The finding of orexin/hypocretin deficiency in narcolepsy patients suggests that this hypothalamic neuropeptide plays a crucial role in regulating sleep/wakefulness states. However, very little is known about the synaptic input of orexin/hypocretin-producing neurons (orexin neurons). We applied a transgenic method to map upstream neuronal populations that have synaptic connections to orexin neurons and revealed that orexin neurons receive input from several brain areas. These include the amygdala, basal forebrain cholinergic neurons, GABAergic neurons in the preoptic area, and serotonergic neurons in the median/paramedian raphe nuclei. Monoamine-containing groups that are innervated by orexin neurons do not receive reciprocal connections, while cholinergic neurons in the basal forebrain have reciprocal connections, which might be important for consolidating wakefulness. Electrophysiological study showed that carbachol excites almost one-third of orexin neurons and inhibits a small population of orexin neurons. These neuroanatomical findings provide important insights into the neural pathways that regulate sleep/wakefulness states.

In this paper, there was an error in the description of the fusion protein used in the transgenic construct. We described the construct as TTC::GFP in the text and in Figure 1A. The order of the components of the fusion protein was wrong. The fusion protein used in this study should be described as GFP::TTC (the tetanus toxin C-terminal fragment is fused to the C terminus of GFP). Although this correction does not affect the data or the conclusions of the paper, the authors would like to apologize to readers who have been misled by these mistakes. The authors also wish to correct the affiliations of Natsuko Tsujino and Yoshimasa Koyama as listed above.

The purpose of this present study was to compare the physiological effects of the hydrophilic and hydrophobic properties of the fabrics investigated in exercising and resting subjects at an ambient temperature of 30 degrees C and a relative humidity of 50% with and without wind. Three kinds of clothing ensemble were tested: wool and cotton blend with high moisture regain (A), 100% cotton with intermediate moisture regain (B), 100% polyester clothing with low moisture regain (C). The experiments were performed using seven young adult women as subjects. They comprised six repeated periods of 10-min exercise on a cycle ergometer at an intensity of 40% maximal oxygen uptake followed by 5 min of rest (20 min for the last rest). The experiments comprised two sessions. During session I (first three repetitions of exercise and rest) the subjects were exposed to an indifferent wind velocity and during session II (last three repetitions of exercise and rest) they were exposed to a wind velocity of 1.5 m x s(-1). Rectal temperature and skin temperatures at eight sites, pulse rate and clothing microclimate were recorded throughout the whole period. The main findings can be summarized as follows: rectal temperature during session II was kept at a significantly lower level in A than in B and C. Clothing microclimate humidity at the chest was significantly lower in A than in B and C during session II. Skin and clothing microclimate temperatures at the chest were significantly lower in A than in B and C during session II. Pulse rate was significantly higher in C than in A and B during sessions I and II. It was concluded that the hydrophilic properties of the fabrics studied were of physiological significance for reducing heat strain during exercise and rest especially when influenced by wind.

No abstract

C/EBP-homologous protein (CHOP)/gadd153 (or CHOP) is a transcription factor induced by endoplasmic reticulum (ER) stress. Forcible overexpression of CHOP causes apoptosis in keratinocytes in culture. Here, we asked whether CHOP might be increased in the skin after UVB (280-320 nm) exposure, thus implicating CHOP in sunburn cell (SBC) formation. SKH-1 hairless mice were exposed to a ultraviolet (UV) source (80 mJ per cm2; approximately 74% UVB, approximately 16% UVA), and skin biopsies examined by immunohistology and immunoprecipitation. Compared with non-irradiated epidermis, CHOP expression was significantly increased at 30 min, and reached maximal levels by 24 h. Similar increases in CHOP following UVB exposure were observed in human buttock skin. The time course of CHOP expression preceded SBC formation and another marker of apoptosis, caspase-3 cleavage. Intracellular CHOP accumulated mainly in cytoplasmic and perinuclear locations, with little remaining in the nucleus. To examine mechanisms, cultured keratinocytes were irradiated in vitro and examined by western blotting. Under conditions that eliminated ER stress because of cell handling, CHOP did not accumulate (and was in fact decreased) in the cells. Thus, induction of CHOP in keratinocytes requires factors present only in the native skin. Overall, the data suggest that CHOP participates in adaptive responses of the epidermis following UVB/UVA exposure in vivo.