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Biomedical subjects

K Mano

Publications and source records attributed to K Mano.

At least 37 records · Page 2Linked to original sources
PubMed1995

[The relationship among hematocrit, platelet aggregation and the time of onset in patients with acute stage-cerebral infarction].

We evaluated time relation among hematocrit (Ht), platelet aggregation (PA) and the onset of acute stage-cerebral infarction in 221 patients. Lacunar infarctions were likely to occur in the evening or at midnight. The elevated Ht value was frequently found in patients with infarctions occurring at midnight, suggesting that the elevation of blood viscosity has an intimate etiology to the onset. The decrease of PA was often found in those who suffered from their stroke while awake in the morning or at midnight, and frequently had been associated with elevated Ht in the latter patients. Decrease of PA is often reported during acute stage-cerebral infarction. Our results indicate that increased platelet aggregation may play an important role in developing cerebral infarction, especially in those who had onset of illness in the morning.

Acute Disease↗
PubMed1994

Efficacy of recombinant human granulocyte-macrophage colony-stimulating factor for chemotherapy-induced leukopenia in patients with non-small-cell lung cancer.

To assess the feasibility and efficacy of rhGM-CSF in ameliorating chemotherapy-induced leukopenia in patients with advanced non-small-cell lung cancer, we conducted a double-blind placebo controlled phase III study in a multicenter setting. Patients were eligible if they had cytologically or histologically proven cancer, no prior chemotherapy, stage IIIB or IV disease, an Eastern Cooperative Oncology Group (ECOG) performance status of 0-2, an age of less than 76 years, and no symptomatic brain metastasis, disseminated bone metastasis, or previous vertebral/pelvic irradiation. The chemotherapy regimen consisted of mitomycin given at 8 mg/m2 on day 1, cisplatin given at 100 mg/m2 on day 1, and vindesine given at 3 mg/m2 i.v. on days 1 and 8 (MVP). If the granulocyte nadir count recorded after the first cycle of MVP was less than 1,000/mm3, patients were randomly assigned to receive recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) or placebo during the second cycle of MVP. The dose of rhGM-CSF was 125 micrograms/m2 given daily s.c. for 14 consecutive days starting on day 2. Of the 52 patients enrolled, 45 were evaluable. The nadir of granulocytes was significantly lower in the placebo group (P = 0.007). The period during which the granulocyte count was less than 1,000/mm3 was significantly longer in the placebo group (median, 6 vs 10 days; P = 0.04). The incidence of adverse effects related to rhGM-CSF, such as fever (> or = 38 degrees C) and skin rash, was significantly higher in the rhGM-CSF group (P = 0.011). The rate of response to chemotherapy did not significantly differ between the two groups. In conclusion, rhGM-CSF reduced the duration of chemotherapy-induced granulocytopenia. The clinical usefulness of this agent may be deminished because of the adverse effects encountered when it is used in combination with a moderately myelotoxic chemotherapy regimen.

Adult↗
PubMed1994

[Cytokine production by human airway epithelial cells and its modulation].

There is increasing evidence that airway epithelial cells play an active role in allergic inflammation, including bronchial asthma. We showed that human airway epithelial cells in culture release GM-CSF, G-CSF, M-CSF, IL-6, and IL-8, using a serum-free culture system. These cytokines are known to modulate the bioactivities of inflammatory cells that accumulate at the site of inflammation. Among them, GM-CSF, IL-8, or both may be important because they influence the bioactivities of eosinophils, which are characteristic of allergic inflammation. Here we report on the effects of air pollutants such as suspended particulate matter and diesel exhaust particulates on release of cytokines from airway epithelial cells. All air pollutants we tested stimulated epithelial cells to release GM-CSF. These results suggest that one cause of the recent increase in the prevalence of allergic disorders is direct stimulation of airway epithelial cells by air-pollutants. Furthermore, anti-inflammatory agents such as steroids and anti-allergic drugs were found to suppress the release of GM-CSF from airway epithelial cells in vitro.

Air Pollutants↗
PubMed1994

[Clinical evaluation of combination therapy of sulbactam/cefoperazone and aminoglycoside in respiratory tract infections].

We compared clinical efficacy and safety of sulbactam/cefoperazone (SBT/CPZ) with those of SBT/CPZ combined with aminoglycoside (amikacin (AMK), tobramycin (TOB), etc.) in treatment of respiratory tract infections in patients with underlying respiratory diseases, with cancer, or with acute exacerbation of chronic respiratory infections. Clinical evaluations of monotherapy with SBT/CPZ in a total of 30 patients showed excellent results in 5, good results in 17. Clinical effects of combined therapy of SBT/CPZ plus different aminoglycosides in a total of 33 patients were excellent in 18, good in 5. The efficacy rates (excellent plus good) were 73.3% in the monotherapy and 69.7% in the combined therapy. AMK was used concomitantly with SBT/CPZ in 16 of 33 patients. Clinical effects of SBT/CPZ plus AMK were excellent in 10, good in 3, and the efficacy rate was 81.3%. Bacteriological effects were evaluable against 11 strains in the monotherapy group, and against 17 strains in the combined therapy group. The eradication rates were 54.5% in the monotherapy group, and 81.3% in the combination therapy group. Diarrhea was observed in a patient who received the monotherapy. Abnormal laboratory test results were observed on in 5 patients who received the monotherapy, and in 4 patients who received one of the combined therapies. All abnormalities disappeared after the completion or discontinuation of therapies. We considered SBT/CPZ combined with an aminoglycoside is a useful chemotherapy for respiratory tract infections in patients with underlying diseases and acute exacerbation of chronic respiratory tract infections.

Adult↗
PubMed1993

Expression of a novel form of Tec kinase in hematopoietic cells and mapping of the gene to chromosome 5 near Kit.

The Tec kinase was initially identified as a novel cytoplasmic protein tyrosine kinase that is preferentially expressed in the liver and is highly homologous to the Drosophila Dsrc28C src-related tyrosine kinase. In screening of interleukin 3 (IL-3)-dependent myeloid leukemia cells for protein tyrosine kinases, we observed that all cell lines examined expressed high levels of Tec transcripts. However, characterization of Tec cDNAs indicated that they differed significantly from the published sequence. Most strikingly, an insertion of 41 bp in the 5' region affects the initiation codon and results in replacing the published 13 amino acid amino-terminal sequences with 94 amino acids. Using polymerase chain reaction (PCR) analysis, only the form containing the insertion was detected in hematopoietic cells. In addition, we found an in-frame insertion of 66 bp that introduces an additional 22 amino acids into the SH3 domain. This insertion restores conserved SH3 sequences that are found in the src gene family and in the Dsrc28C gene. By PCR analysis, approximately equal levels of Tec transcripts containing the intact SH3 domain and containing the 22 amino acid deletion were found in hematopoietic cells. Lastly, by interspecies backcross analysis, we show that the Tec gene is tightly linked to the c-Kit gene on mouse chromosome 5.

Amino Acid Sequence↗
PubMed1993

[A case of marked eosinophilia in peripheral blood induced by rhGM-CSF].

A 53-year-old man underwent chemotherapy (CDDP, VDS, MMC) for treatment of lung cancer. He was given 125 micrograms/m2 of GM-CSF subcutaneously every day for 8 consecutive days, in order to prevent neutropenia. Three days after starting GM-CSF therapy, marked eosinophilia in peripheral blood was observed. The maximum eosinophil count was 89% of leukocytes. Nine days after stopping the treatment with GM-CSF, the number of eosinophils had normalized spontaneously. There were no clinical symptoms except for slight fever, up to 37.5 degrees C. Moreover, there was no relationship between the number of eosinophils and the serum levels of cytokines (IL-3, IL-5, GM-CSF), although we observed minimal but significant elevation of serum ECP level. This case indicates that GM-CSF may induce marked eosinophilia rather than widely stimulating granulocytes and monocytes.

Blood Proteins↗
PubMed1993

Remission of myasthenia gravis: clinical, electrophysiological and immunological studies.

The prognosis of 142 patients with myasthenia gravis (MG) was clinically investigated. Forty-nine (35%) had clinical remission (CR) and 23 (16%) good improvement (GI), while 70 (49%) remained in poor condition. Favorable clinical factors for CR were the onset of MG before the age of 20 years, a pre-thymectomy period of less than one year, and a post-thymectomy period of six years or more. Single-fiber electromyography (SFEMG) showed abnormal jitter in nine (47%) of the 19 CR patients, while abnormal jitter was shown in 13 (81%) of the 16 GI patients. Abnormal jitter in CR patients was correlated with the following clinical factors: complication with the thymoma, a period of three or more years from thymectomy to remission, and a remission period of less than six years. An anti-acetylcholine receptor (anti-AChR) antibody was positive in 12 CR patients (63%) as well as in 13 GI patients (81%). Based upon these facts, we point out that true remission seldom occurs in MG patients, and that there exist clinical features that may favorably induce clinical remission. We would like to postulate that electrophysiological and immunological follow-up is indispensable even in CR patients to predict recurrence.

Adult↗
PubMed1992

Genetic disease patterns in Japan: a review.

Comprehensive genetic studies in which the genetic structure of a population is considered against the background of ecological factors, including environmental and social variables, often supply valuable information for the solution of a number of problems in human biology, including reproductive compensation and inbreeding depression. In the first section of this paper we consider the incidence of genetic diseases in Japan in reference to other populations. Some of the genetic disorders found elsewhere do not occur or are of lower frequencies in Japan. On the other hand, a number of genetic diseases occur at higher than usual frequencies, leading to an incidence of genetic disease of the order of about 1 per 100 in newborn Japanese. We next review the studies of consanguinity in Japan and report evidence of very high levels, ranging from 8.6% to 58.0%, for villages during the early part of the twentieth century. The rates are declining rapidly for the country but, because of traditional social values, inbreeding rates remain significant in many small villages. In the final section we consider the probable trends in the frequency of inbreeding on a worldwide basis and point out that frequencies of certain genetic diseases are likely to remain high and even increase in some societies because of various socially prescribed mating patterns.

Consanguinity↗
PubMed1992

[Clinical course of asthmatics with severe asthma attack].

This study was conducted on 39 patients whose severe attacks of bronchial asthma with disturbance of consciousness required admission to the ICU of our hospital between 1984 and 1989. Among the 39 patients, there were 16 deaths. Most patients collapsed suddenly at home and were taken to our hospital. Arterial blood gas analysis at the time of admission to the ICU revealed that the PaO2 levels were as high as 252.6 +/- 57.6 (mean +/- S.E.) Torr in non-survivors and 221.0 +/- 29.7 Torr in survivors, with no significant difference because of prior oxygen therapy in almost all cases. Systolic blood pressure was 14.8 +/- 10.8 (mean +/- S.E.) mmHg, with marked circulatory disturbance in the fatal cases. Most patients displayed marked disturbance of consciousness, but maintenance of blood pressure led to recovery without sequelae despite marked disturbance of consciousness in most patients.

Adolescent↗
PubMed1991

[A family with autosomal dominant hereditary myoedema, muscular irritability, stiffness and hypertrophy].

A familial case with autosomal dominantly transmitted myoedema, muscular irritability, stiffness and hypertrophy was reported. The patient is 54 years old and his father, two sisters and niece had suffered from the similar symptoms. He had noticed a feeling of stiffness and pain in the femoral muscles after several minutes of erect position from the age of 5-6 years. He had observed that light tapping of muscles caused a bulge which persisted for several seconds in the whole body. These symptoms were not progressive. The patients had an athletic appearance, hypertrophy of gastrocnemius muscles, pes cavus and hammer toes. Mild muscular weakness and wasting were noted in the intrinsic hand muscles and the anterior tibial muscles. Myoedema was seen in the muscles of the whole body. His thyroid functions were normal. EMG studies showed no myotonic discharges. Light microscopy of biopsy specimens from the biceps brachii muscle showed unspecific myopathic changes. Electron microscopy showed many vacuoles between myofibrils. The symptoms and signs of this case are very like to those of the cases which Torbergsen described in 1975 and only four families were reported after that. The family presented here is the first report in Japan.

Edema↗
PubMed1990

Demyelinating changes in sural nerve biopsy of patients with HTLV-I-associated myelopathy.

We describe the sural nerve pathology in 3 patients with HTLV-I-associated myelopathy (HAM). These patients showed remarkable symptoms of myelopathy and had high HTLV-I titers in the serum and CSF. The common pathologic findings in the sural nerves were as follows: slightly decreased density in myelinated fibers (6,567/mm2, 6,488/mm2, and 7,159/mm2; control 9,999 +/- 3,446/mm2), frequent occurrence of demyelinated and remyelinated fibers, and many degenerating fibers with globule-like myelin changes. Teased-fiber analysis indicated the globule-like changes (Dyck's G change) to be accompanied by the formation of adjacent demyelinated segments. The globules result from slowly repetitive degenerative changes of myelin and are considered to be a form of demyelination. However, they have seldom been found in other demyelinating neuropathies, indicating the demyelination process with globule formation in HAM to be rather specific for this disease.

Axons↗
PubMed1990

[A case of long-term survival of a patient with complicated diffuse metastatic leptomeningeal carcinomatosis secondary to lung adenocarcinoma].

A case of long-term survival of a female patient with complicated diffuse metastatic leptomeningeal carcinomatosis (DMLC) secondary to lung cancer is reported. A 36-year-old woman, hospitalized with a chief complaint of headache and unproductive cough, was diagnosed as having primary lung adenocarcinoma (T4N1M1 oss) and was given systemic chemotherapy. Although progressive deterioration of her headache continued, repeated neurological examination, cerebrospinal fluid (CSF) examination, and cranial CT scans failed to show evidence of metastasis to the central nervous system, and the only finding suggesting CNS involvement was an elevated CEA level in CSF. Later in the course of her treatment, the patient suddenly lost her vision and subsequently consciousness due to acute increased intracranial pressure, and emergency ventricular drainage was performed for therapeutic and diagnostic purposes. Malignant cells were found in CSF obtained from a ventricular drainage and she was treated successfully by systemic and intrathecal chemotherapeutic agents. She was discharged after a ventriculoperitoneal shunt operation for hydrocephalus; a double-dome reservoir was used for continuous intrathecal administration of the anticancer drugs, and a shunt filter was located in the tube to prevent the dissemination of cancer cells. In addition to methotrexate and cytosine arabinoside, ACNU and interleukin-2 were administered intrathecally without serious adverse effects, but no apparent therapeutic effects were noted either. She survived over 2 years after DMLC was first diagnosed. At autopsy DMLC secondary to lung adenocarcinoma was confirmed, but no evidence of leukoencephalopathy due to aggressive intrathecal chemotherapy was found. Current therapy for patients with DMLC and its clinical problems are discussed in relation to our experience in this case.

Adenocarcinoma↗
PubMed1989

Effect of deuterium oxide (D2O) on the IgE-mediated Ca2+ influx, arachidonic acid and histamine release in rat basophilic leukemia cells.

Deuterium oxide (D2O), which is known to stimulate microtubule aggregation, enhanced the IgE-mediated 45Ca2+ influx, (14C)-arachidonic acid and histamine release in rat basophilic leukemia cells (RBL-2H3) in the same dose-dependent manner (up to 90% (v/v]. We compared the interaction between D2O and a variety of groups of pharmacological agents. A microtubule depolymerizing agent, demecolcine, which inhibited the IgE-mediated (14C)-arachidonic acid and histamine release without affecting 45Ca2+ influx, was counteracted by 45% D2O. Taxol, a microtubule stabilizing agent, which had an inhibitory effect on the above three steps, was also reversed by 45% D2O. These results would support the previous data on the interaction between D2O and microtubules and would further suggest that the status of microtubule aggregation may be related to the secretory process. Calmodulin inhibitors (W-7, trifluoperazine) blocked the IgE-mediated 45Ca2+ influx, (14C)-arachidonic acid and histamine release in the same dose-dependent manner, but were counteracted by 45% D2O. In contrast, the effects of proteinase inhibitors (TPCK, TLCK), an adenylate cyclase inhibitor (ddAdo), a phosphodiesterase inhibitor (aminophylline), a phospholipid methylation inhibitor (DZA + Hcy) and microfilament blockers (cytochalasin B and D) were not counteracted by 45% D2O. These results would suggest that D2O may be associated with calmodulin directly or indirectly possibly through some relationship between calmodulin and microtubules.

Animals↗
PubMed1989

[Study of development of autoantibody to beta-adrenergic receptors in asthmatics].

An (125I) iodohydroxybenzyl pindolol (125IHYP) binding inhibition assay was performed. Various dilutions (1:5-1:500) of sera from asthmatics and controls were incubated with canine lung membranes for 60 minutes at 30 degrees C. 125IHYP was added to the membranes for 30 minutes at room temperature in the presence and absence of 10 microM 1-propranolol, and the samples were washed through a Gelman (Type A-E) glass fiber filter using a washing buffer. Radio activity was measured with Aloka gamma counter. In the presence of various serum dilutions from asthmatics, 125IHYP specific bindings of 0.16 fmol to 4.38 fmol were measured. 125IHYP binding was inhibited in a dose-related and nonspecific manner. Serum, albumin, L-histidine and L-cysteine also inhibited 125IHYP specific binding to beta-receptors. Percentages of inhibition of serum from asthmatics on 125IHYP specific finding to beta-receptors were -17.6% to +9.3%, which were compared with identical dilutions of control serum. There was no significant difference in 125IHYP binding inhibition assay between asthmatics and controls. From these results, development of autoantibody to beta-adrenergic receptors could not be detected in this study.

Animals↗
PubMed1989

Allergenicity of Chironomidae in asthmatic patients.

In order to clarify the relation between asthma and Chironomidae, we examined the cross-reactivity between Chironomidae and other common allergens. We noted significant correlations between positive skin tests with Chironomidae and with other allergens. The radioallergosorbent inhibition test, however, suggested that there may be no cross-reactivity or, if any, only very low cross-reactivity between midge allergens and mite, house dust (HD), silk, shrimp, or mosquito allergens.

Allergens↗