The fuel test loop consisted an in-pile test section (IPS) and an out-pile system (OPS) is an nuclear fuel irradiation test facility installed in HANARO and its operating temperature and pressure are similar to those of commercial nuclear power plant’s. Penetration pipe connecting the IPS and OPS at the reactor concrete wall is supported by pool-wall pipe support. The existing pool-wall pipe support established in the HANARO have insulations even thought the leak tightness is not ensured. So, the need for an isolation of the insulations from the HANARO cooling water makes the existing pool-wall pipe support newly designed. In this study a structural evaluation for the pool-wall pipe support in accordance with the 2001 ASME B&PV Section III NF is implemented. The most critical primary and secondary stress intensities occur at the modified connection area of the main cooling water pipe and plate ring, but those values are less than the allowable stress. It is concluded that the existing pool-wall pipe support could be modified to a newly designed shape having an isolated insulation from a HANARO cooling water.

The purpose of the present study was to examine the role of peripheral nitric oxide (NO) pathways in the onset of interleukin (IL)-1β-induced mechanical allodynia in the orofacial area. Experiments were carried out on male Sprague-Dawley rats weighing 230-280 gm and surgical procedures were performed under pentobarbital sodium (40 mg/kg, i.p.). Under anesthesia, a polyethylene tube (PE10) was implanted into the subcutaneous area of one vibrissa pad, which enabled the injection of IL-1β or other chemicals. We subcutaneously injected 50 μL of IL-1β into a vibrissa pad through the implanted polyethylene tube with a 100 Hamilton syringe. After the administration of 0.01, 0.1, 1, or 10 pg of IL-1β, withdrawal behavioral responses were examined. The subcutaneous injection of saline had no effects on the air-puff thresholds. Following the subcutaneous injection of 0.01, 0.1, 1, or 10 pg of IL-1, the threshold of air puffs decreased significantly to 12± 3, 7 ± 2, 5 ±1, or 5 ± 1 psi, respectively, in a dose dependent manner. Pretreatment with L-NAME, a nitric oxide synthase (NOS) inhibitor, blocked IL-1β-induced mechanical allodynia. However, neither D-NAME, an inactive isomer of L-NAME, nor vehicle affected the IL-1β-induced mechanical allodynia. Subcutaneous injection of IL-1 increased the number of c-fos-like immunoreactive neurons, whereas pretreatment with L-NAME decreased this number, in the trigeminal caudal nucleus. These results suggest that pro-inflammatory cytokines and NO are important contributors to the pathogenesis of persistent and exaggerated IL-1β-induced pain states. Based on these observations, peripheral application of NOS inhibitors may be of therapeutic value in treating pain disorders in the clinic.