За кадры. 1971. № 50 (1564)

"Горжусь дипломом ТПИ" / [беседа с] В. Попералов ; [беседа с] В. Скорых ; [беседовал] Н. ГригорьеваВ свете решений съезда / В. ЕрмолинЭкзамен по АСУ / Ф. И. ПерегудовПрямая линия. Рассказы о молодых коммунистах / М. АлейниковЗрелость молодостиНаш долг - учеба / В. КиселевНас ждут на селе / А. ПузыревичХимики не подведут / В. ЗерновКомандиром снова Оля / С. ПетровЯ молодой побег нашел... / А. РодионовВетер волосы раздувает... / Л. ГромоваМежду нами глухой овраг или даже зияет пропасть... / В. ФоновНИИ машиностроения - трудности и задачи / В. Ф. ГорбуновВ едином строю / П. Семенов, Г. ГерасимовССО: где, что, сколько?Через 30 летСоциалистические обязательства ТПИ по благоустройству / И. И. Каляцкий [и др.]Наши интервью / [беседа с] С. Т. Мальцев ; [беседа с] В. ТихоновКаким должно быть учебное пособие / И. Д. КутявинПолитехник - участник международной фотовыставки / Б. ИвановПолкилометра под землей / Е. Гребенщиков2300 инженеров дал стране в этом году наш дважды орденоносный институ

The Aldo-Keto Reductase AKR1B10 Is Up-Regulated in Keloid Epidermis, Implicating Retinoic Acid Pathway Dysregulation in the Pathogenesis of Keloid Disease

Keloid disease is a recurrent fibroproliferative cutaneous tumor of unknown pathogenesis for which clinical management remains unsatisfactory. To obtain new insights into hitherto underappreciated aspects of keloid pathobiology, we took a laser capture microdissection-based, whole-genome microarray analysis approach to identify distinct keloid disease-associated gene expression patterns within defined keloid regions. Identification of the aldo-keto reductase enzyme AKR1B10 as highly up-regulated in keloid epidermis suggested that an imbalance of retinoic acid metabolism is likely associated with keloid disease. Here, we show that AKR1B10 transfection into normal human keratinocytes reproduced the abnormal retinoic acid pathway expression pattern we had identified in keloid epidermis. Cotransfection of AKR1B10 with a luciferase reporter plasmid showed reduced retinoic acid response element activity, supporting the hypothesis of retinoic acid synthesis deficiency in keloid epidermis. Paracrine signals released by AKR1B10-overexpressing keratinocytes into conditioned medium resulted in up-regulation of transforming growth factor-β1, transforming growth factor-β2, and collagens I and III in both keloid and normal skin fibroblasts, mimicking the typical profibrotic keloid profile. Our study results suggest that insufficient retinoic acid synthesis by keloid epidermal keratinocytes may contribute to the pathogenesis of keloid disease. We refocus attention on the role of injured epithelium in keloid disease and identify AKR1B10 as a potential new target in future management of keloid disease

Multicenter study of wound healing in neurofibromatosis and neurofibroma

Based on clinical experience, the senior author has become convinced that wounds produced to correct the deformities of patients with neurofibromatosis (NF-1) have produced remarkably good scars, the interesting feature being that progression to keloid or hypertrophic scar is rare. The other point noted was that this situation did not change, no matter the patient's race or skin color. There have been few reports describing or discussing this hypothesis. The purpose of this study was to investigate whether wounds produced in the patients with NF-1 produce keloid or hypertrophic scars. The patients with solitary neurofibroma were also included in this study; these were compared with the NF-1 group. This was conducted as a multicenter study. Patients with neurofibromatosis/solitary neurofibroma, who were operated on from 1990 to 2000, were evaluated by reviewing their medical charts and photographs retrospectively. The patients were treated in centers from five different countries. The analysis was undertaken based on the following points: 1) age and sex at surgery; 2) race of the patients; 3) past and family histories of hypertrophic scar and keloid; 4) surgical site(s); 5) diagnosis, NF1 or solitary neurofibroma; 6) surgical complications; 7) number of reoperations to manage the complications; 8) adjuvant therapy for the tumor; 9) depth of the tumors; and 10) incidence of malignant degeneration. A total of 101 cases with neurofibromatosis or solitary neurofibroma was analyzed. The age at surgery ranged from 1 year 6 months to 74 years; sex ratio was 47 males and 54 females. The racial distribution of the patients was 13 white, 13 black, 3 Hispanic, and 58 Asian. There was no past or family history of hypertrophic scar or keloid. The surgical sites were head and neck in 70 cases, trunk in 20 cases, upper extremities in 22 cases, and lower extremities in 20 cases. The clinical diagnosis was NF-1 in W cases, solitary neurofibroma in 35 cases, plexiform neurofibroma in four cases, and no distinct clinical diagnosis in five cases. There were no other types of neurofibiomatosis. Hematoma and white wide scar were the main postoperative complications found in six cases of NF-1. Infection was also noted in four cases. However, no patient developed hypertrophic scar or keloid in the neurofibromatosis group, whereas two cases showed hypertrophic scar in the solitary neurofibroma group. The outcome showed that the patients with NF-1 and plexiform neurofibroma, no matter the racial group, produce good scars without keloid or hypertrophic changes, whereas solitary neurofibroma has a potential to cause hypertrophic scar.Providence Hosp, Inst Craniofacial & Reconstruct Surg, Southfield, MI 48037 USAJikei Univ, Sch Med, Dept Plast & Reconstruct Surg, Tokyo, JapanUniv Fed Sao Paulo, Dept Plast Surg, Sao Paulo, BrazilLady Davis Carmel Med Ctr, Haifa, IsraelUniv Fed Sao Paulo, Dept Plast Surg, Sao Paulo, BrazilWeb of Scienc