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Biomedical subjects

A Masuda

Publications and source records attributed to A Masuda.

At least 73 records · Page 4Linked to original sources
PubMed1999

Comparison of survival rates of patients with nasopharyngeal carcinoma treated with radiotherapy, 5-fluorouracil and vitamin A ("FAR" therapy) vs FAR therapy plus adjunctive cisplatin and peplomycin chemotherapy.

The overall survival rate (OSR) of 36 patients with nasopharyngeal carcinomas (NPC) treated at Kyushu University hospital between 1983 to 1992 was analyzed. As primary treatment, 16 patients received a combination therapy of 5-fluorouracil, vitamin A, and radiation (FAR therapy); two patients received radiotherapy only; 18 patients received FAR therapy plus adjunctive systemic chemotherapy consisting of cisplatin and peplomycin. The radiation dose to the nasopharynx was 6000 to 7050 cGy while that to the neck was 4000-6000 cGy. The 5-year OSR of all the patients was 49%. Histological type (moderately differentiated squamous cell carcinoma) and patient age (> or = 55) were found to be significant prognostic factors for a worse OSR. Although survival decreased with increasing T stage, no significant difference was observed. The 5-year OSR of the patients treated with FAR therapy was 53% and was 51% with FAR therapy plus chemotherapy. Compared to FAR therapy alone, adjunctive chemotherapy did not increase OSR of the patients with NPC.

Adult↗
PubMed1999

Modified functional hemispherectomy in hemimegalencephaly.

We report a case of hemimegalencephaly in a 13-month-old girl successfully treated with modified functional hemispherectomy. Instead of total temporal lobectomy, medial temporal lobectomy with excision of the hippocampus and amygdala was carried out. The central region including the parasagittal tissue was preserved. A few days after the surgery seizures completely ceased. Administration of anticonvulsants was stopped 5 months after the surgery, and she has been seizure-free for 42 months.

Amygdala↗
PubMed1999

Hearing immaturity found by ABR and its clinical impact on otoneurological evaluation.

Auditory Brainstem Response (ABR) is the most reliable and most frequently used procedure to evaluate audiological conditions in early infancy. However, several reports have demonstrated that developmental change in the central nervous system may affect the results of ABR in audiological evaluations. We examined statistically the reliability of ABR for the diagnosis of profound deafness in early childhood according to our experience over the past 12 years of follow-up in our facility. Subjects included 371 children among 1,041 children who were admitted to Kanariya-Gakuen (institute for pre-school deaf children) from April 1985 to March 1997. These children were examined with ABR to determine their hearing levels. In five cases with an abnormal hearing threshold determined by ABR and other audiological tests, repeated examinations carried out during a 5- to 6-month follow-up period revealed that they had normal hearing. Three of these children had been diagnosed previously with mental retardation and the remaining two were infants < 5 months old. The specificity and sensitivity of ABR were calculated as 97.3% and 100%, respectively. The predictive value of a positive result was 94.7%. There remains the possibility of a false negative for such cases, although the rate seems to be very low (< 0.2%).

Audiometry↗
PubMed1999

A gene for fluctuating, progressive autosomal dominant nonsyndromic hearing loss, DFNA16, maps to chromosome 2q23-24.3.

The sixteenth gene to cause autosomal dominant nonsyndromic hearing loss (ADNSHL), DFNA16, maps to chromosome 2q23-24.3 and is tightly linked to markers in the D2S2380-D2S335 interval. DFNA16 is unique in that it results in the only form of ADNSHL in which the phenotype includes rapidly progressing and fluctuating hearing loss that appears to respond to steroid therapy. This observation suggests that it may be possible to stabilize hearing through medical intervention, once the biophysiology of deafness due to DFNA16 is clarified. Especially intriguing is the localization of several voltage-gated sodium-channel genes to the DFNA16 interval. These cationic channels are excellent positional and functional DFNA16 candidate genes.

Adolescent↗
PubMed1999

An unusual regressive germinal center, the 'FDC-only lymphoid follicle,' in lymph nodes of organ transplant recipients.

Follicular lesions include germinal center (GC) hyperplasia, regressive transformation of GCs, and follicle lysis. The present histologic, electron microscopic, and immunohistochemical study of six autopsy cases after organ transplantation accompanied by the administration of immunosuppressive drugs revealed a peculiar regression of lymph node GCs in two cases, which has not been noted previously. The histologic findings of the regressive GCs were classified into three patterns. In pattern A, the GCs had few or no lymphocytes and were surrounded by a poorly developed mantle zone-like structure. Apoptotic cell death of GC lymphocytes was found in a few GCs, but most GCs lacked tingible body macrophages. In pattern B, the GC lymphocytes and tingible body macrophages were absent, showing crowded follicular dendritic cells (FDCs) in a corpuscular shape. In pattern C, the lymphocytic mantle was absent. The GCs were smaller than those in the other patterns, and the shape was irregular because of disintegration of FDCs. The immunostaining for FDC markers revealed dispersed growth of FDCs. On electron microscopy, the lesions were composed of a dense mass of elliptical and oval cells without prominent cytoplasmic processes, a labyrinthlike structure, and emperipolesis of lymphocytes. The distinct desmosomelike adhesive junctions, specific electron microscopic features of FDCs, were evident. We propose to call these follicular lesions "FDC-only lymphoid follicles." It is speculated that this follicle may be evoked after preceding follicular hyperplasia with a complicated mechanism including increased apoptosis of GC lymphocytes and decreased lymphocyte migration to lymph node GCs caused by immunosuppressive drugs.

Adult↗
PubMed1999

Volatile anesthetics reduce calcium current in parasympathetic neurons from bullfrog hearts.

UNLABELLED: Although the autonomic nervous system regulates cardiac function, the cellular mechanism(s) of general anesthetics on the activities of parasympathetic neurons have not been directly assessed. We therefore studied the volatile anesthetic actions on the Ca2+ current of parasympathetic neurons isolated from bullfrog hearts. Neurons were enzymatically isolated from the interatrial septum of bullfrog heart and maintained in a short-term tissue culture. The Ca2+ current was recorded with a whole-cell voltage-clamp method under a Na+, K+ -free condition. Isoflurane (2.5 vol%) and sevoflurane (5.0 vol%) reduced the peak amplitude of the Ca2+ current (to 79% and 72% of control, respectively) without changing the reversal potential. The curve-fit analysis of the inactivation kinetics revealed that isoflurane and sevoflurane accelerated the inactivation of the current and that isoflurane shifted the midpoint of the steady-state inactivation curve of the Ca2+ current toward negative by 13.6 mV. The results indicate that volatile anesthetics reduce the Ca2+ current of parasympathetic neurons and modify the inactivation kinetics. IMPLICATIONS: The anesthetic reduction of the Ca2+ current of parasympathetic neurons can induce a decrease of acetylcholine release from the post-ganglionic endings. These findings, in part, account for the anesthetic attenuation of the vagal efferent activities observed in humans and experimental animals.

Anesthetics, Inhalation↗
PubMed1999

Effects of propofol on contractile response and electrophysiological properties in single guinea-pig ventricular myocyte.

Effects of propofol on contractile response, action potential, resting membrane potential and L-type voltage-dependent calcium channel current were examined in guinea-pig single cardiac myocyte. Propofol (10(-4) M) inhibited contractile response induced by electrical stimulation (83.6% of control, n = 5), but did not change the resting membrane potential. On the other hand, propofol reduced the overshoot of action potential (10(-4) M), and shortened the duration of action potential (10(-5) and 10(-4) M). Whole-cell voltage clamp experiment showed inhibition of L-type calcium channel current (ICa, 10(-5) M: 90.8+/-1.39, 10(-4) M: 83.4+/-1.53% of control, n = 5). In addition, propofol showed use-dependent block of ICa. It is concluded that negative inotropic effect of propofol is caused by suppression of action potential, and that inhibition of ICa plays a role in shortening of the duration of action potential.

Action Potentials↗
PubMed1999

Effects of unilateral stellate ganglion block on the spectral characteristics of heart rate variability.

The effect of unilateral stellate ganglion block on cardiovascular regulation remains controversial, so the present study used power spectral analysis of heart rate variability to investigate its effect on the autonomic neural control of the heart. In 20 young healthy volunteers (mean age: 25 years), heart rate variability was determined before and after unilateral stellate ganglion block (right side 11, left side 9) using 8 ml of 1% mepivacaine during supine rest. Using autoregressive spectrum analysis, power spectra were quantified by measuring the area in 3 frequency bands: high-frequency power (lnHF, parasympathetic influence) from 0.15 to 0.40 Hz, low-frequency power (lnLF, predominantly sympathetic influence) from 0.04 to 0.15 Hz, and total-frequency power (lnTF) less than 0.40 Hz. Right stellate ganglion block decreased not only the lnLF component from 6.55+/-0.84 to 5.77+/-0.47 but also the lnHF component from 4.40+/-0.95 to 3.42+/-1.12 (p<0.05). In contrast, left stellate ganglion block changed neither the lnLF nor the lnHF component. The lnTF component was also decreased significantly by right stellate ganglion block from 7.80+/-0.95 to 7.01+/-0.36 (p<0.05), but was unchanged following left stellate ganglion block. Neither right nor left stellate ganglion block induced any significant change in both the RR and corrected QT intervals. However, changes in the RR interval induced by right stellate ganglion block showed significant positive correlation with changes in lnHF (p<0.005) and lnTF (p<0.05). These results suggest that (1) autonomic innervation to the sinus node is mainly through the right-sided stellate ganglion, (2) pharmacological right-sided stellate ganglion block may attenuate not only sympathetic but also parasympathetic activity and (3) following right stellate ganglion block the decrease in both the sympathetic and parasympathetic influence on the sinus node may inconsistently counterbalance and change the RR interval.

Adult↗
PubMed1999

A case of Graves' disease associated with autoimmune hepatitis and mixed connective tissue disease.

The patient was a woman of forty-eight. Liver dysfunction was pointed out at the age of forty-five. She was admitted to hospital because of her hyperthyroidism. Her palmar skin was wet and her fingers were swollen like sausages. She had a diffuse and elastic hard goiter with a rough surface. The serum levels of free T3 (9.6 pg/mL) and free T4 (3.76 ng/dL) were high and that of TSH (0.11 microU/mL) was low. The activity of TSH-binding inhibitory immunoglobulin (TBII) was 89%. The uptake rate of 123I to the thyroid was 55.1% and the uptake pattern was nearly diffuse. The goiter was proved to contain several nodules by ultrasonography, but aspiration cytology showed no malignant cells. She was diagnosed to have Graves' disease with adenomatous goiter. She also had high ALT (34 IU/L) and gamma-globulin (1.97 g/dL). She had positive antinuclear antibody (speckled type), positive anti-ribosomal nuclear protein antibody, and positive LE cell phenomenon. The liver biopsy revealed mononuclear cell infiltration with fibrosis in the portal area. These data indicated that she also had autoimmune hepatitis (AIH) and mixed connective tissue disease (MCTD). The analysis of human leukocyte antigen (HLA) showed positive A11 which had been reported to relate to Graves' disease, and positive DR4 which had been reported to relate to AIH and MCTD. These results suggested that HLA would determine susceptibility to three distinct autoimmune diseases in this case.

Alanine Transaminase↗
PubMed1999

[Multicenter prospective survey of prognosis of hypertensive elderly outpatient under antihypertensive treatment--morbidity and mortality of cardiovascular diseases and cancer].

Although calcium-channel blockers and angiotensin-I-converting enzyme inhibitors are often used for treatment of hypertension in the elderly in Japan compared to those in the United States and in European countries, there have been few investigations on the prognosis of the elderly receiving these antihypertensive treatments. The Research Group for "Guidelines on the Treatment of Hypertension in the Elderly" collaborated with the Comprehensive Research Projects on Aging and Health group of the Ministry of Health and Welfare of Japan in performing a 3-year survey on the outcome of 700 hypertensive elderly outpatients (> or = 60 years) receiving treatment of antihypertensive drugs. Antihypertensive drugs including dihydropyridine-type calcium channel blockers, beta blockers, angiotensin-I-converting enzyme inhibitors, diltiazem, diuretics and old-type antihypertensives (hydralazine, budralazine, and centrally acting drugs such as clonidine, methyldopa and guanabenz) were administered to 71.3%, 30.4%, 26.2%, 14.0%, 8.6%, and 6.4% of the 642 elderly patients surveyed for three years, at the time of registration, respectively. Morbidity and mortality rates of total cerebro-cardiovascular diseases, stroke, and heart diseases, were 27.6 and 7.81/1,000 patient-years, 15.1 and 3.6/1,000 patient-years, 10.4 and 4.2/1,000 patient-years, respectively. These results were similar or even better than those of megatrials of antihypertensive treatments for elderly patients in Europe and United States. After adjustment for potential confounding factors, multiple logistic analysis revealed that a past history of ischemic heart disease, use of the old-type antihypertensive drugs, male gender, and diastolic high blood pressure were independent risk factors for the morbidity of cerebro-cardiovascular diseases taking the group of non-cerebro-cardiovascular disease as the reference group. We also identified 22 cases of newly occurred malignancies including 7 fatal cases. However, none of the antihypertensives was significantly related to the occurrence of malignancies. These results lead support to the tendencies in the use of antihypertensive drugs in Japan.

Aged↗
PubMed1999

Follicular dendritic cell dysfunction and disorganization of lymphoid structures in MRL/lpr mice.

The follicular dendritic cell (FDC) in secondary lymphoid organs plays a key role in the function of the germinal center (GC) of the lymphoid follicle (LF) for regulation of the humoral immune response. MRL MpJ-lpr/lpr (MRL/lpr) mice, which have an abnormal humoral immune response, are a model for autoimmune disease. The present study was undertaken to investigate FDC dysfunction and LF disorganization in the spleen and lymph nodes of MRL/lpr mice. In 12-week-old MRL/lpr mice, antigen (Ag) trapping of FDC and half-life of trapped Ag on FDC was reduced. Although immunohistochemistry revealed well-developed FDC networks positive for complement receptors and having in vitro immune complex trapping in cryostat sections, Ag-trapping was not detected in 16-week-old MRL/lpr mice. Moreover a marked decrease in the number of GC and that of GC cell of residual GC in the MRL/lpr mice was observed by 12 weeks of age. Also reduced expression of intercellular adhesion molecule-1, FcgammaRII/III, and FDC-specific Ag (FDC-M1) on FDC was detected in 16-week-old MRL/lpr mice. The accumulation of double negative (CD4-CD8-) T cells, which is a characteristic feature of MRL/lpr mice, was observed around LF; however they did not infiltrate the LF and FDC network. In conclusion the loss of Ag-trapping on FDC and simultaneous disorganization of the lymphoid structure may be related closely to the immunologic abnormality observed in MRL/lpr mice.

Animals↗
PubMed1999

Cochlear implantation for symptomatic hereditary deafness.

Recently, the effectiveness of cochlear implantation for hereditary deafness has been reported. We performed cochlear implantation for two patients with symptomatic hereditary deafness. Deafness in one patient was thought to be a result of albinism-deafness syndrome and in the other patient, a result of chronic progressive external ophthalmoplegia syndrome. Since their speech perception abilities improved dramatically, we believe that cochlear implantation should be actively performed for these two syndromes.

Adult↗
PubMed1998

Immunization of bovines with an aspartic proteinase precursor isolated from Boophilus microplus eggs.

The capacity of the Boophilus Yolk pro-Cathepsin (BYC) to induce a protective immune response in cattle against Boophilus microplus infestation was tested by vaccination experiments and by inoculation of monoclonal antibody (MAb) against BYC into fully engorged tick females. In immunization experiments the measurement of various biological parameters demonstrated a partial protection against B. microplus. A continuous decrease in the levels of specific antibodies was observed over 11 months when six bovines were maintained in field conditions. The inoculation of the MAb into tick females produced a dose-dependent decrease in oviposition and survival of the ectoparasite compared to the control.

Animals↗
PubMed1998

GABAergic mechanisms in the action of general anesthetics.

1. The effects of volatile and intravenous anesthetics were studied on evoked field potentials in rat hippocampal CA1 neurons in vitro to determine the role of GABAergic mechanisms in the action of general anesthetics. 2. It was observed that both volatile (halothane, isoflurane, sevoflurane) and intravenous (thiopental, pentobarbital, propofol) anesthetics decreased population spike (PS) amplitudes. 3. Using paired-pulse paradigms, it was revealed that volatile agents enhance paired-pulse facilitation (PPF), and intravenous agents reduce PPF. Use-dependent effects on PS amplitudes were observed following application of the intravenous anesthetics, whereas volatile agents did not show use-dependency. The effects of the intravenous anesthetics were blocked by the GABA(A) receptor antagonist, bicuculline. 4. It is suggested that agent specific actions of general anesthetics are a result of differential effects on GABAergic mechanisms that modulate synaptic transmission.

Anesthetics, General↗
PubMed1998

Regulation of cytosol-nucleus pH gradients by K+/H+ exchange mechanism in the nuclear envelope of neonatal rat astrocytes.

In order to study the subcellular heterogeneity of intracellular H+ concentration in reactive astrocytes, the pH in the nucleus and cytosol of cultured astrocytes was measured using a confocal laser scanning microscope (CLSM) and pH indicator dye, 5'(and 6')-carboxyseminaphthofluorescein (carboxy SNAFL-1). The change in intracellular pH was indexed by the fluorescence ratio (F535/F610) at an excitation wavelength of 514.5 nm. The in vitro fluorescence ratio increased as pH decreased. This ratio in the nucleus was significantly lower than that in the cytosol of astrocytes when perfused by HEPES-buffered Hanks' balanced salt solution (HHBSS) at pH 7.4. Acid stimulations of cells (pH 5.0) raised the fluorescence ratio in both nucleus and cytosol. However, the increase in the fluorescence ratio of the nucleus was less than that of cytosol. Treatment with a K+/H+ ionophore, nigericin (20 microM), reversibly nullified this cytosol-nucleus pH gradient. These findings suggest that a buffering mechanism(s) for maintaining of intracellular pH exists between the nucleus and cytosol, and a K+/H+ exchanger may act on the nuclear envelope to eventuate intranuclear pH maintenance in the living cells.

Animals↗
PubMed1998

Induction of apoptosis by Smad3 and down-regulation of Smad3 expression in response to TGF-beta in human normal lung epithelial cells.

Smad family members are essential intracellular signaling components of the transforming growth factor-beta (TGF-beta) superfamily involved in a range of biological activities. Two highly homologous molecules, Smad2 and Smad3, have so far been identified as receptor-activated Smads for TGF-beta signaling and have become the focus of intensive studies. However, no definite differences in regulation or function have been established between these TGF-beta signaling molecules. In the present study, we show that the expression of Smad3, but not its close relative, Smad2, is down-regulated by TGF-beta mediated signals themselves in human lung epithelial cells. This down-regulation of Smad3 by TGF-beta treatment did not appear to result from shortening of the half-life of Smad3 mRNA. Constitutive expression of Smad3 in the presence of TGF-beta induced apoptotic cell death, with an adverse effect on the cell growth of human lung epithelial cells. Apoptotic cell death could also be induced by forced expression of Smad2 in the presence of TGF-beta, but less efficiently than by that of Smad3. These findings clearly define the distinctions between Smad2 and Smad3 for the first time in that a qualitative difference was observed with regard to the regulation of their expression in response to TGF-beta, while Smad2 and Smad3 appeared to have quantitatively different capabilities regarding the induction of apoptotic cell death in human lung epithelial cells.

Apoptosis↗
PubMed1998

p27KIP1 in human lung cancers: differential changes in small cell and non-small cell carcinomas.

Small cell lung cancers (SCLCs) and non-small cell lung cancers (NSCLCs), two major categories of human lung cancers, have been shown to exhibit considerably different clinicopathological, biological, and molecular genetic characteristics. Inactivation of cyclin-dependent kinase inhibitors is now thought to play an important part in the pathogenesis of this fatal disease. In the present study, we show that in vitro p27KIP1 expression was associated with cell density-dependent growth inhibition in human lung epithelial cells in vitro, whereas in vivo, p27KIP1 expression in lung cells showed an inverse correlation with proliferative activity in the developing and adult normal lungs. Our immunohistochemical examination of 166 lung tumor specimens also revealed a striking difference in p27KIP1 expression between SCLCs and NSCLCs. Of 149 NSCLCs, 107 (72%) showed reduced p27KIP1 expression, with 8 being virtually negative. Furthermore, p27KIP1 expression status was found to be a significant prognostic factor for patient survival in the analysis of the 149 primary, resected NSCLC cases (P = 0.03 by the log-rank test). In contrast, all SCLC specimens thus far examined exhibited significantly increased staining when compared to the corresponding normal lung epithelium. These findings provide additional evidence for the heterogeneity prevalent in human lung cancers and suggest that p27KIP1 might play distinct biological roles in the pathogenesis of the two major histological categories, warranting additional studies to elucidate the functional consequences of such differences.

Adult↗