A nomogram prediction model for postoperative seroma/hematoma in elderly subjects after TAPP.

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.

Erratum: [Corrigendum] miR‑590‑5p may regulate colorectal cancer cell viability and migration by targeting PDCD4.

[This corrects the article DOI: 10.3892/etm.2020.

Modified Frailty Index and Albumin-Fibrinogen Ratio Predicts Postoperative Seroma After Laparoscopic TAPP.

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).

miR-590-5p may regulate colorectal cancer cell viability and migration by targeting PDCD4.

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 and transfected with miR-590-5p inhibitor.

Blocking of the EGFR-STAT3 signaling pathway through afatinib treatment inhibited the intrahepatic cholangiocarcinoma.

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).

Silencing of survivin by YM155 induces apoptosis and growth arrest in hepatocellular carcinoma cells.

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.