Mesenteric arteriovenous dysplasia/vasculopathy (MAVD/V) is a rare vasculopathy involving both mesenteric arteries and veins with unique vascular lesions. The diagnosis requires comprehensive analysis with histological and clinically relevant examination data, as well as differentiation from Crohn′s disease and other chronic ischemic bowel diseases. This paper summarizes the clinicopathological features of two cases of MAVD/V and reviews the literature in order to improve the understanding of MAVD/V among clinicians and pathologists.

Mesenteric arteriovenous dysplasia/vasculopathy (MAVD/V) is a rare vasculopathy involving both mesenteric arteries and veins with unique vascular lesions. The diagnosis requires comprehensive analysis with histological and clinically relevant examination data, as well as differentiation from Crohn′s disease and other chronic ischemic bowel diseases. This paper summarizes the clinicopathological features of two cases of MAVD/V and reviews the literature in order to improve the understanding of MAVD/V among clinicians and pathologists.

Metabolic-associated fatty liver disease (MAFLD), which is previously known as non-alcoholic fatty liver disease (NAFLD), represents a major health concern worldwide with limited therapy. Here, we provide evidence that ferroptosis, a novel form of regulated cell death characterized by iron-driven lipid peroxidation, was comprehensively activated in liver tissues from MAFLD patients. The canonical-GPX4 (cGPX4), which is the most important negative controller of ferroptosis, is downregulated at protein but not mRNA level. Interestingly, a non-canonical GPX4 transcript-variant is induced (inducible-GPX4, iGPX4) in MAFLD condition. The high fat-fructose/sucrose diet (HFFD) and methionine/choline-deficient diet (MCD)-induced MAFLD pathologies, including hepatocellular ballooning, steatohepatitis and fibrosis, were attenuated and aggravated, respectively, in cGPX4-and iGPX4-knockin mice. cGPX4 and iGPX4 isoforms also displayed opposing effects on oxidative stress and ferroptosis in hepatocytes. Knockdown of iGPX4 by siRNA alleviated lipid stress, ferroptosis and cell injury. Mechanistically, the triggered iGPX4 interacts with cGPX4 to facilitate the transformation of cGPX4 from enzymatic-active monomer to enzymatic-inactive oligomers upon lipid stress, and thus promotes ferroptosis. Co-immunoprecipitation and nano LC-MS/MS analyses confirmed the interaction between iGPX4 and cGPX4. Our results reveal a detrimental role of non-canonical GPX4 isoform in ferroptosis, and indicate selectively targeting iGPX4 may be a promising therapeutic strategy for MAFLD.

Objective To develop a new method of presurgical nasoalveolar molding based on computer-aided design technique.Methods Twenty patients(1 6 boys, 4 girls) with complete unilateral cleft lip and palate(UCLP) who received presurgical nasoalveolar molding were recruited as the treatment group.Twenty patients(15 boys, 5 girls) with complete UCLP who did not receive presurgical orthopedic treatment were selected as the control group.All parameters of the digital maxillary model were measured using the Rapidform XOR3 software.The statistical analysis was performed with SPSS 15.0.Results A'-X and B-Il were reduced significantly after presurgical nasoalveolar molding.However, the mean alveolar height [F-hight (3.7± 1.1) mm, F'-height (4.6±0.9) mm] decreased significantly after treatment(P＜ 0.05).There were significant differences between the treatment group and the control group(P＜0.05).Conclusions Maxillary alveolar morphology could be improved in UCLP infants treated with computer-aided presurgical nasoalveolar molding.The width of the cleft could be reduced and the maxillary midline corrected effectively.However, the alveolar height decreased significantly after the treatment.