SciCombinator

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To evaluate the associations between adiposity measures (body mass index, waist circumference, and waist-to-height ratio) with decline in glomerular filtration rate (GFR) and with all cause mortality.

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Artificial intelligence is likely to perform several roles currently performed by humans, and the adoption of artificial intelligence-based medicine in gastroenterology practice is expected in the near future. Medical image-based diagnoses, such as pathology, radiology, and endoscopy, are expected to be the first in the medical field to be affected by artificial intelligence. A convolutional neural network, a kind of deep-learning method with multilayer perceptrons designed to use minimal preprocessing, was recently reported as being highly beneficial in the field of endoscopy, including esophagogastroduodenoscopy, colonoscopy, and capsule endoscopy. A convolutional neural network-based diagnostic program was challenged to recognize anatomical locations in esophagogastroduodenoscopy images, Helicobacter pylori infection, and gastric cancer for esophagogastroduodenoscopy; to detect and classify colorectal polyps; to recognize celiac disease and hookworm; and to perform small intestine motility characterization of capsule endoscopy images. Artificial intelligence is expected to help endoscopists provide a more accurate diagnosis by automatically detecting and classifying lesions; therefore, it is essential that endoscopists focus on this novel technology. In this review, we describe the effects of artificial intelligence on gastroenterology with a special focus on automatic diagnosis, based on endoscopic findings.

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Endoscopic transpapillary or transanastomotic pancreatic duct drainage (PD) is the mainstay of drainage in symptomatic pancreatic duct obstruction or leakage. However, transpapillary or transanastomotic PD can be technically difficult due to the tight stricture or surgically altered anatomy (SAA), and endoscopic ultrasound (EUS)-guided PD (EUS-PD) is now increasingly used as an alternative technique. There are two approaches in EUS-PD: EUS-guided rendezvous (EUS-RV) and EUS-guided transmural drainage (EUS-TMD). In cases with normal anatomy, EUS-RV should be the first approach, whereas EUS-TMD can be selected in cases with SAA or duodenal obstruction. In our literature review, technical success and adverse event rates were 78.7% and 21.8%, respectively. The technical success rate of EUS-RV appeared lower than EUS-TMD due to the difficulty in guidewire passage. In future, development of dedicated devices and standardization of EUS-PD procedure are necessary.

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The impact of diabetes on perioperative outcomes remains incompletely understood. Our purpose is to evaluate post-operative complications and mortality in patients with diabetes. Using the institutional and clinical databases of three university hospitals from 2009⁻2015, we conducted a matched study of 16,539 diabetes patients, aged >20 years, who underwent major surgery. Using a propensity score matching procedure, 16,539 surgical patients without diabetes who underwent surgery were also selected. Logistic regressions were used to calculate the odds ratios (ORs) with 95% confidence intervals (CIs) for post-operative complications and in-hospital mortality associated with diabetes. Patients with diabetes had a higher risk of postoperative septicemia (OR 1.33, 95% CI 1.01⁻1.74), necrotizing fasciitis (OR 3.98, 95% CI 1.12⁻14.2), cellulitis (OR 2.10, 95% CI 1.46⁻3.03), acute pyelonephritis (OR 1.86, 95% CI 1.01⁻3.41), infectious arthritis (OR 3.89, 95% CI 1.19⁻12.7), and in-hospital mortality (OR 1.51, 95% CI 1.07⁻2.13) compared to people without diabetes. Previous admission for diabetes (OR 2.33, 95% CI 1.85⁻2.93), HbA1c >8% (OR 1.96, 95% CI 1.64⁻2.33) and fasting glucose >180 mg/dL (OR 1.90, 95% CI 1.68⁻2.16) were predictors for post-operative adverse events. Diabetes patients who underwent surgery had higher risks of infectious complications and in-hospital mortality compared with patients without diabetes who underwent similar major surgeries.

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Background/Study context: Posture and gait are complex sensorimotor functions affected by age. These difficulties are particularly apparent when performing cognitively demanding tasks. Characterizing the functional organization of brain networks involved in these associations remains a challenge because of the incompatibility of brain imagery techniques with gross body movements. The present study aimed at testing whether resting-state functional connectivity of sensorimotor networks is associated with posture and gait performance recorded offline, in young and older adults.

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Background Intrauterine growth retardation ( IUGR ) is related to pulmonary artery hypertension in adults, and mi croRNA -206 (miR-206) is proposed to affect the proliferation and apoptosis of pulmonary artery smooth muscle cells ( PASMC s) via post-transcriptional regulation. Methods and Results In an IUGR rat model, we found that the expression and function of potassium voltage-gated channel subfamily A member 5 (Kv1.5) in PASMC s was inhibited, and pulmonary artery hypertension was exaggerated after chronic hypoxia ( CH ) treatment as adults. micro RNA expression was investigated in PASMC s from 12-week-old male IUGR rats with CH by microarray, polymerase chain reaction, and in situ hybridization. The expression levels of Kv1.5 in primary cultured PASMC s and pulmonary artery smooth muscle from IUGR or control rats were evaluated with and without application of an miR-206 inhibitor. Right ventricular systolic pressure, cell proliferation, luciferase reporter assay, and IKv were also calculated. We found increased expression of miR-206 in resistance pulmonary arteries of IUGR rats at 12 weeks compared with newborns. Application of an miR-206 inhibitor in vivo or in vitro increased expression of Kv1.5 α-protein and KCNA 5. Also, decreased right ventricular systolic pressure and cell proliferation were observed in PASMC s from 12-week-old control and IUGR rats after CH , while inhibitor did not significantly affect control and IUGR rats. Conclusions These results suggest that expression of Kv1.5 and 4-aminopyridine (Kv channel special inhibitor)-sensitive Kv current were correlated with the inhibition of miR-206 in PA rings of IUGR - CH rats and cultured IUGR PASMC s exposed to hypoxia. Thus, miR-206 may be a trigger for induction of exaggerated CH-pulmonary artery hypertension of IUGR via Kv1.5.

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Background Cardiac ischemic/reperfusion (I/R) injury leads to brain damage. A new antihyperlipidemic drug is aimed at inhibiting PCSK 9 (proprotein convertase subtilisin/kexin type 9), a molecule first identified in a neuronal apoptosis paradigm. Thus, the PCSK 9 inhibitor ( PCSK 9i) may play a role in neuronal recovery following cardiac I/R insults. We hypothesize that PCSK 9i attenuates brain damage caused by cardiac I/R via diminishing microglial/astrocytic hyperactivation, β-amyloid aggregation, and loss of dendritic spine. Methods and Results Adult male rats were divided into 7 groups: (1) control (n=4); (2) PCSK 9i without cardiac I/R (n=4); (3) sham (n=4); and cardiac I/R (n=40). Cardiac I/R rats were divided into 4 subgroups (n=10/subgroup): (1) vehicle; (2) PCSK 9i (10 μg/kg, IV) before ischemia; (3) PCSK 9i during ischemia; and (4) PCSK 9i at the onset of reperfusion. At the end of cardiac I/R protocol, brains were removed to determine microglial and astrocytic activities, β-amyloid aggravation, and dendritic spine density. The cardiac I/R led to the activation of the brain’s innate immunity resulting in increasing Iba1+ microglia, GFAP + astrocytes, and CD 11b+/ CD 45+high cell numbers. However, CD 11b+/ CD 45+low cell numbers were decreased following cardiac I/R. In addition, cardiac I/R led to reduced dendritic spine density, and increased β-amyloid aggregation. Only the administration of PCSK 9i before ischemia effectively attenuated these deleterious effects on the brain following cardiac I/R. PCSK 9i administration under the physiologic condition did not affect the aforementioned parameters. Conclusions Cardiac I/R injury activated microglial activity in the brain, leading to brain damage. Only the pretreatment with PCSK 9i prevented dendritic spine loss via reduction of microglial activation and Aβ aggregation.

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Background Morphine administration is a strong predictor of delayed onset of action of orally administered ticagrelor in patients with ST-segment-elevation myocardial infarction, likely because of impaired gastrointestinal motility. The aim of this study was to evaluate whether the peripheral opioid antagonist methylnaltrexone could improve pharmacodynamics and pharmacokinetics of orally administered ticagrelor in patients with ST-segment-elevation myocardial infarction receiving morphine. Methods and Results The MOVEMENT (Methylnaltrexone to Improve Platelet Inhibition of Ticagrelor in Morphine-Treated Patients With ST-Segment Elevation Myocardial Infarction) trial was a multicenter, prospective, randomized, controlled trial in patients with ST-segment-elevation myocardial infarction treated with morphine and ticagrelor. Upon arrival to the catheterization laboratory, patients were randomized to a blinded intravenous injection of either methylnaltrexone (8 or 12 mg according to weight) or 0.9% sodium chloride. The proportion of patients with high on-treatment platelet reactivity and plasma concentrations of ticagrelor and AR -C124910XX were assessed at baseline (arrival in the catheterization laboratory) and 1 and 2 hours later. A total of 82 patients received either methylnaltrexone (n=43) or placebo (n=39). Median (interquartile range) time from ticagrelor administration to randomization was 41 (31-50) versus 45.5 (37-60) minutes ( P=0.16). Intravenous methylnaltrexone administration did not significantly affect prevalence of high on-treatment platelet reactivity at 2 hours after inclusion, the primary end point, when compared with placebo (54% versus 51%, P=0.84). Plasma concentrations of ticagrelor and its active metabolite, the prespecified secondary end points, did not differ significantly between the groups over time. There was no significant difference in patient self-estimated pain between the groups. Conclusions Methylnaltrexone did not significantly improve platelet reactivity or plasma concentrations of orally administered ticagrelor in patients with ST-segment-elevation myocardial infarction receiving morphine. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 02942550.

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Background The prognostic significance of obstructive sleep apnea ( OSA ) in patients with acute coronary syndrome ( ACS ) in the contemporary era is unclear. We performed a large, prospective cohort study and did a landmark analysis to delineate the association of OSA with subsequent cardiovascular events after ACS onset. Methods and Results Between June 2015 and May 2017, consecutive eligible patients admitted for ACS underwent cardiorespiratory polygraphy during hospitalization. OSA was defined as an apnea-hypopnea index ≥15 events·h-1. The primary end point was major adverse cardiovascular and cerebrovascular event ( MACCE ), including cardiovascular death, myocardial infarction, stroke, ischemia-driven revascularization, or hospitalization for unstable angina or heart failure. OSA was present in 403 of 804 (50.1%) patients. During median follow-up of 1 year, cumulative incidence of MACCE was significantly higher in the OSA group than in the non- OSA group (log-rank, P=0.041). Multivariate analysis showed that OSA was nominally associated with incidence of MACCE (adjusted hazard ratio, 1.55; 95% CI, 0.94-2.57; P=0.085). In the landmark analysis, patients with OSA had 3.9 times the risk of incurring a MACCE after 1 year (adjusted hazard ratio, 3.87; 95% CI, 1.20-12.46; P=0.023), but no increased risk was found within 1-year follow-up (adjusted hazard ratio, 1.18; 95% CI, 0.67-2.09; P=0.575). No significant differences were found in the incidence of cardiovascular death, myocardial infarction, and ischemia-driven revascularization, except for a higher rate of hospitalization for unstable angina in the OSA group than in the non- OSA group (adjusted hazard ratio, 2.10; 95% CI, 1.09-4.05; P=0.027). Conclusions There was no independent correlation between OSA and 1-year MACCE after ACS . The increased risk associated with OSA was only observed after 1-year follow-up. Efficacy of OSA treatment as secondary prevention after ACS requires further investigation.

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