Endoluminal vacuum-assisted therapy (EVT) has been introduced recently to treat colorectal anastomotic leaks in clinically stable non-peritonitic patients. Its application has been mainly reserved to low colorectal and colo-anal anastomoses. The main advantage of this new procedure is to ensure continuous drainage of the abscess cavity, to promote and to accelerate the formation of granulation tissue resulting in a reduction of the abscess cavity. The reported results are promising allowing a higher preservation of the anastomosis when compared to conventional treatments that include trans-anastomotic tube placement, percutaneous drainage, endoscopic clipping of the anastomotic defect or stent placement. Nevertheless, despite this procedure is gaining acceptance among the surgical community, indications, inclusion criteria and definitions of success are not yet standardized and extremely heterogeneous, making it difficult to reach definitive conclusions and to ascertain which are the real benefits of this new procedure. Moreover, long-term and functional results are poorly reported. The present review is focused on critically analyzing the theoretical benefits and risks of the procedure, short- and long-term functional results and future direction in the application of EVT.

The phosphorylation status of β-arrestin1 influences its function as a signal strongly related to sorafenib resistance. This retrospective study aimed to develop and validate radiomics-based models for predicting β-arrestin1 phosphorylation in hepatocellular carcinoma (HCC) using whole-lesion radiomics and visual imaging features on preoperative contrast-enhanced computed tomography (CT) images.

To develop and validate radiomics-based models for predicting β-arrestin1 phosphorylation in HCC using radiomics with contrast-enhanced CT.

Ninety-nine HCC patients (training cohort

= 69; validation cohort

= 30) receiving systemic sorafenib treatment after surgery were enrolled in this retrospective study. Three-dimensional whole-lesion regions of interest were manually delineated along the tumor margins on portal venous CT images. Radiomics features were generated and selected to build a radiomics score using logistic regression analysis. Imaging features were evaluated by two radiologists independently. cal usefulness confirmed in both the training and validation cohorts using decision curve analysis. The risk of β-arrestin1 phosphorylation predicted by the CRR model was significantly associated with overall survival in the training and validation cohorts (log-rank test,

< 0.05).

The radiomics signature is a reliable tool for evaluating β-arrestin1 phosphorylation which has prognostic significance for HCC patients, providing the potential to better identify patients who would benefit from sorafenib treatment.

The radiomics signature is a reliable tool for evaluating β-arrestin1 phosphorylation which has prognostic significance for HCC patients, providing the potential to better identify patients who would benefit from sorafenib treatment.

Liver transplantation is a therapy for irreversible liver failure; however, at present, donor organs are in short supply. Cell transplantation therapy for liver failure is still at the developmental stage and is critically limited by a shortage of human primary hepatocytes.

To investigate the possibility that hepatic progenitor cells (HPCs) prepared from the portal branch-ligated hepatic lobe may be used in regenerative medicine, we attempted to enable the implantation of extracellular matrices containing organoids consisting of HPC-derived hepatocytes and non-parenchymal cells.

liver organoid tissue has been generated by accumulating collagen fibrils, fibroblasts, and HPCs on a mesh of polylactic acid fabric using a bioreactor; this was subsequently implanted into syngeneic wild-type mice.

The

liver organoid tissues generated transplantable tissues in the condensed collagen fibril matrix and were obtained from the mouse through partial hepatectomy.

Liver organoid tissue was produced from expanded HPCs using an originally designed bioreactor system. This tissue was comparable to liver lobules, and with fibroblasts embedded in the network collagen fibrils of this artificial tissue, it is useful for reconstructing the hepatic interstitial structure.

Liver organoid tissue was produced from expanded HPCs using an originally designed bioreactor system. This tissue was comparable to liver lobules, and with fibroblasts embedded in the network collagen fibrils of this artificial tissue, it is useful for reconstructing the hepatic interstitial structure.Primary biliary cholangitis and primary sclerosing cholangitis (PSC) are the most common cholestatic liver diseases (CLD) in adults and are both characterized by an immune pathogenesis. While primary biliary cholangitis is a model autoimmune disease, with over 90% of patients presenting very specific autoantibodies against mitochondrial antigens, PSC is considered an immune mediated disease. Osteoporosis is the most common bone disease in CLD, resulting in frequent fractures and leading to significant morbidity. Further, sarcopenia is emerging as a frequent complication of chronic liver diseases with a significant prognostic impact and severe implications on the quality of life of patients. The mechanisms underlying osteoporosis and sarcopenia in CLD are still largely unknown and the association between these clinical conditions remains to be dissected. Although timely diagnosis, prevention, and management of osteosarcopenia are crucial to limit the consequences, there are no specific guidelines for management of osteoporosis and sarcopenia in patients with CLD. International guidelines recommend screening for bone disease at the time of diagnosis of CLD. However, the optimal monitoring strategies and treatments have not been defined yet and vary among centers. We herein aim to comprehensively outline the pathogenic mechanisms and clinical implications of osteosarcopenia in CLD, and to summarize expert recommendations for appropriate diagnostic and therapeutic approaches.An enhanced cascade of care should include a younger population, helping to achieve the goal of the World Health Organization with a focus on elimination in the pediatric population. Furthermore, enhanced screening and awareness efforts and continued education of health care providers will improve the outcomes of chronic hepatitis C virus (HCV) infection in the pediatric population. The present work discusses and comments on the topic „cascade of care in HCV chronic pediatric patients”.Hepatocellular adenoma (HCA) is a benign hepatocellular neoplasm, commonly occurs in young women with a history of oral contraceptive use. Complications including hemorrhage and malignant transformation necessitate the need for a thorough understanding of the underlying molecular signatures in this entity. Recent molecular studies have significantly expanded our knowledge of HCAs. The well-developed phenotype-genotype classification system improves clinical management through identifying „high risk” subtype of HCAs. In this article, we attempt to provide updated information on clinical, pathologic and molecular features of each subtype of HCAs.A study addressing the influence of type 2 diabetes on the prognosis of acute-on-chronic liver failure patients was reviewed. Some statistical deficiencies were found in the reviewed article, and the sample size was too small to support the study. In addition, age should have been considered as one of the prognostic factors.

Heterotopic pancreas (HP) is an aberrant anatomic malformation that occurs most commonly in the upper gastrointestinal tract. While the majority of heterotopic pancreatic lesions are asymptomatic, many manifest severe clinical symptoms which require surgical or endoscopic intervention. Understanding of the clinical manifestations and symptoms of HP is limited due to the lack of large volume studies in the literature. The purpose of this study is to review symptomatic cases at a single center and compare these to a systematic review of the literature in order to characterize common clinical manifestations and treatment of this disease.

To classify the common clinical manifestations of heterotopic pancreas.

A retrospective review was conducted of pathologic samples containing heterotopic pancreas from 2000-2018. Review was limited to HP of the upper gastrointestinal tract due to the frequency of presentation in this location. Symptomatic patients were identified from review of the medical records and clinreatitis (

= 260, 28%); (3) Gastrointestinal bleeding (

= 80, 9%); and (4) Gastric outlet obstruction (

= 80, 9%). The majority of cases (

= 832, 90%) underwent surgical or endoscopic resection with 85% reporting resolution or improvement in their symptoms.

Heterotopic pancreas can cause significant clinical symptoms in the upper gastrointestinal tract. Better understanding and classification of this disease may result in more accurate identification and treatment of this malformation.

Heterotopic pancreas can cause significant clinical symptoms in the upper gastrointestinal tract. Better understanding and classification of this disease may result in more accurate identification and treatment of this malformation.Insulin, a key pleiotropic hormone, regulates metabolism through several signaling pathways in target tissues including skeletal muscle, liver, and brain. In the brain, insulin modulates learning and memory, and impaired insulin signaling is associated with metabolic dysregulation and neurodegenerative diseases. At the receptor level, in aging and Alzheimer’s disease (AD) models, the amount of insulin receptors and their functions are decreased. Clinical and animal model studies suggest that memory improvements are due to changes in insulin levels. Furthermore, diabetes mellitus (DM) and insulin resistance are associated with age-related cognitive decline, increased levels of β-amyloid peptide, phosphorylation of tau protein; oxidative stress, pro-inflammatory cytokine production, and dyslipidemia. Recent evidence shows that deleting brain insulin receptors leads to mild obesity and insulin resistance without influencing brain size and apoptosis development. Conversely, deleting insulin-like growth factor 1 ra specific target for therapeutic strategies to decrease alterations associated with age-related cognitive decline.Diabetic kidney disease (DKD) is one of the major chronic complications of diabetes mellitus (DM), as well as a main cause of end-stage renal disease. Over the last few years, substantial research studies have revealed a contributory role of gut microbiota in the process of DM and DKD. Metabolites of gut microbiota like lipopolysaccharide, short-chain fatty acids, and trimethylamine N-oxide are key mediators of microbial-host crosstalk. However, the underlying mechanisms of how gut microbiota influences the onset and progression of DKD are relatively unknown. Besides, strategies to remodel the composition of gut microbiota or to reduce the metabolites of microbiota have been found recently, representing a new potential remedial target for DKD. In this mini-review, we will address the possible contribution of the gut microbiota in the pathogenesis of DKD and its role as a therapeutic target.