BackgroundDisorders of endocrine substances in epicardial adipose tissue are known causes of coronary artery disease (CAD). Adiponectin is associated with cardiovascular disease. However, expression of adiponectin in epicardial adipose tissue and its function in CAD pathogenesis is unclear. This study investigates adiponectin expression in epicardial adipose tissue in CAD patients.MethodsVessels or adipose tissue samples collected from CAD patients and non-CAD controls were examined after immunochemical staining. Adiponectin, cytokines of interleukin-6 (IL-6) and necrosis factor-α (TNF-α) and toll-like receptor 4 (TLR4) expression level in adipose tissue were measured using real-time quantitative RT-PCR. Adiponectin concentrations in peripheral and coronary sinus vein plasma were measured with enzyme-linked immunosorbent assay. Peripheral vein plasma biochemistries were performed with routine laboratory techniques. Monocytes were collected from blood using lymphocyte separation medium. Expression level of cytokines and transcription factor NF-κB were measured to learn the effect of adiponectin on stearic acid-stimulated monocytes. Percentage of TLR4 positive monocytes was analyzed using flow cytometry.ResultsHistological examination revealed increased macrophage infiltration into epicardial adipose tissue of CAD patients. Decreased adiponectin displayed by real-time quantitative RT-PCR was associated with enhanced cytokines of IL-6 and TNF-α or TLR4 expression level in epicardial adipose tissue, suggesting decreased circulating adiponectin may be useful as a more sensitive predictor for coronary atherosclerosis than routine laboratory examinations. Adiponectin suppressed secretion of IL-6 and TNF-α in stimulated monocytes and TLR4 was expressed on cell surfaces.ConclusionsEndocrine disorders in epicardial adipose tissue are strongly linked to CAD, and adiponectin has a protective effect by inhibiting macrophage-mediated inflammation.

Background: Diabetic retinopathy (DR) is a specific neurovascular complication of diabetes mellitus (DM). Clinically, family history is a widely recognized risk factor for DR, assisting diagnosis and risk strata. However, among a great amount of DR patients without hereditary history like hypertension and diabetes, direct and simple risk factors to assist clinical decisions are still required. Herein, we intend to investigate the associated risk factors for these DR patients based on systemic inflammatory response indexes, neutrophil-to-lymphocyte ratio (NLR) and platelet-tolymphocyte ratio (PLR). Methods: We consecutively enrolled 1030 patients with a definite diagnosis of type 2 diabetes mellitus (T2DM) from the endocrinology department of the Second hospital of People in Yun Nan. Based on funduscopy and family history checking, we excluded patients with a family history of hypertension and diabetes and finally enrolled 264 patients with DR and 206 patients with non-diabetic retinopathy (NDR). Through correlation analysis, univariate and multivariate regression, we further explore the association between NLR, PLR, and DR. On top of that, we investigate the effect of NLR and PLR on risk reclassification of DR. Results: Compared with NDR patients, NLR and PLR levels are significantly higher among DR patients (NLR: 2.36 ± 1.16 in DR group versus 1.97 ± 1.06 in NDR group, p < 0.001; PLR: 11.62 ± 4.55 in DR group versus10.56 ± 4.45 in NDR group, p = 0.012). According to univariate analysis, NLR and PLR add risks to DR. After fully adjusting co-founders, NLR, as both continuous and categorical variate, remains an independent risk factor for DR (OR (95%CI): 1.37 (1.06, 1.78) P = 0.018). And though PLR was not independently associated with DR as a continuous variable (OR (95%CI) 1.05 (0.99, 1.11) p = 0.135), the highest quantile of PLR add twofold increased risk (OR (95%CI) 2.20 (1.05, 4.59) p = 0.037) in the fully adjusted model for DR. In addition, addition of PLR and NLR to the established factor hemoglobin (Hb) improved the discriminability of the model and assisted the reclassification of DR. After combining PLR and NLR the

BACKGROUNDHypoparathyroidism with basal ganglia calcification is clinically rare. Here, we report a case of Fahr’s syndrome due to hypoparathyroidism and review the literature in terms of etiology, clinical manifestation, diagnosis, and treatment.CASE SUMMARYA 62-year-old man experienced repeated twitching of both hands in recent 10 years. On July 28, 2017, the patient was admitted to our hospital due to slow response and speech difficulties. On medical examinations, he had a positive Chvostek sign, while no Albright’s hereditary osteodystrophy signs or history of neck surgery or radiation, and his family members had no similar medical history. Laboratory examinations revealed hypocalcemia, hyperphosphatemia, and low parathyroid hormone (PTH) levels. Computed tomography revealed basal ganglia calcification. Based on these investigations, a diagnosis of Fahr’s syndrome due to hypoparathyroidism was suggested. After receiving intravenous calcium gluconate to relieve symptoms, the patient continued to take oral calcium carbonate and calcitriol for treatment.CONCLUSIONThe possibility of hypoparathyroidism should be considered in patients with chronic hypocalcemia, recurrent tetany, and even neuropsychiatric symptoms. Hypoparathyroidism is a common cause of basal ganglia calcification. Therefore, it is recommended that blood calcium, phosphorus, and PTH levels should be measured in all individuals with basal ganglia calcification to exclude hypoparathyroidism.

Background: Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in patients with type 2 diabetes (T2DM). Carotid intima-media thickness (CIMT) is considered a preclinical stage of atherosclerosis. Therefore, it is necessary to identify the related risk factors for CIMT to facilitate the early prevention of CVD. Previous studies have shown that visceral fat area (VFA) is a risk factor for T2DM and CVD. However, few studies have focused on the effects of VFA on CIMT associated with T2DM. Moreover, considering that the body fat distribution shows regional and racial heterogeneity, the purpose of this study was to investigate the predictive value of VFA and other risk factors for CIMT associated with T2DM in Western China. Methods: In a cross-sectional study, a total of 1372 patients with T2DM were divided into the CIMT (−) group (n = 965) and the CIMT (+) group (n = 407) based on CIMT values. In addition to the univariate analyses, logistic regression analysis and a decision tree model were simultaneously performed to establish a correlation factor model for CIMT. Results: Univariate analyses showed that sex, smoking status, age, heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP), height, weight, body mass index (BMI), waist circumference, hip circumference, waist-hip ratio, VFA, subcutaneous fat area, and the levels of 2-h C-peptide, serum creatinine, urea nitrogen and uric acid were significantly different between the two groups (all p < 0.05). Smoking, increased VFA, female sex and increased BMI were risk factors in the logistic regression analyses (OR = 5.759, OR = 1.364, OR = 2.239, OR = 1.186, respectively). In the decision tree model, smoking was the root node, followed by sex, waist circumference, VFA and chronic kidney disease (CKD) in order of importance. Conclusions: In addition to smoking, sex and BMI, VFA has a significant effect on CIMT associated with T2DM in the Chinese Han population in Western China. In addition, the decision tree model could help clinicians make more effective decisions, with its simplicity and intuitiveness, making it worth promoting in future medical research.