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BACKGROUND: Formation of seroma/hematoma is one of the most common postoperative complications following laparoscopic inguinal hernia repair. This study aimed to identify risk factors associated with seroma/hematoma and construct a prediction model. METHODS: Elderly subjects undergoing laparoscopic Transabdominal preperitoneal Patch Plasty (TAPP) were included in this study. The observation endpoint was set as the occurrence of seroma/hematoma within 3 months after TAPP surgery. Independent risk factors were identified through preliminary univariate screening and binary logistic regression analysis. These risk factors were then used to construct a nomogram predictive model using R software. RESULTS: A total of 330 patients were included in the analysis, of which 51 developed seroma/hematoma, resulting in an incidence rate of 15.5%. Obesity (OR: 3.54, 95%CI: 1.45-8.66, P = 0.006), antithrombotic drug use (OR: 2.73, 95%CI: 1.06-7.03, P = 0.037), C-reactive protein (CRP) ≥ 8 (OR: 2.72, 95%CI: 1.04-7.10, P = 0.041, albumin/fibrinogen ratio (AFR) < 7.85 (OR: 2.99, 95%CI: 1.28-7.00, P = 0.012), and lymphocyte/monocyte ratio (LMR) < 4.05 (OR: 12.62, 95%CI: 5.69-28.01, P < 0.001) were five independent risk factors for seroma/hematoma. The nomogram model has well predictive value for seroma/hematoma, with an AUC of 0.879. CONCLUSIONS: The nomogram model based on obesity, antithrombotic drug, CRP, AFR, and LMR has a proved good predictive value and it has potential in clinical practice.

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[This corrects the article DOI: 10.3892/etm.2020.9183.].

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Background: Postoperative seroma is the most common minor complication after inguinal hernia repair surgery and can have negative consequences. The objective of this study was to identify potential risk factors for postoperative seroma. Methods: This study consecutively included 354 elderly patients with inguinal hernia who underwent laparoscopic Transabdominal preperitoneal Patch Plasty (TAPP). Seroma diagnosis was conducted by the same experienced surgeon based on the physical examinations combined with ultrasound. Risk factors for seroma were identified through univariate analysis and subsequently included in the binary multivariate logistic regression model. Results: A total of 40 patients experienced postoperative complications of seroma, with an incidence rate of 11.3% (40/354). The binary logistic regression analysis revealed that obesity (OR: 2.98, 95% CI: 1.20-7.41, P = 0.018), disease duration ≥ 4.5 years (OR: 4.88, 95% CI: 2.14-11.18, P < 0.001), albumin-fibrinogen ratio (AFR) level < 9.25 (OR: 6.13, 95% CI: 2.00-18.76, P = 0.001), and modified frailty index (mFI) score ≥ 0.225 (OR: 6.38, 95% CI: 2.69-15.10, P < 0.001) were four independent risk factors for postoperative seroma. Conclusion: Obesity, prolonged disease duration, decreased AFR level, and increased mFI score independently predict postoperative seroma after laparoscopic TAPP.

Asunto(s)

Fragilidad , Hernia Inguinal , Laparoscopía , Anciano , Humanos , Fibrinógeno , Seroma/diagnóstico por imagen , Seroma/epidemiología , Seroma/etiología , Obesidad/cirugía , Albúminas , Laparoscopía/efectos adversos , Complicaciones Posoperatorias/epidemiología , Complicaciones Posoperatorias/etiología

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Recent studies have revealed that microRNAs (miRs) are involved in the pathogenesis of colorectal cancer (CRC); however, the roles of miR-590-5p in CRC are not completely understood. Therefore, the present study investigated the expression of miR-590-5p and programmed cell death 4 (PDCD4) in CRC tissues and healthy adjacent tissues via reverse transcription-quantitative PCR. Furthermore, human CRC cells were cultured in vitro and transfected with miR-590-5p inhibitor. CRC cell viability, migration and invasion were evaluated by conducting MTT, wound healing and Transwell assays, respectively. Additionally, the relative expression of PDCD4 and phosphorylated-Smad2/3 was analyzed via western blotting. miR-590-5p was significantly upregulated and PDCD4 was significantly downregulated in CRC tissues compared with healthy adjacent tissues. Moreover, the results indicated that miR-590-5p knockdown inhibited cell viability and migration by altering the expression of PDCD4, transforming growth factor-ß and phosphorylated-Smad2/3. PDCD4 was identified as a direct target of miR-590-5p. In conclusion, the results of the present study suggested that miR-590-5p may regulate CRC cell viability and migration, indicating that miR-590-5p may serve as a potential therapeutic target for CRC.

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Epidermal growth factor receptor (EGFR) and downstream signal transducer and activator of transcription 3 (STAT3) signaling have been extensively implicated in various human neoplasms. Recently, a novel EGFR inhibitor, known as afatinib, has exhibited broad antitumor activities in a variety of tumors. Therefore, the present study attempted to investigate the impact of this agent on intrahepatic cholangiocarcinoma (ICC). Initially, immunohistochemical assays were performed on 15 human ICC specimens and their adjacent tissues in order to assess the protein levels of phosphorylated EGFR (pEGFR) and pSTAT3. Subsequently, the human ICC cell lines JCK and OZ were exposed to different doses of afatinib, and then cell viability and apoptosis were determined by MTT assay and flow cytometry, respectively. Furthermore, immunoblotting was applied to detect any variations in the phosphorylated protein levels of EGFR and STAT3 in afatinib-treated ICC cells. The results of the current study demonstrated that ICC specimens had evidently increased pEGFR and pSTAT3 protein levels as compared with the adjacent noncancerous tissues. Further in vitro experiments indicated that afatinib evidently blocked ICC cell growth and induced cell apoptosis. At the protein level, pEGFR and pSTAT3 were evidently attenuated by afatinib-administration. In conclusion, the present study clearly determined that afatinib exerts an antitumor effect on ICC cells by silencing the EGFR-STAT3 signaling pathway. This novel agent deserves further investigation as a potential therapeutic strategy for ICC.

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Survivin overactivation is a frequent event in human hepatocellular carcinoma (HCC), due to its function in the induction of hepatocyte proliferation and apoptotic dysfunction. Recently, a novel survivin inhibitor named YM155, has demonstrated broad antitumor effects against various malignant tumors. Therefore, the present study aimed to explore how this agent may impact on HCC and elucidate its underlying mechanism of action. Immunohistochemical analysis was performed on 8 specimens of human HCC, to assess the protein expression of survivin and phosphorylated retinoblastoma tumor suppressor (p-Rb). In addition, in vitro, HepG2 and Huh7 human HCC cell lines were exposed to 100 µM YM155 for up to 72 h and the cell viability was subsequently determined using MTT assay. Furthermore, the apoptotic status of YM155-treated HCC cells was investigated by flow cytometry, and the protein levels of survivin, procaspase-3 and p-Rb in YM155-treated HCC cells were assessed by immunoblotting analysis. The results demonstrated that HCC specimens expressed high levels of survivin and p-Rb protein compared with those of adjacent noncancerous liver tissues. In vitro, YM155 significantly induced HCC cell apoptosis and growth arrest. At the protein level, YM155 markedly inhibited survivin and p-Rb expression, and elevated procaspase-3. YM155 demonstrated significant antitumor effects on HCC cells in the present study. These effects were associated with its anti-proliferative and apoptosis-induction activities. YM155 requires further investigation as a novel agent for potential use as a therapeutic strategy for the treatment of HCC.