Biliary reconstruction with localized creation: One case report of repairing bile duct injury and defect with autografts.

INTRODUCTION: Bile duct injuries caused by any reason are a disaster for patients and pose a significant psychological and technical challenge for surgeons. The use of Ligamentum teres hepatis and gallbladder flap as autografts is showing promising results in the repair of bile duct injury. CASE PRESENTATION: This article presents a challenging case of a patient with Mirizzi syndrome who experienced a complex bile duct defect and injury during cholecystectomy. We describe the successful reconstruction of the bile duct using ligamentum teres hepatis and remnant gallbladder flap simultaneously. DISCUSSION: Ligamentum teres hepatis and remnant gallbladder flap are ideal repair materials for repairing and reconstructing bile duct injuries due to their easy availability, good tissue compatibility, and low incidence of postoperative complications. It is essential to seek the assistance of an experienced biliary surgeon when bile duct injury occurs during operation. CONCLUSION: Ligamentum teres hepatis and gallbladder flap, as suitable autologous tissues, are viable options for repairing bile duct injuries and defects.

[Interpretation of the World Society of the Emergency Surgery/the Global Alliance for Infection in Surgery/the Surgical Infection Society-Europe/the World Surgical Infection Society/the American Association for the Surgery of Trauma global clinical pathways for patients with intra-abdominal infections].

Intra-abdominal infections (IAI) is common surgical emergencies and have been reported as major contributors to non-trauma deaths in hospitals worldwide. The principles of IAI management included early diagnosis, adequate source control, appropriate antimicrobial therapy, and prompt physiologic stabilization using critical care resources, combined with an optimal surgical approach. In order to facilitate clinical management, establish a global standard and provide guidance for clinicians, the World Society of Emergency Surgery (WSES), the Global Alliance for Infection in Surgery (GAIS), the Surgical Infection Society-Europe (SIS-E), the World Surgical Infection Society (WSIS), and the American Association for the Surgery of Trauma (AAST) worked together to complete an international multi-society document, which provided the evidence-based clinical pathways. Herein, we made a comprehensive interpretation for the clinical pathways combined with the latest domestic and international research developments, aiming to provide evidence for domestic doctors on the diagnosis and treatment of IAI, and ultimately benefit patients.

[Interpretation of acute abdomen in the immunocompromised patients: WSES/SIS-E/WSIS/AAST/GAIS guideline].

World Society of Emergency Surgery (WSES), in conjunction with Surgical Infection Society Europe (SIS-E), World Surgical Infection Society (WSIS), American Association for the Surgery of Trauma (AAST), and Global Alliance for Infection in Surgery (GAIS) developed guideline about the management of acute abdomen in immunocompromised patients, which was published in the World Journal of Emergency Surgery (WJES) on August 9, 2021. The guidelines elaborate on the definition, classification, diagnosis and treatment of immunocompromised patients. In addition, based on evidence-based medicine, it provides guidance and suggestion on the management of specific acute abdominal infections in immunocompromised patients, common acute abdominal infections in transplanted patients, patients with human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS), as well as perioperative steroid management. An interpretation of the guideline was performed to accomplish a better understanding the current status and recommendations for the management of acute abdominal conditions in immunocompromised patients, and to make forward suggestions on its limitations.

Pre-transplant infusion of donor leukocytes treated with extracorporeal photochemotherapy induces immune hypo-responsiveness and long-term allograft survival in murine models.

Recipients of solid organ transplantation (SOT) rely on life-long immunosuppression (IS), which is associated with significant side effects. Extracorporeal photochemotherapy (ECP) is a safe, existing cellular therapy used to treat transplant rejection by modulating the recipient's own blood cells. We sought to induce donor-specific hypo-responsiveness of SOT recipients by infusing ECP-treated donor leukocytes prior to transplant. To this end, we utilized major histocompatibility complex mismatched rodent models of allogeneic cardiac, liver, and kidney transplantation to test this novel strategy. Leukocytes isolated from donor-matched spleens for ECP treatment (ECP-DL) were infused into transplant recipients seven days prior to SOT. Pre-transplant infusion of ECP-DL without additional IS was associated with prolonged graft survival in all models. This innovative approach promoted the production of tolerogenic dendritic cells and regulatory T-cells with subsequent inhibition of T-cell priming and differentiation, along with a significant reduction of donor-specific T-cells in the spleen and grafts of treated animals. This new application of donor-type ECP-treated leukocytes provides insight into the mechanisms behind ECP-induced immunoregulation and holds significant promise in the prevention of graft rejection and reduction in need of global immune suppressive therapy in patients following SOT.

Identification of a novel nine-SnoRNA signature with potential prognostic and therapeutic value in ovarian cancer.

BACKGROUND: Increasing evidence has been confirmed that small nucleolar RNAs (SnoRNAs) play critical roles in tumorigenesis and exhibit prognostic value in clinical practice. However, there is short of systematic research on SnoRNAs in ovarian cancer (OV). MATERIAL/METHODS: 379 OV patients with RNA-Seq and clinical parameters from TCGA database and 5 paired clinical OV tissues were embedded in our study. Cox regression analysis was used to identify prognostic SnoRNAs and construct prediction model. SNORic database was adopted to examine the copy number variation of SnoRNAs. ROC curves and KM plot curves were applied to validate the prognostic model. Besides, the model was validated in 5 paired clinical tissues by real-time PCR, H&E staining and immunohistochemistry. RESULTS: A prognostic model was constructed on the basis of SnoRNAs in OV patients. Patients with higher RiskScore had poor clinicopathological parameters, including higher age, larger tumor size, advanced stage and with tumor status. KM plot analysis confirmed that patients with higher RiskScore had poorer prognosis in subgroup of age, tumor size, and stage. 7 of 9 SnoRNAs in the prognostic model had positive correlation with their host genes. Moreover, 5 of 9 SnoRNAs in the prognostic model correlated with their CNVs, and SNORD105B had the strongest correction with its CNVs. ROC curve showed that the RiskScore had excellent specificity and accuracy. Further, results of H&E staining and immunohistochemistry of Ki67, P53 and P16 confirmed that patients with higher RiskScore are more malignant. CONCLUSIONS: In summary, we identified a nine-SnoRNAs signature as an independent indicator to predict prognosis of OV, providing a prospective prognostic biomarker and potential therapeutic targets for ovarian cancer.

Taking the Next Step: a Neural Coaptation Orthotopic Hind Limb Transplant Model to Maximize Functional Recovery in Rat.

Limb transplant in particular and vascularized composite allotransplant (VCA) in general have wide therapeutic promise that have been stymied by current limitations in immunosuppression and functional neuromotor recovery. Many animal models have been developed for studying unique features of VCA, but here we present a robust reproducible model of orthotopic hind limb transplant in rats designed to simultaneously investigate both aspects of current VCA limitation: immunosuppression strategies and functional neuromotor recovery. At the core of the model rests a commitment to meticulous, time-tested microsurgical techniques such as hand sewn vascular anastomoses and hand sewn neural coaptation of the femoral nerve and the sciatic nerve. This approach yields durable limb reconstructions that allow for longer lived animals capable of rehabilitation, resumption of daily activities, and functional testing. With short-term treatment of conventional immunosuppressive agents, allotransplanted animals survived up to 70 days post-transplant, and isotransplanted animals provide long lived controls beyond 200 days post-operatively. Evidence of neurologic functional recovery is present by 30 days post operatively. This model not only provides a useful platform for interrogating immunological questions unique to VCA and nerve regeneration, but also allows for in vivo testing of new therapeutic strategies specifically tailored for VCA.

Kidney-intrinsic factors determine the severity of ischemia/reperfusion injury in a mouse model of delayed graft function.

Delayed graft function due to transplant ischemia/reperfusion injury adversely affects up to 50% of deceased-donor kidney transplant recipients. However, key factors contributing to the severity of ischemia/reperfusion injury remain unclear. Here, using a clinically relevant mouse model of delayed graft function, we demonstrated that donor genetic background and kidney-intrinsic MyD88/Trif-dependent innate immunity were key determinants of delayed graft function. Functional deterioration of kidney grafts directly corresponded with the duration of cold ischemia time. The graft dysfunction became irreversible after cold ischemia time exceeded six hours. When cold ischemia time reached four hours, kidney grafts displayed histological features reflective of delayed graft function seen in clinical kidney transplantation. Notably, kidneys of B6 mice exhibited significantly more severe histological and functional impairment than kidneys of C3H or BALB/c mice, regardless of recipient strains or alloreactivities. Furthermore, allografts of B6 mice also showed an upregulation of IL-6, neutrophil gelatinase-associated lipocalin, and endoplasmic reticulum stress genes, as well as an increased influx of host neutrophils and memory CD8 T-cells. In contrast, donor MyD88/Trif deficiency inhibited neutrophil influx and decreased the expression of IL-6 and endoplasmic reticulum stress genes, along with improved graft function and prolonged allograft survival. Thus, kidney-intrinsic factors involving genetic characteristics and innate immunity serve as critical determinants of the severity of delayed graft function. This preclinical murine model allows for further investigations of the mechanisms underlying delayed graft function.