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Biomedical subjects

A Nagai

Publications and source records attributed to A Nagai.

At least 145 records · Page 8Linked to original sources
PubMed1996

Leukoencephalopathy-related cerebral amyloid angiopathy with cystatin C deposition.

BACKGROUND: We have described sporadic cases of cerebral amyloid angiopathy with cerebral hemorrhage showing a low cystatin C level in the cerebrospinal fluid detected by enzyme-linked immunosorbent assay. Recently, several cases of leukoencephalopathy in patients with cerebral amyloid angiopathy have been reported. We describe a sporadic case of leukoencephalopathy with cystatin C-type cerebral amyloid angiopathy diagnosed during life by enzyme-linked immunosorbent assay. CASE DESCRIPTION: A 74-year-old man who had suffered from progressive dementia for 3 years was admitted with right hemiparesis, dysarthria, and ataxia. MRI revealed pontine infarction and multiple lacunar state with leukoaraiosis. We suspected cystatin C-type cerebral amyloid angiopathy because of the low level of cystatin C in the cerebrospinal fluid. The patient died of sepsis 3 months later, and the presence of leukoencephalopathy with cerebral amyloid angiopathy was confirmed by autopsy. Immunohistological examination disclosed cystatin C and beta-protein deposition in amyloid structures of the cortical cerebral arteries. CONCLUSIONS: Measurement of cystatin C in the cerebrospinal fluid by enzyme-linked immunosorbent assay is a useful method of diagnosing leukoencephalopathy related to sporadic cystatin C-type cerebral amyloid angiopathy.

Aged↗
PubMed1996

Alveolar destruction in guinea pigs chronically exposed to diesel engine exhaust. A light- and electron-microscopic morphometry study.

Guinea pigs were exposed 16 h a day, 6 d a week, for 6, 12, 18, or 24 mo to filtered air or diesel-exhaust at low (NO2 = 0.22 +/- 0.03 ppm; SO2 = 0.60 +/- 0.19 ppm; particles = 0.21 +/- 0.07 mg/m3), medium (NO2 = 1.07 +/- 0.09; SO2 = 2.83 +/- 0.73; particles = 1.14 +/- 0.26) or high (NO2 = 2.88 +/- 0.29; SO2 = 6.49 +/- 1.75; particles = 2.94 +/- 0.69) concentrations, or at a medium concentration without particles (NO2 = 1.01 +/- 0.09; SO2 = 2.66 +/- 0.64; particles = 0.01 +/- 0.01). We quantitated the holes in the alveolar wall and alveolar size by using scanning electron microscopy (SEM). After 12 mo of exposure, the ratio of the area of alveolar holes to that of the alveolar wall, and the number of holes per alveolus, rose as the concentration and duration of exposure increased. There were no differences in alveolar size between the study groups. Animals exposed to the medium concentration of diesel exhaust without particles showed less of an increase in the development of holes than animals exposed to the same concentration of diesel exhaust with particles. These findings suggest that diesel exhaust causes alveolar destruction (alveolar holes) without an enlargement in alveolar size in a concentration- and duration-dependent manner. Particulate matter in diesel exhaust may play some role in the development of these lesions.

Animals↗
PubMed1996

New evidence for the involvement of oxygen radicals in triggering neonatal chronic lung disease.

We measured the plasma concentration of allantoin, an oxidation product of uric acid and an "in vivo" marker of free radical generation, within 24-48 h after birth in 10 premature infants who subsequently developed chronic lung disease (CLD) and 9 infants without CLD (non-CLD). The plasma allantoin level (mean +/- SD, 25.9 +/- 9.8 microM for CLD versus 11.0 +/- 5.7 microM for non-CLD, p < 0.01) and the allantoin/urate ratio (5.8 +/- 2.0% for CLD infants versus 2.4 +/- 0.9% for non-CLD infants, p < 0.01) were significantly higher in the CLD group than those in the non-CLD group. These observations suggest the possible involvement of oxygen radicals in triggering CLD. In addition, the plasma allantoin concentration and the allantoin/urate ratio may be useful early predictors of the development of CLD.

Allantoin↗
PubMed1996

Angiotensin II induces ovulation and oocyte maturation in rabbit ovaries via the AT2 receptor subtype.

The present study was undertaken to investigate the role of angiotensin II (Ang II) in ovulation and ovarian steroidogenesis and prostaglandin (PG) production via the Ang II receptors in rabbit ovaries. In in vitro perfused rabbit ovaries, PD123319, a selective nonpeptide antagonist for AT2 receptors, reduced the Ang II-induced ovulation in a dose-dependent manner, whereas CV-11974, a selective nonpeptide antagonist for AT1 receptor, did not affect the Ang II-induced ovulation. Ang II also significantly stimulated the meiotic maturation of ovulated ova and follicular oocytes in the absence of gonadotropin. The addition of PD123319 at 10 (-6) M to the perfusate significantly inhibited the Ang II-induced oocyte maturation. Ang II did not stimulate the production of progesterone by perfused rabbit ovaries but significantly stimulated the production of estradiol (E2) and PGs. When PD123319 at 10(-6) M was added to the perfusate 30 min before the onset of Ang II administration, the Ang II-stimulated production of E2 and PGs was significantly blocked. Saralasin, a peptide analog of Ang II, inhibited the specific binding of [125I] iodo-[Sar1, Ile8] Ang II to rabbit ovarian membranes in a concentration-dependent manner, yielding an inhibitory constant (IC50) value of 1.58 x 10(-9) M. PD123319 and CV-11974 also inhibited the binding of [125I]iodo-[Sar1, Ile8] Ang II; however, PD123319 and CV-11974 were 15 and 40 times less potent than saralasin, respectively. Autoradiographic study revealed that an intense localization of Ang II receptors in the rabbit ovaries was present in the granulosa cell layers and the stroma of the preovulatory follicles. AT2 receptors were predominantly located in granulosa cells, whereas AT1 receptors were more concentrated in the stroma and thecal cell layers. In summary, Ang II induced ovulation and oocyte maturation and stimulated the production of E2 and PG by perfused rabbit ovary in vitro via the AT2 receptor. Thus, locally produced Ang II may be part of a novel intraovarian paracrine or autocrine control mechanism during the ovulatory process.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1996

Immunological, genetic, and microbiological study of family members manifesting early-onset periodontitis.

From the standpoint of host-parasite interactions, family studies help us understand the host defensive factors and the molecular mechanisms involved in the periodontal immune response. In this study, we report the immunological profile of host-defensive functions, human leukocyte antigen (HLA) phenotypes, and the microflora of a mother (rapidly progressive periodontitis), an older son (periodontally healthy), a younger son (localized juvenile periodontitis), and a daughter (localized juvenile periodontitis). We examined the peripheral neutrophil functions, phenotypic and functional analysis of peripheral lymphocytes, serum immunoglobulin G (IgG) antibody titers against periodontopathic bacteria, serological type of HLA class II antigens, and bacterial flora in all periodontal pockets. The results showed that Actinobacillus actinomycetemcomitans was dominant in the pockets of all subjects. The mother and two sons showed a depressed neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine. All subjects except the older son exhibited low T4/T8 ratios. The mother and daughter had raised levels of IgG titers to Porphyromonas gingivalis. All subjects had HLA phenotypes of DRw52 and DQ1 in common. We found that the family members had similar disorders in certain defensive functions. This family has been a model for our understanding of the host defensive factors in the development of early-onset periodontitis.

Adolescent↗
PubMed1996

Host defensive functions in a family manifesting early-onset periodontitis.

Family case studies help us identify host risk factors in periodontal disease. In this study we examine a family consisting of a mother (40 years old, with rapidly progressive periodontitis), her elder daughter (14 years old, with localized juvenile periodontitis), and younger daughter (13 years old, with simple gingivitis). We examined 1) the peripheral neutrophil functions (chemotactic migration, phagocytosis, superoxide production); 2) lymphocyte functions (proliferative activity and cytokine productivity of T cells, immunoglobulin [Ig] M productivity of B cells when stimulated with pokeweed mitogen); 3) phenotypic analyses of peripheral lymphocyte subpopulations; 4) serum IgG antibody titers against periodontopathic bacteria; and 5) serological type of HLA class II. All the subjects exhibited high T4/T8 ratios due to high percentage of CD4-positive cells, showed high IgG titers to Actinobacillus actinomycetemcomitans, and had a HLA DQw1 in common. The mother showed a slight deficiency of neutrophil chemotactic migration to N-formyl methyonyl leucyl phenylalanin (fMLP), raised interleukin-2 productivity of T cell, and high levels of IgG titers to Porphyromonus gingivalis and Fusobacterium nucleatum. Both daughters showed weak T cell proliferative response to anti-CD3 monoclonal antibody and low IgM productivity. Low lymphocyte responsiveness may be involved in the pathogenesis of periodontal disease of these daughters; therefore, the lymphocyte dysfunctions shown should be considered in relation to the progression of periodontal disease.

Adolescent↗
PubMed1996

HLA Class II genotypes associated with early-onset periodontitis: DQB1 molecule primarily confers susceptibility to the disease.

DNA typing was performed on 24 Japanese patients with early-onset periodontitis (EOP) using the PCR-RFLP method to investigate an association of the susceptibility to EOP with the particular HLA class II alleles (HLA-DRB1, -DQA1, and -DQB1). DRB1*1401, DRB1*1501, DQB1*0503, and DQB1*0602 were found more frequently ("susceptible") in the EOP patients than in healthy controls. In contrast, DRB1*0405 and DQB1*0401 were found less frequently ("resistant") in EOP patients. All patients carrying DQB1*0602 had an atypical BamHI site in the intron upstream of the third exon of the DQB1 gene, which in our previous studies appeared to be a susceptible marker for EOP. A comparative analysis of the amino acid sequences of these susceptible and resistant HLA-DRB1 and DQB1 alleles elucidated some differences in antigen-derived peptide binding sites related to the susceptible or resistant alleles. Especially, DQB1*0503 and DQB1*0602 alleles carrying aspartic acid at position 57 and glycine at position 70 are increased significantly in EOP. Since amino acid residues at positions 57 and 70 on the DQB1 molecule are supposed to be involved in antigen binding, amino acid substitutions at these positions may affect the immune responsiveness to the periodontopathic antigen. Our results suggest that the DQB1 molecule plays a crucial role in the pathogenesis of EOP and that the susceptibility to EOP may be determined by the binding ability between the peptide and HLA-DQ antigens.

Adult↗
PubMed1996

[Study on the sclerosing agent for the treatment of simple renal cysts].

BACKGROUND: The objective of this study is to evaluate the sclerosing agents for simple renal cysts. METHODS: Thirty-three renal cysts of 30 patients were treated by injection of sclerosing agents with the guidance of ultrasonography. Among them, 22 were treated with ethanol, and 11 with minocycline-hydrochloride (MINO). RESULTS: Clinical efficacy rates and volume reduction rates in each treatment group of ethanol or MINO, were 100% and 90.9%, and 91.2 +/- 13.1% (mean +/- SD) and 83.2 +/- 28.5%, respectively. Although several complications including pain and intoxication were observed in ethanol (47.4%), no complications were observed in MINO. CONCLUSION: The instillation of MINO into renal cysts is an effective, safe and simple treatment. It is thought that it can be the first choice of treatment for simple renal cysts.

Adult↗
PubMed1996

[Pleural fibroma with a cavity-like air space].

A 45-year-old man was admitted to the hospital because of an increase in the size of an abnormal shadow on chest X-ray films over the preceding 5 years. A chest X-ray film on admission revealed a round air space in a mass-like shadow in the right upper lung field. Results of physical examination, sputum cytologic examination, and Ziehl-Neelsen staining were negative. Histopathological examination of a percutaneous lung biopsy specimen revealed a benign fibrous tumor of the pleura. Thoracotomy revealed a pedunculated tumor arising from the visceral pleura at the apical segment of the right upper lobe. A wedge resection was done. Histological examination revealed that the tumor consisted of regularly-shaped spindle cells with densely collagenous tissue. Normal lung tissue was found to be invaginated into the tumor tissue. These findings are consistent with the radiologic findings.

Fibroma↗
PubMed1996

Isoelectric focusing differences in the mobility of blood and semen PGM1 bands--the role of hemoglobin as a cause.

When using isoelectric focusing for the analysis of phosphoglucomutase isoenzymes, differences between the mobility of the first locus phosphoglucomutase (PGM1) bands have been noted in blood and semen samples from the same individual. This study was thus initiated to determine whether hemoglobin is responsible for these differences. Results revealed that the mobility of the PGM1 bands in diluted hemolysate and hemoglobin-removed hemolysate was similar to that seen in non-treated seminal plasma. Further, the mobility of PGM1 bands in hemoglobin-added seminal plasma was also similar to that seen in non-treated hemolysate. Additionally, on isoelectric focusing of the pI-markers, as well as non-treated hemolysate, hemoglobin-removed hemolysate, hemoglobin-added seminal plasma, and non-treated seminal plasma, distortions of iso-pH lines, i.e., "crank" formations were seen in the lanes of the non-treated hemolysate and hemoglobin-added seminal plasma. The above findings appear to indicate that differences in the mobility of PGM1 bands in the blood and semen result from the presence of high concentrations of hemoglobin in the analyzed samples.

Hemoglobins↗
PubMed1996

[Six patients with pneumonitis related to blended Chinese traditional medicines].

We encountered six patients with pneumonitis related to blended chinese traditional medicine (Kampo). The duration of treatment with kampo ranged from 14 to 110 days (mean: 38 days). The most common complaints were dyspnea, fever, and dry coughing. Fine crackles were heard at the bases of both lungs. Abnormal laboratory findings included high values of C-reactive protein and glutamic-oxaloacetic transaminase in all patients, lactate dehydrogenase in 5 patients, and eosinophil count in 1 patient. Chest X-ray films and CT films revealed diffuse reticulo-nodular interstitial shadows with consolidation in both lung fields in 3 patients and pleural effusion in 1 patient. Bronchoalveolar lavage was done in 4 patients; examination of the lavage fluid showed lymphocyte alveolitis, either pure or associated with neutrophilia and eosinophilia in 3 patients. Inverted CD4/CD8 lymphocyte ratios were found in 3 patients. Transbronchial lung biopsy was done in 4 patients and specimens from 3 of those 4 showed organizing pneumonitis with thickening of alveolar septa. Lymphocyte stimulation tests were positive in 4 patients. Discontinuation of the drug (2 patients) or administration of corticosteroids (4 patients) was followed by rapid improvement. Patients being treated with kampo preparations should be observed for signs and symptoms of drug-induced pneumonitis.

Aged↗
PubMed1996

[Progressive stroke during the acute state of cerebral infarction in the territory of the internal carotid artery].

Diagnosis of deterioration of neurological deficits in the early stage after hospital admission immediately after the onset of cerebral infarction is important in establishing a treatment plan. This study investigated the clinical characteristics of progressive stroke on admission. The subjects were 309 patients admitted on the day of the onset of symptoms and showed a low density area on CT images within 5 days. There were 202 with cerebral infarction in the territory of the deep perforate arteries, 77 with cerebral infarction in the territory of the cortical branch of the middle cerebral artery (MCA), and the remaining 36 had cerebral infarction in the territory of MCA. The results were as follows: 1) Progressive stroke was observed in 71 patients (23.0%): 60 with completed stroke and 11 with reversible ischemic neurological deficits (RIND). 2) The patients with progressive stroke were clearly older than those with non progressive stroke (p < 0.05: Cochran Cox's test). 3) Progressive stroke was seen more frequently in patients with cerebral infarction of the cortical branch of the MCA and patients with occlusion of the internal carotid artery and MCA trunk than patients with cerebral infarction of the deep perforate arteries (p < 0.001: chi 2 test). 4) All patients with progressive stroke had initial evidence of deterioration of neurological deficits within 5 days after the onset, with 39 patients showing deterioration on day 2 and 13 patients showing deterioration on day 3. 5) Deterioration of neurological deficits usually stopped the day after the start of progression. The maximum period from the beginning to the end of the deterioration of neurological deficits was 7 days. 6) Progressive stroke was not seen in 11 patients who were admitted with higher cortical dysfunction and without sensory or motor disturbances, and was seen in only 8 (4%) of the 187 patients with sensory or motor disturbances without higher cortical dysfunction. 7) Progressive stroke was seen in 63 (57%) patients with sensory or motor disturbances and higher cortical dysfunction. 8) Progressive stroke was seen frequently in patients with atrial fibrillation (Af) on the ECG [P < 0.001). 9) Fifty-six of 71 patients with progressive stroke showed persistent severe motor impairment in the upper limbs. Therefore, to diagnose progressive stroke, it is useful to assess the higher cortical dysfunction and examine for Af on admission.

Aged↗
PubMed1995

Enhancement of damage-specific DNA binding of XPA by interaction with the ERCC1 DNA repair protein.

The human XPA and ERCC1 proteins, which are involved in early steps of nucleotide excision repair of DNA, specifically interacted in an in vitro binding assay and a yeast two-hybrid assay. A stretch of consecutive glutamic acid residues in XPA was needed for binding to ERCC1. Binding of XPA to damaged DNA was markedly increased by the interaction of the XPA and ERCC1 proteins. ERCC1 did not enhance binding to DNA when a truncated XPA protein, MF122, was used in place of the XPA protein. MF122 retains damaged DNA binding activity but lacks the region for protein-protein interaction including the E-cluster region. These results suggest that the XPA/ERCC1 interaction may participate in damage-recognition as well as in incision at the 5' site of damage during nucleotide excision repair.

Binding Sites↗
PubMed1995

DNA repair protein XPA binds replication protein A (RPA).

XPA is a zinc finger DNA-binding protein, which is missing or altered in group A xeroderma pigmentosum cells and known to be involved in the damage-recognition step of the nucleotide excision repair (NER) processes. Using the yeast two-hybrid system to search for proteins that interact with XPA, we obtained the 34-kDa subunit of replication protein A (RPA, also known as HSSB and RFA). RPA is a stable complex of three polypeptides of 70, 34, 11 kDa and has been shown to be essential in the early steps of NER as well as in replication and recombination. We also demonstrate here that the RPA complex associates with XPA. These results suggest that RPA may cooperate with XPA in the early steps of the NER processes.

Base Sequence↗
PubMed1995

A microbiological and immunological study of endodontic-periodontic lesions.

The microflora and humoral immune response in tissue from the periodontal pockets and root canals of five teeth with endodontic-periodontic lesions were examined. We found more microbes in the periodontal pockets than in the root canals. The flora in the periodontal pockets was dominated by rods and motile organisms, whereas that in the root canals was largely rods and cocci. We detected no spirochetes in the root canals. The cultivable microflora in the periodontal pockets comprised a high number of different species of bacteria, whereas those in the root canals included only a small number of species. There was no correlation between microbial isolates and antibody titer in the apical tissues or periodontal pockets. We conclude from these studies that the microflora of infected root canals is simple and limited, and that the local humoral immune response does not seem to affect the pathogenesis of disease directly.

Antibodies, Bacterial↗
PubMed1995

Clinical, microbiological and host defense parameters associated with a case of localized prepubertal periodontitis.

A 4-year-old Japanese boy was referred to Osaka University Dental Hospital because of severe mobility and pain of the right lower primary canine. The canine had severe bone loss and a pocket depth exceeding 5-6 mm. The left lower canine showed slight mobility and moderate alveolar bone loss. The other primary teeth showed no pathogenic findings. The subgingival microflora from the right lower canine was dominated by gram-negative rods, especially capnocytophaga and fusobacterium, while actinomyces sp. were the most common gram-positive bacteria. While neutrophil functions of the patient were within the normal ranges of healthy subjects, some lymphocyte functions such as IL-2 production and IgG and IgM syntheses were lower in the patient. 7 months after the extraction of the right lower primary canine, the patient complained of pain around the right lower primary lateral incisor. In 3-4 weeks, the alveolar bone was lost rapidly and mobility of the lower anterior teeth increased significantly. The primary lateral incisor was extracted and the other primary teeth were treated by sealing and systemic and local administration of antibiotics. After treatment, the lower anterior teeth became less mobile and the gram-positive cocci predominated.

Actinomyces↗
PubMed1995

Erythromycin shortens neutrophil survival by accelerating apoptosis.

Erythromycin is reported to have an anti-inflammatory action, which may account for its clinical effectiveness in the treatment of chronic inflammatory diseases such as diffuse panbronchiolitis. To evaluate the anti-inflammatory action of erythromycin, we examined the survival of isolated neutrophils with and without erythromycin. Erythromycin shortened neutrophil survival in a dose-dependent fashion, with a maximum effect at 10 micrograms/ml [corrected] and above. Survival at 24 h was 63.4% in medium with 10 micrograms of erythromycin per ml compared with 82.7% in control medium (P < 0.01). This shortening of survival was brought about by acceleration of apoptosis, as evidenced by transmission electron microscopy. In a manner similar to that of erythromycin, other macrolide antibiotics, i.e., clarithromycin, roxithromycin, and midecamycin, also shortened neutrophil survival, but neither the beta-lactams ampicillin and cefazolin nor the aminoglycoside gentamicin affected their survival. Erythromycin increased intracellular levels of cyclic AMP (cAMP) to 150% of control levels in neutrophils. Forskolin, rolipram, and dibutyryl-cAMP, which are known to increase intracellular cAMP levels, also shortened neutrophil survival. H-89, an inhibitor of cAMP-dependent protein kinase A, partially blocked the survival-shortening effect of erythromycin. Our findings suggest that erythromycin shortens neutrophil survival at least in part through elevation of intracellular cAMP levels.

Apoptosis↗