Search PubMed⌕ Search

Biomedical subjects

J Watanabe

Publications and source records attributed to J Watanabe.

At least 73 records · Page 4Linked to original sources
PubMed2001

T-large granular lymphocyte leukemia accompanied by an increase of natural killer cells (CD3-) and associated with ulcerative colitis and autoimmune hepatitis.

Clonal expansion of large granular lymphocyte(LGL) have been classified into T-LGL and NK-LGL leukemia. T-LGL leukemia cells have a CD3+ phenotype and show clonal T-cell receptor(TCR) gene rearrangement. NK-LGL leukemia cells have a CD3- phenotype and no TCR gene rearrangement. We report a case of T-LGL leukemia accompanied by NK LGL expansions in a 65-year-old man who was observed 3 years earlier to have a LGL lymphocytosis in association with ulcerative colitis(UC) and autoimmune hepatitis (AIH). Phenotypic analysis of peripheral blood by flow cytometry disclosed an increase of both T-LGL(CD3+,CD56-,CD57+,and TCRalphabeta+) and NK-LGL (CD3-,CD16+,CD56+, and CD57+). Clonal rearrangement of the TCR beta gene was detected. A diagnosis of UC and AIH was made on the basis of the X-ray and mucosal biopsy findings of the large intestine, and on the scoring system for diagnosis of AIH, respectively. The disease was nonprogressive, and mesalazine and prednisolone were successful for treatment of UC and AIH. Previously reported cases of T-LGL, NK-LGL leukemia, or NK cell lymphocytosis had no association with UC or AIH, and there have been no reports having both T-LGL leukemia with T-cell receptor gene rearrangement and chronic NK cell lymphocytosis co-existing in a single patient.

Anti-Inflammatory Agents↗
PubMed2001

An unusual association of monoclonal gammopathy, paroxysmal nocturnal haemoglobinuria and myelodysplastic syndrome transformed into acute myeloid leukaemia: coexistence of triple clonal disorders.

An unusual association of paroxysmal nocturnal haemoglobinuria (PNH), myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML) and monoclonal gammopathy is reported. A 60-year old male, who had a history of IgA monoclonal gammopathy, presented with haemoglobinuria and colic pain. Flow cytometry showed CD55negative/59dim peripheral red cells, and bone marrow examination disclosed MDS. Eleven months, he developed later AML with disappearance of the PNH clones, although the monoclonal gammopathy persisted. The relationship between PNH and MDS has not fully been assessed, although our findings indicate that these triple clonal disorders, all coexisted in one patient.

Acute Disease↗
PubMed2001

Effect of transient stretch on intracellular Ca2+ during triggered propagated contractions in intact trabeculae.

Transient stretch of cardiac muscle during a twitch contraction may dissociate Ca2+ from myofilaments into the cytosol at the moment of quick release of the muscle. We studied the effect of stretch and quick release of trabeculae on changes in intracellular Ca2+ ([Ca2+]i) during triggered propagated contractions (TPCs). Trabeculae were dissected from the right ventricle of 9 rat hearts. [Ca2+]i was measured using electrophoretically injected fura-2. Force was measured using a silicon strain gauge and sarcomere length was measured using laser diffraction techniques. Reproducible TPCs (n = 13) were induced by trains of electrical stimuli (378 +/- 19 ms interval) for 7.5 s at [Ca2+]o of 2.0 mM (27.9 +/- 0.2 degrees C). The latency of the TPC force and the underlying increase in [Ca2+]i was calculated from the time (TimeF) between the last stimulus and the peak of TPC force (PeakF), or the time (TimeCa) between the last stimulus and the peak of the increase in [Ca2+]i during the TPCs (PeakCa). As a result of a 10% increase in muscle length for 150-200 ms during the last stimulated twitches, TimeF and TimeCa decreased and PeakF and PeakCa increased significantly (n = 13). In addition, transient stretch sometimes induced a twitch contraction subsequent to the accelerated TPC and its underlying increase in [Ca2+]i. These results suggest that Ca2+ binding and dissociation from the myofilaments by the stretch and quick release of muscle may modulate the TPC force and the underlying increases in [Ca2+]i and play an important role in the induction of arrhythmias.

Actin Cytoskeleton↗
PubMed2001

[Utilization of emergency ambulances in Yokohoma City, Japan].

OBJECTIVE: In recent years, the annual number of emergency ambulance (EA) calls has increased in Yokohama city, Japan. A questionnaire study was carried out to describe behavioral features of the users in Yokohama city, and to investigate their relationship with the increase in EA utilization. METHODS: We randomly recruited 2,910 citizens, aged 15 years or older, for the questionnaire study and a total of 2,294 (78.8%) replied. The questionnaire included questions about their demographic characteristics, history of EA use, existence of family doctors, and knowledge of emergency medical services and emergency medical information centers. Additionally, respondents who had used EA previously were asked about their reasons for this. RESULTS: A total of 513 (22.4%) respondents answered that they had used EA previously. A slightly higher rate of EA use was shown among elderly people, 65 years old or over (a rate of 26.2%). The major reason for requesting EA use was the urgency of the disease or the injury (61.8%). 182 respondents answered that they requested EA as a means of transportation. However, most of them also mentioned that the urgency of the disease or the injury was one of the reasons for their request. This survey showed no evidence that the citizens of Yokohama have used EA improperly. Elderly people, among whom the annual number of EA uses has increased rapidly over the years, tended to employ EA in a way more in line with regulations than other generations. CONCLUSION: This study suggested that the basic reason for the increase of EA utilization in Yokohama city was not due to inappropriate demand but to the aging of the population.

Adolescent↗
PubMed2001

Accuracy of technetium-99m tetrofosmin myocardial perfusion imaging in the detection of spontaneous recanalization in patients with acute anterior myocardial infarction.

To avoid the haemorrhagic risk of unnecessary thrombolysis in acute myocardial infarction (MI), early and precise diagnosis of spontaneous recanalization (SR) of the infarct-related artery is required. To clarify the accuracy of technetium-99m tetrofosmin myocardial single-photon emission tomography (SPET) in the detection of SR in patients with acute anterior MI, electrocardiography (ECG), echocardiography and 99mTc-tetrofosmin SPET imaging were performed in 49 patients with acute anterior MI before emergency coronary angiography. Defect score was calculated as the sum of the perfusion defects of each segment: from 3 (complete defect) to 0 (normal perfusion). Echocardiographic asynergic score (the sum of asynergic grades) and the greatest ST elevation of the 12-lead ECG on admission were also measured. SR was defined as Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow on emergency coronary angiography. Defect score in 11 patients with SR (9.2 +/- 3.7) was significantly lower than that in 38 patients without SR (18.5 +/- 5.0) (P < 0.001), whereas there were no significant differences in asynergic score and ST elevation between the two groups. From the receiver operating characteristic curves, the optimal cut-off points of defect score, asynergic score and ST elevation for the detection of SR were calculated to be 12, 13 and 3.5, respectively. The sensitivity and specificity of the scintigraphic defect score (91% and 89%) were significantly higher than those of the asynergic score (64% and 68%) and ST elevation (73% and 71%). Thus, 99mTc-tetrofosmin SPET imaging on admission is a very accurate method for the detection of SR in patients with acute anterior MI.

Acute Disease↗
PubMed2001

[Prostate cancer associated with hemorrhagic cyst: a case report].

A 68-year-old man consulted our department for sudden onset of dysuria and perineal pain. On digital rectal examination, soft and a hen-egg-sized mass was palpated. Serum PSA value was elevated to 11.4 ng/ml. Pelvic magnetic resonance imaging (MRI) suggested a large hemorrhagic cyst associated with prostate cancer. In addition to a pathological diagnosis as poorly differentiated adenocarcinoma (Gleason grade 5/4), which was established by transurethral biopsy, aspirated cyst contents revealed an elevated PSA value (3,090 ng/ml). Clinical staging was determined as T4N0M0. Following administration of androgen-deprivation therapy for 3 months, radiation therapy (64 Gy) was administered to the prostate. Twelve months after the diagnosis, the serum PSA value has remained within normal limits, and no local recurrence of the disease was detected.

Aged↗
PubMed2001

[Vesicoureteral reflux in a family].

We treated 3 cases of primary familial vesicoureteral reflux (VUR). Case 1: A 6-year-old boy had a grade III VUR in the left. Case 2: A 9-year-old boy, who was the elder brother of case 1, had grade III VUR in the right and grade V VUR in the left. Case 3: An 11-year-old girl, who was the elder sister of case 1 and case 2, had bilateral grade V VUR. VUR disappeared after anti-reflux operations in all cases.

Child↗
PubMed2000

Induced antiferroelectric smectic- C(*)(A) phase by doping ferroelectric- C* phase with bent-shaped molecules

Doping of the ferroelectric Sm-C(*) phase with bent-shaped molecules induces the antiferroelectric Sm-C(*)(A) phase. The effect was observed by means of electro-optic and dielectric measurements in systems with weak interlayer interactions in which the relative strength of anticlinic-synclinic order between molecules in adjacent layers is easily controlled by external factors. Fourier-transform infrared spectroscopy studies suggest that the bent-shaped molecules are not flat. They reorient upon the electric field-induced antiferroelectric-ferroelectric transition to adopt a position in which the average direction of the carbonyl groups is in the smectic plane and a bending tip along the C2 symmetry axis.

Journal Article↗
PubMed2000

Effect of phenobarbital on intralobular expression of CYP2B1/2 in livers of rats: difference in the expression between single and repetitive administrations.

Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers. The present study was undertaken to determine whether the spread of enzyme induction to midzonal and periportal hepatocytes is caused by the increase in total dose of the drug by repetitive injections or by the repetitive injections of the drug themselves. Male adult rats were administered PB by a single injection (80 mg/kg) or repetitive injections (20 mg/kg once a day for 4 days; a total dose of 80 mg/kg), and the molar content of CYP2B1/2 was measured by quantitative immunohistochemistry in the cytoplasm of perivenular, midzonal, and periportal hepatocytes. In addition, the molar content of total CYP in the cytoplasm was measured by microphotometry, and the expression of CYP2B2 mRNA was examined by in situ hybridization. When animals received the single injection, the isoforms and CYP2B2 mRNA increased markedly in perivenular hepatocytes, increased somewhat in midzonal hepatocytes, and remained unchanged in periportal hepatocytes. If animals received the repetitive injections, however, although the isoforms and the mRNA increased markedly in perivenular hepatocytes, they also increased markedly in midzonal hepatocytes and somewhat in periportal hepatocytes. These findings demonstrated that the enlargement of the sublobular area in which induction of the isoforms occurred was caused by the repetitive injections of PB themselves.

Analysis of Variance↗
PubMed2000

Mild mitral regurgitation was associated with increased prevalence of thromboembolic events in patients with nonrheumatic atrial fibrillation.

Although several studies demonstrated that the presence of significant mitral regurgitation was associated with reduced occurrence of thromboembolism, little data is available concerning the effect of mild mitral regurgitation on the occurrence of thromboembolic events. To evaluate the association between mild mitral regurgitation and thromboembolic events, we reviewed 232 patients' records between January 1996 and September 1997 who had nonrheumatic atrial fibrillation. There were 59 patients (25%) with mitral regurgitation > or = grade 2, 69 patients (30%) with grade 1 mitral regurgitation, and 104 patients (45%) with no mitral regurgitation. Patients with grade 1 mitral regurgitation had significantly higher prevalence of thromboembolic events (28%) than those with mitral regurgitation > or = grade 2 (8%, P=0.006) or those with no mitral regurgitation (11%, P=0.007). A history of previous thromboembolic events were compared between 173 patients with grade 1 mitral regurgitation and those with no mitral regurgitation using the logistic regression analysis adjusted for age, sex, administration of warfarin, and presence of hypertension, diabetes mellitus, structural heart disease, enlarged left atrium (> or = 40 mm), chronic atrial fibrillation, and grade 1 mitral regurgitation. Grade 1 mitral regurgitation (odds ratio=2.689, 95% confidence interval=1.039-7.189, P=0.0434) and no warfarin administration (odds ratio=0.045, 95% confidence interval=0.002-0.242, P=0.0036) were significantly associated with the history of thromboembolic events. The presence of mild mitral regurgitation in nonrheumatic atrial fibrillation was associated with higher prevalence of thromboembolic events.

Aged↗
PubMed2000

Carrier-mediated transport of riboflavin in the rat colon.

Carriers involved in riboflavin transport have generally been presumed to be localized in the upper small intestine. However, using a closed loop technique, we found that in the rat colon the absorption of riboflavin could be significantly reduced by raising the concentration from 0.1 to 200 microM and by adding lumiflavin, an analogue of riboflavin. These results suggest that saturable transport by the carrier that is specific for riboflavin and analogues may also be involved in riboflavin absorption in the colon. At the lower concentration of 0.1 microM, carrier-mediated transport was suggested to prevail, compared with passive transport, both in the colon and the small intestine. Furthermore, carrier-mediated transport in the colon was comparable with that in the small intestine. This study is the first to suggest carrier-mediated riboflavin transport in the colon. Although the riboflavin transport system in the colon needs to be subjected to more detailed investigation of its transport functions and role in riboflavin absorption after oral administration, it would be of interest to explore potential use of this carrier as a system for drug delivery.

Animals↗
PubMed2000

Cytochemical and ultrastructural examination of apoptotic odontoclasts induced by bisphosphonate administration.

Since odontoclasts share similar characteristics with osteoclasts, this study has examined whether odontoclasts exhibit cytological alteration after treatment with bisphosphonate, which induces apoptosis of osteoclasts. After the administration of bisphosphonate to 6-day-old rabbits, many odontoclasts detached from the dentine surface of the deciduous teeth, resulting in the reduction of tartrate-resistant acid phosphatase (TRAP-ase) and immunoreactivity for cathepsin K. Transmission electron microscopy revealed a number of odontoclasts showing poorly developed or a lack of ruffled borders, a Golgi apparatus markedly reduced in size, and numerous cytoplasmic vesicles. The bisphosphonate-treated odontoclasts displayed fragmented DNA in the pyknotic nuclei evidenced by terminal deoxynucleotidyl-transferase-mediated dUTP-biotin nick-end labeling, indicating that bisphosphonate can induce apoptosis of the odontoclasts. Ultrastructural observations of the apoptotic odontoclasts revealed condensed heterochromatin at the margin of the nuclear envelope, assembled arrays of rough endoplasmic reticulum, and many vacuoles and vesicles. Some apoptotic odontoclasts showed ladder-like structures between the adjacent nuclear envelopes, enlargement of the nuclear envelopes, and the formation of a ribosome-like granular structure in the nuclei. Thus, odontoclasts are able to undergo apoptosis after bisphosphonate treatment; this results in cytological alterations, including reduced resorption activity and the inhibition of protein synthesis/transport as indicated by the diminished TRAPase and cathepsin K and the poorly developed Golgi apparatus, respectively. Nuclear alteration as evidenced by the appearance of ladder-like and ribosome-like structures was characteristic of apoptotic odontoclasts.

Acid Phosphatase↗
PubMed2000

Cell biology of cytochrome P-450 in the liver.

Cytochromes P-450 (P-450) are members of a multigene superfamily of hemoproteins consisting the microsomal monooxygenase system with NADPH P-450 reductase (reductase) and/or reducing equivalents. Expression of many P-450 isoforms in hepatocytes is shown to be regulated at the level of transcription through interaction between cis-acting elements in the genes and DNA-binding (transacting) factors. Some isoforms of the CYP1A, 2B, 2E, and 3A subfamilies are regulated at the posttranscriptional level. For the topology of P-450 and reductase molecules in ER membrane of hepatocytes, models from stopped flow analysis and electron spin resonance are proposed. The densities of total P-450 and reductase molecules are revealed to be high enough to support the cluster model, suggesting that about ten P-450 molecules form an aggregate and surround one reductase molecule, and therefore the two enzymes form large micelles. ER proliferation after PB administration, which had been correlated with increase in P-450 level, is shown to be probably independent of the increase in P-450 level. There are considerable discrepancies among results reported on sublobular expression of various P-450 isoforms. Causes of the discrepancies are likely to be differences in experimental conditions of histochemical detection carried out and/or in species, strain, and/or sex.

Animals↗
PubMed2000

Induction of apoptosis in human cancer cells by TZT-1027, an antimicrotubule agent.

TZT-1027, a newly synthesized dolastatin 10 derivative, is a potent antitumor agent which inhibits microtubule polymerization and perturbs microtubule dynamics. In this report, we investigated whether TZT-1027 inhibited the growth of various human cancer cells, and the cell death caused by TZT-1027 was due to apoptosis. In addition, we elucidated the apoptosis machinery induced by treatment with TZT-1027. The 50% growth-inhibitory concentrations (IC50 values) of TZT-1027 on cancer cells derived from various sources were not more than 5.9 ng/ml. TZT-1027 showed superior cytotoxicity than any other antitumor agents. Next, we evaluated morphological nuclear change, namely, chromatin condensation and DNA fragmentation. We used three cancer cell lines derived from different types in view of having apoptosis related protein, human leukemia HL-60 (in the presence of both Caspase-3 and Bcl-2), human breast cancer MCF-7 (in the absence of Caspase-3), and human prostate cancer DU145 (in the absence of Bcl-2). TZT-1027 induced DNA fragmentation in the presence but not absence of Caspase-3. Nevertheless, apoptic chromatin condensation was observed in all cancer cells even if there was no Caspase-3. Furthermore, we examined whether TZT-1027, microtubule-disrupting agent, influenced cell cycle progression. Flow cytometric analysis revealed the cells treated with TZT-1027, and with the other antimicrotubule agents, to be arrested at the G2/M phase and subsequently to show fragmented DNA smaller than that of G1 phase cells. Moreover, we tested TZT-1027 for its ability to induce Bcl-2 phosphorylation in human cancer cell lines. TZT-1027 and other agents which interacted with microtubules induced Bcl-2 phosphorylation, whereas DNA-damaging agents did not. The present results suggested an association of the growth-inhibitory effect of TZT-1027 with the induction of apoptosis and indicated that the apoptosis induced by TZT-1027 was followed by G2/M arrest even if there was no Caspase-3 or Bcl-2.

Antineoplastic Agents↗
PubMed2000

Insulin modulation of intracellular free magnesium in heart: involvement of protein kinase C.

In the present study of rat heart using (31)P-nuclear magnetic resonance, we examined the interaction between beta-adrenergic and insulin receptors in terms of the intracellular free Mg(2+) concentration ([Mg(2+)](i)) regulation. [Mg(2+)](i) was estimated from the separation of the chemical shifts of the alpha- and beta-adenosine triphosphate (ATP) peaks, using the dissociation constant of MgATP 87 microM (established recently). In normal (phosphate-free Krebs-Henseleit) solution, [Mg(2+)](i) was approximately 1.02 mM. Insulin at physiological and pathological concentrations increased [Mg(2+)](i) and contractility in a dose-dependent manner. Insulin (more than 100 micro(u) ml(-1)) suppressed the decrease in [Mg(2+)](i) caused by isoprenaline (100 nM), and these effects of insulin on [Mg(2+)](i) and contractility were blocked by LY333531 (macrocyclic bis (indolyl) maleimide, 100 nM), a protein kinase C (PKC) inhibitor. The isoprenaline-induced decrease in the concentrations of ATP ([ATP]) with insulin application was significantly smaller than that without insulin. Insulin modulates [Mg(2+)](i) and haemodynamics, presumably via activation of PKC, thereby antagonizing the reduction of [Mg(2+)](i) induced by beta-adrenoceptor stimulation.

Adenosine Triphosphate↗