Isolated traumatic gallbladder injury: A case report.

BACKGROUND: Isolated gallbladder injury (GI) (IGI) directly induced by abdominal trauma is rare. Symptoms, indications, and imaging examinations of IGI are frequently non-specific, posing tremendous diagnostic challenges, which are simple to overlook and may have severe implications. Improving doctors' understanding of gallbladder injury (GI) facilitates early detection and decreases the likelihood of severe consequences, including death. CASE SUMMARY: We report a case of IGI caused by blunt violence (after falling from three meters with the umbilicus as the stress point) and performed laparoscopic repair of the gallbladder rupture, which helps clinicians understand IGI and reduce the severe consequences of delayed diagnosis. Through extensive medical history and dynamic abdominal ultrasound evaluation, doctors can identify GI early and begin surgery, thereby decreasing the devastating repercussions of delayed diagnosis. CONCLUSION: This article aims to improve clinicians' understanding of IGI and propose a method for the diagnosis and treatment of GI.

Excellent Dark/Light Dual-Mode Photoresponsive Activities Based on g-C3N4/CMCh/PVA Nanocomposite Hydrogel Using Electron Beam Radiation Method.

Photocatalytic technology for inactivating bacteria in water has received much attention. In this study, we reported a dark-light dual-mode sterilized g-C3N4/chitosan/poly (vinyl alcohol) hydrogel (g-CP) prepared through freeze-thaw cycling and an in situ electron-beam radiation method. The structures and morphologies of g-CP were confirmed using Fourier infrared spectroscopy (FTIR), X-ray diffraction spectroscopy (XRD), X-ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM), solid ultraviolet diffuse reflectance spectroscopy (UV-vis DRS), and Brunauer-Emmett-Teller (BET). Photocatalytic degradation experiments demonstrated that 1 wt% g-CP degraded rhodamine B (RhB) up to 65.92% in 60 min. At the same time, g-CP had good antimicrobial abilities for Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) within 4 h. The shapes of g-CP were adjustable (such as bar, cylinder, and cube) and had good mechanical properties and biocompatibility. The tensile and compressive modulus of 2 wt% g-CP were 0.093 MPa and 1.61 MPa, respectively. The Cell Counting Kit-8 (CCK-8) test and Hoechst33342/PI double staining were used to prove that g-CP had good biocompatibility. It is expected to be applied to environmental sewage treatment and wound dressing in the future.

Intervention of Compound Xueshuantong Capsule on the incidence of heart failure in patients with acute myocardial infarction after PCI based on the combination of disease and syndrome: A multi-center, randomized, double-blind, controlled trial.

BACKGROUND: Heart failure (HF), manifested as a severe or end stage of various cardiac diseases, is characterized by increased incidence, mortality, re-hospitalization, and economic burden. Myocardial infarction (MI) is one of the most common and important causes of HF. Since 2005, acute MI (AMI)-associated mortality in China has been on the rise, and MI accounts for 23.1% of the causes of HF. Traditional Chinese medicine (TCM) has the unique advantages of controlling angina pectoris and HF symptoms, and improving patients' quality of life. Compound Xueshuantong Capsule (CXSTC), also named as Fufang Xueshuantong Capsule, has the effect of increasing cardiac output and protecting myocardial function. In this trial, we aim to investigate the efficacy and safety of CXSTC in the prophylactic treatment of post-infarction HF and attempt to provide a clinical evidence-based basis for the prophylactic treatment of HF after AMI using TCM. METHODS: This will be a multi-center, randomized, double-blind, placebo-parallel controlled trial. A total of 300 patients diagnosed with AMI and undergoing percutaneous coronary intervention within 12 hours of diagnosis will be randomized 1:1 into 2 groups: the control group that will be administered conventional Western medicine plus placebo and the trial group that will be administered XST along with the conventional Western medicine. The duration of treatment will be 3 months and the follow-up will be up to 6 months for both groups. The main efficacy indicator is the incidence of HF. The secondary efficacy indicators are cardiac function classification, 6-minute walk test score, TCM syndrome score, survival quality score, brain natriuretic peptide level, ultrasensitive C-reactive protein level, and cardiac ultrasound result. Data will be collected to analyze the underlying mechanisms by using IBM SPSS 23.0 software. DISCUSSION: By investigating the efficacy and safety of CXSTC, this study will provide a clinical evidence base for the use of TCM in the prophylactic treatment of post-infarction HF.

Comparative transcriptome analysis of differentially expressed genes and pathways in Procambarus clarkii (Louisiana crawfish) at different acute temperature stress.

Procambarus clarkii is an important economic species in China, and exhibit heat and cold tolerance in the main culture regions. To understand the mechanisms, we analyzed the hepatopancreas transcriptome of P. clarkii treated at 10 °C, 25 °C, and 30 °C, then 2092 DEGs and 6929 DEGs were found in 30 °C stress group and 10 °C stress group, respectively. KEGG pathway enrichment results showed that immune pathway is the main stress pathway for 10 °C treatment and metabolic pathway is the main response pathway for 30 °C treatment, which implies low temperature stress induces the damage of the immune system and increases the susceptibility of bacteria while the body response to high temperature stress through metabolic adjustment. In addition, flow cytometry proved that both high and low temperature stress caused different degrees of apoptosis of hemocytes, and dynamic transcription heat map analysis also identified the differential expression of HSPs family genes and apoptosis pathway genes under different heat stresses. This indicates that preventing damaged protein misfolding and accelerating cell apoptosis are necessary mechanisms for P. clarkii to cope with high and low temperature stress. Our research has deepened our understanding of the complex molecular mechanisms of P. clarkii in response to acute temperature stress, and provided a potential strategy for aquatic animals to relieve environmental duress.

A circular intronic RNA ciPVT1 delays endothelial cell senescence by regulating the miR-24-3p/CDK4/pRb axis.

Circular RNAs (circRNAs) have been established to be involved in numerous processes in the human genome, but their function in vascular aging remains largely unknown. In this study, we aimed to characterize and analyze the function of a circular intronic RNA, ciPVT1, in endothelial cell senescence. We observed significant downregulation of ciPVT1 in senescent endothelial cells. In proliferating endothelial cells, ciPVT1 knockdown induced a premature senescence-like phenotype, inhibited proliferation, and led to an impairment in angiogenesis. An in vivo angiogenic plug assay revealed that ciPVT1 silencing significantly inhibited endothelial tube formation and decreased hemoglobin content. Conversely, overexpression of ciPVT1 in old endothelial cells delayed senescence, promoted proliferation, and increased angiogenic activity. Mechanistic studies revealed that ciPVT1 can sponge miR-24-3p to upregulate the expression of CDK4, resulting in enhanced Rb phosphorylation. Moreover, enforced expression of ciPVT1 reversed the senescence induction effect of miR-24-3p in endothelial cells. In summary, the present study reveals a pivotal role for ciPVT1 in regulating endothelial cell senescence and may have important implications in the search of strategies to counteract the development of age-associated vascular pathologies.

circGNAQ, a circular RNA enriched in vascular endothelium, inhibits endothelial cell senescence and atherosclerosis progression.

Endothelial cell senescence is one of the most important causes of vascular dysfunction and atherosclerosis. Circular RNAs (circRNAs) are endogenous RNA molecules with covalently closed-loop structures, which have been reported to be abnormally expressed in many human diseases. However, the potential role of circRNAs in endothelial cell senescence and atherosclerosis remains largely unknown. Here, we compared the expression patterns of circRNAs in young and senescent human endothelial cells with RNA sequencing. Among the differentially expressed circRNAs, circGNAQ, a circRNA enriched in vascular endothelium, was significantly downregulated in senescent endothelial cells. circGNAQ silencing triggered endothelial cell senescence, as determined by a rise in senescence-associated ß-galactosidase activity, reduced cell proliferation, and suppressed angiogenesis; circGNAQ overexpression showed the opposite effects. Mechanistic studies revealed that circGNAQ acted as an endogenous miR-146a-5p sponge to increase the expression of its target gene PLK2 by decoying the miR-146a-5p, thereby delaying endothelial cell senescence. In vivo studies showed that circGNAQ overexpression in the endothelium inhibited endothelial cell senescence and atherosclerosis progression. These results suggest that circGNAQ plays critical roles in endothelial cell senescence and consequently the pathogenesis of atherosclerosis, implying that the management of circGNAQ provides a potential therapeutic approach for limiting the progression of atherosclerosis.

Circular RNAs as Competing Endogenous RNAs in Cardiovascular and Cerebrovascular Diseases: Molecular Mechanisms and Clinical Implications.

Circular RNAs (circRNAs) represent a novel class of widespread and diverse endogenous RNA molecules. This unusual class of RNA species is generated by a back-splicing event of exons or introns, resulting in a covalently closed circRNA molecule. Accumulating evidence indicates that circRNA plays an important role in the biological functions of a network of competing endogenous RNA (ceRNA). CircRNAs can competitively bind to miRNAs and abolish the suppressive effect of miRNAs on target RNAs, thus regulating gene expression at the posttranscriptional level. The role of circRNAs as ceRNAs in the pathogenesis of cardiovascular and cerebrovascular diseases (CVDs) has been recently reported and highlighted. Understanding the underlying molecular mechanism could aid the discovery of therapeutic targets or strategies against CVDs. Here, we review the progress in studying the role of circRNAs as ceRNAs in CVDs, with emphasis on the molecular mechanism, and discuss future directions and possible clinical implications.

Long non-coding RNA BX357664 inhibits gastric cancer progression by sponging miR-183a-3p to regulate the PTEN expression and PI3K/AKT pathway.

Lately, long non-coding RNA (lncRNA) is recognized as a key regulator of gastric cancer (GC) which has aroused great interest in the fields of medicine, toxicology, and functional food. Studies related to LncRNA expression microarray data indicate that BX357664 is down-regulated in GC specimens. However, the expression pattern and molecular mechanism of BX357664 in GC have not been studied so far. The purpose of this study was to investigate the expression of lncRNA BX357664 in GC and its function in GC cell lines. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the level of BX357664 in 50 pairs of cancer tissues and adjacent non-cancer tissues collected from GC patients. It was found that BX357664 level was lowered in cancer specimens than adjacent non-cancer tissues and correlated with tumor size and TNM stage. Also, we used cell counting kit 8 (CCK8), cell clone formation assay and transwell assay, which affirmed that up-regulation of BX357664 inhibited the proliferation, migration, and invasion of GC cells, but promoted apoptosis. In the dual-luciferase report analysis, BX357664 acted as a miR-183-3p ceRNA to target and regulate the expression of PTEN and affect the PI3K/AKT pathway. These results indicate that BX357664 can inhibit the proliferation and metastasis of GC through the miR-183-3p/PTEN/PI3K/AKT pathway, which may serve as potential targets for the treatment of GC in the future.

Transcriptome reveals the important role of metabolic imbalances, immune disorders and apoptosis in the treatment of Procambarus clarkii at super high temperature.

Temperature is an important environmental factor in the living environment of crustaceans. Changes in temperature can affect their normal growth and metabolism and even cause bacterial disease. Currently, the potential anti-reverse molecular reaction mechanism of crustaceans during high-temperature conditions has not yet been fully understood. Therefore, in this study, we characterised the transcriptome of Procambarus clarkii using RNA sequencing and performed a comparison between super-high-temperature treated samples and controls. After assembly and annotation, 81,097 unigenes with an average length of 069 bp and 358 differentially expressed genes (DEGs) were identified. Among these DEGs, 264 were differentially upregulated and 94 were differentially downregulated. To obtain comprehensive gene function information, we queried seven databases, namely, Nr, Nt, Pfam, KOG, Swiss-Prot, KEGG, and GO to annotate gene functions. Transcriptome analysis revealed that the identified DEGs have significant effects on immune-related pathways, including lysosomal and phagosomal pathways, and that super-high-temperature conditions can cause disease in P. clarkii. Some significantly downregulated genes are involved in oxidative phosphorylation and the PPAR signalling pathway; this suggests a metabolic imbalance in P. clarkia during extreme temperature conditions. In addition, elevated temperature changed the expression patterns of key apoptosis genes XIAP, CASP2, CASP2, CASP8, and CYTC, thereby confirming that high-temperature conditions caused immune disorders, metabolic imbalance, and, finally, triggered apoptosis. Our results provide a useful foundation for understanding the molecular mechanisms underlying the responses of P. clarkii during high-temperature conditions.

Risk Factors for Severe Complications After Laparoscopic Surgery for T3 or T4 Rectal Cancer for Chinese Patients: Experience from a Single Center.

BACKGROUND Patients with rectal cancer are usually at advanced stage with or beyond serosa invasion in China. Severe complications after laparoscopic rectal surgery leads to prolonged hospitalization and high medical cost. This study aimed to explore risk factors for severe complications after laparoscopic surgery of T3 or T4 rectal cancer. MATERIAL AND METHODS A total of 287 patients diagnosed with T3 or T4 rectal cancer were enrolled from the Department of Gastrointestinal Surgery of Anhui Provincial Hospital from February 2012 to February 2017. Univariate analysis and multivariable logistic regression model were used to analyze the risk factors for severe complications (Clavien-Dindo grade ≥III) after laparoscopic surgery. RESULTS Eighteen patients (6.25%) had severe complications; 15 patients were categorized as Clavien-Dindo grade III, and 3 patients were categorized as Clavien-Dindo grade IV. Univariate analysis showed that male gender, high preoperative white blood cells (WBC), diabetes mellitus, pulmonary dysfunction, and tumor distance from anus were associated with increased risk of severe complications after laparoscopic surgery for rectal cancer. Multivariate analysis showed that preoperative WBC ≥6.9×109/L (OR=5.54 (1.58-19.45), P=0.008), diabetes mellitus (OR=13.07 (3.31-51.67), P=0.000) and pulmonary dysfunction (OR=7.75 (1.69-35.63), P=0.008) were independent risk factors for postoperative severe complications. CONCLUSIONS Preoperative high white blood cells, diabetes mellitus and pulmonary dysfunction were independent risk factors for severe complications after laparoscopic surgery for T3 or T4 rectal cancer.

Enhanced Effect of IL-1ß-Activated Adipose-Derived MSCs (ADMSCs) on Repair of Intestinal Ischemia-Reperfusion Injury via COX-2-PGE2 Signaling.

Adipose-derived mesenchymal stem cells (ADMSCs) have been used for treating tissue injury, and preactivation enhances their therapeutic effect. This study is aimed at investigating the therapeutic effect of activated ADMSCs by IL-1ß on the intestinal ischaemia-reperfusion (IR) injury and exploring potential mechanisms. ADMSCs were pretreated with IL-1ß in vitro, and activation of ADMSCs was assessed by α-SMA and COX-2 expressions and secretary function. Activated ADMSCs was transplanted into IR-injured intestine in a mouse model, and therapeutic effect was evaluated. In addition, to explore underlying mechanisms, COX-2 expression was silenced to investigate its role in activated ADMSCs for treatment of intestinal IR injury. When ADMSCs were pretreated with 50 ng/ml IL-1ß for 24 hr, expressions of α-SMA and COX-2 were significantly upregulated, and secretions of PGE2, SDF-1, and VEGF were increased. When COX-2 was silenced, the effect of IL-1ß treatment was abolished. Activated ADMSCs with IL-1ß significantly suppressed inflammation and apoptosis and enhanced healing of intestinal IR injury in mice, and these effects were impaired by COX-2 silencing. The results of RNA sequencing suggested that compared with the IR injury group activated ADMSCs induced alterations in mRNA expression and suppressed the activation of the NF-κB-P65, MAPK-ERK1/2, and PI3K-AKT pathways induced by intestinal IR injury, whereas silencing COX-2 impaired the suppressive effect of activated ADMSCs on these pathway activations induced by IR injury. These data suggested that IL-1ß pretreatment enhanced the therapeutic effect of ADMSCs on intestinal IR injury repairing via activating ADMSC COX-2-PGE2 signaling axis and via suppressing the NF-κB-P65, MAPK-ERK1/2, and PI3K-AKT pathways in the intestinal IR-injured tissue.

[Effects of IL-1ß Pretreated Adipose Tissue-derived Mesenchymal Stem Cells on VEGF Secretion and Macrophage M2 Polarization].

OBJECTIVE: To investigate the effects of interleukin (IL)-1ß preteated adipose tissue-derived mesenchymal stem cells (ADMSCs) on vascular endothelial growth factor (VEGF) secretion and macrophages M2 polarization. METHODS: After IL-1ß pretreated ADMSC for 24 h, the expression of cyclooxygenase-2 (COX-2) was detected using Western blot, and the secretions of prostaglandin E2 (PGE2) and VEGF were measured by ELISA method. Conditioned media collected from ADMSCs was used for culturing PMA-U937 macrophages for 72 h, and the expressions of CD163 and IL-10 mRNAs were detected using qRT-PCR. After inhibition of COX-2 expression in ADMSCs by Lentivirus silencing, secretion of VEGF and CD163 and IL-10 mRNA expressions were detected. RESULTS: IL-1ß pretreating ADMSCs increased the expression level of COX-2, enhanced PGE2 and VEGF secretions (P<0.05). In addition, the mRNA levels of CD163 and IL-10 were upregulated when ADMSCs were pretreated by IL-1ß in PMA-U937 cells. After downregulation of COX-2 in ADMSCs, the secretion of VEGF was suppressed, and the mRNA levels of CD163 and IL-10 were also significantly down-regulated. CONCLUSION: IL-1ß pretreatment enhanced the secretion of PGE2 and VEGF, and induced macrophage M2 polarization, which depended on COX-2-PGE2 signal pathway.

[Expression and significance of tumor susceptibility gene 101 in hepatocellular carcinoma tissues].

AIM: To study the expression and clinical significance of tumor susceptibility gene 101 (TSG101) expression in hepatocellular carcinoma (HCC) tissues. METHODS: The expression of TSG101 in HCC and corresponding non-tumor tissues was detected by immunohistochemistry and Western blotting. Statistical analyses were conducted to test the relationships of TSG101 expression with clinical parameters such as age, gender, TNM stage, tumor metastasis, and so on. RESULTS: Immunohistochemistry and Western blotting showed that the expression of TSG101 in HCC was significantly higher than that in corresponding non-tumor tissues (P<0.05), and the expression rate was also higher in HCC (53/66, 80.3%) than in non-cancer tissues(18/66, 20.7%)(P<0.05). Higher TSG101 expression in HCC was significantly correlated with TNM stage (P<0.05) and metastasis (P<0.05), but not with age, gender and HBsAg (P>0.05). Multiple regression analysis indicated that TSG101 expression rate was significantly associated with TNM stage and metastasis (P<0.05), but not with gender, age and HBsAg (P>0.05). CONCLUSION: The expression of TSG101 in HCC is higher than that in corresponding non-cancer tissues and the expression level is closely correlated with TNM stage and metastasis of HCC.

1-(2,4-Difluoro-phen-yl)-2-(1H-1,2,4-triazol-1-yl)ethanol.

In the title compound, C(10)H(9)F(2)N(3)O, the dihedral angle between the rings is 22.90 (4)°. In the crystal, C-H⋯F and O-H⋯N hydrogen bonds link the mol-ecules into chains along [010].

1-(4-Fluoro-phen-yl)-2-(1H-imidazol-1-yl)ethanol.

In the title compound, C(11)H(11)FN(2)O, the dihedral angle between the mean planes of the two rings is 1.30 (4)°. In the crystal, O-H⋯N hydrogen bonds link the mol-ecules into chains along the b axis.

1-(4-Fluoro-phen-yl)-2-(1H-1,2,4-triazol-1-yl)ethanone hemihydrate.

In the title compound, C(10)H(8)FN(3)O·0.5H(2)O, the dihedral angle between the mean planes of the rings is 99.80 (4)°. The water mol-ecule lies on a twofold axis. Weak inter-molecular O-H⋯N and C-H⋯O hydrogen bonds link one water mol-ecule with four phenyl-ethanone mol-ecules, while inter-molecular C-H⋯O hydrogen bonds involving the ketone group link phenyl-ethanone mol-ecules into layers parallel to (100).

1-(4-Fluoro-phen-yl)-2-(1H-imidazol-1-yl)ethanone.

In the title compound, C(11)H(9)FN(2)O, the dihedral angle between the rings is 87.50 (4)°. In the crystal, inter-molecular C-H⋯N hydrogen bonds link the mol-ecules in a stacked arrangement along the c axis.

7-Fluoro-2-(prop-2-en-1-ylsulfan-yl)-3-(1H-1,2,4-triazol-1-yl)-4H-thio-chromen-4-one.

The asymmetric unit of the title compound, C(14)H(10)FN(3)OS(2), contains two independent mol-ecules which differ in the relative orientations of the triazole and allyl-sulfanyl groups with respect to the planar thio-chromen-4-one frameworks. The N-N-C-C torsion angles are 128.2 (5) and -120.9 (5)°, while the C-S-C-S torsion angles are -17.4 (4) and 16.4 (4)°. In the crystal, inter-molecular C-H⋯O and C-H⋯N hydrogen bonds link the mol-ecules in a stacked arrangement along the a axis.

Methyl 7-chloro-2-ethyl-sulfanyl-6-fluoro-4-oxo-4H-thio-chromene-3-carboxyl-ate.

In the title compound, C(13)H(10)ClFO(3)S(2), the two-ring system is essentially planar, the mean plane of the benzene ring being inclined at 6.0 (2)° to the plane of the remaining four atoms. The ethyl-sulfanyl group is almost coplanar with the two rings [dihedral angle = 6.4 (2)°], while the carboxyl-ate group is almost perpendicular to it [dihedral angle = 72.4 (2)°]. In the crystal structure, inter-molecular C-H⋯O and C-H⋯F hydrogen bonds link the mol-ecules in a stacked arrangement along the a axis.