PubMed Health⌕ Search

Biomedical subjects

Z Nambu

Publications and source records attributed to Z Nambu.

17 recordsLinked to original sources

Isolation of a cDNA encoding a putative SPARC from the brine shrimp, Artemia franciscana.

SPARC (Secreted protein, acidic, rich in cysteine) is an extracellular matrix-associated and anti-adhesive glycoprotein extensively studied in vertebrates. Its presence among invertebrates has been reported in nematodes and flies. We cloned a cDNA containing a complete open reading frame for SPARC from the brine shrimp, Artemia franciscana. The amino acid sequence identity between the Artemia and the fly SPARCs was 55%, whereas that of the Artemia and the nematode proteins was 45%. Artemia and vertebrates exhibited a sequence identity of 30% in the predicted aa sequences. The SPARC consisted of four domains commonly found among reported SPARCs. The protein comprised 291 amino acids, having a signal peptide, a follistatin-like domain, one N-glycosylation site and one calcium-binding EF-hand motif. Fourteen cysteine residues conserved among all the secreted forms of SPARCs were present in the Artemia SPARC, and four extra cysteine residues were also found in it. The extra residues were conserved among SPARCs of the arthropods and the nematode. Phylogenetic analyses showed that the sequences of SPARCs were grouped into those of vertebrates and invertebrates. Though the structural organization of SPARC was conserved among all the species studied, SPARC within a group was highly conserved within that group, but divergent between the two. Northern blots revealed the presence of a 1.1 kb mRNA, which was faintly expressed in embryos and considerably detected in prenauplii and nauplii. The isolation of a SPARC cDNA from Artemia franciscana provides intriguing features of the divergent protein, SPARC.

Amino Acid Motifs↗

[A method for culturing Artemia].

Artemia sp. is classified into phylum Arthropoda and class Crustacea. Ecological and experimental studies of this animal have been reported using wild species. In order to isolate inbred strains of Artemia, we have established a subculturing method for siblings of Artemia. Details of our practice on the culturing method of Artemia are described and the recent classification of Artemia is presented.

Animal Husbandry↗

Gene expression of trehalase during post-dormant development of the brine shrimp, Artemia: comparison of the two species.

Based on a homology screening approach, two degenerate oligonucleotides were employed as primers in a polymerase chain reaction to amplify a fragment of DNA encoding trehalase with a template of cDNA derived from embryos of American Artemia. Sequence analysis revealed that the fragment was composed of 228 bp comprising 76 amino acids, and highly homologous to trehalases of Tenebrio molitor (mealworm beetle), rabbit, Caenorhabditis elegans, Bombyx mori (silkworm) and Escherichia coli treA and treF (58-38%, in order of description). This fragment was used as a hybridization probe. A Northern blot analysis on American Artemia showed three transcripts of 5.0, 2.7 and 2.2 kb, and the two larger transcripts were also detected in Chinese Artemia. The developmental profile of the gene expression and the trehalase activity suggest that the transcripts of 5.0 and (or) 2.7 kb in both Artemia may be directly or indirectly related to translation of the trehalase. A Southern blot analysis on both Artemia suggested the existence of two highly homologous genes or one gene having an intron within the region where the probe binds in their haploid genome.

Amino Acid Sequence↗

Comparison of Two Questionnaires on Respiratory Symptoms in a Nicaraguan Population: Value in Diagnosis of Chronic Bronchitis.

Two questionnaires about respiratory symptoms were evaluated for reliability and ability to diagnose chronic bronchitis in a study population of 129 Nicaraguans (110 workers and 19 patients with chronic bronchitis). The first questionnaire (AQ) had symptom questions that were based on British Medical Research Council (MRC) questions, adapted to local Spanish. The second questionnaire (MRCQ) contained MRC symptom questions translated directly into Spanish. The reliability of the questions was measured in a test-retest procedure. The questionnaire-based diagnosis of chronic bronchitis was compared with the diagnosis made by a physician (for workers) or from the hospital records (for patients). The questions concerning symptoms in both questionnaires were of acceptable reliability. For the diagnosis of chronic bronchitis in workers, the AQ showed similar sensitivity, a somewhat higher specificity, and a substantially higher positive predictive value (90%) than the MRCQ (57%). Among the patients, the AQ identified 17 patients as positive (sensitivity 89%), while the MRCQ identified 15 (sensitivity 79%). respiratory questionnaire; reliability; chronic bronchitis; Nicaragua Hanley & Belfus, Inc. Int J Occup Environ Health 1077-3525 2 2 1996 April/June Chronic Exposure to Cigarette Smoke Inhibits the Stimulating Effects of Mineral Fibers on the Production of Tumor Necrosis Factor by Alveolar Macrophages of Rats 95 98 EN Yasuo Morimoto Department of Environmental Health Engineering, University of Occupational and Environmental Health, Japan 1-1, Iseigaoka, Yahatanishiku, Kitakyushu 807, Japan. Ziro Nambu Hajime Hori Tohru Tsuda Hiroshi Yamato Toshiaki Higashi Yasuyuki Yokosaki Masamitsu Kido Isamu Tanaka The objective of this study was to evaluate the chronic combined effects of mineral fibers and cigarette smoke on the production of tumor necrosis factor (TNF) by alveolar macrophages. The authors chronically exposed ten rats to cigarette smoke in vivo and measured the production of TNF by alveolar macrophages in the presence of mineral fibers in vitro. For smoke exposure, rats were divided into two groups. Five rats were exposed daily to a concentration of 10 mg/m(3) of cigarette smoke for six hours a day, five days a week, for four weeks, and five rats (control) were not exposed to smoke. A broncho-alveolar lavage was performed after the smoke exposure, and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibers on a microplate for 24 hours. TNF activity in the supernatant was determined by the L929 bioassay. When alveolar macrophages were not stimulated by mineral fibers, TNF production tended to be lower in smoke-exposed alveolar macrophages than in unexposed ones, although the difference was not significant statistically. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibers, both fibers stimulated TNF production, but TNF production in smoke-exposed alveolar macrophages was lower than that in unexposed macrophages. These results revealed that long-term exposure to cigarette smoke inhibited the stimulating effect of mineral fibers on the production of TNF.

Journal Article↗

Effects of nickel oxide on the production of tumor necrosis factor by alveolar macrophages of rats.

To evaluate the effect of green nickel oxide (NiO) on the production of tumor necrosis factor (TNF) by alveolar macrophages, alveolar macrophages were exposed to NiO in vitro and in vivo. For the in vitro study, rats alveolar macrophages were incubated with NiO on a microplate for 24 h. TNF activity in the culture supernatant was determined by the L929 bioassay. Rats alveolar macrophages cultured with 100 and 200 micrograms/mL of NiO in vitro induced the production of TNF, however, it was not statistically significant compared with the control that was free from NiO exposure. For exposure in vivo, rats were divided into two groups. Five were exposed to a daily concentration of 11.7 +/- 2.0 mg/m3 of NiO for an 8-hr/d, 5 d/wk, for 4 wk, and five rats (control) were kept in a cage and not exposed to NiO. Bronchoalveolar lavage was performed and the recovered alveolar macrophages were incubated on a microplate for 24 h. TNF production by exposed alveolar macrophages was significantly higher than that of controls.

Acid Phosphatase↗

Pulmonary response to exposure to ozone of emphysematous rats.

Rats were treated with a single intratracheal instillation of 6.5 units elastase or normal saline. Seven weeks after treatment, the animals were exposed for 24 hr to filtered air or 1 ppm O3, and their lung functions were measured. The exposure to O3 resulted in functional changes depending mainly on peripheral airway obstruction, and the direction and degree of those functional changes were in general similar between the saline- and elastase-treated animals. Another group of saline- or elastase-treated rats were exposed to 3 ppm O3 for 3 hr and the edematous response of their lungs was again similar. These results indicate that elastase-treated lungs responded to the exposure to O3 in a fashion similar to normal lungs in rats, but lung damage caused by the exposure to O3 superimposed over preexisting emphysematous damage, resulted in an additional lessening of the margin of pulmonary reserve capacity.

Animals↗

An emphysema model in rats treated intratracheally with elastase.

Pulmonary functions, morphology, and morphometry were examined in rats at 3, 7, and 10 weeks after a single intratracheal administration of 6.5 units of porcine pancreatic elastase in order to obtain a model of pulmonary emphysema which would be suitable for studying the responses of emphysematous lungs to atmospheric pollutants. Functional residual capacity and residual volume of the elastase-treated rats increased at all the times studied, but their total lung capacity increased only at 7 and 10 weeks compared with those of the saline-treated control rats. The increase in static lung compliance and the decrease in peak flow and maximum flow at 50% of total lung capacity during forced expiration were also observed in all except the 3-week elastase animals. The elastase-treated lungs showed morphological changes characteristic of emphysematous lesions. The increase in mean linear intercept length and the decrease in total alveolar surface area were demonstrated by these elastase-treated lungs. Based on these results, we conclude that an adequate and suitable model of pulmonary emphysema could be obtained in rats 7-10 weeks after treatment with the present dose of elastase.

Animals↗

Tolerance to ozone in emphysematous rats.

Pulmonary emphysema was induced in rats by a single intratracheal instillation of swine pancreatic elastase. After adequate development of the pulmonary emphysema, the animals were initially exposed to 1.9 ppm ozone for 3 hrs, and 3 days later, challenge-exposed to 5.1 ppm ozone for 3 hrs and immediately sacrificed to investigate the extent of the development of tolerance to ozone judged by the formation of edema. Although the body weights of the pulmonary emphysematous rats were the same as those of the saline-treated control rats, the lung weights of the former were heavier. The extent of the edema formation by ozone and of the tolerance to ozone of the pulmonary emphysematous rats seemed to be quite similar to those of the saline-treated control rats. On the other hand, although the exposure of the saline-treated control rats to 1.9 ppm ozone for 3 hrs resulted in an increase in lung weight without edema 3 days after the exposure, the pulmonary emphysematous rats did not show such a response.

Animals↗

Respiratory effects of intermittent exposure to ozone of rats.

Intermittent exposures of rats to ozone (O3) of 1 and 0.5 ppm were performed. Flow resistance of the lungs left in situ in the chest cavity opened after the sacrifice was measured at different levels of elastic pressure, and it was shown that daily 3-hr exposures to 1 ppm O3 for 30 consecutive days mainly produced increased resistance of more-central airways, while daily 6-hr exposures to 0.5 ppm O3 for 60 consecutive days mainly increased the resistance of peripheral airways. Morphological changes of the lungs caused by both exposures were in general similar in nature, but differences in secretion were noticed: it was more evident in larger to middle-sized bronchi in the animals intermittently exposed to 1 ppm O3, but more evident in the peripheral airway region in the animals intermittently exposed to 0.5 ppm O3. No change in the pulmonary static volume-pressure curve, indicative of the altered retractive forces of alveoli, was observed in both exposures, although a slight reduction in lung distensibility was suggested.

Airway Resistance↗

Antioxidant system and ozone tolerance.

Rats were initially exposed to 2 ppm ozone for 3 hr in order to induce ozone tolerance. The time course of the content of nonprotein SH as well as the activities of glutathione peroxidase, glutathione reductase, and glucose 6-phosphate dehydrogenase (so-called antioxidant system) in lungs of the animals was compared to the development of tolerance in the animals to a challenge exposure of 5.6 ppm ozone for 3 hr. An enhancement of a part of the antioxidant system was detected on the second day and thereafter following the initial exposure, but the clear and complete tolerance to ozone was demonstrated 1 day before the enhancement of the antioxidant system. Alternatively, the induction of tolerance to ozone was found to be experimentally suppressed by actinomycin D or colchicine, but the levels of the antioxidant system in animals thus treated were not significantly different from the matched controls, or only partly enhanced. These events suggest that the tolerance to ozone is not related to an enhancement of the antioxidant system.

Adaptation, Physiological↗

Protection with cycloheximide or emetine against pulmonary edema induced by ozone or nitrogen dioxide.

Pretreatment with cycloheximide or emetine provided significant protection against pulmonary edema in rats exposed to ozone or nitrogen dioxide. Other inhibitors of protein-synthesis, actinomycin D or puromycin, failed to show such effects. Possible actions of these agents as well as the doses and times that afforded the significant protection were investigated. These agents, by themselves, did not alter the water content of the lungs. In vitro study revealed that both cycloheximide and emetine hardly acted as scavengers of oxidant. Pretreatment with either agent was associated with a significant increase in the activity of glucose 6-phosphate dehydrogenase of the lungs, but the increase did not necessarily coincide with the protection. Activity levels of non-protein SH, glutathione-peroxidase and -reductase in the lungs of rats treated with either agent were scarcely altered. The effect of these agents administered in vivo or in vitro on the in vitro lipid peroxidation by air was also investigated. Other possible mechanisms of these agents responsible for the protective effect against pulmonary edema induced by oxidants were also discussed.

Animals↗

The effect of age on the ozone-induced pulmonary edema and tolerance in rats.

Effects of the age on the lung injury caused by ozone and on the development of ozone tolerance were examined in male rats by measuring pulmonary weight response. The pulmonary susceptibility to ozone was found to be proportional to the logarithm of body weight from 70 to 300 g, but extraordinarily enhanced beyond 300 g (about 9 weeks old). The developmental process of ozone tolerance in young rats were found to be similar to that in young adults, but apparently different from that in older rats. Pulmonary ability to induce ozone tolerance was higher in young rats weighing less than 300 g than in older rats. These results suggest that the rat lung response to ozone alters as the rats grow older beyond 9 weeks.

Aging↗

High affinity binders for cyclic adenosine 3', 5'-monophosphate on plasma membranes isolated from rat liver and ascites hepatomas.

Plasma membranes from rat liver were found to contain at least two types of specific binding sites for cyclic [3H] adenosine 3', 5'-monophosphate (c[3H]AMP) with apparent dissociation constants of 0.51 +/- 0.14 and 2.9 +/- 0.6 nM (O degrees), respectively. The levels of these binding sites in liver plasma membranes were about 0.60 +/- 0.20 and 1.3 +/- 0.5 pmole/mg protein. The highest affinity binders for c[3H]AMP were found to be reduced in amount in plasma membranes of ascites hepatomas to 1/3 to 1/4 as compared with liver membranes in the cases of AH-130 and AH-7974 and to an almost undetectable level in the case of AH-130F(N). No difference in the endogenous phosphorylation of plasma membranes by (gamma-32P])ATP was, however, detected among liver and hepatoma plasma membranes. Addition of cAMP or cGMP at various concentrations did not affect the endogenous phosphorylation of plasma membranes of these cells.

Animals↗