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Ameloblastic fibroma (AF) is a rare benign mixed tumor composed of odontogenic mesenchyme and epithelial tissue. AF typically develops in mandibular molars of young patients during childhood and adolescence, and rarely in adult. The primary treatment for AF is conservative enucleation of the tumor considering the patient's age and tumor size. However, mandibulectomy was performed for large and multilocular lesions. Computer-aided surgery has recently become popular in the field of oral and maxillofacial surgery. Here, we report a rare case of extensive AF in an elderly woman, as well as a summary of their clinical features based on a review of 24 cases, which we successfully treated using a radical surgical approach of a computer-assisted surgery system. A 60-year-old woman presented with right posterior buccal gingival swelling in the mandible. Based on incisional biopsy results, the lesion was suspected to be caused by AF. With the assistance of virtual surgical planning, hemi-mandibulectomy was performed followed by immediate mandibular reconstruction with fibula osteocutaneous free flap and patient-specific titanium plate. The final diagnosis of AF was made based on the postoperative resection specimen. The patient's recovery period was uneventful. The patient returned to functional and aesthetic success, and a postoperative 3D-reconstructed computed tomography image revealed little clinical difference between the preoperative planning and postoperative results. This case demonstrates that a computer-aided surgery system can be an effective treatment option for the extensive AF radical approach. Long-term monitoring is required because AF has the potential for recurrence and malignant transformation, especially in adult. [ABSTRACT FROM AUTHOR]

Exosomes are extracellular vesicles primarily responsible for intercellular communication, and they contain nucleic acids and proteins. Exosome secretion has been observed in the intestines, suggesting their physiological effects on the receptor cells of target tissues. It is possible that intestinal epithelial cells recognize food components as ligands, resulting in exosome secretion. However, research on intestine‐derived exosomes regulated by food ingredients is limited. In this study, Caco‐2 cells were utilized as an intestinal epithelial model for proteomic profiling. NanoLC‐MS/MS analysis revealed the alteration of exosome properties by epigallocatechin gallate (EGCG) in differentiated Caco‐2 cells. This natural polyphenol reduced both the number and size of secreted exosomes and altered the expression of exosomal proteins. The enriched proteins in exosomes were involved in immune response and cell proliferation. In contrast, those in the EGCG‐treated group had distinctive functions in the maintenance of skin homeostasis. We also found variable expression of galectin‐3‐binding protein and fibronectin as molecular signatures in exosomes derived from EGCG‐treated cells. These results could help elucidate the expression and mechanism of exosomal proteins related to food components. [ABSTRACT FROM AUTHOR]

The abundance of the cyclin-dependent kinase (CDK) inhibitor p5[7.sup.Kip2], an important regulator of cell cycle progression, is thought to be controlled by the ubiquitin-proteasome pathway. The Skp1/ Cul1/F-box (SCF)-type E3 ubiquitin ligase complex SC[F.sup.skp2] has now been shown to be responsible for regulating the cellular level of p5[7.sup.Kip2] by targeting it for ubiquitylation and proteolysis. The elimination of p5[7.sup.Kip2] was impaired in Skp[2.sup.-I-] cells, resulting in abnormal accumulation of the protein. Coimmunoprecipitation analysis also revealed that Skp2 interacts with p5[7.sup.Kip2] in vivo. Overexpression of WT Skp2 promoted degradation of p5[7.sup.Kip2], whereas expression of a dominant negative mutant of Skp2 prolonged the half-life of p5[7.sup.Kip2]. Mutation of the threonine residue (Thr-310) of human p5[7.sup.Kip2] that is conserved between the COOH-terminal QT domains of p5[7.sup.Kip2] and p2[7.sup.Kip1] prevented the effect of Skp2 on the stability of p5[7.sup.Kip2], suggesting that phosphorylation at this site is required for SC[F.sup.Skp2]-mediated ubiquitylation. Finally, the purified recombinant SC[F.sup.Skp2] complex mediated p5[7.sup.Kip2] ubiquitylation in vitro in a manner dependent on the presence of the cyclin E-CDK2 complex. These observations thus demonstrate that the SC[F.sup.Skp2] complex plays an important role in cell-cycle progression by determining the abundance of p5[7.sup.Kip2] and that of the related CDK inhibitor p2[7.sup.Kip1].

Non-alcoholic fatty liver disease (NAFLD) is a manifestation of metabolic syndrome closely linked to dyslipidemia and gut microbiome dysbiosis. Bilberry anthocyanins (BA) have been reported to have preventive effects against metabolic syndrome. This study aimed to investigate the protective effects and mechanisms of BA in a Western diet (WD)-induced mouse model. The results revealed that supplementation with BA attenuated the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-c), fat content in liver, 2-thiobarbituric acid reactive substances (TBARS) and α-smooth muscle actin (α-SMA) caused by WD. Furthermore, gut microbiota characterized by 16S rRNA sequencing revealed that BA reduced remarkably the ratio of Firmicutes/Bacteroidetes (F/B) and modified gut microbiome. In particular, BA increased the relative abundance of g_Akkermansia and g_Parabacteroides. Taken together, our data demonstrated that BA might ameliorate WD-induced NAFLD by attenuating dyslipidemia and gut microbiome dysbiosis. [ABSTRACT FROM AUTHOR]