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Biomedical subjects

Kenichi Yamada

Publications and source records attributed to Kenichi Yamada.

At least 19 recordsLinked to original sources
PubMed2006

Brain developmental abnormalities in Prader-Willi syndrome detected by diffusion tensor imaging.

OBJECTIVE: The purpose of this work was to detect brain developmental abnormalities in Prader-Willi syndrome by using diffusion tensor imaging based on a high-field MRI system. METHODS: Eight patients with Prader-Willi syndrome and 8 age- and gender-matched normal control subjects were examined using a high-field (3.0 T) MRI system. Trace value and fractional anisotropy were assessed simultaneously in multiple representative brain regions: the deep gray matter (putamen, caudate head, and dorsomedial thalamus) and the white matter structures (frontal and parietal white matter, posterior limb of internal capsule, and corpus callosum). RESULTS: In Prader-Willi syndrome patients, trace value was found to be significantly higher in the left frontal white matter and the left dorsomedial thalamus, whereas fractional anisotropy was significantly reduced in the posterior limb of the internal capsule bilaterally, the right frontal white matter, and the splenium of the corpus callosum. The observed diffusivity characteristics indicate developmental abnormalities in these areas, which are highly consistent with the clinical features of Prader-Willi syndrome. CONCLUSIONS: The study provides the first objective evidence that Prader-Willi syndrome patients indeed have developmental abnormalities in specific areas of the brain, providing a new window toward understanding the pathophysiology of Prader-Willi syndrome.

Adolescent↗
PubMed2006

Rupture of a normal-sized, non-dissected distal aortic arch in a Marfan patient.

We successfully repaired a rupture of a normal-sized, non-dissected distal aortic arch in a patient with Marfan syndrome. Six years previously she had undergone repair of the thoraco-abdominal aortic aneurysm with a 24-mm knitted Dacron graft for type B chronic aortic dissection. The rupture site was located at the back of the native distal aortic arch just 10 mm above the proximal anastomosis, and just below the left subclavian artery. This unexpected situation might be related to dilatation of the knitted Dacron graft up to 34 mm (142%), thus stretching out the fragile native aorta in this Marfan patient.

Adult↗
PubMed2005

Thioredoxin-1 suppresses lung injury and apoptosis induced by diesel exhaust particles (DEP) by scavenging reactive oxygen species and by inhibiting DEP-induced downregulation of Akt.

Diesel exhaust particles (DEP) are reactive oxygen species (ROS)-inducing toxic agents that damage lungs. Thioredoxin-1 (Trx-1) is a thiol protein with antioxidant and redox-regulating effects. In this study, we demonstrate that Trx-1 scavenges ROS generated by DEP and attenuates the lung injury. Intratracheal instillation of DEP resulted in the generation of more hydroxyl radicals in control mice than in human Trx-1 (hTrx-1)-transgenic mice as measured by noninvasive L-band in vivo electron spin resonance. DEP caused acute lung damage with massive infiltration of inflammatory cells in control mice, but much less damage in hTrx-1-transgenic mice. The hTrx-1 transgene protected the mice against DEP toxicity. To investigate further the molecular mechanism of the protective role of Trx-1 against DEP-induced lung injury, we used hTrx-1-transfected L-929 cells and recombinant hTrx-1 (rhTrx-1)-pretreated A-549 cells. DEP-induced ROS generation was suppressed by hTrx-1 transfection or pretreatment with rhTrx-1. Endogenous Trx-1 expression was induced by DEP in control cells. The downregulation of Akt phosphorylation by DEP resulted in apoptosis, which was prevented by Trx-1. Moreover, an Akt inhibitor canceled this protective effect of Trx-1. Collectively, the results suggest that Trx-1 exerts antioxidant effects in vivo and in vitro and that this plays a role in protection against DEP-induced lung damage by regulating Akt-mediated antiapoptotic signaling.

Animals↗
PubMed2005

[Personal exposures of benzene treated workers and a simple biological monitoring].

A simple method of biological monitoring has been developed for occupational benzene exposure. Personal benzene exposure monitoring using a passive sampler and GC/FID was carried out on 74 workers from a benzene-treated company. Their urines were collected before and after work-shift. After treatment of urine samples using solid phase extraction (SPE), trans, trans-muconic acid(t, t-MA) concentration in the elute was analysed by HPLC. Correlation between benzene exposure (X: ppm) and urinary t, t-MA concentration (Y: mg/g x creatinine) for non-smokers was Y = 0.948X + 0.586 (r = 0.798, P < 0.01) and Y = 0.885X + 0.894 (r = 0.871, P < 0.01) for smokers, respectively. The t, t-MA concentration on 1 ppm TLV exposure to benzene was estimated as 1.5 and 1.8 (mg/g creatinine) for non-smokers and smokers, respectively. These values are in agreement with some investigators. This indicates that our simple method for biological monitoring of benzene exposure can be of great service.

Acetylcysteine↗
PubMed2005

Effects of muscle potential depression and muscle stimulation caused by different insulation coating configurations on cardiac pacemakers.

Insulation coating was added to the external pacemaker surface to prevent unnecessary electric current leakage to the periphery because the pulse generator body is used as an anode in unipolar pacing. However, a model without insulation coating has recently been used, so we studied the effects on muscle potential inhibition and muscle stimulation of pacemakers in unipolar pacing with different parts of the pacemaker body coated with insulation. Case comparisons were made for the following models: insulated except for the center of one side (33, group C), insulated except for the peripheral zone (10, group E), and noncoated models (11, group N). The muscle detection threshold voltage, muscle detection threshold pulse duration, muscle potential sensing threshold (MP), and lead resistance were measured. A comparison was made of the amount of energy (En) needed to reach the muscle stimulation threshold. For MP values, there was no significant statistical difference between group C and E, whereas a significant difference was present between group C and N and between group E and N. For En values, there was a significant difference between group C and E and between group C and N, but there was no significant difference between group E and N. The muscle potential sensing threshold dose not have a change in group E and much muscle stimulation energy is needed. The muscle potential sensing threshold was low in group N, requiring much muscle stimulation energy. Based on these results, it is usually not necessary to coat the pacemaker with insulation for unipolar pacing.

Aged↗
PubMed2004

Induction of uPA release in human peripheral blood lymphocytes by [deamino-Cysl,D-Arg8]-vasopressin (dDAVP).

[deamino-Cys(l),d-Arg(8)]-vasopressin (dDAVP), known to be an arginine vasopressin (AVP) V(2) receptor agonist, is an agent that increases fibrinolytic activity levels in plasma after its infusion into the human body. However, mechanisms underlying an increase and exact localization of the extrarenal dDAVP-responsive V(2) receptor remain unclarified. Two AVP receptors, V(1a) and V(2), and a related oxytocin (OT) receptor were found to be expressed in human lymphocytes. Furthermore, we found an increase of fibrinolytic activity in the medium of peripheral lymphocytes obtained from human volunteers less than 20 min after dDAVP infusion. The increased activity was also detected in the medium after incubating the lymphocytes in the presence of dDAVP in vitro, being highest at 20 min after the incubation. In accord with the increased fibrinolytic activity, the levels of urokinase-type plasminogen activator (uPA) in the medium were also increased. However, there was no significant difference of plasminogen activator inhibitor-1 (PAI-1), pro-uPA, and tissue-type plasminogen activator (tPA) concentrations in the medium between dDAVP treatment and control. When lymphocytes were preincubated with a V(2) receptor antagonist [Adamantaneacetyl(1),O-Et-d-Tyr(2),Val(4),Aminobutyryl(6),Arg(8,9)]-vasopressin, the dDAVP-induced uPA increase was diminished. In contrast, preincubation with a V(1) receptor antagonist, [beta-Mercapto-beta,beta-cyclopentamethylenepropionyl(1),O-Me-Tyr(2),Arg(8)]-vasopressin, prior to dDAVP treatment resulted in a greater increase of the uPA concentration in the medium than with the dDAVP treatment alone. Thus it was suggested that dDAVP may induce uPA release from human lymphocytes via V(2) receptor-mediated reaction, and also via cross-talk between V(1) and V(2) receptors.

Arginine Vasopressin↗
PubMed2004

Factors influencing nitroxide reduction and cytotoxicity in vitro.

Nitroxides have been shown to be effective antioxidants, radiation protectors, and redox-active probes for functional electron paramagnetic resonance (EPR) imaging. More recently, the nitroxide 4-hydroxy-2,2,6,6-tetramethylpiperidinyl-N-oxyl (Tempol) has been shown to exert differential cytotoxicity to tumor compared with normal cell counterparts. Nitroxides are readily reduced in tissues to their respective hydroxylamines, which exhibit less cytotoxicity in vitro and do not provide radiation protection or an EPR-detectable signal for imaging. In order to better understand factors that influence nitroxide reduction, the rate of reduction of Tempol in mouse and human cell lines and in primary cultures of tumor cells was measured using EPR spectroscopy. Additionally, the cytotoxicity of high concentrations of Tempol and the hydroxylamine of Tempol (Tempol-H) was evaluated in wild-type and glucose-6-phosphate dehydrogenase (G6PD)-deficient Chinese hamster ovary cells. The results show that in general Tempol was reduced at a faster rate when cells were under hypoxic compared with aerobic conditions. Neither depletion of intracellular glutathione nor treatment of cells with sodium cyanide influenced Tempol reduction rates. G6PD-deficient cells were found to reduce Tempol at a significantly slower rate than wild-type cells. Likewise, Tempol-induced cytotoxicity was markedly less for G6PD-deficient cells compared with wild-type cells. Tempol-H exhibited no cytotoxicity to either cell type. Tempol-mediated cytotoxicity was enhanced by glutathione depletion and inhibition of 6-phosphogluconate dehydrogenase in wild-type cells, but was unaltered in G6PD-deficient cells. Collectively, the results indicate that while the bioreduction of Tempol can be influenced by a number of factors, the hexose monophosphate shunt appears to be involved in both nitroxide reduction as well as cytotoxicity induced by high levels of exposure to Tempol.

Animals↗
PubMed2004

Relationship between NMF (lactate and potassium) content and the physical properties of the stratum corneum in healthy subjects.

Natural moisturizing factor (NMF) of the stratum corneum (SC) has been established to play important roles in the physical properties of the SC. Few studies, however, have investigated the specific influences of NMF components other than the amino acids. In this study, therefore, we focus on the relationship between the ion content and physical properties of the SC in 40 healthy subjects. Changes in the physical properties of the SC induced by the extraction of NMF were equivalent to the changes that took place from summer to winter, demonstrating the important role of NMF in the physical properties of the SC in healthy subjects. The seasonal changes in the physical properties of the SC from summer to winter were accompanied by significant decreases in the levels of lactate, potassium, sodium, and chloride in the SC. Lactate and potassium were the only components found to correlate significantly with the state of hydration, stiffness, and pH in the SC. Interestingly, the levels of lactate and potassium in the SC were also significantly correlated. Moreover, potassium lactate restored the SC hydration state decreased by extraction of NMF. These results suggest that lactate and potassium may play roles in maintaining the physical properties of the SC in healthy subjects.

Adult↗
PubMed2004

Oxidative stress is enhanced in correlation with renal dysfunction: examination with the redox state of albumin.

BACKGROUND: Cardiovascular disease is known to be the most important complication among patients with renal failure, and oxidative stress has been proposed to play a major role as the source of such complications. Human serum albumin (HSA) is composed of human mercaptoalbumin (HMA) with cysteine residues having reducing powers, of reversibly oxidized human non-mercaptoalbumin-1 (HNA-1), and strongly oxidized human non-mercaptoalbumin-2 (HNA-2). METHODS: We used the "redox state of HSA" as a marker to investigate the current status of oxidative stress in predialysis patients with renal failure. The subjects were 55 nondialysis patients (31 males and 24 females) with chronic renal diseases, and having various degrees of renal function. The subjects' redox state of HSA was determined by a high-performance liquid chromatographic (HPLC) procedure, and the results presented in terms of the ratios between HNA-total(HNA-1 + HNA-2) and HNA-2. RESULTS: The values for each fraction of HNA-total (f(HNA-total)) and f(HNA-2) were increased with a decrease of renal functions, and a significant positive correlation with serum creatinine (R= 0.529, P < 0.0001 and R= 0.618, P < 0.0001) was detected. Multiple (forward stepwise) regression analysis using f(HNA-total) and f(HNA-2) as the criterion variables was performed, and creatinine was adopted as significant explanatory variable in both equations. CONCLUSION: We found that even before dialysis, oxidative stress was enhanced in correlation with the level of renal dysfunction among patients with chronic renal failure. In the future, antioxidant strategies should become part of treatment for predialysis renal failure.

Adult↗
PubMed2004

Renoprotective effect of losartan in comparison to amlodipine in patients with chronic kidney disease and hypertension--a report of the Japanese Losartan Therapy Intended for the Global Renal Protection in Hypertensive Patients (JLIGHT) study.

A 12-month, multicenter (57 clinical institutions), randomized, open-labeled trial was undertaken to compare the efficacy of the angiotensin II receptor antagonist losartan and the calcium channel blocker amlodipine in patients with proteinuric chronic kidney disease (CKD) and hypertension. A total of 117 patients (79, chronic glomerulonephritis; 14, diabetic nephropathy; 24, other CKD) were randomly allocated into two treatment groups. Losartan and amlodipine exerted the same efficacy for blood pressure (BP) control; however, losartan significantly reduced the 24-h urinary protein excretion at months 3, 6, and 12, with the reduction of 20.7%, 35.2%, 35.8%, whereas amlodipine did not change the amount of proteinuria over the 12-month study period. When patients were stratified into groups according to the level of BP control at 3 months, the reduction in urinary protein excretion by losartan was evident in the group for which a BP of <140/90 mmHg was achieved, as well as in the group for which the goal BP (<130/85 mmHg) for treatment of CKD was not achieved. When patients were stratified according to baseline urinary protein excretion, those with > or = 2 g/day showed a reduction in proteinuria by losartan of 23.3%, 39.4%, and 47.9% at months 3, 6, and 12, and those with <2 g/day showed a reduction of 18.5% and 31.2% at months 3 and 6, respectively. No fatal adverse events were experienced in either drug group. We conclude that losartan reduced proteinuria in patients with CKD and hypertension. This positive effect may contribute to the renal protective benefit of losartan, and is beyond the magnitude of BP control.

Aged↗
PubMed2003

Prediction of chronic renal allograft dysfunction from evaluations of TGFBeta1 and the renin-angiotensin system.

BACKGROUND: Growth factors, cytokines, and the renin-angiotensin system (RAS) are involved in chronic allograft dysfunction. However, it is unclear whether clinical evaluations of TGFBeta1 and the RAS in longterm stable transplant patients can predict the development of chronic allograft dysfunction. METHODS: Urinary TGFBeta1 excretion and the response of plasma renin activity (PRA) to angiotensin I converting-enzyme inhibition (ACE-I) were prospectively examined in transplant patients who had had stable graft function (n = 16) for at least 1 year after renal transplantation. Four-year follow-up studies were undertaken to evaluate the impact of these parameters on the development of chronic allograft dysfunction. RESULTS: Urinary TGFBeta1 excretion and PRA response to ACE-I in renal transplant patients who developed chronic allograft nephropathy 4 years after the evaluations (n = 7) were significantly higher and greater, respectively, than these values in those who did not ( n = 9; P < 0.01). If the cutoff level for urinary TGFBeta1 excretion was 250 pg/min, the 4-year positive predictive value (PPV) with respect to the development of chronic allograft nephropathy was 83% and the negative predictive value (NPV) was 78% (sensitivity [sen.], 71%; specificity [sp.], 88%). If the cutoff level for PRA at 60 min after ACE-I was 4.0 ng/ml per h, the 4-year PPV was 71% and NPV was 75% (sen., 70%; sp., 75%). The stable transplant patients with high TGFBeta1 excretion and exaggerated PRA response showed significantly higher rates of chronic allograft dysfunction than those with low TGFBeta1 excretion and weak PRA response. CONCLUSIONS: This study demonstrates that some transplant patients with longterm stable graft function show increases in the activities of the TGFBeta system and the RAS. Evaluations of urinary TGFBeta1 excretion and PRA response to ACE-I present a possibility for predicting the development of chronic allograft dysfunction, with significant 4-year predictive values.

Adrenergic alpha-Antagonists↗
PubMed2003

Interim evidence of the renoprotective effect of the angiotensin II receptor antagonist losartan versus the calcium channel blocker amlodipine in patients with chronic kidney disease and hypertension: a report of the Japanese Losartan Therapy Intended for Global Renal Protection in Hypertensive Patients (JLIGHT) Study.

BACKGROUND: Insufficiency of renal function and high blood pressure influence each other and eventually result in life-threatening endstage renal disease. It has been proposed that proteinuria per se is a determinant of the progression of chronic kidney disease (CKD). The therapeutic strategy for patients with proteinuric CKD and hypertension should therefore be targeted with a view not merely toward blood pressure reduction but also toward renoprotection. METHODS: We examined the effect of the angiotensin (AT)1 receptor antagonist losartan and the calcium channel blocker amlodipine, throughout a period of 12 months, on reduction of blood pressure and renoprotection. This was done by assessing amounts of urinary protein excretion, serum creatinine (SCr), and creatinine clearance (CCr) in patients with hypertension (systolic blood pressure [SBP] > or = 140 mmHg or diastolic blood pressure [DBP] > or = 90 mmHg) and CKD (male, body weight [BW] > or = 60 kg: 1.5 < or = SCr < 3.0 mg/dl; female or male BW < 60 kg: 1.3 < or = SCr < 3.0 mg/dl), manifesting proteinuria of 0.5 g or more/day. Losartan was administered once daily at doses of 25 to 100 mg/day, and amlodipine was given once daily at 2.5 to 5 mg/day. No antihypertensive combination therapy was allowed during the first 3-month period. RESULTS: A 3-month interim analysis revealed that, despite there being no difference in blood pressure between the two groups, there was a significant reduction in 24-h urinary protein excretion in the losartan group ( n = 43), but there was no change in the amlodipine group ( n = 43). Analysis of stratified subgroups with proteinuria of 2 g or more/day and less than 2 g/day showed that losartan lowered proteinuria by approximately 24% in both subgroups, while amlodipine lowered proteinuria by 10%, but only in the subgroup of less than 2 g/day (NS). SCr and CCr did not change throughout the period of 3 months in either group. No severe or fatal adverse event was experienced in either group during the study period. CONCLUSIONS: Losartan appeared to be efficacious for renoprotection in patients with proteinuric CKD and hypertension, with the mechanism being independent of its antihypertensive action.

Adult↗
PubMed2003

Coronary artery bypass grafting without cardiopulmonary bypass: a five-year experience.

The current drive to practice less invasive surgery is changing surgical practice towards safer and simpler procedures. The practice of coronary artery bypass grafting (CABG) on a beating heart without cardiopulmonary bypass (CPB), off-pump CABG or OPCAB, has been gaining great attention as an alternative approach to conventional CABG. Since the first adoption of OPCAB in 1997 at our department, 181 patients have undergone OPCAB. OPCAB was indicated for patients who were possibly at risk for CPB, i.e., those who were elderly, who had a history of cerebrovascular disease, whose ascending aorta was severely atherosclerotic with calcification, whose respiratory function was compromised, or whose renal function was compromised. A patient with a concomitant malignant neoplastic disorder was also a candidate for OPCAB because of the possible deleterious effect of CPB on the immune system. More recently, when the coronary anatomy was suitable for OPCAB, even in younger or less risky patients, OPCAB was indicated. The OPCAB procedure was performed through a median sternotomy in 146 patients (80.6%), a left thoracotomy in 27 (14.9%), a subxiphoid approach in 6 and a combined one in 2. One hundred and eleven patients (61.3%) received 1 or 2 grafts (Group I) and 70 (38.7%) received 3 or more grafts (Group II). The number of grafted vessels in Group II patients was 3 to 5 with a mean of 3.44. The mean operative time was 163 minutes in Group I and 209.5 minutes in Group II. The frequency of the use of arterial grafts such as LITA, RITA and RA was significantly higher in Group II than in Group I. Death occurred in 3 patients with acute coronary syndrome who had to undergo urgent surgery. Angiographic examination was performed within 3 months, postoperatively, in 98 patients (54.1%) revealing the overall patency rate of each graft: LITA82/83 (98.8%), RITA 33/33 (100%), GEA 15/16 (93.8%), RA 20/20 (100%), and SVG 15/16 (93.8%). We conclude that, in light of our 5-year experience, off-pump CABG on a beating heart can be safely and effectively performed, with acceptable angiographic results even in patients with multi-vessel coronary disease requiring multiple revascularization. This procedure enables us to perform successful coronary bypass surgery for those who otherwise would not have been candidates for conventional CABG.

Aged↗