Low-density lipoprotein particle size as an independent predictor of glycated low-density lipoprotein level.
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Adult↗
Biomedical subjects
H Matsui
Publications and source records attributed to H Matsui.
Influence of age on diurnal variability in measurements of spirometric indices and respiratory pressures.
We evaluated variations in spirometric indices (i.e., forced vital capacity [FVC], peak expiratory flow [PEF], and forced expiratory volume in 1 sec [FEV1]) and static respiratory muscle pressures (i.e., maximum static inspiratory pressure [PImax] and maximum static expiratory pressure [PEmax]) within a span of 12 hr in 60 healthy elderly subjects, 60 young subjects, and 30 Chronic Obstructive Pulmonary disease (COPD) patients. There were no differences among data of FVC, PEF, FEV1, PImax, and PEmax on three separate occasions within a day in the elderly or the young. The mean coefficient of variation (CV) values of PEF and PImax on three occasions were 3.0 +/- 0.3% and 4.2 +/- 0.4% in the elderly, and 2.4 +/- 0.2% and 3.7 +/- 0.3% in the young, respectively. No subjects had more than 9% CV on each measurement in the study, suggesting that there is nosignificant daytime variation in measurement of expiratory flow and respiratory pressures in young and elderly people. However, FVC, PEF FEV1, and PImax values in the morning were smaller than those measured at the other two occasions in COPD patients. The results indicate that COPD affects diurnal variation in pulmonary function, but age alone has little impact on diurnal variation.
Adult↗
[An elderly case with pseudogout exacerbated by the administration of granulocyte-colony stimulating factor during drug-induced granulocytopenia].
A 82-year-old woman was admitted because of dehydration and chronic renal failure. Although her renal function was improved by hydration, granulocytopenia (granulocyte number 645/mm3) occurred. Treatment with a relatively high dose of H2 blocker for one month before admission may have caused the granulocytopenia. To prevent possible infection in the patient, we administered 75 g of granulocyte-colony stimulating factor (G-CSF) for 5 consecutive days but 4 days after commencement of administration of G-CSF, pain in both knee joints suddenly appeared. Synovial fluid aspiration revealed granulocytosis (10,400/mm3) and deposition of calcium pyrophosphate dihydrate in the knee joints. The level of G-CSF in the synovial fluid was increased in the joints (700 pg/ml), compared with the serum concentration (62 pg/ml). Furthermore, the concentrations of interleukin-6 and interleukin-8 were markedly increased in the synovial fluid. The results indicated that her pseudogout exacerbation by G-CSF was at least in part explained by the increased production of cytokines in the knee joints. Because the prevalence of pseudogout and gout is overwhelming in the elderly, the possibility of GCSF induced exacerbation of joint pain should be carefully considered in elderly patients.
Aged↗
[Molecular genetic analysis of rumen microbes and its application].
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Animals↗
[Effect of mechanical damage on ex vivo DNA virus vector-mediated gene transduction in epithelial cells of murine trachea].
The mechanism of Adenovirus (Ad) and Adeno-associated virus (AAV) vector-mediated gene transduction in murine tracheae has not been fully understood. Excised tracheae from mice were exposed to either Ad vector (Ad-CMV-LacZ) or AAV vector (AAV-CMV-LacZ) for 1 hour. LacZ gene expression in tracheal epithelial cells was detected by X-gal staining. Only patch distributions of LacZ expressing cells were observed. The percentage of LacZ expressing cells to total cells was less than 1% with either vector. Ad-mediated LacZ transduction was increased by mechanical damage using forceps. AAV-mediated gene transduction in tracheal epithelial cells was also increased by mechanical damage. Furthermore, this increased expression of vector LacZ by damaged epithelial cells was not affected by pretreatment with anti-ICAM-1 mAb or platelet-activating factor receptor antagonist. Although the Ad and AAV vectors were inefficient in transferring genetic material to murine trachea ex vivo, our results suggest that mechanical damage can enhance their transduction efficiency.
Adenoviruses, Human↗
Prolapse of the neovagina in Mayer-Rokitansky-Kuster-Hauser syndrome. A case report.
BACKGROUND: Mayer-Rokitansky-Kuster-Hauser syndrome is a rare entity. The creation of a sigmoid vagina was performed in some patients with this syndrome in the past, though it is not widely used now. We report on a patient who developed prolapse of a sigmoid vagina 33 years after the operation. CASE: A 57-year-old woman presented with a "falling-out" sensation in the vagina, pain, leukorrhea and dyspareunia. She had undergone an operation for creation of a sigmoid vagina 33 years earlier in our hospital. She and her husband desired conservation of the ability for sexual intercourse. The transabdominal method of retroperitoneal sacropexy of the sigmoid vagina was performed. The patient has maintained a satisfactory sexual life with her husband since the operation. CONCLUSION: There are a few cases of prolapse of a sigmoid vagina in the literature, while the repair methods are not described in detail. To our knowledge, this is the first report of reconstruction of a sigmoid vaginal prolapse. Although the reasons for the neovaginal prolapse were not understood, the retroperitoneal sacropexy was successful in this case.
Bioprosthesis↗
[The simple swallowing provocation test as a means of screening for swallowing disorders: a comparison with the water swallowing test].
The sensitivity and specificity of the simple swallowing provocation test (S-SPT) were evaluated in a group of patients who were being examined for aspiration pneumonia (ASP) (ASP group: 72.5 +/- 3.9 years old) and in a group of age-matched control subjects (CTRL group: 69.5 +/- 2.9 years old). The S-SPT was evaluated in terms of the swallowing response and latent time (LT) for swallowing after a bolus injection of 0.4 ml of distilled water at the suprapharynx. Responses to the S-SPT were classified as normal or abnormal, dependent on induction of the swallowing reflex within 3 seconds after bolus injection. The sensitivity and specificity of the S-SPT in detecting ASP were calculated. Of the 40 patients in the ASP group, 18 were given a diagnosis of ASP on the basis of clinical findings and laboratory examinations. The sensitivity and specificity of the S-SPT were 94.4% and 86.4%, respectively, compared to 77.8% and 68.1%, respectively, for the water swallowing test. Because the S-SPT can be performed without any need for special patient effort or cooperation, it should be effective in diagnosing ASP in a wide variety of patients, including those who are bedridden.
Aged↗
An outbreak of pharyngitis caused by food-borne group A Streptococcus.
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DNA, Bacterial↗
Axial symptoms after en bloc cervical laminoplasty.
Eighty-two patients were evaluated after cervical laminoplasty to explore measures that could minimize future postoperative axial complaints. Patients were divided into two groups: Group A--severe postoperative axial symptoms, and Group B--mild axial complaints. Japanese Orthopaedic Association outcomes scores were similar for the two groups. Radiologic studies demonstrated greater restriction of range of motion in Group A patients who had undergone longer and more extensive surgical procedures.
Adult↗
Shear-dependent functions of the interaction between soluble von Willebrand factor and platelet glycoprotein Ib in mural thrombus formation on a collagen surface.
Recent flow studies have clearly established the function of von Willebrand factor (vWF) in initial platelet adhesion, in which the interaction of surface-immobilized vWF with platelet glycoprotein (GP) Ib, particularly at high shear rates, leads to the transient capture of flowing platelets onto the surface. This interaction is thought to trigger activation of platelet GP IIb/IIIa, leading to irreversible platelet adhesion and subsequent mural thrombus growth. The role of vWF-GP Ib interaction in secondary thrombus growth remains to be clarified, however. In this study, time-course images of the thrombus formation process were obtained using a whole blood flow system that allows real-time visualization of fluorescence-labeled platelet thrombus formation. The system employs a collagen-coated surface in a parallel plate flow chamber mounted on an epifluorescence microscope, which is then subjected to computer-assisted image analysis. In perfusion of blood preincubated with anti-vWF antibody NMC-4, which blocks the vWF-GP Ib interaction in solution, neither primary platelet adhesion nor subsequent thrombus growth on a collagen surface was detected at high shear rates (> or = 1210/s). In addition, even under experimental conditions in which initial platelet adhesion normally occurred, NMC-4-treated blood perfusion showed an apparent defect of secondary thrombus growth at the same high shear rates. The overall process of thrombus formation at low shear rates (< or = 340/s) was not affected by specific blockers of the vWF-GP Ib interaction. These findings indicate that, in addition to the interaction of surface-immobilized vWF with GP Ib in platelet adhesion, the interaction of soluble vWF with GP Ib is required for secondary thrombus growth selectively at high shear rates.
Antibodies, Monoclonal↗
Purely laparoscopic pylorus-preserving gastrectomy with extraperigastric lymphadenectomy for early gastric cancer: a case and technical report.
For the purpose of prevention of postgastrectomy syndrome and a less invasive and yet curative oncological resection, a purely laparoscopic pylorus-preserving gastrectomy with extraperigastric lymphadenectomy was performed for a patient with early gastric cancer located in the middle third of the stomach. The patient's postoperative course was uneventful. During his postoperative recovery, the patient experienced very little pain and used analgesic medication only one time. This operation appeared to be oncologically adequate. As of the seventh postoperative month, the patient never experienced dumping syndrome or alkaline reflux gastritis. This procedure is technically feasible and an excellent option because of its reduced surgical invasiveness and better postoperative quality of life.
Adenocarcinoma↗
Epidermal growth factor protects rat epithelial cells against acid-induced damage through the activation of Na+/H+ exchangers.
We examined the effect of epidermal growth factor (EGF) on acid-induced cell damage in rat gastric epithelial cells (RGM1) and investigated the mechanisms of this effect. Cells were incubated with EGF for 5, 15, 30, and 60 min, and then immersed in an acidified medium (pH 4.0) for 30 min to induce cell damage. EGF prevented cell damage in a concentration- and time-dependent manner. EGF reduced the effects of the acidified medium on the cells, preventing the reduction of intracellular pH. Replacement of Na+ with K+ in the acidified medium canceled the effect of EGF. Indomethacin and W-7 (a Ca-calmodulin inhibitor) did not alter the protective effect of EGF. In contrast, genistein (a tyrosine kinase inhibitor), amiloride (a Na+/H+ exchangers I and II inhibitor), and wortmannin (a phosphatidylinositol 3-kinase inhibitor) significantly decreased the effect of EGF. Expression of Na+/H+ exchangers type I and type II was confirmed by reverse transcription-polymerase chain reaction. Our results demonstrate that EGF prevents acid-induced cell damage, most likely through the activation of a Na+/H+ exchanger II via phosphatidylinositol 3-kinase.
Animals↗
Evidence for periciliary liquid layer depletion, not abnormal ion composition, in the pathogenesis of cystic fibrosis airways disease.
The pathogenesis of cystic fibrosis (CF) airways infection is unknown. Two hypotheses, "hypotonic [low salt]/defensin" and "isotonic volume transport/mucus clearance," attempt to link defects in cystic fibrosis transmembrane conductance regulator-mediated ion transport to CF airways disease. We tested these hypotheses with planar and cylindrical culture models and found no evidence that the liquids lining airway surfaces were hypotonic or that salt concentrations differed between CF and normal cultures. In contrast, CF airway epithelia exhibited abnormally high rates of airway surface liquid absorption, which depleted the periciliary liquid layer and abolished mucus transport. The failure to clear thickened mucus from airway surfaces likely initiates CF airways infection. These data indicate that therapy for CF lung disease should not be directed at modulation of ionic composition, but rather at restoring volume (salt and water) on airway surfaces.
Absorption↗
Angiotensin II interferes with leukemia inhibitory factor-induced STAT3 activation in cardiac myocytes.
Recently, we reported that leukemia inhibitory factor (LIF), a member of the interleukin (IL)-6 cytokine family, transduced hypertrophic and cytoprotective signals via Januas Kinase-signal transducer and activator of transcription (JAK-STAT) pathway in cardiac myocytes. Angiotensin II (AII) is also known to activate STATs and reported to induced apoptosis in adult rat ventricular myocytes. In the present study, we investigated potential interactions between gp130 dependent and AII signaling pathways, by examining AII regulation of LIF-induced anti-apoptotic effect and STAT3 activation in cardiac myocytes. Although LIF attenuated the DNA fragmentation induced by serum depletion, AII augmented the DNA fragmentation in cultured neonatal rat cardiac myocytes. Furthermore, LIF-mediated cytoprotective effect was inhibited by AII pretreatment. LIF rapidly and transiently tyrosine phosphorylated STAT3 in cardiac myocytes which was not observed by AII. AII pretreatment inhibited LIF-induced phosphorylation of STAT3 in a dose dependent manner. This inhibitory effect of AII on STAT3 activation was blocked by the AII type I (AT1) receptor antagonist CV11974. These results demonstrate that negative crosstalk between gp130 and AT1 receptor dependent signaling exists in cardiac myocytes. This crosstalk may contribute to the modulation of pathophysiological process in myocardial disease.
Angiotensin II↗
Induction of apoptotic DNA fragmentation by nonsteroidal anti-inflammatory drugs in cultured rat gastric mucosal cells.
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause apoptosis in several cell lines including transformed chicken embryo fibroblasts and human colon cancer cells. We herein report the apoptotic effect of NSAIDs in a non-transformed cell line derived from the rat gastric mucosa, RGMI (rat gastric mucosa cell first). 1-[p-Chlorobenzoyl]-5-methoxy-2-methylindole-3-acetic acid (indomethacin) and sodium 2-(2,6-dichloroanilino)phenylacetate (sodium diclofenac), potent and non-selective inhibitors of cyclooxygenase, were found to induce DNA fragmentation in RGM1 cells in a time- and concentration-dependent manner. The expression of mRNA for cyclooxygenase-2 was hardly detected in the intact cells but was clearly enhanced when the cells were incubated with the two NSAIDs. In contrast, the expression of mRNA for cyclooxygenase-1 was constitutive and was never affected by NSAIDs. The effect of [3,4-di(4-methoxyphenyl)-5-isoxazolyl] acetic acid (mofezolac), a potent and highly preferential inhibitor of cyclooxygenase-1, and N-[2-(cyclohexyloxy)-4-nitrophenyl]methanesulphonamide (NS-398), a selective inhibitor of cyclooxygenase-2, on DNA fragmentation and cyclooxygenase-2 mRNA expression was weak compared to the effect of indomethacin or sodium diclofenac. The DNA fragmentation induced by sodium diclofenac was hardly affected by the exogenous addition of 16,16-dimethyl prostaglandin E2 but was inhibited by caspase inhibitors such as Ac-YVAD-CHO and Ac-DEVD-CHO. The present data provide the first evidence that NSAIDs, such as indomethacin and sodium diclofenac, cause apoptotic DNA fragmentation in cultured gastric mucosal cells, and also indicate the involvement of caspases rather than the inhibition of cellular prostaglandin synthesis in the apoptotic process.
16,16-Dimethylprostaglandin E2↗
Preventive measures of back muscle injury after posterior lumbar spine surgery in rats.
STUDY DESIGN: Postoperative back muscle injury was studied in rats. Postoperative findings were compared among three groups: 2-hour continuous back muscle retraction, 5-minute retraction release after 1 hour of retraction, and 5-minute release at every 40 minutes of retraction. OBJECTIVE: To determine whether intermittent release of the retractor during surgery is effective to prevent severe muscle injury. SUMMARY OF BACKGROUND DATA: In surgery performed on the extremities using a tourniquet, intermittent reperfusion intervals can permit extended tourniquet application when the operation is prolonged. However, there have been no specific studies on the effects of intermittent retraction release for postoperative back muscle injury. METHODS: The back muscle of rats was retracted using a self-retaining retractor for 2 hours. The 36 rats were divided equally into the following three groups: Group 1, 2 hours of continuous retraction; Group 2, two 1-hour retractions interposed with a 5-minute retraction release; and Group 3, three 40-minute retractions interposed with a 5-minute retraction release. In each group, the multifidus muscle was histologically analyzed at 48 hours, 1 week, and 6 weeks after surgery. The muscles were stained by a variety of histochemical methods. The level of serum CPK-MM isoenzyme was measured 48 hours after surgery. RESULTS: Postoperative back muscle degeneration was the most severe in Group 1. The concentration of CPK-MM in Group 1 was significantly higher than that in Groups 2 and 3. One week after surgery, the lesser diameter of regenerated fibers in Group 1 was smaller than that in Groups 2 and 3. The incidence of neurogenic muscle damage was the highest in Group 1. CONCLUSIONS: During posterior lumbar spine surgery, 5-minute retraction release after 1 hour or after 40 minutes of retraction was effective in preventing severe back muscle injury after surgery.
Animals↗
Coordinated clearance of periciliary liquid and mucus from airway surfaces.
Airway surface liquid is comprised of mucus and an underlying, watery periciliary liquid (PCL). In contrast to the well-described axial transport of mucus along airway surfaces via ciliary action, theoretical analyses predict that the PCL is nearly stationary. Conventional and confocal microscopy of fluorescent microspheres and photoactivated fluorescent dyes were used with well-differentiated human tracheobronchial epithelial cell cultures exhibiting spontaneous, radial mucociliary transport to study the movements of mucus and PCL. These studies showed that the entire PCL is transported at approximately the same rate as mucus, 39.2+/-4.7 and 39.8+/-4.2 micrometer/sec, respectively. Removing the mucus layer reduced PCL transport by > 80%, to 4.8+/-0.6 micrometer/sec, a value close to that predicted from theoretical analyses of the ciliary beat cycle. Hence, the rapid movement of PCL is dependent upon the transport of mucus. Mucus-dependent PCL transport was spatially uniform and exceeded the rate expected for pure frictional coupling with the overlying mucus layer; hence, ciliary mixing most likely accelerates the diffusion of momentum from mucus into the PCL. The cephalad movement of PCL along airway epithelial surfaces makes this mucus-driven transport an important component of salt and water physiology in the lung in health and disease.
Biological Transport↗
Modulation of LDL particle size after an oral glucose load is associated with insulin levels.
Individuals with a predominance of small low-density lipoprotein (LDL) particles appear to be at increased risk for coronary artery disease. The purpose of this study was to determine whether the LDL particle size was modulated in response to a 75-g oral glucose load. Overall, there were no significant changes in the LDL particle size after glucose load. However, the difference in LDL particle size (deltaLDL size) between the fasting and 2-h post-load states was inversely correlated with the fasting LDL particle size. Also, deltaLDL size was positively correlated with BMI and the post-load glucose levels. Forward stepwise regression analysis revealed three parameters as independent factors capable of modulating LDL particle size: BMI, fasting insulin, and post-load glucose levels. After adjustment for BMI and glucose levels, the levels of fasting and 2-h post-load insulin remain independent determinants of deltaLDL size. These results suggest that plasma insulin levels during glucose load modulate LDL particle size.
Adult↗