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The spontaneous healing process of the tympanic membrane starts from the outer epithelial layer, with later healing of the lamina propria and the mucosal layer.

Highlights Approximately 650,000 people will be diagnosed this year with cancers of the oral cavity and pharynx worldwide. The absence of biomarkers for the disease early detection contributes to the late diagnosis. Despite some advances with regards to treatment, overall survival has not significantly improved in decades. We have shown that increased relative mRNA expression of KLK5 to LEKTI is associated with disease’s poor outcome. This work supports the relative expression of KLK5 to LEKTI as a valuable prognostic marker.

Insulin accelerated the healing process of TMs traumatic perforations.

Skeletal muscle has the intrinsic ability to self-repair through a multifactorial process, but many aspects of its cellular and molecular mechanisms are not fully understood. There is increasing evidence that some members of the mammalian β-galactoside-binding protein family (galectins) are involved in the muscular repair process (MRP), including galectin-3 (Gal-3). However, there are many questions about the role of this protein on muscle self-repair. Here, we demonstrate that endogenous Gal-3 is required for: i) muscle repair in vivo using a chloride-barium myolesion mouse model, and ii) mouse primary myoblasts myogenic programming. Injured muscle from Gal-3 knockout mice (GAL3KO) showed persistent inflammation associated with compromised muscle repair and the formation of fibrotic tissue on the lesion site. In GAL3KO mice, osteopontin expression remained high even after 7 and 14 days of the myolesion, while MyoD and myogenin had decreased their expression. In GAL3KO mouse primary myoblast cell culture, Pax7 detection seems to sustain even when cells are stimulated to differentiation and MyoD expression is drastically reduced. The detection and temporal expression levels of these transcriptional factors appear to be altered in Gal-3-deficient myoblast. Gal-3 expression in WT states, both in vivo and in vitro, in sarcoplasm/cytoplasm and myonuclei; as differentiation proceeds, Gal-3 expression is drastically reduced, and its location is confined to the sarcolemma/plasma cell membrane. We also observed a change in the temporal–spatial profile of Gal-3 expression and muscle transcription factors levels during the myolesion. Overall, these results demonstrate that endogenous Gal-3 is required for the skeletal muscle repair process.

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retinal neuron apoptosis is a key component of diabetic retinopathy (dr), one of the most common complications of diabetes. Stress due to persistent hyperglycaemia and corresponding glucotoxicity represents one of the primary pathogenic mechanisms of diabetes and its complications. apoptosis of retinal neurons serves a critical role in the pathogenesis of dr observed in patients with diabetes and streptozotocin (STZ)-induced diabetic rats. retinal neuron apoptosis occurs one month after STZ injection, which is considered the early stage of dr. The molecular mechanism involved in the suppression of retinal neuron apoptosis during the early stage of dr remains unclear. rna-dependent protein kinase (PKr) is a stress-sensitive pro-apoptotic kinase. our previous study indicated that PKR-associated protein X, a stress-sensitive activator of PKr, is upregulated in the early stage of STZ-induced diabetes. in order to assess the role of PKr in dr prior to apoptosis of retinal neurons, immunofluorescence and western blotting were performed to investigate the cellular localization and expression of PKr in the retina in the early stage of STZ-induced diabetes in rats. PKr activity was indirectly assessed by expression levels of phosphorylated eukaryotic translation initiation factor 2α (p-eiF2-α) and the presence of apoptotic cells in the retina was investigated by Tunel assay. The findings revealed that PKR was localized in the nucleus of retinal ganglion and inner nuclear layer cells from normal and diabetic rats. To the best of our knowledge, the present study is the first to demonstrate nuclear localization of PKR in retinal neurons. Immunofluorescence analysis demonstrated that PKR was expressed in the nuclei of retinal neurons at 3 and 6 days and its expression was decreased at 15 days after STZ treatment. in addition, p-eiF2-α expression and cellular localization followed the trend of PKr, suggesting that this pro-apoptotic kinase was active in the nuclei of retinal neurons. These findings are consistent with the hypothesis that nuclear translocation of PKr may be a mechanism to sequester active PKr, thus preventing upregulation of cytosolic signalling pathways that induce apoptosis in retinal neurons. apoptotic cells were not detected in the retina in the early stage of dr. a model was proposed to explain the mechanism by which apoptosis of retinal neurons by PKr is suppressed in the early stage of dr. The possible role of mitochondrial rna (mtrna) and Alu rna in this phenomenon is also discussed since it was demonstrated that the cellular stress due to prolonged hyperglycaemia induces the release of mtrna and transcription of Alu rna. Moreover, it mtrna activates PKr, whereas Alu rna inhibits the activation of this protein kinase.