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A 30-year-old man had been treated for malignant rheumatoid arthritis from 1989 with a non-steroidal anti-inflammatory drug, then bucillamine for six months and prednisolone. Mild proteinuria appeared in May 1994, 4 years after bucillamine therapy was conducted. The patient was admitted to our hospital for a renal biopsy in July 1994. The specimen revealed secondary amyloidosis and membranous nephropathy (MGN). These findings suggest that MGN unrelated to bucillamine therapy might have occurred with secondary amyloidosis in rheumatoid arthritis.

We have already reported that decreased renal medullary blood flow and retention of sodium play an important role in the development of hypertension during chronic systemic L-NAME (NG-nitro-L-arginine methyl ester) administration, despite the absence of measurable changes in renal cortical blood flow as determined from fibers implanted for laser-Doppler flowmetry. In the present experiment, to investigate the interaction between nitric oxide and angiotensin II on renal hemodynamics, the effect of chronic intravenous infusion of L-NAME on blood pressure, sodium and water retention, and intrarenal blood flow distribution were studied in a separate group of rats pretreated with captopril and in which optical fiber for laser-Doppler flowmetry had been implanted. Captopril completely prevented sustained hypertension, sodium retention, and decreased medullary blood flow during chronic L-NAME infusion. These date indicated that angiotensin plays an important role in the regulation of renal medullary blood flow and sodium excretion by modulating the effects of nitric oxide in renal medullary blood flow.

The treatment of a 14-membered ring macrolide, clarithromycin (CAM), prolongs the survival time of patients with unresectable nonsmall cell lung cancer, and improves the host factor. As we previously reported, one of the underlying mechanisms is that the treatment of CAM increases the bioactivity of interleukin-12 (IL-12). In the present study, we administered CAM to murine lung cancer treatment models with Lewis lung carcinoma and to 18 patients with unresectable non-small lung cancer whose anticancer treatment had been terminated. The timing of CAM administration was examined and the time course of NK activity was measured. In the murine lung cancer treatment models, administration of CAM 7 days after anticancer chemotherapy more strongly inhibited the tumor growth and more rapidly and significantly increased NK activity, compared to the concomitant use of CAM with an anticancer chemotherapy. In humans, the NK activity which had decreased after anticancer treatment, tended to be increased after one month of treatment with CAM (p = 0.06). One month of treatment with CAM significantly increased the NK activity (p0.05) of the following subjects: patients with stage III in the clinical stages, patients with squamous cell carcinoma, patients who had received radiotherapy alone as pretreatment therapy, and patients whose pretreatment therapy effect was partial response (PR). We conjectured that increasing NK activity was one of the underlying mechanisms of the macrobiotic effect of CAM. CAM was especially effective for patients in the early clinical stages and patients who responded well to pretreatment therapy. Murine lung cancer models showed that non-concomitant use of CAM with anticancer chemotherapy was more effective.

Dramatic effects of chitin and chitosan on wound healing were demonstrated in field cases of many small animals (dogs and cats), food animals (338 cows) and 142 zoo animals. In comparison with conventional therapy with irrigation and antibiotic administration to wound, new treatment with chitin and chitosan permitted a substantial decrease in treatment frequency with minimum scar formation.

Apoptosis of peripheral leukocytes in 9 patients with myelodysplastic syndromes (MDS) was examined in vitro, using peripheral blood that had been gently incubated at 37 degrees C for 5 hours. The MDS patients included 3 with refractory anemia, 2 with refractory anemia with ringed sideroblasts, and 4 with refractory anemia with excess blasts. Peripheral blood specimens were also obtained from a control group consisting of 10 patients with iron deficiency anemia (IDA), 10 with idiopathic thrombocytopenic purpura (ITP) and 10 healthy individuals. Apoptotic granulocytes (Apo-Gs) were identified by morphological changes, including nuclear fragmentation, and expressed as a percentage of every 300 granulocytes counted. Apo-Gs were counted 1, 2, 3, 4, and 5 hours after incubation. Although the percentage of apo-Gs climbed over time in the MDS patients, a small number of apo-Gs were also observed in the healthy individuals. In the MDS patients, the proportions of apo-Gs 5 hours after incubation (37 degrees C) were significantly higher than those in the IDA and ITP patients and healthy individuals (15.7 +/- 8.0% in MDS patients vs. 2.8 +/- 1.2% in IDA patients, 2.3 +/- 1.7% in ITP patients, and 0.7 +/- 0.6% in healthy individuals; p0.005). No significant differences were observed in the proportions of apo-lymphocytes. DNA fragments were observed in blood lymphocyte from an MDS patient examined. Negative correlations between the percentages of granulocytes and Apo-Gs tended to be observed in the MDS patients. These results suggest that a strong susceptibility to peripheral granulocyte apoptosis is one of possible causes of granulocytopenia in MDS patients.

A 66 year-old man was found to have pointed out a 1-cm tumor shadow, on a chest X-ray film when he underwent a gastrectomy because of advanced gastric cancer. Five months after the operation, edema and proteinuria developed, and a chest X-ray film revealed enlargement of the tumor. There was no sign of recurrence of the gastric cancer. Nephrotic syndrome due to IgA-nephropathy and small cell lung cancer was diagnosed. Chemotherapy (carboplatin and etoposide) was effective against both the lung tumor and the nephrotic syndrome. Small cell lung cancer may have been involved in the pathogenesis of the nephrotic syndrome in this patient.

The high incidence of loss of heterozygosity (LOH) on chromosome 18q in advanced non-small cell lung carcinomas indicates the presence of tumor suppressor gene(s) on this chromosome arm, which plays an important role in the acquisition of malignant phenotypes in lung cancers. In the present study, we examined 62 lung cancer specimens and 54 lung cancer cell lines for allelic imbalance at 11 microsatellite loci to define common regions of 18q deletions. Allelic imbalance of 18q was detected in 24 (55.8%) non-small cell lung carcinoma specimens and in 6 (31.6%) small cell lung carcinoma specimens, whereas a similar frequency of LOH was statistically inferred to occur in cell lines by analyzing marker homozygosity as an indirect measure of LOH. Five specimens and 11 cell lines showed partial or interstitial deletions of chromosome 18q, and 2 of them had homozygous deletions at the 18q21.1 region. A commonly deleted region was assigned between the D18S46 and y953G12R loci. The size of this region is less than 1 Mb, and the coding exons of three candidate tumor suppressor genes, Smad2, Smad4, and DCC, were mapped outside the region. This result suggests that the common region harbors a novel tumor suppressor gene involved in the progression of lung cancer.

We present a 31-year-old female patient with systemic lupus erythematosus (SLE) which was accompanied by prolactinoma. Her SLE flared when the plasma levels of prolactin (PRL) increased, and subsided when these levels decreased following the administration of bromocriptine, irrespective of the glucocorticoid dosage. For the 29 plasma samples obtained during the clinical course, PRL levels were significantly correlated to the serum anti-DNA antibody titers (r = 0.55, p0.05) and inversely to the serum complement activity (r = -0.33, p0.05). This result suggests that PRL may play a role in the pathogenesis of SLE in some patients.

The activity of the medaka beta-actin promoter as a ubiquitous expression vector in transgenic medaka was examined using complementary DNA of the green fluorescent protein (GFP). Plasmid pOBA-GFP contained both the medaka beta-actin promoter and cDNA of the wild-type GFP, while pOBA-hGFP contained the medaka beta-actin promoter and cDNA of the mutant GFP in which serine was substituted for threonine at position 65 and codon usage was humanized to promote translation in vertebrate cells. The ApaI-SmaI fragment of both plasmids was microinjected into the nuclei of oocytes or the cytoplasm of embryos at the one-cell stage. The gene expression was detected, using a fluorescent stereomicroscope, from early stages of development to 1 week after hatching. The expression of the wild-type GFP was detected in early embryos, in the yolk sac and in small portions of the muscle and epidermis. This expression pattern was similar to that of the Escherichia coli beta-galactosidase reporter gene (lacZ), driven by the medaka beta-actin promoter, which was examined in our previous studies. The mutant GFP was expressed in early embryos and in many tissues such as the epidermis, blood vessels, muscle, notochord, fin ray, gut, eyes, and yolk sac, and the fluorescence was much stronger than that of the wild-type GFP. Thus, the usefulness of the medaka beta-actin promoter as a ubiquitous expression vector was confirmed using the mutant GFP as a reporter gene.

We compared clinical and demographic features, MRI findings, and HLA profiles of 57 Japanese patients with multiple sclerosis (MS) between groups with and without oligoclonal IgG bands (OCB) in the cerebrospinal fluid (CSF). Patients with the optic–spinal form of MS (OpS-MS) or acute transverse myelopathy (ATM), which are distinctive and relatively common in Japanese MS, were excluded in this study. The OCB-positive rate was only 56.1% (32/57) among these 57 `conventional' MS patients, of whom clinical features were similar to those of Western MS patients. The demographic features, clinical course, disability, and cerebral abnormalities seen on MRI were similar in the OCB-negative and OCB-positive patient groups. HLA-DR2 antigen, which has been confirmed to be associated with MS in many populations, was more common in the OCB-positive than in the OCB-negative and control groups. Furthermore, DR4 antigen was statistically more common in the OCB-negative patient group. These results raise the possibility that the presence of OCB is related to the immunogenetic background of the patient, and that there may be at least two subpopulations in Japanese patients with `conventional' MS from the viewpoint of immunogenetics. In one subpopulation, MS is associated with the DR2 antigen, and shows a stronger humoral immune response in the CSF, while in the other MS is associated with DR4, which has a milder humoral response. Further investigations involving more patients are warranted.

Androgen insensitivity syndromes are due to defects in the androgen receptor gene. In this study, we analyzed the androgen receptor gene in four cases with complete androgen insensitivity syndrome. In patient 1, one substitutional mutation [arginine (codon CGC) to cysteine (codon TGC) at position 774] of exon F was identified. This position was located in the hormone binding domain and appeared to be one hot spot of mutations because the mutations at the same position in several unrelated cases were reported before. In patient 2, one substitutional mutation [tyrosine (codon TAT) to cysteine (codon TGT) at position 571] of exon B was identified. This position was located in the DNA binding domain. In patients 3 and 4 (siblings), one substitutional mutation [arginine (codon CGA) to glutamine (codon CAA) at position 752] of exon E was identified. Taken together, these abnormalities might be related to the pathogenesis of complete androgen insensitivity.

Objective To evaluate the histological structure of benign prostatic hyperplasia (BPH) and its relationship with the density of α1-adrenoceptors in smooth muscle. Materials and methods Specimens from hyperplastic tissues obtained from 14 patients with BPH were evaluated for the density of α1-adrenoceptors in smooth muscle using autoradiography, Mallory-Azan staining and computer-assisted image analyses. The binding of [3H] tamsulosin (a selective α1-blocker) and the ratio of smooth muscle area was calculated, and the density of α1-adrenoceptors per area of smooth muscle determined by dividing the degree of binding by the ratio of smooth muscle to total area. Results There was a significant difference between the ratio of smooth muscle area in the hyperplastic acinar nodule and the surrounding stroma (P

A 59 year old woman developed pronounced thirst, increased water intake, and increased urinary output followed by slowly progressive cerebellar symptoms. Brain MRI showed abnormal hyperintensity on T2 weighted studies in the region of both dentate nuclei without atrophy of the cerebellum or the brainstem. A 99mTC diphosphonate bone scan showed bone lesions in the distal parts of both femurs as well as distal and proximal parts of both tibias. The diagnosis of Erdheim-Chester disease was made by bone biopsy. This is the first case of Erdheim-Chester disease presenting as a slowly progressive cerebellar syndrome and diabetes insipidus, and also showing high signal lesions in deep cerebellar nuclei on MRI. Skeletal surveys are indicated for patients with otherwise unexplained slowly progressive cerebellar symptoms.

We investigated the outcome of patients with asbestos pleurisy. The mean follow-up period of 12 patients was 6.5 +/- 3.7 years. Recurrence occurred in 5 patients (41.7%). Six of the cases recurred contralateral to the original lesion, while one recurred ipsilaterally. The mean period from onset to recurrence was 2.8 +/- 2.8 years. Five of the cases ended in death, and the mean period from onset to death was 5.0 +/- 3.1 years. Two patients died from pneumonia, 2 died from respiratory failure due to progressive pleural fibrosis, and 1 died from lung cancer. One of the 2 patients with progressive pleural fibrosis had leukopenia. It has been reported that the majority of cases of asbestos pleurisy resolve spontaneously, with a good prognosis. However, because of the possible mortality associated with respiratory failure caused by progressive pleural fibrosis, it seems prudent to follow patients with asbestos pleurisy closely.

In 1994, Barnes found the new method "long PCR method" where over 10 kb DNA was easily amplified, compared with conventional PCR method in which only a few kb DNA was amplified. He devised the new enzyme in this system which included Taq DNA polymerase plus a little amount of 3'--5' exonuclease activity (proofreading activity). We tried to apply this method to detect mitochondrial DNA deletions in mitochondrial encephalomyopathies. We detected mtDNA deletions easily, however, we could not quantify mtDNA deletions. This method can be performed within one day, compared with about 1 week required to perform Southern blotting and/or several sets of conventional PCR. Although Southern blotting is needed for quantifying mtDNA deletions, this method will become a useful screening method for detecting mtDNA deletions.

Percutaneous vertebroplasty is a radiologically guided therapeutic procedure that consists of percutaneous injection of surgical cement into a vertebral osteolytic metastatic lesion. This procedure has the advantage of providing rapid pain relief and bone strengthening. We report a 46-year-old male patient with osteolytic L3 vertebral metastasis from lung adenocarcinoma treated by percutaneous vertebroplasty under CT and fluoroscopic guidance. After this treatment, definite pain relief and stabilization of the vertebra were achieved. Vertebroplasty for osteolytic metastasis may be a minimally invasive procedure that provides immediate, long-term pain relief and contributes to spinal stabilization.

Facial palsy occurred in 21 (19.6%) of 107 Japanese patients with multiple sclerosis (MS) during a mean follow-up period of 4.3 years. We observed residual signs of facial palsy in five other patients in whom acute onset was confirmed from medical records. Facial palsy began on average 7.6 years after the onset of MS but in five patients (4.7%) was the first symptom of MS, preceding the next MS symptom by 0.5-3 years. Facial palsy was usually associated with other brainstem signs, while two patients showed only facial palsy 1 and 3 years after the onset of MS. Twenty-one (84.0%) of the 25 patients who underwent brain magnetic resonance imaging (MRI) showed brainstem lesions in the pontine tegmentum ipsilateral to the facial palsy. However, the two patients without other symptoms or signs had no apparent causal lesion on MRI, which suggests difficulty in differentiating idiopathic Bell's palsy from MS- associated facial palsy by MRI, although it has an excellent capacity to detect causal lesions of facial palsy associated with MS.

Apoptosis of lymphocytes in infectious mononucleosis (IM) was studied. Apoptotic cells (APCs) were defined by morphological characteristics, such as nuclear fragmentation, undergoing apoptosis. Among 10 of 27 IM patients (37.0%) APCsor = 3 per 500 peripheral white blood cells were observed on admission, but not in normal individuals. Sequential changes of proportions of both APCs and atypical lymphocytes (examined in 2 cases) showed a similar pattern, although APCs began to appear somewhat later and peak level of APCs were lower in comparison with those of atypical lymphocytes. APCs were positive for both anti-T cell and anti-Fas antigen monoclonal antibodies. Fas-positive cells were frequent in the early stage of IM, and returned to the normal range with the decrease of atypical lymphocytes. Sequential analyses of DNA fragmentation, done in one case, revealed that DNA fragmentation appeared with increase of APCs and disappeared with the decrease of APCs. These results suggest that apoptosis of T-cells in IM participates in the reconstitution of a proportion of lymphocytes disturbed by EB virus.

Overexpressing or restoring the basal levels of tumor suppressor genes in cancer cells can suppress tumorigenicity of cancer cells. In this communication, we compared tumor suppressive activities of three well-defined tumor suppressive genes (p53, p21WAF1/CIP1, and p16CDKN2) delivered individually to prostate cancer cells with adenoviral vector (Ad).Efficacy of growth inhibition by recombinant adenoviruses bearing p53, p21WAF1/CIP1, or p16CDKN2 (Ad5CMV-p53, Ad5CMV-p21, Ad5CMV-p16) genes were tested in vitro on androgen-dependent (LNCaP) and androgen-independent (C4-2, DU-145, and PC-3) human prostate cancer cells, ex vivo and in vivo on PC-3 tumor.Ad5CMV-p53 was observed to exert the greatest growth inhibitory action on all of the cell lines tested; inhibition appeared to be cytolytic. In comparison to control Ad5CMV-PA added samples, the growth inhibitory action of Ad5CMV-p21 and Ad5CMV-p16 appeared to be cytostatic. Ad5CMV-p53 is more effective than Ad5CMV-p16 and Ad5CMV-p21 in inhibiting the tumor "take" rate. A similar order of antitumor activity was observed when recombinant adenoviruses were injected intratumorily to previously established PC-3 tumors in vivo.p53 is the most effective tumor suppressor gene to target human prostate cancer.

We studied a dominant hereditary disorder showing progressive spastic paraparesis. The symptoms began in early childhood, with cerebellar deficits and mild mental deterioration, and the subsequent appearance of limb spasticity resulted in severe disability in the 3rd-4th decades of life. None of the patients were associated with any somatic abnormalities. Brain MRI showed diffuse white-matter involevement in all affected patients, but not in unaffected siblings. Although dominant, recessive, or X-linked leukodystrophies cause similar clinical features, our family did not show any known biochemical or gene deficits characteristic of these disorders. The clinical, radiological, and biochemical findings of this family are reported and suggest a possible novel genetic disorder.

A 45-year-old woman was admitted to Nara Medical University Hospital because of right-sided chest pain. Both a chest X-ray film and a chest CT scan revealed bilateral hilar and mediastinal lymphadenopathy and right pleurisy. She underwent fiberoptic bronchoscopy and mediastinoscopy. Biopsy specimens of the lung and mediastinal lymph nodes showed non-caseous epithelioid cell granulomas. After on ophthalmologic examination, she was given a diagnosis of sarcoidosis with a pleural lesion and uveal involvement. The pleurisy become less severe and the lymph nodes shrank without any treatment. About one year later, she complained of right-sided chest pain again and a chest X-ray film revealed diffuse thickening of the pleural on the right side. Examination of pleural biopsy specimens revealed malignant mesothelioma. We know of no previous report from Japan of malignant pleural mesothelioma in a patient with sarcoidosis.

To evaluate the role of tissue polypeptide antigen (TPA) as a biological marker of malignant pleural mesothelioma (MPM), we used immunohistochemical techniques to detect TPA in tumor cells, and we measured the content of TPA in serum from patients with MPM. In 14 of 16 patients with MPM, TPA was detected in the cytoplasm of tumor cells. Epithelial-type cells from 11 of 12 patients were stained positively (91.7%), and sarcomatous-type cells from 7 of 8 patients were stained positively (87.5%). Serum TPA levels were abnormally high in 7 of 9 patients. Two of three patients with stage-I disease had normal serum TPA levels, and all patients whose disease was at stage II or higher had abnormal serum TPA levels. Serum TPA levels increased as MPM progressed. These results suggest that the serum TPA level can be used as a biological marker of MPM.

A 40-year-old woman who worked as a nurse and had suffered from progressive exertional dyspnea for about 14 years underwent open lung biopsy with surgical treatment for pneumothorax. The diagnosis was lymphangiomyomatosis and she was treated with danazol to suppress ovarian function. Her condition improved temporarily, but she died of respiratory failure when she was 47 years old. The survival time after the onset of respiratory symptoms was 21 years, and after the biopsy it was 8 years. At autopsy a retroperitoneal cystic tumor was found (9 x 7 x 5 cm), which had been evident clinically. Histologic examination showed that the tumor was an extrapulmonary manifestation of the lumphangiomyomatosis lesion. Some paraaortic lymph nodes has similar lesions. Aggregates of small red spots were seen on acute surface of the liver. These were diagnosed as peliosis hepatis, they may have been caused by the danazol.

NS-21 ((+/-)-4-diethylamino-1,1-dimethylbut-2-yn-1-yl 2-cyclohexyl-2-hydroxy-2-phenylacetate monohydrochloride monohydrate, CAS 129927-33-4) is a novel compound designed for the treatment of bladder dysfunction. The effects of NS-21 and its active metabolite, RCC-36 ((+/-)-4-ethylamino-1,1-dimethylbut-2-yn-1-yl 2-cyclohexyl-2-hydroxy-2-phenylacetate monohydrochloride), on the urodynamics of decerebrated dogs are reported. Dogs were decerebrated at the precollicular-postmamillary level and the urodynamic effects of intravenously administered NS-21, RCC-36, and various reference drugs were compared by cystometry. NS-21 (0.3-1 mg/kg) and RCC-36 (0.1 mg/kg) caused an increase in bladder capacity without affecting the micturition pressure or residual volume, and thus caused a significant increase in functional bladder capacity. Oxybutynin caused a dose-dependent increase in bladder capacity at 0.1 mg/ kg and higher doses; however, the associated decrease in micturition pressure resulted in a significant increase in residual volume and a decrease in functional bladder capacity. These effects of oxybutynin were similar to those of atropine. Propiverine (0.1-10 mg/kg) and terodiline (0.1-10 mg/kg) caused no significant increase in bladder capacity. In conclusion, in decerebrated dogs, NS-21 and RCC-36 increased the bladder capacity without increasing the residual volume. NS-21 thus had more favorable therapeutic effects than any of the reference drugs tested and is therefore a promising candidate drug for the treatment of pollakiuria and urinary incontinence.

NS-21 ((+/-)-4-diethylamino-1,1-dimethylbut-2-yn-1-yl 2-cyclohexyl-2-hydroxy-2-phenylacetate monohydrochloride monohydrate, CAS 129927-33-4) and its active metabolite, RCC-36 ((+/-)-4-ethylamino-1,1-dimethylbut-2-yn-1-yl 2-cyclohexyl-2-hydroxy-2-phenylacetate monohydrochloride), have both anticholinergic and calcium antagonistic activities. NS-21 is under development for the treatment of bladder dysfunction. This study was designed to compare the effects of NS-21 and RCC-36 on the bladder function of monkeys with the effects of various reference drugs. Male rhesus monkeys were anesthetized with a mixture of enflurane and nitrous oxide, a transurethral catheter was inserted into the urinary bladder from the external urethral orifice, and cystometrograms were recorded. Drugs were administered intravenously. NS-21 at doses of 0.3 and 1 mg/kg caused an increase in bladder capacity without affecting the micturition pressure. RCC-36 also caused an increase in bladder capacity, but it was accompanied by a significant decrease in micturition pressure. Oxybutynin, atropine and verapamil all caused decreases in micturition pressure at doses which caused an increase in bladder capacity. Of the drugs examined, only NS-21 caused an increase in the bladder capacity of rhesus monkeys without affecting the micturition pressure. This drug is therefore a promising candidate for the clinical treatment of pollakiuria and urinary incontinence.

Metal contamination level will be decreased in order to maintain a device reliability according to device size reduction. Metal contamination from various processes are surveyed. The influence of metal contamination for 7–15nm thick gate oxides is discussed in order to clarify the critical concentration to gate oxides. NIG(Non Intrinsic Gettering) substrates are used in a worst case for gettering. Fe contamination with 4×1010 cm−2 strongly affects the TDDM characteristics, although there is no serious influence in the breakdown voltage even at the concentration of 5×1011 cm−2. The same tendency is observed for Cu contaminant and the critical concentration for TDDB characteristics is around 3×1011 cm−2. High energy B implantation is carried out to form gettering sites near device region. Breakdown voltage and TDDB characteristics are almost the same as epitaxial substrates at Fe concentration up to l×1012 Cm−2. Detailed examination such as SIMS, C-t and DLTS measurements is also supported the effectiveness in high energy gettering.

Competition between symmetric fission and asymmetric one for double charged sodium clusters with cluster size around 40 is discussed in terms of fission barriers calculated by the Kohn-Sham equation with deformed jellium positive ion cores. It is shown that the fission barrier heights for these processes depend on the shell correction energy of parent and daughter clusters.

The ITER central solenoid (CS) must be capable of driving inductively 30 000 15 MA plasma pulses with a burn duration of 400 s. This implies that during the lifetime of the machine, the CS, comprised of six independently powered coil modules, will have to sustain severe and repeated electromagnetic cycles to high current and field conditions. The design of the CS calls for the use of cable-in-conduit conductors made up of Nb3Sn and pure copper strands, assembled in a five-stage, rope-type cable around a central cooling spiral that is inserted into a circle-in-square jacket made up of a special grade of high manganese stainless steel. Since Nb3Sn cable-in-conduit conductors are known to exhibit electromagnetic cycling degradation, prior to the launch of production, the conductor design and potential suppliers must be qualified through the successful testing of full-size conductor samples. These tests are carried out at the SULTAN test facility. In this paper, we report the results of the on-going CS conductor performance qualification and we present the options under consideration for the different modules constituting the CS coil.

The International Thermonuclear Experimental Reactor (ITER) cable-in-conduit conductor used in the superconducting magnet system consists of a cable made of 300 to 1440 strands housed in a stainless steel tube (called as jacket or conduit). There are circular, square, as well as circle-in-square jackets, made of either a very low carbon AISI 316LN and AISI 316L grade stainless steels, or a high Mn austenitic stainless steel developed for ITER called JK2LB. Selected mechanical properties of the base material and weld joint were tested at room temperature and/or cryogenic temperatures (

The purpose of this study was to examine the effects of physical exercise on the expression of clusters of differentiation (CD)11b, CD18 and CD 54 on granulocytes and complement 3bi (C3bi)-dependent functions in rats.The rats were separated into two groups: the control group (n = 21) and the training group (n = 14). The rats in the training group were subjected to a program that consisted of swimming 6 days in a week for 7 weeks.The phagocytic and hydrogen peroxide (H2O2) generating activities and the expression of receptors on granulocytes were measured using flow cytometric techniques.The acute swimming and the 7 weeks of swim training caused high C3bi-dependent phagocytic activity of granulocytes. Swim training led to an increase of H2O2 generating activity together with C3bi-dependent phagocytosis both immediately after and 24 hrs after the 120 min swimming. The 24 hrs recovery from the 120 min swimming in trained and untrained rats caused an increase of H2O2 generating activity of granulocytes. In the training group, an increase in this activity could be observed immediately after the 120 min swimming exercise. The upregulation of the CI1b on granulocytes was induced by the 120 min of swimming regardless of swim training.These results suggest that the increase of C3bi receptor-dependent phagocytosis and H2O2 generating activities induced by the physical exercise might depend on the upregulation of the CD11b that is the component of C3bi receptor.

The gene for SCA2 has been mapped to chromosome 12q23-q24.1, but the mutant gene remained to be identified. When studying a Japanese family with SCA2, we noted that clinical features and disability varied among patients, with the central feature being progressive ataxia-slow eye movement-hyporeflexia syndrome. Additional symptoms were parkinsonism with minor cerebellar deficits, and severe ataxia with choreoathetosis. Our experience plus related literature documentation indicates that choreoathetosis is not so rare at the advanced stage of the disease, with onset at an early age, and that the variety of SCA2 phenotype depends on age at onset and duration of the disorder.

Tissue factor (TF) is a cell surface glycoprotein that initiates the extrinsic coagulation protease cascade and it is expressed in some tumor cells. TF belongs to the interferon receptor family, and it is one of the early immediate genes, suggesting that TF has a biological function other than hemostasis. We investigated the expression of TF in gliomas. Immunocytochemistry showed the expression of TF in 3 glioma cell lines. Immunohistochemical analysis of 44 surgical specimens revealed that all gliomas were positive for TF, and 19 (95%) of 20 glioblastomas, 12 (86%) of 14 anaplastic astrocytomas and 1 (10%) of 10 benign gliomas were moderately or strongly positive for TF. Our study showed that TF is expressed in gliomas, and that the level of TF expression is correlated with the grade of malignancy of the glioma, suggesting that TF may participate in cell growth.

A 66-year-old man was admitted to Nara Medical University Hospital because of sputum production and fevre. A chest X-ray film obtained on admission revealed many cysts and an infiltrative shadow in the right upper lung field. The patient was treated with antimycobacterial drugs (isoniazid 400 mg, streptomycin 0.75 g, and rifampicin 450 mg) because acid-fast bacilli were detected in his sputum. Although the symptoms and laboratory data improved, a new infiltrative shadow developed in the right lower lung field two months after the start of treatment. Transbronchial biopsy specimens showed intraluminal organizing exudate and alveolitis. The new lesion resolved when treated with the same antimycobacterial drugs. Mycobacterium xenopi was cultured from the sputum 80 days later. This is the third reported case of atypical mycobacteriosis (non-tuberculous mycobacteriosis) due to M. xenopi in Japan with the "initial aggravation" seen in some patients with typical pulmonary tuberculosis.

We report MRI changes in a spontaneous intracranial hypotension(SIH). The patient was 29-year-old woman, who developed headaches in upright position, nausea, and vomiting preceded by pressure feeling of ears. Neurological examination was unremarkable except for hyperreflexia in the lower extremities. Lumbar punctures revealed very low opening pressure, a mild elevated CSF protein and a mild pleocytosis. No evidence of underlying systemic or neoplastic diseases was noted. The brain and cervical MRI showed diffuse and continuous pachymeningeal enhancement with gadolinium. Her symptoms gradually improved within two months without any treatment, and follow-up MRI showed resolution of the abnormalities within five months. The dural enhancement with gadolinium seen in the SIH should be kept in mind in case of hypertrophic pachymeningitis of unknown etiology, and be differentiated from such diseases as hypertrophic pachymeningitis associated with infectious, neoplastic diseases or sarcoidosis.

In most cervical cancers, the function of p53 is down regulated. To explore the potential use of p53 in gene therapy for cervical cancer, we introduced wild-type p53 into cervical cancer cell lines via a recombinant adenoviral vector, Ad5CMV-p53, and analyzed its effects on cell and tumor growth. The transduction efficiencies of all cell lines were 100% at a multiplicity of infection of 100 or greater. The p53 protein was detected in Ad5CMV-p53-infected cells. Protein expression peaked at day 3 after infection and lasted 15 days. The Ad5CMV-p53-infected cells underwent apoptosis, and cell growth was greatly suppressed. The Ad5CMV-p53 treatment significantly reduced the volumes of established s.c. tumors in vivo. These results indicate that transfection of cervical cancer cells with the wild-type p53 gene via Ad5CMV-p53 is a potential novel approach to the therapy of cervical cancer.