Diagnosis and treatment of diabetic foot ulcer complicated with lower extremity vasculopathy: Consensus recommendation from the Chinese Medical Association (CMA), Chinese Medical Doctor Association (CMDA).

Diabetic foot ulcer complicated with lower extremity vasculopathy is highly prevalent, slow healing and have a poor prognosis. The final progression leads to amputation, or may even be life-threatening, seriously affecting patients' quality of life. The treatment of lower extremity vasculopathy is the focus of clinical practice and is vital to improving the healing process of diabetic foot ulcers. Recently, a number of clinical trials on diabetic foot ulcers with lower extremity vasculopathy have been reported. A joint group of Chinese Medical Association (CMA) and Chinese Medical Doctor Association (CMDA) expert representatives reviewed and reached a consensus on the guidelines for the clinical diagnosis and treatment of this kind of disease. These guidelines are based on evidence from the literature and cover the pathogenesis of diabetic foot ulcers complicated with lower extremity vasculopathy and the application of new treatment approaches. These guidelines have been put forward to guide practitioners on the best approaches for screening, diagnosing and treating diabetic foot ulcers with lower extremity vasculopathy, with the aim of providing optimal, evidence-based management for medical personnel working with diabetic foot wound repair and treatment.

Association of body mass index and waist circumference with type 2 diabetes mellitus in older adults: a cross-sectional study.

BACKGROUND: The prevalence of obesity and diabetes is rising. The aim of this study was to determine the association of body mass index (BMI) and waist circumference (WC) with type 2 diabetes mellitus (T2DM) in the elderly and to compare the discriminatory abilities of BMI, WC and other anthropometric indicators, including waist-to-height ratio (WHtR), body adiposity estimator (BAE) and body roundness index (BRI) for T2DM. METHODS: This cross-sectional study included 69,388 subjects aged ≥ 60 years living in Xinzheng, Henan Province, from January to December 2020. The data came from the residents' electronic health records of the Xinzheng Hospital Information System. Logistic regression was used to examine the relationships. Fully adjusted models adjusted for age, sex, place of residence, alcohol consumption, smoking, physical exercise, SBP and RHR. The area under the receiver operating characteristic curve (AUC) was used to compare the discriminatory ability of different anthropometric indicators for T2DM under the influence of potential risk factors. RESULTS: After adjusting for multiple covariates, compared with the first BMI quintile, the odds ratios (ORs) and 95% confidence intervals (CIs) from the second to fifth quintile for T2DM were 1.416 (1.335-1.502), 1.664 (1.570-1.764), 1.879 (1.774-1.990) and 2.156 (2.037-2.283), respectively. Compared with the first WC quintile, the ORs and 95% CIs from the second to fifth quintiles for T2DM were 1.322 (1.244-1.404), 1.549 (1.459-1.643), 1.705 (1.609-1.807) and 2.169 (2.048-2.297), respectively. Among men, compared with other anthropometric indicators (BMI, WHtR, BAE and BRI), WC showed the highest AUC (AUC: 0.629; 95% CI: 0.622-0.636). Among women, the AUCs of BMI (AUC: 0.600; 95% CI: 0.594-0.606), WC (AUC: 0.600; 95% CI: 0.593-0.606) and BAE (AUC: 0.600; 95% CI: 0.594-0.607) were similar, and the AUCs of BMI, WC and BAE were higher than WHtR, BRI. CONCLUSIONS: All anthropometric indicators were positively associated with T2DM. In men, WC with the strongest positive association with T2DM was the best predictor of T2DM. In women, BMI was most strongly associated with T2DM, and the predictive powers of BMI, WC and BAE were similar. After adjusting the potential confounding factors including age, sex, place of residence, alcohol consumption, smoking, physical exercise, SBP and RHR, the effect of these factors was eliminated, the findings were independent of the covariates considered.

Deletion of HNF1A-AS1 Suppresses the Malignant Phenotypes of Breast Cancer Cells In Vitro and In Vivo Through Targeting miRNA-20a-5p/TRIM32 Axis.

Background: Hepatocyte nuclear factor 1 homeobox A-antisense RNA 1 (HNF1A-AS1) is a long noncoding RNA and controls human tumor development and progression. However, its expression and role in breast cancer, the most overwhelmingly occurring malignancy in women globally, remain poorly illuminated. Materials and Methods: Expression of HNF1A-AS1, miRNA (miR)-20a-5p, and tripartite motif containing 32 (TRIM32) was detected using quantitative real-time polymerase chain reaction and Western blotting. Cell proliferation, apoptosis, migration, and invasion were measured by cellTiter 96 AQueous one solution cell proliferation assay kit, flow cytometry, and transwell assays, respectively. Epithelial-mesenchymal transition (EMT) was evaluated by Western blotting, analyzing E-cadherin, N-cadherin, and vimentin expression. Mice xenograft model was generated to investigate tumor growth in vivo. The target binding among miR-20a-5p, HNF1A-AS1, and TRIM32 was confirmed by dual-luciferase reporter assay. Results: Expression of HNF1A-AS1 and TRIM32 was upregulated and miR-20a-5p was downregulated in breast cancer tumors and cell lines. Deletion of HNF1A-AS1 induced cell apoptosis rate, but suppressed cell proliferation, EMT, migration, and invasion in MDA-MB-231 and MCF-7 cells. Furthermore, HNF1A-AS1 downregulation impeded tumor growth in vivo. Interestingly, miR-20a-5p overexpression elicited the similar suppressive effects in MDA-MB-231 and MCF-7 cells, which was partially reversed by TRIM32 upregulation; besides, miR-20a-5p silencing could abolish the antitumor role of HNF1A-AS1 deletion. Notably, HNF1A-AS1 positively modulated TRIM32 expression through acting as a molecular "sponge" for miR-20a-5p. Conclusions: Knockdown of HNF1A-AS1 suppressed breast carcinogenesis presumably through targeting miR-20a-5p/TRIM32 axis, suggesting that HNF1A-AS1 might be a promising therapy target for breast cancer.

Gastrodin relieved complete Freund's adjuvant-induced spontaneous pain by inhibiting inflammatory response.

The analgesic effects of gastrodin (GAS), an active component derived from the Chinese herb Tian ma (Gastrodia elata Blume), on chronic inflammatory pain of mice and the involved molecular mechanisms were investigated. GAS significantly attenuated mice chronic inflammatory pain induced by hindpaw injection of complete Freund's adjuvant (CFA) and the accompanying anxiety-like behaviors. GAS administration reduced CFA-induced up-regulation of GluR1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, GluN2A- and GluN2B-containing N-methyl-d-aspartate (NMDA) receptors, and Ca2+/calmodulin-dependent protein kinase II-alpha (CaMKII-α) in the anterior cingulate cortex (ACC). The GluN2A and GluN2B subunits of NMDA receptors, the GluR1 type of AMPA receptor, and CaMKII-α are key molecules responsible for neuroplasticity involved in chronic pain and the accompanying anxiety. Moreover, GAS administration reduced the activation of astrocyte and microglia and the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice. Therefore, GAS administration relieved chronic pain, exerted anxiolytic effects by regulating neuroplasticity molecules, and attenuated the inflammatory response by reducing the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice.

A moderate static magnetic field enhances TRAIL-induced apoptosis by the inhibition of Cdc2 and subsequent downregulation of survivin in human breast carcinoma cells.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) exhibits its potent antitumor activity via membrane receptors on cancer cells without deleterious side effects for normal tissue. However, as many other cancer types, breast cancer cells develop a resistance to TRAIL. In the present study, we reported that exposure to 3.0 mT static magnetic field (SMF) mediated the sensitization of breast cancer cells to TRAIL-induced apoptosis. This effect was significantly reduced by the forced expression of survivin, suggesting the sensitization was mediated at least in part through the inhibition of survivin expression. In addition, SMF alone or in combination with TRAIL induced a cell cycle arrest within the G2 /M phase, and the reduction in the survivin protein level was associated with the downregulated expression of Cdc2, a cyclin B-dependent kinase that is necessary for the entry into the M phase. Taken together, our results demonstrated that SMF promoted TRAIL-induced apoptosis by inhibiting the expression of Cdc2 and, subsequently, survivin. Of note, SMF did not sensitize untransformed human mammary epithelial cells to TRAIL-mediated apoptosis. Therefore, the combined treatment of SMF and TRAIL may offer an attractive strategy for safely treating resistant breast cancers.