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Biomedical subjects

M Takeuchi

Publications and source records attributed to M Takeuchi.

At least 415 records · Page 23Linked to original sources
PubMed1997

[A risk of pulmonary edema associated with G-CSF pretreatment].

We reported a case of severe pulmonary edema in the normal adult after bone marrow harvesting (BMH), who had received granular cell stimulating factor (G-CSF) pretreatment. The patient was 38 year old healthy man who was a donor to his son suffering from SCID (severe complicated immunodefficiency). He was administered total of G-CSF 750 mcg for three days before BMH. At the end of the BMH procedure, the patient was becoming dyspneic followed by severe pulmonary edema that continued about 8 hours. The levels of TNF alpha and IL-6 in his plasma and endotracheal exudate were abnormally as high as 10 and 130 pg.ml-1 of TNF alpha in plasma and exudate respectively and as 51.8 pg.ml-1 of IL-6 in plasma. We speculate that G-CSF activates white cells and induces leaking of cytokines from white cells, and the severity of pulmonary edema is associated with the cytokines.

Adult↗
PubMed1997

[Non-uremic neuropathy in hemodialysis patients].

We have reviewed 20 clinical records of hemodialysis patients with neuropathy admitted to the Department of Neurology during 1978 april through 1995 march. The clinical diagnosis was made based on clinical findings, neurophysiological examinations, and histopathological findings of sural nerve and peroneal muscle biopsies. Four out of twenty hemodialysis patients with neuropathy were non-uremic neuropathy. The diagnosis of neuropathy of four patients were chronic inflammatory demyelinating polyneuropathy, neuropathy with graft versus host disease, Guillain-Barré syndrome, and subacute combined degeneration of the spinal cord. All patients improved after the treatment. It is important to consider the possibility of association of non-uremic neuropathy in hemodialysis patients.

Adult↗
PubMed1997

[Anesthetic and perioperative management of a neonatal vein of Galen malformation with multiple organ failure].

We treated a neonate in intractable cardiac failure due to a vein of Galen malformation. She manifested severe multiple organ failure. Perioperative problems are cardiac failure, respiratory failure, renal as well as hepatic dysfunction, and coagulopathy. Direct clipping of the feeding arteries improved her symptoms. Anesthetic problems encountered in this patient are massive bleeding and drastic circulatory changes while clipping the feeding arteries, increased intracranial pressure and brain ischemia, and other underlying complications; hepatic and renal dysfunction, respiratory failure and coagulopathy.

Anesthesia, General↗
PubMed1997

[Successful treatment for advanced and refractory chronic lymphocytic leukemia with fludarabine phosphate].

53-year-old man with chronic lymphocytic leukemia resistant to alkylating agent containing regimens, was treated with fludarabine phosphate. Hematological data before the administration of fludarabine phosphate was as follows: RBC 216 x 10(4)/microliter, Hb 7.7 g/dl, WBC 69,400/microliter (lymphocyte 96%), PLT 0.2 x 10(4)/microliter. Bone marrow was fully occupied with lymphocytes. Red blood cells and platelets transfusions were frequently required. Fludarabine phosphate was administered at a dose of 40 mg (23 mg/m2) intravenously for 5 days every 4 weeks. After the start of the therapy, peripheral lymphocyte counts were markedly decreased and recovery of normal hematopoiesis was observed in bone marrow. Any transfusions were no longer necessary. Fludarabine phosphate may be active even for advanced, refractory and terminal stage chronic lymphocytic leukemia.

Antineoplastic Agents↗
PubMed1997

[A case of paradoxical cerebral embolism with 'spectacular shrinking deficit'].

A 66-year-old woman was admitted to our hospital because of abrupt onset of left hemiparesis and confusional state. Ten hours prior to admission, she developed difficulty in left hand movement, and her family noticed cloudiness of consciousness and gait disturbance. Neurological examination revealed only a hollow hand sign of the left hand without other neurological deficits. Cranial CT showed a low density area in the right superior parietal region, and the follow up CT on 6th hospital day exhibited contrast enhancement and hemorrhagic transformation in this area. Cerebral angiography demonstrated capillary blush and early venous filling in the right posterior parietal region. Transesophageal color-coded Doppler echocardiography (TEE-CD) showed a shunt flow via patent foramen ovale (PFO). Thus, we diagnosed this case as paradoxical cerebral embolism through PFO, which is characterized by rapid recovery of clinical manifestation, so-called spectacular shrinking deficit. Even in elderly patients with embolic stroke of unknown origin, TEE-CD should be performed to investigate PFO.

Aged↗
PubMed1997

Recovery of perfusion, glucose utilization and fatty acid utilization in stunned myocardium.

We describe the clinical features and results of cardiac catheterization, PET ([13N]ammonia, 18F-fluorodeoxyglucose (FDG)) and SPECT [123I-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP)], in a patient with acute myocardial infarction successfully treated with intracoronary thrombolytic therapy. We compared the clinical and electrocardiographic changes with the myocardial glucose and fatty acid metabolism in stunned myocardium over a period of several months. The patient we studied illustrates the features of stunned myocardium. In the subacute phase, there was a concordant depression of myocardial [13N]ammonia and FDG uptake, and the metabolic abnormalities persisted even after regional wall motion at rest had returned to normal. The electrocardiographic recovery of deep negative T waves appeared to be related to the metabolic recovery in regions of stunned myocardium in this patient.

Ammonia↗
PubMed1997

[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis].

We presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.

Acute Disease↗
PubMed1997

[Neurosarcoidosis with an alternating and recurrent external ophthalmoplegia].

We report a 62-year-old woman who was admitted to our hospital because of abrupt onset of ptosis, and alternating and recurrent bilateral external ophthalmoplegia in a short period without pupillary sphincter muscle abnormality. She had been suffering from uveitis of unknown origin for four years before admission, which was improved with the local administration of steroid. Her brain CT and MRI showed a parasellar mass lesion, and cerebral angiography revealed total occlusion of the right internal carotid artery with little arteriosclerotic change in other blood vessels. She was diagnosed as having sarcoidosis because of elevated serum creatinine kinase and lysozyme levels, and the pathological finding of granuloma in muscle biopsy. The oral administration of prednisolone resulted in disappearance of her external ophthalmoplegia completely in ten months. We postulate that in this patient, the alternating and recurrent external ophthalmoplegia in a short period was related to ischemic neuropathy caused by vascular lesion of neurosarcoidosis.

Cranial Nerve Diseases↗
PubMed1996

The tumor necrosis factor receptor 2 signal transducers TRAF2 and c-IAP1 are components of the tumor necrosis factor receptor 1 signaling complex.

The two cell surface receptors for tumor necrosis factor (TNF) interact with a number of intracellular signal transducing proteins. The association of TRADD, a 34-kDa cytoplasmic protein containing a C-terminal death domain, with aggregated TNF receptor 1 (TNF-R1) through their respective death domains leads to NF-kappa B activation and programmed cell death. In contrast, TNF receptor 2 (TNF-R2) interacts with the TNF receptor associated factors 2/1 (TRAF2/TRAF1) heterocomplex, which mediates the recruitment of two cellular inhibitor of apoptosis proteins (c-IAP1 and c-IAP2) to TNF-R2. Here we show that the TNF-R2 signal transducers TRAF2 and c-IAP1 are a part of the TNF-R1 signaling complex. The recruitment of TRAF2 and c-IAP1 to TNF-R1 is TNF-dependent, is mediated by TRADD, and is independent of TNF-R2. These data establish the physiological involvement of TRAF2 and c-IAP1 in TNF-R1 signaling and help provide a molecular explanation for both the overlapping and distinct signals generated by the two TNF receptors.

Antigens, CD↗
PubMed1996

TRAF6 is a signal transducer for interleukin-1.

Many cytokines signal through different cell-surface receptors to activate the transcription factor NF-kappaB. Members of the TRAF protein family have been implicated in the activation of NF-kappaB by the tumour-necrosis factor (TNF)-receptor superfamily. Here we report the identification of a new TRAF family member, designated TRAF6. When overexpressed in human 293 cells, TRAF6 activates NF-kappaB. A dominant-negative mutant of TRAF6 inhibits NF-kappaB activation signalled by interleukin-1 (IL-1) but not by TNF. IL-1 treatment of 293 cells induces the association of TRAF6 with IRAK, a serine/threonine kinase that is rapidly recruited to the IL-1 receptor after IL-1 induction. These findings indicate that TRAF proteins may function as signal transducers for distinct receptor families and that TRAF6 participates in IL-1 signalling.

Amino Acid Sequence↗
PubMed1996

Anatomy of TRAF2. Distinct domains for nuclear factor-kappaB activation and association with tumor necrosis factor signaling proteins.

The tumor necrosis factor (TNF) receptor-associated factor (TRAF) family of proteins interact with and transduce signals for members of the TNF receptor superfamily. TRAF1, TRAF2, and TRAF3 share a conserved C-terminal TRAF domain. TRAF2 plays a key role in transducing signals for activation of the transcription factor nuclear factor-kappaB (NF-kappaB). We have performed extensive mutational analysis on TRAF2, examining the requirements for NF-kappaB activation, self-association, and interaction with other molecules involved in TNF signaling. Examination of point mutants and TRAF2-TRAF3 chimeric proteins indicates that the N-terminal RING finger and two adjacent zinc fingers of TRAF2 are required for NF-kappaB activation. The two distinct TRAF-N and TRAF-C subdomains of the TRAF domain appear to independently mediate self-association and interaction with TRAF1. Interaction of TRAF2 with TNF-R2 and TRADD requires sequences at the C terminus of the TRAF-C domain, whereas interaction with the protein kinase receptor-interacting protein V(RIP) occurs via sequences at the N terminus of the TRAF-C domain. Thus, distinct domains of TRAF2 are involved in recruitment and signaling functions.

Antigens, CD↗
PubMed1996

Negative chronotropic effect of beta-blockade therapy reduces myocardial oxygen expenditure for nonmechanical work.

BACKGROUND: The negative chronotropic effect of beta-blocking agents is likely to provide hemodynamic and energetic advantages. However, the negative chronotropic effect on cardiac energetics observed on the initiation of beta-blockade therapy has not been fully elucidated. METHODS AND RESULTS: In 18 patients with heart failure, left ventricular pressure and volume, external work (EW), myocardial oxygen consumption per beat (total Vo2), mechanical efficiency (EW/total Vo2), and Vo2 for nonmechanical work (total Vo2-2.EW) were measured with the use of conductance catheter and Webster catheter at the following three states: under control conditions and after beta-blockade (0.15 +/- 0.07 mg/kg propranolol IV) with and without atrial pacing to keep the heart rate at control levels. Heart rate decreased after atrial pacing was stopped. EW decreased during beta-blockade with pacing and returned to the control level after pacing was stopped. Total Vo2 did not change during beta-blockade with or without pacing, whereas Vo2 for nonmechanical work increased with pacing and returned to the control level after pacing was stopped. As a result, mechanical efficiency decreased during beta-blockade with pacing and returned to the control level after pacing was stopped. CONCLUSIONS: The negative chronotropic effect of a beta-blocking agent may offset the mechanoenergetical deterioration resulting from its negative inotropic effect through a reduction in oxygen expenditure for nonmechanical work. These findings suggest that the negative chronotropic effect is an important aspect of beta-blockade therapy.

Adrenergic beta-Antagonists↗
PubMed1996

Carnosine sustains the retention of cell morphology in continuous fibroblast culture subjected to nutritional insult.

L- Carnosine (beta-alanyl L-histidine), occurring abundantly in skeletal muscles, has been suggested to possess antioxidant and anti-aging properties. Using three different experimental approaches (microscopic, flow cytometric and ELISA for one of the markers of DNA oxidative damage) this study on rat embryonic fibroblasts demonstrates that L-carnosine at 30 mM concentration sustains the retention of cell morphology even during a nutritional insult for five weeks. Also, L-carnosine significantly reduces the formation of 8-hydroxy deoxyguanosine (8-OH dG) in the cells after four weeks of continuous culture. Thus it could be inferred that the anti-senescent effect of L-carnosine is probably linked to its inhibition of formation of intracellular 8-OH dG during oxidative stress.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Defective anion transport and marked spherocytosis with membrane instability caused by hereditary total deficiency of red cell band 3 in cattle due to a nonsense mutation.

We studied bovine subjects that exhibited a moderate uncompensated anemia with hereditary spherocytosis inherited in an autosomal incompletely dominant mode and retarded growth. Based on the results of SDS-PAGE, immunoblotting, and electron microscopic analysis by the freeze fracture method, we show here that the proband red cells lacked the band 3 protein completely. Sequence analysis of the proband band 3 cDNA and genomic DNA showed a C --> T substitution resulting in a nonsense mutation (CGA --> TGA; Arg --> Stop) at the position corresponding to codon 646 in human red cell band 3 cDNA. The proband red cells were deficient in spectrin, ankyrin, actin, and protein 4.2, resulting in a distorted and disrupted membrane skeletal network with decreased density. Therefore, the proband red cell membranes were extremely unstable and showed the loss of surface area in several distinct ways such as invagination, vesiculation, and extrusion of microvesicles, leading to the formation of spherocytes. Total deficiency of band 3 also resulted in defective Cl-/HCO3- exchange, causing mild acidosis with decreases in the HCO3- concentration and total CO2 in the proband blood. Our results demonstrate that band 3 indeed contributes to red cell membrane stability, CO2 transport, and acid-base homeostasis, but is not always essential to the survival of this mammal.

Animals↗
PubMed1996

Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: increased oxygen cost of contractility.

BACKGROUND: Although the use of inotropic agents to treat congestive heart failure (CHF) in patients with coronary artery disease has yielded short-term hemodynamic improvement, long-term mortality has shown less improvement. The loss of cardiac muscle as a result of infarction not only decreases the pumping ability of the heart but also leads to some dramatic changes in myocardial energetics. However, little is known about the mechanoenergetics of the heart in patients with left ventricular (LV) dysfunction after myocardial infarction. METHODS AND RESULTS: The present study was designed to compare by means of the Vo2-pressure-volume area relation (PVA, a measure of total mechanical energy) and Emax (LV contractility index), the incremental oxygen cost of contractility measured as nonmechanical energy per unit increment in contractility in patients with various kinds of LV dysfunction. We assessed Emax, Vo2, and PVA using conductance and Webster catheters under control conditions and during different rates of dobutamine infusion (3 and 6 micrograms x kg-1 x min-1) in 30 patients with coronary artery disease. Patients were divided into three groups according to LV ejection fraction (EF): 10 without LV dysfunction (EF>/= 60%), 10 with mild LV dysfunction (40% </= EF < 60%), and 10 with severe LV dysfunction (EF < 40%). Under control conditions, the Vo2-PVA relation was linear in each group. Contractile efficiency, the reciprocal of the slope of this relation, was comparable among the three groups. The oxygen cost of contractility in the severe LV dysfunction group was significantly greater than in the groups without and with mild LV dysfunction (0.022 +/- 0.014 versus 0.005 +/- 0.002 and 0.0012 +/- 0.005 mL O2 x mL x mm Hg-1 per beat, P <.05). CONCLUSIONS: These findings suggest that the alteration in mechanoenergetics in patients with severe LV dysfunction after myocardial infarction may result from the increased oxygen cost of excitation-contraction coupling rather than from a reduction in the efficiency of chemomechanical energy transduction.

Adult↗
PubMed1996

Does coronary flow reserve assessed by blood flow velocity analysis reflect absolute coronary flow reserve?

Doppler guidewire enables us to measure phasic coronary velocity and has been used for the measurement of coronary flow reserve (CFR). Although CFR is usually calculated by the quotient of peak flow velocity during papaverine infusion and flow velocity at rest, this assumption is true only if conduit vessel size is constant. To determine the accuracy of measurement of CFR using average peak velocity (APV) with Doppler guidewire, we investigated the influence of intracoronary papaverine on coronary flow velocity and coronary arterial diameter (CAD) and examined the correlation between CFR derived using APV and that derived using coronary blood flow (CBF) in 26 patients with normal coronary arteries. We measured phasic coronary flow velocity, and performed quantitative coronary angiography in the proximal left coronary artery at control and during 10 mg of intracoronary papaverine. Compared to control value, papaverine induced a significant increase in APV (% increase: 182 +/- 101%; P < 0.001). Papaverine also significantly increased CAD (16 +/- 10%; P < 0.001). Thus, CFR derived from APV was significantly lower than that derived from CBF (2.8 +/- 1.0 vs. 4.0 +/- 1.5, P < 0.001). Although there was a significantly strong positive correlation between these two methods (R2 = 0.83, P < 0.001), there was also considerable variability with regard to predicting one variable from the other. These results suggest the importance of standardizing the conditions in which coronary flow velocity is measured with regard to either controlling or measuring changes in epicardial coronary arterial diameter during changes in distal resistance vessel tone.

Adult↗