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T Takeda

Publications and source records attributed to T Takeda.

At least 559 records · Page 31Linked to original sources
PubMed1994

Significance of distributed representation in the output layer of a neural network in a pattern recognition task.

In the cerebral cortex, it is assumed that information is represented by the activity pattern of an assembly of neurons and the synaptic efficacies among them. A distributed representation of pattern is incorporated in the output layer of a neural network with an error back-propagation algorithm, in order to study its technological merits. The network has three layers, which consist of a 32 x 32 array of units (1024) for the input layer, 6-25 units for the hidden layer and 12 units for the output layer. 12 triangular patterns with a variety of parameters are presented to the input layer. Three output-layer units are assigned to each input figure. After initial learning, the network responds to the learned pattern with high accuracy. In addition, it responds with high accuracy to similar but unpresented patterns, showing a generalisation for patterns. The network shows resistance to unit de-activation procedures. When the input layer is exposed to the learned pattern, the hidden-layer units show associative activation pattern. These results indicate that the organisation of information representation in the output layer in a neural network strongly influences both the performance of the whole network and information representation in the hidden layer.

Association↗
PubMed1994

What is the benefit of aggressive chemotherapy for advanced neuroblastoma with N-myc amplification? A report from the Japanese Study Group for the Treatment of Advanced Neuroblastoma.

In 1985, a nationwide single protocol (cyclophosphamide, vincristine, tetrahydropyranyl Adriamycin, and cisplatin) for the treatment of advanced neuroblastoma was begun in Japan and was found to significantly increase the 3-year survival rate--to 70% for stage III, and to 45% for stage IV. In this study, the authors investigated the efficacy of this protocol for advanced neuroblastoma with or without N-myc amplification. In 159 of the 233 patients with advanced neuroblastoma treated with this protocol (between January 1985 and March 1993), genomic amplification of N-myc was determined. These 159 patients were divided into two groups according to the number of N-myc copies, ie, those with fewer than 10 copies (105 patients) and those with 10 or more copies (54 patients). The survival curves for the two groups were significantly different. The 5-year survival rate for patients with 10 or more copies was 43.9%; this is surprisingly high in comparison to results of previous studies in which no survivors were expected in cases of advanced neuroblastoma with highly amplified N-myc. Persistent bone marrow suppression was common, but there were no deaths attributable to drug side effects. Five patients with fewer than copies of N-myc amplification died more than 3 years after initial treatment. Three of the five had tumors with an unfavorable Shimada classification, and two had diploid nuclear DNA content. The authors conclude that the protocol resulted in dramatic improvement in the patients with advanced neuroblastoma, even with high N-myc amplification.(ABSTRACT TRUNCATED AT 250 WORDS)

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Accelerated aging of dermal fibroblast-like cells from senescence-accelerated mouse (SAM). 1. Acceleration of population aging in vitro.

Fibroblast-like cells were isolated from the senescence accelerated mouse (SAM) and cultured, after which evidence of accelerated senescence was sought. Fibroblast-like cell lines were established from the dorsal dermis of neonate mice of both the accelerated senescence-prone strain, SAMP11 and the accelerated senescence-resistant strain, SAMR1. All cell lines from both strains showed a crisis in growth and were immortalized. At crisis, all cultures were composed of morphologically characteristic senescent cells. However, in cell lines from SAMP11, this change was more rapid and at earlier population doublings (PDs) than seen in cell lines from SAMR1. Crises (SAMP11; SAMR1) were also operationally taken to be the point of the least change in PDs (11.2 +/- 1.1; 15.4 +/- 0.5 PDs), the least saturation density (11.3 +/- 0.8; 19.1 +/- 2.6 PDs), and the longest population doubling time (10.1 +/- 0.8; 14.2 +/- 0.6 PDs). Crisis occurred significantly earlier (P < 0.05) and the aging process was accelerated in cell lines from SAMP11, compared with lines from SAMR1. This evidence tends to support various observations made in the accelerated senescence-prone strains of SAMP, in vivo.

Aging↗
PubMed1994

Acute brain swelling in cerebral embolization model of rats. I: Epidural pressure monitoring.

The authors measured epidural pressure of rats using a microballoon to monitor brain swelling after cerebral embolism. Rats with embolization of the major cerebral artery frequently demonstrated acute brain swelling. Within 5 hours of embolization, the increase in epidural pressure was 29.7 +/- 20.3 mm Hg (mean +/- SD), ranging from 3 to 68 mm Hg. The increase in epidural pressure tended to reach a near-maximal value within 30 minutes of embolization and thereafter stayed at that point until the end of the experiment. These results suggest that measuring epidural pressure can quantitatively assess acute brain swelling in rats.

Acute Disease↗
PubMed1994

Localization of atrophy-prone areas in the aging mouse brain: comparison between the brain atrophy model SAM-P/10 and the normal control SAM-R/1.

Mouse inbred strain "SAM-P/10" (Senescence Accelerated Mouse) is a model of age-related brain atrophy. In this strain there is an earlier and more severe age-related deterioration in the conditional avoidance learning than the normal control inbred SAM-R/1 strain. The present study analysed age-related changes in brain area size using a computerized morphometric method. The region most vulnerable to age-related atrophy in SAM-P/10 was the frontal region of the cerebral cortex, including the prefrontal cortex. Other neocortical regions underwent diffuse atrophy. Posterior piriform cortex, entorhinal cortex, anterior olfactory nucleus, amygdala, caudate-putamen, nucleus accumbens and cerebellar cortex were atrophy-prone regions. The septum also underwent atrophy but other basal forebrain structures were intact. The hippocampus, diencephalon and brainstem structures showed no atrophic change. White matter structures did not change in size with aging except for the forceps minor of the corpus callosum, which showed age-related atrophy. On the contrary, SAM-R/1 showed a significant age-related atrophy only in a restricted part of the cerebral cortex, mainly in the parietal region. Other cortical regions, subcortical structures, diencephalon, brainstem structures, cerebellum and white matter were atrophy-resistant in SAM-R/1. The prefrontal cortex, entorhinal cortex, piriform cortex and striatum are closely interconnected and also connect with the amygdala which plays a key role in conditioning in the rodent. Age-related atrophy in all these structures in SAM-P/10 presumably accounts for the age-related deficits in conditional avoidance learning in this strain of mouse. Comparison between SAM-P/10 and SAM-R/1 or other well-known rodents indicates that SAM-P/10 is a unique rodent that spontaneously and rapidly develops progressive generalized cerebral atrophy, which is considered to be a pathological process rather than an accelerated aging process.

Aging↗
PubMed1994

Age-related hearing impairment in senescence-accelerated mouse (SAM).

The auditory brainstem response and histopathology of the cochlea were investigated in an accelerated senescence-prone strain, SAM-P/1 mice and a senescence-resistant strain, SAM-R/1 mice. Each strain displayed an age-related auditory loss expressed as elevated thresholds similar to human hearing loss in that high-frequency losses occurred earlier than middle- or low-frequency losses. SAM-P/1 showed a more rapid decline of hearing with age than did SAM-R/1. Interpeak intervals I-III and I-IV were prolonged with age in both strains, especially at high frequency. The prolongation was more marked in SAM-P/1 than in SAM-R/1. The decrease in amplitude of wave I observed in both strains was greater in SAM-P/1 than in SAM-R/1. The auditory function assessed by thresholds, interpeak intervals and amplitudes of wave I in SAM-P/1 at 12 months of age corresponded roughly to that in SAM-R/1 at 20 months of age. In morphological studies, there was an age-related decrease in the cell density as well as in the size of spiral ganglion neurons in both strains, but these changes were more pronounced in SAM-P/1 than in SAM-R/1. These results reveal that age-related hearing impairment associated with morphological changes in the cochlea is manifested earlier and progresses more rapidly in SAM-P/1 than in SAM-R/1. Thus, the SAM-P/1 strain should prove useful as a model of presbycusis.

Aging↗
PubMed1994

Modification of strain-specific femoral bone density by bone marrow-derived factors administered neonatally: a study on the spontaneously osteoporotic mouse, SAMP6.

SAMP6 is a recently developed strain of osteoporotic mice, and SAMP2 is a control for SAMP6 and has a higher peak bone mass. The bone mass of SAMP6 was increased until 2 months of age when a lysate of cells derived from the bone marrow of SAMP2 was injected at 1 or 4 days of age, but it was not increased when the lysate was injected at 21 days of age. No effect on bone mass was observed when lysates of other cells, bovine serum albumin or heat-inactivated lysate of bone marrow-derived cells of SAMP2, were injected. The ability to increase bone mass was not in the supernatant but in the pellet obtained by ultracentrifugation (105,000 g) of the lysate of bone marrow-derived cells of SAMP2. The lysate did not change the osteoclast surface but changed the appositional bone formation. In conclusion, the lysate of cells derived from the bone marrow of SAMP2 contains factors which can increase the bone mass of SAMP6, and these factors are present in the pellet obtained by ultracentrifugation.

Animals↗
PubMed1994

Heparin inhibits endothelin-1 production in cultured rat mesangial cells.

The present study was designed to examine whether heparin inhibits basal or stimulated endothelin-1 production by arginine vasopressin (AVP) and platelet-derived growth factor (PDGF) in cultured rat mesangial cells. In addition, the reversibility of the heparin effect on mesangial cell endothelin-1 production was examined. AVP and PDGF stimulated endothelin-1 secretion in a concentration-dependent manner in these cells. Heparin (10 to 100 U/ml) exhibited concentration-related inhibition of AVP- and PDGF-stimulated endothelin-1 secretion. Heparin also had weak but significant inhibitory effects on basal endothelin-1 secretion in these cells. The protein kinase (PKC)-activating phorbor ester, phorbor myristate acetate (PMA), stimulated endothelin-1 secretion and heparin inhibited PMA-stimulated endothelin-1 secretion. In addition, the inhibitory effect of heparin was completely abolished in PKC-depleted mesangial cells. Mesangial cells which were exposed to a high concentration (100 U/ml) of heparin for 24 hours were capable of producing endothelin-1 after a short lag period of removal of heparin from the culture medium. These mesangial cells also showed recovery of responses to AVP and PDGF by secreting a significantly greater amount of endothelin-1 than the non-stimulated level. These results indicate that heparin potently inhibits mesangial cell endothelin-1 production, especially when stimulated by AVP or PDGF. This inhibitory effect of heparin is probably PKC dependent, and reversible.

Animals↗
PubMed1994

Dentatorubral and pallidoluysian atrophy expansion of an unstable CAG trinucleotide on chromosome 12p.

Dentatorubral and pallidoluysian atrophy (DRPLA) is an autosomal dominant neurodegenerative disorder characterized by combined systemic degeneration of the dentatofugal and pallidofugal pathways. We investigated a candidate gene and found that DRPLA patients had an expanded CAG trinucleotide repeat in a gene on the short arm of chromosome 12. The repeat size varied from 7-23 in normal individuals. In patients one allele was expanded to between 49-75 repeats or occasionally even more. Expansion was usually associated with paternal transmission and only occasionally with maternal transmission. Repeat size showed a close correlation with age of onset of symptoms and disease severity. We conclude that DRPLA is the seventh genetic disorder known to be associated with expansion of an unstable trinucleotide repeat.

Alleles↗
PubMed1994

Transforming growth factor beta 1 and extracellular matrix gene expression in isoprenaline induced cardiac hypertrophy: effects of inhibition of the renin-angiotensin system.

OBJECTIVE: The aim was to investigate changes in cardiac transforming growth factor beta 1 (TGF-beta 1), fibronectin, and collagen types I and III mRNA levels in isoprenaline induced cardiac hypertrophy, and the effects of delapril, an angiotensin converting enzyme inhibitor, and TCV-116, an angiotensin II type 1 receptor antagonist, on this hypertrophy. METHODS: Rats were continuously infused with saline and low or high dose of isoprenaline (0.5 or 3 mg.kg-1.d-1) by an osmotic minipump for 24 h, 48 h or 7 d. Treatment with delapril (100 mg.kg-1.d-1) or TCV-116 (10 mg.kg-1.d-1) was started from 1 d before the implantation of minipump to the end of experiments. After the experimental periods, left ventricular weight was measured and the mRNA was extracted and measured by northern blot hybridisation. RESULTS: Both low and high doses of isoprenaline infusion resulted in increased left ventricular weight. With low dose infusion, cardiac TGF-beta 1 mRNA was not stimulated throughout the infusion, while fibronectin mRNA and collagen types I and III mRNAs began to increase at 24 h and 48 h, respectively, after the infusion. In high dose isoprenaline infusion, not only was extracellular matrix mRNA but also TGF-beta 1 mRNA in the ventricle significantly increased. TCV-116 prevented isoprenaline induced left ventricular hypertrophy as much as delapril. However, with delapril or TCV-116, the time course of TGF-beta 1 and ECM mRNA expression was almost similar to isoprenaline infusion only. CONCLUSIONS: The extracellular matrix mRNA expressions are enhanced in myocardial hypertrophy by a low dose of isoprenaline, which is probably not mediated by TGF-beta 1. The preventive effects of TCV-116 on this hypertrophy indicate that the inhibitory effects of angiotensin converting enzyme inhibitor on cardiac hypertrophy are due to the inhibition of angiotensin II and that angiotensin II type I receptor plays an important role in isoprenaline induced left ventricular hypertrophy. However, the renin-angiotensin system may play a minor role in isoprenaline induced cardiac fibrosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Molecular genetic characterization of the senescence-accelerated mouse (SAM) strains.

Senescence-Accelerated Mouse (SAM) is a murine model of accelerated senescence, which consists of the senescence-prone P series and the senescence-resistant R series of strains. In order to characterize these SAM strains molecular genetically, we have performed a series of Southern hybridization experiments using oligonucleotide probes designed to recognize the endogenous mouse retrovirus sequences. The repertoires of endogenous retroviruses in different SAM strains indicated that each SAM strain is distinct. Comparisons of the SAM strains with the parental AKR/J strain revealed significant differences between them, suggesting the involvement of other strains in the course of the development of SAM. While some of the endogenous retroviruses were found in all of the SAM strains, others were found to be distributed uniquely, indicating their potential usefulness as genetic markers in the analysis of strain-specific phenotypes, and possibly of the phenomenon of accelerated senescence itself.

Aging↗
PubMed1994

Spread of Vibrio cholerae O139 Bengal in India.

Vibrio cholerae serogroup O139 Bengal, a novel strain with epidemic potential, completely displaced V. cholerae serogroup 01 in Calcutta in January 1993, which was followed by an epidemic caused by V. cholerae O139 in March-May 1993. From November 1992 to July 1993, 95.6% of 916 V. cholerae isolates submitted to the National Institute of Cholera and Enteric Diseases from 28 locations in India were confirmed as serogroup O139. As of July 1993, V. cholerae O139 had been isolated from 13 Indian states and a union territory, and large outbreaks of cholera caused by the O139 serogroup had occurred in several cities. The extent of spread of V. cholerae O139 Bengal in India and its ability to swiftly disseminate leaves little doubt that this is the beginning of the eighth pandemic of cholera.

Adolescent↗
PubMed1994

Accommodation toward diameter change of a spotlight in a dark room.

The three-dimensional optometer (TDO III) was used to measure accommodative responses when gazing at a spotlight that changed its diameter in an otherwise completely dark room. Three emmetropic females served as subjects and the stimuli were presented at 33 cm (-3 D) from the subjects. The subjects felt that the spotlight approached them when its diameter increased. However, the magnitude of accommodation when viewing the smaller diameter spotlight was greater than that for the larger diameter spotlight. This means that the eye accommodated less, although the spotlight was felt to be nearer, and contradicts the common belief based on the subjectively measured data reported earlier. By conducting several supplemental experiments, we infer that this phenomenon comes from the effort in reducing accommodation lag dynamically in order to see the smaller target more clearly.

Accommodation, Ocular↗
PubMed1994

Eosinophil cationic protein in the sera of patients with Mycoplasma pneumonia.

In 1985 we reported that eosinophilia was found in many children with Mycoplasma pneumonia. We measured the serum concentrations of eosinophil cationic protein (ECP) produced by eosinophils in 25 children with Mycoplasma pneumonia, 25 with asthma and 11 with no disease (normal controls). The mean concentrations (+/- SD) of serum ECP in children with Mycoplasma pneumonia, with asthma and the normal controls were 18.7 +/- 12.6, 23.7 +/- 12.2 and 6.5 +/- 1.4 micrograms/ml, respectively. When compared with those of normal controls, these higher serum concentrations of ECP in children with Mycoplasma pneumonia and asthma were statistically significant (P < 0.001). The data were directly correlated with the presence of eosinophilia (r = 0.349). There was no relationship between the amount of ECP and the age of children with Mycoplasma pneumonia. These results suggest that ECP may work as a factor causing a persistent cough similar to asthma in children with Mycoplasma pneumonia.

Adolescent↗
PubMed1994

The capacity of dog lung to release prostaglandin I2 as a biochemical parameter for evaluating lung damage during preservation.

The release of prostaglandin I2 (PGI2) from the vasculature is thought to reflect damage to the vessels. Basal and bradykinin (BK)-stimulated release of PGI2 from isolated dog lungs after 6-hr preservation were investigated to evaluate lung damage after preservation. Maximal PGI2 release induced by BK decreased significantly after preservation at 24 degrees C (room temperature), but not after hypothermic preservation at 4 degrees C, although basal PGI2 release without BK stimulation did not change in either group of lungs after preservation. The function of allotransplanted lungs assessed by arterial oxygen tension was impaired by preservation at room temperature but not by hypothermic preservation. No differences were observed by light microscopy in either group in the pulmonary tissues, including the pulmonary artery, after preservation. In summary, damage to the lung after preservation may be reflected by the maximal PGI2 release from the lung after BK infusion. Therefore the maximal PGI2 releasing capacity induced by BK may be a useful biochemical parameter for estimating the viability of preserved lungs.

Animals↗
PubMed1994

Vibrio mimicus with multiple toxin types isolated from human and environmental sources.

A collection of 13 strains of Vibrio mimicus, including both clinical and environmental isolates from different geographic regions, was examined for various toxins. One strain of environmental origin produced cholera-like toxin (CT) which was completely absorbed with anti-CT immunoglobulin G, five strains produced a haemolysin that cross-reacted with the thermostable direct haemolysin of V. parahaemolyticus and DNA from two strains hybridised with a DNA probe specific for the heat-stable enterotoxin of V. cholerae non-O1. Culture supernates of all strains produced a factor that was cytotoxic to Vero and Chinese hamster ovary cells. In this study, we were able to identify strains of V. mimicus that produced, or had the genetic potential to produce, several toxin types simultaneously. The role of these strains as genetic reservoirs is discussed.

Animals↗