The sensitivity of serum TFF3 for monitoring CD activity was 100% and the specificity was 76.2%. CONCLUSIONS TFF3 level increased with CD activity, which is of significance for diagnosis and for evaluation of mucosal healing. TFF3 could also be a marker in pediatric UC, as TFF3 positively correlated with UCAI. IMPACT The diagnosis and evaluation of IBD is difficult; endoscopy provides objective assessment; TFF3 can be a useful marker instead of endoscopy.TFF3 was increased in active CD of children; TFF3 can be used as a clinical marker of pediatric CD; TFF3 can diagnose and evaluate mucosal healing of CD.Pediatrician should pay attention to clinical marker; TFF3 level may be a key evaluation of mucosal healing of CD; the value of diagnosis of TFF3 in CD is important.BACKGROUND Mechanical ventilation of preterm neonates is associated with neuroinflammation and an increased risk of adverse neurological outcomes. Human amnion epithelial cells (hAECs) have anti-inflammatory and regenerative properties.  https://www.selleckchem.com/products/vorapaxar.html  We aimed to determine if intravenous administration of hAECs to preterm lambs would reduce neuroinflammation and injury at 2 days of age. METHODS Preterm lambs were delivered by cesarean section at 128-130 days' gestation (term is ~147 days) and either ventilated for 48 h or humanely killed at birth. Lambs received 3 mL surfactant (Curosurf) via endotracheal tube prior to delivery (either with or without 90 × 106 hAECs) and 3 mL intravenous phosphate-buffered saline (with or without 90 × 106 hAECs, consistent with intratracheal treatment) after birth. RESULTS Ventilation increased microglial activation, total oligodendrocyte cell number, cell proliferation and blood-brain barrier permeability (P  less then  0.05, PBS + ventilation and hAEC + ventilation vs. control), but did ntion to the preterm neonate is safe.Considering that hAECs are being used in phase 1 trials for the treatment of BPD in preterm infants, with future trials planned for neonatal neuroprotection, we believe these observations are highly relevant.Familial hypercholesterolemia (FH) is considered the genetic cause of coronary heart disease and ischemic stroke. FH is mainly an autosomal codominant pattern-based disorder and is primarily determined by point mutations within the low-density lipoprotein receptor, apolipoprotein B, and proprotein convertase subtilisin/kexin type 9 genes, causing increased low-density lipoprotein cholesterol levels in the serum of untreated individuals. The accumulation will eventually lead to atherosclerotic cardiovascular disease. Although clinical criteria comprising several prognosis scores, such as the Simon Broome, Dutch Lipid Clinic Network, Make Early Diagnosis to Prevent Early Death, and the recently proposed Montreal-FH-SCORE, are the conventional basis of diagnosing FH, the genetic diagnosis made by single nucleotide polymorphism genotyping, multiplex ligation-dependent probe amplification analysis, and sequencing (both Sanger and Next-Generation sequencing) offers unequivocal diagnosis. Given the heterogeneity of known mutations, the genetic diagnosis of FH is often difficult to establish, despite the growing evidence of the causative mutations, as well as the polygenic aspect of this pathology and the importance of cascade screening of the FH patient‚s healthy family members. This review article details different genetic techniques that can be used in FH identification when there is a clinical FH suspicion based on criteria comprised in prognosis scores, knowing that none of these are exhaustive in the diagnosis, yet they efficaciously overlap and complement each other for confirming the disease at the molecular level.OBJECTIVE Heart failure (HF) is a progressive clinical syndrome. SELFIE-TR is a registry illustrating the overall HF patient profile of Turkey. Herein, all-cause mortality (ACM) data during follow-up were provided. METHODS This is a prospective outcome analysis of SELFIE-TR. Patients were classified as acute HF (AHF) versus chronic HF (CHF) and HF with reduced ejection fraction (HFrEF), HF with mid-range ejection fraction, and HF with preserved ejection fraction and were followed up for ACM. RESULTS There were 1054 patients with a mean age of 63.3±13.3 years and with a median follow-up period of 16 (7-17) months. Survival data within 1 year were available in 1022 patients. Crude ACM was 19.9% for 1 year in the whole group. ACM within 1 year was 13.7% versus 32.6% in patients with CHF and AHF, respectively (p less then 0.001). Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, beta blocker, and mineralocorticoid receptor antagonist were present in 70.6%, 88.2%, and 50.7%, respectively. In the whole cohort, survival curves were graded according to guideline-directed medical therapy (GDMT) scores ≤1 versus 2 versus 3 as 28% versus 20.2% versus 12.2%, respectively (p less then 0.001). Multivariate analysis of the whole cohort yielded age (p=0.009) and AHF (p=0.028) as independent predictors of mortality in 1 year. CONCLUSION One-year mortality is high in Turkish patients with HF compared with contemporary cohorts with AHF and CHF. Of note, GDMT score is influential on 1-year mortality being the most striking one on chronic HFrEF. On the other hand, in the whole cohort, age and AHF were the only independent predictors of death in 1 year.OBJECTIVE To the best of our knowledge, there is no up-to-date information regarding the presentation, management, and clinical course of patients with acute myocardial infarction (MI) in Turkey. The TURKMI registry is designed to provide an insight into the characteristics, management from the symptoms onset to the hospital discharge, and outcome of patients with acute MI in Turkey. METHODS The TURKMI study, as a nationwide registry, will be conducted in 50 percutaneous coronary intervention-capable centers, selected from each EuroStat NUTS region in Turkey according to their population sampling weight, prioritizing the hospital volume in each region. All consecutive patients with acute MI admitted to the coronary care units within the 48 hours of the symptoms onset will be prospectively enrolled during a predefined 2-week period. The first step of the study has a cross-sectional design in which baseline information such as symptoms, risk factors, time periods at each step from the symptoms onset to revascularization, way of arrival to hospital, biochemical analysis, and in-hospital management and outcome will be assessed.