Registered state and a two-dimensional Bose liquid of 4He in mesopores of hectorite.
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Biomedical subjects
Publications and source records attributed to K Torii.
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Each L-amino acid (AA) in plasma and brain remains unchanged while normal diet is available. Once L-lysine (Lys) deficient diet was offered to rats, Lys in plasma and brain declined, and anorexia occurred. When solutions of AAs were offered, they selected the Lys solution, and their food intake and growth normalized. The single neuron activity in the lateral hypothalamic area of these rats suggested that neural plasticity occurred, specifically responding to Lys, both by iontophoretic application and during ingestion of AA. The recognition site for deficient nutrient intake in the brain of rats with Lys deficiency was identified by non-invasive magnetic resonance imaging (MRI 4.7 tesla, 40 cm bore in diameter) developed to monitor changes in cerebral blood flow and oxygenation in rat brain. Wistar strain young male rats fed with Lys deficient diet for 4 days, were adapted to be settled in the center of the bore. When they received a Lys injection intraperitoneally (0.2 M, 10 mL/kg), a signal intensity decrease in the medial and lateral hypothalamus appeared 30 minutes later in T2 weighted images, reflecting increased oxygenation which lasted for 30 minutes, and then gradually recovered. These changes never occurred in any other areas of the brain of rats with Lys deficiency, i.e., the thalamus, the cortex, the hippocampus, etc. There were no changes in the signal intensity with control injection of saline. In addition, oxygen consumption in the brain of rats without Lys deficiency was not altered by intraperitoneal Lys injection. The present results suggest that in essential AA deficiency, the medial and lateral hypothalamus may play important roles in recognition responses to particular deficient nutrients in order to maintain homeostasis.
Three case reports of thymolipoma are herein presented. One patient presented with myasthenia gravis, while the other patients were asymptomatic. The tumors in our cases all had histopathologically different features: case 1, lipoma of the thymus; case 2, involuted thymic hyperplasia; and case 3, typical thymolipoma. The histopathological findings of thymolipoma are discussed in the context of the pathogenesis of thymolipoma.
The effect of continuous L-lysine (Lys) infusion on dietary choice between Lys deficient and protein-free diets in Sprague-Dawley rats was studied to determine the sensing site of Lys deficiency. After daily intake of each diet became constant, Lys was continuously infused for 11 days via intraperitoneal (IP), intragastric (IG) or intracerebroventricular (ICV) route, with an osmotic pump. Daily intake of each diet was measured. Intake of the Lys deficient diet compared with protein-free diet in either IP or IG Lys-infused group increased significantly (p < 0.001) vs. the intake in the baseline period. The selection of the Lys deficient diet was quite comparable between IP and IG groups. But the intake of the ICV group was unchanged. Hepatic vagotomy during IP infusion transiently delayed selection of the Lys deficient diet. These results imply the roles of postabsorptive mechanisms in sensing an amino acid deficiency, and possible involvement of the hepatic branch of the vagus in the sensing. However, sensing in the brain or indeed in the intestine was not excluded.
The Long Evans Cinnamon (LEC) rat spontaneously develops fulminant hepatitis, which is usually lethal due to excess copper accumulation in the liver and is considered an animal model of Wilson's disease. LEC rats show a strong appetite for proline solution. Daily oral (p.o.) administration of proline resulted in significant delay of mortality. Feeding a copper-deficient diet greatly delayed the onset of jaundice and mortality and voluntary consumption or p.o. administration of proline further delayed jaundice and prevented mortality. LEC rats also consume ascorbic acid solutions, and p.o. administration of ascorbate also results in a significant delay in the appearance of jaundice and mortality. Combined treatment with ascorbic acid and proline is additive to delay further jaundice and mortality. An endogenous antioxidant protein, thioredoxin, when infused by minipump IP, could also inhibit the incidence of jaundice. These results indicate that antioxidant treatment combined with proline may be of benefit in Wilson's disease and possibly other forms of hepatic dysfunction.
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A randomized study was conducted for 4 weeks to evaluate the effect of twice daily inhalation of beclomethasone dipropionate (BDP) inhalation (group A) as compared to four times a day inhalation (group B) in chronic asthma. Patients were randomly allocated to receive BDP at a dosage of eight puffs twice daily (800 micrograms/day, group A) or four puffs four times daily (800 micrograms/day, group B). Forty four patients entered the study but eleven were excluded because of their insufficient records or unfitness to eligibility criteria. There was no significant difference in patients' characteristics such as types, and severity of diseases between the two groups. Daily keeping of symptom scores, twice daily measurement of morning and night peak expiratory flow (PEF) and checking of the drug consumption were performed throughout the study. There was no significant difference in the mean %PEF either at 2 and 4 weeks at the study between the two groups. Symptom scores, asthmatic scores, bronchial hyperresponsiveness, pulmonary function tests (FVC, FEV1, FEV1%) and serum cortisol levels also showed no significant difference between the two groups. These results indicate that twice daily inhalation of BDP (800 micrograms/day) for four weeks caused the same effects on the patients with chronic bronchial asthma as 4 times daily inhalation did. Therefore, twice daily inhalation therapy with BDP is recommended for chronic bronchial asthma patients.
As a test for specific hunger for amino acids with the goal of identifying brain regions which might mediate motivation to alleviate L-lysine (Lys) deficiency, rats were trained to lever press to receive complete diet. Rats were given Lys deficient (Lys-def) diet ad lib. Intraperitoneal (IP) injection of Lys, 2 h before the test session, inhibited lever pressing. Lys injected animals pressed at nearly the same low rate as did animals fed ad lib complete diet, although the response of saline injected animals was also partially decreased. Next, osmotic minipumps were implanted IP and animals given Lys-def diet ad lib. Chronic Lys infusion also strongly inhibited lever pressing. Rats allowed ad lib access to Lys to drink drank significantly more Lys than when given complete diet. Lys chronically infused by minipump into the lateral hypothalamus, also inhibited pressing by rats given Lys-def diet. Therefore, animals lacking Lys in the diet will work to receive complete diet, but replacement of Lys by drinking, chronic IP infusion, or directly into the lateral hypothalamic area inhibits bar pressing behavior.
Functional roles of the glossopharyngeal (GL) nerve on food and fluid intake were studied by examining effects of the GL denervation on two biologically different activities induced by specific diets using mice and rats. First, we examined whether GL section alters the acceptability of a bitter tasting essential amino acid, L-lysine (Lys), by Lys-deficiency in mice. The aversion threshold for Lys, normally about 3 uM in mice, increased to about 300 uM when mice were fed the Lys-deficient diet for 10 days. This increase of the Lys aversion threshold (increase of acceptability for Lys) by Lys-deficiency was also evident in mice with the chorda tympani denervation but was not observed in mice with the GL denervation. Next, we examined whether GL section alters the induction of a salivary protein, cystatin S (a cysteine proteinase inhibitor), by a diet containing papain (a cysteine proteinase) in rats. GL denervation largely inhibited the induction of cystatin S in the rat submandibular glands by papain. These results collectively suggest that chemosensory information conveyed by the GL nerve plays important roles on recognition of both nutrient and toxic compounds in the diet and induction of biological responses that protect the animal from both nutritional deficiency and exogenous toxic compounds.
A case of idiopathic plasmacytic lymphadenopathy with hyperimmunoglobulinemia is reported. A 71-year-old man was admitted to the hospital because of the abnormal shadow on chest roentgenogram. Chest X-ray taken on admission showed remarkable diffuse infiltration and pleural thickening. Laboratory examinations revealed an elevated total protein level of 10.1 g/dl, and a gammaglobulin level of 7.0 g/dl including 6,790 mg/dl IgG. Mediastinal lymphadenopathy was observed on a chest CT. The patient underwent open lung biopsy. Heavy infiltration of lymphocytes and plasma cells were seen in the moderately fibrotic pulmonary interstitium. LIP was diagnosed. Lymph node biopsy was also performed. Follicular hyperplasia with prominent germinal centers and plasma cell proliferation in the interfollicular area were seen. Treatment with prednisolone resulted in an improvement in the chest X-ray findings, as well as a diminished polyclonal hypergammaglobulin level.
There is much evidence that the cysteinyl-leukotrienes (C-LTs) are important in the pathogenesis of asthma. The clinical effect of a new leukotriene antagonist, ONO 1078 (4-oxo-8-[4-phenylbutoxy)benzoylamino]-2-(tetrazol-5-yl)-4H- 1-benzopyran hemihydrate, CAS 103177-37-3) on symptoms, pulmonary lung function and bronchial hyperresponsiveness was evaluated in patients with bronchial asthma. Eleven patients were treated for 24 weeks with 450 mg of ONO 1078 twice daily. The score of asthma symptom severity and the number of inhaled procaterol were significantly reduced after 2 weeks of ONO 1078 treatment and remained decreased for another 22 weeks. Their FEV1 and PC20 to histamine significantly improved 12 and 24 weeks after ONO 1078 treatment. The effectiveness of ONO 1078 suggests that the C-LTs play an important role in the pathogenesis of asthma. ONO 1078 might help to favorably modify the pathophysiologic condition in patients with bronchial asthma.
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Core I protein is the largest subunit of ubiquinol-cytochrome c reductase. We have isolated a complete cDNA clone of 1575 bp encoding the precursor to this protein by screening a human fibroblast cDNA library. Nucleotide sequence comparison showed that the human core I protein cDNA is about 85% homologous with the reported bovine counter part but with a large difference in the length of coding region which consists of 480 amino acids in human and 362 amino acids in bovine. Human core I protein is presumed to contain a presequence of 34 amino acids. Amino acid sequence alignment study showed that the predicted human core I protein has a significant homology with other members of matrix processing peptidase (MPP) and processing enhancing protein (PEP) family.
When a L-lysine (Lys)-deficient diet is given to rats, Lys in plasma and brain declines and rats will then select a Lys solution from among other L-amino acids (AAs). The recording of single-unit activity in the lateral hypothalamic area of these rats suggested that neural plasticity occurred, specifically responding to the deficient nutrient, Lys, centrally and during ingestion of AA. Possible neurotrophic factors in serum from rats with or without deficiency of either protein or Lys was assayed by Hydra japonica. An increase in serum inhibin and activin A was observed in rats fed a Lys-sufficient and nonprotein diet, respectively. However, serum activin A-like activity was severely suppressed under Lys deficiency. Additionally, the immunohistochemical distribution of activin A in the brain was found in the nucleus tractus solitarius, the area postrema, and the arcuate nucleus. These facts indicate that ingestion of Lys-deficient or nonprotein diet caused a change in serum levels of activin A as a possible neurotrophic factor. This release may elicit plasticity in the sensitivity of neurons to deficient AA in the nuclei that could selectively drive ingestive behavior for its particular AA (e.g., Lys) to maintain AA homeostasis.
Human blood monocytes cultured in various serum conditions were stimulated with Mycobacterium leprae or M. bovis BCG and their cytokine-inducing abilities were compared. BCG, either live or killed, induced production of interleukin 1 (IL-1), IL-6, tumor necrosis factor (TNF), and IL-1 receptor antagonist (IL-1ra). Live BCG at a lower bacterial number was more potent than killed BCG in the induction of IL-6 and TNF. In contrast to BCG, killed M. leprae induced few cytokines except for IL-1ra. Similar results were obtained when monocytes were cultured in the presence of untreated or heat-inactivated fetal bovine serum (FBS). When FBS and human serum (HS) were compared and the effect of heat inactivation was investigated, monocytes in HS produced the most cytokines, then those in FBS, irrespective of heat inactivation, and those in heat-inactivated HS produced the least cytokines. There were no differences between live and killed M. leprae, and BCG were far more potent than M. leprae in all of our experimental conditions, indicating that the poor cytokine (IL-1, IL-6 and TNF)-inducing ability of M. leprae was not due to their viability. Cytokine production was partially in parallel with the phagocytosis of the mycobacteria. These results suggest that M. leprae favor their infection by evoking little host reaction through the induction of only low levels of immunostimulatory or proinflammatory cytokines but a substantial amount of immunosuppressive cytokine.
The purpose of this study was to elucidate the effects of aging on diaphragmatic mitochondrial function. Diaphragm mitochondria were prepared from specific pathogen-free rats aged 7 wk (n = 7), 35 wk (n = 7), and 55 wk (n = 7). The activities of various portions of the mitochondrial electron transport chain, i.e., complexes I, II, III, and IV, were measured enzymatically. The specific activities of complex I decreased significantly (P less than 0.01) in 35-wk-old rats (726 +/- 90 nmol/min/mg protein) compared with 7-wk-old rats (1,018 +/- 121), and the decrease was more remarkable in 35-wk-old rats (565 +/- 64; P less than 0.01 versus 35-wk-old). The activities of complex IV also decreased significantly (P less than 0.01) in 55-wk-old rats (1,222 +/- 191) compared with 7-wk-old rats (1,797 +/- 208); however, no significant changes in complex IV activities between 7-wk-old rat and 35-wk-old rats were observed. In contrast, the activities of complex II and III were not affected by aging. Limb muscle, heart, and liver mitochondria were also prepared from the same rats. The same tendency was observed in limb muscle mitochondria; however, in heart and liver mitochondria, activities of all four complexes were not changed in rats of all age groups. These results indicate that vulnerability of mitochondrial electron transport chain to aging differs from organ to organ and that it also differs from portion to portion in the electron transport chain and the most vulnerable site was complex I.(ABSTRACT TRUNCATED AT 250 WORDS)