New Brunswick's mental health action plan: A quantitative exploration of program efficacy in children and youth using the Canadian Community Health Survey.

In 2011, the New Brunswick government released the New Brunswick Mental Health Action Plan 2011-2018 (Action Plan). Following the release of the Action Plan in 2011, two progress reports were released in 2013 and 2015, highlighting the implementation status of the Action Plan. While vague in their language, these reports indicated considerable progress in implementing the Action Plan, as various initiatives were undertaken to raise awareness and provide additional resources to facilitate early prevention and intervention in children and youth. However, whether these initiatives have yielded measurable improvements in population-level mental health outcomes in children and youth remains unclear. The current study explored the impact of the Action Plan by visualizing the trend in psychosocial outcomes and service utilization of vulnerable populations in New Brunswick before and after the implementation of the Action Plan using multiple datasets from the Canadian Community Health Survey. Survey-weighted ordinary least square regression analyses were performed to investigate measurable improvements in available mental health outcomes. The result revealed a declining trend in the mental wellness of vulnerable youth despite them consistently reporting higher frequencies of mental health service use. This study highlights the need for a concerted effort in providing effective mental health services to New Brunswick youth and, more broadly, Canadian youth, as well as ensuring rigorous routine outcome monitoring and evaluation plans are consistently implemented for future mental health strategies at the time of their initiation.

Characteristics of metabolic inflammatory syndrome among inpatients with type 2 diabetes: A cross-sectional study in China.

BACKGROUND: As meta-inflammation is a common feature for obesity, type 2 diabetes (T2D), nonalcoholic fatty liver disease and atherosclerosis, we have proposed a new concept, metabolic inflammatory syndrome (MIS), to cluster such diseases. We aimed to characterize MIS and explore its association with coronary heart disease (CHD) among T2D inpatients in China. METHODS: A total number of 8344 T2D participants were enrolled. Each component of MIS and metabolic syndrome (MS) was analyzed. Their association with the risk of CHD was assessed using a binary logistic analysis. RESULTS: Among the T2D inpatients, the detection rate of MIS was much higher than that of MS (93.6 % vs. 53.2 %). Among all the components of MIS and MS, carotid atherosclerosis (71.9 %) was most commonly detected, which increased with aging in subgroups. Surprisingly, the most common combination of MIS was with all 4 components in T2D patients, with a constituent ratio of 30.9 %. According to the odds ratios (ORs), MIS was a better predictor of CHD than MS, especially after adjustment for age, sex, smoking, and alcohol consumption (adjusted OR for MIS: 3.083; for MS: 1.515). The presence of more components of MIS was associated with a higher detection rate of CHD (P < 0.001). Among all the components of MIS and MS, carotid atherosclerosis best predicted the risk of CHD (adjusted OR: 1.787). CONCLUSIONS: MIS is an independent risk factor for CHD, with a bigger OR value than MS. Carotid atherosclerosis, with the highest detection rate, was the best individual predictor of CHD and thus a critical component of MIS. The concept of MIS represents the understanding of metabolic diseases from the perspective of holistic integrative medicine.

Consensus of Chinese experts on strengthening personalized prevention and treatment of type 2 diabetes.

Up to now, there has not yet been guidance or consensus from Chinese experts in the field of personalized prevention and treatment of type 2 diabetes. In view of the above, the endocrinology diabetes Professional Committee of Chinese Non-government Medical Institutions Association, the integrated endocrinology diabetes Professional Committee of the integrated medicine branch of Chinese Medical Doctor Association, and the diabetes education and microvascular complications group of the diabetes branch of the Chinese Medical Association organized relevant experts to discuss and reach the "Chinese expert consensus on strengthening personalized prevention and treatment of type 2 diabetes" for reference in clinical practice.

Long Non-coding RNA DLGAP1-AS1 and DLGAP1-AS2: Two Novel Oncogenes in Multiple Cancers.

BACKGROUND: The change of lncRNA expression is known to affect the progression of tumors. This has fueled numerous investigations aiming at the mystery of lncRNA. Clear lncRNA has been the hotspot of antisense RNAs research. More and more lncRNAs have been proven to take effect as oncogenes of multitudinous cancers and accelerate tumor progression. This review elucidates the pathophysiological functions of lncRNA DLGAP1-AS1 and lncRNA DLGAP1-AS2 in a variety of tumors. METHODS: Via systematic analysis and in-depth study about relevant articles in PubMed, this article analyzes and summarizes the mechanism of antisense transcripts DLGAP1- AS1 and DLGAP1-AS2 in tumor development. RESULTS: DLGAP1-AS1 and DLGAP1-AS2 can exert their effect as oncogenes on various cancers. The expression of DLGAP1-AS1 is aberrantly high in various tumors, including GC, BC, HCC, glioblastoma and CRC. Concurrently, in LC, RC, HCC, GC, glioma and CCA, DLGAP1-AS2 is also discovered to be highly expressed. And they have a strong pertinence with a poor prognosis. The disorder of DLGAP1-AS1 and DLGAP1- AS2 in different tumors has different malignant impacts on tumors, not only to invasion, apoptosis, multiplication and EMT of tumor cells but also to drug resistance and radioresistance. In addition, DLGAP1-AS2 was revealed to have the ability to predict the prognosis of WT and RCC. CONCLUSION: The regulatory effects of DLGAP1-AS1 and DLGAP1-AS2 on tumors make them possible to be clinical markers for the early diagnosis of tumors and effective therapeutic targets.

ROS-Mediated Enamel Formation Disturbance Characterized by Alternative Cervical Loop Cell Proliferation and Downregulation of RhoA/ROCK in Ameloblasts.

Reactive oxygen stress (ROS) is generally accepted as a signal transducer for coordinating the growth and differentiation of tissues and organs in the oral and maxillofacial region. Although ROS has been confirmed to affect the development of enamel, it is not yet known that the specific mechanism of ROS accumulation induced enamel defects. Given the lack of knowledge of the role of ROS in enamel, the aim of the study is to determine how oxidative stress affects cervical cells and ameloblast cells. Using SOD1 knockout mice, we identified a relationship between ROS fluctuations and abnormal enamel structure with HE staining, micro-CT, and scanning electron microscope. Increased ROS induced by H2O2, certified by the DCFH probe, has resulted in a dual effect on the proliferation and differentiation of cervical cells, indicating a higher tendency to proliferate at low ROS concentrations. Ameloblasts transfected with SOD1 siRNA showed a significant reduction of RhoA and ROCK. This study investigates for the first time that SOD1-mediated ROS accumulation disrupted normal enamel structure through alternative cervical loop cell proliferation and downregulation of RhoA and ROCK in ameloblasts, demonstrating the convoluted role of ROS in monitoring the progress of enamel defects.

BMSC-Derived Small Extracellular Vesicles Induce Cartilage Reconstruction of Temporomandibular Joint Osteoarthritis via Autotaxin-YAP Signaling Axis.

Background: Temporomandibular joint osteoarthritis (TMJOA) seriously affects the health of patients, and the current treatments are invasive and only used for advanced cases. Bone marrow mesenchymal stem cell (BMSC)-derived small extracellular vesicles (BMSC-sEVs) may represent a safer and more effective treatment, but their role in TMJOA has not been elucidated. This study attempted to analyze the cartilage reconstruction effect of BMSC-sEVs on TMJOA and the mechanism underlying this effect. Methods: BMSC-sEVs were isolated and purified by microfiltration and ultrafiltration and were subsequently characterized by nanoparticle tracking analysis, electron microscopy, and immunoblotting. TMJOA models were established in vivo and in vitro, and hematoxylin-eosin staining, immunohistochemistry, and histological scoring were performed to analyze the histological changes in TMJOA cartilage tissues treated with BMSC-sEVs. The proliferation, migratory capacity, and cell cycle distribution of TMJOA cartilage cells treated with BMSC-sEVs were detected. Furthermore, the related mechanisms were studied by bioinformatic analysis, immunoblotting, and quantitative PCR, and they were further analyzed by knockdown and inhibitor techniques. Results: The acquisition and identification of BMSC-sEVs were efficient and satisfactory. Compared with the osteoarthritis (OA) group, the condylar tissue of the OA group treated with BMSC-sEV (OAsEV) showed an increase in cartilage lacuna and hypertrophic cartilage cells in the deep area of the bone under the cartilage. Significantly upregulated expression of proliferating cell nuclear antigen and cartilage-forming factors and downregulated expression of cartilage inflammation-related factors in OAsEV were observed. In addition, we found higher rates of cell proliferation and migratory activity and alleviated G1 stagnation of the cell cycle of OAsEV. Autotaxin was found in the BMSC-sEVs, and key factors of the Hippo pathway, Yes-associated protein (YAP), phosphorylated Yes-associated protein (p-YAP), etc. were upregulated in the OAsEV group. Treatment with BMSC-sEVs after autotaxin knockdown or inhibition no longer resulted in expression changes in cartilage-forming and inflammation-related factors and key factors of the Hippo pathway. Conclusions: These results suggest that the autotaxin-YAP signaling axis plays an important role in the mechanism by which BMSC-sEVs promote cartilage reconstruction in TMJOA, which may provide guidance regarding their therapeutic applications as early and minimally invasive therapies for TMJOA, and provide insight into the internal mechanisms of TMJOA.

The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition.

The status of reactive oxygen species (ROS) correlates closely with the normal development of the oral and maxillofacial tissues. Oxidative stress caused by ROS accumulation not only affects the development of enamel and dentin but also causes pathological changes in periodontal tissues (periodontal ligament and alveolar bone) that surround the root of the tooth. Although previous studies have shown that ROS accumulation plays a pathologic role in some oral and maxillofacial tissues, the effects of ROS on alveolar bone development remain unclear. In this study, we focused on mandibular alveolar bone development of mice deficient in superoxide dismutase1 (SOD1). Analyses were performed using microcomputerized tomography (micro-CT), TRAP staining, immunohistochemical (IHC) staining, and enzyme-linked immunosorbent assay (ELISA). We found for the first time that slightly higher ROS in mandibular alveolar bone of SOD1(-/-) mice at early ages (2-4 months) caused a distinct enlargement in bone size and increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and expression of alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and osteopontin (OPN). With ROS accumulation to oxidative stress level, increased trabecular bone separation (Tb.Sp) and decreased expression of ALP, Runx2, and OPN were found in SOD1(-/-) mice at 6 months. Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN. These results indicate that redox imbalance caused by SOD1 deficiency has dual effects (promotion or inhibition) on mandibular alveolar bone development, which is closely related to the concentration of ROS and the stage of growth. We present a valuable model here for investigating the effects of ROS on mandibular alveolar bone formation and highlight important roles of ROS in regulating tissue development and pathological states, illustrating the complexity of the redox signal.

The application of a new clear removable appliance with an occlusal splint in early anterior crossbite.

BACKGROUND: The effectiveness of anterior crossbite treatment in preschool-aged children depends on the treatment design and patient compliance. Common early treatment appliances with steel wires and acrylic resin can bring about numerous problems, such as toothache, sore gums and mucous membrane injury. The aim of this study was to propose a new clear removable appliance to provide preschool-age children with an improved experience of early occlusal interference treatment. METHODS: Appliances were designed with the help of 3-dimensional (3D) digital reconstruction oral models and fabricated using 3D printing technology and the pressed film method. Then, the mechanical properties of the original dental coping sheet and thermoformed aligners were assessed in a simulated intraoral environment. Preschool-age participants who displayed anterior crossbite were recruited in this study. Records (photographs and impressions) were taken before the treatment (T1), during the treatment (T2) and at the end of the treatment (T3). The effects of treatment were evaluated by clinical examination and questionnaires. RESULTS: Normal degrees of overbite and overjet in the primary dentition were achieved using this new appliance. Dental and soft tissue relationships were improved. Questionnaires showed that the safety evaluation, degree of comfort and convenience grades of the appliance were all relatively high. CONCLUSION: This explorative study demonstrates that our new clear removable appliance is able to correct early-stage anterior crossbite in a safe, comfortable, convenient and efficient way. Thus, it is a promising method to correct a certain type of malocclusion, and its clinical use should be promoted in the future.

miR-18a Inhibitor Suppresses Leukemia Cell Proliferation by Upregulation of PTEN Expression.

BACKGROUND Leukemia is common in aging adults and has very high mortality worldwide. The present study was designed to investigate the therapeutic efficacy of miR-18a inhibitor against WEHI-3 and THP-1 leukemia cells. MATERIAL AND METHODS The changes in miR-18a inhibitor-transfected WEHI-3 and THP-1 cell proliferative potential was measured by use of the Cell Counting Kit-8 assay. Apoptotic changes were analyzed by electron microscopy, and evaluation of PI3K, AKT, mTOR, and PTEN expression was assessed by RT-qPCR assay. RESULTS Transfection of miR-18a inhibitor significantly (P<0.05) suppressed the proliferative potential of WEHI-3 and THP-1 cells. The WEHI-3 cells showed the presence of characteristic apoptotic bodies on transfection with miR-18a inhibitor at 48 h. Flow cytometry showed that miR-18a inhibitor transfection significantly (P<0.05) increased the WEHI-3 cell percentage in G1 phase. The transfection of miR-18a inhibitor significantly (P<0.05) promoted apoptosis in WEHI-3 cells. In WEHI-3 cells, miR-18a inhibitor transfection markedly suppressed the expression of PI3K, AKT, and mTOR mRNA. The expression of PTEN mRNA was significantly (P<0.05) upregulated by miR-18a inhibitor transfection in WEHI-3 cells. CONCLUSIONS The present study investigated the therapeutic efficacy of miR-18a inhibitor against WEHI-3 and THP1 leukemia cells. The study demonstrated that miR-18a inhibitor suppressed the proliferative potential of WEHI-3 and THP1 cells and activated apoptotic process through upregulation of PTEN mRNA expression. Therefore, miR-18a inhibitor can be of therapeutic importance for the treatment of leukemia.

CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury.

C1q/tumor necrosis factor (TNF)-related protein 12 (CTRP12) is a secretory protein that participates in the regulation of glucose and lipid metabolism in obesity and diabetes. Its role in cardiovascular disease, particularly sepsis-induced cardiac injury, is unclear. Here, we stimulated cardiomyocytes with lipopolysaccharide (LPS) to establish an in vitro cardiomyocyte injury model and CTRP12 was overexpressed with an adenovirus delivery system. Overexpression of CTRP12 reduced the transcription and release of pro-inflammatory cytokines from LPS-stimulated cardiomyocytes, including TNFα, interleukin-1 (IL-1), and IL-6. Reactive oxygen species (ROS) level increased and the oxidation/redox system was disturbed in LPS-stimulated cardiomyocytes, as evident from the decrease in superoxide dismutase activity and an increase in reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and malondialdehyde level. CTRP12 overexpression decreased the increasing level of ROS and ameliorated the unbalance in the oxidation/redox system in LPS-stimulated cardiomyocytes. The viability of cardiomyocytes decreased after LPS stimulation, and the cells underwent apoptosis. CTRP12-overexpressing cardiomyocytes showed a decrease in the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells, and the ratio of B cell lymphoma (Bcl)-1/Bax in these cells was recovered. In comparison with the control group, LPS-stimulated cardiomyocytes showed reduced expression of nuclear factor E2-related factor 2 (NRF2), while CTRP12-overexpressing cardiomyocytes showed elevated NRF2 expression. Small-interfering RNA-mediated silencing of NRF2 expression in cardiomyocytes resulted in the inhibition of the protective effects of CTRP12. Thus, CTRP12 ameliorated injury in LPS-stimulated cardiomyocytes in an NRF2-dependent manner.

Entry-Prohibited Effect of kHz Pulsed Magnetic Field Upon Interaction Between SPIO Nanoparticles and Mesenchymal Stem Cells.

OBJECTIVE: The interaction between superparamagnetic iron oxide (SPIO) nanoparticles and mesenchymal stem cells (MSCs) in the presence of pulsed magnetic field (PMF) has become an important area of research in recent years. METHODS: A parameter-adjustable pulsed magnetic field was developed based on the principle of insulated gate bipolar translator transistor-controlled discharge of large capacitances. The internalizations of SPIO nanoparticles by MSCs were investigated under the treatment of PMF in both intermittent stimulation mode and continuous stimulation mode. RESULTS: The intensities and frequencies of pulsed magnetic field can be adjustable in the range of 1.9-4.6 mT and 3-5 kHz, respectively. This PMF was safe to the MSCs. However, the uptake of SPIO nanoparticles by MSCs was significantly prohibited under the treatment of kHz-ranged PMF while the 10 Hz PMF enhanced the cellular uptake of nanoparticles. This phenomenon was relative with the magnetic effect of the PMF with different frequency. CONCLUSION: The PMF can be used to effectively regulate the cellular uptake of SPIO nanoparticles and the mechanism lies in the magnetic effect. SIGNIFICANCE: The interaction between SPIO nanoparticles and the MSCs is a fundamental and important issue for nanomedicine and stem cell research. Our results demonstrate that the external magnetic field can be used to regulate their interaction. We believe that this safe, facile, and flexible method will greatly promote the development and clinical translation of regenerative medicine and nanomedicine.

Aptamer-antibody dual probes on single-walled carbon nanotube bridged dielectrode: Comparative analysis on human blood clotting factor.

Haemophilia is a blood clotting disorder known as 'Christmas disease' caused when the blood has defect with the clotting factor(s). Bleeding leads various issues, such as chronic pain, arthritis and a serious complication during the surgery. Identifying this disease is mandatory to take the necessary treatment and maintains the normal clotting. It has been proved that the level of factor IX (FIX) is lesser with haemophilia patient and the attempt here is focused to quantify FIX level by interdigitated electrode (IDE) sensor. Single-walled carbon nanotube (SWCNT) was utilized to modify IDE sensing surface. On this surface, dual probing was evaluated with aptamer and antibody to bring the possible advantages. The detection limit with antibody was found to be 1 pM, while aptamer shows 100 fM. Further, a fine-tuning was attempted with sandwich pattern of aptamer-FIX-antibody and antibody-FIX-aptamer and compared. Specific elevation of detection with 10 folds was noticed and displayed the detection at 100 f. in both sandwich patterns. In addition, FIX was detected in the diluted human serum by aptamer-FIX-antibody sandwich, it was found that FIX detected from the dilution factor 1:640. A novel demonstration is with higher discrimination against other clotting factors, XI and VII.

Effect of canonical NF-κB signaling pathway on the differentiation of rat dental epithelial stem cells.

BACKGROUND: Nuclear factor-κB (NF-κB), an important transcription factor, participates in many physiological and pathological processes such as growth, differentiation, organogenesis, apoptosis, inflammation, and immune response, including tooth development. However, it is still unknown whether NF-κB participates in the regulation of dental epithelial stem cells (DESCs) in postnatal rat incisors. Here, we investigated the specific differentiation regulatory mechanisms of the canonical NF-κB signaling pathway in DESCs and provided the mechanism of cross-talk involved in DESC differentiation. METHODS: After adding the activator or inhibitor of the NF-κB signaling pathway, Western blot and quantitative real-time PCR were used to analyze the expressions of amelogenesis-related genes and proteins and canonical transforming growth factor-ß (TGF-ß) signaling. In addition, we used amelogenesis induction in vitro by adding the activator or inhibitor of the NF-κB signaling pathway to the amelogenesis-induction medium, respectively. Recombinant TGF-ß was used to activate the TGF-ß pathway, and SMAD7 siRNA was used to downregulate the expression of SMAD7 in DESCs. RESULTS: We found that the expression of amelogenesis-related genes and proteins as well as TGF-ß signaling were downregulated, while SMAD7 expression was increased in NF-κB-activated DESCs. In addition, NF-κB-inhibited DESCs exhibited opposite results compared with NF-κB-activated DESCs. Furthermore, the canonical NF-κB signaling pathway suppressed the canonical TGF-ß-SMAD signaling by inducing SMAD7 expression involved in the regulation of DESC differentiation. CONCLUSIONS: These results indicate that the canonical NF-κB signaling pathway participated in the regulation of DESC differentiation, which was through upregulating SMAD7 expression and further suppressing the canonical TGF-ß-SMAD signaling pathway.

Exendin-4 enhances expression of Neurod1 and Glut2 in insulin-producing cells derived from mouse embryonic stem cells.

INTRODUCTION: Stem cells involved cell replacement therapies for type 1 diabetes mellitus is promising, yet time-consuming and inefficient. Exendin-4 is a glucagon-like peptide-1 (GLP-1) receptor agonist which has been reported to possess anti-apoptotic effects, thereby increasing ß-cell mass and improving ß-cell function. The present study aimed to investigate whether exendin-4 would enhance the differentiation of embryonic stem cells into insulin-secreting cells and improve the pancreatic differentiation strategy. MATERIAL AND METHODS: R1 embryonic stem cells were treated with different concentrations of exendin-4 and divided into three groups. In the high dosage group (group H), exendin-4 was added at the dosage of 10 nmol/l. In the low dosage group (group L), exendin-4 was added at the dosage of 0.1 nmol/l. Group C was a control. Expression of genes related to the ß-cell phenotype and immunofluorescence staining of insulin and C-peptide were detected. RESULTS: Compared with groups L and C, group H had the highest mRNA expression levels of Isl1, Pdx1, Ngn3, and Insulin1 (p < 0.05). Neurod1 and Glut2 only emerged at the final stage of differentiation in group H. Immunofluorescence analysis revealed that exendin-4 upregulated the protein expression of insulin and C-peptide. CONCLUSIONS: Exendin-4 remarkably facilitated Neurod1 and Glut2 gene transcription, and was able to induce differentiation of embryonic stem cells into endocrine and insulin-producing cells.

Glycemic control rate of T2DM outpatients in China: a multi-center survey.

BACKGROUND: Type 2 diabetes mellitus (T2DM)-associated mortality and morbidity are strongly dependent on glycemic control. With T2DM prevalence increasing in China, we aimed to assess glycemic control rates in Chinese T2DM outpatients. MATERIAL/METHODS: A total of 9065 adult T2DM outpatients (5035 men) were assessed in 26 Chinese medical centers between August 2010 and April 2012. Patients were stratified according to BMI (kg/m2): <24, 24-28, and >28. Successful glycemic control was defined as glycated hemoglobin A1c (HbA1c) ≤7% or fasting plasma glucose (FPG) <7.0 mmol/L. RESULTS: Among the participants included in this study, 2939 had BMI <24, 3361 had BMI of 24-28, and 2764 had BMI >28. The glycemic control rate was only 32.6%, and the triple control rate for glycemia, blood pressure, and lipidemia was only 11.2%. Glycemic control rates by BMI group were 33.7% (<24), 33.8% (24-28), and 30.2% (>28) (p=0.005), and corresponding incidences of cardiovascular diseases (CVD) were 12.2%, 15.7%, and 15.9% (p<0.001). Multivariate logistic regression analysis demonstrated that older age (p<0.001), higher BMI (p=0.026), larger waist circumference (p<0.001), less education (p<0.001), and recent diagnosis (p<0.001) were independent risk factors for poor glycemic control. CONCLUSIONS: The T2DM glycemic control rate in China is currently low, especially in older obese patients with poor education and recent diagnosis.

Epidemiology of type 2 diabetic foot problems and predictive factors for amputation in China.

To determine incidence and clinically relevant risk factors for diabetic amputation in a large cohort study of diabetic foot ulceration patients in China, we investigated a total of 669 diabetic foot ulceration patients, who were assessed at baseline for demographic information, medical and social history, peripheral neuropathy screening, periphery artery disease screening, assessment of nutritional status and diabetic control, physical examination including foot deformity in 15 Grade III-A hospitals. Of the 669 patients, 435 were male and 201 were female, with the mean age being 64.0 years. Of all patients, 110 had neuropathic ulcers, 122 had ischemic ulcers, 276 had neuroischemic ulcers, and 12 cases were unclassified. Wagner classification showed 61 cases were grade I, 216 cases grade II, 159 cases grade III, 137 cases grade IV, and 7 cases grade V. The overall amputation rate among diabetic foot patients was 19.03%, and major and minor amputation rates were 2.14% and 16.88%, respectively. By univariate analysis, statistically significant differences were found in smoking, rest pain, ulcer history, revascularization history, amputation history, gangrene, infection, Wagner grades, duration of diabetes, and postprandial blood glucose, aldehyde, total protein, globulin, albumin, white blood cell (WBC), hemoglobin, HbA1c, ulcer property, body mass index, as well as creatinine. Binary logistic regression model showed that increased WBC (odds ratio 1.25) and ulcer history (odds ratio 6.8) were associated with increased risks from diabetic foot ulcer to major amputation; increased duration of diabetes (odds ratio 1.004), WBC (odds ratio 1.102), infection (odds ratio 2.323), foot deformity (odds ratio 1.973), revascularization history (odds ratio 2.662), and decreased postprandial blood sugar (odds ratio 0.94) were associated with increased risks from diabetic foot ulcer to minor amputation. It is of great importance to give better management to diabetic patients at early stages. Following a diagnosis of DFU more intensive surveillance and aggressive care may improve outcome.

Glycemic control among patients in China with type 2 diabetes mellitus receiving oral drugs or injectables.

BACKGROUND: The prevalence of type 2 diabetes mellitus (T2DM) is increasing rapidly among Chinese adults, and limited data are available on T2DM management and the status of glycemic control in China. We assessed the efficacy of oral antidiabetes drugs (OADs), glucagon-like peptide-1 (GLP-1) receptor agonists, and insulin for treatment of T2DM across multiple regions in China. METHODS: This was a multicenter, cross-sectional survey of outpatients conducted in 606 hospitals across China. Data from all the patients were collected between April and June, 2011. RESULTS: A total of 238,639 patients were included in the survey. Eligible patients were treated with either OADs alone (n=157,212 [65.88%]), OADs plus insulin (n=80,973 [33.93%]), or OADs plus GLP-1 receptor agonists (n=454 [0.19%]). The OAD monotherapy, OAD + insulin, and OAD + GLP-1 receptor agonist groups had mean glycosylated hemoglobin (HbA1c) levels (±SD) of 7.67% (±1.58%), 8.21% (±1.91%), and 7.80% (±1.76%), respectively. Among those three groups, 34.63%, 26.21%, and 36.12% met the goal of HbA1c <7.0%, respectively. Mean HbA1c and achievement of A1c <7.0% was related to the duration of T2DM. CONCLUSIONS: Less than one third of the patients had achieved the goal of HbA1c <7.0%. Glycemic control decreased and insulin use increased with the duration of diabetes.