Biomedical subjects
T Kondo
Publications and source records attributed to T Kondo.
Cold milk accelerates oro-cecal transit time during the luteal phase but not the follicular phase in women.
The effect of the menstrual cycle on oro-cecal transit time (OCTT) has been controversial. Since poor reproducibility of OCTT measurements by lactulose might be responsible for this controversy, we measured OCTT with either milk or a solid test meal during the luteal and follicular phases of the menstrual cycle. Nine healthy young women (21.9 +/- 0.42 years old) with regular menstruation were studied for 4 consecutive menstrual cycles. Control (37 degrees C) or cold (10 degrees C) milk was used as a liquid meal, and the OCTT measurements were taken 3 times at each milk temperature during each of the 2 phases for 3 consecutive menstrual cycles. OCTT after a solid test meal (cooked rice, miso soup, a boiled egg, and cooked soybeans with mixed vegetables) was studied twice in 1 menstrual cycle. Breath hydrogen was determined every 15 min for 6 h. OCTT was defined as the time when breath hydrogen showed a sustained rise of 3 ppm or more from baseline. OCTT was not different between the luteal and follicular phases when the test meal was control milk or the solid meal. When cold milk was used as the test meal, OCTT was significantly shorter during the luteal phase (134 +/- 15 min) than during the follicular phase (165 +/- 21 min). In conclusion, cold milk accelerates OCTT during the luteal phase but not the follicular phase of the menstrual cycle in women.
[The pattern of mediastinal nodal involvement in lung cancer according to tumor-located lobe].
To clarify the pathway of the metastases from each pulmonary lobe to mediastinal nodes, we examined the pattern of mediastinal nodal involvement in 462 resected pN2 non-small cell lung cancer. Carcinomas of the right upper lobe frequently involved #3 (78/133) and #4 (70/133) nodes, whereas those of the right middle or lower lobe frequently metastasized to #7 nodes (18/23 and 86/113, respectively). On the other hand, carcinoma of left upper lobe frequently involved #5 nodes (81/118), whereas those of the left lower lobe most frequently metastasized to #7 nodes (50/75). Of 462 pN2 patients, 95 (20.6%) had skip metastases to the mediastinal nodes. Skip metastasis was observed more frequently in carcinomas of right upper and middle lobe. One of the reasons of skip metastasis may be the direct lymph drainage through subpleural space to mediastinum.
Vocal fold injection of collagen for unilateral vocal fold paralysis caused by chest diseases.
BACKGROUND: Patients having malignant chest diseases sometimes suffer from vocal fold paralysis. Treatment for vocal fold paralysis is important for such patients, because vocal fold paralysis causes lack of the versatility of the human voice which is essential for our communication. METHODS: Seventeen patients suffering from unilateral vocal fold paralysis were treated with vocal fold injections of collagen. Three patients received twice, and 20 treatments were conducted. A flexible bronchofiberscope was used under local anesthesia in order to observe the whole procedure of vocal fold injection. Using an injector and a long needle, collagen was injected with transcutaneous technique mainly through the cricothyroid membrane. The amount of collagen was determined with bronchoscopic findings. RESULTS: During and after treatment, no complication was observed. Of 20 treatments, a marked improvement was observed in 8, and moderate improvement was observed in 9 treatments. CONCLUSIONS: Vocal fold injection of collagen is a very useful and safe treatment for unilateral vocal fold paralysis caused by chest diseases.
[Clinical study of carcinoma of the penis].
We reviewed six cases of carcinoma of the penis seen at our department during the last 12 years. The mean age and mean followup period were 56 +/- 11 years and 53 +/- 42 months, respectively. Inguinal lymphadenopathy was evident in all patients, one of whom was diagnosed as having nodal metastasis because of the persistence of adenopathy after antimicrobial therapy. Four patients, had Jackson Stage 1, 1 Stage 2 and 1 Stage 3 cancer. The patient with Stage 3 cancer underwent total penectomy and bilateral inguinal lymphadenectomy. He died of cancer 2 years after the operation. The 5 patients with stage 1 or 2 underwent partial penectomy without lymphadenectomy. Pathological examination showed moderately differentiated squamous cell carcinoma (SCC) in 2 patients with stage 2 and 3 cancer, well differentiated SCC in 3 and verrucous carcinoma in the other patient with stage 1 cancer. Prophylactic external radiation therapy to the groin was performed in 3 of the 4 patients with invasion to corpus spongiosum (pT2). Two of the 3 patients developed mild radiation dermatitis, and no major complications were observed. The 5 patients with clinically negative nodes showed no evidence of recurrence after surgery. As reported by others, inguinal node metastasis appears to worsen the prognosis of patients with carcinoma of the penis.
[Clinical evaluation of acute and chronic pulmonary thromboembolism using intravascular ultrasound and angioscopy].
Pulmonary artery thrombi and parietal lesions were observed in 13 patients (mean age 58 +/- 18 years) with acute pulmonary thromboembolism (n = 4) and chronic pulmonary thromboembolism (n = 9) using intravascular ultrasound and angioscopy at the time of right heart catheterization. Patients with acute pulmonary thromboembolism without underlying disease mainly had non-echogenic intraluminal mass, and good pulsatile vessel without intimal thickening. Angioscopy directly showed red thrombi with white fibrin coating, and no parietal lesions. Patients with chronic pulmonary thromboembolism could be classified into 3 groups: 1) Poor extensibility of the vessel wall and intimal thickening with non-echogenic thrombi on intravascular ultrasound, and relatively fresh parietal thrombi consisting of a mixture of red blood cell and fibrin, and spider web-like fibrin net on angioscopy (6 patients). 2) Crescent parietal thrombi and wall irregularity on intravascular ultrasound, and probably organized thrombi with a mixture of red and white surface on angioscopy (one patient). 3) Marked and echogenic intimal thickening and poor extensibility on intravascular ultrasound, and intimal surface irregularities and yellowish changes on angioscopy (one patient). All patients suffering acute deterioration in the chronic phase belonged to groups 1) or 2). Intravascular ultrasound and angioscopy are useful for characterizing the thrombi and related pulmonary artery lesions in patients with pulmonary thromboembolism. The pulmonary artery intima and thrombus differ between acute and chronic pulmonary thromboembolism.
[A 73-year-old woman with familial Parkinson's disease].
We report a 73-year-old Japanese woman with familial Parkinson's disease. The patient was well until her 67 years of the age, when she noted rest tremor in her right hand. Soon after her gait became short stepped. She visited our clinic on October 6, 1992 when she was 68 years old. She was alert and well oriented without dementia. She showed masked face, small voice, small stepped gait, retropulsion, resting tremor in her right hand, rigidity in the neck, and bradykinesia. She was treated with 400 mg/day of levodopa-carbidopa, which improved her symptoms, however, she developed wearing off phenomenon 3 years after the initiation of levodopa treatment. On August 26, 1998, she developed abdominal pain, diarrhea, and vomiting. She was admitted to another hospital, where abdominal plain x-ray revealed an evidence of intestinal obstruction (ileus). She was treated with nasogastric suction and intravenous fluid. Her condition did not improve and she was transferred to our hospital on August 29, 1998. Her family history revealed no consanguineous marriage. She had two elder brothers and three elder sisters. One of her brothers had been diagnosed as Parkinson's disease. Her husband also suffered from Parkinson's disease, however, her parents apparently did not have Parkinson's disease. On admission, she appeared to be drowsy. Her blood pressure was 102/70 mmHg, body temperature 36.2 degrees C. The lungs were clear and no cardiac murmur was present. Abdomen was flat and bowel sound was audible. No abnormal mass was palpable. Neurologic examination revealed mild consciousness disturbance, masked face, and small voice. No motor paralysis was noted. Muscle tone was hypotonic. No abnormal involuntary movement was noted. Abnormal laboratory findings on admission were as follows; WBC 11,300/microliter, amylase 1,373 IU/l, CK 446 IU/l, BUN 50 mg/dl, creatinine 1.17 mg/dl, CRP 22.7 mg/ dl, Na 134 mEq/l, K 3.1 mEq/l, and Cl 81 mEq/l. A chest x-ray film revealed pneumonic shadows in both lower lung fields. She was treated by nasointestinal suction, intravenous fluids, and chemotherapy for her infection. Her BP started to drop on September 2 and she developed cardiac arrest on the same day. She was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had a form of autosomal dominant familial Parkinson's disease. As parents did not have Parkinson's disease, some of the participants raised the possibility of autosomal recessive inheritance. But the age of onset was too late for autosomal recessive inheritance. Majority thought that the mode of inheritance was autosomal dominant with low penetrance. alpha-Synuclein mutation causes an autosomal dominant familial Parkinson's disease, but this type is very rare in non-Greek populations and the penetrance is high. Chromosome 2-linked autosomal dominant familial Parkinson's disease shows low penetrance. There are many other autosomal dominant forms of familial Parkinson's disease linked to yet unknown chromosome loci. Majority thought that this patient also had a form of Lewy-body positive autosomal dominant familial Parkinson's disease of unknown chromosome locus. Post mortem examination revealed ischemic intestinal lesion with strangulation. This was thought to be the cause of her death. In the central nervous system, the brain appeared to be normal by inspection. In the coronal sections, the substantia nigra and the locus coeruleus showed marked depigmentation. Histologic examination revealed marked neuronal loss and Lewy body formation in the remaining neurons. Pathologic examination was consistent with Parkinson's disease. Mutational analysis for the parkin gene was negative.
Field evaluation of who hemoglobin color scale in West Java.
The results obtained with a WHO hemoglobin (Hb) colour scale were evaluated in a field study in Chibubur district in Java island by comparison with hemoglobin values obtained by an automated blood cell analyzer K-800 (Sysmex. Kobe, Japan). When the color scale test was performed following the instructions for use. Hb values observed were usually higher than the values obtained by the analyzer. Thirty microl blood was loaded on the filter paper and an 60 sec waiting period was used. The sensitivity of results obtained with the color scale was 23.3% (14/60), and specificity was 96.6% (58/60). We propose an additional testing method based on our results.
Vectorcardiographic evaluation of myocardial infarct size: comparisons with thallium myocardial scintigraphy.
OBJECTIVE: To determine the usefulness of vectorcardiography (VCG) in assessing myocardial infarct size. METHODS: The correlation of spatial and scalar parameters of VCG with the percent defect volume (%DV) of thallium myocardial single photon emission computed tomography (SPECT) was investigated in 63 patients with first-onset myocardial infarction (MI). VCG parameters included: (1) spatial parameters: magnitude, azimuth and elevation of the maximal vector, vectors at 20 ms and 30 ms, and (2) scalar parameters: amplitudes of 20 ms and 30 ms vectors at X, Y, and Z scalar leads abbreviated as X20, Y20, Z20, X30, Y30 and Z30, respectively. RESULTS: For anteroseptal MI, the azimuth of 30 ms vector and Z20 showed a significant correlation with %DV (r = 0.572, P < 0.05 and r = 0.832, P < 0.001) while in anteroseptal MI with involvement of lateral wall, the azimuth of 30 ms vector and X30 were correlated with %DV significantly (r = 0.775, and r = 0.780, P < 0.01). For inferior and inferoposterior MI, the elevation of 30 ms vector and Y30 were correlated well with %DV (r = 0.871, P < 0.01, r = 0.928, P < 0.001 for inferior MI and r = 0.678, P < 0.01, r = 0.760, P < 0.001 for inferoposterior MI). CONCLUSION: VCG parameters, especially scalar parameters, can be used to evaluate myocardial infarct size easily and non-invasively with remarkable accuracy.
Effects of mouth cleansing on the levels of exhaled nitrous oxide in young and older adults.
Nitrous oxide (N2O) is produced by denitrification, i.e. by microbial reduction of nitrate (NO3-). Our previous studies have established an analytical method for demonstrating the existence of N2O in exhaled air, and we showed that levels of N2O in exhaled air increase with age after puberty. However, the source of this change and its biological significance are still unclear. The purpose of this study was to examine whether the oral microorganisms are the main source of N2O. We measured exhaled N2O in 35 young adults (aged 19-29 years) and 34 older adults (aged 61-79 years) before and after mouth cleansing. N2O was measured using an infrared-photoacoustic analyzer equipped with an optical filter (UA0985, 2215 cm-1). Participants were classified as producers and non-producers according to the levels of exhaled N2O relative to the level in the atmosphere. N2O production differed significantly between the young adult producers and the older adult producers. Mouth cleansing resulted in an immediate reduction in exhaled N2O in both groups. We only found seven (20.0%) producers in the young, and 32 (94.1%) producers in the older after mouth washing. The differences before and after mouth cleansing were significant in both groups (P < 0.01 in the young and P < 0.05 in the older). The oral cavity is a major source of N2O. However, since approximately half-levels of N2O were still observed in exhaled air after mouth, cleansing, there may exist another N2O source in the human body.
Glutathione downregulates the phosphorylation of I kappa B: autoloop regulation of the NF-kappa B-mediated expression of NF-kappa B subunits by TNF-alpha in mouse vascular endothelial cells.
Nuclear factor-kappa B (NF-kappa B) regulates gene expression upon immune and inflammatory responses. It has been demonstrated that redox regulation by thiols is involved in the signal-transduction cascade. In this study, we examined the effect of glutathione (GSH) on the NF-kappa B activity and the expression of NF-kappa B subunits induced by tumor necrosis factor-alpha (TNF-alpha) using mouse vascular endothelial cells. GSH inhibited the serine phosphorylation of I kappa B-alpha by TNF-alpha, leading to the downregulation of NF-kappa B-DNA binding activity followed by decreased expression of p65/p50 and I kappa B mRNAs. The regulation of the autoregulatory loop for the NF-kappa B activation and the expression of NF-kappa B subunits may be important in endothelial cells in response to cytokines.
Mutagenicities of 2,4- and 2,6-dinitrotoluenes and their reduced products in Salmonella typhimurium nitroreductase- and O-acetyltransferase-overproducing Ames test strains.
Mutagenicities of 2,4- and 2,6-dinitrotoluene (2,4-and 2,6-DNT), and reduced metabolites formed by the incubation of 2,4- and 2,6-DNT with Salmonella typhimurium TA98, were tested using S. typhimurium YG strains possessing high level of nitroreductase (NR) and/or O-acetyltransferase (OAT) activities. All compounds tested showed greatest mutagenic activities toward strains YG1041 and YG1042, which possess high levels of NR and OAT activities. The relative mutagenic activities of 2,4-DNT and its related compounds toward YG1041 and YG1042 were aminonitrotoluenes<2,4-DNT<2,2'-dimethyl-5, 5'-dinitroazoxybenzene (2,2'-DM-5, 5'-DNAOB)4-hydroxylamino-2-nitrotoluene (4HA2NT)<<4, 4'-dimethyl-3,3'-dinitroazoxybenzene (4,4'-DM-3,3'-DNAOB), and aminonitrotoluenes (2A4AT, 4A2NT)<2,4-DNT<4HA2NT4,4'-dimethyl-3, 3'-dinitroazoxybenzene (4,4'-DM-3,3'-DNAOB)<2HA4NT, respectively. In addition, the relative mutagenic activities of 2,6-DNT and its related compounds toward YG1041 and YG1042 were 2, 6-DNT<2-hydroxylamino-6-nitrotoluene (2HA6NT)<2,2'-dimethyl-3, 3'-dinitroazoxybenzene (2,2'-DM-3,3'-DNAOB), and 2-amino-6-nitrotoluene (2A6NT)<2,6-DNT<2HA6NT, respectively. These results, together with previous findings, suggested that aminohydroxylamino dimethylazoxybenzenes or aminohydroxylamino dimethylazobenzenes produced either by the reduction of hydroxylaminonitrotoluenes or by the reduction of dimethyl dinitroazoxybenzenes are active metabolites responsible for the mutagenic activities of 2,4- and 2,6-DNT.
Decreased expression of bcl-2 and bcl-x mRNA coincides with apoptosis following intracerebral administration of 3-nitropropionic acid.
The mitochondrial toxin, 3-nitropropionic acid (3-NP), is an irreversible inhibitor of succinate dehydrogenase that induces apoptosis in vitro and in vivo. We injected 3-NP into the striatum of rats to examine the potential role of Bcl-2 or Bcl-x, proteins that can inhibit apoptosis, in brain injury due to 3-NP. Electrophoretic examination of striatal tissue indicated that 3-NP induced internucleosomal fragmentation typical of apoptosis. There was also histologic evidence of apoptosis based on staining by the terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) method. Apoptosis was first observed 6 h after injection, was maximal at 1 day, and was still observed on day 7. Expression of bcl-2, bcl-x, and c-jun mRNA expression was evaluated 1, 3, 6, and 12 h and 1, 3, 5, and 7 days after injection using in situ hybridization. Both bcl-2 and bcl-x mRNA expression in the striatum decreased starting at 6 h and continued to 5 days after injection. This was in contrast to an apparent increase in c-jun expression. The similarity in the time course of apoptosis to that of suppression of bcl-2 and bcl-x mRNA suggests that changes in expression of these genes may contribute to apoptosis following 3-NP injection.
Expression of a gene cluster kaiABC as a circadian feedback process in cyanobacteria.
Cyanobacteria are the simplest organisms known to have a circadian clock. A circadian clock gene cluster kaiABC was cloned from the cyanobacterium Synechococcus. Nineteen clock mutations were mapped to the three kai genes. Promoter activities upstream of the kaiA and kaiB genes showed circadian rhythms of expression, and both kaiA and kaiBC messenger RNAs displayed circadian cycling. Inactivation of any single kai gene abolished these rhythms and reduced kaiBC-promoter activity. Continuous kaiC overexpression repressed the kaiBC promoter, whereas kaiA overexpression enhanced it. Temporal kaiC overexpression reset the phase of the rhythms. Thus, a negative feedback control of kaiC expression by KaiC generates a circadian oscillation in cyanobacteria, and KaiA sustains the oscillation by enhancing kaiC expression.
Familial essential thrombocythemia associated with one-base deletion in the 5'-untranslated region of the thrombopoietin gene.
Familial essential thrombocythemia (ET) is inherited in an autosomal-dominant manner. This finding implies that familial ET may arise as a consequence of a mutation(s) that activates platelet production. In 1994, the thrombopoietin (TPO) gene was isolated and cloned. The TPO-TPO receptor, encoded for by the c-mpl gene, are essential regulators of thrombopoiesis. Alterations of TPO or c-Mpl thus may constitute a pathogenic event leading to familial ET. In a case of familial ET presented in our institute, serum TPO levels were significantly elevated in affected members of the family as compared with nonaffected members. Moreover, we identified a one-base deletion in the 5'-untranslated region of the TPO gene in affected but not in nonaffected family members. In vitro experiments showed that the identified mutation increased TPO production. Based on our findings, we propose that this region of the TPO gene may play a crucial role in regulating TPO expression. Our results strongly suggest that the identified mutation leads to familial ET.