Biomedical subjects

J Tanabe

Publications and source records attributed to J Tanabe.

At least 73 records · Page 4Linked to original sources

PubMed1993

[Study of bacterial flora in the stomach and the upper and lower respiratory tracts--the mechanism of lower respiratory tract infection].

To evaluate the mechanism of lower respiratory tract infection in the hospital, gastric juice, throat secretions, secretions in tracheal cannulae or tubes and aspirated sputum were cultured simultaneously in seven patients with tracheostomy and seven patients with tracheal intubation. Thirty-six strains of bacteria were isolated from gastric juice and only 22.2% of them were the same bacteria as those in the throat secretions. This suggested that there was little correlation between gastric and oropharyngeal flora. The bacteria isolated from throat secretions and aspirated sputum showed 38.5% coincidence in tracheostomized patients and 80% coincidence in intubated patients. In addition, the rate of agreement was 33.3% in tracheostomized patients and 88.9% in intubated patients between throat secretions and tracheal cannulae or tubes. These findings suggested that the correlation of bacterial flora between the upper and lower respiratory tracts was high in intubated patients and low in tracheostomized patients. Identical bacteria in the stomach and the upper and lower respiratory tracts (which may cause nosocomial infection) were isolated in only four of the 14 patients. It has been suggested that bacterial flora in the lower respiratory tract are transmitted from the stomach to the oropharynx and then cause lower respiratory tract infection in hospital. However, our study suggested that this was not a common pathogenic mechanism.

Aged↗

PubMed1993

[A comparative study of VEPA and ACOMEP-BD regimen for the patients with non-Hodgkin's lymphoma].

Between 1981 and 1990, ACOMEP-BD regimen (adriamycin, cyclophosphamide, vincristine, methotrexate, etoposide, prednisolone, bleomycin, dacarbazine) was compared with VEPA regimen (vincristine, cyclophosphamide, prednisolone, adriamycin) in 66 newly diagnosed patients younger than 65 of age, with non-Hodgkin's lymphoma (NHL). The median age of the patients was 47.5 years (range 22-64 years), 43 males and 23 females. One patients were in stage I, 6 were in II, 27 were in III, 32 were in IV. Twenty-seven patients received VEPA and 39 received ACOMEP-BD. The therapeutic results of 66 patients with ACOMEP-BD or VEPA were as follows: complete remission (CR) rate of 54% and 48%; relapse rate of 29% and 77%; CR duration of 2-34 months (mean: 22 months) and 2-74 months (16 months); freedom-from-relapse survival (at 3 years) of 71% and 38%; and overall survival (at 4 years) of 62% and 26%, respectively. In these results, only relapse rate was significant and the others were not. Prognostic factors were performance status (PS) and lactate dehydrogenase level for ACOMEP-BD, and PS and marrow involvement for VEPA. Received dose intensity was 0.85 in ACOMP-BD and 0.41 in VEPA. It was expected that outcome of patients with NHL can be improved by increasing dose intensity.

Adult↗

PubMed1993

[Neutrophilic myelofibrosis; a case report].

A 53-year-old male was admitted to our hospital with abdominal pain. Physical examination revealed marked splenomegaly. The white blood cell count increased to 5.8 x 10(4)/microliters. Bone marrow biopsy showed hypercellularity with a moderate increase in reticulin fiber. Chromosomal analysis showed 47, XY, +9q-, -9q- without Ph1 chromosome and bcr-abl rearrangement. MCNU therapy was successful in reducing the white blood cell count and splenomegaly. It is likely that the diagnosis of our patient is compatible with the neutrophilic myelofibrosis described by Stewart, et al.

Blood Cell Count↗

PubMed1993

Functional domains of c-Myc involved in the commitment and differentiation of murine erythroleukemia cells.

In the early event of the induction of mouse erythroleukemia (MEL) cell differentiation, c-myc mRNA levels show a drastic change. The elevated expression of a transfected c-myc gene inhibits the commitment and differentiation of MEL cell transformants. In the present work, we have introduced human c-myc mutants into MEL cells under the inducible promoter to define the functional domains of c-Myc involved in erythroid differentiation. The c-Myc domains necessary for commitment and differentiation are not co-localized; almost entire regions are required for inhibition of commitment, whereas domains II and IV that are essential for co-transforming activity with ras are required for inhibition of differentiation. Interestingly, mutants that delete domains for c-Myc dimerization motifs enhanced differentiation. These results suggest that c-Myc may regulate commitment and differentiation by interacting with proteins through different domains.

Animals↗

PubMed1992

Evaluation of retinal integrity in eyes with retained intraocular metallic foreign body by ERG and EOG.

In three eyes with a retained intraocular metallic foreign body, the neural retina and retinal pigment epithelial (RPE) integrity were evaluated by means of ERG (a-wave, b-wave, oscillatory potentials) and non-photic EOG responses from the RPE (hyperosmolarity response, Diamox response, bicarbonate response). All three cases were judged in an early stage of retinal impairment on the basis of a well-preserved or supernormal b-wave amplitude and showed good postoperative prognosis. Out of three non-photic responses from the RPE, only the bicarbonate response was preoperatively reduced in two out of the three eyes.

Adult↗

PubMed1992

Spectral characteristics of rapid off-response in congenital deuteranomaly in one of monozygotic female twins.

The spectral sensitivity of the rapid off-response in the electroretinogram was studied in monozygotic female twins. One case was diagnosed as congenital deuteranomaly, and the other was normal. The log ratio of the sensitivity at 480 nm to the sensitivity at 620 nm (log S480/S620) was within the deutan range in the first case and within the normal range in the second. The two case were determined to be different at the retinal receptor level by study of the rapid off-response. This result of the rapid off-response was consistent with the results of the psychophysical examinations.

Adult↗

PubMed1992

The CBF threshold and dynamics for focal cerebral infarction in spontaneously hypertensive rats.

Two strategies were used to estimate the blood flow threshold for focal cerebral infarction in spontaneously hypertensive rats (SHRs) subjected to permanent middle cerebral artery and common carotid artery occlusion (MCA/CCAO). The first compared the volume of cortical infarction (24 h after ischemia onset) to the volumes of ischemic cortex (image analysis of [14C]iodoantipyrine CBF autoradiographs) perfused below CBF values less than 50 (VIC50) and less than 25 ml 100 g-1 min-1 (VIC25) at serial intervals during the first 3 h of ischemia. The infarct process becomes irreversible within 3 h in this model. In the second, measurements of CBF at the border separating normal from infarcted cortex at 24 h after ischemia onset were used as an index of the threshold. During the first 3 h of ischemia, VIC50 increased slightly to reach a maximum size at 3 h that closely matched the 24 h infarct volume. VIC25, in contrast, consistently underestimated the infarct volume by a factor of 2-3. CBF at the 24 h infarct border averaged 50 ml 100 g-1 min -1. Taken together, the results indicate that the CBF threshold for infarction in SHRs approaches 50 ml 100 g-1 min-1 when ischemia persists for greater than or equal to 3 h. This threshold value is approximately three times higher than in primates. Since cortical neuronal density is also threefold greater in rats than in primates, the higher injury threshold in the rat may reflect a neuronal primacy in determining the brain's susceptibility to partial ischemia.

Animals↗

PubMed1992

Role of c-Myc on erythroid differentiation.

In the early event of the induction of mouse erythroleukemia (MEL) cell differentiation, c-myc mRNA levels show a biphasic change. The elevated expression of a transfected c-myc gene inhibits the commitment and differentiation of MEL cell transformants. In the present work, we have introduced human c-myc mutants into MEL cells under the inducible promoter to define the functional domains of c-Myc involved in erythroid differentiation. The c-Myc domains necessary for commitment and differentiation are not colocalized; almost entire regions are required for inhibition of commitment, whereas domains II and IV that are essential for co-transforming activity with ras are required for inhibition of differentiation. Interestingly, mutants that delete domains for c-Myc dimerization motifs enhanced differentiation. Thus, c-Myc interferes with MEL cell differentiation by interacting with c-Myc partners and the induced protein(s) through dimerization domains. These results suggest that c-Myc may regulate commitment and differentiation by interacting with proteins through different domains.

Animals↗

PubMed1992

[Three M-components (IgG kappa, IgA kappa, IgM kappa) in a patient with non-Hodgkin's lymphoma].

Co-existence of three M-components in the serum or urine is rare. A case of non-Hodgkin's lymphoma was associated with three M-components. A 64-year-old woman was referred to our hospital because of M-proteinemia in June, 1989. On admission, serum electrophoresis on cellulose acetate membrane disclosed a triple M-peak. Immunoelectrophoresis showed M-bows for anti-IgG, anti-IgA, anti-IgM and anti-kappa simultaneously. In the urine, kappa type only Bence Jones protein was found. Scanning computed tomography revealed bulky masses in the lower abdomen, and the tumor masses were removed and diagnosed as non-Hodgkin's lymphoma. Immunohistochemical staining with antibodies to each immunoglobulins revealed the cells producing single M-component of each isotype of immunoglobulins. Although surgical removal of tumor caused a marked decrease in M-component especially IgA kappa, consistent presence of plasmacytoid lymphocyte was observed in peripheral blood. Combination therapy with melphalan and procarbazine resulted in disappearance of IgG kappa and IgA kappa from the serum. In January 1990, she achieved partial remission and was discharged. The patient has remained in remission for 16 months.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1992

[Study of the duration of antimicrobial chemotherapy in mycoplasmal pneumonia].

We assessed the period of administration of antibiotics required for cases of mycoplasmal pneumonia. The subjects were 38 patients with mycoplasmal pneumonia admitted to our hospital. These patients were treated with 100 mg minocycline or 500 mg erythromycin by intravenous infusion twice a day. They were divided into a 6 day-administration group (Group A; 16 cases) and a 9 day-administration group (Group B; 17 cases). Administration was discontinued on the 4th day or earlier in 5 cases due to side effects. A comparative assessment was made between Groups A and B with respect to body temperature, WBC, erythrocyte sedimentation rate, CRP, and chest X-ray on the 3rd, 6th, and 9th days of treatment, but no significant difference was observed. Residual shadows at the end of treatment were present in 100% of Group A and in 47% of Group B, but they disappeared gradually in both groups. No cases of recurrence were observed in either Group A or B within 1 month after the completion of treatment. Regarding the treatment period for mycoplasmal pneumonia by intravenous infusion of minocycline or erythromycin, no significant clinical difference was observed between the 6 day-administration group and the 9 day-administration group, suggesting that 6 days of administration is sufficient for treatment.

Adolescent↗

PubMed1992

[Myelodysplastic syndrome associated with marked eosinophilia and basophilia].

Myelodysplastic syndrome (refractory anemia with excess of blasts; RAEB) with marked basophilia and eosinophilia is described. An 82-year-old male was admitted to our hospital because of severe normocytic normochromic anemia (Hb 5.6 g/dl). The white cell count was 9,200/microliters with marked basophilia (34.5%) and eosinophilia (19.5%). The bone marrow aspiration also revealed both basophilia and eosinophilia, with blast contents of 9%. Diagnosis of RAEB was established. Although the treatment with red cell transfusion and ubenimex (Bastatin) was started, anemia was not improved. A karyotype of the bone marrow cells from this patient showed 47, XY, +8, i (17q), which has been observed as additional chromosomal abnormalities in blastic crisis of chronic myelogenous leukemia. The diagnosis of CML was not compatible with this case, because Ph1 chromosome and bcr gene rearrangement were negative. It is concluded that eosinophilia and basophilia might be derived from clonal abnormalities associated with MDS.

Aged↗

PubMed1991

Dynamics of interstitial and intracellular pH in evolving brain infarct.

We examined the relationships between intracellular pH (pHi) and interstitial pH (pHe) in a rat model of focal ischemia. Interstitial pH was measured with pH-sensitive microelectrodes, and the average tissue pH was measured with the [14C]dimethadione method in rats subjected to occlusion of the right middle cerebral and common carotid arteries (MCA-CCAO). In normal cortex, pHe and pHi were 7.24 +/- 0.97 and 7.01 +/- 0.13 (means +/- SD, n = 6), respectively. In the ischemic cortex, pHe fell to 6.43 +/- 0.13, whereas pHi decreased only to 6.86 +/- 0.11 (n = 5) 1 h after MCA-CCAO. After 4 h of ischemia, the pHe was 6.61 +/- 0.09 and pHi was 6.62 +/- 0.20 (n = 4). Treatment with glucose before ischemia markedly lowered the pHe (5.88 +/- 0.17) but not pHi (6.83 +/- 0.03, n = 4) measured 1 h after ischemia. In the ischemic cortex of animals made hypoglycemic by pretreatment with insulin, neither pHe (7.25 +/- 0.06) nor pHi (6.99 +/- 0.13, n = 4) decreased. The demonstrated difference in pHi and pHe indicates that some cells remained sufficiently functional to maintain a plasma membrane gradient of protons within the evolving infarct. If the calculated pHi values accurately reflect the true pHi of cells within zones of severe focal ischemia, then cerebral infarction can proceed at pHi levels not greatly altered from normal.

Animals↗

PubMed1991

Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia.

We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.

Analysis of Variance↗

PubMed1991

[A case of pulmonary embolism following acute respiratory failure with hypercapnia].

A 18-year-old boy was admitted to hospital in an unconsciousness state as a result of taking a large dose of several psychotropic drugs simultaneously in an attempt to commit suicide. Blood studies revealed hypoxia (55.7 mmHg) and hypercapnia (59.7 mmHg). Hypoxia (74.3 mmHg) and hypercapnia (46.7 mmHg) were still present on the fourth day after admission, and the patient was becoming lethargic. Reduced vascular markings in the right upper lung field on chest roentgenogram in spite of hypercapnia suggested that the persistent hypoxia was the result of a pulmonary embolism. This diagnosis was supported by a perfusion defect on 99mTc-MAA scintigram and arterial obstruction in right pulmonary angiogram. Hypercapnia is an unusual finding in pulmonary embolism, and in this case was considered due to depression of respiration by psychotropic drugs.

Acute Disease↗

PubMed1991

[Observations of the fibrosing process in paraquat lung injury by chest X-ray and CT].

A 42-year-old woman with a known history of paraquat ingestion was admitted to our hospital on the 10th day after ingestion complaining of dyspnea and general fatigue. Steroid therapy and low dose oxygen therapy were administered. She recovered and was discharged on the 190th day after paraquat ingestion. A chest X-ray film on admission disclosed a bilateral ground-glass shadow. As time passed, a reticular shadow with a loss of lung volume leaving a peripherally clear zone appeared on chest X-rays and shrank gradually toward the peri-hilar area during the course. CT of the lung clearly demonstrated progress of the pulmonary fibrosing process. In the early phase of paraquat poisoning, CT revealed diffuse high density areas dominant in the posterior part of the lungs with a subpleural intact area. The high density area was sharply demarcated from the subpleural intact area. As time passed, the high density area shrank toward the central zone, causing bullous changes in the subpleural area. The dominant fibrotic change in the intermediate and central zones seems to be one of the characteristic findings in paraquat induced pulmonary fibrosis.

Adult↗

PubMed1990

Pre- and post-treatment with MK-801 but not pretreatment alone reduces neocortical damage after focal cerebral ischemia in the rat.

The effect of treatment with the potent, non-competitive NMDA receptor-channel antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a, d] cyclohepten-5,10-imine maleate (MK-801) on ischemia-induced brain damage was studied in a well-characterized model of focal neocortical infarction in spontaneously hypertensive rats. Anesthesia exposure was minimized to the surgical procedure and the infarcts were allowed to mature over a 24-h period. Pretreatment with 5 mg/kg i.p. MK-801 (n = 11 control, n = 12 treated animals) 30 min before induction of focal cerebral ischemia had no statistically significant influence on infarct volumes. However, pre- and post-treatment with MK-801 5 mg/kg i.p. 30 min before induction of ischemia and 2.5 mg/kg each at 8 and 16 h after onset of ischemia, reduced infarct volumes in two separate studies by 29% (investigator J.T., n = 5 control and n = 7 treated animals) and 20% (investigator U.D., n = 8 control and n = 8 treated animals), respectively. The combined reduction in infarct volume in MK-801-treated animals for both investigators was 23% (P = 0.016, ANOVA). The findings indicate a smaller neuroprotective effect of MK-801 in spontaneously hypertensive rats subjected to focal ischemia than in previous reports using normotensive animals.

Animals↗

PubMed1990

Continuous nimodipine treatment attenuates cortical infarction in rats subjected to 24 hours of focal cerebral ischemia.

Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 micrograms/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10-15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20-60% smaller cortical infarct volumes than controls (p less than 0.002). Cortical edema was reduced proportionately to the decrease in infarct volume and constituted approximately 36% of the infarct volume. Nimodipine caused a mild hypotensive response that did not aggravate ischemic brain damage. The results indicate that continuous nimodipine treatment, started before induction of focal cerebral ischemia, can attenuate ischemic brain damage and edema as late as 24 h after the onset of ischemia.

Animals↗

PubMed1990

Nimodipine pretreatment improves cerebral blood flow and reduces brain edema in conscious rats subjected to focal cerebral ischemia.

The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 micrograms/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a "vascular steal" and reduced the volume of the ischemic core (cortex with CBF of less than 25 ml/100 g/min) and accompanying edema by approximately 50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50-75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20-30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.

Animals↗