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Biomedical subjects

R Nakamura

Publications and source records attributed to R Nakamura.

At least 55 records · Page 3Linked to original sources

Chemoradiotherapy followed by surgery for thoracic esophageal cancer potentially or actually involving adjacent organs.

The objective of this study was to evaluate the therapeutic usefulness of chemoradiotherapy (CRT) followed by surgery in patients with clinically T4 (cT4) esophageal cancer involving adjacent organs such as the trachea, main bronchi, and large vessels. Thirty-seven patients with cT4 squamous cell carcinoma of the thoracic esophagus were enrolled in this study. The CRT regimen comprised cisplatin (70 mg/m2) on day 1, 5-fluorouracil (700 mg/m2) on days 1-4 and external irradiation (200 cGy/day, total 30 Gy) on either days 8-26 (sequential schedule, n=15) or days 1-19 (concurrent schedule, n022). Two courses of CRT were given. The results of CRT were complete response in nine patients, partial response in 19, no change in three (minor response in two), and progressive disease in six patients. The median response duration in all responders was 172 days (range: 56-2469, n=19). After CRT, 13 patients received surgery. In 12 of these patients, tumors were completely resected. Histopathologic examination of the resected specimen revealed a discrepancy between clinical response and histopathologic effect. The median duration of survival and the 1-, 2- and 5-year survival rates were 304 days (84-3155), 45%, 35% and 23% in all patients, respectively, 866 days (190-3155), 83%, 83% and 57% in the 13 patients whose tumors were resected, and 187 days (84--2630), 25%, 5% and 5% in the 24 patients whose tumors were not resected. Grade 3 toxicity, especially hematological reactions, was noted in 13.5% (5/37) of the patients. There was one toxicity-related death (sepsis). A good outcome may be obtained with CRT, followed by surgery when feasible. However, CRT can cause toxic reactions, and close monitoring of patients is required.

Aged↗

Histologic analysis of the tibial bone tunnel after anterior cruciate ligament reconstruction using solvent-dried and gamma-irradiated fascia lata allograft.

Anterior cruciate ligament (ACL) reconstruction using free tendon graft requires biologic fixation in the bone tunnel. This report describes the intratunnel histology retrieved from a 47-year-old woman who underwent high tibial osteotomy 17 months after ACL reconstruction using a hybrid graft (a solvent-dried and gamma-irradiated fascia lata allograft as a core wrapped with iliotibial autograft). The patient underwent revision because of pain resulting from osteoarthrotic change, and the graft appeared to be taut and healthy on second-look arthroscopy. The sample was taken from the site of the metaphyseal osteotomy site. Histologic examination of the samples was performed with a light microscope (H&E and Masson trichrome stain). Biologic fixation of the graft to the bone was evident from observation of collagen fiber continuities, resembling Sharpey fibers. Integration of the autograft and allograft seemed to have occurred; the junction between the allograft and the autograft could not be determined. However, there was a difference in ligamentization depending on location. In the peripheral region of the graft (the autograft region), the collagen fibers showed a distinct crimped pattern; the fibroblasts were arranged regularly along the major axis of the collagen fiber bundle. In the central part of the graft (the allograft region), remodeling seemed to be delayed. There were acellular, bubbly or myxoid degeneration areas in which the fiber bundles were less oriented and there was increased vascularity.

Anterior Cruciate Ligament↗

Role of intraoperative insulin monitoring in surgical management of insulinoma.

BACKGROUND AND PURPOSE: Precise localization and surgical excision is the therapeutic strategy for insulinomas. However, it is often difficult to localize the insulinomas, because of their small size. Surgeons may not localize and remove all of them together, particularly in patients with multiple insulinomas. We reviewed our experience to confirm the efficacy of blood glucose and intraoperative immunoreactive insulin (IRI) monitoring for surgical management of insulinomas. PATIENTS AND METHODS: Thirty-nine patients with insulinoma were surgically treated in our department. Perioperative blood glucose monitoring was performed in 14 patients, intraoperative quick IRI assay of the peripheral blood in 10 patients, and assay of a portal sample in 4 patients by an IMX analyzer. RESULTS: Rebound response of blood glucose to insulinoma removal was not always noted (8/14; 57%). Seven of ten patients showed a decrease of peripheral serum IRI levels within 15 minutes after removal of the insulinoma. The other two patients showed a rebound response of peripheral blood glucose or portal IRI. All the patients who had intraoperative monitoring of peripheral blood and peripheral and portal IRI had no recurrent insulinoma syndrome after surgical removal of their insulinomas. CONCLUSION: Combined monitoring of peripheral blood glucose and peripheral and portal IRI are helpful in the surgical management of insulinomas, as they can indicate that no insulinoma remains.

Adolescent↗

Independent predictors of restenosis after percutaneous coronary revascularization in haemodialysis patients.

BACKGROUND: Percutaneous balloon angioplasty has become a well-established and routine procedure for coronary revascularization of haemodialysis patients with coronary artery disease. However, the incidence of restenosis after balloon angioplasty is significantly higher in haemodialysis patients than in the general population. We performed a retrospective study comparing balloon angioplasty with coronary stenting in haemodialysis patients. We evaluated the long-term clinical and angiographic outcome after successful percutaneous coronary revascularization in haemodialysis patients. METHODS: A total of 103 consecutive haemodialysis patients (123 lesions) underwent procedurally and clinically successful percutaneous revascularization. Patients were treated with three different strategies: (i) balloon angioplasty in 55 patients (69 lesions); (ii) coronary stenting with balloon angioplasty in 23 patients (25 lesions); and (iii) coronary stenting with rotational atherectomy in 25 patients (29 lesions) who had severely calcified stenotic coronaries. RESULTS: The rates of in-hospital mortality were similar in the three groups. The 1-year incidence of overall events and major adverse cardiac events (MACE) were significantly higher in the balloon group than in the stent with/without rotational atherectomy groups (75% vs 36 and 28%, P<0.01; 71% vs 32 and 28%, P<0.01). Use of coronary stenting (relative risk=0.006, P<0.001) and the presence of calcified coronary lesion (relative risk=68.2, P<0.001) were independent predictors of the 1-year MACE-free survival after percutaneous revascularization. The 3-year MACE-free survival rate was significantly lower in the balloon group than in the stent with/without rotational atherectomy groups (11% vs 33 and 47%, P<0.005 and P<0.001). CONCLUSIONS: This study shows that coronary stenting reduces the incidence of MACE in haemodialysis patients with/without calcified coronary lesions. Moreover, coronary stenting reduces the restenosis rate of both complex and restenotic lesions, and rotational atherectomy prior to coronary stenting reduces the restenosis rate of the severely calcified coronary lesions. These results suggest that coronary stenting with/without rotational atherectomy has led to an improved long-term outcome in the haemodialysis patients with coronary artery disease.

Aged↗

Positive inotropic effects of calcium sensitizers on normal and failing cardiac myocytes.

Calcium sensitizers increase myocardial contractile function without affecting Ca2+ homeostasis, which might be beneficial in the treatment of patients with heart failure. However, it remains uncertain whether Ca sensitizers induce quantitatively similar inotropic responses in control and failing hearts. To compare their effects in normal versus failing hearts at the cellular level, shortening mechanics and intracellular calcium ([Ca2+]i) transient were simultaneously measured in the left ventricular myocytes isolated from normal dogs (n = 8) and dogs with rapid pacing-induced heart failure (n = 7). CGP 48506 and EMD 57033 exerted a positive inotropic effect in a dose (0.1-3 microM)-dependent manner in both normal and heart failure myocytes. The percent increase of cell shortening magnitude was comparable between the two groups. CGP 48506 and EMD 57033 did not affect the diastolic cell length and resting [Ca2+]i level. They did not affect the duration of [Ca2+]i transient dynamics. Thus Ca2+ sensitizers exerted comparable positive inotropic effects without affecting the rest cell length and rest [Ca2+]i in normal and heart failure myocytes.

Animals↗

Increased inactivation of nitric oxide is involved in coronary endothelial dysfunction in heart failure.

Recent evidence suggests the possibility that enhanced inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) may cause endothelial dysfunction in heart failure (HF). To test this hypothesis, we examined the effect of antioxidant therapy on endothelium-dependent vasodilation of the coronary circulation in a canine model of tachycardia-induced HF. Endothelium-dependent vasodilation was less than that in controls, and OFR formation in coronary arterial and myocardial tissues was greater in HF dogs than those in controls. The immunohistochemical staining of 4-hydroxy-2-nonenal, OFR-induced lipid peroxides was detected in coronary microvessels of HF dogs. Intracoronary infusion of the cell-permeable OFR scavenger Tiron inhibited OFR formation and improved endothelium-dependent vasodilation in HF dogs but not in controls. The NO synthesis inhibitor N(G)-monomethyl-L-arginine (L-NMMA) diminished the beneficial effect of Tiron in HF dogs. Endothelium-independent vasodilation was similar between control and HF dogs, and no change in its response was noted by Tiron or Tiron plus L-NMMA in either group. In summary, antioxidant treatment with Tiron improved coronary vascular endothelium-dependent vasodilation by increasing NO activity in tachycardia-induced HF. Thus coronary endothelial dysfunction in HF may be, at least in part, due to increased inactivation of NO by OFR.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

Alpha1-adrenoceptor-Gq-RhoA signaling is upregulated to increase myofibrillar Ca2+ sensitivity in failing hearts.

Alpha1-adrenergic stimulation, coupled to Gq, has been shown to promote heart failure. However, the role of alpha1-adrenergic signaling in the regulation of myocardial contractility in failing myocardium is still poorly understood. To investigate this, we observed 1) the effect of phenylephrine on myofibrillar Ca2+ sensitivity in alpha-toxin-skinned cardiomyocytes, and 2) protein expression of Gq, RhoA, and myosin light chain phosphorylation using tachypacing-induced canine failing hearts. Phenylephrine significantly increased myofibrillar Ca2+ sensitivity in failing but not in normal cardiomyocytes. Whereas Y-27632 (Rho kinase inhibitor) blocked the phenylephrine-induced Ca2+ sensitization in the failing myocytes, calphostin C (protein kinase C inhibitor) had no effect on Ca2+ sensitization. The protein expression of Galpha(q) and RhoA and the phosphorylation level of regulatory myosin light chain significantly increased in the failing myocardium. Our results suggest that alpha1-adrenoceptor-Gq signaling is upregulated in the failing myocardium to increase the myofibrillar Ca2+ sensitivity mainly through the RhoA-Rho kinase pathway rather than through the protein kinase C pathway.

Amides↗

Increased inactivation of nitric oxide is involved in impaired coronary flow reserve in heart failure.

Recent evidence suggests that increased inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) formation is involved in the pathogenesis of endothelial dysfunction in heart failure (HF). However, it is unclear whether increased OFR limits coronary flow reserve in HF. To test this hypothesis, we examined the effects of antioxidant therapy on coronary flow reserve in a canine model of tachycardia-induced HF. The flow reserve (percent increase in coronary blood flow) to adenosine or to 20-s ischemia was less and OFR formation (electron-spin resonance spectroscopy) in myocardial tissues was greater in HF dogs than in controls. Immunohistochemical staining of 4-hydroxy-2-nonenal, an OFR-induced lipid peroxide, was detected in coronary microvessels of HF dogs. Intracoronary infusion of a cell-permeable OFR scavenger, tiron, suppressed OFR formation and improved the vasodilating capacity to adenosine or brief ischemia in HF dogs but not in controls. A NO synthesis inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), diminished the beneficial effects of tiron in HF dogs. Vasodilation to sodium nitroprusside was similar between control and HF dogs, and no change in its response was noted with tiron or tiron + L-NMMA in either group. In summary, antioxidant treatment with tiron improved coronary flow reserve by increasing NO bioactivity in HF dogs. Thus increased OFR formation may impair coronary flow reserve in HF by reducing NO bioactivity.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

The order of reacquirement of activity of daily living functions in people with spinal cord injury during rehabilitation after initial medical treatment and its affecting factors.

The purpose of this study was to investigate the order of reacquisition of activity of daily living (ADL) functions during inpatient rehabilitation at our spinal cord injury unit following the individual's initial medical care and to investigate what initial medical and biological factors would affect the ADL functions which the individual with spinal cord injury could perform 14 weeks after the beginning of inpatient rehabilitation. Fifty-two patients with spinal cord injuries who were hospitalized in the rehabilitation unit after their initial medical care participated in this study. The participants' ADL abilities were measured using the Barthel Index every four weeks after hospitalization for a period of 26 weeks. The order of reacquisition of ADL functions included in the Barthel Index was analyzed. Multiple regression analysis was performed to analyze the initial medical and biological factors affecting ADL reacquisition 14 weeks after hospitalization. The order of reacquisition of the ADL functions was almost the same in each individual. The multiple regression equations of the Barthel Index score and number of ADL functions after 14 weeks were both significant and the explanatory variables in both equations included the patients' age, complications on the initial stage and traumatic brain injury as an associated injury with spinal cord injury. We concluded that the patient's score on the Barthel Index and what the patient could actually perform 14 weeks after hospitalization could be predicted from the patient's status at hospitalization in the rehabilitation unit. This predictable correlation can contribute to the rehabilitation management for spinal cord injuries.

Activities of Daily Living↗

Coronary artery disease as a definitive risk factor of short-term outcome after starting hemodialysis in diabetic renal failure patients.

Cardiovascular disease is a major cause of morbidity and mortality in patients with diabetes who are receiving dialysis. It is known that cardiac mortality is high in the first year of hemodialysis (HD). The purpose of this study was to clarify the prevalence of coronary artery disease (CAD) in patients with diabetes at the initiation of HD, and to investigate the relationship between short-term outcomes after starting hemodialysis and CAD. We performed coronary angiography (CAG), whether or not patient had angina, within one month of initiation of maintenance HD in 17 of 34 consecutive unselected diabetic patients. We studied the two-year survival rate of those with CAD. Eleven patients (65%) were classified CAD-positive. Nine (82%) of these 11 had multivessel disease. Clinical and hematologic factors did not differ significantly between the groups with and without CAD. During the two-year follow-up period, 28 (82%) of 34 patients survived. In patients with CAD the two-year survival rate was 60%. None of the patients without CAD died within 2 years after starting HD. These results suggest that the presence of CAD at the initiation of HD may play a critical role in short-term outcomes after starting HD. We believe that an evaluation of CAD should be performed at the initiation of HD.

Chi-Square Distribution↗

Radioimmunoassay for somatostatin receptor type 2.

OBJECTIVE: To develop radioimmunoassay for somatostatin receptor type 2 (SSTR2) and search for its presence in certain rat tissues. METHODS: Anti-SSTR2 antiserum has been raised in New Zealand white rabbits immunized with a conjugate of synthetic SSTR2 with bovine serum albumin. Radioiodination of SSTR2 was performed by chloramin T method followed by purification of radioiodinated material on Sephadex G-25 column. RESULTS: The obtained antibody did not crossreact with SSTR1, SSTR3, SSTR4, SSTR5, hypothalamic hormones, pituitary hormones, neuropeptides or gut hormones. The assay was performed with a double antibody system. SSTR2 was extracted from the tissues with acid acetone. The dilution curve of acid acetone-extracts of rat hypothalamus in the radioimmunoassay system was parallel to the standard curve. The recovery of tissue SSTR2 was about 89 %, and the intra-assay and inter-assay variations were 4.9 % and 7.8 %, respectively. SSTR2 was found in the hypothalamus, cerebrum, cerebellum, pituitary, stomach and testis. CONCLUSIONS: These data suggest that this assay system is suitable for the estimation of SSTR2 in the tissues.

Acetone↗

[An autopsied case of presenile dementia with tangles].

We report an autopsied case of presenile dementia showing neuropathologically abundant neurofibrillary tangles(NFT) without senile plaques(tangle only dementia). A Japanese woman developed memory disturbance when she was 60 years old. At age of 65, her ability to understand deteriorated and euphoria and wandering manifested but neither psychotic symptoms, including hallucination and delusion nor a change in character were observed. The patient was hospitalized at age 66 and a cranial CT scan revealed bilateral moderate atrophy of the cortex and moderate enlargement of the lateral ventricle, especially in the inferior horn. No lobar atrophy was detected. She exhibited an oral tendency and became appallic at her final stage and died at the age of 75. Autopsy showed that her brain weighed 850 g and neuropathological study showed numerous NFT mainly in the entorhinal (trans-entorhinal) region, subiculum, CA1-CA4, dentate gyrus, amygdara, subthalamic nucleus, basal nucleus of Meynert, substantia nigra and locus coeruleus. Severe neuronal loss with gliosis was noted in the temporal lobes including the hippocampal region. No senile plaque was detected in any of the brain regions. There have been some recent reports of patients with abundant NFT with the predominant involvement of the allocortex but no or very little senile plaque. All the patients in the reported cases were very elderly at onset(over 80 years of age). In our case, the onset was presenile and we could exclude any other diseases, that usually present with NFT, and to our knowledge, this is the first report of a presenile dementia with tangles.

Aged↗

Diagnosis of ulnar wrist pain.

In the diagnosis of ulnar wrist pain, physical examinations including provacative tests are primary elements in identifying the site and nature of ulnar wrist pain. Imagings techniques are helpful for diagnosing occult fractures and distal radioulnar subluxation, but unsatisfactory for diagnosing ulnocarpal impaction syndrome, tears of the triangular fibrocartilage complex and lunotriquetral ligament, and joint mouse, imagings. Therefore, prior to surgical intervention arthroscopy is recommended for patients with persistent ulnar wrist pain that interferes with their daily activity.

Arthroscopy↗

The correlation between spontaneous and radiation-induced apoptosis in T3B bladder cancer (histological grade G3), and the precedence between the two kinds of apoptosis for predicting clinical prognosis.

PURPOSE: The correlation between the frequency of spontaneous and radiation-induced apoptosis, and the precedence between those for predicting prognosis were studied at clinical level. METHODS AND MATERIALS: Twenty-one patients (mean age, 65.8 years; 16 men and 5 women) with bladder cancer (transitional cell carcinoma Grade 3, T3bN0M0, Stage IIIb) underwent intraoperative radiotherapy: single 30-Gy 12-MV electron beam irradiation to bladder, followed by total cystectomy 6 h after irradiation. The specimens of pretreatment and irradiated bladder cancer were assayed for apoptosis, using TUNEL staining with counter staining of hematoxylin. The apoptotic index (AI) was calculated by dividing the number of apoptotic cells by the total number of cells and multiplying by 100. The Pearson's linear fitting was used to test the correlation between spontaneous and radiation-induced apoptosis. The Kaplan-Meier product-limit estimation was used for overall survival (OS) and freedom from recurrence (FFR). The precedence between spontaneous and radiation-induced apoptosis for predicting the clinical prognosis was estimated using the proportional hazard regression. RESULTS: The mean AI of spontaneous and radiation-induced apoptosis was 1.18 +/- 0.16 and 2.63 +/- 0.45, respectively, which was significantly different. There was strong correlation between spontaneous and radiation-induced apoptosis (r(2) = 0.864, adjusted r(2) = 0.857). Radiation-induced apoptosis was estimated by equation: y (radiation-induced apoptosis) = 2.67 x (spontaneous apoptosis) -0.52. However, the proportional hazard regression test indicated that only spontaneous apoptosis was significant for predicting OS and FFR (&z.sfnc;t&z.sfnc; > 0.2), but radiation-induced apoptosis was not. CONCLUSION: Estimating AI in radiation-induced apoptosis from AI in spontaneous apoptosis is possible. However, spontaneous apoptosis is more accurate in predicting clinical prognosis.

Aged↗

Causal influences in primate cerebral cortex during visual pattern discrimination.

Anatomical studies of the visual cortex demonstrate the existence of feedforward, feedback and lateral pathways among multiple cortical areas. Yet relatively little evidence has previously been available to show the causal influences of these areas on one another during visual information processing. We simultaneously recorded event-related local field potentials (LFPs) from surface-to-depth bipolar electrodes at six sites in the ventral region of the right hemisphere visual cortex in a highly trained macaque monkey during performance of a visual pattern discrimination task. Applying a new statistical measure, the short-time directed transfer function (STDTF), to the LFP data set, we charted the changing strength and direction of causal influence between these cortical sites on a fraction-of-a-second time scale. We present results showing, for the first time, the dynamics of distinct feedforward, feedback and lateral influences in the ventral portion of the primate visual cortex during visual pattern processing.

Action Potentials↗

Atomic force microscopy to study the effects of ITIM-bearing FcgammaRIIB on the activation of RBL-2H3 cells.

We have studied here the effects of ITIM-bearing FcgammaRIIB2 on the FcvarepsilonRI-dependent activation of rat basophilic leukemia (RBL-2H3) cells by atomic force microscopy (AFM). AFM images showed that ruffling and degranulation of RBL-2H3 cells were significantly reduced but the cell spreading was not by the co-clustering of FcgammaRIIB2 and FcvarepsilonRI. From the results it was shown that the co-clustering of ITIM-bearing negative co-receptors in a single RBL cell hardly induce the degranulation though the [Ca(2+)](i) increased transiently in the cell. This suggested that secretory responses and the membrane ruffling which were induced by the crosslinkng of FcgammaRII should be negatively controlled by the co-clustering of FcgammaRII.

Animals↗