Biological therapy with IFX enables mucosal healing in pediatric patients with CD. Induction therapy with infliximab was found to be clinically effective in 72% of Polish pediatric patients with CD and induced a remission in 33% of them. Induction therapy with infliximab helps to increase BMI.

The progression of non-alcoholic fatty liver (NAFL) into non-alcoholic steatohepatitis implicates multiple mechanisms, chief of which is mitochondrial dysfunction. However, the sequence of events underlying mitochondrial failure are still poorly clarified. In this work, male C57BL/6J mice were fed with a high-fat plus high-sucrose diet for 16, 20, 22, and 24 weeks to induce NAFL. Up to the 20th week, an early mitochondrial remodeling with increased OXPHOS subunits levels and higher mitochondrial respiration occurred. Interestingly, a progressive loss of mitochondrial respiration along “Western diet” feeding was identified, accompanied by higher susceptibility to mitochondrial permeability transition pore opening. Importantly, our findings prove that mitochondrial alterations and subsequent impairment are independent of an excessive mitochondrial reactive oxygen species (ROS) generation, which was found to be progressively diminished along with disease progression. Instead, increased peroxisomal abundance and peroxisomal fatty acid oxidation-related pathway suggest that peroxisomes may contribute to hepatic ROS generation and oxidative damage, which may accelerate hepatic injury and disease progression. We show here for the first time the sequential events of mitochondrial alterations involved in non-alcoholic fatty liver disease (NAFLD) progression and demonstrate that mitochondrial ROS are not one of the first hits that cause NAFLD progression.

Nonalcoholic fatty liver disease (NAFLD) is characterized by the development of steatosis, which can ultimately compromise liver function. Mitochondria are key players in obesity-induced metabolic disorders; however, the distinct role of hypercaloric diet constituents in hepatic cellular oxidative stress and metabolism is unknown. Male mice were fed either a high-fat (HF) diet, a high-sucrose (HS) diet or a combined HF plus HS (HFHS) diet for 16 weeks. This study shows that hypercaloric diets caused steatosis; however, the HFHS diet induced severe fibrotic phenotype. At the mitochondrial level, lipidomic analysis showed an increased cardiolipin content for all tested diets. Despite this, no alterations were found in the coupling efficiency of oxidative phosphorylation and neither in mitochondrial fatty acid oxidation (FAO). Consistent with unchanged mitochondrial function, no alterations in mitochondrial-induced reactive oxygen species (ROS) and antioxidant capacity were found. In contrast, the HF and HS diets caused lipid peroxidation and provoked altered antioxidant enzyme levels/activities in liver tissue. Our work provides evidence that hepatic oxidative damage may be caused by augmented levels of peroxisomes and consequently higher peroxisomal FAO-induced ROS in the early NAFLD stage. Hepatic damage is also associated with autophagic flux impairment, which was demonstrated to be diet-type dependent. The HS diet induced a reduction in autophagosomal formation, while the HF diet reduced levels of cathepsins. The accumulation of damaged organelles could instigate hepatocyte injuries and NAFLD progression.

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An atypical type A thymoma is a newly added entity to the last World Health Organization (WHO) histological classification [2015] of uncertain prognosis. The conventional type A and AB thymomas are usually locally aggressive neoplasms that rarely metastasize with distant metastases to the central nervous system (CNS) occurring extremely exceptionally. We present a history of a woman with a mediastinal tumor originally considered to be a Masaoka-Koga stage II "mixed thymoma with well-differentiated thymic carcinoma component" according to the historic Müller-Hermelink nomenclature. By applying the criteria of the new WHO classification the tumor should be reclassified as an AB thymoma with an atypical A component. The patient developed metastases to the lung and brain 10 and 15 years after the original diagnosis, respectively. All metastases morphologically corresponded to an atypical A component of primary thymoma. Molecular study revealed GTF2I mutations in the primary and one of the metastatic tumors. To our knowledge, this is the first description of a GTF2I mutation in AB thymoma with atypical A component and its metastases. The presented case highlights the necessity of an accurate microscopic search for atypical areas in A or AB thymomas because of their potentially negative impact on prognosis.