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M Koide

Publications and source records attributed to M Koide.

At least 109 records · Page 6Linked to original sources
PubMed1995

In vivo administration of IL-1 beta accelerates silk ligature-induced alveolar bone resorption in rats.

The effects of recombinant human interleukin-1 beta (rhIL-1 beta) on alveolar bone resorptive activity in rats were examined. Continuous administration of rhIL-1 beta or phosphate-buffered saline (PBS) was given via osmotic pumps for 3, 7 and 14 days to rats with silk ligatures around second maxillary molars. Other animals without ligatures received insertion of pumps containing rhIL-1 beta or remained untreated. Sections were subject to three different stains:--hematoxylin and eosin (H-E) for histology, acid phosphatase (ACPase) activity for osteoclast detection, and immunohistochemistry using anti-rat monocyte/macrophage monoclonal antibody (ED 1). In addition, body weight, plasma calcium and phosphorus levels were monitored. The mean body weight of rats receiving rhIL-1 beta was significantly lower (P < 0.05 to P < 0.01) compared with untreated rats throughout the experimental period. On Day 7, plasma calcium and phosphorus levels were significantly lower in rats receiving rhIL-1 beta than in rats receiving PBS only (P < 0.05). Sections revealed a moderate inflammatory cell infiltrate reaching near the alveolar crest in both groups with ligatures on Day 3. Only rats receiving rhIL-1 beta exhibited enhancement of inflammatory cell invasion on Days 7 and 14. In rats receiving rhIL-1 beta with ligatures, numerous resorption lacunae containing ACPase-positive multinucleated giant cells (MNGCs), coinciding with ED1-positive cells, were located on the mesial side of the septum where extensive bone resorption had occurred throughout the experimental period. In animals receiving rhIL-1 beta without ligatures, compared with untreated rats, increased ACPase-positive cells were observed on the mesial side of the septum on Day 3. In animals receiving PBS only, a few ACPase-positive cells were observed confined to the mesial regions where slight bone resorption occurred on Days 7 and 14. These results indicate that the administration of rhIL-1 beta accelerated alveolar bone destruction in ligature-induced periodontal tissue inflammation over a two-week period.

Acid Phosphatase↗
PubMed1995

Detection of Mycobacterium tuberculosis in clinical specimens by polymerase chain reaction method.

An insertion sequence repeated multiple times in the chromosome of Mycobacterium tuberculosis was used as a target for amplification using the polymerase chain reaction (PCR) assay for detecting Mycobacterium tuberculosis in clinical specimens. The sequences of primers were 5'-CCTGCGAGCGTAGGCGTCGG-3' (primer 1) and 5'-CTCGTCCAGCGCCGCTTCGG-3' (primer 2). One cycle of amplification consisted of denaturing at 94 degrees C for 2 min, primer annealing at 68 degrees C for 2 min, and extension at 72 degrees C for 2 min. DNA (5 fg) extracted from M. tuberculosis was detected by gel electrophoresis and Southern blot hybridization after 40 cycles of amplification. The amplification products were not obtained by DNA extracted from M. kansasii, M. intracellulare, M. avium, M. fortuitum, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Legionella pneumophila and Staphylococcus aureus; only from the M. tuberculosis complex. PCR results were compared with conventional cultural, pathological and microscopic findings in the detection of M. tuberculosis in 112 clinical specimens. There were 25 specimens that were positive for M. tuberculosis by cultural or pathological examination, of which 20 (80%) were positive by PCR. PCR detected the organism in 5 (83%) of 6 smear-positive specimens and 15 (79%) of 19 smear-negative specimens in which culture or pathology revealed M. tuberculosis. In addition, 2 smear-negative specimens and 8 smear-negative and culture-negative specimens were positive by PCR. These 10 samples were collected from the patients suspected as having tuberculosis by the clinical diagnosis based on the clinical history, characteristic radiographs, a positive PPD skin test and the effectiveness of anti-tuberculous drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1995

[An outbreak of Pontiac fever due to Legionella pneumophila serogroup 7. I. Clinical aspects].

In August 1994, an epidemic of acute febrile illness occurred at the Education Center Building of a company in Shibuya-ku, Tokyo. All 43 trainees attended in two groups and 2 staff members of the Center fell ill. The 45 patients came to one of our hospitals in two groups, and 35 patients were treated. The patients were 4 males and 31 females, and the average age was 29.0 years. The duration until falling ill was 36 to 90 hours after entering the Center. Symptoms were fever, lumbago arthralgia, headache, dyspnea, general fatigue, etc. Physical examination revealed slightly injected mucosa of the pharynx in a patient who complained of a sore throat. On laboratory examination, leukocytosis with a left shift of the nucleus and elevation of serum CRP levels were found. Erythromycin (600 mg, daily) and nonsteroidal antiinflammatory drugs (NSAIDs) were given by mouth to almost every patient. Two patients were hospitalized. The illness was self-limited, generally lasting from two to five days. Strains of legionellae isolated from the water of the cooling tower located at the top of the Center, were identified as L. pneumophila serogroup 7. Since seroconversion in a patient against the cooling tower strain from 1:16 to 1:256 was determined and the clinical courses agreed with the definition of Pontiac fever by Glick et al, we concluded that the epidemic was an outbreak of Pontiac fever due to L. pneumophila serogroup 7. Pontiac fever is considered to be one of the community-acquired diseases. Thus, we have to note that Pontiac fever may be misdiagnosed as we examine patients who complain of the symptoms noted above.

Adolescent↗
PubMed1995

[An outbreak of Pontiac fever due to Legionella pneumophila serogroup 7. II. Epidemiological aspects].

From August 20 to 22, 1994, an outbreak of acute febrile illness occurred in a Training Center building of a company in Shibuya-ku, Tokyo. All 43 trainees attended in two groups and 2 Center staffs were attacked. Illness was self- limiting, generally lasting three days. Though strains of legionellae, isolated from the water of the cooling tower located at the top of the building, were identified as Legionella pneumophila by microplate DNA-DNA hybridization, they failed to agglutinate with antisera against L. pneumophila serogroups 1 through 6. Two strains were sent to the Centers for Disease Control, Atlanta, Georgia, USA, and determined as serogroup 7 of the species. Since the clinical courses agreed with the definition of Pontiac fever by Glick et al. and seroconversion in a patient against the cooling tower strain (EY3698)from 1:16 to 1:256 was determined by indirect fluorescent antibody technique, the epidemic of acute febrile illness was concluded as an outbreak of Pontiac fever due to L. pneumophila serogroup 7. The cooling tower was a cylindrical open style, with volumetric flow rate of 130 liter/min, and was used for air- conditioning exclusively to the third floor of the building. The building equipped no air-inlet, and indoor-air of the training room exchanged at every break time through windows of 168 cm in height and 72 cm in width. The cooling tower was not operated for five days before the Group A trainees checked in the Center on 18 August followed by Group B trainees on 19 August. It was speculated that high atmospheric temperature and stagnation of cooling water during this period would lead L. pneumophila to overly multiply, which could be a source of infection by flowing in through opened windows to the training rooms.

Disease Outbreaks↗
PubMed1995

[Identification of Legionella pneumophila strains by polymerase chain reaction method which isolated from cooling tower water].

We studied the polymerase chain reaction (PCR) method with 5 strains of Legionella pneumophila serogroup 4, 7 strains of L. pneumophila serogroup 5, 7 strains of L. pneumophila UT and 15 strains of Legionella like organisms (LLO). We used mip-primers reported by Mahbubani et al and LEG-primers reported by Starnbach et al. Positive PCR results were obtained by all strains of L. pneumophila serogroup 4, L. pneamophila serogroup 5, L. pneumophila UT and 11 strains of LLO using mip-primers. Using LEG-primers, positive results were obtained by 2, 6, 5 and 8 strains respectively. All strains that showed positive results using LEG-primer PCR, were contained by the strains that showed positive results using mip-primer PCR. Conversely, there were some strains that were positive in mip-primer PCR and negative in LEG-primer simultaneously. Therefore, mip-primers is recommended to detect L. pneumophila in clinical specimens by PCR method.

Base Sequence↗
PubMed1995

Marked increase of activated factor VII in uremic patients.

We investigated plasma activated factor VII (FVIIa) levels in uremic patients (nondialysis group: n = 38; dialysis group: n = 36) and healthy controls (n = 32). We also measured the plasma levels of thrombomodulin (an indicator of endothelial cell injury) and tissue factor. Plasma FVIIa showed a marked increase in the nondialysis group (mean [95% confidence interval]: 4.6 [4.1-5.1] ng/ml, p < 0.0001) with the progressive impairment of renal function, as indicated by the serum creatinine level, when compared with the 32 controls (2.8 [2.5-3.1] ng/ml), and was further increased in the dialysis group (6.1 [5.5-6.8] ng/ml, p < 0.001 vs. nondialysis group). Plasma levels of thrombomodulin and tissue factor were also higher in the nondialysis group than the control group, and were further increased in the dialysis group. Plasma tissue factor levels did not show any correlation with FVIIa or thrombomodulin in both the nondialysis and dialysis groups. Thus, circulating tissue factor appears to be released by a different mechanism from thrombomodulin and may not contribute to the direct activation of factor VII in uremic patients. On the other hand, the plasma level of thrombomodulin was positively correlated with that of FVIIa in the nondialysis group, and this correlation was independent of renal function. Thus, enhanced conversion of factor VII zymogen to FVIIa, probably related to endothelial cell injury, may be a risk factor for cardiovascular events in uremic patients.

Aged↗
PubMed1995

High lipoprotein (a) levels in chronic hemodialysis patients are closely related to the acute phase reaction.

To study the mechanism underlying the high lipoprotein (a) [Lp(a)] level in uremic patients on chronic hemodialysis, we investigated the levels of Lp(a), acute phase reactants (C-reactive protein and sialic acid), and interleukin-6 (IL-6) in 54 dialysis patients. The mean [95% CI] Lp(a) level was increased in the hemodialysis patients compared with the 30 controls (30 [25-36] vs. 18 [14-23] mg/dl, p < 0.005). Among dialysis patients, 46% had an Lp(a) level > 30 mg/dl, which was significantly higher than the percentage in the control group (17%). The levels of C-reactive protein, sialic acid, and IL-6 were also increased in dialysis subjects compared with controls (200 [134-299] vs. 37 [24-58] micrograms/dl, p < 0.0001; 63 [59-66] vs. 54 [52-56] mg/dl, p < 0.002; and 9.2 [7.8-11] vs. 5.5 [5.0-6.1] pg/ml, p < 0.0005, respectively). The Lp(a) level was positively correlated with that of C-reactive protein (r = 0.415, p < 0.002), sialic acid (r = 0.426, p < 0.002), and IL-6 (r = 0.298, p < 0.05) in the hemodialysis patients, but not in the controls or non-dialysis uremic patients. The Lp(a) level in the dialysis patients was also positively correlated with activation markers of coagulation (thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex, p < 0.005). These results indicate that the Lp(a) level is closely related to the acute phase reaction and hypercoagulability in chronic hemodialysis patients.

Acute-Phase Reaction↗
PubMed1994

Soluble intercellular adhesion molecule-1 (sICAM-1) in atopic dermatitis.

The serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) were determined by enzyme-linked immunosorbent assay, in 88 patients with atopic dermatitis (AD), 29 patients with eczematous dermatitis (ED) and in 33 healthy controls. The sICAM-1 levels were significantly higher in both AD and ED patients than in normal individuals. The longitudinal study of patients with AD revealed a significant decrease in the levels of sICAM-1 (P < 0.05) with improvements in disease activity. In AD patients, the sICAM-1 level correlated significantly with the total numbers of leukocytes and lymphocytes (P < 0.01 and P < 0.05, respectively), whereas no such correlation was found in patients with ED. Our studies show that the levels of sICAM-1 may be a useful immunologic parameter for monitoring disease activity in some of the individuals with AD.

Dermatitis, Atopic↗
PubMed1994

Potentiating effect of insulin on exocrine secretory function in isolated rat pancreatic acini.

BACKGROUND/AIMS: Insulin is shown to exert various regulatory effects on the exocrine pancreatic function. We investigated the direct effect of insulin on exocrine pancreatic secretion. METHODS: The effects of insulin on amylase release, 125I-secretin binding and Na(+)- and K(+)-activated adenosine triphosphate phosphohydrolase (Na+,K(+)-ATPase) activity were measured using the isolated rat pancreatic acini. RESULTS: Insulin potentiated the amylase release elicited by secretin plus cholecystokinin (CCK), but not by either secretin or CCK alone. The potentiating effect of insulin was dependent on the concentration and preincubation time. Insulin had no effect on 125I-secretin binding. Ouabain, a specific Na+,K(+)-ATPase inhibitor, caused a concentration-dependent inhibition of the potentiated secretion by insulin without affecting the secretory response to secretin plus CCK. In membranes prepared from acini treated with insulin, Na+,K(+)-ATPase activity was significantly increased. Similar results were obtained when acini were treated with insulin in combination with secretin plus CCK. CONCLUSIONS: Insulin exerts a direct effect on pancreatic acinar cells and potentiates exocrine secretion elicited by secretin in combination with CCK, in part, by increasing Na+,K(+)-ATPase activity.

Amylases↗
PubMed1994

[Serodiagnosis of Legionella pneumonia--data of our laboratory in the recent 3 years].

We had examined antibody titers against Legionella spp. of patients' sera which were mainly sent from other hospitals, performed with the indirect fluorescent antibody (IFA) method. The clinical status of the cases diagnosed as Legionella pneumonia serologically, were also studied. Out of 105 cases with clinically suspected Legionella pneumonia, 15 cases (14.3%) were seropositive. In 9 out of the 15 cases (60.0%) were caused by Legionella pneumophila serogroup 1. Clinical outline of these 15 cases did not contradict those reported in the literature, and erythromycin was effective in many cases. Significant rises (more than four times) of the titer were observed 3 to 4 weeks after onset in most of cases. We would like to emphasize that this should be performed serodiagnosis of Legionella pneumonia.

Adult↗
PubMed1994

[Usefulness of polymerase chain reaction method in the early diagnosis of Pneumocystis carinii pneumonia].

We evaluated the sensitivity and specificity of polymerase chain reaction (PCR) method in the detection of Pneumocystis carinii, and compared its clinical usefulness with that of a previous method, toluidine blue-O (TBO) staining in diagnosis of P. carinii pneumonia (PCP) using clinical samples such as sputum and bronchoalveolar lavage fluid (BALF). Using P. carinii obtained from BALF of the infected rats, we showed that PCR showed 100 fold more sensitivity than TBO staining as indicated by the comparison of their detection limits (78 cysts/ml vs 7800 cysts/ml). In addition, the detection using PCR in this study was specific for P. carinii because all other pathogens examined were not positive. In the clinical study we analyzed 44 patients including 10 with definite PCP, 8 with portable PCP and 26 with other diagnosis. In the sputum, the sensitivity and specificity were 100% and 95%, respectively, in PCR, while 13% and 100% in TBO staining. These results revealed that PCR was much superior to TBO staining in sensitivity especially when the sputum was used as samples, and suggested that examination of the sputum by PCR was clinically very useful in early diagnosis of P. carinii pneumonia.

Adult↗
PubMed1994

Expression of nitric oxide synthase by cytokines in vascular smooth muscle cells.

In cultured vascular smooth muscle cells, the baseline mRNA and protein levels of an inducible type of nitric oxide synthase were barely detectable. Interferon gamma, tumor necrosis factor-alpha, and interleukin-1 beta each markedly increased mRNA and protein levels of this enzyme in parallel with the production of nitrite, a stable oxidative metabolite of nitric oxide. Actinomycin D abolished the cytokine-induced increases in mRNA levels and nitrite production. Cycloheximide, which abolished the cytokine-induced increase in nitrite production, had no effect on the interferon-gamma-induced increase in mRNA levels but partially inhibited that induced by interleukin-1 beta and markedly inhibited that induced by tumor necrosis factor-alpha. Transforming growth factor-beta 1, which inhibited the interferon gamma-, interleukin-1 beta-, and tumor necrosis factor-alpha-induced nitrite production, did not affect the increases in mRNA levels caused by these cytokines. Transforming growth factor-beta 1, however, significantly inhibited the increase in protein levels caused by these cytokines. These findings suggest that interferon gamma directly induces the expression of the inducible nitric oxide synthase gene, whereas tumor necrosis factor-alpha and interleukin-1 beta induce it, at least in part, via the induction of intermediary protein(s), and that transforming growth factor-beta 1 inhibits cytokine-induced nitric oxide production by blocking the posttranscriptional synthesis of inducible nitric oxide synthase.

Amino Acid Oxidoreductases↗
PubMed1994

[Left ventricular wall stress and contractile function immediately after arterial switch operation in neonates].

Dynamic changes in left ventricular function immediately after arterial switch operation in neonates are poorly understood. Accordingly we determined left ventricular end-systolic wall stress (ESWS) and rate corrected mean velocity of fiber shortening (mVcfc) by echocardiography immediately after arterial switch operation in the intensive care unit (ICU) in 11 neonates. Stress-velocity index (S-V Index: number of standard deviations from the population mean mVcfc for ESWS) was calculated from the ESWS-mVcfc relation as a load independent index of myocardial contractility. The dicrotic notch of radial arterial wave form was used to determine the end-systolic pressure (radial Pes). Left ventricular ejection time was obtained from the pulse Doppler wave form sampled from the ascending aorta. Mean ESWS after the operation was 37.8 +/- 17.3 g/cm2 (mean +/- SD) and mean S-V index was normal (0.80 +/- 3.11). S-V index was normalized within 12 hours after operation in 9 cases. In one case, which showed acute heart failure because of accidentally elevated afterload just after pump perfusion, S-V index had not recovered until 24 hours after operation. In another case, preoperative LV/RV pressure ratio was 0.63 and resulted in prolonged low level of S-V index. Preoperative conditions of left ventricle were compared with postoperative ESWS and S-V index. Preoperative end-diastolic posterior wall thickness of left ventricle (LVPWTd) was correlated with postoperative S-V index (r = 0.74, p = 0.015). Preoperative LVPWTd/LVDd (end-diastolic internal diameter of left ventricle) ratio was inversely correlated with postoperative ESWS (r = 0.66, p = 0.037) and correlated with S-V index (r = 0.80, p = 0.006). Preoperative LV/RV pressure ratio showed correlation with S-V index (r = 0.67, p = 0.023).(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography↗
PubMed1994

[Left ventricular characteristics after Jatene operation for transposition of the great arteries with intact ventricular septum--comparative study of neonatal primary and two stage repairs].

Left ventricular characteristics in late postoperative period after the arterial switch operation (ASO) was evaluated in fifty-nine patients with transposition of the great arteries and intact ventricular septum. They included 22 neonates who underwent a neonatal ASO (Group I) and 37 patients who underwent a two-stage ASO (Group II). Group II was subdivided into two groups according to the presence or absence of aortic regurgitation in the late postoperative period as group IIa (aortic regurgitation [-], 22 patients) and group IIb (aortic regurgitation [+], 15 patients). Age at ASO ranged from 4 to 27 days (average 12.7 days) in the group I, 5 to 43 months (average 12.7 months) in the group IIa, and 4 to 54 months (average 16.3 months) in the group IIb. Postoperative follow-up period ranged from 8 to 68 months (average 25.0 months) in the group I, 12 to 74 months (average 59.0 months) in the group IIa, and 19 to 66 months (average 48.5 months) in the group IIb. Left ventricular end-diastolic volume was significantly smaller in the group I (123 +/- 19% of normal) than the group IIa (146 +/- 38 of normal) and the group IIa (183 +/- 53% of normal). And left ventricular ejection fraction was significantly higher in the group I (67 +/- 5%) than the group IIa (62 +/- 11%) and the group IIb (58 +/- 8%). Left ventricular normalized mass was significantly smaller in the group I (85 +/- 11% of normal) than the group IIa (113 +/- 14% of normal) and the group IIb (130 +/- 9% of normal).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Cyclic AMP-elevating agents induce an inducible type of nitric oxide synthase in cultured vascular smooth muscle cells. Synergism with the induction elicited by inflammatory cytokines.

In cultured vascular smooth muscle cells, interferon gamma (IFN-gamma) induced the accumulation of nitrite, a stable metabolite of nitric oxide, in a dose- and time-dependent manner. In parallel with this reaction, this cytokine increased the mRNA and protein levels of an inducible macrophage-type of nitric oxide synthase (iNOS). Forskolin, a direct activator of adenylate cyclase, or dibutyryl cAMP alone caused small increases in nitrite accumulation and iNOS mRNA and protein levels and synergistically enhanced the IFN-gamma-stimulated reactions. 8-Bromo-cGMP neither increased by itself nor synergized with IFN-gamma to increase the same reactions. Prostaglandin E1 and beraprost, a stable analogue of prostaglandin I2, which by themselves showed only marginal effects on these reactions, also synergized with IFN-gamma to stimulate the reactions. Interleukin 1 beta or tumor necrosis factor alpha stimulated the same reactions which were similarly enhanced by forskolin. These results indicate that an elevation of intracellular cAMP, particularly in combination with inflammatory cytokines, positively regulates nitric oxide production at the level of iNOS mRNA expression in vascular smooth muscle cells.

Amino Acid Oxidoreductases↗
PubMed1993

Cytokine-induced expression of an inducible type of nitric oxide synthase gene in cultured vascular smooth muscle cells.

In unstimulated cultured vascular smooth muscle cells (VSMC), mRNA of an inducible macrophage-type of nitric oxide synthase (iNOS) was barely detectable. Interferon gamma (IFN gamma) and tumor necrosis factor alpha (TNF alpha) markedly increased iNOS mRNA levels in time- and dose-dependent manners. The induction of iNOS mRNA paralleled the cytokine-induced nitrite production. Actinomycin D abolished the IFN gamma- and TNF alpha-induced increases in iNOS mRNA and nitrite production. Cycloheximide, which abolished both the IFN gamma- and TNF alpha-induced increases in nitrite production, had no effect on the IFN gamma-induced increase in iNOS mRNA but markedly inhibited the TNF alpha-induced one. These results suggest that IFN gamma directly induces the expression of the iNOS gene whereas TNF alpha mainly induces it via the induction of an intermediary protein in cultured VSMC.

Amino Acid Oxidoreductases↗