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To examine the hypothesis that normalization of low circulating leptin levels in patients with anorexia nervosa ameliorates hyperactivity, three seriously ill females with hyperactivity were treated off-label with metreleptin (recombinant human leptin) for up to 14 days. Drive for activity, repetitive thoughts of food, inner restlessness, and weight phobia decreased in two patients. Surprisingly, depression improved rapidly in all patients. No serious adverse events occurred. Due to obvious limitations of uncontrolled case series, placebo-controlled clinical trials are mandatory to confirm the observed rapid onset of beneficial effects. Our findings suggest an important role of hypoleptinemia in the mental and behavioral phenotype of anorexia nervosa.Phosphoglycerate mutase 1 (PGAM1) is a recently identified key catalytic enzyme in aerobic glycolysis. Recent literature has documented that dysregulated PGAM1 expression is associated with tumorigenesis in various cancers. However, the expression status and biological function of PGAM1 in non-small-cell lung cancer (NSCLC) are poorly elucidated. In this study, we found that PGAM1 was overexpressed in NSCLC tissues and that high expression of PGAM1 was associated with poor prognosis in NSCLC patients. Functionally, gain- and loss-of-function analysis showed that PGAM1 promoted proliferation and invasion in vitro, and facilitated tumor growth in vivo. Mechanistically, the transforming growth factor-β (TGF-β) signaling pathway was also markedly impaired in response to PGAM1 silencing. Additionally, we verified that PGAM1 was inhibited by miR-3614-5p via direct targeting of its 3'-untranslated regions in a hypoxia-independent manner. Furthermore, overexpression of miR-3614-5p attenuated NSCLC cell proliferation and invasion, and these effects could be partially reversed by reintroduction of PGAM1. Conclusively, our results suggest that the miR-3614-5p/PGAM1 axis plays a critical role during the progression of NSCLC, and these findings may provide a potential target for the development of therapeutic strategies for NSCLC patients.BACKGROUND Gestational weight gain (GWG) is an important index influencing perinatal outcomes. Inappropriate weight gain during pregnancy is strongly associated with multiple pregnancy complications. In pregnant liver transplant recipients whose risk of adverse pregnancy outcomes is already high, this aspect may be even more significant. The present study analyzed the gestational weight gain in female liver transplant recipients and its effect on neonatal complications. MATERIAL AND METHODS A cohort study of retrospective data was performed in the 1st Department of Obstetrics and Gynecology, Medical University of Warsaw. There were 23 patients who fulfilled all inclusion criteria. The gestational weight gain was analyzed in the context of pre-pregnancy BMI, immunosuppression, and perinatal outcomes. RESULTS The preterm delivery rate was 39.13% and GWG increased according to the duration of pregnancy. The model adjusted to week of delivery revealed no association between weight gain and the length of pregnancy (p=0.82). GWG in liver transplant recipients did not affect hypotrophy incidence, adverse perinatal outcomes, or caesarian delivery rate. A positive correlation between GWG and neonatal birth weight was observed (p=0.06). One patient, with coexisting PIH, had a stillbirth at 23 weeks. In all other cases, the 5-min Apgar score was 10 points. CONCLUSIONS Current obstetrical recommendations do not consider patients with chronic diseases undergoing immunosuppressive treatment. Proper counselling and preparing liver transplant recipients for pregnancy, especially optimizing maternal pre-pregnancy BMI, may be an important element in improving perinatal outcomes by lowering the risk of maternal complications. GWG itself is not relevant as a predictor of term gestation, but it might be important in achieving eutrophic fetus growth.BACKGROUND Pancreas transplantation has proven to be the most effective therapeutic option for insulin-dependent diabetes mellitus. However, despite advances in surgical technique and continuously improving outcomes, pancreas transplantation has the highest complication rate among all solid-organ transplants. Vascular complications in particular can be catastrophic, with graft- and life-threatening potential. Ectopic variceal bleeding is less common and is rarely reported in the literature. CASE REPORT A 51-year-old man presented with recurrent intermittent gastrointestinal bleeding (GIB) associated with hepatic dysfunction and portal hypertension 4 years after a successful pancreas-after-kidney transplant. Sodium oxamate purchase Apart from positive serology for hepatitis E virus, all the other liver disease screening results were negative. He was extensively investigated with 6 computed tomography (CT) scans, 3 esophago-gastro-duodenoscopies (EGD), 3 colonoscopies, and 1 visceral arteriogram before the plausible diagnosis of ectopic trans-anastomotic variceal bleeding involving the pancreas transplant was established. Selective variceal catheterization and embolization were done with 3% sodium tetradecyl sulphate (STD). He remained free of bleeding after embolization. CONCLUSIONS This case report adds to the scanty literature on the management of ectopic variceal bleeding in a pancreas transplant recipient. Diagnosis of ectopic varix is usually challenging and frequently requires a visceral arteriogram. We describe a novel minimally-interventional technique to obtain source control and also discuss the complexity involved in the management, along with future implications.BACKGROUND Chronic hypertension changes the function and structure of the heart and blood vessels. This study aimed to explore the role of the NOD1/Rip2 (nucleotide-binding oligomerization domain 1/receptor-interacting protein 2) signaling pathway in myocardial remodeling in spontaneously hypertensive rats (SHRs). MATERIAL AND METHODS Blood pressure was measured using a tail cuff. The cardiac structure was observed using echocardiography. Slices of the myocardium were stained with hematoxylin and eosin. The expression of NOD1 and Rip2 was detected using real-time polymerase chain reaction, western blot, and immunohistochemistry. The content and distribution of collagen in the myocardium were observed using Van Gieson staining. Enzyme-linked immunosorbent assay was used to detect the interleukin-1 (IL-1) concentrations. SHRs were treated with the NOD1 agonist iE-DAP and NOD1 inhibitor ML130. RESULTS The NOD1 agonist increased blood pressure in SHRs, and the NOD1 inhibitor decreased blood pressure; the interventricular septum thickness (IVST) and left ventricular posterior wall thickness (LVPWT) of the agonist-treated group were thicker than those of the control group, and the antagonist exerted the opposite effects.
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