Background and Objectives: Galectin-3 promotes fibroblast-to-myofibroblast differentiation and facilitates injury repair. Previous studies have shown that exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) promote the differentiation of myocardial fibroblasts into myofibroblasts under inflammatory environment. Whether hucMSC-ex derived Galectin-3 (hucMSC-ex-Galectin-3) plays an important role in fibroblast-to-myofibroblast differentiation is the focus of this study. Methods: and Results: Galectin-3 was knocked-down by siRNA in hucMSCs, and then exosomes were extracted. Fibroblasts were treated with LPS, LPS＋hucMSC-ex, LPS＋negative control-siRNA-ex (NC-ex), or LPS＋ Galectin-3-siRNA-ex (si-ex) in vitro. The coronary artery of the left anterior descending (LAD) branch was permanently ligated, followed by intramyocardial injection with phosphate buffered saline(PBS), hucMSC-ex, hucMSC-NC-ex, or hucMSC-si-ex in vivo. Western blot, RT-PCR, and immunohistochemistry were used to detect the expression of markers related to fibroblast-to-myofibroblast differentiation and inflammatory factors. Migration and contraction functions of fibroblasts were evaluated using Transwell migration and collagen contraction assays, respectively. β-catenin expression was detected by western blot and immunofluorescence. The results showed that hucMSC-ex increased the protein expression of myofibroblast markers, anti-inflammatory factors, and β-catenin. HucMSC-ex also reduced the migration and promoted the contractility of fibroblasts. However, hucMSC-si-ex did not show these activities. Conclusions HucMSC-ex-Galectin-3 promoted the differentiation of cardiac fibroblasts into myofibroblasts in an inflammatory environment, which was associated with increased β-catenin levels.

Background and Objectives: Galectin-3 promotes fibroblast-to-myofibroblast differentiation and facilitates injury repair. Previous studies have shown that exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) promote the differentiation of myocardial fibroblasts into myofibroblasts under inflammatory environment. Whether hucMSC-ex derived Galectin-3 (hucMSC-ex-Galectin-3) plays an important role in fibroblast-to-myofibroblast differentiation is the focus of this study. Methods: and Results: Galectin-3 was knocked-down by siRNA in hucMSCs, and then exosomes were extracted. Fibroblasts were treated with LPS, LPS＋hucMSC-ex, LPS＋negative control-siRNA-ex (NC-ex), or LPS＋ Galectin-3-siRNA-ex (si-ex) in vitro. The coronary artery of the left anterior descending (LAD) branch was permanently ligated, followed by intramyocardial injection with phosphate buffered saline(PBS), hucMSC-ex, hucMSC-NC-ex, or hucMSC-si-ex in vivo. Western blot, RT-PCR, and immunohistochemistry were used to detect the expression of markers related to fibroblast-to-myofibroblast differentiation and inflammatory factors. Migration and contraction functions of fibroblasts were evaluated using Transwell migration and collagen contraction assays, respectively. β-catenin expression was detected by western blot and immunofluorescence. The results showed that hucMSC-ex increased the protein expression of myofibroblast markers, anti-inflammatory factors, and β-catenin. HucMSC-ex also reduced the migration and promoted the contractility of fibroblasts. However, hucMSC-si-ex did not show these activities. Conclusions HucMSC-ex-Galectin-3 promoted the differentiation of cardiac fibroblasts into myofibroblasts in an inflammatory environment, which was associated with increased β-catenin levels.

The signaling pathways involved in acupuncture intervention in post-stroke depression (PSD) mainly include cAMP signaling pathway, MAPK signaling pathway, PI3K/Akt/mTOR signaling pathway, NF-κB signaling pathway, CREB signaling pathway, and CaMK signaling pathway. A variety of regulatory networks are formed between these signaling pathways, which play a key role in reducing inflammation, inhibiting apoptosis, improving neuroplasticity, promoting angiogenesis, and protecting neurons.

Objective:To investigate the correlation between serum levels of heme oxygenase-1 (HO-1) and lipoxin A4 (LXA4) and diabetic nephropathy, and to analyze the value of HO-1 and LXA4 in the diagnosis of diabetic nephropathy.Methods:A prospective cohort study was conducted in 185 patients with type 2 diabetes admitted to the Department of Endocrinology, Yan'an Hospital Affiliated to Kunming Medical University from January 2016 to January 2020. There were 96 cases with diabetic nephropathy (nephropathy group) and 89 cases without diabetic nephropathy (non nephropathy group). According to the stage of chronic kidney disease,the nephrotic group was divided into three subgroups: stage 1-2 group (31 cases), stage 3-4 group (40 cases) and stage 5 group (25 cases). Another 82 healthy volunteers were selected as the control group.Serum HO-1, LXA4, oxidative stress,inflammatory factors, glucose metabolism and renal function were detected. Pearson analysis of HO-1, LXA4 and oxidative stress, inflammatory factors, glucose metabolism and renal function index correlation, binary logistic regression analysis of diabetic nephropathy factors.Results:The serum HO-1 ((0.60 ± 0.20) μg/L) and LXA4 levels ((435.12 ± 22.42) ng/L) in nephrotic group were lower than those in non nephrotic ((0.72 ± 0.23) μg/L, (498.21 ± 29.48) ng/L)( t=29.351, 24.135, all P<0.05). The serum HO-1 and LXA4 levels in the 5 stage group were lower than those in the 3-4 stage and 1-2 stage group (all P<0.05). The serum HO-1 and LXA4 levels in the 3-4 stage group were lower than those in the 1-2 stage group (all P<0.05). Pearson correlation analysis showed that HO-1 was positively correlated with total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and estimated glomerular filtration rate (EGFR) ( r=0.516, 0.602, 0.617; all P<0.05), and was positively correlated with malondialdehyde (MDA) and homeostasis model insulin resistance (homeostasis model insulin resistance) Model assessment insulin resistance (HOMA-IR), urinary albumin creatinine ratio (UACR) LXA4 was negatively correlated with T-AOC, SOD and EGFR ( r=-0.559, 0.597, 0.637; all P<0.05), and positively correlated with MDA, IL-6, TGF-β1, HOMA-IR and UACR There was a negative correlation ( r=-0.498, -0.623, -0.725; all P<0.05). Binary logistic regression analysis showed that malondialdehyde ( OR=1.587, 95% CI 1.402-1.603, P=0.016), TGF-β1 ( OR=1.679, 95% CI 1.642-1.739, P=0.012), HOMA-IR ( OR=1.699、95% CI 1.534-1.739, P=0.009) were risk factors of diabetic nephropathy (all P<0.05). HO-1 ( OR=0.506, 95% CI 0.423-0.653, P<0.001) and LXA4 ( OR=0.492, 95% CI 0.409-0.535, P<0.001) were protective factors for DN ( P<0.001). After adjusting for MDA, TGF-β1 and HOMA-IR, HO-1 ( OR=0.485, 95% CI:0.402-0.564, P<0.001) and LXA4 ( OR=0.416, 95% CI:0.386-0.475, P<0.001) were still associated with DN. ROC analysis showed that the area under curve (AUC) of HO-1 and LXA4 were 0.820 (95% CI:0.760-0.880, P<0.001) and 0.763 (95% CI:0.691-0.836, P<0.001), respectively. The sensitivity and specificity were 71.88%, 80.90%, 75.00% and 84.27%, respectively. Conclusion:The decrease of serum LXA4 and HO-1 levels is closely related to diabetic nephropathy, which can be used as a biological indicator for the diagnosis of diabetic nephropathy.

Objective:To investigate the nutritional and metabolic risk factors associated with recurrence in patients with newly diagnosed ulcerative colitis (UC), so as to allow better clinical prediction of recurrence.Methods:A retrospective cohort study was conducted. Patients newly diagnosed with UC (mild and moderate) from the People's Hospital of Xinjiang Uygur Autonomous Region were screened based on prespecified inclusion and exclusion criteria from January 2016 to January 2019. Patients were followed up regularly for three years. Subgroups were determined according to the presence or absence of recurrence. The patients in the UC recurrence group were further stratified according to the time to recurrence into short-term (0-6 months), mid-term (6-12 months) and long-term (12-36 months) recurrence groups. The nutritional and metabolic risk factors related to recurrence were evaluated by univariate analysis and multifactorial logistic regression analysis, and the predictive value was evaluated via receiver operating characteristic curve. The risk factors were then compared across the 3 subgroups with recurrence.Results:A total of 210 patients newly diagnosed with UC (mild and moderate) were included, including 38 experiencing recurrence within 0-6 months, 27 within 6-12 months, 24 within 12-36 months, and 121 without recurrence. There were no statistically significant differences in gender, age, smoking history, and family history in the recurrence group compared with the non-recurrence group. Univariate analysis suggested significant differences in homocysteine, folate, total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A/B (ApoA/B), 25-hydroxy vitamin D 3, and body mass index (BMI) between recurrence and non-recurrence groups ( P < 0.05). Multifactorial binary logistic regression analysis suggested that homocysteine ( OR = 0.869, 95% CI: 0.782 to 0.965, P = 0.009), triglycerides ( OR = 0.176, 95% CI: 0.060 to 0.519, P = 0.002), LDL ( OR = 0.256, 95% CI: 0.089 to 0.733, P = 0.011), 25-hydroxy vitamin D 3 ( OR = 0.937, 95% CI: 0.895 to 0.0.982, P = 0.006), and BMI ( OR = 1.319, 95% CI: 1.162 to 1.498, P < 0.01) were independent risk factors for UC recurrence. The predictive efficiency of individual risk factors in descending order was as following: LDL (AUC = 0.762, Youden's index [YI] = 0.42, cut-off value = 2.345), triglycerides (AUC = 0.718, YI = 0.361, cut-off value = 1), homocysteine (AUC = 0.666, YI = 0.283, cut-off value = 13.265). There were no statistically significant differences in gender, age, smoking history, and family history across the short-term, mid-term and long-term recurrence groups. There were significant differences in HDL and ApoA/B levels between the short-term and the long-term recurrence groups ( P < 0.05). Conclusions:Recurrence of the disease in UC patients results from the combined effects of multiple factors. The changes in homocysteine, triglycerides, LDL, 25-hydroxy vitamin D 3, and BMI in UC patients should be proactively monitored to prevent recurrence.

Short-chain fatty acids (SCFAs), as the main energy source for colonic epithelial cells, are becoming one of the important nutritional agents in the treatment of E1 (proctitis) and E2 (left-sided) subtypes of ulcerative colitis. To date, the therapeutic effects of topical SCFAs as primary or adjuvant induction therapy have been studied. However, the specific mechanism of action for SCFAs in the pathogenesis and progression of ulcerative colitis needs further investigation. High-quality prospective studies are required to verify current opinions on the selection of SCFA mixtures and the choice of topical or systemic routes of administration. In addition, SCFA is considered as a promising agent to prevent the occurrence and progression of ulcerative colitis-related colorectal cancer. Therefore, the optimal timing to integrate SCFAs into the treatment of ulcerative colitis represents another future research direction.

Background: In China, secondary cytoreductive surgery (SCR) has been widely used in ovarian cancer (OC) over the past two decades. Although Gynecologic Oncology Group-0213 trial did not show its overall survival benefit in first relapsed patients, the questions on patient selection and effect of subsequent targeting therapy are still open. The preliminary data from our pre-SOC1 phase II study showed that selected patients with second relapse who never received SCR at recurrence may still benefit from surgery. Moreover, poly(ADP-ribose) polymerase inhibitors (PARPi) maintenance now has been a standard care for platinum sensitive relapsed OC. To our knowledge, no published or ongoing trial is trying to answer the question if patient can benefit from a potentially complete resection combined with PARPi maintenance in OC patients with secondary recurrence. Methods SOC-3 is a multi-center, open, randomized, controlled, phase II trial of SCR followed by chemotherapy and niraparib maintenance vs chemotherapy and niraparib maintenance in patients with platinum-sensitive second relapsed OC who never received SCR at recurrence. To guarantee surgical quality, if the sites had no experience of participating in any OC-related surgical trials, the number of recurrent lesions evaluated by central-reviewed positron emission tomography–computed tomography image shouldn't be more than 3. Eligible patients are randomly assigned in a 1:1 ratio to receive either SCR followed by 6 cyclesof platinum-based chemotherapy and niraparib maintenance or 6 cycles of platinum-based chemotherapy and niraparib maintenance alone. Patients who undergo at least 4 cycles of chemotherapy and must be, in the opinion of the investigator, without disease progression, will be assigned niraparib maintenance. Major inclusion criteria are secondary relapsed OC with a platinum-free interval of no less than 6 months and a possibly complete resection. Major exclusion criteria are borderline tumors and non-epithelial ovarian malignancies, received debulking surgery at recurrence and impossible to complete resection. The sample size is 96 patients. Primary endpoint is 12-month non-progression rate.