gastroscope-assisted-trans-trocar-gastrostomy-abdominal

Gastroscope-assisted Trans-Trocar Gastrostomy and Abdominal Exploration

Advanced endoscopic technologies have revolutionized gastrointestinal surgical procedures, transitioning from open or laparoscopic methods to endoscopic ...

Sun Yat-sen University

Colorectal cancer (CRC) is the third most common malignancy in developed countries, and its incidence rate has been continuously increasing in developing countries over the past few decades. Taurine-upregulated gene 1 (TUG1) plays an important role in signal transduction, regulation of cell morphology, migration, proliferation and apoptosis. The aim of the present study was to evaluate the role of TUG1 in CRC, and whether knockdown of TUG1 expression could affect cell proliferation, migration and invasion of CRC cell lines. Here, we reported that TUG1 was upregulated in CRC. Further experiments revealed that TUG1 knockdown significantly inhibited cell proliferation, migration and invasion of CRC in vitro. Above all, knockdown of TUG1 may represent a rational therapeutic strategy for CRC patients in future.

Long non-coding RNA TUG1 promotes colorectal cancer metastasis via EMT pathway.

To observe the safety and efficacy of biological patch (Biodesign Surgisis mesh, SIS) in hybrid technique for incisional herniorrhaphy.

[Observation of the efficacy of biological patch in hybrid technique for incisional herniorrhaphy: 5-year follow-up results from a single center].

Nowadays, biological matrix has become more widely applied than synthetic mesh for the surgical management of ventral hernia. Conventionally, such biodegradable matrix is commonly placed in an intraperitoneal or extraperitoneal position to reinforce the abdominal wall during surgery. Herein, we introduce our novel idea to deliver such biological material.

Deperitoneum biological mesh repair for abdominal wall hernia: a novel wound healing promotion idea.

Gastric cancer is a deadly disease. Some microRNAs are involved in tumor invasion and metastasis. Underexpression of miR-375 has been correlated with tumorigenesis, treatment resistance, and poor prognosis. In this study, we first analyzed the profiles and prognostic values of miR-375 expression in gastric cancer tissues from a public database, and the expression level of miR-375 in gastric cancer samples and gastric cancer cell lines was then analyzed by quantitative real- time polymerase chain reaction. Significant underexpression of miR-375 was seen in all the gastric cancer samples compared to paired paracarcinoma tissues, and the expression level of miR-375 in the gastric cancer cell lines was negatively associated with the cell migration ability. A Cell proliferation (CCK-8) assay was performed to examine cell viability. Overexpression of miR-375 suppressed the proliferation of gastric cancer cells. A Western blot analysis was carried out to test protein expression. Overexpression of miR-375 inhibited autophagy through the AKT/ mammalian target of rapamycin signaling pathway. MiR-375 regulated invasion and migration via AKT/ mammalian target of rapamycin pathway-mediated epithelial-to-mesenchymal transition. Wound healing and migration assays were used to determine the motility of gastric cancer cells. A gastric cancer xenograft nude mouse model was used for an in vivo efficacy evaluation. Overexpression of miR-375 significantly suppressed cell proliferation in the established gastric cancer xenograft nude mouse model. Our results demonstrate that increasing the expression level of miR-375 suppresses proliferation in vitro and in vivo, and they provide a mechanistic and applicable rationale for the future clinical evaluation of miR-375 in gastric cancer treatment. Our findings provide not only new information about the molecular mechanism of microRNAs in regulating invasion and migration in gastric cancer but also a theoretical principle for a potential targeted therapy for gastric cancer.

Deregulation of MicroRNA-375 Inhibits Proliferation and Migration in Gastric Cancer in Association With Autophagy-Mediated AKT/mTOR Signaling Pathways.

The shiitake mushroom (), known as Xiang-gu in China, has been an important component of Asian cuisine for hundreds of years. Although not easily digestible, there are few reports of them causing bowel obstruction. We present two cases of small bowel obstruction due to a shiitake mushroom requiring surgical intervention. Two patients who did not have any teeth and did not use dentures presented with intestinal bowel obstruction and were referred to the Emergency Department of our hospital after eating a meal including shiitake mushrooms without cutting. The first patient underwent an emergency laparotomy and a semental small bowel resection and the other underwent laparoscopic small bowel incision for removal of a foreign body. The causes of the small bowel obstruction for the two patients were uncut shiitake mushrooms in the small bowel. The two patients recovered uneventfully post-operatively.

Two cases of small bowel obstruction due to a shiitake mushroom.

The adipocyte precursors (APs) located in white adipose tissue (WAT) are functionally significant in adipose plasticity and browning. Modifying adipogenesis or WAT browning targeted on APs is a promising mechanism for anti-obesity drug. We herein explored the in vitro actions and mechanisms of glucose-dependent insulinotropic polypeptide (GIP), a gut-derived peptide, in human adipose-derived mesenchymal stem cells (hADSCs) isolated from omentum. The hADSCs were cotreated with 100 nM GIP with or without equimolar concentration of GIP3-42 (a GIP receptor antagonist), and subsequently examined in vitro. CCK-8, EdU incorporation, and flow cytometry assays were used to assess cellular proliferation. Annexin V FTIC/PI double stain, TUNEL staining, and Western blot were applied for apoptosis evaluation. Adipogenesis was reflected by Western blot, real-time PCR, Oil Red O staining, mitochondrial staining, and mitochondrial DNA analysis. Results showed that GIP promoted proliferation and inhibited apoptosis of hADSCs via pleiotropic effects. Besides, GIP facilitated de novo beige adipogenesis, by accelerating mitotic clonal expansion (MCE), upregulating core adipogenic regulators (C/EBPα and PPARγ), augmenting beige-related genes (UCP1, PGC1α, and PRDM16), increasing mitochondrial content and improving beige adipocyte functionalities. Above all, our study expands knowledge on the mechanisms of GIP modifying adipogenesis especially in inducing beige adipogenesis, and thus provides a theoretical support for clinical usage of GIP on obesity treatment.

Glucose-dependent insulinotropic polypeptide modifies adipose plasticity and promotes beige adipogenesis of human omental adipose-derived stem cells.

Bronchogenic cyst is congenital aberration of bronchopulmonary malformation, which is rarely encountered in the abdomen and retroperitoneum. We present a case report and literature review of retroperitoneal bronchogenic cyst.

Ectopic bronchogenic cyst in the retroperitoneal region: a case report and literature review of adult patients.

Peritoneal fibrosis is a common complication of peritoneal dialysis (PD) with a complicated pathogenesis and limited treatments. Parthenolide (PTL), a recognized nuclear factor-κB (NF-κB) inhibitor extracted from Tanacetum balsamita, has been widely used to treat various inflammatory diseases and has been proven to improve peritoneal fibrosis in PD mice by selectively inhibiting the phosphorylation of Smad2/3. Transforming growth factor-β1 (TGF-β1), via Smad-dependent signaling, has a pivotal role in promoting pathogenic of fibrosis. To investigate whether PTL can inhibit peritoneal fibrosis, we affected the interaction between NF-κB and the TGF-β/Smad2/3 pathway. Long dwell peritoneal dialysis fluid (PDF) and peritoneum tissues were collected from continuous ambulatory peritoneal dialysis (CAPD) patients. PTL was administered intragastrically into a PD mouse model by daily infusion of 4.25% dextrose-containing PDF. Treated HMrSV5 cells or rat peritoneal mesothelial cells (RPMCs) were treated with high glucose(138 mM) at the same concentration as 2.5% dextrose-containing PDF and PTL. PD-related peritoneal fibrosis samples indicated an increase in inflammation, and PTL decreased the levels of inflammatory cytokines (L-6, TNF-α, and MCP-1). PTL inhibited high glucose-induced mesothelial-to-mesenchymal transition (MMT), as indicated by a reduced expression of fibrosis markers (fibronectin, collagen I, and α-SMA) and increased expression of the epithelial marker E-cadherin. PTL also significantly decreased TGF-β1 expression and the phosphorylation of IκBα and NF-κBp65. The changes in the levels of TGF-β1 expression and p-p65 or p65 showed similar trends according to western blot, immunohistochemistry, and immunofluorescence assays in vitro and in vivo. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were used to confirm that PTL regulates the transcription of TGF-β1 induced by high glucose through NF-κBp65. In summary, PTL induces a therapeutic effect in peritoneal fibrosis by inhibiting inflammation via the NF-κB/ TGF-β/Smad signaling axis.

Weidong Feng

Division of Gastrointestinal Surgery Center,
The First Affiliated Hospital,
Center of Endoscopy,
Division of Gastrointestinal Surgery Center, The First Affiliated Hospital,
Center of Endoscopy, The First Affiliated Hospital

Sun Yat-sen University

Gastroscope-assisted Trans-Trocar Gastrostomy and Abdominal Exploration

Weidong Feng

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Division of Gastrointestinal Surgery Center,The First Affiliated Hospital,Center of Endoscopy,Division of Gastrointestinal Surgery Center, The First Affiliated Hospital,Center of Endoscopy, The First Affiliated Hospital

Sun Yat-sen University

Gastroscope-assisted Trans-Trocar Gastrostomy and Abdominal Exploration

Division of Gastrointestinal Surgery Center,
The First Affiliated Hospital,
Center of Endoscopy,
Division of Gastrointestinal Surgery Center, The First Affiliated Hospital,
Center of Endoscopy, The First Affiliated Hospital