Objective To explore the feasibility of prediction of subacute infarct lesion volumes by processing ADC maps based on ADC cut-off values in patients with acute stroke.Methods MRI was performed in 20 patients with clinically diagnosed acute infarct less than 6 h after stroke onset.The MRI included a DWI and conventional MRI.The follow-up MR examinations of all the patients were carried out within 4-7 days after admission.The brain tissue, which showed abnormal high intensity both in DWI at the baseline and FLAIR at the reexamination , was regarded as the area of the initial ischemia core.Graphic-penumbra was regarded as the difference between initial DWI and follow-up FLAIR.The ADC values of the ischemia core, graphic-penumbra and the contralateral normal brain tissue , the relative ADC (rADC) were measured.The rADC value of the graphic-penumbra was defined as the ADC cut-off values.GE medical system based on ADC cut-off values was also tested in these patients to obtain ADC maps.The lesion volumes, the abnormal area seen on the DWI , ADC maps and follow-up FLAIR, were also measured.rADC values in different areas were analyzed by paired Student t test.Relationship between baseline DWI , ADC map and follow-up FLAIR was analyzed using Spearman rank-order correlation test , and Kruskal-Wallis H test was used to compare the volumes among three groups.Results Absolute ADC and rADC values gradually increased from the core to the periphery of the ischemic lesion.The absolute ADC values statistically differed from those on the contralateral side for both ischemia core and graphic-penumbra.The rADC values were significantly decreased in the ischemia core ( 0.620 ±0.116 ) compared with the graphic-penumbra values (0.809 ±0.097;t =8.083,P <0.01).The lesion volume of follow-up FLAIR [16.3 (4.7, 29.0) cm3 ] correlated highly with both volume predicted with the ADC map [13.5 (4.8, 25.4) cm3] (r=0.967, P<0.01) and baseline DWI volume [11.0 (4.4,30.4) cm3] (r=0.950, P<0.01).There was no difference between the volume of DWI , ADC map and follow-up FLAIR(H=0.168, P>0.05).Conclusions Data shows the high feasibility of prediction of subacute infarct lesion volumes by processing ADC maps based on ADC cut-off values in patients with acute stroke , without intravenous contrast material, and it provides a new method for outcome prediction.

As a major cause of disability, depression is expected to become the second highest burden of disease worldwide by the year 2020. The shift of research in depression from monoamine hypothesis to the realm of neurotrophic hypothesis, neural plasticity hypothesis, and enhancing neurogenesis as an antidepressant-like agent brings about crucial insights to find novel mediator of antidepressant activity. Studies have shown that the neuropeptide VGF participates in the regulation of hippocampal neurogenesis and neuroplasticity and also plays an important role in the regulation of neuronal proliferation and survival, suggesting that the neuropeptide VGF may be a novel regulator in antidepressant treatment. The authors review the latest progress in the regulatory mechanisms of neuropeptide VGF on neurogenesis, neurotrophic and synaptic activity in depression. Further understanding of the role of neuropeptide VGF in depression can identify novel targets for pharmacological interventions.
Animals ; Antidepressive Agents ; Depression ; physiopathology ; Humans ; Neurogenesis ; Neuropeptides ; physiology ; Synaptic Transmission

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.

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.