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Takayuki Fujita

Publications and source records attributed to Takayuki Fujita.

At least 19 recordsLinked to original sources
PubMed2007

Comparison of 4 MV photon surface dose among Varian, Siemens, and Elekta linear accelerators for tangential breast treatment: a phantom study.

PURPOSE: We have compared the differences in a 4-MV photon surface dose among Varian, Siemens, and Elekta linear accelerators (linacs) with wedges for tangential breast treatment. MATERIALS AND METHODS: The wedge factor and the surface dose were measured using a solid water phantom and an ion chamber for each linear accelerator with various field sizes and wedge angles. A tangential treatment plan was applied to an elliptical hollow cylinder water phantom with a radiochromic film placed thereon. A dose was delivered to a simulated target in the phantom, and the resulting dose distribution was analyzed using a film scanner. RESULTS: Varian's wedges resulted in the highest wedge factors, ranging from 0.37 to 0.75 depending on the wedge angles. Varian's wedges led to the highest normalized skin doses, ranging between 0.40 and 0.73 depending on the wedge angles and field sizes. In the cylinder phantom test with two tangential beams, the Varian linac provided a nearly 20% higher maximum dose than the Siemens and Elekta linacs. CONCLUSION: The Varian linac resulted in the highest surface doses, and the Elekta linac led to the lowest for nearly all the measurement conditions we employed, including open beams.

Breast Diseases↗
PubMed2006

Correction of copper deficiency improves erythropoietin unresponsiveness in hemodialysis patients with anemia.

We have encountered five hemodialysis patients who had received enteral nutrition and recovered from erythropoietin-resistant anemia with neutropenia after the correction of copper deficiency. We reduced the required doses of recombinant human erythropoietin (rHuEPO) to maintain the target hematocrit levels and three patients were finally weaned from the rHuEPO therapy. Thus, copper deficiency is involved in erythropoietin-resistant anemia in hemodialysis patients.

Anemia↗
PubMed2005

Serum mannose-binding lectin levels in maintenance hemodialysis patients: impact on all-cause mortality.

BACKGROUND/AIMS: Mannose-binding lectin (MBL) is characteristic of an acute-phase-reacting protein like C-reactive protein (CRP). However, the prognostic value of the serum MBL level has not been examined. The aim of this study was to evaluate whether the serum MBL level can predict all-cause mortality in hemodialysis (HD) patients. METHODS: A total of 131 patients without active infection, who had been on maintenance HD for at least 2 years, were included in this study. The serum MBL, high-sensitivity CRP (hs-CRP) level, nutrition markers, and biochemical parameters were measured in June 1999. The cohort was then followed prospectively for 36 months, and clinical data were recorded. RESULTS: The MBL level of the 131 HD patients was 9.054 +/- 5.115 microg/ml (mean +/- SD). During the follow-up period, 18 patients (9 males and 9 females) died and 113 (64 males and 49 females) survived. The two leading causes of death were cardiovascular events (n = 6, 33.3%) and infection (n = 4, 22.2%). The serum MBL level was significantly lower among the nonsurvivors (6.596 +/- 4.990 microg/ml) than among the survivors (9.445 +/- 5.046 microg/ml; p < 0.05). There was a significant, although very weak, correlation between the MBL level and albumin level (p < 0.05), but there was no correlationbetween the MBL level and the hs-CRP level. The patients were divided into two groups according to the serum MBL level (< 5 and > 5 microg/ml). Multivariate analysis of factors predicting all-cause mortality in multivariate logistic regression analysis identified a serum MBL level < 5 microg/ml as a variable that independently predicted all-cause mortality (adjusted odds ratio: 7.632; 95% CI: 2.244-25.961; p = 0.0011). Other significant and independent predictors for mortality included the hs-CRP level (every 100 microg/dl increase), hypertension and diabetes mellitus. CONCLUSIONS: Our findings suggest that the serum MBL level is a significant predictor of outcome in HD patients. HD patients with a low level of serum MBL should be carefully monitored.

Adult↗
PubMed2005

[A case of chronic renal failure complicated with tuberculous meningitis successfully diagnosed by nested polymerase chain reaction (PCR)].

A 44 year-old woman was diagnosed as having chronic renal failure due to rapidly progressive glomerulonephritis (RPGN) from one year earlier. She has been managed with steroid therapy and hemodialysis. The patient was admitted to our hospital because of fever and sudden disturbance of consciousness with generalized convulsion on October 30, 2003. She showed mild meningeal irritation. Cerebrospinal fluid (CSF) examination demonstrated a cell count of 60/microl, protein level of 70 mg/dl, glucose level of 52 mg/dl, and chloride (Cl) level of 116 mEq/l. Both the CSF culture for Mycobacterium (M.) tuberculosis and the conventional single polymerase chain reaction (PCR) for M. tuberculosis DNA in CSF were negative results on admission. In contrast, nested PCR of preserved CSF samples obtained at admission demonstrated positive results. We diagnosed her conditions as tuberculous meningitis (TBM) and administered a total of 3 anti-tuberculosis agents over a period of about 2 months. Her clinical condition and CSF examinations improved immediately in response to anti-tuberculosis treatment. Serial CSF cultures for M. tuberculosis and the serial single PCRs for M. tuberculosis DNA in CSF were all negative during the course of anti-tuberculosis treatment. However, serial nested PCR results gradually converted from positive to negative, correlating with the improvement in clinical conditions during the course of anti-tuberculosis treatment. Therefore, nested PCRs were much more useful for the rapid and accurate diagnosis of TBM and for assessment of the clinical course and anti-tuberculosis treatment response of TBM than conventional CSF cultures and single PCRs. To the best of our knowledge, there have been few previous reports of diachronic study in which the serial nested PCR was used to test CSF samples obtained earlier in the clinical course of TBM. In conclusion, our findings suggest that nested PCR for M. tuberculosis DNA in CSF was highly useful not only for rapid and accurate diagnosis of TBM, but also for assessment of the antituberculous treatment response in cases highly suspected of TBM despite negative results on conventional cultures and single PCRs.

Adult↗
PubMed2004

Glomerular deposition and urinary excretion of complement factor H in idiopathic membranous nephropathy.

BACKGROUND/AIMS: The complement system plays an important role in the pathogenesis of membranous nephropathy (MN). In order to elucidate the regulatory mechanism of complement activation, we demonstrated glomerular deposition and urinary excretion of complement factor H, which controls the alternative pathway and the amplification loop at the C3 step, in patients with idiopathic MN. METHODS: Renal biopsy specimens from 20 patients with idiopathic MN were studied immunohistochemically using monoclonal antibodies against complement components including factor H. SDS-PAGE and Western blotting analysis of urine samples were performed, and the urinary excretion of factor H and C5b-9 were measured by quantitative sandwich ELISA. RESULTS: Intense glomerular deposition of factor H was observed with C3b.C3c and C5b-9 at an early stage of the disease. Factor H was detected in Western blots of urine samples, but factor H-like protein 1 (FHL-1) was not. The mean level of urinary factor H was elevated (86.30 +/- 21.93 U/mg urinary creatinine) in comparison to that of normal controls (4.76 +/- 1.03 U/mg urinary creatinine). Urinary factor H level exhibited no correlation with clinical parameters; however, a negative correlation was found between urinary C5b-9/factor H and creatinine clearance (r = 0.662, p < 0.01). CONCLUSION: The source of glomerular and urinary factor H is supposedly a 150-kD protein. There was no evidence to suggest that FHL-1 is synthesized at the site of inflammation. The urinary C5b-9 to urinary factor H ratio is indicative of the degree of ongoing complement activation in the glomeruli and complement-mediated renal injury. These findings suggest that factor H contributes to the control mechanism of in situ complement activation and prevents renal damage in idiopathic MN.

Alternative Splicing↗
PubMed2004

Worsening fluid retention in a patient with hereditary angioedema and end-stage renal disease.

A 60-year-old woman who was diagnosed with hereditary angioedema (HAE) developed nephrotic syndrome, with end-stage renal disease (ESRD) occurring about 2.5 years later. During her slide toward ESRD, she experienced three severe episodes of angioedema that each resulted in significant fluid retention. Though the therapeutic administration of C1-inhibitor concentrate was effective in controlling her angioedema, seemed ineffective in preventing her from developing ESRD requiring hemodialysis treatment. We theorized that the patient's low colloid osmolality and glomerular perfusion were important facilitators of her attacks of angioedema.

Angioedema↗
PubMed2003

Autoimmune hemolytic anemia occurred prior to evident nephropathy in a patient with chronic hepatitis C virus infection: case report.

BACKGROUND: Renal involvement in patients with chronic hepatitis C virus infection has been suggested to be due to a variety of immunological processes. However, the precise mechanism by which the kidneys are damaged in these patients is still unclear. CASE PRESENTATION: A 66 year old man presented with the sudden onset of autoimmune hemolytic anemia. Concomitant with a worsening of hemolysis, his initially mild proteinuria and hemoglobinuria progressed. On admission, laboratory tests revealed that he was positive for hepatitis C virus in his blood, though his liver function tests were all normal. The patient displayed cryoglobulinemia and hypocomplementemia with cold activation, and exhibited a biological false positive of syphilic test. Renal biopsy specimens showed signs of immune complex type nephropathy with hemosiderin deposition in the tubular epithelial cells. CONCLUSIONS: The renal histological findings in this case are consistent with the deposition of immune complexes and hemolytic products, which might have occurred as a result of the patient's underlying autoimmune imbalance, autoimmune hemolytic anemia, and chronic hepatitis C virus infection.

Aged↗
PubMed2003

Nicotinic acetylcholine receptor alpha 7 regulates cAMP signal within lipid rafts.

Neuronal nicotinic acetylcholine receptors (nAChRs) are made of multiple subunits with diversified functions. The nAChR alpha 7-subunit has a property of high Ca2+ permeability and may have specific functions and localization within the plasma membrane as a signal transduction molecule. In PC-12 cells, fractionation by sucrose gradient centrifugation revealed that nAChR alpha 7 existed in low-density, cholesterol-enriched plasma membrane microdomains known as lipid rafts where flotillin also exists. In contrast, nAChR alpha 5- and beta2-subunits were located in high-density fractions, out of the lipid rafts. Type 6 adenylyl cyclase (AC6), a calcium-inhibitable isoform, was also found in lipid rafts and was coimmunoprecipitated with nAChR alpha 7. Cholesterol depletion from plasma membranes with methyl-beta-cyclodextrin redistributed nAChR alpha 7 and AC6 diffusely within plasma membranes. Nicotine stimulation reduced forskolin-stimulated AC activity by 35%, and this inhibition was negated by either treatment with alpha-bungarotoxin, a specific antagonist of nAChR alpha 7, or cholesterol depletion from plasma membranes. The effect of cholesterol depletion was negated by the addition of cholesterol. These data suggest that nAChR alpha 7 has a specific membrane localization relative to other nAChR subunits and that lipid rafts are necessary to localize nAChR alpha 7 with AC within plasma membranes. In addition, nAChR alpha 7 may regulate the AC activity via Ca2+ within lipid rafts.

Adenylyl Cyclases↗
PubMed2003

Ischemic preconditioning prevents ischemia-induced beta-adrenergic receptor sequestration.

Preconditioning enables endogenous protection to repeated myocardial ischemia. However, the effect of preconditioning on beta1 adrenergic receptor (AR) signal remains controversial. We have recently developed receptor assay system using whole cells, in which overexpressed cell surface beta ARs can be readily quantitated without disrupting the cell. Using this technique, we examined the effects of chemical/metabolic ischemia on the beta1 AR sequestration and adenylyl cyclase activity. Isoproterenol treatment, but not forskolin treatment, of HEK293T cells overexpressing beta1 ARs led to a rapid decrease (within 2 hours) in the number of the cell surface receptor, which was negated in the presence of concanavalin A. Similarly, treatment of cells with potassium cyanide and 2-deoxy-D-glucose (chemical/metabolic ischemia) induced similar receptor sequestration. When isoproterenol was superimposed on chemical/metabolic ischemia, the degree of sequestration became greater. However, when cells were pre-exposed to potassium cyanide on the preceding day (chemical preconditioning), the sequestration induced by either isoproterenol or chemical/metabolic ischemia was attenuated. Adenylyl cyclase catalytic activity as assessed by stimulation with forskolin was decreased by chemical/metabolic ischemia but fully recovered after 24 hours, suggesting that chemical/metabolic ischemia treatment did not alter cell viability. Putting together, chemical/metabolic ischemia induced beta1 AR sequestration in a similar manner to isoproterenol. In addition, preconditioning prevented the beta1 AR sequestration induced by both isoproterenol and chemical/metabolic ischemia. Pre-conditioning may play a role in preserving the cell surface beta ARs by inhibiting the sequestration that is usually induced by an ischemic event or beta adrenergic stimulation.

Adenylyl Cyclases↗
PubMed2003

Lipoxygenase products regulate nitric oxide and inducible nitric oxide synthase production in interleukin-1beta stimulated vascular smooth muscle cells.

In cultured vascular smooth muscle cells (VSMCs), interleukin-1beta (IL-1beta) stimulates inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production. IL-1beta also activates phospholipase A2 (PLA2), and induces lipoxygenase (LOX) and cyclooxygenase-2 (COX-2). The present study investigated whether these metabolites are involved in the regulation of IL-1beta-induced NO production and iNOS expression. Pretreatment with ONO-RS-082, the secretory PLA2 (sPLA2) inhibitor, at 1 to 10 micromol/l reduced IL-1beta-stimulated nitrite production and iNOS expression. Nordihydroguaiaretic acid (NDGA, 1 to 10 micromol/l), the LOX inhibitor, also reduced IL-1beta (10 ng/ml)-stimulated nitrite production and iNOS expression in a dose-dependent manner. Exogenous 12(S)-hydroxyeicosatetraenoic acids (HETE) enhanced the IL-1beta-stimulated nitrite production and iNOS expression. On the other hand, the COX inhibitors, indomethacin and NS-398, had little effect on nitrite production or iNOS expression. These results suggest that LOX products play important roles in the regulation of stimulus-induced NO production in VSMCs.

Aminobenzoates↗
PubMed2003

Characterization of beta-adrenergic receptor sequestration by newly developed whole cell binding assays.

Upon agonist binding, beta-adrenergic receptors sequestrate from the cell surface plasma membrane to cytosol. In the present study, we examine the kinetics of sequestration of beta1-adrenergic receptor and beta3-adrenergic receptor subtypes by radioligand binding assays using whole cells ('whole cell binding assays'). We found that HEK293T cells, but not COS1 cells, were readily and uniformly detached from the culture dish upon exposure to ice-cold phosphate-buffered saline. Using this property of HEK293T cells, we conducted whole cell binding assays using a hydrophilic antagonist ([3H]CGP-12177) and HEK293T cells transiently overexpressing human beta1-adrenergic receptor or beta3-adrenergic receptor. The Bmax and Kd values were 5.96 +/- 0.97 pmol/mg protein and 1 +/- 0.23 nM for the beta1-adrenergic receptor, and were 1.84 +/- 0.13 pmol/mg protein and 44.7 +/- 2.5 nM for the beta3-adrenergic receptor, respectively. Isoproterenol treatment, but not 6-[3-(dimethylamino)propionyl]forskolin treatment, for 2 h resulted in a dose-dependent loss of the number of the cell surface beta1-adrenergic receptor. At 100 microM, 36.6 +/- 5.7% of the cell surface beta1-adrenergic receptor was lost. In contrast, the cell surface beta3-adrenergic receptor number remained unchanged with isoproterenol treatment. Thus, beta1-adrenergic receptor sequestrates upon agonist stimulation but the same agonist stimulation does not induce beta3-adrenergic receptor sequestration, as demonstrated by our whole cell binding assays.

Animals↗
PubMed2002

Significant elevations in serum mannose-binding lectin levels in patients with chronic renal failure.

BACKGROUND/AIMS: Mannose-binding lectin (MBL), a liver-derived C-type serum lectin, activates the complement cascade through the lectin pathway. Since the complement system contributes to the host defense against infections and mediates inflammatory processes including atherosclerosis, and since chronic renal failure (CRF) patients are prone to the development of infectious complications and cardiovascular disease, we focused on serum MBL levels in CRF patients who were either uremic, or who were receiving hemodialysis treatment. METHODS: MBL levels were measured in the sera of subjects with CRF before they began dialysis treatment (pre-HD patients; n = 23) and in the sera of subjects who were receiving maintenance hemodialysis (HD patients; n = 178), by ELISA using polyclonal anti-rabbit IgG and a monoclonal antibody directed against MBL (3E7). METHODS: Mean levels (+/- SD) of serum MBL were significantly higher in pre-HD subjects (4.343 +/- 2.533 microg/ml, p < 0.05) and in HD subjects (8.897 +/- 4.920 microg/ml, p < 0.05), than in healthy controls (1.452 +/- 0.692 microg/ml). Levels were also significantly higher in HD subjects than in pre-HD subjects (p < 0.05). CONCLUSIONS: Elevated serum MBL levels in patients with CRF might have significantly influence pathologic conditions such as alterations of the immune system and acceleration of atherogenesis.

Adult↗
PubMed2002

Urinary complement factor H in renal disease.

BACKGROUND: Complement factor H (hCFH) plays a key inhibitory role in the control of the alternative complement pathway. We examined whether urinary hCFH (U-hCFH) levels is useful as an indirect indicator of renal damage. METHODS: Urine samples were obtained from 104 patients with renal disease. Urine was collected with 10 mM EDTA and U-hCFH levels were measured using the BTA TRAK Assay Kit. RESULTS: In the 62 patients with nephritis, the levels of U-hCFH were elevated (range 15-52,198 U/ml) over the normal range (0-14 U/ml). U-hCFH levels of patients with chronic renal failure, lupus nephritis, membranoproliferative glomerulonephritis, focal glomerulosclerosis were higher than that of IgA nephropathy patients (p < 0.05). In the patients with minimal change disease, showed high levels of U-hCFH during the nephrotic syndrome. U-hCFH was correlated significantly with urinary protein and urinary N-acetyl-beta-D-glucosaminidase. CONCLUSIONS: We demonstrated that U-hCFH was detected in the urine of nephritis patients.

Biomarkers↗
PubMed2002

Nephrotic syndrome with portal, splenic and renal vein thrombosis. A case report.

BACKGROUND: Thromboembolism is known as a major complication of nephrotic syndrome, but only 4 cases of portal vein thrombosis have been reported as a complication of nephrotic syndrome. All of these 4 cases had acute symptoms, and 3 of 4 were in relapsing phase of nephrotic syndrome when thrombi were found. We describe here a case of 51-year-old woman with fresh nephrotic syndrome that was asymptomatically complicated by portal, splenic and renal vein thrombosis. CONCLUSIONS: In the presence of fresh nephrotic syndrome of minimal change, asymptomatic and widely distributed, including portal vein, thrombus formation occurred. If the clinical course shows resistance to therapy, we must consider the complication of venous thrombosis. Anticoagulant therapy with heparin and warfarin was effective and all thrombi disappeared without any other complications.

Acute Disease↗