To characterize the fixation and macular integrity of subjects with multiple sclerosis (MS) with and without previous optic neuritis (ON) using microperimetry (MP). Fifty-five eyes of MS patients, subdivided into three groups (28 eyes without ON, 16 with previous ON, and 11 eyes with previous ON in the contralateral eye), and 43 healthy eyes were enrolled (January-November 2018). All cases were evaluated using the MAIA microperimeter (Centervue), analyzing the following parameters average macular threshold (AT), fixation indexes (P1 and P2), bivariate contour ellipse area (BCEA) for 95% and 63% of points, and horizontal (H) and vertical (V) axes of the ellipse of fixation. All MS groups showed a significant reduced AT compared with the control group (p < 0.001). This reduction was more representative (p < 0.001) in eyes with previous ON. No statistically significant differences were found between MS patients with and without previous ON (p > 0.05). Mean AT was correlated with the examination time in all three groups (between ρ = - 0.798 p < 0.001 and ρ = - 0.49 p < 0.001). Significant differences in fixation parameters were only found between control and MS with ON groups (p < 0.02). The ratio of the disease showed a significant correlation with fixation parameters in MS groups (p < 0.02), but not with AT. In MS patients, macular sensitivity is altered, especially in eyes with previous ON. Likewise, a fixational instability is present in MS patients with ON, with more increase of the V axis of the fixation area than of the H. The ratio of the disease also affects the patient fixation pattern. In MS patients, macular sensitivity is altered, especially in eyes with previous ON. #link# Likewise, a fixational instability is present in MS patients with ON, with more increase of the V axis of the fixation area than of the H. The ratio of the disease also affects the patient fixation pattern. Several studies reported that excessive correction of severe genu varum deformity with total knee arthroplasty or high tibial osteotomy (HTO) could result in ankle joint pain and osteoarthritis progression. However, few studies have evaluated the change in the weight-bearing-line (WBL) ratio of the ankle joint after knee arthroplasty or HTO in patients with genu varum deformities. This study aimed to investigate the change in the WBL ratio of the ankle joint and ankle joint line orientation after knee arthroplasty or HTO in patients with genu varum deformities. We retrospectively evaluated 40 patients (mean age, 69.9 ± 8.0years) with genu varum deformities of > 5° and underwent knee arthroplasty or HTO. Three radiologic parameters, including (1) the hip-knee-ankle (HKA) angle, (2) WBL ratio of the ankle joint, and (3) ankle joint line orientation relative to the ground (AJLO-G), were assessed using pre-operative and post-operative orthoradiographs. A paired t test was used to evaluate post-operative chnt line orientation.Solid dispersion is one of the most effective ways to improve the dissolution of insoluble drugs. When the carrier can highly disperse the drug, it will increase the wettability of the drug and reduce the surface tension, thus improving the solubility, dissolution, and bioavailability. However, amorphous solid dispersions usually have low drug loading and poor stability. Therefore, the goal of this work is to study the increased dissolution and high stability of high drug-loading crystalline solid dispersion (CSD), and the difference in dissolution and stability of high-loading and low-loading amorphous solid dispersion (ASD). A CSD of nimodipine with a drug loading of 90% was prepared by wet milling, with hydroxypropyl cellulose (model HPC-SL) and sodium dodecyl sulfate as stabilizers and spray drying. At the same time, the gradient drug-loaded ASD was prepared by hot melt extrusion with HPC-SL as the carrier. Each preparation was characterized by DSC, PXRD, FT-IR, SEM, and in vitro dissolution testing. The results indicated that the drug in CSD existed in a crystalline state. The amorphous drug molecules in the low drug-loading ASD were uniformly dispersed in the carrier, while the drug state in the high drug-loading ASD was aggregates of the amorphous drug. At the end of the dissolution assay, the 90% drug-loading CSD increased cumulative dissolution to 60%, and the 10% drug-loading ASD achieved a cumulative dissolution rate of 90%. Despite the high prevalence of non-alcoholic fatty liver disease (NAFLD) and its associated co-morbidities, no efficient treatment in a high percentage of individuals is available. Beneficial effects of sodium-glucose co-transporter2 inhibitors on fatty liver have been investigated in people with type2 diabetes (T2DM). The aim of this study was to explore the effect of empagliflozin on liver steatosis and fibrosis in patients with NAFLD without T2DM. In this prospective randomized, double-blind, placebo-controlled clinical trial, participants with NAFLD were randomized to empagliflozin (10mg/day) (n = 43) or placebo (n = 47) for 24weeks. Hepatic steatosis and fibrosis were assessed using transient elastography to measure the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM). The primary outcome was the change in CAP score at 24weeks. There was https://www.selleckchem.com/products/2-d08.html in CAP score in both groups but no significant difference was observed between the two groups (P = 0.396). LSM was significantly decreased in the empagliflozin-treated group (6.03 ± 1.40 to 5.33 ± 1.08kPa; P = 0.001), while no change was found in the placebo group. In subgroups analysis of patients with significant steatosis at baseline (CAP ≥ 302dB/m), steatosis significantly improved in the empagliflozin group (37.2% vs. 17%; P = 0.035). There was a significant decrease in the grade of liver fat on visual analysis of ultrasound images, AST, ALT, and fasting insulin levels in the empagliflozin group, while no changes were observed in the placebo group. Empagliflozin improves liver steatosis and, more importantly, measures of liver fibrosis in patients with NAFLD without T2DM. ClinicalTrials.gov identifier, IRCT20190122042450N1. ClinicalTrials.gov identifier, IRCT20190122042450N1.