Protein-losing enteropathy in Crohn's disease

Protein-losing enteropathy (PLE) is a rare but severe complication of Crohn's disease (CD) and hypoalbuminemia can be one of the presenting symptoms of this illness. The diagnosis of PLE can only be made after exclusion of malnutrition and liver or kidney failure. Significant intestinal leakage can be caused by mucosal injury, increased lymphatic pressure or dilated lymphatics and has been reported in a large number of diseases. The protein-losing can be diagnosed by assessing the excretion of different radiolabeled macromolecules in the faeces or by the clearance of alpha-1-antitrypsine in stools. The primary approach should be the optimization of the nutritional status. Medical treatment of the underlying disease is primordial. In other cases surgical resection of the most affected areas is inevitable. We report a case of a 21-year-old male with a 4 year history of CD, who developed significant hypoproteinemia with pitting oedema, initially in the absence of any other sign of severe disease activity. A "Cr-chloride albumin excretion confirmed our hypothesis of protein-losing enteropathy. Because of sub-obstruction signs some months later, a laparotomy was performed which revealed a severely affected loop with dilatation of the proximal jejunum. Interestingly, multiple large lymph nodes and dilated lymphatics were seen. A partial jejunal resection was performed for stricturing Crohn's disease. Histology showed severe mesenteric granulomatosis, dilated lymph vessels and granulomatous vasculitis. After the resection our patient improved without further albumin infusions and the oedema resolved.     

MiR-210: A potential therapeutic target against radiation-induced enteropathy

A previously undescribed and robust miR210 overexpression is shown in intestinal samples obtained from patients with radiation enteropathy and fibrotic cultured cells. In addition, miR-210 overexpression is repressed by antifibrotic treatment combining pentoxifylline and α-tocopherol.     

Combined Use of Modal Analysis and Machine Learning for Materials Classification

The present study deals with modal work that is a type of framework for structural dynamic testing of linear structures. Modal analysis is a powerful tool that works on the modal parameters to ensure the safety of materials and eliminate the failure possibilities. The concept of classification through this study is validated for isotropic and orthotropic materials, reaching up to a 100% accuracy when deploying the machine learning approach between the mode number and the associated frequency of the interrelated variables that were extracted from modal analysis performed by ANSYS. This study shows a new classification method dependent only on the knowledge of resonance frequency of a specific material and opens new directions for future developments to create a single device that can identify and classify different engineering materials.     

Seladin-1 is a novel lipopolysaccharide (LPS)-responsive gene and inhibits the tumour necrosis factor-�� production and osteoclast formation in response to LPS

Selective Alzheimer disease indicator‐1 (seladin‐1) is a broadly expressed oxidoreductase and is related to Alzheimer disease, cholesterol metabolism and carcinogenesis. The effect of lipopolysaccharide (LPS) on the expression of seladin‐1 was examined using RAW 264.7 macrophage‐like cells and murine peritoneal macrophages. Lipopolysaccharide induced the expression of seladin‐1 protein and messenger RNA in those macrophages. The seladin‐1 expression was also augmented by a series of Toll‐like receptor ligands. The LPS augmented the expression of seladin‐1 via reactive oxygen species generation and p38 activation. Seladin‐1 inhibited LPS‐induced activation of p38 but not nuclear factor‐κB and inhibited the production of tumour necrosis factor‐α in response to LPS. Moreover, seladin‐1 inhibited LPS‐induced osteoclast formation and enhanced LPS‐induced alkaline phosphatase activity. Therefore, it was suggested that seladin‐1 might be an LPS‐responsible gene product and regulate the LPS‐induced inflammatory response negatively.