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[Climate therapy of uveitis in a mountain environment].

Climatotherapy as part of treatment of intraocular inflammatory diseases has a worldwide renaissance due to recent research. The stimulating climate in high mountains leads to induction of defence mechanisms in the organism. In these mechanisms participates in particular the neurovegetative, cardiovascular, thermoregulating and immune system. An important effect of climatotherapy is marked vascularization of tissues and increased ACTH and glucocorticoid secretion, and this along with the immunosuppressive action of light during heliotherapy leads to physiological immunosuppression. This fact is significant in particular in the treatment of uveitis and raises hope of reduced doses of corticoids and immunosuppressive drugs which reduces the risk of undesirable side-effects of this treatment. The results of climatotherapy is in many instances a reduced number of relapses of inflammatory diseases, shortening of the period of the acute attack and a milder course of the attack.

Altitude↗

Sunburn related to UV radiation exposure, age, sex, occupation, and sun bed use based on time-stamped personal dosimetry and sun behavior diaries.

OBJECTIVE: To assess when sunburn occurs and who experiences sunburn by personal UV dosimetry and diaries. DESIGN: Open prospective observational study. SETTING: University hospital. PARTICIPANTS: A convenience sample of 340 Danish volunteers: children, adolescents, indoor workers, sun worshippers, golfers, and gardeners (age range, 4-68 years). MAIN OUTCOME MEASURES: Subjects recorded sunburn and sun-exposure behavior in diaries and carried personal, electronic, wristwatch UV radiation (UVR) dosimeters that measured time-stamped UVR doses continuously for a median of 119 days covering 346 sun-years (1 sun-year equals 1 subject participating during 1 summer half-year). RESULTS: A typical sunburn day was a day off work (91%; odds ratio, 4.1) with risk behavior (sunbathing/exposing shoulders) (79%; odds ratio, 15.9) in May, June, or July (90%) for 6.4 exposure hours (interquartile range, 5-7.7 hours), of which 2.8 hours fell between noon and 3 pm. Subjects had a median of 1 sunburn per sun-year; adolescents, sun worshippers, and indoor workers had more than children, golfers, and gardeners (P<.05). Sunburn peaked at age 20 years, and female subjects had more sunburns than male subjects (P<.01). Skin type IV had fewer sunburns than types I through III (P<.01). Sunburned persons had more risk-behavior days and lower skin type (P<.01) than nonsunburned persons. The median UVR doses received were significantly higher on sunburn days than on nonsunburn days with risk behavior (P<.01). There was a significant correlation between sunburn size and severity; sunburn and sunscreen use; and sunburn and sun-bed use (P<.01 for all 3 comparisons). CONCLUSIONS: Sunburn was highly correlated with risk behavior. Reduction of risk-behavior days and/or exposure hours around noon can reduce sunburn. Sunburn was not found during breaks on normal full-time indoor work or school days.

Adolescent↗

"Sunbath polyneuritis": subacute axonal neuropathy in perazine-treated patients after intense sun exposure.

This article aims at drawing attention to the peculiar association of intense exposure to sunlight and subacute development of sensory neuropathy which was seen in 7 psychiatric patients treated with the phenothiazine derivative, perazine. Three patients additionally developed bilateral VII nerve palsy. Symptoms followed a monophasic course with almost complete remission. Routine neurophysiology suggested axonal neuropathy confirmed by sural nerve biopsy in 1 patient. A toxic origin of neuropathy is supposed, possibly induced by phenothiazine photoproducts, which may cause cell damage via lipid peroxidation.

Adult↗

Novel regulators of vitamin D action and metabolism: Lessons learned at the Los Angeles zoo.

We undertook an investigation of an outbreak of rachitic bone disease in the Emperor Tamarin New World primate colony at the Los Angeles Zoo in the mid-1980s. The disease phenotype resembled that observed in humans with an inactivating mutation of the vitamin D receptor (VDR), hypocalcemia, high 1,25-dihydroxyvitamin D (1,25-(OH)(2)D) levels, and rickets in rapidly growing adolescent primates. In contrast to the human disease, the New World primate VDR was functionally normal in all respects. The proximate cause of vitamin D hormone resistance in New World primates was determined to be the constitutive overexpression of a heterogeneous nuclear ribonucleoprotein in the A family which we coined the vitamin D response element binding protein (VDRE-BP). VDRE-BP competed in trans with the VDR-retinoid X receptor (RXR) for binding to the vitamin D response element. VDRE-BP-legislated resistance to 1,25-(OH)(2)D was antagonized (i.e., compensated) by another set of constitutively overexpressed proteins, the hsp-70-related intracellular vitamin D binding proteins (IDBPs). IDBPs, present but expressed at much lower levels in Old World primates including man, exhibited a high capacity for 25-hydroxylated vitamin D metabolites and functioned to traffic vitamin Ds to specific intracellular destinations to promote their action and metabolism.

Animals↗