Short chain fatty acids acetate and propionate have been demonstrated protective function in the intestinal mucosa. However, their impact on gastric mucosa has not yet been elucidated. The current study aimed to investigate the potential protective effects of acetate and propionate against ethanol-induced gastric mucosal lesion and the underlying mechanism in mice. ICR mice were orally treated with acetate and propionate, respectively, 30 min prior to the establishment of gastric mucosal injury model by challenge with absolute ethanol. The gastric samples were collected for the detection of oxidative, inflammatory and apoptotic related parameters. Acetate, but not propionate, attenuated the severity of gastric mucosal damage as evidenced by the gross changes of gastric mucosa, pathological aberrations. Acetate alleviated oxidative stress as shown by the increase in glutathione (GSH) content and superoxide dismutase (SOD) activities, and the decrease of malondialdehyde (MDA) level. The elevated concentrations of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and IL-6, and the activation of nuclear factor-kappaB (NF-κB) p65 by ethanol stimulation was also reduced by acetate. Moreover, the anti-inflammatory factors, IL-4, LXA4 and IL-10, were up-regulated in acetate treated group. With respect to gastric mucosal apoptosis, acetate suppressed caspase-3 activity and BAX expression in favor of cell survival. These favorable actions were maybe associated with up-regulation of the gastric MUC5AC, the key defense factor of gastric mucosal system. These findings accentuate the gastroprotective actions of acetate in ethanol-induced gastric injury which were mediated via concerted multiprolonged actions, including suppression of gastric oxidation, inflammation and apoptosis and promotion of MUC5AC expression.

The present study aimed to explore the expression and effects of microRNA (miR)-155 in synovial fibroblasts of patients with rheumatoid arthritis (RA). A total of 89 synovial tissues from RA patients and 49 control synovial tissues were collected, and the levels of miR-155 were measured by reverse transcription quantitative-PCR and western blotting. Fibroblast-like synoviocytes (FLS) were isolated from synovial tissues from the control group and were used to evaluate the roles of miR-155 and forkhead box protein O3a (FOXO3a). MTT assay was used to measure the proliferation of FLS. The expression of miR-155 in RA synovial tissues was significantly higher than that in the control group, but the expression of FOXO3a was significantly lower. In RA synovial tissues, miR-155 expression was negatively correlated with FOXO3a expression, but was positively correlated with the release of inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α). A dual-luciferase reporter system showed that miR-155 inhibited the expression of FOXO3a in FLS cells. miR-155 also promoted secretion of the inflammatory cytokines IL-1β, IL-6 and TNF-α by FLS and proliferation of these cells by targeting FOXO3a.

SummaryTumour necrosis factor (TNF)-a plays a critical role in the pathogenesis of T helper type 1-mediated colitis such as Crohn's disease. However, the roles of its two receptors in mediating pathology remain largely unknown. In this study, trinitrobenzene sulphonic acid (TNBS) was used to induce colitis in TNF-receptor single or double knock-out (DKO) BALB/c mice and in wildtype counterparts. TNF-R1 -/-mice had significantly less weight loss, reduced mortality, colon shortening and oedema, colon histological damage and lower levels of colon myeloperoxidase compared with wild-type (WT) BALB/c mice. A similar manifestation was also observed in TNF-R2-/-and TNF-R1 -/-TNF-R2-/-(TNF-R DKO) mice. Strikingly, systemic inflammatory response (including splenomegaly and monocyte expansion) was found in WT and TNF-R1 -/-mice after TNBS, instead of TNF-R2 -/-and TNF-R DKO mice. Attenuated pathology of colitis in TNF-R1-/-or TNF-R2 -/-mice correlated with lower amounts of interleukin (IL)-6, IL-1b, monocyte chemotactic protein (MCP)-1, IL-12p70 and interferon (IFN)-g production in the colons. Importantly, ablation of TNF-R1 or TNF-R2 reduced the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick endlabelling (TUNEL)-positive apoptotic epithelial cells in the affected colons compared with WT TNBS-instilled controls, which might be due to the heightened ratio of Bcl-2/Bax and reduced activity of nuclear factor (NF)-kB. These findings suggest that either TNF-R1 or TNF-R2 plays a pathogenic role in the pathology of colitis and TNF signalling via TNF-R1 or TNF-R2 alone is not sufficient for inducing mucosal damage.

BackgroundHepatocellular carcinoma (HCC) is the fifth most common malignancy in China, and China’s annual number of new cases accounts for about 45% of the world total. This research was aimed to study the expression of TBX3 protein in HCC and exploring its clinical significance.Material/MethodsWe collected tumor tissues and adjacent non-tumoral tissues of 174 patients with HCC undergoing surgical resection. The expression of TBX3 protein in different tissues and cell lines in vitro (LO2, HHL-5, MHC97-L, MHC97-H) was detected by immunohistochemistry or Western blotting, and the relationship between TBX3 expression and clinical data of patients with HCC was analyzed.ResultsThe expression of TBX3 protein in HCC was significantly correlated with histological grade, tumor size, cancer cell metastasis, hepatitis B surface antigen, and the expression of Ki-67 in tumor tissues (P<0.05), and it was positively correlated with serum AFP level (r=0.766, P<0.05). The expression of TBX3 increased with increased histological grade in HCC (P<0.05). Cox regression analysis showed that the expression of TBX3 protein in HCC was an independent risk factor for prognosis (OR=0.524, 95% CI=0.283–0.964). The 5-year survival rate of patients with HCC that highly expressed TBX3 protein was 20.83%, which was significantly lower than the 40.20% rate in patients with low expression (P<0.05).ConclusionsThe expression of TBX3 in HCC patients undergoing surgical resection is high, and its expression increases with the degree of tumor differentiation. It is related to the metastasis of tumor cells and is positively correlated with the serum level of AFP and may affect the survival time of HCC patients undergoing surgical resection.

Ultrasound biomicroscopy could be used for a noninvasive, accurate, and dynamic analysis of aortic atherosclerosis in LDL-R knockout mice.

Objectives To compare cardiac function and systolic dyssynchrony of fetuses not exposed to and those exposed to maternal autoimmune antibodies using two-dimensional speckle tracking echocardiography (2DSTE). Methods An observational study of 52 fetuses, 18 from mothers with autoimmune antibodies (anti-SSA/Ro60, anti-Ro52 or/and anti-SSB/La) and 34 from healthy mothers without antibodies, was conducted. Maternal baseline characteristics, fetoplacental Doppler parameters, and conventional echocardiographic data were prospectively collected. Systolic global and regional longitudinal strain of left and right ventricle (LV and RV) and the time to peak strain of regional myocardium were measured using 2DSTE. We also calculated the differences in time to peak strain between the LV free wall and RV free wall (two-chamber dyssynchrony, 2C-DYS) and the LV dyssynchrony between the septum and LV free wall (one-chamber dyssynchrony, 1C-DYS). Results There were no significant differences in conventional systolic and diastolic functional parameters for the LV and RV. No effect modification was demonstrated in a myocardial deformation analysis. However, 1C-DYS was significantly more prolonged in the maternal autoimmune disease group (19.50 [8.00 to 29.25] vs. 28.50 [13.50 to 39.25], P = 0.042). Conclusions LV systolic mechanical dyssynchrony in fetuses of mothers with autoimmune antibodies suggests in-utero subclinical damage of the cardiac conduction system. Key points• The left ventricular systolic dyssynchrony was significantly more prolonged in the maternal autoimmune disease (AD) fetuses.• Subclinical damage to the left ventricular conduction system of the fetal heart in maternal AD was observed.• Systolic and diastolic functional of the left and right ventricle were preserved in fetuses exposed to maternal autoimmune disease.

A 13-year-old girl was referred to our hospital with a history of chest tightness and shortness of breath after activity for 1 year.Systolic murmurs were audible on auscultation of the left sternal border second intercostal. Electrocardiography indicated a normal sinus rhythm. Transthoracic echocardiography (TTE) revealed a large cavity connected to the lateral wall of the right atrium (RA).The apical four-chamber view revealed this large cavity, measuring 33 × 38 mm and communicating with the RA via a broad neck, the diameter of which was 20 mm (Figure 1A, arrow). The anatomical position and structure of the tricuspid valve (TV) were normal. The right ventricle (RV) and TV annular were moderately compressed by the abnormal cavity, whereas tricuspid regurgitation was mild.No thrombus was observed within the abnormal chamber. Color Doppler flow imaging (CDFI) showed free bi-directional flow between the RA and large cavity ( Figure 1B-C, arrow). In addition, a 10-mm atrial septal defect (ASD) was noted, through which a leftto-right shunt signal was detected on CDFI. Other cardiac parameters were within the normal ranges. Thus, the patient was diagnosed

Supravalvular aortic stenosis is a type of congenital heart disease in which membrane-like stenosis rarely occurs. Herein, we present the case of a 52-year-old female patient who was admitted to the hospital because of palpitation. Two-dimensional echocardiography and real-time three-dimensional echocardiography showed supravalvular membrane-like stenosis with aortic insufficiency. The patient underwent surgery, with the ascending aortic fiber stenosis ring removed intraoperatively. She was followed up closely after discharge[If there is no word count limitation, please provide the implication of this case.