Localization of CCK-1R in the omasum and role of CCK in the regulation of omasal contractions in sheep.

The present study examined localization of cholecystokinin receptor (CCK-R) mRNA in the muscle layer of the ovine omasum and role of CCK-R type 1 (CCK-1R) in the regulation of muscle contraction of the omasum. We demonstrated that not only CCK-R type 2 (CCK-2R) mRNA but also CCK-1R mRNA is highly expressed in the muscle layer of the ovine omasum. Application of CCK-8 to muscle strips of the greater curvature of the ovine omasum at 1-100 nM induced tonic contraction in a concentration-dependent manner, and the contractile effect of CCK-8 was inhibited by both CCK-1R antagonist lorglumide (IC(50) 2.7 and 7.9 microM in the longitudinal and circular muscle, respectively) and CCK-2R antagonist PD135,158 (IC(50) 51.4 microM in the longitudinal muscle), indicating that not only CCK-2R but also CCK-1R is functionally expressed in the plasma membrane of smooth muscles in the omasum and mediates action of exogenous CCK. Contractile effect of intravenous infusion of CCK-8 (1-30 pmol/kg/min) on omasal contraction was also confirmed in the in vivo experiments using conscious sheep in the absence and presence of atropine infusion (14.4 nmol/kg/min), and showed that circulating CCK increases omasal electromyographic (EMG) activity at lower plasma concentration than that it inhibits ruminal contractions. Taking account of our previous results in the in vivo study using other CCK-1R antagonist, it is suggested that circulating CCK, even at normal range of plasma concentration, plays a physiological role as a regulator of omasal contractions in sheep and CCK-1R mediates the action of CCK.

A case of sick building syndrome in a Japanese office worker.

The adverse health effects caused by indoor air pollution are termed "sick building syndrome". We report such a patient whose symptoms appeared in the workplace. A 36-year-old female office worker developed nausea and headache during working hours in a refurbished office. After eight months of seeking help at other clinics or hospitals without improvement, she was referred to our hospital. At that time she reacted to the smells of various chemicals outside of the office building. Biochemical findings were all within normal ranges. Specific IgE antibody to cedar pollen was positive and the ratio of TH1/TH2 was 4.5. In the Eye Tracking Test (ETT), vertical eye movement was saccadic. Her anxiety level was very high according to the State-Trait Anxiety Inventory (STAI) questionnaire. Subjective symptoms, ETT findings and anxiety levels on STAI gradually improved during two years of follow-up. One year after the onset of her illness, the formaldehyde concentrations in the building air ranged from 0.017-0.053 ppm. Even though relatively low, chemical exposure from building materials such as formaldehyde induced a range of symptoms. Also, lack of recognition by superiors and doctors that sick building syndrome might have been the source of her illness coupled with her high state of anxiety may have exacerbated her symptoms and led to the onset of multiple chemical sensitivity. Thus psychosocial factors may contribute to sick building syndrome in the workplace.

Efficacy of a detector tube method in formaldehyde measurement.

In order to determine the efficacy of a detector tube method in formaldehyde (HCHO) measurement, we performed a chamber experiment and a field study. The experiment clearly showed that the value obtained by the detector tube method was significantly correlated to that obtained using an active-DNPH method, and was not influenced by the coexistence of toluene, xylene or carbon monoxide, but was by acetaldehyde. In the field study, we investigated 171 rooms in 81 houses. Indoor air was simultaneously sampled for 30 minutes by both an active-DNPH method and the detector tube method. The mean HCHO concentration in the 171 rooms was 0.110 +/- 0.089 ppm determined by the active-DNPH method and 0.12 +/- 0.10 ppm by the detector tube method. Regression analysis showed that the two measures closely correlated with a regression equation Y=1.057 X + 0.002 (r=0.912, p<0.0001), where X is the HCHO concentration determined by the active-DNPH method and Y is that determined by the detector tube method. The mean acetaldehyde concentration in the 171 rooms was 0.024 +/- 0.018 ppm using the active-DNPH method, and no correlation was found between acetaldehyde concentrations using the active-DNPH method and the values obtained by the detector tube method. Therefore, this study clearly showed that the detector tube method is not only simple and fast but also precise in measuring HCHO in indoor air.