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Y Kajimoto

Publications and source records attributed to Y Kajimoto.

At least 37 records · Page 2Linked to original sources
PubMed2000

New concept for the pressure setting of a programmable pressure valve and measurement of in vivo shunt flow performed using a microflowmeter. Technical note.

The aim of this study was to establish a standard method for determining the pressure setting of the Codman Hakim valve (CHV) in patients with hydrocephalus. The authors' investigation was twofold. It focused on: 1) the relationships among CHV setting, intracranial pressure (ICP), intraabdominal pressure (IAP), hydrostatic pressure (HP), and perfusion pressure (PP); and 2) the shunt flow in 18 patients with normal-pressure hydrocephalus. With the patient in a sitting position, the pressure environment around the ventriculoperitoneal shunt stabilized when PP became equal to the CHV setting. The lower the CHV setting, the lower the ICP obtained in patients in a sitting position (ICPsit) settled. This indicated the possibility of calculating the CHV setting by the equation CHV setting = HP + ideal ICPsit - IAP, where the ideal ICPsit was estimated to be between -70 and -140 mm H2O. The CHV setting was individually determined for 18 patients by using this method. The ICPsit, was controlled at a level equal to the estimated ICPsit in most cases, which supported the rationality of our concept. Shunt flow was intermittent or very low when the patient assumed a supine position and between 200 and 600 microl/minute when the patient was seated. Determining the CHV setting by using the equation CHV setting = HP + ideal ICPsit - IAP was found to be useful when directly measuring HP and IAP in patients and estimating the ideal ICPsit to be between -70 and -140 mm H2O. Postoperative shunt control performed using this method was satisfactory, and shunt complications and the number of CHV resettings were lower than in those published in previous reports. Shunt-flow measurement performed in vivo and in real time by using a microflowmeter should be useful not only in testing the functioning of shunt systems, but also in clarifying the pathophysiology of hydrocephalus.

Abdomen↗
PubMed2000

Posture-related changes in the pressure environment of the ventriculoperitoneal shunt system.

OBJECT: The purpose of this study is to clarify the whole pressure environment of the ventriculoperitoneal (VP) shunt system in patients with successfully treated hydrocephalus and to determine which factor of the pressure environment has a preventive effect on overdrainage. METHODS: Thirteen patients with hydrocephalus who had been treated with VP shunt therapy by using a Codman-Hakim programmable valve without incidence of overdrainage were examined. The authors evaluated intracranial pressure (ICP), intraabdominal pressure (IAP), hydrostatic pressure (HP), and the perfusion pressure (PP) of the shunt system with the patients both supine and sitting. With patients supine, ICP, IAP, and HP were 4.6 +/- 3 mm Hg, 5.7 +/- 3.3 mm Hg, and 3.3 +/- 1 mm Hg, respectively. As a result, the PP was only 2.2 +/- 4.9 mm Hg. When the patients sat up, the IAP increased to 14.7 +/- 4.8 mm Hg, and ICP decreased to-- 14.2 +/- 4.5 mm Hg. The increased IAP and decreased ICP offset 67% of the HP (42.9 +/- 3.5 mm Hg), and consequently the PP (14 +/- 6.3 mm Hg) corresponded to only 33% of HP. CONCLUSIONS: The results observed in patients indicated that IAP as well as ICP play an important role in VP shunt therapy and that the increased IAP and the decreased ICP in patients placed in the upright position allow them to adapt to the siphoning effect and for overdrainage thereby to be avoided.

Aged↗
PubMed1999

Identification of oxidative stress-regulated genes in rat aortic smooth muscle cells by suppression subtractive hybridization.

A suppression subtractive hybridization technique was used to identify reactive oxygen species (ROS)-regulated genes in rat vascular smooth muscle cells. Three genes out of 89 clones, identified as fibronectin, p105 coactivator and ECA39, showed increased expression after treatment with H(2)O(2). The mRNA expressions of these three genes were induced in a time- and dose-dependent manner, independent of protein kinase C activation. Immunohistochemical staining showed that the p105 coactivator expression was markedly induced in the neointima of balloon-injured rat carotid arteries. These results suggest that ROS may play an important role in the development of atherosclerosis by regulating the gene expressions we identified in this study.

Animals↗
PubMed1999

Human insulin gene is a target gene of hepatocyte nuclear factor-1alpha (HNF-1alpha) and HNF-1beta.

Maturity-onset diabetes of the young (MODY) is a monogenic form of diabetes characterized by autosomal dominant inheritance, early-onset, and impaired insulin secretion. The type 3 and type 5 forms of MODY result from mutations in the genes encoding the transcription factor, hepatocyte nuclear factor (HNF)-1alpha and HNF-1beta, respectively. The mechanism by which mutations in one allele of the HNF-1 gene impair pancreatic beta cell function is unclear. We studied the effects of wild-type and four mutant (L12H, R263C, P379fsdelCT, and L584S585fsinsTC) HNF-1alpha, which were identified in Japanese subjects with MODY3 on human insulin gene transcription. Both wild-type (WT) HNF-1alpha and HNF-1beta bound to the oligonucleotide containing the A3 element sequence in the human insulin promoter and transactivated the insulin-luciferase reporter gene by 30- and 31-fold, respectively. In contrast, binding of L12H, R263C and L584S585fsinsTC-HNF-1alpha to the probe was impaired. Transactivation activity by the four mutant HNF-1alpha was reduced (4.3 to 43.3% of WT). These data suggest that the insulin gene is a candidate target gene of HNF-1alpha/HNF-1beta and the impairment of insulin gene transcription by mutations in the HNF-1 gene might be involved in the pathogenesis of MODY.

Animals↗
PubMed1999

Association study of a polymorphism of nonerythroid alpha-spectrin gene with schizophrenia.

The specificity of cytoarchitectural abnormalities in limbic structures of patients with schizophrenia and their contributions towards the etiology of schizophrenia remain unknown. We have recently reported an increased breakdown of nonerythroid alpha-spectrin (fodrin), a major component of neuronal cytoskeletal proteins, in schizophrenic left superior temporal cortices [Kitamura et al., 1998: Biol Psychiatry 43:254-262], suggesting that polymorphisms of the alpha-spectrin gene might contribute to the vulnerability to schizophrenia. We screened for genetic variations associated with schizophrenia through the C-terminus sequences of the human nonerythroid alpha-spectrin gene (SPTAN1) spanning two EF-hands and also tested a possible contribution of the polymorphism to the development of schizophrenia by an association study. We found a polymorphic region of an intron located in the second EF-hand of SPTAN1 gene. There was no significant difference between patients with schizophrenia and controls in allele frequencies or genotype distribution. There is evidence that the Psh BI SPTAN1 gene polymorphism does not play a major role in the genetic component of schizophrenia.

Adult↗
PubMed1999

Oxidative stress induces p21 expression in pancreatic islet cells: possible implication in beta-cell dysfunction.

AIMS/HYPOTHESIS: Prolonged poor glycaemic control in patients with Type II (non-insulin-dependent) diabetes mellitus often causes pancreatic beta-cell dysfunction accompanied by decreases in insulin biosynthesis and beta-cell proliferation. This is well known as a clinical concept called glucose toxicity. Whereas oxidative stress is provoked under diabetic conditions, we examined the possible implication of cyclin-dependent kinase (Cdk) inhibitor p21 (WAF1/CIP1/Sdi1) in beta-cell dysfunction mediated by oxidative stress. METHODS: Oxidative stress was induced in isolated rat pancreatic islet cells by treatment with H(2)O(2) and mRNA expression of p21 and insulin was examined by northern blot analyses. Also, the expression of p21 and insulin mRNA was examined in Zucker diabetic fatty rat. In islet cells p21 was overexpressed using adenovirus and its effect on insulin gene transcription was examined. RESULTS: When oxidative stress was charged on isolated rat pancreatic islet cells, p21 mRNA expression was induced whereas insulin mRNA was decreased. Also, when diabetes developed in Zucker diabetic fatty rats, p21 expression was induced and the insulin mRNA expression was reduced. As support for the implication of p21 in impairment of beta-cell function, the p21 overexpression in the islet cells suppressed the insulin gene transcription. CONCLUSIONS/INTERPRETATION: The expression of cyclin-dependent kinase inhibitor p21, which can be induced by oxidative stress, increases in pancreatic islet cells upon development of diabetes. By suppressing cell proliferation and insulin biosynthesis, the p21 induction is likely to be implicated in the beta-cell glucose toxicity.

Animals↗
PubMed1999

Induction of glycation suppresses glucokinase gene expression in HIT-T15 cells.

AIMS/HYPOTHESIS: Chronic hyperglycaemia in patients with Type II (non-insulin-dependent) diabetes mellitus often leads to a decline in glucose-responsive insulin secretion from pancreatic beta cells, a phenomenon called glucose toxicity. Upon hyperglycaemia, glycation reaction occurs in the beta cells and induces oxidative stress. To understand the molecular basis of the beta-cell glucose toxicity, we investigated the possible effects of glycation on the expression and enzymatic activity of glucokinase, which plays a crucial part in glucose-responsive insulin secretion. METHODS: Glycation and reactive oxygen species were induced in HIT-T15 cells by treatment with D-ribose and effects on glucokinase gene transcription, glucokinase protein amount, glucose phosphorylation activity, and DNA-binding activities of putative glucokinase gene transcription factors were evaluated. RESULTS: When glycation was induced in HIT-T15 cells, the activity of the human glucokinase gene beta-cell-type promoter was suppressed substantially (83% reduction at 60 mmol/l D-ribose). Also, similar reductions in mRNA and protein amounts of glucokinase and in the Vmax of its enzymatic activity were observed. In agreement with the reduction in the promoter activity, the two major transcription factors of the glucokinase gene, the Pal-binding factor and PDX-1, reduced their binding to their target sequences in the glucokinase gene promoter in glycation-induced HIT cells. Because these effects of D-ribose were counteracted by aminoguanidine or N-acetylcysteine, reactive oxygen species, generated by the glycation reaction, appears to be involved in the phenomena. CONCLUSION/INTERPRETATION: The induction of the glycation reaction, which is known to occur in pancreatic beta cells in chronic hyperglycaemia, suppresses the glucokinase gene transcription and its enzymatic activity. Thus, hyperglycaemia-dependent inhibition of glucokinase activity could in part explain beta-cell glucose toxicity.

Acetylcysteine↗
PubMed1999

A clinical survey of hydrocephalus and current treatment for hydrocephalus in Japan: analysis by nationwide questionnaire.

We analyzed current treatment for hydrocephalus in Japan by means of a nationwide questionnaire. Ventriculoperitoneal (VP) shunting was the most common form of cerebrospinal fluid (CSF) shunting, and in 66% of cases the ventricular catheter was inserted via the anterior horn. Various types of flow-control valves were used in 46% of CSF shunting procedures, and the proportion of cases in which such valves are used seems to be increasing. The Codman-Hakim valve was used most frequently, followed by the Sophy valve. The initial pressure setting of programmable pressure valves was selected in 82% of institutes on the basis of the CSF pressure obtained during the shunt operation. Most flow-control valves were implanted in the retroauricular region; however, Sophy valves were implanted in the chest wall in a high percentage of cases. The rate of shunt complications was significantly lower among VP shunt cases with flow-control valves than in those without flow-control valves. The most common cause of shunt complications was trouble with the abdominal catheter. These results will contribute to progress in the treatment for hydrocephalus.

Adult↗
PubMed1999

Diamox((R)) challenge test to decide indications for cerebrospinal fluid shunting in normal pressure hydrocephalus.

OBJECTIVE: The indications for cerebrospinal fluid (CSF) shunting in patients with normal pressure hydrocephalus (NPH) have not been established. Establishment of clear-cut indications for this procedure is essential to ensure cost-effective, and safe treatment. We report the usefulness of the Diamox((R)) challenge test in evaluating indications for CSF shunting in patients with NPH. METHODS: Pre- and post-operative responses in cerebral blood flow (CBF) and intracranial pressure (ICP) to intravenous administration of Diamox((R)) 1000mg (Diamox((R)) administration) were analysed in 41 patients with NPH who were treated by ventriculoperitoneal (VP) shunt with a programmable valve and an on-off valve. RESULTS: The preoperative response of ICP to Diamox((R)) administration was more than 10 mmHg in most patients in whom the shunt was effective (shunt effective group), however, it was less than 10 mmHg in most patients in whom the shunt was ineffective (shunt non-effective group). Furthermore, the postoperative response of ICP to Diamox((R)) administration decreased to less than 10 mmHg in most patients in the shunt effective group. The increases in CBF in response to Diamox((R)) administration were similar in the two groups both before and after placement of the VP shunt. CONCLUSION: Patients in whom ICP increased by more than 10 mmHg in response to Diamox((R)) administration were regarded to have poor CSF circulation and to thus be candidates for CSF shunting. The Diamox((R)) challenge test is a simple, safe procedure, useful in evaluating the response to treatment.

Acetazolamide↗
PubMed1999

Surgical management for supratentorial astrocytic tumors.

To compare the surgical treatment of supratentorial astrocytic tumors, various methods were performed by the same surgeon. Removal of the tumor was performed using stereotactic open surgery, the fluorescein surgical microscope, and a frameless stereotactic system, and these methods were compared. The method using the stereotactic technique was useful because there was no disturbance by the shifting of the brain during the operation. However, its limitation was that only points can be marked. The fluorescein surgical microscope was very useful in the cases where neuroradiological images were enhanced by the contrast medium, but deep lesions could not be identified from the brain surface. This method could not be used, either, in the case of images that were not enhanced. By the method using the frameless stereotactic system, identification of tumors including deep lesions was possible from every direction, but the problems were the mobility of the registered skin and the shifting of the brain during the operation. On the basis of these results, the combined method of the fluorescein surgical microscope and the frameless stereotactic system appeared to be useful when neuroradiological images of lesions were enhanced because these methods were complementary towards each other, and the frameless stereotactic system supplemented by the stereotactic open surgery technique (such as leaving a marker in deep lesions just before the start of microsurgery) seemed useful when images could not be enhanced.

Adult↗
PubMed1999

Comparison between operative findings on malignant glioma by a fluorescein surgical microscopy and histological findings.

Using a fluorescein surgical microscope that we developed, we performed surgery on 30 cases of malignant glioma. Operative findings and histological findings were then compared in five of these cases. Fluorescein sodium was systemically administered intravenously as a fluorescent dye. About 20 min after intravenous administration, fluorescein activity in the blood decreased, and the fluorescence was observed only in the area lacking the blood-brain barrier function, such as tumors; then, resection of the tumor was started. The fluorescent regions coincided with the enhanced regions on CT and MRI. Fluorescein spread to the surrounding brain edematous region with time, but its intensity was very different from the tumor-associated one. In the histological examination of intensely fluorescent regions, abnormal tumor blood vessels with a thick wall and a small caliber, or with a thin wall and a large caliber, were observed. Dense tumor cells were found in these regions. On the other hand, in regions with weak or no fluorescence, infiltration of tumor cells was scant, and no abnormal blood vessels were found. Fluorescence was not observed in necrotic regions of the tumor center. These histological findings coincided with those obtained in large surgical specimen or autopsy, and tumor-cell rich regions seemed to be removed by resecting abnormal vascular regions (fluorescent regions). Enhanced regions on CT and MRI disappeared after operation by resecting intensely fluorescent regions. These results indicate that the fluorescein surgical microscope developed by us is a useful aid in operations on malignant glioma.

Brain Neoplasms↗
PubMed1999

Overexpression of the aldose reductase gene induces apoptosis in pancreatic beta-cells by causing a redox imbalance.

To determine the role of the polyol metabolizing pathway under hyperglycemic conditions, the effects of aldose reductase (AR) on the cellular functions of pancreatic beta-cells were examined. Stable transfectants of rat AR cDNA were obtained with a pancreatic beta-cell line, HIT, in which a negligible amount of AR was originally expressed. Overproduction of AR triggered DNA fragmentation, as judged with the TUNEL method and agarose gel electrophoresis. Morphological analysis by electron microscopy also clearly showed apoptosis of the AR-overexpressing HIT cells. Induction by interleukin-1beta of gene expression such as those of an inducible form of nitric oxide synthase (NOS-II) and Mn-superoxide dismutase (Mn-SOD), was much lower in the transfectants than in the control cells, while the expression of constitutively expressed genes such as those for Cu,Zn-superoxide dismutase and insulin was not changed. The susceptibility to interleukin-1beta stimulation of the expression of the NOS II and Mn-SOD genes was due to suppressed NF-kappaB activity, which is essential for the expression of these genes. In addition, the intracellular NADPH/NADP+ ratio was considerably lower in the AR-transfected cells than in control cells. Thus, the overexpression of AR in pancreatic beta-cells induced apoptosis that may be caused by a redox imbalance.

Aldehyde Reductase↗
PubMed1999

Identification of a portable repression domain and an E1A-responsive activation domain in Pax4: a possible role of Pax4 as a transcriptional repressor in the pancreas.

Pax4 is a paired-domain (PD)-containing transcription factor which plays a crucial role in pancreatic beta/delta-cell development. In this study, we characterized the DNA-binding and transactivation properties of mouse Pax4. Repetitive rounds of PCR-based selection led to identification of the optimal DNA-binding sequences for the PD of Pax4. In agreement with the conservation of the optimal binding sequences among the Pax family transcription factors, Pax4 could bind to the potential binding sites for Pax6, another member of the Pax family also involved in endocrine pancreas development. The overexpression of Pax4 in HIT-T15 cells dose dependently inhibited the basal transcriptional activity as well as Pax6-induced activity. Detailed domain mapping analyses using GAL4-Pax4 chimeras revealed that the C-terminal region of Pax4 contains both activation and repression domains. The activation domain was active in the embryonic kidney-derived 293/293T cells and embryonal carcinoma-derived F9 cells, containing adenoviral E1A protein or E1A-like activity, respectively but was inactive or very weakly active in other cells including those of pancreatic beta- and alpha-cell origin. Indeed, the exogenous overexpression of type 13S E1A in heterologous cell types could convert the activation domain to an active one. On the other hand, the repression domain was active regardless of the cell type. When the repression domain was linked to the transactivation domain of a heterologous transcription factor, PDX-1, it could completely abolish the transactivation potential of PDX-1. These observations suggest a primary role of Pax4 as a transcriptional repressor whose function may involve the competitive inhibition of Pax6 function. The identification of the E1A-responsive transactivation domain, however, indicates that the function of Pax4 is subject to posttranslational regulation, providing further support for the complexity of mechanisms that regulate pancreas development.

Adenovirus E1A Proteins↗
PubMed1999

New bipolar diathermy forceps with automatic dripping and flushing--technical note.

A new bipolar diathermy forceps system was developed to solve the problems of constant, pressure-limited flow rate, and one-sided irrigation. A roller pump, activated synchronously by pressing a foot switch, feeds dripping and flushing solution to the target tissue via the tip at both ends of the forceps. This system is volume-limited. Continuous compression of the foot switch first activates the flushing function, which continues for less than 1 second, during which time bleeding spots can be detected. The flow then changes automatically to the dripping function to suppress tip burning and prevent damage to the surrounding tissues from heat and current leakage. Repeated pressing of the foot switch initiates the jet irrigation function (continuous high flow rates), allowing irrigation of hematomas and removal of excess debris.

Electrocoagulation↗
PubMed1999

Beneficial effects of antioxidants in diabetes: possible protection of pancreatic beta-cells against glucose toxicity.

Oxidative stress is produced under diabetic conditions and possibly causes various forms of tissue damage in patients with diabetes. The aim of this study was to examine the involvement of oxidative stress in the progression of pancreatic beta-cell dysfunction in type 2 diabetes and to evaluate the potential usefulness of antioxidants in the treatment of type 2 diabetes. We used diabetic C57BL/KsJ-db/db mice, in whom antioxidant treatment (N-acetyl-L-cysteine [NAC], vitamins C plus E, or both) was started at 6 weeks of age; its effects were evaluated at 10 and 16 weeks of age. According to an intraperitoneal glucose tolerance test, the treatment with NAC retained glucose-stimulated insulin secretion and moderately decreased blood glucose levels. Vitamins C and E were not effective when used alone but slightly effective when used in combination with NAC. No effect on insulin secretion was observed when the same set of antioxidants was given to nondiabetic control mice. Histologic analyses of the pancreases revealed that the beta-cell mass was significantly larger in the diabetic mice treated with the antioxidants than in the untreated mice. As a possible cause, the antioxidant treatment suppressed apoptosis in beta-cells without changing the rate of beta-cell proliferation, supporting the hypothesis that in chronic hyperglycemia, apoptosis induced by oxidative stress causes reduction of beta-cell mass. The antioxidant treatment also preserved the amounts of insulin content and insulin mRNA, making the extent of insulin degranulation less evident. Furthermore, expression of pancreatic and duodenal homeobox factor-1 (PDX-1), a beta-cell-specific transcription factor, was more clearly visible in the nuclei of islet cells after the antioxidant treatment. In conclusion, our observations indicate that antioxidant treatment can exert beneficial effects in diabetes, with preservation of in vivo beta-cell function. This finding suggests a potential usefulness of antioxidants for treating diabetes and provides further support for the implication of oxidative stress in beta-cell dysfunction in diabetes.

Acetylcysteine↗
PubMed1998

Asymmetrical changes in the fodrin alpha subunit in the superior temporal cortices in schizophrenia.

BACKGROUND: We examined possible abnormalities in neural structural proteins that may underlie morphometric changes reported in the left superior temporal cortices (Brodmann's area 22) of schizophrenics. METHODS: Particulate proteins of the superior temporal cortices taken at autopsy from 11 schizophrenic and 9 control brains were fractionated by gel electrophoresis. Target proteins, identified by reading their amino acid sequences, were immunoquantified using the specific antibody. RESULTS: Amino acid sequences of the 150-kDa proteins on sodium dodecyl sulfate/polyacrylamide gel electrophoresis, which were significantly increased on the left side of schizophrenic superior temporal cortices, revealed that they were proteolytic fragments of the alpha subunit of fodrin, a major cytoskeletal protein underlying the plasma membrane. Immunoquantification using the specific antibodies against alpha and beta subunits of fodrin indicated that there exist concomitant decreases in the full-length 240-kDa form and increases in the 150-kDa form of alpha-fodrin with no changes of the 235-kDa form of beta-fodrin in the left superior temporal cortices of the schizophrenic brains. CONCLUSIONS: The findings may be a possible molecular basis for linking morphometric changes to neurochemical pathophysiology in schizophrenia.

Aged↗