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Cutaneous collagenous vasculopathy is a rare microangiopathy first described by Salama and Rosenthal in 2000. Several cases have been reported to date, describing distinct histological findings of thick hyaline collagenous blood vessel walls in the superficial dermis. Clinical confusion can arise with generalised essential telangiectasia. We report a case occurring in a 76-year-old woman who presented with a 2-year history of a telangiectatic rash progressing from her knees upwards. The diagnosis was confirmed on skin biopsy and treatment with pulsed dye laser was later initiated at the patient's [Dural modulation effects of mesenchymal stem cells implantation on myocardial collagen remodeling in a rat model of myocardial infarction].OBJECTIVE: To investigate the modulation effects of mesenchymal stem cells (MSCs) implantation on the collagen remodeling in myocardial infarction. METHODS: Acute myocardial infarction (AMI) was induced in SD rats by left anterior descending coronary artery ligation, and the animals were assigned randomly into the Sham group, MI + PBS group and MI + MSCs group. Echocardiography and hemodynamic examinations were performed to evaluate the cardiac function. HE staining and Masson trichrome staining were used to evaluate the myocardial infarction size. Infarcted area and infarcted expansion index were calculated. The expression of collagens in infarcted hearts was evaluated by immunohistochemistry, RT-PCR and Western blot.Cardiac function was significantly improved post MSCs transplantation [MI + MSCs vs. MI + PBS: FS(%): 298 ± 40 vs. 233 ± 34, P = 005; LVSP (mm Hg, 1 mm Hg = 033 kPa): 1133 ± 101 vs. 995 ± 166, P < 05; LVEDP (mm Hg): 120 ± 48 vs. 208 ± 46, P < 05; +dp/dtmax (mm Hg/s): 46163 ± 3634 vs. 39125 ± 2489, P < 05; -dp/dtmax (mm Hg/s): 42543 ± 3244 vs. area and decreased in non-infarcted area post MSCs transplantation (P < 05).CONCLUSIONS: MSCs transplantation could enhance the collagen synthesis in infarcted area while decrease the deposition of collagen in non-infarcted area in this MI model. squalene may be one of the mechanisms by which ventricular remodeling is attenuated post MSCs transplantation. Composition and adaptation of human myotendinous junction and neighboring muscle Bispebjerg Hospital, Copenhagen, Denmark.Hospital and Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.for Biochemistry, Medical Faculty, University of Cologne, Cologne, Germany.The myotendinous junction (MTJ) is a common site of strain injury and yet understanding of its composition and ability to adapt to loading is poor. The main aims of this study were to determine the profile of selected collagens and macrophage density in human MTJ and adjoining muscle fibers, and to investigate whether heavy exercise loading would alter this profile. Fifteen individuals scheduled for anterior cruciate ligament repair surgery were randomized into three groups: control, acute or 4 weeks heavy resistance training. MTJ samples were collected from the semitendinosus and gracilis muscles and were sectioned and stained immunohistochemically for collagen types I, III, VI, XII, XIV, XXII, Tenascin-C and CD68. Macrophage density and distribution was evaluated and the amount of each collagen type in muscle and MTJ was graded. Collagen XXII was observed solely at the MTJ, while all other collagens were abundant at the MTJ and in muscle perimysium or endomysium. The endomysial content of collagen XIV, macrophages and Tenascin-C increased following 4 weeks of training. These findings illustrate the heterogeneity of collagen type composition of human MTJ. The increase in collagen XIV following 4 weeks of training may reflect a training-induced protection against strain injuries in this region.Structural proteins of the dermal-epidermal junction targeted by autoantibodies The dermal-epidermal junction consists of a network of several interacting structural proteins that strengthen adhesion and mediate signalling events. This structural network consists of hemidesmosomal-anchoring filament complexes connecting the basal keratinocytes to the basement membrane. The anchoring filaments in turn interact with the anchoring fibrils to attach the basement membrane to the underlying dermis. Several of these structural proteins are recognized by autoantibodies in pemphigoid diseases, a heterogeneous group of clinically and immunopathologically diverse entities. Targeted proteins include the two intracellular plakins, plectin isoform 1a and BP230 (also called bullous pemphigoid antigen (BPAG) 1 isoform e (BPAG1e)). Plectin 1a and BP230 are connected to the intermediate filaments and to the cell surface receptor α6β4 integrin, which in turn is connected to laminin 332, a component of the anchoring filaments. Further squalane cleanser the ordinary are BP180, a transmembrane protein, laminin γ1 and type VII collagen. Latter protein is the major constituent of the anchoring fibrils. Mutations in the corresponding genes of these adhesion molecules lead to inherited epidermolysis bullosa emphasizing the importance of these proteins for the integrity of the dermal-epidermal junction.