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001). Conclusion Our software can automatically evaluate temporal changes of JSN, which might free rheumatologists / radiologists from the burden of scoring hand radiography.Objective To determine the ability of multidetector computed tomography (MPR-MDCT) to identify and classify the juxtapapillary duodenal diverticulum (JPDD), with ERCP findings as the gold standard. Methods We retrospectively reviewed all ERCP examinations (n 455) performed between January 2010 to December 2018 and selected 105 patients with JPDD as the inclusion criteria. Of those, 28 patients were excluded because of advanced pancreatic carcinoma, incomplete MDCT examinations and biliary catheter insertion. Finally, MDCT examinations of 77 patients with JPDD were assessed for the presence and type of JPDD. Results MPR-MDCT was able to identify 71 (92.2%) JPDD in 77 cases with 88.9% accuracy, 83.3% sensitivity, and 91.6% specificity in classifying the type of JPDD. MPR-MDCT performed best in determining type 1 JPDD, with accuracy of 95.4% compared with type 2 (83.3%) and type 3 (87.8%). There was no significant difference between age, gender, incidence of biliary stones and pancreatitis between each type of JPDD. No correlation of sizes with types of JPDD was found. Conclusions MPR-MDCT can accurately identify and classify JPDD. This information will be useful in determining the difficulty of ERCP.Aims To compare diabetes patients with hyperglycaemic hyperosmolar state (HHS), diabetic ketoacidosis (DKA), and patients without decompensation (ND). Methods In total, 500,973 patients with type 1 or type 2 diabetes of all ages registered in the diabetes patient follow-up (DPV) were included. Analysis was stratified by age (≤ / > 20 years) and by manifestation/follow-up. Patients were categorized into three groups HHS or DKA-during follow-up according to the most recent episode-or ND. Results At onset of diabetes, HHS criteria were met by 345 (68.4% T1D) and DKA by 9824 (97.6% T1D) patients. DKA patients had a lower BMI(-SDS) in both diabetes types compared to ND. HbA1c was higher in HHS/DKA. During follow-up, HHS occurred in 1451 (42.2% T1D) and DKA in 8389 patients (76.7% T1D). In paediatric T1D, HHS/DKA was associated with younger age, depression, and dyslipidemia. Pump usage was less frequent in DKA patients. In adult T1D/T2D subjects, metabolic control was worse in patients with HHS/DKA. HHS and DKA were also associated with excessive alcohol intake, dementia, stroke, chronic kidney disease, and depression. Conclusions HHS/DKA occurred mostly in T1D and younger patients. However, both also occurred in T2D, which is of great importance in the treatment of diabetes. Better education programmes are necessary to prevent decompensation and comorbidities.Background Recent clinical and animal studies have shown that renal denervation (RDN) improves insulin sensitivity and endothelial dysfunction. However, the specific mechanism remains incompletely understood. The purpose of this study is to investigate the effects of RDN on endothelial dysfunction of type 2 diabetes mellitus (T2DM) rat models with insulin resistance and to explore the underlying molecular mechanisms. Methods Male Sprague-Dawley rats were fed with or without high-fat diet allocated in different groups, combined with low-dose streptozotocin which induces a rat model to develop T2DM with insulin resistance. RDN was conducted 1 week after the rat models fully developed T2DM. The animals were sub-divided into four groups randomly control group (CON, n = 6), diabetic group (T2DM, n = 6), diabetic with sham surgery group (Sham, n = 6) and diabetic with RDN group (RDN, n = 6). Rats in all groups were studied at baseline, both preoperatively and 4 weeks after RDN, respectively. Western blot was used t, ACE2 activated p-AMPK and inhibited p-mTOR, thus promoting autophagy. click here Conclusions RDN may not only increase the expression of ACE2 in the vascular endothelium, but also can via ACE2 activate p-AMPK and inhibit p-mTOR, thus promoting autophagy and improving endothelial dysfunction.Introduction Cholecystokinin type 2 receptor (CCK2R), which mediates the action of gastrin and cholecystokinin (CCK), has been demonstrated to promote the proliferation of colorectal cancer (CRC). A number of studies showed that CCK2R overexpressed in gastric cancer and pancreatic cancer but few in CRC. The correlation between CCK2R expression and clinicopathological characteristics is also not clear. Methods This study investigated CCK2R expression in a wide range of cell lines and clinical CRC samples, and explored expression pattern and prognostic value of CCK2R in relation to clinicopathological parameters. The location and expression levels of CCK2R were measured by immunocytochemical (ICC), qRT-PCR and Western blot. The druggability and antineoplastic effects of CCK2R as a therapeutic target were investigated using an anti-CCK2R targeting recombinant toxin named rCCK8PE38 by CCK-8 assay. Results Compared with paracarcinoma tissues, tumor samples showed overexpression of CCK2R (p = 0.028) including both CRC tissue and plasma samples, with plasma detection showing a significant indication for CCK2R evaluation. Aberrant expression correlated significantly with histological type (p = 0.032) and p53 status (p less then 0.01), and patients with CCK2R overexpression had significantly lower disease-free survival. Application of rCCK8PE38 demonstrated the specificity and druggability of CCK2R as a therapeutic target, providing a strategy for clinical case screening of drugs targeting CCK2R. Conclusion This study highlighted the aberrant expression and clinical correlation of CCK2R and reveals its diagnostic, prognostic and treatment value in CRC. We hypothesize that CCK2R serve as a target for the diagnosis and treatment of this cancer.Purpose Cervical cancer metastasis results in poor prognosis and increased mortality, which is not separated from inflammatory reactions accumulated by prostaglandin E2 (PGE2). As a specific G-protein coupled PGE2 receptor, EP3 is demonstrated as a negative prognosticator of cervical malignancy. Now, we aimed to investigate the pathological mechanism of EP3 in modulating cervical cancer carcinogenesis. Methods Bioinformatics analysis was used to identify PAI-1 and uPAR correlations with EP3 expression, as well as the prognosis of cervical cancer patients. In vitro analyses were carried out to investigate the role of EP3 on cervical cancer proliferation and migration. Results In vitro studies showed that sulprostone (an EP3 agonist) enhanced the proliferation and migration of cervical cancer cells, whereas silencing of EP3 inhibited their proliferation and migration. Furthermore, EP3 knockdown increased the expression of plasminogen activator inhibitor type 1 (PAI-1), urokinase-type plasminogen activator receptor (uPAR), and phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2), but decreased p53 expression.
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