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[Dental imaging procedures in the particular One Health Program as well as the continuing development of extra care: sequence among 2000-2016].
OBJECTIVE Punch-grafting is a traditional technique to enhance wound healing, which has been associated with significant pain reduction. There are few studies measuring pain reduction after punch grafting, our study was designed to measure this outcome. Lomerizine METHOD Patients with hard-to-heal wounds treated with punch grafting were included in a single centre prospective study. Wound pain intensity was measured using a Visual Analogue Scale (VAS) at baseline (before the procedure) and at three time points after the procedure. Punch grafting was performed in an outpatient setting. Patient demographic data, wound aetiology and percentage of graft take were recorded. RESULTS A total of 136 patients were included (62 men and 74 women). Mean age was 60±35 years and 51 (38%) had venous leg ulcers (VLU), 29 (21%) had postoperative wounds, 15 (11%) Martorell ulcers, 15 (11%) traumatic wounds, four (3%) arterial ulcers and 22 (16%) 'other' ulcers. Of the patients, 38 (28%) did not present with painful ulcers and, after punch grafting, all of them remained painless; 29 (21%) patients obtained >70% pain reduction, whereas 73 (54%) patients achieved pain suppression. Pain suppression did not depend on the percentage of graft take. CONCLUSION Punch-grafting is a simple, technique that not only promotes wound healing but also reduces pain. It can also be performed on an outpatient basis. Further studies should be performed to achieve a better understanding of this beneficial finding. Declaration of interest The authors have no conflicts of interest to declare.Purpose To report a case of unilateral acute idiopathic maculopathy (UAIM) following vaccination for type A influenza virus (H1N1).Methods Clinical, fundus autofluorescence (FAF), fluorescein angiography (FA) and optical coherence tomography (OCT) findings are presented.Results A 25-year old white male presented with an acute decrease of vision in his left eye eight days after immunization with influenza A vaccine. Clinical evaluation revealed a deep yellowish-white lesion at the macula, early hyperfluorescence at the level of retinal pigment epithelium (RPE), and leakage and staining during the late phase of FA. OCT demonstrated disruption of the photoreceptor ellipsoid zone, as well as heterogeneous reflectivity changes and thickening at the level of the outer retina-RPE. Three months after presentation, fundus examination showed resolution of the yellowish foveal lesion, with persistence of mild RPE atrophic changes.Conclusion This is the first reported case of UAIM following H1N1 vaccination to date.Purpose To evaluate the role of angiogenic growth factors in the pathogenesis of intraocular tuberculosis.Methods Retinal Pigment Epithelium (RPE) cells were infected with varying dilution of Mycobacterium tuberculosis (MTB), ranging from several thousand to a few MTB bacilli to replicate paucibacillary conditions. Angiogenesis growth factors were evaluated using multiplex fluorescent bead based flow cytometry in the culture supernatant of RPE cells infected with MTB, vitreous fluids and tear samples of uveitis patients visiting retina clinic.Results Vascular endothelial growth factor (VEGF) levels were elevated and fibroblast growth factors (FGFs) were down regulated in RPE-infected MTB cells. Similar pattern of VEGF and FGF was observed in the vitreous of IOTB patients. However, no changes were observed in tear samples.Conclusions MTB exploits the angiogenesis growth factors for pathogenesis by decreasing FGF with concomitant surge of VEGF in MTB infected RPE as well in the vitreous of IOTB patients.Vascular smooth muscle cells (VSMCs) are an important source of foam cells in atherosclerosis. The mechanism for VSMC-derived foam cell formation is, however, poorly understood. Here, we demonstrate that the P2RY12/P2Y12 receptor is important in regulating macroautophagy/autophagy and VSMC-derived foam cell formation in advanced atherosclerosis. Inhibition of the P2RY12 receptor ameliorated lipid accumulation and VSMC-derived foam cell formation in high-fat diet-fed apoe-/- mice (atherosclerosis model) independent of LDL-c levels. Activation of the P2RY12 receptor blocked cholesterol efflux via PI3K-AKT, while genetic knockdown or pharmacological inhibition of the P2RY12 receptor inhibited this effect in VSMCs. Phosphoproteomic analysis showed that the P2RY12 receptor regulated the autophagy pathway in VSMCs. Additionally, activation of the P2RY12 receptor inhibited MAP1LC3/LC3 maturation, SQSTM1 degradation, and autophagosome formation in VSMCs. Genetic knockdown of the essential autophagy gene Atg5 significeceptor 1; ORO oil Red O; ox-LDL oxidized low-density lipoprotein; SQSTM1/p62 sequestosome 1; TEM transmission electron microscopy; TIC ticagrelor; ULK1 unc-51 like autophagy activating kinase 1; VSMCs vascular smooth muscle cells.Trimethyltin chloride (TMT) is widely used as a constituent of fungicides and plastic stabilizers in the industrial and agricultural fields, and is generally acknowledged to have potent neurotoxicity, especially in the hippocampus; however, the mechanism of induction of neurotoxicity by TMT remains elusive. Herein, we exposed Neuro-2a cells to different concentrations of TMT (2, 4, and 8 μM) for 24 h. Proteomic analysis, coupled with bioinformatics analysis, revealed the important role of macroautophagy/autophagy-lysosome machinery in TMT-induced neurotoxicity. Further analyses indicated significant impairment of autophagic flux by TMT via suppressed lysosomal function, such as by inhibiting lysosomal proteolysis and changing the lysosomal pH, thereby contributing to defects in autophagic clearance and subsequently leading to nerve cell death. Mechanistically, molecular interaction networks of Ingenuity Pathway Analysis identified a downregulated molecule, KIF5A (kinesin family member 5A), as a key target in TMT-impaired autophagic flux. TMT decreased KIF5A protein expression, disrupted the interaction between KIF5A and lysosome, and impaired lysosomal axonal transport. Moreover, Kif5a overexpression restored axonal transport, increased lysosomal dysfunction, and antagonized TMT-induced neurotoxicity in vitro. Importantly, in TMT-administered mice with seizure symptoms and histomorphological injury in the hippocampus, TMT inhibited KIF5A expression in the hippocampus. Gene transfer of Kif5a enhanced autophagic clearance in the hippocampus and alleviated TMT-induced neurotoxicity in vivo. Our results are the first to demonstrate KIF5A-dependent axonal transport deficiency to cause autophagic flux impairment via disturbance of lysosomal function in TMT-induced neurotoxicity; manipulation of KIF5A may be a therapeutic approach for antagonizing TMT-induced neurotoxicity.
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