, and brain circularRNAs (circRNAs) profiles in mice. Administration of a HSHF diet-induced dysbacteriosis, damaged the intestinal tract, changed the neurotransmitter metabolism in the intestine and brain, and then caused changes in brain function and circRNA profiles. The GM byproduct trimethylamine-n-oxide could degrade some circRNAs. The basal level of the GM decided the conversion rate of choline to trimethylamine-n-oxide. A change in the abundance of a single bacterial strain could influence neurotransmitter secretion. These findings suggest that a new link between metabolism, brain circRNAs, and GM. Our data could enlarge the "microbiome-transcriptome" linkage library and provide more information on the gut-brain axis. Hence, our findings could provide more information on the interplay between the gut and brain to aid the identification of potential therapeutic markers and mechanistic solutions to complex problems encountered in studies of pathology, toxicology, diet, and nutrition development.

Objective: There is evidence that type 2 diabetes (T2DM) is affected by gut microbiota, and gut microbiota diversity modified by diet. To investigate its modifications in Uyghur patients with different glucose tolerance, we enrolled 561 subjects: newly diagnosed T2DM (n=145), impaired glucose regulation (IGR) patients (n=138) and in normal control (NC) population (n=278). Methods: The nutrient intake in food frequency questionnaire was calculated by R language. The regions V3-V4 of 16S ribosomal RNA were sequenced by using Illumina Miseq platform. Sequences were clustered by operational taxonomy units, gut microbiota composition and diversity was analyzed. Correlations between bacterial composition at different level and dietary factors were evaluated. Results: The α-diversity was highest in NC, followed by T2DM and IGR; β-diversity distinguished between patients and NC. Compared to NC, Saccharibacteria was significantly increased in T2DM and IGR. Deferribacteres was significantly increased in T2DM compared to NC and IGR. Veillonella, Pasteurellaceae and Haemophilus were over-represented in IGR. Abundance of Bacteroidetes was negatively correlated with LDL-C; Abundance of Tenericutes was negatively correlated with hip circumference and total cholesterol, positively correlated with HDL-C and cake intake；Actinobacteria was positively correlated with BMI and folic acid intake, negatively correlated with oil intake. Firmicutes was negatively correlated with beverage and alcohol intake. Spirochaetae was negatively correlated with fungus, fruits, beans, vitamin C, dietary fiber and calcium. Fusobacteria was positively correlated with beans intake, and is negatively correlated with fat intake. Proteobacteria was positively correlated with tuber crops intake. Synergistetes was positively correlated with cholesterol, nicotinic acid, and selenium intake. Deferribacteres was negatively correlated with magnesium intake. Conclusions: At the phylum and genus level, the structure and diversity of intestinal microbiota of T2DM and IGR was altered, the number of OTUs, the relative abundance and diversity were all decreased. The gut microbiota of the newly diagnosed T2DM, IGR and NC were related to age, blood lipids, BMI, blood pressure and dietary nutrient intake. Unbalanced nutrient intake in the three groups may affect the structure and abundance of the gut microbiota, which may play a role in the occurrence and development of T2DM in Uyghur.

Drug combination therapies are common practice in the treatment of cancer. In this study, we evaluated the anticancer effects of myricetin (MYR), methyl eugenol (MEG) and cisplatin (CP) both separately as well as in combination against cervical cancer (HeLa) cells. To demonstrate whether MYR and MEG enhance the anticancer activity of CP against cervical cancer cells, we treated HeLa cells with MYR and MEG alone or in combination with cisplatin and evaluated cell growth and apoptosis using MTT (3 (4, 5 dimethyl thiazol 2yl) 2, 5 diphenyltetrazolium bromide) assay, LDH release assay, flow cytometry and fluorescence microscopy. The results revealed that, as compared to single drug treatment, the combination of MYR or MEG with CP resulted in greater effect in inhibiting cancer cell growth and inducing apoptosis. Cell apoptosis induction, Caspase-3 activity, cell cycle arrest and mitochondrial membrane potential loss were systematically studied to reveal the mechanisms of synergy between MYR, MEG and CP. Combination of MYR or MEG with CP resulted in more potent apoptosis induction as revealed by fluorescence microscopy using Hoechst 33258 and AO-ETBR staining. The combination treatment also increased the number of cells in G0/G1 phase dramatically as compared to single drug treatment. Mitochondrial membrane potential loss (ΛΨm) as well as Caspase-3 activity was much higher in combination treatment as compared to single drug treatment. Findings of this investigation suggest that MYR and MEG combined with cisplatin is a potential clinical chemotherapeutic approach in human cervical cancer.

Pericarpium Citri Reticulatae (PCR, Citrus reticulata 'Chachi', Guangchenpi in Chinese) is one of the most famous Chinese citrus herbal medicines. The in vivo anti-asthmatic activity of 'Chachi' PCR was investigated using a histamine-induced experimental asthma model in Guinea pigs. Two alkaloid-type compounds, synephrine and stachydrine, were analyzed and identified in the 'Chachi' PCR alkaloid fraction. The alkaloid fraction and synephrine protected Guinea pigs against histamine-induced experimental asthma in a dose-dependent manner. The respective application of high, middle, and low doses of the 'Chachi' PCR alkaloid fraction significantly increased specific airway resistance by 284%, 328%, and 355%, and decreased dynamic compliance by 57%, 67%, and 75%. A similar change was observed for synephrine. The expression of eosinophils in bronchoalveolar lavage fluid (BALF) and serum IgE, IL-4, and IL-5 levels in histamine-induced experimental asthmatic Guinea pigs were significantly downregulated by the 'Chachi' PCR alkaloid fraction and synephrine compared to the control group, whereas stachydrine did not impart a statistically significant effect on the expression of tested inflammatory cells (leucocytes, eosinophils, neutrophils, and lymphocytes), immunoglobulin (IgE), or cytokines (IL-4 and IL-5). Pathological changes in lung tissues in each treatment group included the infiltration of inflammatory cells around the bronchia.

BACKGROUND AND OBJECTIVE: Of three first-line anti-tuberculosis (anti-TB) drugs, isoniazid is most commonly associated with hepatotoxicity. Differences in INH-induced toxicity have been attributed to genetic variability at several loci, NAT2, CYP2E1, GSTM1and GSTT1, that code for drug-metabolizing enzymes. This study evaluated whether the polymorphisms in these enzymes were associated with an increased risk of anti-TB drug-induced hepatitis in patients and could potentially be used to identify patients at risk of liver injury. METHODS AND DESIGN: In a cross-sectional study, 2244 tuberculosis patients were assessed two months after the start of treatment. Anti-TB drug-induced liver injury (ATLI) was defined as an ALT, AST or bilirubin value more than twice the upper limit of normal. NAT2, CYP2E1, GSTM1 and GSTT1 genotypes were determined using the PCR/ligase detection reaction assays. RESULTS: 2244 patients were evaluated, there were 89 cases of ATLI, a prevalence of 4% 9 patients (0.4%) had ALT levels more than 5 times the upper limit of normal. The prevalence of ATLI was greater among men than women, and there was a weak association with NAT2*5 genotypes, with ATLI more common among patients with the NAT2*5*CT genotype. The sensitivity of the CT genotype for identifying patients with ATLI was 42% and the positive predictive value 5.9%. CT ATLI was more common among slow acetylators (prevalence ratio 2.0 (95% CI 0.95,4.20) )compared to rapid acetylators. There was no evidence that ATLI was associated with CYP2E1 RsaIc1/c1genotype, CYP2E1 RsaIc1/c2 or c2/c2 genotypes, or GSTM1/GSTT1 null genotypes. CONCLUSIONS: In Xinjiang Uyghur TB patients, liver injury was associated with the genetic variant NAT2*5, however the genetic markers studied are unlikely to be useful for screening patients due to the low sensitivity and low positive predictive values for identifying persons at risk of liver injury.

Myocardial remodeling serves an important role in the pathophysiology of coronary heart disease. The angiotensin-converting enzyme (ACE)2-angiotensin-(1-7) [Ang (1‑7)]‑Mas receptor (MasR) axis is a key regulator in myocardial remodeling and development of heart failure. To investigate how ACE2‑Ang‑(1‑7)‑MasR axis function on myocardial remodeling and cardiac fibrosis in post‑myocardial infarction (MI), male Sprague‑Dawley rats (weight, 200±20 g) were used to establish the model of myocardial infarction by ligating the left coronary artery. The present study suggests that telmisartan (Tel) and olmesartan (Olm) (5 mg/kg/d) can inhibit myocardial remodeling of post‑myocardial infarction through the ACE2‑Ang (1‑7)‑MasR pathway. Administration of Tel or Olm was demonstrated to significantly inhibit collagen deposition using Masson staining. In addition, telmisartan and olmesartan was indicated to antagonize angiotensin II (Ang II) and upregulate ACE2, MasR, Ang (1‑7) expression in myocardial tissue using immunoassay and ELISA test, and the effect of Olm was more marked than that of Tel at the same dosage. Simultaneously, compared with the MI or Sham group, the mRNA and protein expression of ACE2, Ang II and MasR in myocardial tissue demonstrated a remarkable increase in the Olm group, when compared with the Tel group. Taken together, our data demonstrated that ACE2‑Ang (1‑7)‑MasR axis may present a potential protective role in the development of myocardial remodeling and may provide a new target for drug development of cardiac fibrosis. In conclusion, Olm is superior to Tel in inhibiting myocardial local Ang II level reducing myocardial collagen deposition and improving myocardial remodeling by upregulating the expression of ACE2, Ang (1‑7) and MasR.

// Jian Cao 1, 3, 4 , Jun Liu 2 , Ran Xu 1 , Xuan Zhu 1 , Xiaokun Zhao 1 and Bin-Zhi Qian 3 1 Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China 2 Department of Urology, The Fifth Affiliated Hospital of Xinjiang Medical University, Wulumuqi, Xinjiang 830011, P.R. China 3 MRC Centre for Reproductive Health, Queen&rsquo;s Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom 4 Current/Present address: Department of Urology, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, P.R. China Correspondence to: Bin-Zhi Qian, email: Binzhi.Qian@ed.ac.uk Keywords: prostate cancer, tumor-associated macrophages, macrophage scavenger receptor 1, prognosis, meta-analysis Received: September 24, 2016&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Accepted: March 24, 2017&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Published: June 27, 2017 ABSTRACT Recent studies suggested that the tumour associated macrophages may be associated with prostate cancer outcome. A meta-analysis was performed to evaluate the prognostic value of tumor associated macrophages and macrophage scavenger receptor 1, marker for a subset of macrophages, by pooled hazard ratio and 95% confidence intervals from qualified studies following a systemic search. The results indicate that higher infiltration of tumor associated macrophages predicts poor overall survival (HR=1.57, 95%CI: 1.15-1.98), but not biochemical recurrence (HR=1.01, 95%CI: 0.98-1.04) or recurrence-free survival (HR=1.03, 95%CI: 0.05-2.01). In contrast, elevated level of macrophage scavenger receptor 1 was significantly associated with better recurrence-free survival (HR=3.26, 95%CI: 1.22-5.29). Thus, our analysis confirmed the prognostic value of these markers in prostate cancer outcome. We also discussed potential causes of the controversies in the literature and future research directions.

OBJECTIVES: To investigate the prevalence of obesity and hypertension among University students' and their knowledge and attitude towards risk factors of cardiovascular disease (CVD) in Jeddah,: Saudi Arabia. METHODS: A total of 610 male students were selected for present cross sectional study and their blood pressure (BP) and body mass index (BMI) was determined, other data was gathered through a questionnaire, and SPSS-16 was used for analyzing data. RESULTS: Out of 610 students, 7.5% were hypertensive (systolic 2.6% and diastolic 6.3%) while the BMI of 51.6% was in the normal range, 29.8% were overweight and 10.7% were moderately obese and 7.9% were severely obese. Majority of the participants considered that smoking, increased fatty food intake, obesity, high BP, and increased LDL-cholesterol level, are the main causes of the CVD. Most of the participants agreed that one should know his BP, blood sugar, serum cholesterol and one should maintain normal body weight and should do regular exercise. They were also aware that healthy lifestyle could prevent CVD. However, majority of the participants were not practicing healthy lifestyle. CONCLUSION: A huge gap exists in the knowledge, attitude and practice regarding risk factors of CVD among the university students.

N-acetylcysteine is a classic mucolytic agent. This study aimed to investigate the efficacy of N-acetylcysteine on reducing the risk of exacerbations in bronchiectasis patients. A prospective, randomized, controlled trial was conducted between April 1, 2014 and December 31, 2016 in five general hospitals in Shandong Province, China. Adult bronchiectasis patients with at least two exacerbations in the past year were potentially eligible. Patients were randomly assigned to receive oral N-acetylcysteine (600 mg, twice daily, 12 months) or on-demand treatment. A total of 161 patients were eligible for randomization (81 to the N-acetylcysteine group and 80 to the control group). During the 12-month follow-up, the incidence of exacerbations in the N-acetylcysteine group was significantly lower than that in the control group (1.31 vs. 1.98 exacerbations per patient-year; risk ratio, 0.41; 95% CI, 0.17–0.66; P = 0.0011). The median number of exacerbations in the N-acetylcysteine group was 1 (0.5–2), compared with 2 (1–2) in the control group (U = − 2.95, P = 0.003). A total of 24.7% of the N-acetylcysteine group patients and 11.3% of the control group patients remained exacerbation-free throughout the 12-month follow-up (χ2 = 4.924, P = 0.026). Compared with the control group, the volume of 24-h sputum in the N-acetylcysteine group was significantly reduced (t = − 3.091, P = 0.002). Additionally, the N-acetylcysteine group showed a significant improvement in the quality of life. No severe adverse events were reported in the intervention group. The long-term use of N-acetylcysteine is able to reduce the risk of exacerbations for bronchiectasis patients in Shandong Province, China. The results of this study should be verified in a larger randomized controlled trial. ClinicalTrials.gov (NCT02088216) (Registered date: March 5, 2014).

In the study, we evaluated chemical composition and antimicrobial, antibiofilm, and antitumor activities of essential oils from dried leaf essential oil of leaf and flower of Agastache rugosa for the first time. Essential oil of leaf and flower was evaluated with GC and GC-MS methods, and the essential oil of flower revealed the presence of 21 components, whose major compounds were pulegone (34.1%), estragole (29.5%), and p-Menthan-3-one (19.2%). 26 components from essential oil of leaf were identified, the major compounds were p-Menthan-3-one (48.8%) and estragole (20.8%). At the same time, essential oil of leaf, there is a very effective antimicrobial activity with MIC ranging from 9.4 to 42 μg ml(-1) and potential antibiofilm, antitumor activities for essential oils of flower and leaf essential oil of leaf. The study highlighted the diversity in two different parts of A. rugosa grown in Xinjiang region and other places, which have different active constituents. Our results showed that this native plant may be a good candidate for further biological and pharmacological investigations.

A hospital-based case-control study was conducted to investigate potential association between mitochondrial DNA and Type 2 diabetes mellitus (T2DM) in Chinese Uyghur population. We sequenced mitochondrial DNA from 210 Uyghur individuals including 88 T2DM patients and 122 controls. Using haplogroup classification and association test, we found that haplogroup H (odds ratio [OR] = 1.40; 95% confidence interval [CI]: 1.20-1.64; P = 0.0005138) and D4 (odds ratio = 1.47; 95% CI: 1.22-1.77; P = 0.001064) were associated with an increased risk of T2DM in Chinese Uyghur population. Two markers of haplogroup D4 and H, MT-ATP8 m.8414 T > G (p.Leu17Phe) and m.2706 G > A encoding 16S rRNA in mitochondria, were predicted to affect the structure of MT-ATP8 and 16S RNA, respectively, and may be involved in the pathogenesis of T2DM. Our study provides a new clue for mitochondrial DNA in the etiology of T2DM in Chinese Uyghur population.