Connexin 43 (Cx43), known to be the main protein building blocks of gap junctions and hemichannels in mammalian heart, plays an important role in cardiocytes proliferation. Gap junctional intercellular communication has been suggested to be necessary for cellular proliferation and differentiation. However, the effect of Cx43 hemichannel on cardiocytes proliferation and the mechanism remain unclear. In this study, rat heart cell line H9c2 was used. The Cx43 location, the proliferation rate and hemichannel activity of H9c2 cells and Wnt-3a
Purpose
This study aimed to explore risk factors of postoperative complications for adult patients with incarcerated groin hernia (IGH).
Methods
From January 2010 to December 2017, consecutive patients undergoing emergency hernia repair for IGH in our center were retrospectively reviewed. Postoperative complications, such as surgical site infection, seroma, hernia recurrence and mortality, were investigated, with risk factors for such complications analyzed using univariate and multivariate regressions.
Results
Sixty-four patients were included, with 51 males and 13 females (mean age 65.1, range 25–98 years). Ten patients (15.6%) underwent resection of necrotic bowel and anastomosis. 43 patients (67.2%) received open tension-free herniorrhaphy with polypropylene mesh, whereas the rest (32.8%) received herniorrhaphy without mesh. The overall postoperative complication rate was 40.6% (26/64), with an incisional complication rate of 31.2% (20/64) and an infection rate of 6.2% (4/64). At a median follow-up of 32 months, hernia recurrence and mortality were recorded in five cases each (7.8%). Mesh repair was associated with decreased recurrence rate compared with non-mesh repair (2.3% vs. 19.0%,
p
= 0.019). Diabetes mellitus (OR 8.611, 95%CI 1.292–57.405;
p
= 0.026) was an independent risk factor of postoperative complications, together with chronic obstructive pulmonary disease (COPD; OR 14.365, 95%CI 1.652–127.767,
p
= 0.016), intestinal necrosis (OR 14.260, 95%CI 1.079–188.460,
p
= 0.044), and general anesthesia (OR 14.543, 95%CI 1.682–125.711,
p
= 0.015) as risk for incisional complications after surgery.
Conclusions
Diabetes mellitus was an independent risk factor of postoperative complications for IGH, along with COPD, intestinal necrosis and general anesthesia associated with incisional complications. The use of polypropylene mesh did not increase infection or recurrence rate in this cohort.
Circular RNA (circRNA), a type of RNA that is widely expressed in mammalian cells, is considered to be essential in tumorigenesis. CircRNA can regulate target gene expression by interacting with the corresponding microRNA (miRNA). Our preliminary results showed that the expression levels of 1,817 circRNAs were significantly different in colon cancer tissue compared with paracancerous tissue, of which 1,236 were upregulated and 581 were downregulated. By using RT-PCR, we confirmed that the expression of hsa_circ_0007843, hsa_circ_0010575, hsa_circ_0007331, and hsa_circ_0001615 was significantly higher in colon cancer tissue than in normal colonic tissue; however, the expression levels of hsa_circ_0014879 and hsa_circRNA_401801 were not significantly different between normal and neoplastic colonic tissue. Among the circRNAs that were confirmed to be upregulated in colon cancer tissue, hsa_circ_0007843 was also found to be highly expressed in colon cancer SW480 cells. Overexpression of hsa_circ_0007843 promoted the invasion and migration of SW480 cells, whereas its downregulation suppressed their invasion and migration. Overexpression of hsa_circ_0007843 promoted tumor growth, whereas its downregulation inhibited tumor growth. We found that hsa_circ_0007843 interacted with miR-518c-5p and suppressed its expression, and miR-518c-5p interacted with matrix metallopeptidase 2 (MMP2) and promoted its expression and translation. Taken together, this study demonstrated that hsa_circ_0007843 acted as an miRNA sponge to regulate MMP2 expression by removing the inhibitory effect of miR-518c-5p on MMP2 gene translation, which further affected the invasive capability of SW480 cells.
Edited by Robert BaroukiKeywords: SREBP-1c promoter FoxO1 LXRa Insulin a b s t r a c t Recent studies have demonstrated that FoxO1 modulates the expression of SREBP-1c, but the exact mechanism remains unknown. Our results demonstrate that FoxO1 suppresses the SREBP-1c promoter transcriptional activity in HepG2 cells. This repression was independent of FoxO1 binding to the SREBP-1c promoter, but LXR responsive elements (LXREs) were crucial to this phenomenon. Moreover, FoxO1 also strongly inhibited the LXRa-mediated elevated transcription by SREBP-1c promoter. Electrophoretic mobility shift assay and chromatin immuno-precipitation further suggested the ability of FoxO1 to inhibit LXRa binding with the LXRE in the SREBP-c promoter. FoxO1-mediated suppression of SREBP-1c promoter activity could be partially alleviated by insulin.
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