Two-dimensional material assisted-growth strategy: new insights and opportunities.

The exploration and synthesis of novel materials are integral to scientific and technological progress. Since the prediction and synthesis of two-dimensional (2D) materials, it is expected to play an important role in the application of industrialization and the information age, resulting from its excellent physical and chemical properties. Currently, researchers have effectively utilized a range of material synthesis techniques, including mechanical exfoliation, redox reactions, chemical vapor deposition, and chemical vapor transport, to fabricate two-dimensional materials. However, despite their rapid development, the widespread industrial application of 2D materials faces challenges due to demanding synthesis requirements and high costs. To address these challenges, assisted growth techniques such as salt-assisted, gas-assisted, organic-assisted, and template-assisted growth have emerged as promising approaches. Herein, this study gives a summary of important developments in recent years in the assisted growth synthesis of 2D materials. Additionally, it highlights the current difficulties and possible benefits of the assisted-growth approach for 2D materials. It also highlights novel avenues of development and presents opportunities for new lines of investigation.

Ultra-High-Efficiency Corrosion Protection of Metallic Surface Based on Thin and Dense Hexagonal Boron Nitride Coating Films.

Quest for ultrathin and highly effective anticorrosion coating films is critical for both fundamental community of materials science and industrial economics. A two-dimensional hexagonal boron nitride (h-BN) film is a newly developed effective anticorrosion material due to its superior impermeability, thermal stability, and chemical stability. However, research in growth and anticorrosion properties of large-area dense h-BN coating films still lies in its infancy. Here, we report on the synthesis of a large-area and continuous dense few-layer (∼4) h-BN coating film onto a metal surface by chemical vapor deposition (CVD) and its anticorrosion properties both in air and seawater environments. Cu coated in h-BN, which functions as an anticorrosive coating, exhibits an impressively reduced corrosion rate (CR) in a 3.5% NaCl solution (which mimics a seawater environment) when compared to bare Cu (approximately 27 times). At 200 °C, the h-BN coating can prevent Cu foil's surface from oxidizing, although doing so will cause a significant amount of oxide particles to simultaneously form on the bare Cu surface. In the meantime, the performance of the h-BN film remains unaltered after 100 days in an atmospheric environment, demonstrating the ultrahigh stability and corrosion resistance of the as-grown h-BN film.

Deciphering transcriptional dynamics of cardiac hypertrophy and failure in a chamber-specific manner.

Pressure overload-induced pathological cardiac hypertrophy (CH) is a complexed and adaptive remodeling of the heart, predominantly involving an increase in cardiomyocyte size and thickening of ventricular walls. Over time, these changes can lead to heart failure (HF). However, the individual and shared biological mechanisms of both processes remain poorly understood. This study aimed to identify key genes and signaling pathways associated with CH and HF following aortic arch constriction (TAC) at four weeks and six weeks, respectively, and to investigate potential underlying molecular mechanisms in this dynamic transition from CH to HF at the whole cardiac transcriptome level. Initially, a total of 363, 482, and 264 differentially expressed genes (DEGs) for CH, and 317, 305, and 416 DEGs for HF were identified in the left atrium (LA), left ventricle (LV), and right ventricle (RV), respectively. These identified DEGs could serve as biomarkers for the two conditions in different heart chambers. Additionaly, two communal DEGs, elastin (ELN) and hemoglobin beta chain-beta S variant (HBB-BS), were found in all chambers, with 35 communal DEGs in the LA and LV and 15 communal DEGs in the LV and RV in both CH and HF. Functional enrichment analysis of these genes emphasized the crucial roles of the extracellular matrix and sarcolemma in CH and HF. Lastly, three groups of hub genes, including the lysyl oxidase (LOX) family, fibroblast growth factors (FGF) family, and NADH-ubiquinone oxidoreductase (NDUF) family, were determined to be essential genes of dynamic changes from CH to HF.

Enhancing the Strengthening Effect of Graphene-Nanoplates in Al Matrix Composites by Heterogeneous Matrix Design.

In the present work, the properties of graphene-nanoplates/aluminum (GNPs/Al) composites with a heterogeneous matrix design were investigated. The advantage of the heterogeneous matrix was investigated by the finite element method. Then, 0.6 wt.% (GNPs/6061Al)/2024Al (heterogeneous matrix) and 0.6 wt.% GNPs/6061Al composites were prepared by ball milling, pressure infiltration technology, and hot extrusion. The aggregation of GNPs was eliminated and the interlayer slide of GNPs was observed. Mechanical property test results show that the mechanical properties of the heterogeneous matrix composite are better than that of a homogeneous matrix composite, including strength, elastic modulus, and plasticity. It is assumed that the heterogeneous matrix design enhances the non-uniform stress field during the deformation treatment. This improves the dispersion of GNPs, grain refinement, and produces the few-layer graphene (FLG), thus enhancing the strengthening effect of GNPs. Meanwhile, heterogeneous matrix design is thought to introduce more hardening mechanisms to increase the plasticity of materials and improve the intrinsic trade-off of strength and toughness.

Engineering the Optoelectronic Properties of 2D Hexagonal Boron Nitride Monolayer Films by Sulfur Substitutional Doping.

Tuning the optical and electrical properties of two-dimensional (2D) hexagonal boron nitride (hBN) is critical for its successful application in optoelectronics. Herein, we report a new methodology to significantly enhance the optoelectronic properties of hBN monolayers by substitutionally doping with sulfur (S) on a molten Au substrate using chemical vapor deposition. The S atoms are more geometrically and energetically favorable to be doped in the N sites than in the B sites of hBN, and the S 3p orbitals hybridize with the B 2p orbitals, forming a new conduction band edge that narrows its band gap. The band edge positions change with the doping concentration of S atoms. The conductivity increases up to 1.5 times and enhances the optoelectronic properties, compared to pristine hBN. A photodetector made of a 2D S-doped hBN film shows an extended wavelength response from 260 to 280 nm and a 50 times increase in its photocurrent and responsivity with light illumination at 280 nm. These enhancements are mainly due to the improved light absorption and increased electrical conductivity through doping with sulfur. This S-doped hBN monolayer film can be used in the next-generation electronics, optoelectronics, and spintronics.

High-responsivity photodetector based on scrolling monolayer MoS2hybridized with carbon quantum dots.

The monolayer MoS2based photodetectors have been widely investigated, which show limited photoelectric performances due to its low light absorption and uncontrollable adsorbates. In this paper, we present a MoS2-based hybrid nanoscrolls device, in which one-dimensional nanoscrollsof MoS2is hybridized with carbon quantum dots (CQDs). This device architecture effectively enhanced the photodetection performance. The photoresponsivity and detectivity values of MoS2/CQDs-NS photodetectors are respectively 1793 A W-1and 5.97 × 1012Jones, which are 830-fold and 268-fold higher than those of pristine MoS2under 300 nm illumination atVds = 5 V. This research indicates a significant progress in fabricating high-performance MoS2photodetectors.

Properties of Concrete Prepared with Silane Coupling Agent-Impregnated Coral Aggregate and Coral Concrete.

Silane coupling agent (SCA), a kind of organic solvent, was introduced to improve the performance of coral coarse aggregates and enhance the interfacial adhesion between the inorganic coral aggregate and the cement paste of coral concrete. The crushing indicator and water absorption of the coral aggregates over various dipping times were measured, and the slump, interface microhardness, and compressive strength of coral concrete tested. The microscopic appearances of the coral concrete before and after modification were analyzed based on SEM images. The experimental results indicate that SCA can effectively reduce the crushing indicator and water absorption of coral coarse aggregates, and the modification performance becomes better over time. SCA facilitates the generation of chemical forces between the coral aggregates and cement mortars, improves adhesion between the aggregates and mortars, augments the microhardness of the interface, and increases the compressive strength. According to the microscopic appearance of the treated and untreated coral aggregate interfaces, the aggregates and the mortars are in closer combination after modification.

Evaluation of the Effects of Surface Treatment Methods on the Properties of Coral Aggregate and Concrete.

Coral concrete has low cost and convenient materials, making it an excellent raw material for processing. However, its lower strength limits the application of coral concrete. Surface modification is expected to increase the properties of porous coral concrete. In this study, single and compound modification treatments were applied to the surface of a coral aggregate to improve its properties for promoting the mechanical performance of coral concrete. The results showed that the micro-aggregate effect and pozzolanic activity of granulated blast furnace slag (GBFS) and the permeability and polycondensation of sodium silicate (SS) could be mutually promoted. The GBFS and SS could effectively fill the pores of the coral aggregate, enhancing the properties of the aggregate, such as density and load-bearing capacity, and reducing the water absorption and crushing index by more than 50%. GBFS and SS could intensify and accelerate the hydration of cement, and generate a large number of hard hydration products at the interfacial transition zone (ITZ), which could strengthen the bonding between the aggregate and mortar, improving the strength of the ITZ. The compressive strength of the coral concrete was significantly increased.

Design and Evaluation of an Ultrahigh-Strength Coral Aggregate Concrete for Maritime and Reef Engineering.

In this paper, an ultrahigh-strength marine concrete containing coral aggregates is developed. Concrete fabricated from marine sources is considered an effective and economical alternative for marine engineering and the construction of remote islands. To protect sea coral ecosystems, the coral aggregates used for construction are only efflorescent coral debris. To achieve the expected mechanical performance from the studied concrete, an optimal mixture design is conducted to determine the optimal proportions of components, in order to optimize the compressive strength. The mechanical properties and the autogenous shrinkage, as well as the heat flow of early hydration reactions, are measured. The hydration products fill up the pores of coral aggregates, endowing our concrete with flowability and self-compacting ability. The phases in the marine concrete are identified via X-ray diffraction analysis. The 28-day compressive and flexural strength of the developed marine concrete achieve 116.76 MPa and 18.24 MPa, respectively. On account of the lower cement content and the internal curing provided by coral aggregates, the volume change resulting from autogenous shrinkage is only 63.11% of that of ordinary reactive powder concrete.

[Down-regulation of IL-25 accompanied by a decrease in the number of M2 macrophages in patients of non-alcoholic fatty liver disease with significant liver fibrosis].

Objective To observe and analyze the relationships among the level of interleukin 25 (IL-25), the stage of liver fibrosis and the polarization of hepatic M2 macrophages in patients with non-alcoholic fatty liver disease (NAFLD). Methods A total of 36 patients with NAFLD and 20 control patients were enrolled. Fibrotouch, HE staining, and immunohistochemistry were used to evaluate the stage of liver fibrosis. Patients with NAFLD were classified into groups of mild liver fibrosis (F1) (20 cases) and significant liver fibrosis (≥ F2) (16 cases). The level of serum IL-25 in each group was detected by ELISA. Real-time fluorescent quantitative PCR was used to detect the hepatic mRNA expression levels of IL-25, collagen1 (Col1), α mooth muscle actin (α-SMA), macrophage mannose receptor 1 (CD206/MR1) and transglutaminase 2 (TGM2). Immunohistochemistry was used to detect the protein levels of IL-25, α-SMA, CD206 and TGM2. Results There was no significant difference in the level of serum IL-25 among groups. Compared with patients in the control group and the mild liver fibrosis group, patients with significant liver fibrosis showed reduced mRNA expression levels of IL-25, CD206, and TGM2 in addition to lower levels of hepatic IL-25 protein and less polarization of M2 macrophages. Conclusion Down-regulation of IL-25 is accompanied by a decrease in the number of the M2 macrophages with the progression of liver fibrosis in NAFLD patients.

Analysis of clinical and pathological features of primary bilateral macronodular adrenocortical hyperplasia compared with unilateral cortisol-secreting adrenal adenoma.

BACKGROUND: Primary bilateral macronodular adrenocortical hyperplasia (PBMAH) is a rare condition with untypical subclinical symptoms of Cushing's syndrome (CS). This study aimed to compare the clinical and pathological features of PBMAH with unilateral cortisol-secreting adrenal adenoma (UAA). METHODS: We prospectively included 46 PBMAH patients and 205 UAA patients from January 2000 to February 2014. Cortisol levels and 24 hours urine free cortisol (UFC) were determined at baseline and during dexamethasone suppression test (DST) using the chemiluminescence method. Computed tomography (CT) examination of the adrenal glands was performed in all patients. For patients treated with adrenalectomy, hematoxylin, and eosin, staining was performed for pathological examination. RESULTS: The proportion of patients with autonomous cortisol secretion was significantly higher in PBMAH patients (39.1%) than UAA patients (6.8%). The PBMAH patients showed significantly lower levels of basal cortisol, low dose dexamethasone suppressed cortisol, and high dose dexamethasone suppressed cortisol than the UAA patients (452.6±183.3 vs. 578.7±166.4 nmol/L, P=0.003; 394.5±298.9 vs. 549.2±217.7 nmol/L, P=0.002; 397.3±282.3 vs. 544.3±187.6 nmol/L, P=0.003). Similarly, the PBMAH patients had significantly lower levels of basal 24 hours UFC, low dose dexamethasone suppressed 24 hours UFC, and high dose dexamethasone suppressed 24 hours UFC than the UAA patients (1,144.4±1,048.1 vs. 1,674.9±1,520.4 nmol/24 h, P=0.032; 1,157.3±1,483.5 vs. 1,940.1±1,360.9 nmol/24 h, P=0.003; 1,256.4±1,767.0 vs. 1,969.9±1,361.7 nmol/24 h, P=0.011). CONCLUSIONS: PBMAH is often associated with atypical CS symptoms. The clinical and imaging features of PBMAH are useful for the differential diagnosis of this disease.

Enrichment differentiation of human induced pluripotent stem cells into sinoatrial node-like cells by combined modulation of BMP, FGF, and RA signaling pathways.

BACKGROUND: Biological pacemakers derived from pluripotent stem cell (PSC) have been considered as a potential therapeutic surrogate for sick sinus syndrome. So it is essential to develop highly efficient strategies for enrichment of sinoatrial node-like cells (SANLCs) as seed cells for biological pacemakers. It has been reported that BMP, FGF, and RA signaling pathways are involved in specification of different cardiomyocyte subtypes, pacemaker, ventricular, and atrial cells. We aimed to investigate whether combined modulation of BMP, FGF, and RA signaling pathways could enrich the differentiation of SANLC from human pluripotent stem cell (hiPSC). METHODS: During the differentiation process from human induced pluripotent stem cell to cardiomyocyte through small molecule-based temporal modulation of the Wnt signaling pathway, signaling of BMP, FGF, and RA was manipulated at cardiac mesoderm stage. qRT-PCR, immunofluorescence, flow cytometry, and whole cell patch clamp were used to identify the SANLC. RESULTS: qRT-PCR results showed that manipulating each one of bone morphogenetic protein (BMP), fibroblast growth factor (FGF), and retinoid acid (RA) signaling was effective for the upregulation of SANLC markers. Moreover, combined modulation of these three pathways displayed the best efficiency for the expression of SANLC markers, which was further confirmed at protein level using immunofluorescence and flow cytometry. Finally, the electrophysiological characteristics of upregulated SANLC were verified by patch clamp method. CONCLUSION: An efficient transgene-independent differentiation protocol for generating SANLC from hiPSC was developed, in which combined modulating BMP, FGF, and RA signaling at cardiac mesoderm stage generates SANLC at high efficiency. This may serve as a potential approach for biological pacemaker construction.

Atorvastatin attenuates TGF­ß1­induced fibrogenesis by inhibiting Smad3 and MAPK signaling in human ventricular fibroblasts.

Excessive proliferation and myofibroblasts transformation of cardiac fibroblasts play a critical role in the process of cardiac fibrosis. Atorvastatin (ATV), a 3­hydroxy­3­methyl­glutaryl­coenzyme A reductase inhibitor, is commonly used to treat hypercholesterolemia. It has previously been shown that ATV has potential anti­fibrotic effects. However, the underlying mechanisms of ATV against cardiac fibrosis remain to be fully elucidated, and to the best of our knowledge, there are no reports focusing on the effects of ATV on transforming growth factor­ß1 (TGF­ß1)­induced human ventricular fibroblasts (hVFs) activation. In the present study, hVFs were stimulated with TGF­ß1 with or without pretreatment with ATV. Subsequently, hVF proliferation, cytotoxicity, myofibroblast differentiation and pro­fibrotic gene expression were assessed. Canonical and non­canonical signaling downstream of TGF­ß1, such as Smad3 and mitogen­activated protein kinase (MAPK) signaling, were investigated by evaluating the phosphorylation levels of Smad3, extracellular signal­regulated kinase 1/2, p38 MAPK and c­Jun N­terminal kinase. The results indicated that ATV significantly prevented TGF­ß1­induced cell proliferation, myofibroblast differentiation and production of extracellular matrix proteins, such as matrix metalloproteinase­2, collagen I and collagen III, in hVFs. Furthermore, ATV effectively inhibited TGF­ß1­induced activation of Smad3 and MAPK signaling in hVFs. In conclusion, the present results demonstrated that ATV prevented TGF­ß1­induced fibrogenesis in hVFs, at least in part by inhibiting the Smad3 and MAPK signaling pathways. Therefore, these results imply that ATV may be a promising agent to treat myocardial fibrosis.

Fecal microbiota transplantation as an effective initial therapy for pancreatitis complicated with severe Clostridium difficile infection: A case report.

BACKGROUND: Moderately severe acute pancreatitis (MSAP) is a critical form of acute pancreatitis that is related with high morbidity and mortality. Severe Clostridium difficile infection (sCDI) is a serious and rare nosocomial diarrheal complication, especially in MSAP patients. Fecal microbiota transplantation (FMT) is a highly effective treatment for refractory and recurrent CDI (rCDI). However, knowledge regarding the initial use of FMT in patients suffering from sCDI is limited. CASE SUMMARY: Here, we report an MSAP patient complicated with sCDI who was treated by FMT as a first-line therapy. The patient was a 51-year-old man who suffered from diarrhea in his course of acute pancreatitis. An enzyme immunoassay was performed to detect toxins, and the result was positive for toxin-producing C. difficile and toxin B and negative for C. difficile ribotype 027. The colonoscopy revealed pseudomembranous colitis. Due to these findings, sCDI was our primary consideration. Because the patient provided informed consent for FMT treatment, we initially treated the patient by FMT rather than metronidazole. Diarrhea resolved within 5 d after FMT. The patient remained asymptomatic, and the follow-up colonoscopy performed 40 d after discharge showed a complete recovery. Our case is the first reported in China. CONCLUSION: This case explores the possibilities of initially using FMT to treat severe CDI. Moreover, FMT may become a critical component of the treatment for severe CDI in MSAP patients.

miR-499 released during myocardial infarction causes endothelial injury by targeting α7-nAchR.

The surged systemic vascular inflammation after acute myocardial infarction (AMI) aggravates the atherosclerotic endothelial injury. To explore roles of miR-499 released from cardiomyocytes during AMI in endothelial injury. Using qPCR and ELISA, we discovered that patients with AMI had significantly increased plasma miR-499, which was directly correlated with serum thrombomodulin, a marker for endothelial injury. Plasma of AMI patients, when incubated with human umbilical vein endothelial cells (HUVECs), significantly increased the expression of endothelial injury markers, which could be abrogated by antagomiR-499. In vitro, neonatal rat cardiomyocytes subjected to hypoxia/reoxygenation (HX/R) released miR-499 that could be internalized into rat pulmonary microvascular endothelial cells (RPMECs), worsening the high glucose-induced injury. In silico analysis demonstrated that CHRNA7 encoding α7-nAchR is a target of miR-499, which was validated in cell lines expressing endogenous α7-nAchR. In high glucose-induced RPMECs injury model, miR-499 aggravated, whereas forced CHRNA7 expression ameliorated the injury. Moreover, the perfusate from Langendorff perfused rat heart subjected to HX/R contained higher level of miR-499 that significantly impaired the Bradykinin-mediated endothelium-dependent relaxation in both conduit and resistance arteries, which could be partially abrogated by antagomiR-499. Finally, the correlation between plasma miR-499 and endothelial injury was further confirmed in another cohort of AMI patients. We conclude that miR-499 released from injured cardiomyocytes contributes to the endothelial injury by targeting α7-nAchR. This study implies that miR-499 may serve as a potential target for the treatment of the surged vascular inflammation post-AMI.

IL-25 protects against high-fat diet-induced hepatic steatosis in mice by inducing IL-25 and M2a macrophage production.

Interleukin (IL)-25 is a cytokine that has previously been shown to have a protective role against nonalcoholic fatty liver disease (NAFLD), which is associated with the induction of M2 macrophage differentiation. However, the direct relationships between IL-25 expression regulation, M2 induction and NAFLD remain unknown. In this study, we demonstrate that IL-25 promotes hepatic macrophage differentiation into M2a macrophages both in vivo and in vitro via the IL-13/STAT6 pathway. M2 macrophages that were differentiated in vitro were able to ameliorate high-fat diet HFD-induced hepatic steatosis. Furthermore, we found that IL-25 treatment, both in vitro and in vivo, promotes direct binding of STAT6 to the IL-25 gene promoter region. This binding of STAT6 in response to IL-25 treatment also resulted in the increase of IL-25 expression in hepatocytes. Together, these findings identify IL-25 as a protective factor against HFD-induced hepatic steatosis by inducing an increase of IL-25 expression in hepatocytes and through promotion of M2a macrophage production.

Natural history of covert hepatic encephalopathy: An observational study of 366 cirrhotic patients.

AIM: To explore the natural history of covert hepatic encephalopathy (CHE) in absence of medication intervention. METHODS: Consecutive outpatient cirrhotic patients in a Chinese tertiary care hospital were enrolled and evaluated for CHE diagnosis. They were followed up for a mean of 11.2 ± 1.3 mo. Time to the first cirrhosis-related complications requiring hospitalization, including overt HE (OHE), resolution of CHE and death/transplantation, were compared between CHE and no-CHE patients. Predictors for complication(s) and death/transplantation were also analyzed. RESULTS: A total of 366 patients (age: 47.2 ± 8.6 years, male: 73.0%) were enrolled. CHE was identified in 131 patients (35.8%). CHE patients had higher rates of death and incidence of complications requiring hospitalization, including OHE, compared to unimpaired patients. Moreover, 17.6% of CHE patients developed OHE, 42.0% suffered persistent CHE, and 19.8% of CHE spontaneously resolved. In CHE patients, serum albumin < 30 g/L (HR = 5.22, P = 0.03) was the sole predictor for developing OHE, and blood creatinine > 133 µmol/L (HR = 4.75, P = 0.036) predicted mortality. Child-Pugh B/C (HR = 0.084, P < 0.001) and OHE history (HR = 0.15, P = 0.014) were predictors of spontaneous resolution of CHE. CONCLUSION: CHE exacerbates, persists or resolves without medication intervention in clinically stable cirrhosis. Triage of patients based on these predictors will allow for more cost-effect management of CHE.

Low levels of serum 25-hydroxyvitamin D and risk of metabolic syndrome in China.

Recent evidence indicates the potential role of vitamin D in the prevention of Metabolic syndrome (MetSyn). This is an analytical cross sectional study. A total of 3275 subjects were investigated. 25-hydroxyvitamin D(25[OH]D) was detected by electrochemiluminescence immunoassay (ECLIA) technology. Metabolic syndrome was defined according to the definition of International Diabetes Federation (IDF). Among the participants, the prevalence of the MetSyn was 6.0%. The prevalence of vitamin D deficiency and insufficiency was 50.1% and 25.0% respectively. Subjects with MetSyn presented with significantly lower 25(OH)Vit D serum levels compared with non-MetSyn group. The results shows that vitamin D deficiency is common in Chinese adults, and subjects with lower serum 25(OH)D have a higher risk of the MetSyn. The cut-off value of serum 25(OH)D that reflected MetSyn in Chinese adluts was 15.655 ng/mL.

The cutoffs and performance of glycated hemoglobin for diagnosing diabetes and prediabetes in a young and middle-aged population and in an elderly population.

The aims were to compare the appropriate cutoffs of glycated hemoglobin (HbA1c) in a population of varying ages and to evaluate the performance of HbA1c for diagnosing diabetes and prediabetes. A total of 1064 participants in the young and middle-aged group and 1671 in the elderly group were included and underwent HbA1c testing and an oral glucose tolerance test (OGTT). Sensitivity, specificity, and area under the receiver operating characteristic curve (AUC) were calculated to evaluate the optimal HbA1c cutoffs. Kappa coefficients were used to test for agreement between HbA1c categorization and OGTT-based diagnoses. The optimal HbA1c cutoffs for diagnosing diabetes were 5.7% (39 mmol/mol) in the young and middle-aged group with a sensitivity of 66.7%, specificity of 86.7%, and AUC of 0.821 (95% CI: 0.686, 0.955) and 5.9% (41 mmol/mol) in the elderly group with a sensitivity of 80.4%, specificity of 73.3%, and AUC of 0.831 (0.801, 0.861). The optimal cutoffs for diagnosing prediabetes were 5.6% (38 mmol/mol) and 5.7% (39 mmol/mol) in the young and middle-aged group and in the elderly group, respectively. Agreement between the OGTT-based diagnosis of diabetes or prediabetes and the optimal HbA1c cutoff was low (all kappa coefficients <0.4). The combination of HbA1c and fasting plasma glucose increased diagnostic sensitivities or specificities. In conclusion, age-specific HbA1c cutoffs for diagnosing diabetes or prediabetes were appropriate. Furthermore, the performance of HbA1c for diagnosing diabetes and prediabetes was poor. HbA1c should be used in combination with traditional glucose criteria when detecting and diagnosing diabetes or prediabetes.

[Correlation of serum 25-hydroxyvitamin D and parathyroid hormone levels with metabolic syndrome in aged males].

OBJECTIVE: To explore the association of 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone (PTH) with metabolic syndrome (MS) and its components in aged males. METHODS: For this cross-sectional study, 1 729 aged males aged over 60 years were selected from participants in a routine annual health examination at our hospital from May to June 2012. Their mean age was 75 ± 10 years. Height, weight, blood pressure, blood glucose, blood lipids, alkaline phosphatase, calcium, phosphorus, 25(OH) D and PTH were measured. And the associations of 25(OH)D and PTH with the presence of MS and its components were analyzed. RESULTS: The prevalence of MS was 22.0%. The PTH levels were significantly higher in the MS and abnormal blood glucose and HDL-C group than in their control group [(42 ± 16) vs (40 ± 17), (42 ± 16) vs (40 ± 17), (47 ± 18) vs (40 ± 16) ng/L respectively, P < 0.05].However, there were no significant differences of 25(OH)D between these groups. The prevalence of MS showed a gradual increase according to the PTH quintiles (P < 0.05). When comparing the subjects in the highest and lowest quintile of PTH, the former group demonstrated a 1.51-fold increase in odds ratio for MS after adjusting for 25(OH)D levels and other confounding factors. Logistic regression analysis showed that the PTH level was an independent influencing factor for MS in aged males (OR = 1.007, 95%CI: 1.000-1.014, P = 0.047). The levels of 25 (OH) D were not associated with MS in the regression model (OR = 1.004, 95%CI: 0.992-1.016, P = 0.538). CONCLUSION: In aged males, the elevated level of PTH is a risk factor for the prevalence of MS. However, there was no association between 25 (OH) D and MS.