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could enhance prenatal counseling of pregnancies with congenital CMV infection with normal prenatal imaging. © 2020 International Society of Ultrasound in Obstetrics and Gynecology.Childhood trauma (CT) is a well-established risk factor for major depressive disorder (MDD). Selleckchem CW069 However, the underlying mechanism linking CT and MDD remains not fully understood. The present study tested the hypothesis that CT have effects on specific types of anhedonia in depression via reward system. To do so, we evaluated different aspects of anhedonia and resting-state functional connectivity (FC) in reward system among 66 patients with MDD (44 with moderate-to-severe and 22 with no or low CT), and 57 healthy controls (HC; 23 with moderate-to-severe and 34 with no or low CT). Results showed that MDD patients with moderate-to-severe CT suffered more severe state anhedonic depression than patients with no or low level of CT. Individuals with moderate-to-severe CT, irrespective of MDD diagnosis, had elevated physical, social and anticipatory but not consummatory trait anhedonia, and demonstrated decreased left nucleus accumbens (NAcc)-right orbital frontal cortex (OFC) and left ventral caudate-left OFC connectivity compared to those with no or low exposure. Left NAcc-right OFC connectivity mediated relationship between CT and state anhedonia in MDD. The total altered ventral striatum (VS)-OFC connectivity mediated links between CT and physical trait anhedonia in HC. These findings highlight specific types of anhedonia and the core reward system as targets of CT. Blunted hedonic responses via decreased coupling within core reward system may be involved in the mechanism of depression following CT. Implications for clinical interventions are also discussed.

To estimate the effect of elective induction of labour at 39 weeks of gestation on children's educational outcomes as measured by the Australian National Assessment Program-Literacy and Numeracy (NAPLAN) tests at year 3 (~8 years of age), compared with expectant management.

We merged perinatal data, including information regarding all infants in South Australia from 1999 to 2008, with children's school assessment data (i.e., NAPLAN data). The study population included all singleton births born without malformations at 39-42 weeks of gestation in vertex presentation. Children had to have undertaken year-3 NAPLAN (~8 years of age). We excluded births from women who had a contraindication to vaginal delivery and with conditions possibly justifying elective delivery before 39 weeks of gestation. Our outcome of interest was children's educational outcomes as measured by NAPLAN. The NAPLAN included five learning domains (reading, writing, spelling, grammar and numeracy). Each domain was categorised according toCI -0.01 to 0.04)) and numeracy (0.03 (95% CI -0.00 to 0.05)).

Elective induction of labour at 39 weeks of gestation did not affect children's standardised literacy and numeracy testing outcomes at eight years of age when compared with expectant management. This article is protected by copyright. All rights reserved.

Elective induction of labour at 39 weeks of gestation did not affect children's standardised literacy and numeracy testing outcomes at eight years of age when compared with expectant management. This article is protected by copyright. All rights reserved.Autophagy is a mechanism that enables cells to maintain cellular homeostasis by removing damaged materials and mobilizing energy reserves in conditions of starvation. Although nutrient availability strongly impacts the process of autophagy, the specific metabolites that regulate autophagic responses have not yet been determined. Recent results indicate that S-adenosylmethionine (SAM) represents a critical inhibitor of methionine starvation-induced autophagy. SAM is primarily involved in four key metabolic pathways transmethylation, transsulphuration, polyamine synthesis and 5'-deoxyadenosyl 5'-radical-mediated biochemical transformations. SAM is the sole methyl group donor involved in the methylation of DNA, RNA and histones, modulating the autophagic process by mediating epigenetic effects. Moreover, the metabolites of SAM, such as homocysteine, glutathione, decarboxylated SAM and spermidine, also exert important influences on the regulation of autophagy. From our perspective, nuclear-cytosolic SAM is a conserved metabolic inhibitor that connects cellular metabolic status and the regulation of autophagy. In the future, SAM might be a new target of autophagy regulators and be widely used in the treatment of various diseases.

Posterior cortical atrophy (PCA) is a rare neurodegenerative syndrome, defined by a distinctive clinical-radiological profile, with Alzheimer's disease (AD) pathology accounting for the majority of cases. The aim of this report was to present the case of a patient with impairment of visual and constructional abilities as initial manifestations.

The patient underwent a multidimensional assessment, including neuropsychological evaluation, structural and functional imaging and genetic screening.

Neurological and neuropsychological assessment showed an impairment of constructive and visuo-spatial skills, associated with dyscalculia, simultanagnosia, optic ataxia and oculomotor apraxia. In accordance with the latest consensus criteria, a diagnosis of PCA was made. Consistent with the clinical findings, structural and functional imaging showed a peculiar pattern of atrophy with primary involvement of right parieto-occipital cortices, whereas cerebrospinal fluid biochemical analysis did not reveal a profile compatible with AD pathology. Genetic screening identified a known pathogenic GRN mutation.

We present a case of PCA in a GRN mutation carrier in whom a concomitant AD pathological process was excluded. Consequently, although lacking histological data, our case suggests GRN-related pathology causative of PCA. Through this report we provide further evidence for a new neurodegenerative pathway leading to PCA, extending the clinical spectrum of GRN-associated phenotypes.

We present a case of PCA in a GRN mutation carrier in whom a concomitant AD pathological process was excluded. Consequently, although lacking histological data, our case suggests GRN-related pathology causative of PCA. Through this report we provide further evidence for a new neurodegenerative pathway leading to PCA, extending the clinical spectrum of GRN-associated phenotypes.