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Biomedical subjects

A Nagai

Publications and source records attributed to A Nagai.

At least 91 records · Page 5Linked to original sources
PubMed1999

Thiol depletion induces apoptosis in cultured lung fibroblasts.

Thiol antioxidants are implicated in the protection of cells from oxidative injury. We studied the role of thiols in the regulation of apoptosis in cultured lung fibroblasts. Thiol depletion by culturing fibroblasts in cystine-free medium or with thiol-depleting agents induced oxidant accumulation and cell death by apoptosis. The cell death was prevented by the antioxidants ascorbic acid (AA) and catalase. Thiol depletion also induced leukotriene (LT) C4, LTD4, and LTE4 production and selective phosphorylation of p38-mitogen-activated protein kinase (MAPK) and its nuclear substrate ATF2. LT production and p38-MAPK phosphorylation were required for induction of apoptosis because thiol depletion-induced apoptosis was completely blocked by the 5-lipoxygenase inhibitor AA861, the LT antagonists FPL55712 and ONO1078, and the p38-MAPK inhibitor SB203580. LT production was inhibited by AA and p38-MAPK phosphorylation was inhibited by AA, AA861, and FPL55712. In an in vitro scratch wound model, repopulating fibroblasts at the wound margin, but not quiescent cells at the intact site, selectively underwent thiol depletion- induced apoptosis that was completely blocked by AA861, FPL55712, and SB203580. Thus, thiol depletion induces apoptosis through an ordered pathway involving oxidant accumulation, LT production, and p38-MAPK activation. Apoptosis of wound fibroblasts may be responsible for impaired wound healing in various organs, including the lung.

Apoptosis↗
PubMed1999

Effect of cromolyn on adenosine-induced airway microvascular leakage in sensitized rats.

Inhalation of adenosine causes bronchoconstriction in asthmatic subjects, but the effect of this purine nucleotide on airway vascular permeability is unknown. In order to determine whether adenosine produces airway microvascular leakage and, if so, to examine the effect of cromolyn (sodium cromoglycate (SCG)) on this extravasation of Evans blue was measured in the airways of ovalbumin-sensitized Brown Norway rats. Inhaled adenosine caused microvascular leakage in sensitized but not in non-sensitized rats, and the response was abolished by capsaicin pretreatment or the tachykinin neurokinin-1 receptor antagonist FK888. Adenosine-induced vascular leakage became apparent in nonsensitized rats when treated with phosphoramidon, and airway neutral endopeptidase activity was lower in sensitized than in non-sensitized animals. The extravasation induced by adenosine in sensitized rats was dose dependently inhibited by SCG aerosols, SCG likewise inhibited microvascular responses to substance P, but had no effect on those to platelet-activating factor. These results suggest that: 1) adenosine induces airway microvascular leakage in sensitized rats through stimulation of neurokinin-1 receptors; 2) this effect is associated with a sensitization-induced decrease in neutral endopeptidase activity; and 3) sodium cromoglycate inhibits adenosine-induced extravasation, presumably via functional antagonism of tachykinins.

Adenosine↗
PubMed1999

Merits of soft nitriding scalers.

BACKGROUND: It has been demonstrated that nitriding modifies the physical characteristics of metals. The purpose of this study was to evaluate the changes induced by 3 levels of inexpensive soft nitriding treatments on commercial sickle scalers. METHODS: Taglite scalers (NT) were soft nitrided for 30 (SN30), 60 (SN60), or 90 (SN90) minutes. The cumulated scaled material was weighed every 10 strokes x 10 and thereafter every 1,000 to 8,000 strokes by an automatic scaling apparatus against epoxy resin. Weight differences were used to indicate abrasion resistance; the relative efficiency (RE) was calculated as the ratio of scaled amount at a given number of strokes (SN/NT). The hardness and the tensile strengths were determined for each soft nitriding treatment level. The nitrided layer thickness of representative SN scalers was observed by electron probe x-ray microanalysis. RESULTS: The SN60 was not significantly different from SN30 or SN90, but the SN90 was more efficient than SN30 for the first 100 strokes (P<0.01). The RE of all SN scalers was significantly greater (2.3 to 2.7 times) than the NT scalers from the beginning of the study and throughout all time periods (SN90 > SN60 > SN30); it increased further during the first 100 strokes (9.7 to 15.5 times), indicating the NT scalers wore out faster than SN scalers. The untreated scalers' performance decreased to 10% of baseline after 100 strokes; but even after 1,000 strokes, the SN60 and SN90 performed better than new untreated scalers. Thereafter, all scalers' performance, including SN scalers, decreased. While the NT blades ceased to cut measurable amounts after 7,000 to 8,000 strokes, all SN scalers continued to cut. Although SN90 scalers had the thickest soft layer and were the hardest (P<0.01), the SN60 had the highest tensile strength (P <0.01), suggesting that it might be the safest in practice. CONCLUSIONS: Sixty minutes of soft nitriding treatment of commercially available taglite scalers seem to be the optimal treatment duration to increase their durability, on the order of 100 to 1,000 times, without jeopardizing safety for clinical use.

Dental Alloys↗
PubMed1999

Kaposi's sarcoma-associated herpesvirus infection in the lung in multicentric Castleman's disease.

A 32-year-old female was admitted for evaluation of multiple infiltrates on a chest radiograph. A diagnosis of multicentric Castleman's disease was made on the basis of typical clinical manifestations. Transbronchial lung biopsy (TBLB) revealed histological findings reported in lymphocytic interstitial pneumonia. Both the polymerase chain reaction and in situ hybridization with a probe specific for Kaposi's sarcoma-associated herpesvirus (KSHV) sequences demonstrated the presence of KSHV in the TBLB sample.

Adult↗
PubMed1999

[Apoptosis in chronic obstructive pulmonary disease].

Apoptosis is a critical mechanism controlling cellularity in various tissues. It is so far unknown whether apoptosis plays a critical role in the pathogenesis and development of chronic obstructive pulmonary disease (COPD). However, recent evidence suggests that apoptosis may occur in vascular endothelial cells and/or alveolar epithelial cells in COPD lungs, thereby potentially contributing to lung tissue destruction seen in COPD. Apoptosis may also influence cellular infiltrates into the lung, another pathologic feature of COPD, because the survival of inflammatory cells such as neutrophils, lymphocytes, and macrophages are critically determined by the mechanism of apoptosis.

Apoptosis↗
PubMed1999

[Relationship between p 53 gene mutation and MDR 1 gene expression in surgically resected non-small cell lung cancer].

The resistance of tumor cells to chemotherapeutic drugs is a major obstacle to successful cancer chemotherapy. Expression of the MDR 1 gene, which encodes for a transmembrane efflux pump (P-glycoprotein), leads to decreased intracellular accumulation and resistance to a variety of anticancer drugs. Recently, one mutant p 53 form was shown to stimulate the MDR 1 gene promoter in vitro, whereas wild-type p 53 repressed this activity. We examined the relationship between p 53 gene mutation and MDR 1 gene expression in specimens from non-small cell lung cancer patients. Tumor samples were obtained from 21 patients during surgery. Mutations of exon 5 through exon 8 of the p 53 gene were detected by the polymerase chain reaction single strand conformation polymorphism method. MDR 1 expression was semi-quantified by the reverse transcriptase polymerase chain reaction method. We identified p 53 gene mutation in samples from 7 patients. MDR 1 gene expression was observed in samples from 20 patients. The expressivity of the MDR 1 gene tended to be higher in patients with adenocarcinoma. No significant relationship between p 53 mutation and MDR 1 expressivity was observed in our study.

Adenocarcinoma↗
PubMed1999

Blood grouping of mixed bloodstains using immunocytochemical methods.

Immunocytochemical methods to determine the ABO blood group of each blood of mixed bloodstains have been developed. Mixed bloodstains were made on surgical blades and a cedar board. The blades were dipped into blood and then dipped into blood of a different group at intervals of 30, 20, 15, 10 and 5 s. Two drops of blood were dropped on a cedar board and then two drops of blood of a different group were dropped there at the same intervals. The bloodstains were dried for a week. The blood samples were removed from the blades or the cedar board and processed according with a routine histological method. Three serial thin sections were obtained. After deparaffinization, the sections were treated in papain solution for 2 h at 36 degrees C, to unmask antigenic sites on red cell membranes. The labeled streptavidin-biotin (LSAB) and peroxidase-anti-peroxidase (PAP) methods were used to detect A and B antigens, and an indirect immunocytochemical method for H antigen. These immunocytochemical methods showed specific immunologic reactions and allowed determination of the blood group of each blood of mixed bloodstains. Further, these methods indicated a possibility to determine who was stabbed first, in cases where two or more victims were stabbed with a single knife.

ABO Blood-Group System↗
PubMed1998

Atypical adrenoceptor-mediated relaxation of canine pulmonary artery through a cAMP-dependent pathway.

We studied the existence of beta 3-adrenoceptors in canine pulmonary artery smooth muscle under isometric conditions in vitro. A rank order potency of vascular relaxation was isoproterenol > salbutamol > selective beta 3-adrenoceptor agonists, CL 316243 and BRL 37344. A marked desensitization to salbutamol occurred by pretreatment with salbutamol but not with CL 316243. When beta 1-adrenoceptors were blocked, the relaxant responses to salbutamol were competitively antagonized by the beta 2-adrenoceptor antagonist ICI 118551, whereas the response to CL 316243 was not. Cyanopindolol, a non-selective beta-adrenoceptor antagonist, antagonized CL 316243-induced relaxation in a competitive manner with a pA2 of 6.10, and this value was lower than that when salbutamol was used as an agonist (6.69). Intracellular cAMP levels were increased by CL 316243, an effect that was not altered by ICI 118551. Therefore, beta 3-adrenoceptors may be present and functioning in canine pulmonary artery.

Adrenergic beta-Agonists↗
PubMed1998

A human bronchial epithelial cell line releases arginine vasopressin: involvement of Ca2+ -activated K+ channels.

To determine whether airway epithelium releases arginine vasopressin (AVP) and, if so, what the mechanism of the release is, we studied cultured human bronchial epithelial cell line, 16-HBE cells, in vitro. The cells spontaneously released small but significant amounts of AVP, and this release was dose dependently increased by platelet-activating factor (PAF) or bradykinin (BK). The PAF- and BK-induced AVP release was inhibited by 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate, a phospholipase C inhibitor, and thapsigargin but not by Ca2+ -free solution. Pretreatment with the big conductance Ca2+-activated K+ channel blocker iberiotoxin attenuated the stimulated release of AVP, whereas apamin and glibenclamide were without effect. These results suggest that human bronchial epithelial cells release AVP and that the release may be stimulated by phospholipase C activation, mobilization of Ca2+ from internal stores and the concomitant activation of big conductance Ca2+-activated K+ channels.

Arginine Vasopressin↗
PubMed1998

Airway hyperresponsiveness to histamine in mycoplasmal infection: role of histamine N-methyltransferase.

To elucidate the modulatory role of histamine-degrading enzymes in airway constrictor responses in mycoplasmal infection, we studied hamster tracheal segments under isometric conditions in vitro. Nasal inoculation with Mycoplasma pneumoniae potentiated the contractile responses to histamine but not to methacholine. Pretreatment of tissues with the histamine N-methyltransferase inhibitor SKF 91488 abolished the infection-induced potentiation, whereas, the diamine oxidase inhibitor aminoguanidine had no effect. The histamine N-methyltransferase but not diamine oxidase activity in tracheal tissues was decreased in infected animals. These results suggest that M. pneumoniae causes airway hyperresponsiveness to histamine probably through a reduction of endogenous histamine N-methyltransferase activity.

Amine Oxidase (Copper-Containing)↗
PubMed1998

Selective removal of cholesterol esters in an arteriosclerotic region of blood vessels with a free-electron laser.

BACKGROUND AND OBJECTIVE: In advanced atheromatous atherosclerosis, a large amount of lipids, particularly cholesterol esters, accumulates on the arterial wall. The selective removal of cholesterol esters accumulated in the intracellular or extracellular spaces has clinical significance. In the present work, the authors investigated the removal of cholesterol esters by using a free-electron laser (FEL) in an arteriosclerotic region. STUDY DESIGN/MATERIALS AND METHODS: Thin films of cholesteryl oleate and albumin and the cross section of a rabbit artery were placed on an inverted microscope stage, and the changes caused by the FEL irradiation of 5.75 microm and 6.1 microm, with 1.5-3 mW on average, were monitored continuously by using a CCD camera in real time. RESULTS AND CONCLUSION: FEL irradiation at a wavelength of 5.75 microm, which is a stretching vibrational mode of the ester, was able to ablate cholesterol esters without affecting albumin. It can also remove cholesterol esters from rabbit arteriosclerotic arterial walls.

Albumins↗
PubMed1998

No mutations in cystatin C gene in cerebral amyloid angiopathy with cystatin C deposition.

To investigate the relationship between cerebral amyloid angiopathy (CAA) and cystatin C, we studied five CAA patients on whose cerebral blood vessels colocalization of cystatin C and beta-protein was recognized immunohistochemically. One patient was suspected as familial CAA and the other patients were sporadic cases. Two patients had low concentration of cystatin C in their cerebrospinal fluid (CSF) as we have previously reported in CAA patients. Enzyme-linked immunosorbent assay (ELISA) revealed that cystatin C and beta-protein have been included at the ratio of about 1:100 in the crude amyloid fibrils of one patient. Using a monoclonal antibody (MAb) against cystatin C, we performed affinity chromatography and immunoblotting on her amyloid fibril fraction. Eluate showed a band with a mol wt of 14,000 and the N-terminal 14 amino acid residues of 14-kDa protein were identical with that of cystatin C. This molecular weight is not identical to that of the truncated form of cystatin C deposited in hereditary cerebral hemorrhage with amyloidosis in Iceland (HCHWA-I), but that of normal cystatin C. DNA sequence analysis of five patients showed no point mutations in the cystatin C gene. Cystatin C and beta-protein colocalization, which was recognized in amyloid lesions of CAA, suggests that cystatin C deposition may be related to beta-protein deposition. We hypothesize that cystatin C deposition in sporadic cerebral amyloid angiopathy with cystatin C deposition (SCCAA) involves a different mechanism from that in HCHWA-I, which may be related to low CSF concentration of cystatin C without amino acid substitutions.

Aged↗
PubMed1998

Fluorescence based co-amplification and automated detection of the STR loci HUMFIBRA and HUMD21S11 in a Hungarian Caucasian population sample.

Population data were generated for the STR systems HUMFIBRA and HUMD21S11 for a Hungarian Caucasian population sample residing in Baranya County, Hungary (127 unrelated individuals). The loci were coamplified using a fluorescence based PCR method and were typed automatically. For both loci 12 different alleles could be found including some variants. No deviations from Hardy-Weinberg expectations were observed. Both loci proved to be highly discriminating and valuable polymorphisms for forensic analyses.

Alleles↗
PubMed1998

Urodynamic changes after endoscopic correction of vesicoureteral reflux.

Massive bilateral vesicoureteral reflux (VUR) in a 7-year-old girl with spinal scoliosis was successfully treated by endoscopic correction. She was admitted due to a febrile urinary tract infection and urinary incontinence. A cystometrogram demonstrated normal detrusor function during storage. The endoscopic subureteric injection of polytetrafluoroethylene (Teflon) was performed, resulting in the disappearance of the VUR. A postoperative cystometrogram demonstrated overactive detrusor function during storage, necessitating anticholinergic medication. She has been free of febrile urinary tract infections and incontinence for 2 years postoperatively, although self-catheterization is necessary. In a case of neurogenic vesical dysfunction with massive reflux, endoscopic subureteric injection is not only a therapeutic tool, but also a useful diagnostic option for detecting occult detrusor overactivity during storage prior to open surgery.

Child↗
PubMed1998

Granulocyte colony-stimulating factor induces neutrophil sequestration in rabbit lungs.

The effects of intravenous injection of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on circulating neutrophil numbers, pulmonary vascular permeability, and morphologic changes in the lung were examined in rabbits. Intravenous injection of rhG-CSF caused a rapid, profound neutropenia due to neutrophil sequestration primarily within capillaries but also in larger microvessels of the lungs. Examination of neutrophil deformability using microfilters revealed that granulocyte colony-stimulating factor (G-CSF) treatment caused a rapid stiffening of neutrophils through the polymerization of F-actin but not microtubule assembly. The expression of CD11b, CD11c, and CD18 on human neutrophils after G-CSF treatment increased, but CD11a did not. Intravenous injection of rhG-CSF did not induce neutrophil emigration or albumin leakage into alveolar space, wet/dry lung weight ratios were unchanged, and no pathologic changes in lung histology were observed. These studies indicate that injection of rhG-CSF caused a rapid neutropenia and neutrophil sequestration in the lungs that is likely to be mediated through a G-CSF-induced decrease in neutrophil deformability, although neutrophil-endothelial cell adhesion may also play a role. However, this G-CSF-induced neutrophil sequestration did not induce a massive lung injury.

Animals↗
PubMed1998

Vasopressin stimulates ciliary motility of rabbit tracheal epithelium: role of V1b receptor-mediated Ca2+ mobilization.

Arginine vasopressin (AVP) has recently been shown to exist in and to be released from airway epithelial cells, but the physiologic role of this hormone in airway epithelial function is unknown. To determine whether AVP affects ciliary motility, and if so, to elucidate the mechanism of action and the subtype of AVP receptors involved, we measured ciliary beat frequency (CBF) and the intracellular Ca2+ concentration ([Ca2+]i) of cultured rabbit tracheal epithelium with a photoelectric method and the fura-2 fluorescence method, respectively. Addition of AVP caused a rapid increase in CBF, followed by a decline and a subsequent sustained response. The ciliary stimulatory action was dose dependent, the maximal peak increase from the baseline CBF being 20.6 +/- 4.7% (mean +/- SE, P < 0.001), and this effect was reduced to 5.9 +/- 2. 0% by the V1 receptor antagonist OPC-21268 (P < 0.01), but not by the V2 receptor antagonist OPC-31260. The AVP-induced increase in CBF was not altered by the protein kinase A (PKA) inhibitor Rp-adenosine-3',5'-cyclic monophosphorothioate triethylamine (Rp-cAMPS) or by Ca2+-free solution containing ethylene glycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA), but was abolished by pretreatment with thapsigargin. Exposure of cells to AVP elicited a transient increase in [Ca2+]i, an effect that was likewise abolished by thapsigargin. The rank-order potency of AVP analogues to increase [Ca2+]i was AVP = [deamino1, D-3-(pyridyl) Ala2-Arg8] vasopressin (DP-VP), a specific V1b receptor agonist > [Phe2, Ile3, Orn8] vasopressin (PO-VT), a V1a agonist > 1-desamino-8-D-arginine vasopressin (dDAVP), a V2 agonist. Moreover, OPC-21268 greatly attenuated the action of AVP, whereas OPC-31260 was without effect. These results suggest that AVP stimulates ciliary motility of rabbit tracheal epithelium through mobilization of Ca2+ from thapsigargin-sensitive stores, and that this effect may be mediated by V1b receptors.

Animals↗