Long-Term Tropical Residency Diminishes Central Sudomotor Sensitivities in Male Subjects

Tropical natives (TROP) are capable of tolerating tropical heat because of their long-term adaptation to tropical environments. When exposed to heat stress, these natives tend to respond with lower sweat output, which is generally thought to be the result of heat acclimatization. The main objective of this study was to clarify central mechanisms inherent to suppressed thermal sweating in tropical natives (Malaysians) by comparing their sweating responses to those of temperate native (TEMP) (Koreans). This experiment was conducted in a thermoneutral climatic chamber (24+/-0.5 degrees C, 40+/-3% relative humidity). Heat loads were applied to each subject by the immersion of their lower legs in a hot water bath (43 degrees C for 30 min). Sweat onset-time and sweat volume were compared between TROP and TEMP. The sweat onset-times on four selected points on the body ranged from 10.25 to 13.47 min in TEMP subjects, and from 16.24 to 17.83 min in TROP subjects (p<0.001). The local sweat volumes at the same sites ranged from 4.30 to 9.74 mg/cm2 in TEMP subjects, and from between 1.80 to 4.40 mg/cm2 in TROP subjects (p<0.001). These results demonstrated a significant difference between TROP and TEMP subjects with regard to the manner in which they regulate their body temperatures when exposed to heat loads, and verified that long-term thermal adaptation blunts sweating sensitivities.

Melatonin ameliorates autoimmune encephalomyelitis through suppression of intercellular adhesion molecule-1

Melatonin (N-acetyl-5-methoxytryptamine), a pineal neurohormone, is a hydroxyl radical scavenger and antioxidant, and plays an important role in the immune system. We studied the effect of exogenous melatonin on the pathogenesis of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats by immunization with rat spinal cord homogenates. Subsequent oral administration of melatonin at 5 mg/kg significantly reduced the clinical severity of EAE paralysis compared with administration of the vehicle alone (p<0.01). Infiltration of ED1 macrophages and CD4 T cells into spinal cords occurred both in the absence and presence of melatonin treatment, but melatonin-treated rats had less spinal cord infiltration of inflammatory cells than did the control group. ICAM-1 immunoreactivity in the blood vessels of EAE lesions was decreased in melatonin-treated rats compared to vehicle-treated rats. These findings suggest that exogenous melatonin ameliorates EAE via a mechanism involving reduced expression of ICAM-1 and lymphocyte function associated antigen-1a in autoimmune target organs.