WITHDRAWN: Reply to Dr Ma et al Mukhtar, Ahmed M, MD; Dabous, Hany, MD
Journal of cardiothoracic and vascular anesthesia,
2016
Journal Article
Recenzirano
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The emergency intervention for acute malignant left-sided colonic obstruction remains controversial. Conflicting reports exist regarding the efficacy and safety of endoscopic placement of ...self-expandable metallic stents (SEMS) vs. primary surgery. Most reports focus on SEMS insertion as a bridge to surgery.
An observational nonrandomized study at a single center in Cairo, Egypt included 65 high-risk patients (American Society of Anesthesiologists physical status classification ≥ III, age > 60 years) with acute malignant metastatic (stage IV) colonic obstruction. Twenty-nine patients underwent primary surgery (Hartmann's procedure, HP), and 35 patients underwent SEMS insertion.
All cases that underwent SEMS insertion were technically successful. The 2 procedures were comparable in clinical success rates but a statistically significant difference existed between them regarding the duration of postoperative hospital stay in the HP and SEMS group (7.7 ± 3.1 days vs. 3.5 ± 0.6 days, retrospectively; P < 0.001), the interval before regaining oral feeding (41.8 ± 26.8 hours vs. 27.6 ± 18.5 hours, retrospectively; P = 0.015), and the duration of intensive care unit (ICU) admission (5.0 ± 1.7 days vs. 1.5 ± 0.7 days, retrospectively; P = 0.035). Six patients (20.7%) in the HP group and 2 patients (5.7%) in the SEMS group required postoperative ICU admission.
SEMS placement provides comparable efficacy and safety to HP in managing acute malignant obstruction of the rectosigmoid region in high-risk individuals, with faster recovery and less hospital and ICU admission time.
The emergency intervention for acute malignant left-sided colonic obstruction remains controversial. Conflicting reports exist regarding the efficacy and safety of endoscopic placement of ...self-expandable metallic stents (SEMS) versus primary surgery. Most reports focus on SEMS insertion as a bridge to surgery.
An observational non-randomized study at a single center in Cairo, Egypt included 65 high-risk patients (American Society of Anesthesiologists Preoperative Score: III or more, and age over 60 years) with acute malignant (Stage IV) colonic obstruction. Twenty-nine patients underwent primary surgery (Hartmann's procedure, HP), and 35 patients underwent SEMS insertion.
All cases that underwent SEMS insertion were technically successful. The two procedures were comparable in clinical success rates but a statistically significant difference existed between them regarding the duration of postoperative hospital stay (7.7 ± 3.1 days in the HP group and 3.5 ± 0.6 days in the SEMS group, p < 0.0001), the interval before regaining oral feeding (41.8 ± 26.8 hours in the HP group and 27.6 ± 18.5 hours in the SEMS group, p = 0.0151), and the duration of ICU admission (5 ± 1.7 days in the HP group and 1.5 ± 0.7 days in the SEMS group, p = 0.0348). Six patients (20.7%) in the HP group and 2 patients (5.7%) in the SEMS group required postoperative ICU admission.
SEMS placement provides comparable efficacy and safety to HP in managing acute malignant obstruction of the rectosigmoid region in high-risk individuals, with faster recovery and less hospital and ICU admission time.
Objective To evaluate the effect of intraoperative infusion with terlipressin on the incidence of acute kidney injury (AKI) after living donor liver transplantation (LDLT). Design Retrospective ...case-controlled study. Setting Government hospital. Participants The medical records of 303 patients who underwent LDLT were reviewed retrospectively. Interventions Patients were divided into 2 groups on the basis of intraoperative administration of terlipressin. The primary outcome was AKI, as defined by the Acute Kidney Injury Network criteria. Secondary outcomes included the requirement for postoperative dialysis and in-hospital mortality. Measurements and Main Results The incidence of AKI was 38% (n = 115); AKI occurred in 24 (24.2%) patients who received terlipressin versus 91 (44.6%) in the control group (p = 0.001). The incidence of postoperative dialysis was 9.2% (n = 28). Postoperative dialysis was needed by 8 patients (8.1%) in the terlipressin group versus 20 patients (9.8%) in the control group (p = 0.62). Multivariate logistic regression analysis indicated that terlipressin protected against AKI (odds ratio OR, 0.4; 95% confidence interval CI, 0.2-0.8; p = 0.013) but not the need for dialysis (OR, 0.7; 95% CI, 0.2-2.2; p = 0.53) or the in-hospital mortality (OR, 1.1; 95% CI, 0.5-2.3; p = 0.7). Adjustment, using the propensity score, did not alter the association between the use of terlipressin and AKI reduction (OR, 0.46; 95% CI, 0.22-0.89; p = 0.03). Conclusion These results suggested that intraoperative terlipressin therapy is associated with significant reductions in the risk of AKI in LDLT patients.
The antiviral response against influenza A virus (IAV) infection includes the induction of the interferon (IFN) signaling pathway, including activation of the STATs protein family. Subsequently, ...antiviral myxovirus resistance (MxA) protein and other interferon-stimulated genes control virus replication; however, the molecular interaction of viral-mediated IFN signaling needs more investigation. Host microRNAs (miRNAs) are small non-coding molecules that posttranscriptionally regulate gene expression. Here, we sought to investigate the possible involvement of miR-141 in IAV-mediated IFN signaling. Accordingly, the microarray analysis of A549 cells transfected with precursor miR-141 (pre-miR-141) was used to capture the potentially regulated genes in response to miR-141 overexpression independent of IAV infection. The downregulation of targeted genes by miR-141, in addition to viral gene expression, was investigated by quantitative real-time PCR, western blot analysis, and flow cytometric assay. Our findings showed a significant upregulation of miR-141 in infected A549 cells with different strains of IAV. Notably, IAV replication was firmly interrupted in cells transfected with the miR-141 inhibitor. While its replication significantly increased in cells transfected with pre-miR-141 confirming the crucial role of miRNA-141 in supporting virus replication. Interestingly, the microarray data of miR-141 transduced A549 cells showed many downregulated genes, including MxA, STAT3, IFI27, and LAMP3. The expression profile of MxA and STAT3 was significantly depleted in infected cells transfected with the pre-miR-141, while their expression was restored in infected cells transfected with the miR-141 inhibitor. Unlike interleukin 6 (IL-6), the production of IFN-beta markedly decreased in infected cells that transfected with pre-miR-141, while it significantly elevated in infected cells transfected with miR-141 inhibitor. These data provide evidence for the crucial role of miR-141 in regulating the antiviral gene expression induced by IFN and IL-6 signaling during IAV infection to ensure virus replication.
Abstract Liver cancer is one of the most pivotal global health problems, leading hepatocellular carcinoma (HCC) with a significant increase in cases worldwide. The role of non-coding-RNA in cancer ...proliferation and carcinogenesis has attracted much attention in the last decade; however, microRNAs (miRNAs), as non-coding RNA, are considered master mediators in various cancer progressions. Yet the role of miR-141 as a modulator for specific cellular processes in liver cancer cell proliferation is still unclear. This study identified the role of miR-141 and its potential functions in liver carcinogenesis. The level of miR-141 in HepG2 and HuH7 cells was assessed using quantitative real-time PCR (qRT-PCR) and compared with its expression in normal hepatocytes. A new miR-141 construct has been performed in a CMV promoter vector tagged with GFP. Using microarray analysis, we identified the potentially regulated genes by miR-141 in transfected HepG2 cells. The protein profile of the kallikrein-related peptidase 10 (KLK10) and tumor necrosis factor TNFSF-15 was investigated in HepG2 cells transfected with either an inhibitor, antagonist miR-141, or miR-141 overexpression vector using immunoblotting and flow cytometry assay. Finally, ELISA assay has been used to monitor the produced inflammatory cytokines from transfected HepG2 cells. Our findings showed that t he expression of miR-141 significantly increased in HepG2 and HuH7 cells compared to the normal hepatocytes. Transfection of HepG2 cells with an inhibitor, antagonist miR-141, showed a significant reduction of HepG2 cell viability, unlike the transfection of miR-141 overexpression vector. The microarray data of HepG2 cells overexpressed miR-141 provided a hundred downregulated genes, including KLK10 and TNFSF-15. Furthermore, the expression profile of KLK10 and TNFSF-15 markedly depleted in HepG2 cells transfected with miR-141 overexpression accompanied by a decreasing level of interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α), indicating the role of miR-141 in HepG2 cell proliferation and programmed cell death. Interestingly, the experimental rats with liver cancer induced by Diethylnitrosamine injection further confirmed the upregulation of miR-141 level, IL-10, and TNF-α and the disturbance in KLK10 and TNFSF-15 gene expression compared with their expression in normal rats. The in-silico online tools, IntaRNA and miRWalk were used to confirm the direct interaction and potential binding sites between miR-141 and identified genes. Thus, the seeding regions of potential targeted sequences was cloned upstream of luciferase reporter gene in pGL3 control vector. Interestingly, the luciferase activities of constructed vectors were significantly decreased in HepG2 cells pre-transfected with miR-141 overexpression vector, while increasing in cells pre-transfected with miR-141 specific inhibitor. In summary, these data suggest the crucial role of miR-141 in liver cancer development via targeting KLK10 and TNFSF-15 and provide miR-141 as an attractive candidate in liver cancer treatment and protection.
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