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Kazuhiro Ishikawa

Publications and source records attributed to Kazuhiro Ishikawa.

18 recordsLinked to original sources
PubMed2006

Fhit modulates the DNA damage checkpoint response.

In preneoplastic lesions, the DNA damage checkpoint is induced and loss of heterozygosity at the FRA3B/FHIT common chromosome fragile region precedes or is coincident with activation of the checkpoint response in these early stages. Introduction of exogenous Fhit into cells in vitro led to modulation of expression of checkpoint proteins Hus1 and Chk1 at mid-S checkpoint, a modulation that led to induction of apoptosis in esophageal cancer cells but not in noncancerous primary cultures. Mutation of the conserved Fhit tyrosine 114 resulted in failure of this function, confirming the importance of this residue. The results suggest that the DNA damage-susceptible FRA3B/FHIT chromosome fragile region, paradoxically, encodes a protein that is necessary for protecting cells from accumulation of DNA damage through its role in modulation of checkpoint proteins, and inactivation of Fhit contributes to accumulation of abnormal checkpoint phenotypes in cancer development.

Acid Anhydride Hydrolases↗
PubMed2006

DNA damage-dependent cell cycle checkpoints and genomic stability.

In response to genotoxic stress, which can be caused by environmental or endogenous genotoxic insults such as ionizing or ultraviolet radiation, various chemicals and reactive cellular metabolites, cell cycle checkpoints which slow down or arrest cell cycle progression can be activated, allowing the cell to repair or prevent the transmission of damaged or incompletely replicated chromosomes. Checkpoint machineries can also initiate pathways leading to apoptosis and the removal of a damaged cell from a tissue. The balance between cell cycle arrest and damage repair on one hand and the initiation of cell death, on the other hand, could determine if cellular or DNA damage is compatible with cell survival or requires cell elimination by apoptosis. Defects in these processes may lead to hypersensitivity to cellular stress, and susceptibility to DNA damage, genomic defects, and resistance to apoptosis, which characterize cancer cells. In this article, we have noted recent studies of DNA damage-dependent cell cycle checkpoints, which may be significant in preventing genomic instability.

Animals↗
PubMed2006

[Summary of an electronic chart system in Anjo Kosei hospital and clinical laboratory system].

Many companies are introducing PC systems, and management administration can be done more effectively. Management administration was previously paper-based was, but, with improved PC information systems, their adoption is inevitable. This is the situation facing the Mayor of Ministry of Health and Welfare Health Policy Bureau, the medical and pharmaceutical safety chief of the bureau, the guidelines about "saving medical examination and treatment records on electronic media" by the insurance chief of the bureau joint signature notification on April 22, 1999, the spread of the electronic chart system which changes a patient's paper record, aiming at patient's record disclosure, standardization of data, and equalization of medical quality to no longer be an exception in medical care. At this symposium, I presented a summary of the electronic chart system and the inspection system that this House introduced concentrating on the particularly special functions.

Blood Specimen Collection↗
PubMed2005

Effects of single and repeated administration of methamphetamine or morphine on neuroglycan C gene expression in the rat brain.

The rearrangement of neural networks associated with the behavioural sensitization and tolerance induced by psychostimulants is poorly understood. We have investigated the effects of repeated administration of methamphetamine (chronic MAP), which induces behavioural sensitization, or morphine (chronic morphine), which induces tolerance to its antinociceptive effect, on the mRNA levels of neural network-related genes in the rat brain. A gene of special interest was that for neuroglycan C (NGC), a neural tissue-specific transmembrane chondroitin sulphate proteoglycan. Single MAP (acute MAP) administration significantly decreased NGC mRNA levels in the frontal cortex, ventral tegmental area (VTA), and amygdala compared to vehicle-treated groups. Repeated MAP (chronic MAP) administration significantly increased NGC mRNA levels in the frontal cortex, nucleus accumbens (NAc), striatum, hippocampus, VTA, and amygdala compared to acute MAP treatment. Single morphine (acute morphine) administration significantly increased NGC mRNA levels in the NAc, striatum, hippocampus, VTA, and amygdala compared to vehicle-treated groups. Chronic morphine administration significantly decreased NGC mRNA levels in the NAc, striatum, VTA, and amygdala compared to acute treatment. In addition, the NGC protein level in the NAc was increased after chronic MAP and acute morphine treatment. Dopamine and opioid receptor antagonists attenuated the effect of MAP and morphine respectively on NGC mRNA levels. These results suggest that the sensitization to MAP is associated with up-regulation of NGC gene expression, while the tolerance to the morphine-induced analgesic effect is associated with the down-regulation of NGC gene expression.

Animals↗
PubMed2005

Irinotecan therapy in a 12-year-old girl with recurrent brain stem glioma and without functional polymorphisms in UGT1A1 activity: case report.

A 10-year-old girl was diagnosed with astrocytoma grade 2. Immuno-chemo-radiotherapy (interferon, ranimustine, and radiation), second-line chemotherapy (carboplatin and etoposide, 7 cycles) and third-line chemotherapy (ifosfamide, carboplatin, and etoposide) was given to treat progressive disease. Finally, irinotecan therapy was initiated and led to dramatic clinical improvement. Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) to yield its beta-glucuronide. The polymorphic UGT isoenzyme, UGT1A1 has genetic variants which decrease in SN-38 glucuronidating capacity and could help predict irinotecan-associated toxicity. The patient suffered excessive toxicity with low-dose irinotecan although no functional polymorphism in UGT1A1 was identified. We suggest that irinotecan offers an effective treatment option for children with recurrent brain stem glioma and other genetic variants except UGT1A1 may be a risk factor for irinotecan-induced toxicity.

Antineoplastic Agents, Phytogenic↗
PubMed2005

The role of tissue plasminogen activator in methamphetamine-related reward and sensitization.

In the central nervous system, tissue plasminogen activator (tPA) plays a role in synaptic plasticity and remodeling. Our recent study has suggested that tPA participates in the rewarding effects of morphine by regulating dopamine release. In this study, we investigated the role of tPA in methamphetamine (METH)-related reward and sensitization. Repeated METH treatment dose-dependently induced tPA mRNA expression in the frontal cortex, nucleus accumbens, striatum and hippocampus, whereas single METH treatment did not affect tPA mRNA expression in these brain areas. The METH-induced increase in tPA mRNA expression in the nucleus accumbens was completely inhibited by pre-treatment with R(+)-SCH23390 and raclopride, dopamine D1 and D2 receptor antagonists, respectively. In addition, repeated METH treatment increased tPA activity in the nucleus accumbens. There was no difference in METH-induced hyperlocomotion between wild-type and tPA-deficient (tPA-/-) mice. On the other hand, METH-induced conditioned place preference and behavioral sensitization after repeated METH treatment were significantly reduced in tPA-/- mice compared with wild-type mice. The defect of behavioral sensitization in tPA-/- mice was reversed by microinjections of exogenous tPA into the nucleus accumbens. Our findings suggest that tPA is involved in the rewarding effects as well as the sensitization of the locomotor-stimulating effect of METH.

Amphetamine-Related Disorders↗
PubMed2004

The tissue plasminogen activator-plasmin system participates in the rewarding effect of morphine by regulating dopamine release.

Tissue plasminogen activator (tPA) is a serine protease that catalyzes the conversion of plasminogen (plg) to plasmin, which in turn functions to degrade extracellular matrix proteins in the central nervous system. The tPA-plasmin system plays a role in synaptic plasticity and remodeling. Here we show that this protease system participates in the rewarding effects of morphine by acutely regulating morphine-induced dopamine release in the nucleus accumbens (NAcc). A single morphine treatment induced tPA mRNA and protein expression in a naloxone-sensitive manner, which was associated with an increase in the enzyme activity in the NAcc. The acute effect of morphine in inducing tPA expression was diminished after repeated administration. Morphine-induced conditioned place preference and hyperlocomotion were significantly reduced in tPA(-/-) and plg(-/-) mice, being accompanied by a loss of morphine-induced dopamine release in the NAcc. The defect of morphine-induced dopamine release and hyperlocomotion in tPA(-/-) mice was reversed by microinjections of either exogenous tPA or plasmin into the NAcc. Our findings demonstrate a previously undescribed function of the tPA-plasmin system in regulating dopamine release, which is involved in the rewarding effects of morphine.

Animals↗
PubMed2003

Comparative study of acute effects of single doses of fexofenadine, olopatadine, d-chlorpheniramine and placebo on psychomotor function in healthy volunteers.

Since most classical (first-generation) antihistamines have undesirable sedative effects on the central nervous system (CNS), newer (second-generation) antihistamines have been developed to relieve the sedative effects and to improve the patient's quality of life. However, the psychomotor profiles of second-generation antihistamines are not fully elucidated. In this randomized, double-blind, crossover study, the acute effects of single doses of second-generation antihistamines, fexofenadine (120 mg) and olopatadine (10 mg), on cognitive and psychomotor performance were investigated in comparison with those of placebo and d-chlorpheniramine (4 mg), a first-generation antihistamine, using objective and subjective assessments, in 11 healthy Japanese volunteers. In a battery of psychomotor tests, d-chlorpheniramine impaired tracking ability in the compensatory tracking task and caused a reduction in behavioural activity as continuously measured by wrist actigraphy. Olopatadine, like d-chlorpheniramine, reduced the behavioural activity, while fexofenadine had no effect in any of the tests. No significant changes in the subjects' self-ratings of drowsiness were found with the three antihistamines. These results suggest that d-chlorpheniramine and olopatadine, but not fexofenadine, produce sedative effects on psychomotor performance, and that the CNS profile of fexofenadine is different from that of olopatadine.

Adult↗
PubMed2003

Results of orbital preservation for advanced malignant maxillary sinus tumors.

OBJECTIVE: The purpose of the study was to examine the oncological and functional outcomes of multimodality therapy for patients with advanced malignant maxillary sinus tumors that invaded the orbit. STUDY DESIGN: Retrospective study. METHODS: The medical records of 26 patients with orbital invasion were retrospectively analyzed. The patient group consisted of 16 men and 10 women, with a median age of 58 years. The mean follow-up period was 73 months. The most common disease was squamous cell carcinoma. Seven patients had nodal disease. All patients underwent simultaneous combined therapy consisting of conservative surgery through a sublabial incision, radiotherapy, and regional chemotherapy. Patients with nodal disease were treated with either irradiation or selective neck dissection. RESULTS: The 5- and 10-year overall survival rates were 68% and 51%, respectively. The 5- and 10-year local control rates were 66% and 51%, respectively. Overall survival rates and local control rates were significantly worse in patients with disease other than squamous cell carcinoma. Local control rates were significantly worse in patients with orbital apex disease than in patients without orbital apex disease. All 26 patients, despite orbital involvement, retained their orbital contents. Nineteen of these patients demonstrated adequate ocular function. CONCLUSIONS: Combined therapy with conservative surgery, radiotherapy, and regional chemotherapy is an effective method for local control and preservation of ocular function. However, performing orbital conservation procedure in patients with disease other than squamous cell carcinoma and with orbital apex disease must be considered carefully.

Adult↗
PubMed2002

Phenotype of DFNA11: a nonsyndromic hearing loss caused by a myosin VIIA mutation.

OBJECTIVES/HYPOTHESIS: To characterize the audiovestibular phenotype of DFNA11, an autosomal dominant nonsyndromic hearing impairment caused by a mutation in the myosin VIIA gene (MYO7A), including whether DFNA11-affected subjects have retinal degeneration as is characteristic of Usher syndrome type 1B, caused by different MYO7A mutations. STUDY DESIGN: Retrospective study of audiovestibular and ophthalmological data in a Japanese family linked to DFNA11. METHODS: Otoscopic examination and pure-tone audiometry were performed in all participants in the family. Selected subjects underwent additional examinations including speech discrimination scoring, acoustic reflex measurements, Békésy audiometry, evoked and distortion-product otoacoustic emissions, auditory brainstem responses, and bithermal caloric testing; visual acuity, ocular tonometry, slit-lamp examination, ophthalmoscopy, and electroretinography; and computed tomography of the temporal bone. RESULTS: Most affected individuals had moderate cochlear hearing loss beginning in the second decade and progressing at all frequencies. Variable degrees of asymptomatic vestibular dysfunction were present. Computed tomography showed normal inner and middle ear structures. No evidence suggested retinitis pigmentosa. CONCLUSIONS: The phenotype of DFNA11 is postlingual, nonsyndromic sensorineural hearing loss with gradual progression. Showing moderate hearing loss with asymptomatic variable vestibular dysfunction and no retinal degeneration, the DFNA11 phenotype is mildest among phenotypes caused by MYO7A mutations.

Adaptor Proteins, Signal Transducing↗
PubMed2002

[Adverse reactions to TS-1 for outpatients with recurrent head and neck cancer].

To examine the adverse reactions to TS-1 for patients with recurrent head and neck cancer, five patients with locoregional recurrences and two with distant metastasis were enrolled in the present study and took TS-1 as outpatients. All patients underwent irradiation with or without surgery before administration of TS-1. One patient was given 100 mg of TS-1 daily, and six patients were given 120 mg of TS-1 daily. Thirteen courses consisted of the regimen of four weeks of TS-1 administration followed by two weeks of intermission, nine courses consisted of the regimen of two weeks of administration followed by one week of intermission, and seven courses consisted of the regimen of two weeks of administration followed by two weeks of intermission. Anemia, leukopenia, neutropenia, and liver dysfunction were often observed as adverse reactions to TS-1 administration. Grade 3 bilirubinemia was observed in only one course, but other adverse reactions consisted of grade 1 or grade 2. Almost all adverse reactions returned to normal after the cessation of drug administration. Based on these results, we conclude that TS-1 is a safe drug for the treatment of outpatients with recurrent head and neck cancer.

Adult↗
PubMedDate not supplied

MR features of diseases involving bilateral middle cerebellar peduncles.

BACKGROUND AND PURPOSE: Distribution of lesions or involvement of specific anatomic sites can suggest the diagnosis of disease. The purpose of this study was to investigate what diseases affect both middle cerebellar peduncles (MCPs) and to evaluate other MR features for differential diagnosis. METHODS: MR findings of 27 patients (14 male and 13 female; age range, 4-77 years [mean, 48.5 years]) with bilateral MCP lesions were retrospectively studied. RESULTS: Neurodegenerative diseases were the most frequent diagnoses (n = 11 [41%]: sporadic olivopontocerebellar atrophy, eight; Shy-Drager syndrome, one; spinocerebellar ataxia, two). Also included were metabolic diseases (n = 6 [22%]: adrenoleukodystrophy, two; Wilson disease, two; cirrhosis of the liver, one; and hypoglycemia, one); cerebrovascular diseases, including posterior reversible encephalopathy syndrome (n = 3 [11%]: infarction, one; hypertensive encephalopathy, one; cyclosporin-A encephalopathy, one), demyelinating and inflammatory diseases (n = 4 [15%]: multiple sclerosis, one; acute disseminated encephalomyelitis, one; Behçet disease, one; and HIV encephalopathy, one), and neoplasms (n = 3 [11%]: lymphoma, one; glioma, one; meningeal carcinomatosis, one). All patients showed symmetrical T2 hyperintensity in both MCPs, except for one with malignant lymphoma. Marked atrophy in the posterior fossa was characteristically seen in neurodegenerative diseases. Enlargement of the pons was observed in hypertensive encephalopathy and neoplasms but absent in meningeal carcinomatosis. Lesions were restricted in the posterior fossa in eight patients with neurodegenerative diseases and one with brain stem glioma. Other patients had supratentorial lesions. CONCLUSION: Symmetricity of MCP lesions, morphologic change of the posterior fossa structures, and distribution of other lesions are helpful in the differential diagnosis.

Adolescent↗
PubMedDate not supplied

Mimics of brain tumor on neuroimaging: part I.

Brain tumor is a distinct pathological entity that differs from other diseases, including cerebrovascular, demyelinating, inflammatory, infectious, and various miscellaneous diseases. Insidious onset and gradual progression of signs and symptoms are common in patients with brain tumors, whereas the onset of cerebrovascular diseases is usually acute or sudden. Patients with demyelinating, inflammatory, or infectious diseases show subacute onset. Differentiation of brain tumors from other disorders is usually possible from the clinically and radiologically characteristic features. However, in some diseases other than brain tumors, an atypical clinical course and/or radiological findings may suggest or simulate those of brain tumors. The diagnosis of brain tumor is confirmed histopathologically, and appropriate therapies are given to the patient based on the histopathological type and grade of the tumor. In order to obtain a specimen for histopathological examination, surgical intervention is required. Other diseases are usually diagnosed clinically and radiologically. Invasive procedures should be avoided in making a diagnosis. Therefore, differentiation of brain tumors from other diseases is a critical issue for neuroimaging. Detailed inspection of images is necessary, and characteristic findings, and additional imaging methods, such as diffusion-weighted imaging, are often helpful for the differential diagnosis. We assess the imaging findings of diseases simulating brain tumors and review the literature.

Adult↗
PubMedDate not supplied

Mimics of brain tumor on neuroimaging: part II.

Brain tumor is a distinct pathological entity that differs from other diseases, including cerebrovascular, demyelinating, inflammatory, infectious, and various miscellaneous diseases. Insidious onset and gradual progression of signs and symptoms are common in patients with brain tumors, whereas the onset of cerebrovascular diseases is usually acute or sudden. Patients with demyelinating, inflammatory, or infectious diseases show subacute onset. Differentiation of brain tumors from other disorders is usually possible from the clinically and radiologically characteristic features. However, in some diseases other than brain tumors, an atypical clinical course and/or radiological findings may suggest or simulate those of brain tumors. The diagnosis of brain tumor is confirmed histopathologically, and appropriate therapies are given to the patient based on the histopathological type and grade of the tumor. In order to obtain a specimen for histopathological examination, surgical intervention is required. Other diseases are usually diagnosed clinically and radiologically. Invasive procedures should be avoided in making a diagnosis. Therefore, differentiation of brain tumors from other diseases is a critical issue for neuroimaging. Detailed inspection of images is necessary, and characteristic findings, and additional imaging methods, such as diffusion-weighted imaging, are often helpful for the differential diagnosis. We assess the imaging findings of diseases simulating brain tumors and review the literature.

Brain Neoplasms↗