Petersen's hernia after gastric cancer surgery: Unravelling clinical characteristics and optimal management approaches.

INTRODUCTION: Petersen's hernia is a rare and serious complication that can occur after radical gastrectomy and digestive tract reconstruction for gastric cancer. This article summarises the symptoms, diagnosis and treatment of Petersen's hernia after surgery for gastric cancer. PATIENTS AND METHODS: A retrospective analysis was conducted on 11 male patients who were diagnosed with Petersen's hernia and underwent surgical treatment at our hospital from January 2020 to December 2022. Their clinical manifestations, perioperative conditions and follow-up after treatment were collected. RESULTS: The median age was 58.5 years (range: 45-73), and the median time since gastrectomy was 24 months (range: 4-125). Open distal gastrectomy (45.5%) and open total gastrectomy (27.3%) were the most common procedures. Roux-en-Y (81.8%) was the predominant anastomosis method. All patients underwent emergency surgery within a median time of 30 h (range: 4-45). Intestine necrosis occurred in 36.4% of cases, with a perioperative death rate of 27.3%. CONCLUSION: Petersen's hernia after gastric cancer surgery can quickly lead to necrotising intestinal obstruction and poor prognosis. Enhanced abdominal computed tomography should be performed as soon as possible, and early exploratory laparotomy should be done to avoid intestinal necrosis. Routine closure of the mesenteric defect after gastric cancer resection can prevent the occurrence of Petersen's hernia. This article highlights the need for increased awareness and preventive measures to minimise the occurrence of Petersen's hernia in gastric cancer patients. It emphasises the importance of early detection and appropriate management strategies for improved patient outcomes.

Preparation, characterization, and bioavailability evaluation of antioxidant phosvitin peptide-ferrous complex.

BACKGROUND: Iron deficiency anemia (IDA) is one of the commonest global nutritional deficiency diseases, and the low bioavailability of iron is a key contributing factor. The peptide-iron complex could be used as a novel iron supplement to improve iron bioavailability. RESULTS: In this study, antioxidant low molecular weight (<3 kDa) phosvitin peptide (named PP-4) was separated to prepare a phosvitin peptide-ferrous complex (named PP-4-Fe); then the structural conformation of PP-4-Fe was characterized and its bioavailability by in vitro digestion was evaluated. The results showed that PP-4 had good ferrous-binding activity with 96.14 ± 2.86 µg Fe2+ mg-1 , and had a strong antioxidant effect with 995.61 ± 79.75 µmol TE mg-1 in 2,2'-azinobis'3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 62.3 ± 3.95 µmol FeSO4 mg-1 in ferric ion reducing antioxidant power (FRAP). After ferrous binding, the FRAP activity of PP-4-Fe, enhanced by 1.8 times, formed a more ordered structure with an increase in α-helix and decrease in γ-random coil. The ferrous binding sites of PP-4 involved were the amino, carboxyl, imidazole, and phosphate groups. The PP-4-Fe complex displayed excellent gastrointestinal stability and antioxidant effects during digestion. The iron dialysis percentage of PP-4-Fe was 74.59% ± 0.68%, and increased to 81.10% ± 0.89% with the addition of 0.25 times vitamin C (VC). This indicated that PP-4-Fe displayed excellent bioavailability and VC in sufficient quantities had a synergistic effect on improving bioavailability. CONCLUSIONS: This study demonstrated that antioxidant phosvitin peptide was an efficient delivery system to protect ferrous ions and suggested that the phosvitin peptide-ferrous complex has strong potential as a ferrous supplement. © 2023 Society of Chemical Industry.

Feasibility of preservation of superior rectal artery plus dissection of lymph nodes around inferior mesenteric artery in laparoscopic resection for sigmoid colon cancer.

Background: Limited data are available about superior rectal artery (SRA) preservation in laparoscopic resection for sigmoid colon cancer (SCC). This study aimed to evaluate the short-term and long-term efficacies of SRA preservation in laparoscopic radical resection for SCC. Methods: We retrospectively analyzed 207 patients with SCC who underwent laparoscopic radical resection for SCC from January 2017 to June 2021. A total of 84 patients received lymph node clearance around the inferior mesenteric artery (IMA) root (D3 lymph node dissection) with preservation of SRA (SRA preservation group), and 123 patients received high ligation of the IMA (control group). The clinicopathological data of the two groups were compared, and Kaplan-Meier method was performed to estimate patient survival. Results: Compared with the control group, the operation time of the SRA preservation group was longer (p < 0.001), but the postoperative exhaust and defecation times were significantly shorter (p = 0.003, p < 0.001). Two cases of postoperative ileus and four cases of anastomotic leakage were observed in the control group, whereas the SRA preservation group had none. However, no statistical difference was observed between the groups (p = 0.652, p = 0.248). The overall survival also showed no significant difference in (p = 0.436). Conclusion: Preservation of SRA plus dissection of lymph nodes around IMA did not increase postoperative morbidity and mortality nor affect the prognosis of patients but increased the bowel blood supply, which may have a significant positive effect on the recovery of postoperative intestinal function and reduction of anastomotic leakage.

Functional Macromolecular Adhesives for Bone Fracture Healing.

Compared with traditional internal fixation devices, bone adhesives are expected to exhibit remarkable advantages, such as improved fixation of comminuted fractures and maintained spatial location of fractured scattered bone pieces in treating bone injuries. In this review, different bone adhesives are summarized from the aspects of bone tissue engineering, and the applications of bone adhesives are emphasized. The concepts of "liquid scaffold" and "liquid plate" are proposed to summarize two different research directions of bone adhesives. Furthermore, significant advances of bone adhesives in recent years in mechanical strength, osseointegration, osteoconductivity, and osteoinductivity are discussed. We conclude this topic by providing perspectives on the state-of-the-art research progress and future development trends of bone adhesives. We hope this review will provide a comprehensive summary of bone adhesives and inspire more extensive and in-depth research on this subject.

YY1-induced long non-coding RNA PSMA3 antisense RNA 1 functions as a competing endogenous RNA for microRNA 214-5p to expedite the viability and restrict the apoptosis of bladder cancer cells via regulating programmed cell death-ligand 1.

Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. Our research aimed to explore the function and underlying mechanisms of long noncoding RNA (lncRNA) PSMA3-AS1 in BC. RT-qPCR was utilized to detect the levels of PSMA3-AS1, miR-214-5p, and PD-L1. ChIP assay was employed to confirm the transcription factor of PSMA3-AS1. Luciferase reporter assay was carried out to demonstrate the relationships between miR-214-5p and PSMA3-AS1 or PD-L1. The diagnostic value of PSMA3-AS1 was evaluated by the ROC curve. CCK-8, wound healing, transwell, and flow cytometry assays were applied to analyze cell viability, migration, invasion, and apoptosis. Western blotting was used to confirm the expression of cleaved caspase-3. The present study revealed that BC tissues and cells exhibited an increased expression in PSMA3-AS1. High expression of PSMA3-AS1 was related to poor prognosis in BC patients. Then, the area under the ROC curve for PSMA3-AS1 was up to 0.8954. Moreover, ChIP assay elaborated that YY1 could bind to the PSMA3-AS1 promoter region. Furthermore, it was found that that PSMA3-AS1 knockdown repressed BC cell viability and metastasis, and promoted apoptosis. In addition, miR-214-5p was inversely correlated with PSMA3-AS1 or PD-L1 levels. MiR-214-5p deletion reversed the impacts of PSMA3-AS1 deletion on BC progression, and PD-L1 inhibition also abrogated the influence of miR-214-5p deletion in BC development. In conclusion, YY1-induced PSMA3-AS1 exerted an oncogenic function in BC cells via targeting miR-214-5p and enhancing PD-L1, providing potential biomarkers for BC therapy.

Green tea polyphenols attenuate LPS-induced inflammation through upregulating microRNA-9 in murine chondrogenic ATDC5 cells.

BACKGROUND: Osteoarthritis (OA), a universal chronic musculoskeletal disorder, is closely related to inflammation. More effective drugs for improving OA outcome are definitely needed. Herein, we attempted to verify the protective role of green tea polyphenols (GTP) after treatment with murine in ATDC5 cells to reveal the regulatory mechanism. METHODS: ATDC5 cells were stimulated with lipopolysaccharide (LPS) to mimic an inflammatory response during OA. Cell activity, apoptosis, levels of relative proteins, and prophlogistic factors were tested via a Cell Counting Kit-8 experiment, a flow cytometry experiment, western blot, and RT-qPCR (ELISA and Western blot), separately. miR-9 level was detected by RT-qPCR and altered via miR-9 mimic and inhibitor transfection. We finally studied MAPK and NF-κB pathways in GTP-related modulations using western blot. RESULTS: LPS caused inflammatory cell damage in ATDC5 cells, showing decreased cell activity, enhanced apoptosis, and increased levels of pro-inflammatory cytokines. GTP pretreatments could significantly attenuate LPS-induced alterations. In addition, LPS-induced miR-9 upregulation was further positively regulated in ATDC5 cells. The effects of GTP pretreatments in LPS-caused ATDC5 cells were enhanced via miR-9 upregulation, whereas they were reduced via miR-9 suppression. Finally, we found that GTP pretreatments could suppress the MAPK and NF-κB pathways through miR-9 regulation. CONCLUSION: GTP pretreatments attenuated LPS-induced inflammatory response accompanied by the suppression of the MAPK and NF-κB pathways via positively regulating miR-9 in ATDC5 cells.

lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.

Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.

Long non-coding RNA THRIL promotes LPS-induced inflammatory injury by down-regulating microRNA-125b in ATDC5 cells.

BACKGROUND: Osteoarthritis is an age-related disorder of bone-joint that causes pain and disability in middle and older people. This study aimed to investigate the potential effects of long non-coding RNA (lncRNA) THRIL on lipopolysaccharide (LPS)-induced osteoarthritis cell injury model (ATDC5 cell inflammatory injury), as well as the possible internal molecular mechanisms. METHODS: Cell viability and apoptosis were assessed using CCK-8 assay and Guava Nexin assay, respectively. Cell transfection was conducted to change the expression of THRIL and microRNA-125b (miR-125b) in ATDC5 cells. qRT-PCR was performed to detect the expression of THRIL, miR-125b and pro-inflammatory cytokines IL-6, TNF-α and monocyte chemotactic protein 1 (MCP-1) in ATDC5 cells. ELISA was used to measure the concentrations of IL-6, TNF-α and MCP-1 in culture supernatant of ATDC5 cells. Finally, the protein expression of key factors involved in cell apoptosis, inflammatory response, JAK1/STAT3 and NF-κB pathways were evaluated using western blotting. RESULTS: LPS significantly induced ATDC5 cell inflammatory injury and up-regulated the expression of THRIL. Overexpression of THRIL aggravated the LPS-induced ATDC5 cell inflammatory injury. Suppression of THRIL had opposite effects. Moreover, THRIL negatively regulated the expression of miR-125b in ATDC5 cells. miR-125b participated in the effects of THRIL overexpression on LPS-induced ATDC5 cell inflammatory injury. Furthermore, overexpression of THRIL enhanced the LPS-induced JAK1/STAT3 and NF-κB pathways activation by down-regulating miR-125b. CONCLUSION: THRIL exerted pro-inflammatory roles in LPS-induced osteoarthritis cell injury model. Overexpression of THRIL promoted LPS-induced ATDC5 cell inflammatory injury by down-regulating miR-125b and then activating JAK1/STAT3 and NF-κB pathways.

MiR-337-3p suppresses the proliferation and metastasis of clear cell renal cell carcinoma cells via modulating Capn4.

OBJECTIVE: Renal cancer accounts for about 3% of human cancer, and clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cancer. Recently, microRNAs (miRNAs) are found to be the biomarkers for cancer diagnosis, prognosis and the targets for tumor management. This study aimed to examine the expression of miR-337-3p in ccRCC and to elucidate the molecular mechanisms underlying miR-337-3p-mediated ccRCC progression. METHODS: The miRNA and mRNA expression levels in ccRCC cells and tissues were measured by qRT-PCR. Cell proliferation, cell adhesion, colony growth and cell invasion were examined by CCK-8 assay, cell adhesion assay, colony formation assay and Transwell invasion assay, respectively. The protein levels were detected by western blot assay. The effects of miR-337-3p on tumor growth in vivo was assessed in a nude mice xenograft model. RESULTS: MiR-337-3p was down-regulated in ccRCC cell lines, and miR-337-3p overexpression suppressed cell proliferation, colony growth and invasion, but enhanced cell adhesion in ccRCC; while knockdown of miR-337-3p exerted the opposite effects on ccRCC. Bioinformatics analysis and luciferase reporter assay showed that Calpain small subunit 1 (Capn4) was negatively regulated by miR-337-3p, and overexpression of miR-337-3p attenuated the miR-337-3p-mediated effects on ccRCC cellular functions. In addition, miR-337-3p also suppressed epithelial-mesenchymal transition in ccRCC. The in vivo tumor growth was markedly suppressed after miR-337-3p overexpression. Data from clinical data showed that down-regulation of miR-337-3p and up-regulation of Capn4 mRNA and protein were identified in the ccRCC tissues, and miR-337-3p expression level was inversely correlated with Capn4 mRNA expression level in ccRCC tissues. CONCLUSIONS: Collectively, these data suggested the tumor suppressive role of miR-337-3p in ccRCC. MiR-337-3p suppressed cell proliferation and metastasis in ccRCC partially via targeting Capn4.

Capn4 contributes to tumor invasion and metastasis in clear cell renal cell carcinoma cells via modulating talin-focal adhesion kinase signaling pathway.

Calpain small subunit 1 (Capn4) has been shown to correlate with the metastasis/invasion of clear cell renal cell carcinoma (ccRCC). This study aimed to further elucidate the molecular mechanisms underlying Capn4-mediated ccRCC progression. The mRNA expression levels in ccRCC cells were measured by quantitative real-time PCR. The effects of Capn4 on cell adhesion, invasion, and migration were examined by cell adhesion assay, cell invasion assay, and wound-healing assay, respectively. The protein levels were detected by western blot analysis. The effect of Capn4 on cancer metastasis in vivo was assessed in a nude mice xenograft model. It was found that Capn4 was up-regulated in the ccRCC cells, and Capn4 overexpression suppressed cell adhesion activity and increased cell invasion and migration in 786-O cells, while Capn4 silencing increased cell adhesion activity and impaired the invasion and migration ability of Caki-1 cells. Capn4 overexpression also increased the protein level of cleaved talin in 786-O cells, while Capn4 silencing decreased the protein level of cleaved talin in Caki-1 cells. The focal adhesion kinase (FAK)/AKT/MAPK signaling was activated by Capn4 overexpression in 786-O cells, and was inhibited by Capn4 down-regulation in Caki-1 cells. Capn4 overexpression increased the protein levels of matrix metalloproteinase 2 (MMP-2), vimentin, N-cadherin, and down-regulated E-cadherin in 786-O cells, while Capn4 silencing decreased the protein levels of MMP-2, vimentin, N-cadherin, and up-regulated E-cadherin in Caki-1 cells. Capn4 also promoted cancer metastasis in the in vivo nude mice xenograft model. Our results implicate the functional role of Capn4 in ccRCC invasion and migration, which may contribute to cancer metastasis in ccRCC.

Laparoscopic Versus Open Resection for Gastric Gastrointestinal Stromal Tumors (GISTs): A Size-Location-Matched Case-Control Study.

BACKGROUND: Laparoscopic resection for gastric gastrointestinal stromal tumors (GISTs) is technically feasible, but the long-term effect remains uncertain. This study aims to compare the long-term oncologic outcomes of laparoscopic versus open resection of GISTs by larger cases based on tumor size-location-matched study. METHODS: Between 2006 and 2015, 63 consecutive patients with a primary gastric GIST undergoing laparoscopic resection were enrolled in and matched (1:1) to patients undergoing open resection by tumor size and location. Clinical and pathologic parameters and surgical outcomes associated with each surgical type were collected and compared. RESULTS: The operation time, intraoperative blood loss, return of bowel function and oral intake, nasogastric tube retention time and postoperative stay were all shorter/faster in laparoscopic group than those in open group (P < 0.001). Postoperative complications were comparable except for the higher incidence of abdominal/incision pain in open group (9.52 vs 27%, P = 0.01). There was no statistical difference in recurrence rate (9.52 vs 15.87%, P = 0.29) and long-term recurrence-free survival between the two groups (P = 0.39). CONCLUSIONS: The long-term oncologic outcome of laparoscopic resection of primary gastric GISTs is comparable to that of open procedure, but laparoscopic procedure has the advantage of minimal invasion and is superior in postoperative recovery.

Intrasylvian/Intracerebral Hematomas Associated with Ruptured Middle Cerebral Artery Aneurysms: A Single-Center Series and Literature Review.

OBJECTIVE: Ruptured middle cerebral artery (MCA) aneurysms usually lead to subarachnoid hemorrhage (SAH), and several cases have shown concomitant intrasylvian or intracerebral hematomas. The objective of this study was to compare the clinical and radiographic characteristics with their different outcomes. METHODS: The charts of 30 consecutive patients with ruptured MCA aneurysm-related intracranial hematoma were retrospectively reviewed. These patients were dichotomized into an intrasylvian hematoma (ISH) group and an intracerebral hematoma (ICH) group by the presence of intrahematomal contrast-enhancing vessel; for patients under open surgery, hematoma type was further confirmed by intraoperative observation. The characteristics were compared between these 2 groups (ie, age, gender, history of hypertension, history of smoking, systolic pressure at admission, hematoma volume, size and side of aneurysms, the angle between the pointing direction of the aneurysm and the MCA trunk [denoted as α], middle line shifting, treatment modality, and outcome). All the angles are measured in the anterior-posterior projection. RESULTS: In our series, only hematoma volume, the angle α, and the middle line shift showed statistical significance regarding prognosis between 2 hematoma groups. An angle α between 109.0°and 216.0° is associated with ISH, whereas aneurysm with an angle beyond this range indicates ICH. In our series, patients in the ICH group had a larger hematoma volume compared with the ISH patients (33.3 ± 17.6 vs. 11.5 ± 10.5; P = 0.002). There exists no statistical difference regarding prognosis between these 2 groups, even although there is a trend toward worse recovery for patients in the ISH group (Glasgow Outcome Scale score, 3.0 ± 1.3 vs. 3.8 ± 1.9; P = 0.07). CONCLUSIONS: In our series, the prognosis of patients with ICH was worse than that of patients with ISH. Early discrimination of these 2 types of hematoma helps to predict future outcome; an angle (between the pointing direction of aneurysm and the MCA trunk) between 109.0°and 216.0° is associated with ISH, whereas aneurysm with an angle beyond this range suggests ICH.

Prognostic role of the lymph node ratio in node positive colorectal cancer: a meta-analysis.

The lymph node ratio (LNR) (i.e. the number of metastatic lymph nodes divided by the number of totally resected lymph nodes) has recently emerged as an important prognostic factor in colorectal cancer (CRC). However, the tumor node metastasis (TNM) staging system for colorectal cancer does not consider it as a prognostic parameter. Therefore, we conducted a meta-analysis to evaluate the prognostic role of the LNR in node positive CRC. A systematic search was performed in PubMed, Embase and the Cochrane Library for relevant studies up to November 2015. As a result, a total of 75,838 node positive patients in 33 studies were included in this meta-analysis. Higher LNR was significantly associated with shorter overall survival (OS) (HR = 1.91; 95% CI 1.71-2.14; P = 0.0000) and disease free survival (DFS) (HR = 2.75; 95% CI: 2.14-3.53; P = 0.0000). Subgroup analysis showed similar results. Based on these results, LNR was an independent predictor of survival in colorectal cancer patients and should be considered as a parameter in future oncologic staging systems.

MiR-10b decreases sensitivity of glioblastoma cells to radiation by targeting AKT.

BACKGROUND: Glioblastomas are the most aggressive brain tumors with extremely poor prognosis despite advances in treatment techniques. MiR-10b is highly expressed in glioblastoma and regulates cell proliferation, migration and invasion. Here, we examined the role of MiR-10b on radiotherapy of glioblastomas. METHODS: MiR-10b mimic or anti-MiR-10b inhibitor was transfected in glioblastoma cells. WST-1 assay was used to examine the effect of MiR-10b on proliferation of transfected glioblastoma cells after radiation treatment. Apoptosis was examined by caspase 3/7 activity and TUNEL assay. The western blot was used to evaluate protein expression. RESULTS: Altered expression of MiR-10b changed the radiation-induced inhibitory effect on proliferation of glioblastoma cells with dose-dependent manner. MiR-10b decreased radiation-induced apoptosis in glioblastoma cells by activation of caspase 3/7 and inhibition Bcl-2 expression. MiR-10b enhances migration and invasion of glioblastoma cells in presence of radiation. In addition, MiR-10b decreased the sensitivity of glioblastoma cells to radiotherapy by activation of p-AKT expression. CONCLUSIONS: MiR-10b might be a potential biomarker to predict radiotherapy response and prognosis in glioblastomas.

MiR-194 inhibits cell proliferation and invasion via repression of RAP2B in bladder cancer.

Bladder cancer is the 7th most common cancer type in the world, and microRNAs (miRNAs) play important roles in cancer progression. In the present study, we investigated the roles and molecular mechanisms of miR-194 in bladder cancer. The results demonstrated that the expression level of miR-194 is significantly down-regulated in bladder cancer cell lines and clinical tissues. Overexpression of miR-194 inhibited cell proliferation and invasion in J82 and T24 cells. Further mechanistic study showed that overexpression of miR1-94 induced G0/G1 phase arrest as well as apoptosis in J82 and T24 cells. In addition, by using bioinformatics tool (Targetscan), RAP2B is found to be a target of miR-194, and miR-194 down-regulates the expression level of RAP2B via directly targeting its 3'UTR. Knockdown of RAP2B also inhibited cell proliferation and invasion in J28 cells. More importantly, restoration of RAP2B activity rescued the inhibitory effects of miR-194 on cell proliferation and invasion in J82 cells. Further analysis of bladder cancer clinical samples showed that miR-194 is inversely correlated with RAP2B. Collectively, our study may implicate that miR-194 plays an important role in the regulation of bladder cancer progression. In summary, our study may implicate that miR-194 acts as a tumor suppressor and plays an important role in the regulation of bladder cancer progression.