Poricoic acid A induces mitophagy to ameliorate podocyte injury in diabetic kidney disease via downregulating FUNDC1.

Diabetic kidney disease (DKD) is a devastating complication of diabetes mellitus (DM) and is the most prevalent chronic kidney disease (CKD). Poricoic acid A (PAA), a component isolated from Traditional Chinese Medicine (TCM) Poria cocos, has hypoglycaemic and anti-fibrosis effects. However, the role of PAA in DKD remains largely unclear. To mimics an in vitro model of DKD, the mouse podocyte MPC5 cells were treated with high glucose (25 mM; HG) for 24 h. CCK-8 and flow cytometry assays were conducted for assessing MPC5 cell viability and apoptosis. Meanwhile, streptozotocin (STZ) was used to induce experimental DKD in mice by intraperitoneal injection. PAA notably inhibited the apoptosis and inflammation, reduced the generation of ROS, and elevated the MMP level in HG-treated MPC5 cells. Moreover, PAA obviously reduced blood glucose and urine protein levels, inhibited renal fibrosis in DKD mice. Meanwhile, PAA markedly increased LC3 and ATG5 levels and declined p62 and FUNDC1 levels in HG-treated MPC5 cells and in the kidney tissues of DKD mice, leading to the activation of cell mitophagy. Furthermore, the downregulation of FUNDC1 also inhibited apoptosis, inflammation, and promoted mitophagy in HG-treated MPC5 cells. As expected, the knockdown of FUNDC1 further enhanced the protective role of PAA in MPC5 cells following HG treatment, indicating that induction of mitophagy could attenuate podocyte injury. Collectively, PAA could exert beneficial effects on podocyte injury in DKD by promoting mitophagy via downregulating FUNDC1. These findings suggested that PAA may have great potential in alleviating kidney injury in DKD.

Case report: A novel mutation in TRPS1 identified in a Chinese family with tricho-rhino-phalangeal syndrome I: A therapeutic challenge.

Tricho-rhino-phalangeal syndrome (TRPS) is a rare autosomal dominant malformation caused by mutations involving the TRPS1 gene. Patients with TRPS exhibit distinctive craniofacial and skeletal abnormalities. This report presents three intra-familial cases with TRPS1 gene mutations that showed the characteristic features of TRPS. A 13-year-old boy was admitted to Department of Endocrinology for the evaluation of short stature. Physical examination revealed that the boy had thin sparse hair, pear-shaped nose, protruding ears, small jaw and brachydactyly. A survey of his family history indicated that the boy's sister and mother shared the same clinical features. Radiological techniques demonstrated a different degree of skeletal abnormalities in these siblings. Next-generation sequencing and quantitative PCR were performed and showed a novel deletion mutation in exons 3-5 in the three familial cases, confirming the diagnosis of TRPS I. The healthy father did not carry the deletion mutation. Currently, there was no specific therapy for TRPS I; however, genetic consultation may be useful for family planning.

Case report: Diabetic muscle infarction with diabetic ketoacidosis: A rare complication of diabetes.

Background: Diabetic muscle infarction (DMI), which is also referred to as diabetic myonecrosis, is a rare and long-term complication of poorly controlled diabetes mellitus, while we found that acute diabetes decompensation, such as diabetic ketoacidosis (DKA), could also stimulate the occurrence and development of DMI. Case presentation: A 23-year-old woman with type 1 diabetes presented with a 10-day history of nausea, vomiting, pain, and swelling of her left leg. Her urine ketone test was positive. The 3-beta-hydroxybutyrate and leukocyte counts and creatine kinase levels were elevated. Magnetic resonance imaging of the left thigh revealed extensive deep tissue oedema and an increase in the T2 signal in the involved muscles. Once the diagnosis of DMI was made, she was managed with rest, celecoxib, clopidogrel and aggressive insulin therapy. Three months after treatment, the patient reported complete resolution of symptoms. Conclusion: DMI is a rare DM complication with a high recurrence rate, commonly presenting with chronic complications, while our case report shows that acute diabetes decompensation, such as DKA, can stimulate the occurrence and development of DMI. Timely diagnosis and appropriate treatment could shorten the recovery time.

Prevalence and severity of corona virus disease 2019 (COVID-19): A systematic review and meta-analysis.

BACKGROUND: Since being first reported in Wuhan, China, in December 8, 2019, the outbreak of the novel coronavirus, now known as COVID-19, has spread globally. Some case studies regarding the characteristics and outcome of patients with COVID-19 have been published recently. We conducted a meta-analysis to evaluate the risk factors of COVID-19. METHODS: Medline, SinoMed, EMBASE, and Cochrane Library were searched for clinical and epidemiological studies on confirmed cases of COVID-19. RESULTS: The incidence of fever, cough, fatigue, and dyspnea symptoms were 85.6 % (95CI 81.3-89.9 %), 65.7 % (95CI 60.1-71.4 %), 42.4 % (95CI 32.2-52.6 %) and 21.4 % (95CI 15.3-27.5 %). The prevalence of diabetes was 7.7 % (95CI 6.1-9.3 %), hypertension was 15.6 % (95CI 12.6-18.6 %), cardiovascular disease was 4.7 % (95CI 3.1-6.2 %), and malignancy was 1.2 % (95CI 0.5-1.8 %). The complications, including ARDS risk, ranged from 5.6-13.2 %, with the pooled estimate of ARDS risk at 9.4 %, ACI at 5.8 % (95CI 0.7-10.8 %), AKI at 2.1 % (95CI 0.6-3.7 %), and shock at 4.7 % (95CI 0.9-8.6 %). The risks of severity and mortality ranged from 12.6 to 23.5% and from 2.0 to 4.4 %, with pooled estimates at 18.0 and 3.2 %, respectively. The percentage of critical cases in diabetes and hypertension was 44.5 % (95CI 27.0-61.9 %) and 41.7 % (95CI 26.4-56.9 %), respectively. CONCLUSION: Fever is the most common symptom in patients with COVID-19. The most prevalent comorbidities are hypertension and diabetes which are associated with the severity of COVID-19. ARDS and ACI may be the main obstacles for patients to treatment recovery. The case severe rate and mortality is lower than that of SARS and MERS.

Impact of weight cycling on CTRP3 expression, adipose tissue inflammation and insulin sensitivity in C57BL/6J mice.

Impacts of weight cycling on C1q/tumor necrosis factor (TNF)-related protein-3 (CTRP3) expression, adipose tissue inflammation and insulin sensitivity in C57BL/6J mice were evaluated in the current study. A total of 30 male C57Bl/6J mice were divided randomly into three groups; normal control (n=10), high-fat diet (OB, n=10) and weight cycling (WC, n=10), which were fed with high-fat diet in the first and last 8 weeks and regular chow in between. Systemic glucose metabolic status and insulin sensitivity were detected by intraperitoneal glucose tolerance test and hyperinsulinemic-euglycemic clamp, respectively. Blood levels of interleukin (IL)-6 and TNF-α were determined using ELISA. Relative CTRP3, IL-6, TNF-α and glucose transporter (GLUT)4 mRNA expression in adipose tissue was detected using reverse transcription-quantitative polymerase chain reaction assays. Relative CTRP3, phosphatidylinositide 3-kinases (PI3K) and protein kinase B (PKB; Ser473) protein expression were detected by western blot analysis. Area under the curve of glucose and glucose infusion rate of the WC group were significantly increased compared with the OB group (P<0.01). CTRP3 mRNA and protein levels of the WC group were significantly decreased by 20.3 and 23.1%, respectively, compared with the OB group (P<0.01). IL-6 and TNF-α protein plasma levels and gene expression in adipose tissue of the WC group were significantly increased compared with the OB group (P<0.01). Expression and phosphorylation of insulin signaling molecules PI3K and PKB (Ser473), respectively and GLUT4 gene expression in adipose tissue of the WC group were significantly decreased compared with the OB group (P<0.01). In conclusion, weight cycling impaired glucose metabolism and insulin sensitivity by decreasing CTRP3, PI3K, phosphorylated-PKB (Ser473) and GLUT4 expression, and increasing IL-6 and TNF-α levels.

Inhibition of Miro1 disturbs mitophagy and pancreatic ß-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes.

Mitochondrial function is essential to meet metabolic demand of pancreatic beta cells respond to high nutrient stress. Mitophagy is an essential component to normal pancreatic ß-cell function and has been associated with ß-cell failure in Type 2 diabetes (T2D). Our previous studies have indicated that mitochondrial Rho (Miro) GTPase-mediated mitochondrial dysfunction under high nutrient stress leads to NOD-like receptor 3 (NLRP3)-dependent proinflammatory responses and subsequent insulin resistance. However, the in vivo mechanism by which Miro1 underlies mitophagy has not been identified. Here we show firstly that the expression of Miro is reduced in human T2D and mouse db/db islets and in INS-1 cell line exposed to high glucose and palmitate. ß-cell specific ablation of Miro1 (Miro1f/f: Rip-cre mice, or (IKO) under high nutrient stress promotes the development of hyperglycemia. ß-cells from IKO mice display an inhibition of mitophagy under oxidative stress and induces mitochondrial dysfunction. Dysfunctional mitophagy in IKO mice is represented by damaged islet beta cell mitochondrial and secretory capacity, unbalanced downstream MKK-JNK signalling without affecting the levels of MEK, ERK or p38 activation and subsequently, impaired insulin secretion signaling via inhibition IRS-AKT-Foxo1 pathway, leading to worsening glucose tolerance in these mice. Thus, these data suggest that Miro1 may be responsible for mitophagy deficiency and ß-cell dysfunction in T2D and that strategies target Miro1 in vivo may provide a therapeutic target to enhance ß-cell mitochondrial quality and insulin secretion to ameliorate complications associated with T2D.

Triglyceride to high-density lipoprotein cholesterol ratio and carotid intima-medial thickness in Chinese adolescents with newly diagnosed type 2 diabetes mellitus.

OBJECTIVE: To investigate the relationship between triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio and carotid intima-medial thickness (CIMT) in Chinese youth and adolescents with newly diagnosed type 2 diabetes mellitus (T2DM). METHODS: Ninety-eight subjects aged 10-24 yr with newly-diagnosed T2DM had general inflammation, anthropometric, laboratory and CIMT data collected, and were divided into three groups based on TG/HDL-C tertiles. RESULTS: There were no significant differences in gender, age, fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and carotid arterial diameter (CAD) among the groups based on TG/HDL-C tertiles. Across TG/HDL-C tertiles, there was a significant progressive increase in body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), homeostasis model assessment-estimated insulin resistance (HOMA-IR), TG, total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C) and CIMT (all P < 0.01 or P < 0.05), while HDL-C was decreased significantly across the groups (P < 0.01). In general linear regression model, TG/HDL-C was an independent determinant of CIMT even after adjusting for BMI, SBP, DBP, TG, TC, LDL-C, HDL-C, HbA1c and HOMA-IR. CONCLUSION: TG/HDL-C ratio, the marker of small dense LDL particles, is an independent determinant of CIMT in Chinese youth and adolescents with newly diagnosed T2DM, and may be a simple and helpful tool in predicting the increased CIMT in such patients.

Combined effects of FTO rs9939609 and MC4R rs17782313 on elevated nocturnal blood pressure in the Chinese Han population.

AIM: In this study we investigated the association of FTO rs9939609 and MC4R rs17782313 with elevated blood pressure in the Chinese Han population, and analysed the relationship between the rs9939609 and rs17782313 variants. METHODS: We tested the rs9939609 and rs17782313 variants with the sequence-retrieval method. RESULTS: The increase in odds ratios of the A allele of rs9939609 and the C allele of rs17782313 for nocturnal blood pressure were 1.37 and 1.69. The nocturnal blood pressure of participants simultaneously carrying the A and C alleles was significantly higher than the blood pressure of those carrying neither FTO nor MC4R risk alleles (p < 0.05), and that of the controls carrying only the A or C alleles (p < 0.05). No association between the FTO or MC4R genes with daytime hypertension was found in this Chinese population (p > 0.05). CONCLUSION: Our data suggest that the rs9939609 and rs17782313 variants may be significantly associated with nocturnal but not daytime blood pressure levels and their combined effects were significant in this Chinese Han population.

Low-Grade Inflammation and Increased Arterial Stiffness in Chinese Youth and Adolescents with Newly-Diagnosed Type 2 Diabetes Mellitus.

OBJECTIVE: To investigate the relationship between low-grade inflammation (LI) and increased arterial stiffness in Chinese youth and adolescents with newly-diagnosed type 2 diabetes mellitus (T2DM). METHODS: Ninety-eight subjects aged 10 to 24 years with newly-diagnosed T2DM were investigated for findings of general inflammation. Anthropometric measurements were taken. Data related to arterial stiffness [brachial artery distensibility (Branch D), augmentation index (AIx), carotid-femoral pulse wave velocity (CF-PWV)] were collected. The subjects were divided into a non-LI group (NLI, n=42) and a LI group (n=56) according to their high-sensitivity C-reactive protein (Hs-CRP) levels. RESULTS: There were no significant differences in age and gender between the LI group and the NLI group. CF-PWV and AIx values of the LI group were higher than those of the NLI group (p<0.01), while Branch D values were lower in the LI group (p<0.01). Branch D, CF-PWV, and AIx values correlated significantly with Hs-CRP overall (r=-0.32, 0.34, 0.33, all p<0.01). Multivariate models revealed that in either group (LI or NLI), Hs-CRP, as a continuous variable, was an independent determinant of arterial stiffness parameters even after adjusting for other risk factors. CONCLUSION: Newly-diagnosed T2DM youth and adolescents with LI present a more adverse cardiovascular disease risk profile and stiffer arteries. Hs-CRP levels correlated with arterial stiffness parameters and constituted an independent determinant of arterial stiffness.

Expression of CTRP3, a novel adipokine, in rats at different pathogenic stages of type 2 diabetes mellitus and the impacts of GLP-1 receptor agonist on it.

This study aimed to investigate the expression of C1q/TNF-related protein-3 (CTRP3) in rats at different pathogenic stages of type 2 diabetes mellitus (T2DM) and the impacts of glucagon-like peptide-1 (GLP-1) receptor agonist on it. Male wistar rats were fed with high-fat diet for 10 weeks to induce insulin resistance (IR) and then were given low-dose streptozotocin (STZ) intraperitoneal injection to induce T2DM. Exendin-4 (Ex-4), a GLP-1 receptor agonist, was subcutaneous injected to the IR rats and T2DM rats for 4 weeks. The expression of CTRP3 mRNA and protein in epididymis adipose tissue of rats at the stage of IR was lower significantly than that of normal control (NC) rats and decreased more when they were at the stage of overt T2DM (all P < 0.05 or P < 0.01). After the treatment with Ex-4, the mRNA and protein expressions of CTRP3 were increased by 15.5% (P < 0.01) and 14.8% (P < 0.05), respectively, in IR rats and increased by 20.6% (P < 0.01) and 16.5% (P < 0.05), respectively, in T2DM rats. Overall, this study found that the expression of CTRP3 in visceral adipose tissue was progressively decreased in a T2DM rat model from the pathogenic stage of IR to overt diabetes, while Ex-4 treatment increased its expression in such animals.

CTRP3 improves the insulin sensitivity of 3T3-L1 adipocytes by inhibiting inflammation and ameliorating insulin signalling transduction.

INTRODUCTION: C1q/TNF-related Protein-3 (CTRP3) is a novel adipokine with multiple effects such as lowering glucose levels, inhibiting glyconeogenesis in the liver, and increasing angiogenesis and anti-inflammation. But little is known about the effects of CTRP3 on insulin resistance in adipose tissue. This study aims to investigate the effects and mechanisms of CTRP3 on the insulin sensitivity of 3T3-L1 adipocytes. MATERIAL AND METHODS: Insulin resistant 3T3-L1 adipocytes were induced by palmic acid cultivation. Such adipocytes were treated with recombinant CTRP3 protein at different concentrations (0, 10, 50, 1,250 ng/mL) for 12 hours, and at a concentration of 250 ng/mL for differing times (2, 6, 12, and 24 h). Another group was pre-treated with wortmannin, the special inhibitor of phosphatidylinositol-4,5- bisphosphate 3-kinase (PI3K), for 20 minutes before the treatment with 250 ng/mL CTRP3. The glucose consumption, the glucose uptake, the expression and release of tumour necrosis factor α (TNF-α) and interleukin-6(IL-6) in supernatant, and the protein relative expression of PI3K and protein kinase B (PKB)(ser437) were detected. RESULTS: Compared to the control group, glucose consumption in the CTRP3 intervention group at concentrations of 10, 50, 250, and 1,250 ng/mL was increased by 22.1%, 42.9%, 76.6% and 80.5% respectively (all P < 0.01); the glucose uptake was increased by 39.0%, 68.0%, 108.0% and 111.0% respectively (all P < 0.01); the content of TNF-α in the culture media of CTRP3 (10, 50, 250 ng/mL) intervention group was decreased by 7.6% (P > 0.05), 13.0% (P < 0.05) and 17.4% (P < 0.01) respectively; the content of IL-6 was decreased by 7.1%, 12.4% and 17.1% respectively (all P < 0.01); the protein relative expression of PI3K was increased by 0.63-, 1.00- and 1.36-fold respectively (all P < 0.01), and PKB(ser437) increased by 0.65-, 1.61- and 1.93-fold respectively (all P < 0.01); the mRNA relative expression of GLUT-4 was increased by 23.0%, 47.0% and 62.0% respectively (all P < 0.01). After the treatment with wortmannin, glucose consumption, glucose uptake, PI3K and PKB(ser437) protein relative expression, as well as GLUT-4 mRNA relative expression, was decreased by 53.2%, 44.7%, 43.4%, 56.1 and 30.9% respectively (all P < 0.01). CONCLUSIONS: CTRP3 could improve insulin sensitivity of insulin resistant 3T3-L1 adipocytes by decreasing inflammation and ameliorating insulin signalling transduction, indicating that CTRP3 may be a new target for the prevention and cure of insulin resistance and type 2 diabetes.

CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes.

The objective of this study was to investigate the impact of C1q/TNF related protein 3 (CTRP3), a novel adipokine, on the expression and secretion of adiponectin, leptin, visfatin, and apelin in 3T3-L1 adipocytes. The effect of insulin resistance on the impact was also investigated. 3T3-L1 adipocytes were treated with different concentrations (0, 10, 50, 250, 1250 ng/mL) CTRP3 for 12 h, and with 250 ng/mL CTRP3 for different times (0, 6, 12, 24, 48 h). The expression of adipokines between normal and insulin resistant adipocytes, as well as between the adipocytes pre-treated with and without Compound C were compared. The secretion and gene expression of the adipokines were detected by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR), respectively. The relative expression of AMPK (thr172) was detected by western blot analysis. With the increase in CTRP3 concentration or the duration of the treatment, the secretion of adiponectin, leptin, visfatin and apelin were all increased accordingly, which was significant under the treatment with 250 ng/mL and 1250 ng/mL CTRP3 for 12 h as well as 250 ng/mL CTRP3 for 12 h, 24 h and 48 h. Gene expression showed a similar trend. The secretion and gene expression of adipokines in insulin resistant adipocytes were all decreased significantly in comparison with that of normal adipocytes. The secretion secretion and gene expression of adiponectin, and the relative expression of AMPK (thr172) in adipocytes pre-treated with Compound C were decreased significantly in comparison with that in adipocytes without Compound C pretreatment. Thus, CTRP3 increased the expression and secretion of adiponectin, leptin, visfatin, and apelin in 3T3-L1 adipocytes, while insulin resistance inhibited the effects. CTRP3 up-regulated the expression of adiponectin in 3T3-L1 adipocytes through AMPK signaling pathway.

WITHDRAWN: RIP140 mediates hyperglycemia-induced glucotoxicity in ß-cells via the activation of JNK and ERK1/2 signaling pathways.

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[Association between leptin gene promoter methylation and type 2 diabetes mellitus].

OBJECTIVE: To assess the association between leptin gene promoter methylation and serum leptin concentrations in patients with impaired glucose regulation (IGR) and type 2 diabetes mellitus (T2DM). METHODS: Methylation status of leptin gene promoter was determined with methylation-specific polymerase chain reaction. Serum leptin concentrations were determined using enzyme-linked immunosorbent assay. RESULTS: Among three groups of individuals with different levels of glucose, the methylation rates of leptin gene in IGR and T2DM groups were 43.6 % and 31.5 %, respectively, which were significantly lower than that of healthy subjects (59.2%; Chi-square=22.499 and 5.109, respectively, P<0.05). A lower methylation rate was also observed in T2DM group compared with IGR group (Chi-square=3.962, P<0.05). Leptin levels in both T2DM and IGR groups were elevated compared with normoglycemic subjects, but only T2DM group was significantly higher (q=6.81, P<0.01). Linear regression analysis indicated that serum leptin concentrations has increased along with declining of DNA methylation rate (r=-0.95, P<0.01). CONCLUSION: Lower levels of leptin gene promoter DNA methylation and serum leptin concentrations are associated with the development of diabetes. Measurement of the methylation status of leptin gene promoter and expression can facilitate early intervention of the disease.

Influence of hybridization and cooperativity on the properties of Au-bonding interaction: comparison with hydrogen bonds.

Quantum chemical calculations have been performed to study the hybridization effect in H(2)O-AuCH(2)CH(3), H(2)O-AuCHCH(2), and H(2)O-AuCCH dimers, and the cooperativity between the hydrogen bond and Au bonding in three trimers (T1, T2, and T3) composed of one AuCCH and two H(2)O molecules. With regard to the organic Au compounds, sp-hybridized AuCCH forms the strongest Au bonding, followed by sp(2) and then sp(3). The C-Au bond is elongated, and its elongation becomes larger with the increase of the s character in hybrid orbitals, whereas the corresponding stretch vibration displays a small blue shift. The positive cooperativity is present for the hydrogen bond and Au bonding in T1 and T2 trimers, whereas the negative cooperativity is found in T3 trimer. The results show that the hybridization effect and cooperative interaction in Au bonding are similar to those in hydrogen bonds. Additionally, an OH···Au hydrogen bond is suggested in T1 trimer.

Combined effects of FTO rs9939609 and MC4R rs17782313 on obesity and BMI in Chinese Han populations.

Genetic variants of FTO and MC4R have been linked with obesity and T2DM in populations of Europeans. In this study, we have investigated the association of FTO rs9939609 and MC4R rs17782313 with obesity and T2DM in the Chinese population and analyzed the relationship between rs9939609 and rs17782313. 2351 individuals were recruited. We tested the rs9939609 and rs17782313 by sequences retrieval method. Clinical and biochemical characteristics were measured. The rs9939609 per-A allele and rs17782313 per-C allele increases of OR for obesity was 1.42 (95% CI 1.39-3.74) and 1.39 (95% CI 1.21-3.53).The genotypic OR for obesity was 1.92 (95% CI 1.81-4.67) for AA genotype, 1.71 (95% CI 1.47-4.54) for AT genotype, 1.87 (95% CI 1.72-4.00) for CC genotype, and 1.44 (95% CI 1.20-3.18) for CT genotype. BMI of participants carrying neither FTO nor MC4R risk allele was 25.9 ± 4.9, one risk allele was 26.4 ± 5.1, two risk alleles was 28.1 ± 5.5, and there or four risk alleles was 33.2 ± 6.3. We found no association between FTO and MC4R and the Chinese population with T2DM (P > 0.05). Our data support that the rs9939609 and rs17782313 are strongly associated with obesity and BMI. Their combined effects were significant in Chinese population. No association between FTO and MC4R and Chinese population with T2DM was found.

Some measures for making halogen bonds stronger than hydrogen bonds in H2CS-HOX (X = F, Cl, and Br) complexes.

The properties and applications of halogen bonds are dependent greatly on their strength. In this paper, we suggested some measures for enhancing the strength of the halogen bond relative to the hydrogen bond in the H(2)CS-HOX (X = F, Cl, and Br) system by means of quantum chemical calculations. It has been shown that with comparison to H(2)CO, the S electron donor in H(2)CS results in a smaller difference in strength for the Cl halogen bond and the corresponding hydrogen bond, and the Br halogen bond is even stronger than the hydrogen bond. The Li atom in LiHCS and methyl group in MeHCS cause an increase in the strength of halogen bonding and hydrogen bonding, but the former makes the halogen bond stronger and the latter makes the hydrogen bond stronger. In solvents, the halogen bond in the Br system is strong enough to compete with the hydrogen bond. The interaction nature and properties in these complexes have been analyzed with the natural bond orbital theory.

Variants in the fat mass and obesity associated (FTO) gene are associated with obesity and C-reactive protein levels in Chinese Han populations.

PURPOSE: Various genetic variants of the fat mass and obesity associated gene (FTO) have been linked to obesity in populations of Europeans. Low-grade inflammation is a key feature of obesity, characterized by elevated plasma levels of C-reactive protein (CRP). In the present study, we have investigated whether the FTO-risk variant is associated with obesity and CRP in the Chinese population. METHODS: 1799 individuals aged 50-70 years (896 men and 903 women), including both obese (560 cases) and control individuals, (1200 cases) were recruited. The FTO rs9939609 polymorphism was tested using sequences retrieval. Waist circumference, body fat, hs-CRP, blood total cholesterol, triglycerides and LDL-C were also measured. RESULTS: The FTO rs9939609 polymorphism per-A allele was associated with an increased odds ratio for obesity of 1.42 (95%CI 1.23-1.64). The genotypic odds ratio for obesity was 1.92 (95%CI 1.43-2.57) for the AA genotype, 1.71 (95%CI 1.35-2.16) for the AT genotype. The association between FTO rs9939609 polymorphism and CRP levels was r=0.78. CONCLUSION: Our data support the hypothesis that FTO rs9939609 polymorphism is strongly associated with obesity and CRP levels in the Chinese population as reported in the European population.

Surprising enhancing effect of methyl group on the strength of O⋯XF and S⋯XF (X=Cl and Br) halogen bonds.

The role of methyl group in H(2)O⋯XF and H(2)S⋯XF (X=Cl and Br) halogen-bonded complexes has been investigated with quantum chemical calculations. The halogen bond in the H(2)O⋯XF complexes is stronger than that in the H(2)S⋯XF complexes. However, the S⋯X halogen bond is stronger than the O⋯X one with the increase of methyl number. The result shows that the methyl group in the halogen acceptor has a positive contribution to the formation of halogen bond and there is a positive nonadditivity of methyl groups. Surprisingly, the methyl groups in dimethyl sulfide causes an increase of 150% for the interaction energy of S⋯Cl halogen bond. The natural bond orbital analyses have been performed to unveil the mechanism of the methyl group in the halogen bonding formation.

Prominent effect of alkali metals in halogen-bonded complex of MCCBr−NCM' (M and M' = H, Li, Na, F, NH2, and CH3).

Quantum chemical calculations have been performed for the MCCBr−NCM' (M and M' = H, Li, Na, F, NH2, and CH3) halogen-bonded complexes at the MP2/aug-cc-pVTZ level. The binding energy is in a range of 1.34−23.42 kJ/mol. The results show that the alkali metal has a prominent effect on the strength of halogen bond, and this effect is different for the alkali metal in the halogen and electron donors. The alkali atom in the halogen donor makes it weaken greatly, whereas that in the electron donor causes it to enhance greatly. Natural bond orbital analysis shows that the alkali atom is electron-withdrawing in the halogen donor and electron-donating in the electron donor. In formation of the halogen bond, the former is a negative contribution, whereas the latter is a positive one. A similar charge transfer is also found for the H atom in the halogen and electron donors. These complexes have also been analyzed with the atoms in molecules theory.