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Leopold Kiselev
Leopold Kiselev

Combo Skin Fuiko Trans 1.43 [2021]

Full Text Available INTRODUÇÃO: A obesidade é considerada grave doença crônica que vem atingindo proporções mundiais gerando transtornos sérios para a saúde pública. No Brasil, a prevalência desta doença denota aumento progressivo em relação ao número de pessoas com sobrepeso e/ou obesidade. Apesar disso, as manifestações dermatológicas da obesidade têm sido pouco estudadas. OBJETIVO: Abordar as dermatoses que mais acometem pacientes obesos e seu tratamento, principalmente na aplicação adequada da fisioterapia dermatofuncional. MÉTODO: Revisão da literatura, entre 2000 e 2010, de artigos indexados nas bases Medline/Pubmed, Scielo e Lilacs, livros e monografias das bibliotecas da Universidade de Fortaleza e Universidade Federal do Ceará, Fortaleza, CE, Brasil, cruzando os descritores obesidade, dermatose e fisioterapia. Foram reconhecidas como mais importantes as seguintes situações patológicas: estrias, celulite, acanthosis nigricans, acrocórdons, flacidez, úlcera e impetigo. Entre as formas de tratamento deuse destaque à atuação da fisioterapia dermatofuncional. CONCLUSÃO: O tratamento das dermatoses por meio da fisioterapia dermatofuncional é possível podendo trazer consigo resultados que satisfaçam a expectativa dos pacientes e proporcionando-lhes melhor qualidade de vida.INTRODUCTION: Obesity is a serious chronic disease that has reached global proportions causing problems to public health. In Brazil, the prevalence of this disease shows a progressive increase in the number of people with overweight or obesity. Nevertheless, the skin manifestations have not been well studied. OBJECTIVE: To analyse the dermatosis most affecting obese patients and its treatment, particularly in proper application of dermatological therapy. METHOD: Was made a literature review between 2000 and 2010 of articles published in Medline/ PubMed, SciELO and Lilacs, books and monographs of the libraries of the University of Fortaleza and the Federal

Combo skin Fuiko Trans 1.43

Corynebacterium bovis has been associated with hyperkeratotic dermatitis and acanthosis in mice. We studied 3 different strains of C. bovis: one previously described to cause hyperkeratotic dermatitis (HAC), one that infected athymic nude mice without leading to the classic clinical signs, and one of bovine origin (ATCC 7715). The 3 strains showed a few biochemical and genetic differences. Immunodeficient nude mice were housed in 3 independent isolators and inoculated with pure cultures of the 3 strains. We studied the transmission of these C. bovis studies to isolator-bedding and contact sentinels housed for 5 to 12 wk in filter-top or wire-top cages in the respective isolators. Using a 16S rRNA-based qPCR assay, we did not find consistent differences in growth and transmission among the 3 C. bovis strains, and neither the incidence nor severity of hyperkeratosis or acanthosis differed between strains. Housing in filter-top compared with wire-top cages did not alter the morbidity associated with any of the strains. Our findings confirmed the variability in the gross and histologic changes associated with C. bovis infection of mice. Although bacteriology was a sensitive method for the detection of Corynebacterium spp., standard algorithms occasionally misidentified C. bovis and several related species. Our study demonstrates that PCR of skin swabs or feces is a sensitive and specific method for the detection of C. bovis infection in mice. An rpoB-based screen of samples from North American vivaria revealed that HAC is the predominant C. bovis strain in laboratory mice.

Full Text Available Palmoplantarkeratodermas (PPKs are a heterogeneous group of hereditary and acquired disorders with underlying gene defects, and characterized by hyperkeratosis of palms and soles with or without other ectodermal and systemic abnormalities. Huriez syndrome is a rare autosomal dominant transgradient type of PPK with high frequency of squamous cell carcinoma in the affected skin. We hereby describe a case of a very rare autosomal dominant PPK in a 40-year-old male patient presenting since birth with PPK extending onto the dorsal aspects of hands and feet with peeling of the skin. The complaints were associated with sclerodactyly, hyperhidrosis, and nail abnormalities. Also superadded dermatophyte infection was observed involving abdomen. No history of loss of any digit. No mucosal, dental, or any systemic involvement was present. No sign of malignancy was noted. Baseline investigations, including ultrasonography of abdomen were normal. Histological findings were nonspecific with only orthohyperkeratosis and acanthosis. Diagnosis was mainly done on clinical grounds. The patient is better with oral retinoids and topical emollients and keratolytics along with antifungal treatment for dermatophyte infection. He is under follow up.

Keratin K2 is one of the most abundant structural proteins of the epidermis; however, its biological significance has remained elusive. Here we show that suprabasal type II keratins, K1 and K2, are expressed in a mutually exclusive manner at different body sites of the mouse, with K2 being confined to the ear, sole, and tail skin. Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail epidermis, corneocyte fragility, increased transepidermal water loss, and local inflammation in the ear skin. The loss of K2 was partially compensated by upregulation of K1 expression. However, a significant portion of K2-deficient suprabasal keratinocytes lacked a regular cytoskeleton and developed massive aggregates of the type I keratin, K10. Aggregate formation, but not hyperkeratosis, was suppressed by the deletion of both K2 and K10, whereas deletion of K10 alone caused clumping of K2 in ear skin. Taken together, this study demonstrates that K2 is a necessary and sufficient binding partner of K10 at distinct body sites of the mouse and that unbalanced expression of these keratins results in aggregate formation.

Psoriasis is a chronic skin disease resulting from the dysregulated interplay between keratinocytes and infiltrating immune cells. We report on a psoriasis-like disease model, which is induced by the transfer of CD4(+)CD45RB(hi)CD25(-) cells to pathogen-free scid/scid mice. Psoriasis-like lesions had elevated levels of antimicrobial peptide and proinflammatory cytokine mRNA. Also, similar to psoriasis, disease progression in this model was dependent on the p40 common to IL-12 and IL-23. To investigate the role of IL-22, a Th17 cytokine, in disease progression, mice were treated with IL-22-neutralizing antibodies. Neutralization of IL-22 prevented the development of disease, reducing acanthosis (thickening of the skin), inflammatory infiltrates, and expression of Th17 cytokines. Direct administration of IL-22 into the skin of normal mice induced both antimicrobial peptide and proinflammatory cytokine gene expression. Our data suggest that IL-22, which acts on keratinocytes and other nonhematopoietic cells, is required for development of the autoreactive Th17 cell-dependent disease in this model of skin inflammation. We propose that IL-22 antagonism might be a promising therapy for the treatment of human psoriasis.

Full Text Available Carcinoma cuniculatum, a low grade squamous carcinoma of plantar skin was first described in 1954. Even after 50 years, biopsy errors are common with delay in diagnosis. Clinico-morphologica1 features in 12 patients of carcinoma cuniculatum, in a period of three and a half years are studied. The aim is to draw attention to the sites of occurrence of this tumor other than the sole and to have better understanding of the diagnostic difficulties. The sites of occurrence of these tumors according to frequency were foot followed by flank, leg, face and palm. The tumors presented with ulcerated, fungating masses with fine papillary architecture. Microscopic examination of the tumors revealed bulbous acanthosis, parakeratosis and a well defined lower border, circumscribed by chronic inflammatory cells. No lymph node metastasis were recorded in any of the cases. Wide local excision with at least five mm free surgical margin was the treatment of choice. A transmetatarsal and above wrist amputation was required in two patients. Carcinoma cuniculatum should always be suspected in a nonhealing ulcer or verrucous growth of long standing duration. Superficial and small biopsies are unsatisfactory. Benign appearance on histopathology of this tumor needs to be interpreted in proper clinical settings.

The clinical features, pathology, and immunopathology of chronic graft-versus-host disease (GVHD) developing in the long-term rat radiation chimera are described. At 6 to 12 months post-transplant, the previously stable ACI/LEW chimeras developed patchy to diffuse severe hair loss and thickened skin folds, and had microscopic features resembling scleroderma, Sjogren's syndrome, and chronic hepatitis. Skin histology showed dermal inflammation and acanthosis with atrophy of the appendages, with progression to dermal sclerosis. The liver revealed chronic hepatitis with bile duct injury and proliferation and periportal piecemeal necrosis. The tongue had considerable submucosal inflammation, muscular necrosis, and atrophy and arteritis. The serous salivary glands, lacrimal glands, and bronchi had lymphocytic inflammation and injury to duct, acinar, and mucosal columnar epithelium. The thymus had lymphocyte depletion of the medulla with prominent epithelium. The spleen and lymph nodes had poorly developed germinal centers but increased numbers of plasma cells. IgM was observed along the basement membrane and around the basal cells of the skin and tongue and along the basement membrane of the bile ducts. IgM was present also in the arteries of the tongue. Immunoglobulins eluted from the skin, cross-reacted with the bile duct epithelium and usually with both ACI and Lewis skin. Increased titers of speckled antinuclear antibodies were present in the serum of rats with chronic (GVHD). Chronic GVHD in the long-term rat radiation chimera is very similar to human chronic GVHD and is a potentially excellent model for autoimmune disorders including scleroderma, Sjorgren's syndrome, and chronic hepatitis. 041b061a72


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