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Biomedical subjects

T Kondo

Publications and source records attributed to T Kondo.

At least 523 records · Page 29Linked to original sources
PubMed1998

Chromosome bands 3p14.2, 9p21, and 13q14 are frequently deleted in roentgenographically occult bronchogenic squamous cell carcinoma of the lung.

Roentgenographically occult bronchogenic squamous cell carcinomas are early lung cancers that localize mainly within the bronchial wall and are thought to be a good model for elucidating chromosomal alterations during lung cancer progression. In this study, we analyzed allelic losses on chromosome regions 1p36, 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, in which there are putative tumor suppressor genes that may play roles in lung carcinogenesis. Forty-five cases with roentgenographically occult bronchogenic squamous cell carcinoma (ROC) and 47 cases of bronchogenic carcinoma with abnormal shadows (roentgenographically nonoccult bronchogenic squamous cell carcinoma [RNOC]) were examined. Highly frequent LOHs in both ROCs and RNOCs were observed in chromosome regions 3p14.2, 9p21, and 13q14.1-q14.2. LOHs were more frequently observed in RNOCs than in ROCs at two loci: 10q25.3-q26.1 and 16q24.1-q24.2. These results suggested that (1) putative tumor suppressor genes exist on 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, which may play important roles in lung carcinogenesis; (2) mutations in genes at 3p14.2, 9p21, and 13q14.12-q14.2 represent rather early events in lung carcinogenesis; and (3) mutations in genes on 10q25.3-q26.1 and 16q24.1-q24.2 represent rather late events.

Aged↗
PubMed1998

[An emergent coronary artery bypass grafting to total occlusion of all three coronary arteries in a patient with severe hyperbilirubinemia].

A 69-year-old man was transferred to our hospital because of chest pain and dyspnea. He had been very ill due to acute hepatitis and hyperbilirubinemia. Coronary angiography showed total occlusion of all three coronary arteries. An emergent coronary artery bypass grafting was successfully performed after insertion of IABP. Even though total bilirubin levels rose to 20.5 mg/dl, it gradually decreased without plasmapheresis. He had no hepatic failure and was discharged on foot on the 24th postoperative days.

Cardiac Surgical Procedures↗
PubMed1998

[A 61-year-old man with progressive gait disturbance, freezing, and vertical gaze paresis who developed esophagus cancer].

We report a 61-year-old Japanese man who died of complications of esophagus cancer surgery. He was well until his 55 years of the age, when he had an onset of speech disturbance and hand writing. He was seen by a neurologist who prescribed Menesit 600 mg/day. His symptoms improved with this medication. In 1993, three years after the onset, he started to show gait disturbance and easy to fall. In 1995, he noted difficulty in eye opening. He visited our clinic on October 26, 1996. On examination, he showed vertical gaze paresis, masked face, nuchal rigidity, small step gait, freezing phenomena, and festination. His mental status was normal. He was treated with 800 mg/day of Menesit, 800 mg/day of L-dops, and 10 mg/day of bromocriptine with little improvement in his symptoms. Cranial CT scan revealed some dilatation of the third ventricle. Subsequent clinical course was one of the slow progression of his parkinsonism. In September of 1997, he noted difficulty in swallowing. He was admitted to the gastrointestinal service of our hospital on October 14, 1997. On admission, neurologic status was essentially similar to the previous one, but he showed more advanced state of his parkinsonism. Upper gastrointestinal series revealed a mass lesion of about 11.5 cm in length protruding into the lower esophagus lumen. Subtotal esophagus resection including the mass was performed on December 2, 1997. The stomach was elevated for anastomosis with the upper esophagus. No metastases were found in the mediastinum except for two lymph nodes in the para-esophageal region. The subsequent course was complicated by marked elevation of GOT, GPT, LDH, total bilirubin as well as direct bilirubin, alkaliphosphatase, and amylase starting in the evening of the surgery. On December 7, leukocytosis and pneumonic shadow were seen involving his right lung. On December 10, he developed cardiopulmonary arrest. He was once resuscitated; however, he developed cardiac arrest again seven hours later and pronounced dead. He was discussed in a neurologic CPC. The chief discussant arrived at the conclusion that the patient had PSP and the cause of the death was ascribed to circulatory disturbance to the liver. The discussant also thought that the terminal course was complicated by cholangitis or cholecystitis, sepsis, and pulmonary embolism. Surgical specimen of the esophagus tumor revealed carcinosarcoma. Postmortem examination revealed yellowish discoloration of the peritoneum and mesenterium, and accumulation of clouded ascites indicating the presence of peritonitis. Inflammatory change extended to the mediastinum. On microscopic examination, various kinds of bacilli and candida spores were seen. The liver was enlarged and a perforation was noted in the gallbladder causing biliary necrosis in the adjacent liver. An extensive infarct was seen in the left lobe of the liver; this was found to be due to obstruction of the hepatic artery at the site of the duodenohepatic mesenterium and obstruction of intrahepatic portal vein secondary to retrograde intrahepatic cholangitis in the left lobe. A piece of surgical threads was seen adjacent to the hepatic artery; foreign body granulomatous reaction was seen surrounding the surgical thread. The rupture of the gallbladder appeared to be due to the obstruction of the left branch of the hepatic artery. Neuropathologic examination revealed extensive degeneration of the pallidum, the substantia nigra, and the subthalamic nucleus and presence of neurofibrillary tangles in the remaining neurons. The neuropathologic findings were consistent with progressive supranuclear palsy, although the pathologic changes in the midbrain tegmentum was only mild gliosis.

Carcinosarcoma↗
PubMed1998

[Easy graphical display of beam directions in three-dimensional converging radiation therapy: proposal for a radiation map].

In stereotactic radiosurgery, non-coplanar isocentric beams are employed to concentrate the dose distribution on the planning target volume (PTV). However, the directions of incident beams must be determined with great care by using a digitally reconstructed beam's eye view (BEV) to prevent the irradiation of organs at risk. We present a new method of 2-dimensional graphical representation (radiation map) to facilitate the understanding of 3-dimensional relationships between incident beams and critical organs. After determining the isocenter and beam diameter, beam directions and critical organs are projected onto the imaginary sphere centered on the isocenter. The coordinate of the beam directions and the organs at risk can be expressed by latitude and longitude on the sphere. The contours of the organs at risk are displayed with a margin of the the radius of the radiation beam. Mirror images of the critical organs are also displayed to prevent irradiation by the opposing beams. The radiation map could be produced within 5 minutes using a workstation. Radiation maps, like DVH, will be very useful in the evaluation of radiation treatment planning.

Radiosurgery↗
PubMed1998

Contribution of airway resistance to airway pressure during mechanical ventilation: an experimental study.

Although airway resistance (R) is an important parameter of the pulmonary condition, its determination during mechanical ventilation is not easy. Most physicians estimate R from peak airway pressure during mechanical ventilation. We assessed the relationship between R and peak airway pressure by a computer simulation. The time course of airway pressure (Ptr) during mechanical ventilation was calculated from the airway pressure at end-inspiration and respiratory flow, allowing for the buffering effect of the dead space. The parameters for computer simulation were obtained from 5 paralyzed and mechanically ventilated dogs. The predicted Ptr curve was a function of airway resistance. Since R was not directly determined by the animal experiments, we determined R by using the Ptr curve most closely approximating the original Ptr curve as the true R. The R-peak tracheal pressure relationship predicted by computer simulation showed that the peak airway pressure increased almost linearly with increases in R. However, in computer simulation, when R was increased 10-fold from the value at airway relaxation, the peak airway pressure increased only 6-fold from the corresponding value. We conclude that peak airway pressure is a relatively insensitive parameter for the estimation of airway constriction during mechanical ventilation.

Airway Resistance↗
PubMed1998

Three cases of primary lung cancer undetected by an annual checkup.

An annual check by chest roentgenogram is very important for the early detection of lung cancer. We present three cases of primary lung cancer which were not detected by the double check system or previous examination. The three patients visited our hospital for evaluation of an ill-defined opacity in the upper lobe of the lung. In the three cases, no abnormality had been reported in the previous year's annual chest X-ray, and we concurred in the decisions. The correct diagnoses of the three cases were well or poorly differentiated adenocarcinoma, and were still amenable for surgical therapy. A poorly defined tumor in this region is very difficult to detect because of superimposed opacities of other anatomical structures. When a questionable shadow in this region is found but without the typical radiological features of lung cancer, it is important to search for indirect indications of adenocarcinoma. These may include fibrotic changes and absence of inflammation. In our cases, the increased number of normal-size bronchi penetrating the ill-defined tumor, seem to have diagnostic significance.

Adenocarcinoma↗
PubMed1998

Social support as a function of school counseling.

The objective of this study was to investigate the value of school counseling, particularly in terms of social support. To prepare this report, I conducted a follow-up study on graduates of T high school, on school counseling, based on 185 individuals. I compared the students who received counseling when they were in school (visitants) with students who did not (non-visitants), and examined the correlation between them. As a result, significant statistical differences were detected as follows: 1. The visitants had different concerns from the non-visitants. 2. The visitants had a variety of individual concerns. 3. The visitants differed in the manner of obtaining social support. 4. Both groups had their own characteristic categories of social support. Consequently, two conclusions have been drawn: 1. Extensive informal relationship with friends exists among high school students. In particular, club and extracurricular activities are of major importance. 2. When informal support is not available, help may be sought from formal relationships (counselor, teachers of handicapped students, or classroom teachers). In other words, school counseling can function as a complementary and effective social support for high school students.

Adolescent↗
PubMed1997

Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells.

In this report, we establish a regulatory role of natural killer (NK) cells in experimental autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide induces a mild form of monophasic EAE. When mice were deprived of NK cells by antibody treatment before immunization, they developed a more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion was also seen in beta 2-microglobulin-/- (beta 2m-/-) mice, indicating that NK cells can play a regulatory role in a manner independent of CD8+ T cells or NK1.1+ T cells (NK-T cells). The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55. EAE passively induced by the MOG35-55-specific T cell line was also enhanced by NK cell deletion in B6, beta 2m-/-, and recombination activation gene 2 (RAG-2)-/- mice, indicating that the regulation by NK cells can be independent of T, B, or NK-T cells. We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation. Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

Amino Acid Sequence↗
PubMed1997

Postmortem alcohol analysis of the synovial fluid and its availability in medico-legal practices.

Alcohol analyses using the synovial fluid of the knee joint (synovial alcohol concentration, SAC) as well as blood (BAC) and urine (UAC) were performed by the pulse heating-gas chromatographic method in 12 medico-legal autopsy cases. In 11 of the 12 cases, the regression analysis showed that BAC and UAC had a fairly linear relationship with SAC, and the average ratios of the BAC/SAC and UAC/SAC were 0.76 +/- 0.12 (range 0.60-0.94) and 1.03 +/- 0.11 (range 0.90-1.21), respectively. The measured BACs showed a difference of 11.8 +/- 9.4% (0.9-27.1%) when compared with the calculated BACs by means of the average BAC/SAC ratio. Between the measured UACs and the calculated UACs, there was an average difference of 7.9 +/- 6.0% (0.3-17.8%). The present study demonstrates that the synovial fluid is one of the available biological specimens for the prediction of BAC or UAC within a range in autopsy cases in which suitable blood and/or urine specimens cannot be obtained.

Adult↗
PubMed1997

ERM (ezrin/radixin/moesin)-based molecular mechanism of microvillar breakdown at an early stage of apoptosis.

Breakdown of microvilli is a common early event in various types of apoptosis, but its molecular mechanism and implications remain unclear. ERM (ezrin/radixin/moesin) proteins are ubiquitously expressed microvillar proteins that are activated in the cytoplasm, translocate to the plasma membrane, and function as general actin filament/plasma membrane cross-linkers to form microvilli. Immunofluorescence microscopic and biochemical analyses revealed that, at the early phase of Fas ligand (FasL)-induced apoptosis in L cells expressing Fas (LHF), ERM proteins translocate from the plasma membranes of microvilli to the cytoplasm concomitant with dephosphorylation. When the FasL-induced dephosphorylation of ERM proteins was suppressed by calyculin A, a serine/threonine protein phosphatase inhibitor, the cytoplasmic translocation of ERM proteins was blocked. The interleukin-1beta-converting enzyme (ICE) protease inhibitors suppressed the dephosphorylation as well as the cytoplasmic translocation of ERM proteins. These findings indicate that during FasL-induced apoptosis, the ICE protease cascade was first activated, and then ERM proteins were dephosphorylated followed by their cytoplasmic translocation, i.e., microvillar breakdown. Next, to examine the subsequent events in microvillar breakdown, we prepared DiO-labeled single-layered plasma membranes with the cytoplasmic surface freely exposed from FasL-treated or nontreated LHF cells. On single-layered plasma membranes from nontreated cells, ERM proteins and actin filaments were densely detected, whereas those from FasL-treated cells were free from ERM proteins or actin filaments. We thus concluded that the cytoplasmic translocation of ERM proteins is responsible for the microvillar breakdown at an early phase of apoptosis and that the depletion of ERM proteins from plasma membranes results in the gross dissociation of actin-based cytoskeleton from plasma membranes. The physiological relevance of this ERM protein-based microvillar breakdown in apoptosis will be discussed.

Animals↗
PubMed1997

Dimethoxyphenylethylamine and tetrahydropapaverine are toxic to the nigrostriatal system.

We report the toxic effects of 3,4-dimethoxyphenylethylamine (DMPEA), and tetrahydropapaverine (THP) on the rat nigrostriatal system; THP is a tetrahydroisoquinoline compound which may be derived from DMPEA by conjugation of DMPEA and its oxidative metabolite, dimethoxyphenylacetaldehyde; both are potent inhibitors of mitochondrial complex I. These compounds were introduced to the unilateral caudate-putamen of male Sprague-Dawley rats over 7 days using a 200-microl mini-osmotic pump. Striatal dopamine on the injected side showed a significant decrease to 86% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA, and to 73% of the non-injected side after 7.90 micromol/7 days of THP infusion; as the non-injected side dopamine also reduced in the THP-injected rats, dopamine on the injected side was 55% of the saline control. Tyrosine hydroxylase (TH)-positive nigral neurons were decreased to 76% of the non-injected side after 16.55 micromol/7 days infusion of DMPEA and to 77% after 7.90 micromol/7 days of THP infusion. Dimethoxyphenyl-tetrahydroisoquinoline compounds appear to be potent nigral neurotoxins.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Activation of distinct caspase-like proteases by Fas and reaper in Drosophila cells.

The cytoplasmic region of Fas, a mammalian death factor receptor, shares a limited homology with reaper, an apoptosis-inducing protein in Drosophila. Expression of either the Fas cytoplasmic region (FasC) or of reaper in Drosophila cells caused cell death. The death process induced by FasC or reaper was inhibited by crmA or p35, suggesting that its death process is mediated by caspase-like proteases. Both Ac-YVAD aldehyde and Ac-DEVD aldehyde, specific inhibitors of caspase 1- and caspase 3-like proteases, respectively, inhibited the FasC-induced death of Drosophila cells. However, the cell death induced by reaper was inhibited by Ac-DEVD aldehyde, but not by Ac-YVAD aldehyde. A caspase 1-like protease activity that preferentially recognizes the YVAD sequence gradually increased in the cytosolic fraction of the FasC-activated cells, whereas the caspase 3-like protease activity recognizing the DEVD sequence was observed in the reaper-activated cells. Partial purification and biochemical characterization of the proteases indicated that there are at least three distinct caspase-like proteases in Drosophila cells, which are differentially activated by FasC and reaper. The conservation of the Fas-death signaling pathway in Drosophila cells, which is distinct from that for reaper, may indicate that cell death in Drosophila is controlled not only by the reaper suicide gene, but also by a Fas-like killer gene.

Animals↗
PubMed1997

Introduction of cyclin B induces activation of the maturation-promoting factor and breakdown of germinal vesicle in growing zebrafish oocytes unresponsive to the maturation-inducing hormone.

When treated with 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP), a natural maturation-inducing hormone in fishes, fully grown zebrafish oocytes are induced to mature via the activation of the maturation-promoting factor (MPF), which consists of cdc2 (a catalytic subunit) and cyclin B (a regulatory subunit). In contrast, 17alpha,20beta-DP is unable to induce growing (previtellogenic and vitellogenic) oocytes to mature. To know the reason growing oocytes fail to mature upon 17alpha,20beta-DP treatment, we investigated changes in the components of machinery responsible for MPF activation during zebrafish oogenesis. Immunoblotting experiments using monoclonal antibodies against cdc2, cyclin B, and cdk7 (an activator of cdc2) have revealed that the concentrations of cdc2 and cdk7 are almost constant during oogenesis. Cyclin B was present in mature oocytes but absent in growing and fully grown immature oocytes. These results, which are identical to those in goldfish, strongly suggest that cyclin B is synthesized from stored (masked) mRNA after 17alpha,20beta-DP stimulation and that its binding to the preexisting cdc2 allows cdk7 to activate MPF. Microinjection of cyclin B protein induced MPF activation and germinal vesicle breakdown in growing oocytes, as well as in fully grown oocytes, indicating that cdk7 present in growing oocytes is already active. Northern blot analysis revealed the presence of cyclin B mRNA in both previtellogenic and fully grown oocytes. These results indicate that, as in fully grown oocytes, growing oocytes are already equipped with the catalytic subunit of MPF (cdc2) and its activator (cdk7) and that the appearance of the regulatory subunit of MPF (cyclin B) is sufficient for initiating maturation. Therefore, the unresponsiveness of growing oocytes to 17alpha,20beta-DP is attributable to a deficiency in the processes leading to cyclin B synthesis, which include 17alpha,20beta-DP reception on the oocyte surface, subsequent signal transduction pathways, and unmasking the stored cyclin B mRNA.

Animals↗
PubMed1997

Relation of electrocardiographic left ventricular hypertrophy with and without T-wave changes to systemic blood pressure, body mass, and serum lipids and blood glucose levels in Japanese men.

Left ventricular (LV) hypertrophy, especially combined with an abnormal ST-T, is considered 1 of many coronary risk factors. Seven hundred forty-nine Japanese men were selected according to their electrocardiographic findings, i.e., normal electrocardiogram, LV hypertrophy without an abnormal ST-T segment, LV hypertrophy with a flat T wave, and LV hypertrophy with a negative T wave. Coronary risk factors were compared among these 4 age-matched groups. Groups with LV hypertrophy with negative or flat T waves had larger body mass index (24.9 vs 22.9 kg/m2), higher mean systemic blood pressure (111 vs 95 mm Hg), larger LV mass (265 vs 157 g), higher blood glucose (110 vs 100 mg/dl), higher serum triglyceride (148 vs 122 mg/dl), higher total cholesterol (206 vs 198 mg/dl), and lower high-density lipoprotein cholesterol (47 vs 54 mg/dl) than the normal group or the group with LV hypertrophy without T-wave change. Among these risk factors, blood pressure and glucose remained higher even after the adjustment by body mass index or by body mass index and blood pressure. Electrocardiographic LV hypertrophy with a changed T wave signified higher risk of coronary artery disease in Japanese men.

Blood Glucose↗
PubMed1997

Characterization of the chromatin binding activity of lamina-associated polypeptide (LAP) 2.

Previous studies have shown that the first and the second halves of the LAP2 N-terminal nucleoplasmic domain function independently in targeting LAP2 to the nuclear envelope, and that the second half is involved in association with the nuclear lamina. To further define the role of the nucleoplasmic domain, we have examined the targeting and chromatin binding functions of the first half of its N-terminus. Expressed polypeptides comprising residues 1-67 fused to the LAP2 transmembrane sequence were localized in perinuclear aggregates, while a residue within residues 244-296 was involved in the translocation of LAP2 to the nucleus as well as in DNA binding. Deletion of any of these domains resulted in a loss of the nuclear envelope targeting function. These data suggest that multimeric interactions of LAP2 with specific cellular components are required for correct targeting to the nuclear envelope and that the first N-terminus has function which is at least directly involved in chromatin association.

Amino Acid Sequence↗
PubMed1997

Body-surface distribution of changes in activation-recovery intervals before and after catheter ablation in patients with Wolff-Parkinson-White syndrome: clinical evidence for ventricular 'electrical remodeling' with prolongation of action-potential duration over a preexcited area.

BACKGROUND: T-wave abnormalities after catheter ablation in patients with manifest Wolff-Parkinson-White (WPW) syndrome have been attributed to a continuation of repolarization abnormalities induced by preexcitation (cardiac memory). METHODS AND RESULTS: To clarify changes in repolarization properties, we analyzed the activation-recovery interval (ARI) obtained from body-surface maps and the relationship between the activation time (AT) and ARI in 30 patients with WPW syndrome (group A, 18 patients with manifest left-sided accessory pathway; group B, 7 patients with manifest right-sided accessory pathway; and group C, 5 patients with concealed left-sided accessory pathway) before, 1 day after, and 1 week after ablation. The ARI significantly decreased 1 week after ablation compared with before and 1 day after ablation over the preexcited area in groups A and B. Correlation coefficients between the AT and ARI showed a significantly (P<.01) stronger inverse relationship before (r=-.58) and 1 week after (r=-.64) ablation than 1 day after ablation (r=-.46) in groups A and B. In group C, the ARI and correlation coefficients between the AT and ARI showed no significant changes. CONCLUSIONS: These findings suggest a prolongation of the action-potential duration over the preexcited area before and just after ablation as ventricular "electrical remodeling," a decrease in the inverse relationship between the AT and action-potential duration 1 day after ablation, and a gradual recovery of the action-potential duration over the preexcited area and inverse relationship 1 week after ablation.

Action Potentials↗
PubMed1997

Acute ischemic vulnerability of PKA in the dendritic subfields of the hippocampus CA1.

Alterations of [3H]cyclic AMP (cAMP) binding, an indicator of the binding activity of particulate cyclic AMP-dependent protein kinase (PKA), were examined after 15 and 30 min of ischemia in the gerbil brain. Severe hemispheric cerebral ischemia was induced by occluding the right common carotid artery. Significant reductions in cAMP binding were noted only in the dendritic subfields of the hippocampus CA1 such as the strata oriens, radiatum and lacunosum-moleculare, on the ischemic side after 15 min of ischemia. After 30 min ischemia cAMP binding was significantly decreased not only in each dendritic subfield of the hippocampus CA1, but also in the layer of pyramidal cell bodies (stratum pyramidale) on the occluded side; other brain regions such as the hippocampus CA3, dentate gyrus and cerebral cortices revealed no significant changes in cAMP binding. These findings suggest that derangement of PKA may begin in the dendritic subfields of the hippocampus CA1 after as little as 15 min of severe ischemia, and proceed centrally to the neuronal cell bodies of the hippocampus CA1.

Animals↗