INTRODUCTION For stage III colon cancer (CC), surgery followed by chemotherapy is the main curative approach, although optimum times between diagnosis and surgery, and surgery and chemotherapy, have not been established. MATERIALS AND METHODS We analysed a population-based sample of 1912 stage III CC cases diagnosed in eight European countries in 2009-2013 aiming to estimate (i) odds of receiving postoperative chemotherapy, overall and within eight weeks of surgery; (ii) risks of death/relapse, according to treatment, Charlson Comorbidity Index, time from diagnosis to surgery for emergency and elective cases, and time from surgery to chemotherapy; and (iii) time-trends in chemotherapy use. RESULTS Overall, 97% of cases received surgery and 65% postoperative chemotherapy, with 71% of these receiving chemotherapy within eight weeks of surgery. Risks of death and relapse were higher for cases starting chemotherapy with delay, but better than for cases not given chemotherapy. Fewer patients with high comorbidities received chemotherapy than those with low (P  less then  0.001). Chemotherapy timing did not vary (P = 0.250) between high and low comorbidity cases. Electively-operated cases with low comorbidities received surgery more promptly than high comorbidity cases. Risks of death and relapse were lower for elective cases given surgery after four weeks than cases given surgery within a week. High comorbidities were always independently associated with poorer outcomes. Chemotherapy use increased over time. CONCLUSIONS Our data indicate that promptly-administered postoperative chemotherapy maximizes its benefit, and that careful assessment of comorbidities is important before treatment. The survival benefit associated with slightly delayed elective surgery deserves further investigation. The liver is the most common anatomical site for hematogenous metastases from colorectal cancer. Therefore effective treatment of liver metastases is one of the most challenging elements in the management of colorectal cancer. However, there is rare available clinical consensus or guideline only focusing on colorectal liver metastases. After six rounds of discussion by 195 clinical experts of the Shanghai International Consensus Expert Group on Colorectal Liver Metastases (SINCE) from 29 countries or regions, the Shanghai Consensus has been finally completed, based on current research and expert experience. The consensus emphasized the principle of multidisciplinary team, provided detailed diagnosis approaches, and guided precise local and systemic treatments. This Shanghai Consensus might be of great significance to standardized diagnosis and treatment of colorectal liver metastases all over the world. BACKGROUND cytoreduction surgery (CRS) and heated intraperitoneal chemotherapy (HIPEC) is currently the standard of care for some peritoneal surface malignancies. There is experimental evidence supporting that high Intra Abdominal Pressure (IAP) during HIPEC could enhance the uptake of drugs by tumor tissues. However, few papers are describing the hemodynamic and respiratory effects of increased IAP during HIPEC. AIMS to evaluate the hemodynamic and respiratory association with different IAPs during HIPEC. METHODS This is part of an IRB board approved prospective randomized controlled trial conducted at The National Tumor Institute of Milan from 2014 to 2017 (NCT0294979). Patients diagnosed with Pseudomyxoma (PMP) or Peritoneal Metastasis of Colorectal Cancer (PM-CRC) were submitted to CRS and then randomized to receive low IAP (8-12 mmHg) or high IAP (18-22 mmHg) HIPEC. Hemodynamic and respiratory data were collected in eight different time-points during the whole procedure. RESULTS 33 patients (n low = 15, n high = 18) with PM-CRC and PMP were analysed. The mean IAP in the low IAP HIPEC group was 11.4 mmHg (SD 2.5) and 18.1 mmHg (SD 2.5) in the high IAP HIPEC group (p«0.001). There was no difference in the hemodynamic parameters between both groups, except for the central venous pressure (CVP) that was significantly higher in the high IAP group (p = 0.006). High IAP was well tolerated in the experimental arm with no hemodynamic and ventilation instability observed during the intervention. CONCLUSION We conclude that high IAP at the level of 18-22 mmHg during HIPEC has no significant hemodynamic parameters difference, being feasible and safe in our study. INTRODUCTION Recent reports on gene expression profiling (GEP) show several genes associated with malignant progression of GIST. However, genes associated with malignant transformation have not been clarified. Here, we aimed to reveal distinct genes in aggressive malignant GIST, using comprehensive gene expression analysis. MATERIALS AND METHODS We investigated GEP obtained by microarrays for 43 gastric GISTs, which mostly harbored KIT and PDGFRA mutations and integrated clinicopathological risk information. RT-PCR and immunohistochemistry were performed for FZD7, a receptor of Wnt ligands. RESULTS GEP divided 43 gastric GISTs into two clusters. A cluster included seven of eight high-risk GISTs (88%) in modified NIH classification and was defined as high-risk cluster; the other cluster was defined as low-risk cluster. The number of probes with over 3-fold changes between the two clusters was 1,177, in which probes corresponding to 16 oncogenes were included. Genes involved in the Wnt signaling pathway were the most abundant among the 16 oncogenes. Focusing on 73 Wnt signaling pathway genes of the 21,578 probes, 12 upregulated and 5 downregulated genes were found in the high-risk cluster. Major cascade genes promoting the Wnt/β-catenin signaling pathway, including WNT11, FZD family, and DVL2, were upregulated in the high-risk cluster. SNAI1, SNAI2, and BIRC5, which are activated by this pathway and increase cell proliferation, were also upregulated. These gene expression alterations were consistent in the positive direction of this pathway. GISTs in high-risk cluster strongly expressed FZD7. CONCLUSION Wnt/β-catenin signaling pathway may play an important role in malignant transformation of indolent GIST. INTRODUCTION Although The Bethesda System for Reporting Cervical Cytopathology does not mandate reporting of endocervical glandular involvement (EGI) in Papanicolaou test specimens with high-grade squamous intraepithelial lesions (HSIL), several studies have suggested that EGI diagnosed on surgical specimens is associated with higher rates of residual or recurrent dysplasia. When suspected, EGI is reported for Papanicolaou test specimens at our institution, but the performance of this diagnosis has not been assessed. MATERIALS AND METHODS The archives were queried for Papanicolaou test specimens with a diagnosis of HSIL-EGI (2006-2017). All follow-up surgical pathology specimens within a year of the Papanicolaou test diagnosis were evaluated for cytologic-histologic correlation. This same query was repeated for all surgical pathology specimens with a diagnosis of HSIL-EGI. All preceding Papanicolaou test diagnoses within a year were assessed for cytologic-histologic correlation. Twenty Papanicolaou test specimen glass slides were reviewed by 6 observers to assess for interobserver variability. RESULTS Patients with HSIL-EGI on surgical specimens were more likely to have a preceding Papanicolaou diagnosis of HSIL and atypical squamous cells, cannot exclude high-grade squamous intraepithelial lesion (ASC-H) (32.3% versus 25.5%, P = 0.03, and 16.7% versus 11.8%, P = 0.04, respectively). Patients with an HSIL-EGI diagnosis on a Papanicolaou test were significantly more likely to have HSIL-EGI detected on a follow-up histology (41.6% versus 24.0%, P less then 0.001). Interobserver concordance was poor for the assignment of EGI in Papanicolaou test specimens. CONCLUSIONS Overall, the diagnosis of HSIL-EGI on Papanicolaou test specimens is complicated by poor sensitivity and interobserver concordance. Atrial fibrillation (AF) is the most common arrhythmias, and patients with AF are facing increased risk of heart failure and ischemic stroke. However, the AF pathogenesis, especially the long noncoding RNAs (lncRNA)-related mechanism, has not been fully understood. In this study, we collected RNA sequencing data of the epicardial adipose tissues (EAT) from 6 AF and 6 sinus rhythm (SR) to identify the differentially expressed protein-coding genes (PCGs) and lncRNAs. Functionally, the differentially expressed PCGs were significantly enriched in bone development disease, chronic kidney failure, and kidney disease. Particularly, we found that homeobox (HOX) genes, especially the antisense RNAs, HOTAIRM1, HOXA-AS2 and HOXB-AS2, were significantly downregulated in EAT of AF. The biological function predictions for the dysregulated lncRNAs revealed that TNF signaling pathway was the most frequent pathway that the lncRNAs might participate in. In addition, SNHG16 and RP11-471B22.2 might participate in TGF-beta signaling and ECM-receptor interaction by interacting with the proteins involved in the pathways, respectively. Collectively, we provided some potentially pathogenic lncRNAs in AF, which might be useful for the related researchers to study their functionality and develop new therapeutics. V.The incidence of type 2 diabetes mellitus (T2DM) and diabetic kidney disease (DKD) has significantly increased worldwide in recent decades, and improved treatments for T2DM and DKD are urgently needed. The pathogenesis of aging-related disorders, such as T2DM and DKD, involves multiple mechanisms, including inflammation, autophagy impairment, and oxidative stress, which are closely associated with mitochondrial dysfunction. Therefore, mitochondrial quality control may be a novel therapeutic target for T2DM and DKD. Previous reports have shown that members of the mammalian Sirtuin family, SIRT 1-7, which are recognized as antiaging molecules, play a crucial role in the regulation of mitochondrial function and quality control through the modulation of oxidative stress, inflammation and autophagy. In this review, we summarized the research published in recent years to highlight the role of Sirtuins in mitochondrial quality control as a therapeutic target for T2DM and DKD. Low-renin hypertension (LRH) is a frequent condition in patients with arterial hypertension, accounting for 30% of patients. Monogenic forms can cause LRH in a minority of cases. However, in the large majority of patients, LRH is caused by the combined effects of congenital and acquired factors, comprising dietary habits. Several genetic variants have been proposed as co-factors in the pathogenesis of LRH with normal-low serum aldosterone. Emerging evidences support the hypothesis that a large proportion of LRH with normal-high serum aldosterone is associated with subclinical primary aldosteronism (PA). The recent identification of aldosterone-producing cell clusters (APCCs) as the possible cause of subclinical PA, further supported the concept of a continuous spectrum of autonomous aldosterone secretion, from subclinical forms towards overt PA. In this review we describe the main aspects of LRH, focusing on molecular basis, clinical risk profile and patients’ management.