Mesh erosion causes small bowel obstruction: a rare complication of laparoscopic inguinal hernia repair: case description and review of literature.

Transabdominal preperitoneal (TAPP) and total extraperitoneal (TEP) are the two types of laparoscopic repair of the inguinal hernia. The main advantages of laparoscopic repair, as compared to open repair, are a shorter hospital stay and a quicker recovery to normal activities. However, we cannot be overlooked or neglected the complication of laparoscopic inguinal hernia repair although it brings us lots of benefits. We report a case of small bowel obstruction caused by a displaced mesh used for the laparoscopic inguinal hernia repair and review of literature.

A Study on Mesoporous Silica Loaded With Novel Photosensitizers HCE6 and Oxaliplatin for the Treatment of Cholangiocarcinoma.

PURPOSE: Cholangiocarcinoma (CCA) is a malignant tumor with a high incidence. The therapeutic effect of conventional chemotherapy and radiotherapy is not obvious. Photodynamic therapy (PDT) is an ideal modality to fight cancer, and the nature of photosensitizer limits its application in clinical therapy. The aim of this study was to explore a novel mode of drug delivery for the intervention of bile duct cancer. METHODS: Oxaliplatin and photosensitizer HCE6 were loaded with mesoporous silica nanoparticles (MSNs) to synthesize Oxaliplatin/HCE6-MSNs (OH-MSNs); the structure of OH-MSNs was characterized by transmission electron microscopy (TEM) and dynamic light scattering (DLS), the drug release rate was detected by high performance liquid chromatography; the cellular activity, apoptosis level, and the expression levels of intracellular apoptosis and autophagy-related factors of OH-MSNs on cholangiocarcinoma cells were observed by CCK-8, flow cytometry, colony formation assay, and Western blot; the effects of OH-MSNs on cholangioma growth were observed by mouse tumor formation, immunohistochemistry, and tissue Tunel staining. RESULTS: The release of OH-MSNs to Oxaliplatin was enhanced under acidic conditions; compared with Oxaliplatin or O-MSNs, OH-MSNs showed more potent killing effects against cholangiocarcinoma cells (P<0.05), and exerted notably inhibitory effects on the activity of cholangiocarcinoma cells (P<0.05), promoted their apoptosis (P<0.05), and greatly facilitated the expression of pro-apoptotic factors and autophagic factors in cholangiocarcinoma cells (P<0.05), and markedly inhibited the expression of anti-apoptotic factors and autophagic inhibitory factors (P<0.05); moreover, OH-MSNs could significantly suppress the growth of mouse cholangiocarcinoma (P<0.05) and induce apoptosis of tumor cells compared with Oxaliplatin or O-MSNs (P<0.05). CONCLUSION: MSNs loading greatly increases the killing effect of Oxaliplatin on cholangiocarcinoma cells and upgrades the autophagic level of cholangiocarcinoma cells, while OH-MSNs synthesized by further loading HCE6 have a more apparent killing effect on cholangiocarcinoma cells.

Single-cell RNA-seq reveals a critical role of novel pro-inflammatory EndMT in mediating adverse remodeling in coronary artery-on-a-chip.

A three-dimensional microengineered human coronary artery-on-a-chip was developed for investigation of the mechanism by which low and oscillatory shear stress (OSS) induces pro-atherogenic changes. Single-cell RNA sequencing revealed that OSS induced distinct changes in endothelial cells (ECs) including pro-inflammatory endothelial-to-mesenchymal transition (EndMT). OSS promoted pro-inflammatory EndMT through the Notch1/p38 MAPK-NF-κB signaling axis. Moreover, OSS-induced EC phenotypic changes resulted in proliferation and extracellular matrix (ECM) protein up-regulation in smooth muscle cells (SMCs) through the RANTES-mediated paracrine mechanism. IL-37 suppressed OSS-induced pro-inflammatory EndMT and thereby abrogated SMC proliferation and ECM protein remodeling. Overall, this study provides insights into endothelial heterogeneity under atheroprone shear stress and identifies the mechanistic role of a novel EC subtype in promoting adverse vascular remodeling. Further, this study demonstrates that anti-inflammatory approach is capable of mitigating vascular pathobiology evoked by atheroprone shear stress.

[Effect of atractylodes macrocephalaon polysaccharides for reducing liver ischemia/reperfusion injury in rats after orthotopic liver autotransplantation].

OBJECTIVE: To explore the effect of atractylodes macrocephalaon polysaccharides (AMP) intervention for reducing liver ischemia/reperfusion (I/R) injury in rats after orthotopic liver autotransplantation. METHODS: SD rat I/R injured model was established by liver autotransplantation. SD rats were randomly divided into three groups: the model group, the AMP group and the sham-operated group. They were infused with saline, AMP and saline respectively after operation, and killed in batches at different time points (1, 6 and 24 h after operation), for determining blood levels of alanine aminotransferase (ALT), total bilirubin (TBIL), direct bilirubin (DBIL), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA), and detecting the expression of nuclear factor kappa-B (NF-kappaB) in liver tissue by immunohistochemical method. The pathological examination of liver was performed as well. RESULTS: Compared with the model group, in the AMP group at any time points after operation, the serum levels of ALT, AST, DBIL, TBIL and MDA were lower and of SOD were higher (P < 0.05); the elevated expression of NF-kappaB was weakened (P < 0.05), and the pathologic changes (liver congestion, swelling, hepatocyte necrosis and portal area inflammation cell infiltration) were lessened. CONCLUSION: AMP could reduce the post-transplantation liver I/R injury in rats, which might be associated with its effects on inhibiting NF-kappaB expression, intervening membrane destruction of liver cells by free oxygen radicals, suppressing enzyme, and alleviating morphological damages of liver.

Impact of hypoxic preconditioning on apoptosis and its possible mechanism in orthotopic liver autotransplantation in rats.

BACKGROUND: Hepatocyte apoptosis is a severe form of cell death after hepatic ischemia-reperfusion injury (HIRI), and its relief is an important issue in liver transplantation. Hypoxic preconditioning (HP) is considered to have protective effects on HIRI. This study was designed to explore the impact of HP on apoptosis and its possible mechanism during orthotopic liver autotransplantation. METHODS: A modified orthotopic liver autotransplantation model was used to simulate HIRI. Sprague-Dawley rats were randomly divided into normal control, autotransplantation (AT) and HP groups. The HP group was subjected to an 8% oxygen atmosphere for 90 minutes before surgery. At 1, 6 and 24 hours after surgery, the rats were killed and their liver tissue was sampled to assess the expression of Bcl-2 protein. The samples were subjected to blood chemistry study, morphological study under a light or transmission electron microscope, and quantitative study of mitochondria. RESULTS: The serum levels of ALT and AST in the HP group were lower than those in the AT group at 1, 6 and 24 hours after orthotopic liver autotransplantation (P<0.05). Bcl-2 protein expression was increased in the HP group at each measurement point (P<0.05). Light microscopy showed that hepatic injury in the AT group was much more severe than in the HP group. Hepatocytes in the AT group showed typical apoptosis signs under a transmission electron microscope. The ultrastructural appearance of hepatocytes in the HP group was much better than in the AT group, and the area, perimeter and diameter of the mitochondria were smaller in the HP group than in the AT group (P<0.05). CONCLUSIONS: Hepatocytes sense and respond to decreased tissue oxygenation. Stimulation by HP relieves apoptosis by upregulating expression of Bcl-2 protein and its protection of mitochondria after orthotopic liver autotransplantation.

Intestinal ischemic preconditioning reduces liver ischemia reperfusion injury in rats.

The aim of the current study was to investigate whether intestinal ischemic preconditioning (IP) reduces damage to the liver during hepatic ischemia reperfusion (IR). Sprague Dawley rats were used to model liver IR injury, and were divided into the sham operation group (SO), IR group and IP group. The results indicated that IR significantly increased Bax, caspase 3 and NF­κBp65 expression levels, with reduced expression of Bcl­2 compared with the IP group. Compared with the IR group, the levels of AST, ALT, MPO, MDA, TNF­α and IL­1 were significantly reduced in the IP group. Immunohistochemistry for Bcl­2 and Bax indicated that Bcl­2 expression in the IP group was significantly increased compared with the IR group. In addition, IP reduced Bax expression compared with the IR group. The average liver injury was worsened in the IR group and improved in the IP group, as indicated by the morphological evaluation of liver tissues. The present study suggested that IP may alleviates apoptosis, reduce the release of pro­inflammatory cytokines, ameloriate reductions in liver function and reduce liver tissue injury. To conclude, IP provided protection against hepatic IR injury.

miR-20b overexpression is predictive of poor prognosis in gastric cancer.

BACKGROUND: miR-20b has been shown to be aberrantly expressed in several tumor types. However, the clinical significance of miR-20b in the prognosis of patients with gastric cancer (GC) is poorly understood, and the exact role of miR-20b in GC remains unclear. MATERIALS AND METHODS: The expression of miR-20b was detected in 102 patients with GC by a SYBR Green assay and was compared with the expression in matched adjacent normal tissue specimens. The aim of the present study was to investigate the association of the expression of miR-20b with the clinicopathological characteristics and the overall survival of patients with GC as analyzed by Kaplan-Meier analysis and Cox proportional hazards regression models. RESULTS: Our results showed that miR-20b expression was upregulated in GC tissue compared with normal mucosa (P=0.00). Furthermore, miR-20b expression was positively correlated with advanced lymph node metastasis (P=0.041), tumor node metastasis stage (P=0.000), and deeper and distant metastasis (P=0.031). The overall survival rate of patients with GC was significantly lower in those whose tumors expressed high levels of miR-20b mRNA compared with those whose tumors expressed low levels of miR-20b mRNA (P=0.019). CONCLUSION: miR-20b may serve as a potential molecular marker for the prognosis of GC.

Clinicopathological Significance of MicroRNA-20b Expression in Hepatocellular Carcinoma and Regulation of HIF-1α and VEGF Effect on Cell Biological Behaviour.

miRNA-20b has been shown to be aberrantly expressed in several tumor types. However, the clinical significance of miRNA-20b in the prognosis of patients with hepatocellular carcinoma (HCC) is poorly understood, and the exact role of miRNA-20b in HCC remains unclear. The aim of the present study was to investigate the association of the expression of miR-20b with clinicopathological characteristics and overall survival of HCC patients analyzed by Kaplan-Meier analysis and Cox proportional hazards regression models. Meanwhile, the HIF-1α and VEGF targets of miR-20b have been confirmed. We found not only miR-20b regulation of HIF-1α and VEGF in normal but also regulation of miR-20b in hypoxia. This mechanism would help the tumor cells adapt to the different environments thus promoting the tumor invasion and development. The whole study suggests that miR-20b, HIF-1α, and VEGF serve as a potential therapeutic agent for hepatocellular carcinoma.

Protective effects of Atractylodes macrocephala polysaccharide on liver ischemia-reperfusion injury and its possible mechanism in rats.

Atractylodes macrocephala polysaccharide (AMP), a traditional Chinese medicine, is thought to have protective effects against liver injury. Therefore, this study was designed to explore the effects of AMP on hepatic ischemia-reperfusion injury (IRI) and elucidate the possible mechanisms. Ninety-six Sprague-Dawley rats were randomly divided into four groups with 24 rats per group: a normal control group, an IRI group, an AMP-treated group (0.4 g/kg/d) and a bifendate-treated group (100 mg/kg). Rats were treated with AMP or bifendate once daily for seven days by gastric gavage. The normal control group and the IRI model group received an equivalent volume of physiological saline. At 1, 6 and 24 h after surgery, the rats were killed and liver tissue samples were obtained to determine interleukin-1 (IL-1) expression by Western blotting and nuclear factor-κB (NF-κB) expression by immunohistochemistry. Liver morphology was assessed by microscopy and transmission electron microscopy. Blood samples were obtained to measure liver function (alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin). AMP significantly reduced the elevated expression of markers of liver dysfunction and the hepatic morphologic changes induced by hepatic IRI in rats. AMP also markedly inhibited IRI-induced lipid peroxidation and altered the activities of the antioxidant enzyme superoxide dismutase and malondialdehyde levels. Moreover, pretreatment with AMP suppressed the expression of interleukin-1ß and NF-kB in IRI-treated rats. These results suggest that AMP exerts protective and therapeutic effects against hepatic IRI in rats, which might be associated with its antioxidant properties and inhibition of NF-κB activation. More studies are needed to better understand the mechanisms underlying the protective effects of AMP on hepatic IRI.

[Experimental study on expanded polytetrafluoroethylene as wound covering].

OBJECTIVE: To assess the feasibility of a polymer material-expanded polytetrafluoroethylene (ePTFE) as wound covering. METHODS: Forty-five Sprague Dawley (SD) rats inflicted with open wound on the back were divided into 3 groups, each group 15 rats. Wounds in the autograft group were covered with autologous skin. Wounds in the allograft group were covered with skin from 15 Wistar rats (donor). Wounds in the experiment group were covered with ePTFE. Wound healing in each group was observed with naked eye. Tissue specimens collected on 3rd, 7th, and 14th post-operative day (POD) respectively were stained with HE and examined under light microscope. Macrophages, lymphocytes and fibroblasts were quantified. IL-2 and IFN-gamma levels in the infiltrating mononuclear cells were assessed by immunohistochemistry with expression of gray value. RESULTS: Wounds in rats of autograft group and experiment group healed well without redness, swelling or infection. Rejection was evident in the allograft group rats on 8th POD, including epidermis degeneration and focal necrosis in different degree, plus red swelling on wound edge. The numbers of macrophages, fibroblasts, lymphocytes in allograft group were significantly higher than those in autograft group and experiment group (P < 0.01). The average gray values of IL-2 and IFN-gamma of allograft group on 7th POD were 129 +/- 7 and 113.7 +/- 2.7, which were significantly lower than those in the experiment group (144 +/- 8, 137.3 +/- 1.9, respectively, P < 0.01) and allograft group (189 +/- 6, 180.3 +/- 3.7, respectively, P < 0.01). CONCLUSIONS: ePTFE will induce minimal inflammatory response and foreign body reaction. It is unlikely to cause side effect when applied to wound surface for a prolonged period. Thus, it is suitable to use ePTFE as wound surface covering.