A European Survey to Identify Challenges in the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease.

Background And Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its more severe subtype, metabolic dysfunction-associated steatohepatitis (MASH), are highly prevalent and strongly associated with obesity and type 2 diabetes (T2D). This study sought to identify challenges to the diagnosis, treatment and management of people living with MASLD and MASH and understand the key barriers to adopting relevant clinical guidelines.

Methods: A real-world, cross-sectional study (BARRIERS-MASLD) consisting of a quantitative survey and qualitative interviews of physicians in France, Germany, Italy, Spain and the United Kingdom was conducted from March to September 2023.

Identifying the location-dependent adipose tissue bacterial DNA signatures in obese patients that predict body weight loss.

Recent sets of evidence have described profiles of 16S rDNA sequences in host tissues, notably in fat pads that are significantly overrepresented and can serve as signatures of metabolic disease. However, these recent and original observations need to be further detailed and functionally defined. Here, using state-of-the-art targeted DNA sequencing and discriminant predictive approaches, we describe, from the longitudinal FLORINASH cohort of patients who underwent bariatric surgery, visceral, and subcutaneous fat pad-specific bacterial 16SrRNA signatures.

A Metabolomic Approach to Unexplained Syncope.

This study aims to identify a metabolomic signature that facilitates the classification of syncope and the categorization of the unexplained syncope (US) to aid in its management. We compared a control group (CTRL, = 10) with a transient loss of consciousness (TLC) group divided into the OH group ( = 23) for orthostatic syncope, the NMS group ( = 26) for neuromediated syncope, the CS group ( = 9) for cardiological syncope, and the US group ( = 27) for US defined as syncope without a precise categorization after first- and second-level diagnostic approaches. The CTRL and the TLC groups significantly differed in metabolic profile.

Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson's disease overexpressing human alpha synuclein.

Increasing efforts have been made to elucidate how genetic and environmental factors interact in Parkinson's disease (PD). In the present study, we assessed the development of symptoms on a genetic PD rat model that overexpresses human α-synuclein (Snca) at a presymptomatic age, exposed to a pro-inflammatory insult by intraperitoneal injection of lipopolysaccharide (LPS), using immunohistology, high-dimensional flow cytometry, constant potential amperometry, and behavioral analyses. A single injection of LPS into WT and Snca rats triggered long-lasting increase in the activation of pro-inflammatory microglial markers, monocytes, and T lymphocytes.