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Background: A large number of skin diseases, including atopic dermatitis and psoriasis, appear to be precipitated or exacerbated by psychological stress. Nevertheless, the specific pathogenic role of psychological stress remains unknown. In 3 different murine models of psychological stress, it was recently shown that psychological stress negatively impacts cutaneous permeability barrier function and that coadministration of tranquilizers blocks this stressinduced deterioration in barrier function. Objectives and Methods: The relationship between psychological stress and epidermal permeability barrier function was investigated in 27 medical, dental, and pharmacy students without coexistent skin disease. Their psychological state was assessed with 2 well-validated measures: the Perceived Stress Scale and the Profile of Mood States. Barrier function was assessed simultaneously with the stress measures at periods of presumed higher stress (during final examinations) and at 2 assumed, lower stress occasions (after return from winter vacation [approximately 4 weeks before final examinations] and during spring vacation [approximately 4 weeks after final examinations]). Results: The subjects as a group demonstrated a decline in permeability barrier recovery kinetics after barrier disruption by cellophane tape stripping, in parallel with an increase in perceived psychological stress during the higher vs the initial lower stress occasions. During the follow-up, presumed lower stress period, the subjects again displayed lower perceived psychological stress scores and improved permeability barrier recovery kinetics, comparable to those during the initial lower stress period. Moreover, the greatest deterioration in barrier function occurred in those subjects who demonstrated the largest increases in perceived psychological stress. Conclusion: These studies provide the first link between psychological status and cutaneous function in humans and suggest a new pathophysiological paradigm, ie, stress-induced derangements in epidermal function as precipitators of inflammatory dermatoses.

Although there are no known gender-related differences in permeability barrier function in adults, estrogens accelerate whereas testosterone retards barrier development in fetal skin, and male fetuses demonstrate slower barrier development than female littermates. Moreover, prenatal administration of the androgen receptor antagonist, flutamide, equalizes developmental rates in male and female fetuses. Therefore, we evaluated the effects of changes in testosterone on barrier homeostasis in adult murine and human skin. Hypogonadal mice (whether by castration or by treatment with systemic flutamide) displayed significantly faster barrier recovery at 3, 6, and 12 h than did controls, and testosterone replacement slowed barrier recovery in castrated mice. Moreover, testosterone directly effects the skin, as topical flutamide also accelerated barrier recovery in normal male mice. These findings appear to be of physiologic significance, since prepubertal male mice (age 5 wk) displayed accelerated barrier recovery in comparison with adult postpubertal (11 wk) males. These studies also appear to be relevant for humans, as a hypopituitary human subject demonstrated repeated changes in barrier recovery in parallel with peaks and nadirs in serum testosterone levels during intermittent testosterone replacement. Mechanistic studies showed that differences in epidermal lipid synthesis do not account for the testosterone-induced functional alterations. Instead, epidermal lamellar body (LB) formation and secretion both decrease, resulting in decreased extracellular lamellar bilayers in testosterone-replete animals. These studies demonstrate that fluctuations in testosterone modulate barrier function, and that testosterone repletion can have negative consequences for permeability barrier homeostasis.

This study was conducted with an aim to assess the prevalence and profile of ear diseases in children from the higher and lower socioeconomic strata of society. Two groups of schools within Delhi were selected. Group A comprised of government schools located in slum areas with an average parental income of INR (Indian National Rupees) 1050 per month and group B of elite private schools with an average family income of TNR 35,000 per month. Three thousand children between the ages of 5-12 years were screened with the help of a written proforma and ear examination. Tympanometry and audiometry were done, where required. 19.6 per cent of children of group A were found to be suffering from ear diseases compared to 2.13 per cent of group B children. The two groups were also compared for number of family members, status of hygiene and parental education.

• There is no significant difference in ferritin and hemoglobin levels at 6 weeks among term, Indian neonates who had UCM and DCC and that this study may give support to the practice of UCM in term deliveries when DCC is not feasible.

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We describe an outbreak of Trichosporon asahii in 8 newborn infants with sepsis. Six out of these 8 infants died. The organism was identified on specific culture and morphologic characteristics. The organism was sensitive to amphotericin-B but resistant to fluconazole. Laminar flow unit was suspected to be the source of the outbreak.

The study reasserts functional continuity of the Achilles tendons 4 weeks after tenotomy using clinical and ultrasonographic methods.