Illiteracy and the readability of patient education materials. A look at Health Watch.
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Biomedical subjects
Publications and source records attributed to S R Feldman.
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Differences in the responses to growth factors of normal fibroblasts and scleroderma fibroblasts have been demonstrated previously. Because human dermal fibroblasts are heterogeneous populations, whether known differences between papillary and reticular dermal fibroblasts could account for the noted differences between normal and scleroderma fibroblasts was investigated. Papillary dermal fibroblasts were grown from a dermatome section of normal skin from an adult donor. Reticular dermal fibroblasts were cultured from punch biopsy specimens taken from the same location. In vitro, papillary dermal fibroblasts proliferated more rapidly, had a higher mitotic index and reached greater density at confluence, confirming previous observations. The reticular dermal fibroblasts were more dendritic. Reticular dermal fibroblasts had higher rates of tritiated thymidine uptake and larger increases in mitotic index in response to isoforms of platelet-derived growth factor (PDGF). The characteristic response of scleroderma fibroblasts, potentiation of the mitogenicity of PDGF AA by transforming growth factor-beta (TGF-beta), was not observed in either cell type. Therefore, the phenotypic characteristics of scleroderma fibroblasts cannot be explained by an unusual admixture of papillary and reticular fibroblasts.
BACKGROUND AND DESIGN: Human papillomavirus (HPV) is accepted as a factor in the pathogenesis of genital squamous cell carcinomas. The incidences of both HPV infection and squamous cell carcinoma are increased in immunocompromised renal transplantation patients. The purpose of this study was to determine if HPV DNA is present in squamous cell carcinomas of nongenital skin in immunosuppressed patients. Amplification of HPV DNA was performed using the polymerase chain reaction. The sensitivity and specificity of the polymerase chain reaction was assessed on 19 positive and six negative control specimens. Twenty genital squamous cell carcinomas from nonimmunocompromised patients and 28 nongenital squamous cell carcinomas from renal transplantation patients were then analyzed. RESULTS: Human papillomavirus DNA was identified in 18 of 19 positive control specimens and zero of six negative control specimens. Human papillomavirus DNA was identified in four of 20 genital squamous cell carcinoma specimens. In comparison, no HPV DNA was identified in 28 nongenital squamous cell carcinomas from immunosuppressed hosts (Fisher's Exact Test, P < .025). CONCLUSIONS: These findings support a role for HPV in genital skin cancers and suggest that HPV does not play a role in the increased incidence of squamous cell carcinoma in renal transplantation patients.
The bullous diseases that are neither immune-mediated nor inherited form a heterogeneous group that may be classified according to their major histopathologic characteristics. Such a classification allows clear distinctions to be made between entities that may have clinical similarities such as staphylococcal scalded skin syndrome, toxic shock syndrome, erythema multiforme/toxic epidermal necrolysis, and acute graft-versus-host disease. Proper differentiation of these entities is critical for their study and for appropriate management.
A comparison of the histopathologic features of Shulman's syndrome (diffuse fasciitis with eosinophilia) and the fasciitis associated with the eosinophilia-myalgia syndrome is presented. The study population consisted of eight biopsy specimens of seven patients with Shulman's syndrome and 11 specimens from 10 patients with eosinophilia-myalgia syndrome. Both groups exhibited inflammatory changes in the subcutaneous fat, septa, and fascia; cutaneous changes were more prominent in cases of eosinophilia-myalgia syndrome. Eosinophils and plasma cells were not consistently present in either condition; mast cells and factor XIIIa-positive cells were consistently present in the inflammatory infiltrates. Although there was overlap in the histopathologic findings, Shulman's syndrome tends to involve the subcutis alone and the eosinophilia-myalgia syndrome tends to be a pancutaneous-subcutaneous process.
Testicular feminization, a syndrome of end-organ androgen resistance, has been characterized at the molecular level. Well-defined mutations in the androgen receptor have been identified in this disorder. This receptor belongs to a family of intracellular hormone receptors, which includes receptors for corticosteroids, mineralocorticoids, sex hormones, vitamin D3, thyroid hormone, and retinoids. An understanding of the structure and molecular defects identified for the androgen receptor serves as a model to understand this entire class of receptors, a group directly involved in the biochemical pathways of a wide variety of dermatologic therapeutic interventions.
The localization of receptors for the proteinase inhibitor alpha 2-macroglobulin was studied in human skin by immunohistochemistry using a monoclonal mouse antibody. No epidermal staining was identified. alpha 2-Macroglobulin receptors were identified on dermal fibroblasts and dermal dendritic cells. Endothelial cells did not stain with the antibody, but positive staining cells were concentrated around dermal vessels. The myoepithelial layer of eccrine glands exhibited receptors; however, there was no staining of the eccrine epithelial layer. The distribution of alpha 2-macroglobulin receptors correlates with the reported distribution of alpha 2-macroglobulin: both are present in the dermal connective tissue and absent in epithelium and endothelium. The distribution of alpha 2-macroglobulin and its receptor in the dermis is consistent with a possible role in regulation of dermal proteolytic activity.
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Genes that are involved in the development of cancer have been identified. These genes, called "oncogenes," are related to normal cellular genes called "proto-oncogenes," which code for proteins involved in the regulation of cellular growth and differentiation. Through the study of these genes, we now begin to assess prognosis of several malignant neoplasms. Moreover, specific inhibitors of oncogene activity have potential use in treatment regimens for cancer.
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Desmoplakin-1 is a 280,000 dalton component of the intracellular portion of desmosomes. Complementary DNA (cDNA) coding for a portion of desmoplakin-1 was obtained by screening a lambda gt11 cDNA library constructed specifically for this purpose. A388 cells (a human skin squamous cell carcinoma cell line) were found to produce desmoplakin-1 and mRNA from this cell line was used to prepare a random primed cDNA library. Screening 60,000 recombinants of the library with an affinity purified anti-demoplakin-1 antibody resulted in initial identification of four clones from which one 1500 base pair clone was isolated by plaque purification. The identity of this desmoplakin clone was confirmed by demonstrating that antibody affinity purified on the protein product of the clone bound desmoplakins 1 and 2 in Western blots. Thus, the clone appears to code for the shared region of desmoplakins 1 and 2.
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Botryomycosis is a bacterial infection characterized by the presence of grains of organisms in the tissue. Although Staphylococcus aureus is the most common causative agent, other bacteria have been reported to cause botryomycosis. Several factors have been hypothesized to be important in the pathogenesis of botryomycosis, including foreign bodies, quantity and virulence of organisms, and host immunity. The resulting infection tends to be resistant to antibiotic therapy. We report a case of botryomycosis of the hand caused by Moraxella nonliquefaciens, an organism of low virulence not previously associated with botryomycosis, and discuss the factors that may have led to this infection. This infection was successfully treated by excision and grafting.
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The in vivo catabolism of 125I-labeled alpha 1-antichymotrypsin was studied in our previously described mouse model. Native alpha 1-antichymotrypsin cleared with an apparent t1/2 of 85 min, but alpha 1-antichymotrypsin in complex with chymotrypsin or cathepsin G cleared with a t1/2 of 12 min. Clearance of the complex was blocked by a large molar excess of unlabeled complexes of proteinases with either alpha 1-antichymotrypsin or alpha 1-proteinase inhibitor. These studies indicate that the clearance of alpha 1-antichymotrypsin-proteinase complexes utilizes the same pathway as complexes with the homologous inhibitor alpha 1-proteinase inhibitor. Previous studies have demonstrated that this pathway is also responsible for the catabolism of two other serine proteinase inhibitors, antithrombin III and heparin cofactor II. This pathway is thus responsible for removing several proteinases involved in coagulation and inflammation from the circulation, thereby decreasing the likelihood of adventitious proteolysis.