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Biomedical subjects

N Matsuda

Publications and source records attributed to N Matsuda.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Recurrent episodes of fever of unknown origin as temporal lobe epilepsy].

A 67-year-old woman was admitted to our department for the recurrent fever of unknown origin that occurred once approximately every 1 month for the last 3 years. No clinical and laboratory abnormality were found, except an interictal EEG showing fronto-temporal spike discharges. During hospitalization a characteristic febrile episode was accompanied by automatism, thereby, it became clear that the undetermined periodic febrile episodes were due to temporal lobe epilepsy. In this case, the thermoregulatory center of the hypothalamus might be symptomatic zone of temporal lobe epilepsy.

Aged↗
PubMed1999

Diabetes-induced down-regulation of beta1-adrenoceptor mRNA expression in rat heart.

The present study addressed the question of whether the number of myocardial beta-adrenoceptors in rats with 4- to 6-week streptozotocin-induced diabetes is regulated in a transcriptional or translational manner. Radioligand binding experiments with [3H]CGP 12177 {4-(3-t-butylamino-2-hydroxypropoxy)-[5,7-3H]benzimidazol-2-one} showed that the density of beta-adrenoceptors fell by 50% with no change in affinity in diabetic rat ventricular myocardium compared with age-matched control myocardium. The relative content of beta1-adrenoceptor mRNA in diabetic myocardium also was reduced from the control level by 57%, as determined by northern blot analysis. The reductions in myocardial beta-adrenoceptor number and beta1-adrenoceptor mRNA observed in diabetes were prevented by insulin therapy. These data indicate that the diminished density of myocardial beta-adrenoceptors in diabetes occurred, at least in part, at the mRNA level.

Animals↗
PubMed1999

Healing of segmental bone defects in rats induced by a beta-TCP-MCPM cement combined with rhBMP-2.

A beta-tricalcium phosphate-monocalcium phosphate monohydrate (beta-TCP-MCPM) cement was evaluated as an effective carrier of recombinant human bone morphogenetic protein-2 (rhBMP-2) in rat femoral critical-size defects. Hard cement cylinders (4 x 5 mm) impregnated with two different doses of rhBMP-2 (1.26 or 6.28 microg) were implanted into each defect, and the results were compared with those in rats that had implantations of cylinders only. Implantation of the 6.28 microg dose of rhBMP-2 caused a large bone shell to form around the defect, resulting in osseous union in all cases within 3 weeks. Except for beta-TCP granules, the cement was resorbed and replaced by bone tissue at 6 weeks. A torsion test at 9 weeks showed that the failure torque and bone stiffness had recovered 99% and 141%, respectively, compared with the intact contralateral femur. The defects that received 1.26 microg of rhBMP-2 resulted in 40% union and 41% of the failure torque at 9 weeks. However, no instances of union were observed in the defects implanted with cylinders only. In conclusion, the beta-TCP-MCPM cement was shown to be effective as a rhBMP-2 carrier. Combined with rhBMP-2, this cement was rapidly resorbed and completely healed the defects.

Animals↗
PubMed1999

Intracellular free calcium accumulation in ferret vascular smooth muscle during crystalloid and blood cardioplegic infusions.

OBJECTIVE: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca2+]i) accumulation and microvascular contractile function were examined. METHODS: Isolated ferret hearts were subjected to hyperkalemic (25 mmol/L K+) blood cardioplegic infusion, hypermagnesemic (25 mmol/L Mg2+, K+-free) crystalloid cardioplegic infusion, or hyperkalemic crystalloid cardioplegic infusion for 1 hour. Coronary arterioles were isolated, cannulated, and loaded with fura 2. Reactivity and [Ca2+]i were assessed with videomicroscopy. [Ca2+]i was measured at baseline and after application of 50 mmol/L KCl. In addition, [Ca2+]i and vascular contraction were measured during exposure to Mg2+ and K+ cardioplegic solution at both 4 degrees C and 37 degrees C. RESULTS: From a baseline [Ca2+]i of 177 +/- 52 nmol/L, K+ cardioplegic infusion (302 +/- 80 nmol/L potassium) markedly increased [Ca2+]i, whereas blood cardioplegic infusion (214 +/- 53 nmol/L) and Mg2+ cardioplegic infusion (180 +/- 42 nmol/L) did not alter [Ca2+]i. Although a difference between groups in percentage contraction after application of 50 mmol/L KCl was not observed, [Ca2+]i increased significantly more in vessels in the control group (764 +/- 327 nmol/L) and the K+ crystalloid cardioplegic infusion group (698 +/- 215 nmol/L) than in vessels in the blood cardioplegic infusion group (402 +/- 45 nmol/L) and the Mg2+ cardioplegic infusion group (389 +/- 80 nmol/L). Mg2+ cardioplegic solution induced no microvascular contraction at either 4 degrees C or 37 degrees C, nor was an increase in [Ca2+]i observed. K+ cardioplegic solution induced microvascular contraction at 37 degrees C but not at 4 degrees C; it increased [Ca2+]i at both 4 degrees C and 37 degrees C. CONCLUSION: An Mg2+-based cardioplegic solution, or appropriate Mg2+ or blood supplementation of a K+ crystalloid cardioplegic solution, may decrease the accumulation of [Ca2+]i in the vascular smooth muscle during ischemic arrest.

Animals↗
PubMed1999

Preconditioning improves cardioplegia-related coronary microvascular smooth muscle hypercontractility: role of KATP channels.

OBJECTIVES: The effect of preconditioning before hyperkalemic cardioplegia on the coronary smooth muscle remains to be elucidated. We tested the hypothesis that hypoxic preconditioning could protect coronary smooth muscle against subsequent hyperkalemic cardioplegia-induced coronary vasospasm and that this preconditioning effect could be mediated by K(ATP) channels. METHODS: Rat coronary arterioles (endothelium-denuded) were studied in a pressurized, no-flow, normothermic state. Simultaneous monitoring of luminal diameter and intracellular calcium concentration of vascular smooth muscle loaded with fura-2 was made with microscopic image analysis. All vessels were subjected to 60 minutes of hypoxic hyperkalemic cardioplegia (K(+) = 25.0 mmol/L) and were then reperfused. Six groups were studied: (1) controls, no precardioplegic intervention; (2) preconditioning, achieved with 10 minutes of hypoxia (PO2 < 30 mm Hg) and 10 minutes of reoxygenation; (3) preconditioning plus glibenclamide (10 micromol/L), achieved with 10 minutes of preconditioning in the presence of K(ATP) channel blocker glibenclamide; (4) pretreatment with K(ATP) channel opener pinacidil (100 micromol/L); (5) pretreatment with pinacidil (100 micromol/L) plus glibenclamide (10 micromol/L); and (6) pretreatment with glibenclamide (10 micromol/L) alone. RESULTS: Hypoxic preconditioning significantly (P <.01) reduced hyperkalemic cardioplegia-induced intracellular calcium concentration accumulation and prevented the hypercontractility during and after hyperkalemic cardioplegia compared with control vessels. Pinacidil provided effective microvascular protection similar to hypoxic preconditioning. These vasoprotective effects of preconditioning were significantly antagonized in glibenclamide-treated vessels. CONCLUSIONS: Hypoxic preconditioning can prevent coronary microvascular hypercontractility during and after subsequent cardioplegia by a K(ATP ) channel mechanism that regulates intracellular calcium concentration of the vascular smooth muscle.

Animals↗
PubMed1999

Comparison of parameters of 123I-MIBG scintigraphy for predicting prognosis in patients with dilated cardiomyopathy.

123I-metaiodobenzylguanidine (MIBG) scintigraphy has been used to predict prognosis of patients with dilated cardiomyopathy (DCM), although it is unknown which parameter of MIBG is the most useful clinically. We studied MIBG in 59 patients with DCM, and followed them up to evaluate the prognosis of DCM. Single photon emission tomography (SPET) and planar imaging were performed, both early (e) and 4 h (delayed, d) post-injection. 201Tl (TL) SPET and radionuclide-ventriculography were also investigated. The total defect score of early and delayed MIBG and 201 Tl (MIBGeDS, MIBGdDS, TLDS) was analysed visually for each SPET image. The heart to mediastinum ratio (H/M) for both the early and delayed MIBG planar images and myocardial washout rate at 4 h were analysed quantitatively. Sixteen patients died during follow-up. Cox Hazards univariate analysis selected washout rate (P < 0.0001), H/Me (P = 0.0012), H/Md (P = 0.0001) and left ventricular ejection fraction (P = 0.0004) as indices for the prediction of cardiac death. Multivariate analysis selected washout rate as the most powerful independent predictor of prognosis (P < 0.0001). Survival curves with a threshold value of 52% for washout rate were able to differentiate a negative outcome from survival (P < 0.0001). TLDS, MIBGeDS and MIBGdDS were not useful in the prediction of prognosis. The washout rate of MIBG is the most potent predictor of cardiac death and is considered clinically useful.

3-Iodobenzylguanidine↗
PubMed1999

Coronary microvascular protection with mg2+: effects on intracellular calcium regulation and vascular function.

The use of Mg2+-supplemented hyperkalemic cardioplegia preserves microvascular function. However, the mechanism of this beneficial action remains to be elucidated. We investigated the effects of Mg2+ supplementation on the regulation of intracellular calcium concentration ([Ca2+]i) and vascular function using an in vitro microvascular model. Ferret coronary arterioles (80-150 micrometer in diameter) were studied in a pressurized (40 mmHg) no-flow, normothermic (37 degrees C) state. Simultaneous monitoring of internal luminal diameter and [Ca2+]i using fura 2 were made with microscopic image analysis. The microvessels (n = 6 each group) were divided into four groups according to the content of MgCl2 (nominally 0, 1.2, 5.0, and 25.0 mM) in a hyperkalemic cardioplegic solution ([K+] 25.0 mM). After baseline measurements, vessels were subjected to 60 min of hypoxia with hyperkalemic cardioplegia (equilibrated with 95% N2-5% CO2) containing each concentration of Mg2+ ([Mg2+]) and were then reoxygenated. During hyperkalemic cardioplegia, [Ca2+]i increased in a time-dependent manner in all groups. In the lower [Mg2+] cardioplegia groups, [Ca2+]i was significantly increased at the end of the 60-min cardioplegic period (247 +/- 44 nM and 236 +/- 49 nM in [Mg2+] 0 and 1.2 mM groups, respectively; both P < 0.05 vs. baseline) with 19.6-17.2% vascular contraction. Conversely, there was no significant [Ca2+]i increase in the higher [Mg2+] cardioplegia groups and less vascular contraction (5.4-4.1%, both P < 0.05 vs. [Mg2+] 1.2 mM group). After reperfusion, agonist (U-46619, thromboxane A2 analog)-induced vascular contraction was significantly enhanced in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was normalized in the higher [Mg2+] cardioplegia groups. Intrinsic myogenic contraction was significantly decreased in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was preserved in the higher [Mg2+] cardioplegia groups. These results suggest that supplementation of the solution with >5.0 mM [Mg2+] may prevent hyperkalemic cardioplegia-related intracellular Ca2+ overloading and preserve vascular contractile function in coronary microvessels.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1999

Clinical characteristics of amiodarone-induced thyrotoxicosis and hypothyroidism in Japan.

Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6 years. AIT and AAH developed after 39+/-21 and 20+/-16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9 months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (< 12 microg/dl), accompanied by suppressed TSH (<0.1 microU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinued in two of 13 AIT patients because of extrathyroidal adverse reactions.

Adult↗
PubMed1999

Influence of oxygenation on endothelial modulation of coronary vasomotor function during hyperkalemic cardioplegia.

BACKGROUND: The purpose of this study was to determine the influence of oxygenation of a hyperkalemic cardioplegic solution (K-CP) on endothelial modulation of vasomotor tone and to correlate these changes with the intracellular calcium concentration ([Ca++]i) in microvascular smooth muscle. METHODS: Rat coronary arterioles were studied in a pressurized, no-flow normothermic state. Simultaneous monitoring of luminal diameter and [Ca++]i (fura-2) was performed with use of microscopic image analysis. Vessels were subjected to 60 minutes of oxygenated or hypoxic K-CP (K+ = 25.0 mmol/L) and were then reperfused with oxygenated Krebs-physiologic saline solution for 60 minutes. RESULTS: In oxygenated K-CP, the K-CP-induced contraction and [Ca++]i accumulation were significantly increased in endothelium-denuded (ED) vessels compared with endothelium-intact vessels. The effect of ED in oxygenated K-CP was mimicked by administration of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. Conversely, in hypoxic K-CP the contraction was significantly attenuated in ED vessels compared with endothelium-intact vessels, although there was no significant difference in [Ca++]i. Indomethacin did not affect the endothelium-dependent contraction during hypoxic K-CP. CONCLUSIONS: Endothelium-derived nitric oxide modulates the vascular tone during K-CP by regulating the vascular smooth muscle [Ca++]i, whereas endothelium-derived contracting factor(s), which is not predominantly a product of cyclo-oxygenase, may play a prominent role under hypoxic K-CP by increasing vascular smooth muscle Ca++ sensitivity.

Animals↗
PubMed1999

[Acquisition of evidence and facts for a consulting service in the department of clinical laboratory to support effective usage of laboratory tests].

We are developing an integrated laboratory information database to share the evidences and facts with clinicians for effective application of diagnostic laboratory tests for the care of individual patients. It includes high quality evidence acquired from the clinical trials and systematic reviews as well as basic information about the analytical method, related disorders and so on of each laboratory test. We should also have the skills to appropriately obtain information from articles about relevant subjects and obtain the original facts from the laboratory database combined with the database from the department of medical records to review diagnostic data of individual cases. These strategies to acquire and accumulate those kinds of knowledge and information are essential for the management of a consulting service room as part of the clinical laboratory department. We must contribute to the improvement of clinical diagnoses and treatments, and serve as professional consultants with the expertise.

Clinical Laboratory Information Systems↗
PubMed1999

[Dynamic generation of diagnostic knowledge from a database of well defined case clinical records].

To promote an evidence-based practice of laboratory medicine, we created a database of 1584 typical case records consisting of 30 common diseases. Cases without therapy or major complication were carefully selected. Characteristic clinical symptoms and signs indicating the severity were recorded together with general laboratory test results. A user-friendly computer system for interpretive laboratory diagnosis was also created. It features (1) automatic graphics for visualizing distributions of laboratory values and/or prevalence of clinical symptoms and signs, (2) simultaneous display of distributions of common test values for any combination of diseases, (3) quick subclassification of cases within a disease group by any clinical characteristic, (4) diagnostic guidance by dynamic calculation of a novel similarity index that represents matching of a given set of signs/values with those of typical cases in the database.

Clinical Laboratory Techniques↗
PubMed1999

[A successful surgical case of billowing mitral leaflet syndrome (Barlow syndrome) combined with severe mitral regurgitation].

We report a successful surgical case of billowing mitral leaflet syndrome combined with severe mitral regurgitation. A 45-year-old man suffered from congestive heart failure and admitted our institution for precise examination. A heart murmur was pointed out by a medical examination at his high school, and mitral valve prolapse was detected by echocardiography at 23 year of age. No medication was applied because he showed no symptom. From 44 year of age, he noted palpitation on exercise. Holter monitor showed blocked PAC and Wenckebach A-V block, and transesophageal echocardiography indicated severe mitral regurgitation due to the billowing of voluminous both leaflets. At his operation, we recognized the billowing of both leaflets with torn chordae, and size of the mitral valve orifice was 8.5 x 5 cm. The huge mitral valve was replaced with a CarboMedics 31M prosthetic valve by plicating mattress stitches of native mitral annulus. Histopathologic findings showed accumulation of acid mucopolysaccharide. Postoperative echocardiography showed reduction of the left ventricular volume and preservation of the left ventricular function. Relatively slow progression of the billowing mitral leaflet syndrome did not cause apparent symptoms of heart failure in this patient. Therefore, proper selection of the procedure and timing of surgical treatments might be important for successful long-term results after operation of the billowing mitral leaflet syndrome.

Cardiac Surgical Procedures↗
PubMed1998

Proliferation and differentiation of human osteoblastic cells associated with differential activation of MAP kinases in response to epidermal growth factor, hypoxia, and mechanical stress in vitro.

In an attempt to elucidate the specificity of pathways from environmental stress to cellular outcome via mitogen activated protein kinases (MAPKs) activation, we examined the responsiveness of cultured human osteoblastic periodontal ligament (PDL) cells to epidermal growth factor (EGF), hypoxia, and mechanical stress, in terms of cell proliferation, differentiation, and associated activation of three different types of MAPK. Cell proliferation was promoted in the presence of 10ng/ml of EGF or in hypoxic conditions (5% O2), whereas it was inhibited by cyclic stretch (9% strain, 6 cycles/min), which was used as a model of mechanical stress. Conversely, the alkaline phosphatase activity, a marker for osteoblastic differentiation of the cells, was increased by cyclic stretch but decreased by EGF and hypoxia. The mitogenic response of PDL cells to EGF or hypoxia was associated with the selective phosphorylation and activation of extracellular-related kinase (ERK) 1/2, while phosphorylation and activation of c-Jun N-terminal kinase (JNK) was observed in mechanical stretch loaded cells. No such changes were seen in p38 protein. These findings suggested that stress-responsive changes in proliferation and osteoblastic differentiation of PDL cells are selectively mediated by ERK 1/2 and by JNK, respectively, and that a balance between these two pathways determines the cell fate.

Alkaline Phosphatase↗
PubMed1998

Influence of calcium on proliferation and phenotype alteration of cardiomyocyte in vitro.

An accelerated weight gain is noted in the heart of Ca-deficient, hypertensive chick embryos maintained in a shell-less culture in vitro. We previously observed that the Ca handling property of cardiomyocytes isolated from the shell-less embryo is altered, i.e., faster Ca uptake, suggesting a requirement for adequate Ca supply and/or proper Ca handling in embryonic cardiac development. In this study, we have examined the function of Ca on cardiomyocytes by analyzing the effects of 1) various Ca concentration in the culture medium (NCa, 1.8 mmol/ L; HCa, 2.8 mmol/L; LCa, 0.9 mmol/L), and 2) various modulators of Ca handling on cell proliferation and phenotype regulation in chick embryonic cardiomyocytes. The analytical parameters included cell number, DNA content, expression of cell cycle-specific and cardiomyocyte-specific proteins, and creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) enzyme activities. Cell number and total DNA were significantly larger (P < 0.01) in LCa cultures compared with those in NCa. The level of LDH was elevated (P < 0.01), but that of CPK was lowered in LCa. Expression of the G1-S-specific protein PCNA was raised, but that of the contractile proteins myosin and tropomyosin was substantially suppressed in LCa; in HCa, the cells did not proliferate as well, whereas the level of contractile proteins was higher. Thapsigargin, a sarcoplasmic reticulum (SR)-specific, Ca-ATPase inhibitor, simulated the effects of LCa by enhancing cell proliferation and lowering the expression of tropomyosin. These results suggest that culturing in low Ca concentration and inhibition of SR Ca pumping enhance myocardial cell proliferation and suppress sarcomeric protein expression, perhaps by inducing cellular de-differentiation. The in vitro effects of medium Ca concentration and Ca handling modulators on cardiomyocytes also suggest that the in vivo cardiomegaly of the SL embryos is a direct result of Ca-deficiency, and that Ca is important in the phenotype regulation of cardiomyocytes.

Animals↗
PubMed1998

Regulation of intracellular calcium concentrations by calcium and magnesium in cardioplegic solutions protects rat neonatal myocytes from simulated ischemia.

The effects of calcium and magnesium ions in cardioplegic solutions on cardioprotection and intracellular calcium ion handling during ischemia and reoxygenation were investigated in cultured neonatal rat myocardial cells. Myocytes were subjected to simulated ischemia for 60 min at 37 degrees C in hyperkalemic cardioplegic solutions containing various concentrations of calcium and magnesium ions, followed by 30 min of reoxygenation. For each Ca2+ concentration (0.1, 0.6, 1.2, or 2.4 mM), the Mg2+ concentration was either 0, 1.2, 8, or 16 mM. The increase in intracellular Ca2+ concentration during ischemia and reoxygenation was suppressed by the addition of magnesium ion, independent of cardioplegic Ca2+ concentration. The recovery of spontaneous contraction rate and enzyme leakage (creatine phosphokinase and lactate dehydrogenase) during both ischemia and reoxygenation correlated with the degree of inhibition of intracellular Ca2+ accumulation. However, in the 0.1 mM Ca2+ groups in which the Mg2+ concentration was greater than 8 mM, the intracellular Ca2+ concentration increased during reoxygenation in a dose-dependent fashion of Mg2+, and was associated with increased enzyme leakage. The findings suggest that in immature cardiac myocytes, the concentrations of Ca2+ and Mg2+ present in cardioplegic solutions control the intracellular Ca2+ concentration during ischemia and reoxygenation, which, in turn, influences the cardioprotective effect of the cardioplegic solution.

Animals↗