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Biomedical subjects

H Kikuchi

Publications and source records attributed to H Kikuchi.

At least 235 records · Page 13Linked to original sources
PubMed1997

Induction by interleukin-1 (IL-1) of the mRNA of histidine decarboxylase, the histamine-forming enzyme, in the lung of mice in vivo and the effect of actinomycin D.

It is known that the activity of histidine decarboxylase (HDC), the histamine-forming enzyme, is induced in response to various stimuli. However, it has repeatedly been reported that actinomycin D (Act D), a typical inhibitor of RNA synthesis, is either ineffective, or actually potentiates induction of this enzyme. Thus, it has been suggested that the induction of HDC may not require the formation of mRNA, i.e. that pre-formed, long-lived mRNA molecules may be responsible for the induction. In the present study, we examined the effects of interleukin-1alpha (IL-1alpha) on the amount of HDC mRNA present during the induction of HDC activity. In mice injected with IL-1alpha, HDC mRNA increased in the lung, spleen and stomach, but was hardly detectable in these tissues in control (saline-injected) mice. In the lung, the time course of the rise and fall in HDC mRNA was shorter than that of the rise and fall in HDC activity. In the present study, actinomycin D (Act D) did not inhibit the increase in HDC mRNA induced by IL-1alpha; in fact, it potentiated the elevation of both HDC mRNA and HDC activity. These results suggest that IL-1alpha induces HDC activity or its enzyme protein through the formation of short-lived HDC mRNA molecules. This is the first demonstration that Act D can enhance an increase in HDC mRNA: this potentiating, rather than inhibiting, effect is discussed.

Animals↗
PubMed1997

Rat TAFII31 gene is induced upon programmed cell death in differentiated PC12 cells deprived of NGF.

Typical programmed cell death (PCD) requires de novo macromolecular synthesis and shares common morphological changes referred to as apoptosis. To elucidate the molecular mechanism of apoptosis, we isolated cDNA clones that are induced in differentiated PC12 cells deprived of NGF by differential display method. Among such clones, homology searches revealed that the one clone encodes the rat TATA-binding-protein-associated factor TAFII31, a component of TFIID, and a transcriptional coactivator of the p53 protein. Northern analysis of various organs in human showed one band in heart, brain, skeletal muscle and pancreas, whose size is approximately 1.1 kb which identical to that of human TAFII31 mRNA, although the size of rat human TAFII31 mRNA is approximately 2.7 kb. The deduced amino acid sequence of the rat TAFII31 was 77% identical to that of the human TAFII31. Northern analysis of various organs in adult mice showed that expression levels of TAFII31 mRNA were strong in heart but weak in spleen, although this gene is ubiquitously expressed.

Amino Acid Sequence↗
PubMed1997

Distinct phenotype of leukemic T cells with various tissue tropisms.

There is an emerging concept, the validity of which remains to be proven, that preferential expression of selective adhesion molecules on particular T cell subsets may result in tissue-specific migration. L-selectin, cutaneous lymphocyte-associated Ag (CLA), and integrin alpha4beta7 are proposed to be involved in selective migration of T cell subsets into peripheral lymph nodes, skin, and gastrointestinal mucosa, respectively. Adult T cell leukemia (ATL) is associated with lymphoid infiltration of tissues and secondary lymphoid organs. To clarify the role of these putative homing molecules in vivo, we assessed their expression on circulating ATL cells from patients with lymph node, skin, and gut involvement. L-selectin expression was significantly higher on peripheral ATL cells in patients with lymphadenopathy than in patients without it. CLA was highly expressed on peripheral ATL cells compared with normal T cells: its expression was also significantly higher on peripheral ATL cells from patients with skin involvement compared with cells from patients without it. beta7 was particularly highly expressed on peripheral ATL cells from patients with gastrointestinal involvement. In summary, the differential expression of beta7 and beta1 on peripheral ATL cells correlates with the presence of gastrointestinal involvement. Similarly, the presence of skin involvement is associated with the expression of CLA(high)beta7low on peripheral ATL cells. These results, which are consistent with the molecules CLA and alpha4beta7 mediating preferential T cell migration to the skin and gastrointestinal mucosa, respectively, may allow for a refinement of the classification of lymphoid neoplasms on the basis of differential expression of homing molecules.

Adult↗
PubMed1997

Behçet's disease associated with myelodysplastic syndromes. A case report and a review of the literature.

BACKGROUND: Behçet's disease has rarely been reported in association with myelodysplastic syndromes (MDS). Increased production of reactive oxygen species (ROS) by neutrophils has a primary role in the pathogenesis of Behçet's disease. However, decreased production of ROS by neutrophils has frequently been reported in patients with MDS. The current study was undertaken to determine the role of ROS production in a patient with Behçet's disease and MDS. METHODS: A patient with MDS with trisomy 8 who developed Behçet's disease is described and a review of the literature of patients with Behçet's disease in MDS is presented. The production of ROS by neutrophils was investigated by luminol-enhanced chemiluminescence (CL) assay. RESULTS: Based on a review of the literature, 10 cases of Behçet's disease associated with MDS have been reported to date. Nine patients had undergone cytogenetic analysis of bone marrow cells, 7 of whom (78%) had trisomy 8. Neutrophils taken from the authors' patient during the active phase of Behçet's disease demonstrated an increased CL response. Moreover, serum from this patient increased the CL emission of neutrophils from healthy volunteers. CONCLUSIONS: These data suggest that trisomy 8 predisposes to Behçet's disease in patients with MDS. Furthermore, an increased ROS production by neutrophils may be associated with the diverse clinical findings in this disease. In this study, neutrophils were activated directly by serum factors.

Adult↗
PubMed1997

Simultaneous recording of epileptiform discharges by MEG and subdural electrodes in temporal lobe epilepsy.

Spontaneous epileptiform discharges were recorded by whole head magnetoencephalography (MEG) and subdural electrodes simultaneously from two patients with medically intractable temporal lobe epilepsy. In one patient whose epileptiform discharges emerged from the lateral temporal lobe, simultaneously recorded MEG could estimate equivalent current dipole reliably near the tumor. The amplitude of the dipole was in proportion not only to the amplitude of epileptiform discharge but also to the number of subdural electrodes involved. In the other patient, MEG detected only a small proportion of epileptiform discharges, even when they were recorded by subdural electrodes from the mesial temporal lobe. It is concluded that the amplitude and the depth of epileptiform discharges would largely affect the sensitivity of dipole localization by MEG.

Adult↗
PubMed1997

Induction of apoptosis in multi-drug resistant (MDR) human glioblastoma cells by SN-38, a metabolite of the camptothecin derivative CPT-11.

The overexpression of the multidrug resistance (mdr1) gene and its product, P-glycoprotein (P-gp), is thought to limit the successful chemotherapy of human tumors. Recent studies demonstrate that SN-38, a metabolite of the camptothecin (CPT) derivative CPT-11, has antitumor effects on several tumors, but the mechanisms responsible for its cytotoxicity remain unclear. We therefore determined whether SN-38 has cytotoxic effects on MDR human glioblastoma GB-1 cells and non-MDR human glioblastoma U87-MG cells. Furthermore, we determined what role SN-38 plays in the induction of cytotoxicity in these tumor cells. In this study, we demonstrated that SN-38 had significantly stronger antitumor effects on GB-1 and U-87MG cells than did CPT (P < 0.01 and P < 0.05, respectively). In addition, findings obtained using a DNA fragmentation assay, Hoechst 33258 staining, in situ end-labeling and cell cycle analysis demonstrated that SN-38 induced apoptosis in these tumors. Our results suggest that SN-38 has a stronger antitumor effect on malignant glioma cells regardless of MDR expression than does CPT, and therefore can be considered a new chemotherapeutic agent potentially effective in the treatment of human primary or recurrent malignant gliomas resistant to chemotherapy.

Antineoplastic Agents, Phytogenic↗
PubMed1997

Intrasellar meningioma: case report and review of the literature.

BACKGROUND: Intrasellar meningioma is a rare clinical entity, and surgical resection may be difficult when it is hypervascularized. METHODS: A case of subdiaphragmatic hypervascular intrasellar meningioma with attachment to the dura of the anterior wall of the sella turcica is described. Literature review of 18 cases with operatively confirmed intrasellar meningioma discloses unexpected intraoperative bleeding and relatively low resectability of the tumor are also described. RESULTS: We used preoperative endovascular embolization of feeding arteries, and resected a hypervascular intrasellar meningioma by a combined transsphenoidal-transcranial approach safely and without massive bleeding. CONCLUSIONS: Preoperative endovascular embolization of feeding arteries and combined transsphenoidal-transcranial approach are useful for the surgical resection of hypervascular intrasellar meningiomas.

Combined Modality Therapy↗
PubMed1997

Surgical extirpation of the posterior hippocampal arteriovenous malformation.

BACKGROUND: Surgical extirpation of medial temporal (AVMs) arteriovenous malformations has been one of the most challenging issues in neurosurgery. Yaşargil classified mediobasal AVM into four subtypes: amygdala, anterior hippocampal, middle hippocampal, and posterior hippocampal lesions. The lesions around the trigone extending forward to the temporal horn, and medially adjacent to the midbrain, can be referred to as posterior hippocampal AVMs. The therapeutic indications and operative approaches for these lesions remain controversial. METHODS: Nine patients underwent surgical resection for AVMs of the posterior hippocampus using a laterobasal approach. RESULTS: In four patients, AVMs were located chiefly within the lateral ventricle, and the lesions were resected using a laterobasal approach through the occipitotemporal sulcus, or through a hematoma cavity within the fusiform gyrus. Clinical improvement followed the procedure in three of four patients. In the remaining five patients, the nidi were located chiefly within the ambient cistern, extending upward to the basal ganglia. Contralateral hemiparesis occurred in three patients. Two patients showed marked improvement following an initial decline in neurologic status. CONCLUSIONS: A laterobasal transventricular approach is suitable for ventricular AVMs, whereas only limited exposure can be afforded through a transventricular, transchoroidal fissure route for the AVMs within the ambient cistern. For these lesions, a conventional subtemporal approach to the tentorial incisura is preferable.

Adult↗
PubMed1997

Boron neutron capture therapy: preliminary study of BNCT with sodium borocaptate (Na2B1 2H1 1SH) on glioblastoma.

To plan the optimal BNCT using BSH for glioblastoma patients, the 10B concentration in tumor and blood was investigated in 11 newly diagnosed glioblastoma patients. All patients received 20 mg BSH/kg body weight 2.5-16 hrs prior to tumor removal. The quantitative distribution of 10B was determined by prompt gamma ray spectrometry and/or alpha-track autoradiography. 10B distribution in tumors was heterogeneous, +/- 25% of scattering at the microscopic level, and the distribution was also heterogeneous at the tissue level. 10B concentration in blood decreased in bi-exponential decay as a function of the time after the end of the administration. The T/B ratio showed non-exponential increase with large variation. The maximum T/B ratio would be around 1. The tumor/normal brain (T/N) ratio of 10B concentration was 11.0 +/- 3.2. The 10B content in normal brain is originated in vascular 10B in parenchyma, since the 10B content in normal brain to blood (N/B ratio) being compatible with the blood content in parenchyma. These values allow for BNCT, using thermal neutrons, on brain tumors located less than approximately 3.3 cm in depth from the brain surface of neutron incidence, providing that the dose on the normal endothelium is controlled to less than the tolerance limit. In our preliminary study of BNCT, a 31% 3-year survival was achieved over all for 16 glioblastoma patients and a 50% 2-year survival was achieved on 8 glioblastoma patients in our recent dose escalation study based on these data.

Borohydrides↗
PubMed1997

The involvement of a novel mechanism distinct from the thrombin receptor in the vasocontraction induced by trypsin.

1. The vasocontracting effect of a serine protease trypsin and its mechanisms were investigated by monitoring the isometric tension in endothelium-denuded rings of rabbit thoracic aortae and its effects on intracellular free Ca2+ concentrations ([Ca2+]i) in dispersed rabbit vascular smooth muscle cells with a Ca2+ indicator fura-2. The actions of trypsin were compared with those of thrombin. 2. Both thrombin and trypsin reversibly contracted aortic rings without endothelium in a concentration-dependent manner. The vasocontraction induced by trypsin was well correlated with the protease activity of trypsin actually added to the tissue baths containing the aortic rings and was completely blocked by soybean trypsin inhibitor and phenylmethylsulphonyl fluoride (PMSF), a serine protease inhibitor. 3. The trypsin-induced contractions of the aortic rings were not the result of irreversible damage to vascular smooth muscle cells, since the contractile responses induced by noradrenaline or 30 mM KCl were unaffected by pretreatment with trypsin. 4. The contractions induced by either thrombin or trypsin were reduced to about 30% of control responses after removal of extracellular Ca2+, indicating that most of the contraction is dependent on extracellular Ca2+. By contrast, the contractions induced by either of the proteases were reduced by an antagonist of L-type voltage-operated Ca2+ channels, nifedipine, to about 70% of control responses, indicating that both nifedipine-sensitive and -resistant Ca2+ channels are involved in these contractions. 5. In the aortic rings precontracted by a maximally effective concentration of thrombin, the second application of thrombin virtually failed to induce contractions but trypsin could still induce contractions amounting to 10% of control values by it's protease activity. 6. After the first application of a maximal concentration of thrombin, the second application of thrombin could not induce an increase in [Ca2+]i, but an application of trypsin could still induce an increase in [Ca2+]i in dispersed rabbit vascular smooth muscle cells. 7. These data suggest that in addition to activation of a thrombin receptor, trypsin can contract rabbit aortae by a proteinase-activated receptor 2 or a novel mechanism.

Animals↗
PubMed1997

Hemolytic uremic syndrome following autologous peripheral blood stem cell transplantation in a patient with malignant lymphoma.

Hemolytic uremic syndrome (HUS) has been reported in patients receiving bone marrow transplantation. However, only a few cases of HUS following autologous peripheral blood stem cell transplantation (PBSCT) have been reported. We present a case of HUS developing after autologous PBSCT in a 40-year-old man with non-Hodgkin's lymphoma. It appears that the chemotherapeutic agents administered during the conditioning regimen for PBSCT may have played an important role in the development of HUS in our patient. In the present case, the combination therapy of vincristine, methylprednisolone, and ticlopidine hydrochloride was effective.

Adult↗
PubMed1997

Thiobarbituric acid reactive substances are increased in the subcutaneous fat tissue of patients with end-stage renal disease.

BACKGROUND: Patients with end-stage renal disease are thought to be in a highly peroxidative state, based on studies showing decreased serum antioxidant activity and increased peroxidative products. In this study we confirm these findings by examining lipid peroxidation in subcutaneous fat tissue in uraemia. SUBJECTS AND METHODS: Twenty-seven subcutaneous fat samples were taken from patients with end-stage renal disease when they underwent intervention for arteriovenous fistula for haemodialyis or for catheter insertion for continuous ambulatory peritoneal dialysis. The control samples were taken from 11 patients with normal renal function and without any history of renal disease who had surgical interventions. Lipid peroxides were measured as thiobarbituric acid reactive substance. RESULTS: The concentration of thiobarbituric acid reactive substances in subcutaneous fat tissue in the patients with end-stage renal disease is 1.223 +/- 0.636 nmol/mg fat tissue (mean +/- SD) whereas the level in the control group is 0.097 +/- 0.054 nmol/mg fat tissue. A comparison of the two groups by Student's t test revealed a highly significant difference (P < 0.001). CONCLUSIONS: This study supports the finding of a severe peroxidative state in patients with end-stage renal disease.

Adipose Tissue↗
PubMed1997

Induction of Bip mRNA upon programmed cell death of differentiated PC12 cells as well as rat sympathetic neurons.

We have found that expression of the Bip (immunoglobulin heavy chain binding protein)/GRP78 (glucose regulated protein 78) gene is markedly enhanced specifically among the heat shock protein (HSP) 70 gene family during the neuronal cell death of PC12 (22a) cells, that is induced by removal of nerve growth factor (NGF) and blocked by a transcription inhibitor, actinomycin D. The Bip mRNA induction is suppressed when the NGF-deprivation-dependent cell death of PC12 (22a) cells is inhibited by cAMP, cycloheximide or high K+. The Ca2+ ionophore, A23187, caused neuronal cell death accompanied by up-regulation of Bip, HSP90, and HSP70 mRNAs. In addition, a chelator of intracellular Ca2+ (BAPTA) elevated Bip mRNA and induced cell death in a low Ca2+ medium. Alterations of intracellular calcium homeostasis thus appear to induce Bip mRNA expression as well as apoptosis in PC12 (22a) cells. However, release of Ca2+ from intracellular stores by thapsigargin induced Bip mRNA expression but not cell death, indicating that Bip mRNA induction is not sufficient for neuronal death. Induction of Bip mRNA in association with apoptosis was also observed for NGF-deprived sympathetic ganglion cells in primary culture. These lines of evidence suggest that selective induction of Bip mRNA may play an important role in the programmed cell death of neurons deprived of neurotrophic factors and could be a landmark of the neuronal programmed cell death.

Actins↗
PubMed1997

Importance of 2-O-sulfate groups of uronate residues in heparin for activation of FGF-1 and FGF-2.

Complete drying of heparin with various concentrations of NaOH by lyophilization caused specific 2-O-desulfation to various degrees without detectable depolymerization or other chemical changes. In order to assess the importance of 2-O-sulfate groups in uronate residues to promote FGF-1 and FGF-2 activities, various 2-O-desulfated (2-O-DS-) heparins were quantitatively examined for their effects on FGF-1 and FGF-2-induced proliferation of BALB/c3T3 clone A31 (A31) cells and the chlorate-treated cells. Twenty-seven percent or less loss to the 2-O-sulfate groups had no effect on the ability to activate both FGF-1 and FGF-2, while 44% loss resulted in a significant loss of the ability. Complete loss of the ability was observed in 2-O-DS-heparins with 75% or more 2-O-desulfation. These results suggest that a high content of 2-O-sulfate groups in uronate residues of heparin is required for activation of both FGF-1 and FGF-2.

3T3 Cells↗
PubMed1997

Expression of interleukin-1 beta converting enzyme gene family and bcl-2 gene family in the rat brain following permanent occlusion of the middle cerebral artery.

Recent investigations have been suggesting that some neuronal subpopulations may die via programmed cell death after focal ischemic injury. To clarify the possible roles of the genes involved in the cell-death program, this study examined the expression of three members of the interleukin-1 beta converting enzyme (Ice) gene family (Ice, Nedd2, and Yama/CPP32) and two members of the bcl-2 gene family (bcl-2 and bcl-x) in the rat brain after permanent occlusion of the middle cerebral artery. Northern blot analysis revealed a transient induction of Nedd2 mRNA 8 h after the ischemic insult (3.8-fold) and an increase in Yama/CPP32 mRNA 16 to 24 h after the insult (5.8-fold at 24 h), whereas the expression of Ice remained constant. The expression of bcl-2 and bcl-x remained constant after the ischemic insult. Taking into account the key role of the Ice gene family in the execution of programmed cell death, the induction of Ice gene family might play a causative role in apoptotic cell death.

Animals↗
PubMed1997

Frontopolar ictal epileptiform discharges on scalp electroencephalogram in temporal lobe epilepsy.

We report 3 patients with medically intractable complex partial seizures (CPS) arising from the temporal lobe judged by surgical outcome, in whom scalp electroencephalogram (EEG) showed ictal epileptiform discharges at the frontopolar region. In all patients, results of cranial magnetic resonance imaging (MRI), positron emission tomography (PET), and ictal single photon emission computed tomography (SPECT) were consistent with those of temporal lobe epilepsy (TLE). The epileptogenic area was defined in the temporal lobe by chronic subdural recording in 2 patients. After surgical treatment (amygdalohippocampectomy, anterior temporal lobectomy, and temporal lesionectomy, respectively), all 3 patients became seizure-free and the interictal frontopolar epileptiform discharges on scalp EEG disappeared. Patients with TLE may show ictal scalp EEG with frontopolar onset. This is most likely explained by direction of dipolar orientation of epileptiform discharges in 1 of our patients; rapid spread of ictal activity to the frontopolar area can also be considered in the 2.

Adult↗
PubMed1997

Physiological role of Ca2+-permeable nonselective cation channel in endothelin-1-induced contraction of rabbit aorta.

We previously showed a role for a nonselective cation channel (NSCC) in the ETA-dependent action of endothelin-1 in mouse fibroblast and rabbit aortic smooth-muscle cell. To clarify the physiological significance of NSCCs in endothelin-1 (ET-1)-induced vasocontraction, we examined the effects of NSCC blockers such as mefenamic acid and SK&F 96365 on the contractions of deendothelialized rabbit aortic rings induced by a low (10[-10] M) or high (10[-8] M) concentration of ET-1. Mefenamic acid (< or =10[-3] M) had little effect on the contraction induced by 45 x 10(-3) M K+ or 1 x 10(-6) M Bay K-8644 in combination with 15 x 10(-3) M K+, indicating that it does not affect voltage-operated calcium channels (VOCs) and contractile mechanisms. The contraction by a low concentration of ET-1 was abolished after removal of extracellular Ca2+, but it was reduced only to 50% by a maximally effective concentration (10[-5] M) of nifedipine, an inhibitor of L-type VOCs (L-VOC). Mefenamic acid and SK&F 96365 inhibited the ET-1-induced contraction with 50% inhibitory concentration (IC50) values of 10(-4) M and 2 x 10(-5) M, respectively, and abolished it at 10(-3) M and 10(-4) M. By contrast, nifedipine, mefenamic acid, or SK&F 96365 had little effect on the contraction by a high concentration of ET-1. The contraction induced by a low or high concentration of ET-1 was abolished by an ETA antagonist, BQ-123, but not by an ETB antagonist, BQ-788. These results demonstrate that the contraction induced by ET-1 is totally mediated exclusively by ETA, but that Ca2+ entry through NSCCs in addition to L-VOCs plays an important role in contractions induced by low concentrations of ET-1, whereas it plays only a minor role in contractions induced by high concentrations of ET-1.

Animals↗