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Biomedical subjects

N Adachi

Publications and source records attributed to N Adachi.

At least 127 records · Page 7Linked to original sources
PubMed1996

Purification, characterization, and cDNA cloning of ABP-2 (arylphorin gene-specific binding protein-2) that specifically binds to the ABP-1-binding sequence in the arylphorin gene of Sarcophaga peregrina.

Previously, we demonstrated that ABP-1 (arylphorin gene-specific binding protein-1), which is suggested to be the transcriptional activator of the arylphorin gene of Sarcophaga peregrina, is present in NIH-Sape-4 cells, which do not express arylphorin. As well as ABP-1, these cells were found to contain another protein (ABP-2) that probably binds to the same sequence as that to which ABP-1 binds [Adachi, N., Kubo, T., and Natori, S. (1993) J. Biochem. 114, 55-60]. We purified ABP-2 from a nuclear extract of NIH-Sape-4 cells and compared its DNA-binding activity with that of ABP-1. Both ABP-1 and ABP-2 were found to bind to the same sequence in the arylphorin gene with the same affinity and stability, but an ABP-2-specific hypersensitive site was detected by DNase I footprinting analysis. Analyses of proteolytic fragments suggested that both ABP-1 and ABP-2 have Zn fingers showing high similarity with that of AEF-1, a transcriptional repressor of the Drosophila melanogaster alcohol dehydrogenase gene that binds to a sequence very similar to that binding ABP-1 and ABP-2. We isolated a candidate cDNA for ABP-2, and the protein it encoded contained nine Zn fingers and regions rich in alanine, glutamine, serine/threonine, glycine, histidine, and asparagine.

Amino Acid Sequence↗
PubMed1996

Effects of pre- and postischemic administration of thiopental on transmitter amino acid release and histologic outcome in gerbils.

BACKGROUND: The mechanism by which barbiturates protect neurons against ischemia is unclear, particularly when they are given after ischemia or reperfusion begins. Because an excess release of excitatory neurotransmitters causes postsynaptic membrane depolarization, which triggers neuronal damage in ischemia, the effects of thiopental on histologic outcome, ischemia-induced amino acid release, and anoxic depolarization in gerbils were studied. METHODS: The effects of different doses of thiopental administered before or after ischemia were examined morphologically by assessing delayed neuronal death in hippocampal CA1 pyramidal cells produced by forebrain ischemia for 3 min in gerbils. The ischemia-induced changes in output of aspartate, glutamate, glycine, taurine, and gamma-aminobutyric acid were measured using a microdialysis-high-performance liquid chromatography procedure, and the differences among a halothane-anesthetized group, a thiopental-administered group, and a group given thiopental after a period of ischemia were evaluated. The changes induced in the direct-current potential in the hippocampal CA1 area by forebrain ischemia were compared in animals anesthetized with halothane and those given thiopental. RESULTS: Preischemic administration of thiopental at all doses decreased the risks for delayed neuronal death (P < 0.01). Post-ischemic administration at a dosage of 2 mg.kg-1.min-1 for 60 min protected neurons, but the same dose for 10 min did not ameliorate the cell injury. Forebrain ischemia produced marked increases in all amino acids 3 to 6 min after the start of recirculation in the halothane-anesthetized gerbils, whereas thiopental anesthesia (2 mg.kg-1.min-1) reduced these increases throughout the experimental period, except for glycine (P < 0.01). The initiation of thiopental after reflow did not markedly diminish these increases. Thiopental anesthesia prolonged the onset of anoxic depolarization and reduced its maximal amplitude. CONCLUSIONS: Thiopental helps protect the brain from ischemia, although treatment with this agent after ischemia requires a larger dose than that before ischemia. The effect of preischemic treatment may be related to the suppression of the excitatory amino acid release and the direct-current potential shift.

Animals↗
PubMed1996

Charles Bonnet syndrome in leprosy; prevalence and clinical characteristics.

Charles Bonnet syndrome (CBS) is diagnosed when a visually impaired patient without any mental disorder develops visual hallucinations. A survey of patients in a National Leprosarium revealed that the point prevalence of CBS in leprosy was 0.4%. This prevalence appears to be high, as few cases with CBS have been reported. The semeiology of visual hallucinations was typical of CBS. However, the clinical features were different from previous reported cases because of the history of leprosy and associated multi-sensory loss. Patients with leprosy appear to be at increased risk for CBS, due to frequent eye complications combined with sensory loss, ageing, and intact intellectual functions.

Adult↗
PubMed1996

Differential diagnosis of scalp trichilemmal cyst on MRI.

The characteristic MRI of scalp trichilemmal cysts is reported. The feature of an iso-intense area on T1-weighted images is unique to trichilemmal cysts. MRI is helpful in diagnosing the trichilemmal cyst and useful in distinguishing cystic tumors on the median scalp from a cranial malformation, meningo- or encephalocele.

Adult↗
PubMed1996

[Cardiac impairment of elderly patients with diabetes mellitus as studied with non-invasive myocardial scintigraphy and signal-averaged electrocardiography].

In patients more than 65-year-old with diabetes mellitus, positive late potentials on signal-averaged electrocardiograms were more common than in normal subjects (p < 0.05). This suggests that aged patients with diabetes mellitus are at risk for micromyocardial impairment. Myocardial scintigraphy with 123I-metaiodobenzylguanidine showed abnormally low uptake, in parallel with the data on SA-ECG. Thus, both methods may be clinically useful ways to noninvasively reveal micromyocardial impairment in aged patients with diabetes mellitus. Moreover, trimetazidine hydrochloride may be effective as therapy for micromyocardial impairment: the uptake of 123I-metaiodobenzyl guanidine had increased in some patients when measured 1 year after administration of trimetazidine hydrochloride (18 mg/day) and the late potential changed from positive to negative.

3-Iodobenzylguanidine↗
PubMed1996

[Mouth mask method for fiberoptic tracheal intubation in difficult intubations].

We tried 72 fiberoptic tracheal intubations (FTI) using a mouth mask in difficult intubation cases. In this method, ventilation is performed via only the mouth using a mask applied over the mouth (mouth mask) and FTI can be done via a nostril with no hindrance from the mask in anesthetized patients. We have been using an infant or child type Seal Mask (Gibeck Respiration) for the mouth mask or a specially made mouth mask. An oral airway is usually inserted and the nostril of one side is plugged with cotton. FTI is performed by another anesthesiologist. An endotracheal (ET) tube capped with a rubber diaphragm is passed through another nostril, and a fiberscope is inserted through the ET tube. The subsequent technique is the same as that of the usual FTI for awake patients. Intubations were successful in all cases except 2; in one, ventilation was impaired even with oral airway in place, and in the other, bleeding in upper airway due to jaw injury from traffic accident hindered the sight of the scope. Mouth mask method for FTI is safe, useful and practical in difficult intubations with little discomfort to the patient.

Adolescent↗
PubMed1996

Decreased DNA topoisomerase II alpha expression and cold-sensitive growth in a mouse mammary cancer cell line resistant to etoposide and doxorubicin.

A mouse mammary carcinoma FM3A cell line resistant to the DNA topoisomerase (topo) II-targeting agent, etoposide (VP-16), FM3A/VP-2B, had a markedly reduced growth rate at a low temperature (33 degrees C). The cells had the following properties: (a) FM3A/VP-2B, which had 24-fold higher resistance to VP-16 than its parental line, FM3A, was cross-resistant to doxorubicin, but not to a camptothecin derivative, CPT-11. (b) Cold-resistant revertants from FM3A/VP-2B, R-6 and R-11, remained 8- to 9-fold more resistant to VP-16 and 2- to 3-fold more resistant to doxorubicin. (c) FM3A/VP-2B had one-fourth the level of topo II activity and one-third of the topo II alpha content and mRNA of FM3A. R-6 and R-11, however, had levels similar to FM3A. (d) FM3A/VP-2B and FM3A had a 3-base deletion at position 4170 on one allele on the topo II alpha cDNA, but expression of the wild-type and the deletion allele was not appreciably changed in both cell lines. Decreased topo II alpha expression might have led to the acquisition of drug resistance to etoposide in FM3A/VP-2B, and appeared to be linked with the cold-sensitive growth. We also present a corrected mouse topo II alpha cDNA sequence.

Amino Acid Sequence↗
PubMed1995

Molecular cloning and sequencing of the hcs gene, which encodes 3-hydroxy-3-methylglutaryl coenzyme A synthase of Schizosaccharomyces pombe.

We have cloned and sequenced the hcs gene, which is thought to encode a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase consisting of 447 amino acids, from the fission yeast Schizosaccharomyces pombe. The predicted amino acid sequence of the hcs product of S. pombe has homology with the HMG-CoA synthase of rat (47.8%), chicken (49.2%), hamster (47.1%) and human cells (46.9%). One of the hcs genes was replaced with a marker gene in the diploid cell. No viable hcs-disrupted haploid was isolated after tetrad dissection, suggesting that the hcs gene is essential for growth. However the hcs-defective mutant could be grown on a medium containing 5 mg/ml mevalonate. These results strongly support that the hcs gene encodes HMG-CoA synthase and S. pombe contains a single copy of the hcs gene.

Amino Acid Sequence↗
PubMed1995

Fatal cytomegalovirus myocarditis in a seronegative ALL patient.

Fatal cytomegalovirus (CMV) myocarditis occurred in a 2 year old boy with acute lymphoblastic leukemia (ALL) in remission. The patient showed mild hepatic dysfunction and a rapid progress of pancytopenia after complete remission had been achieved. At the fifth week of complete remission, he presented signs of heart failure such as tachycardia, S4 gallop on auscultation and decreased ejection fraction on echocardiography. However, no significant electrocardiographic changes were recognized. In addition to the cardiac dysfunction, the patient presented a marked tachypnea and dyspnea associated with hypoxemia. These were dramatically improved by methylprednisolone pulse therapy (30 mg/kg per day, for 3 days) and CMV high titer immunoglobulin (400 mg/kg per day, for 3 days). On the sixth day after signs of respiratory failure were improved, the patient suddenly presented a paroxysmal atrial tachycardia followed by a fatal ventricular fibrillation. Although we could detect neither a specific IgM antibody, a significant increase of IgG antibody, nor CMV genome by DNA hybridization techniques during the course of the illness, microscopic examination of necropsy specimens of the heart showed a marked disruption and disintegration of muscle bands associated with cytomegalic inclusion bodies. Polymerase chain reaction (PCR) yielded a 305 bp amplification product in the heart and lung tissues, supporting the view that myocarditis was caused by CMV.

Antibodies, Viral↗
PubMed1995

A late-appearing Philadelphia chromosome in acute lymphoblastic leukemia confirmed by expression of BCR-ABL mRNA.

We report two cases of acute lymphoblastic leukemia (ALL) with a late-appearing Philadelphia chromosome (Ph1), confirmed by the expression of BCR-ABL mRNA, using the reverse transcriptase/polymerase chain reaction (RT/PCR) technique. The first patient was a 10-year-old boy with precursor B cell type ALL-L1 (FAB classification). At diagnosis, no metaphase cells were found by chromosome analysis and BCR-ABL mRNA was not observed. At the beginning of relapse, which occurred after 7 months of complete remission, a normal karyotype was observed. At the terminal stage, leukemic cells with Ph1 and BCR-ABL mRNA for the P190 variety were observed. The second patient was a 12-year-old boy with immature T cell type ALL-L1. The metaphase cells showed a 9p- chromosome at diagnosis and Ph1 appeared in addition to 9p- at relapse. Hybrid mRNA for the P210 variety was detected only when Ph1 had developed. The blast cells with Ph1 were derived from the original leukemic clone through clonal evolution, since the same clonal rearrangements of IGH or TCRB were detected in leukemic cells obtained both at diagnosis and relapse in both patients. Thus, in both cases, Ph1 was detected only in the course of ALL along with expression of BCR-ABL mRNA. This observation also confirmed that, as in de novo Ph1-positive ALL, both the P190 and P210 varieties of BCR-ABL mRNA are observed in ALL with late-appearing Ph1.

Base Sequence↗
PubMed1995

[Partial status epilepticus developed 41 years after psychosurgery--an electroencephalographic and neuropathological study].

The authors report an 85-year-old man with schizophrenia, who had undergone bilateral frontal gyrectomy at the age of 44 and had a single series of convulsions 6 months after the psychosurgery. Forty-one years later, he had developed partial seizures with secondary generalized seizures, and died of partial status epilepticus. Ictal EEG showed generalized high-amplitude spikes or sharp waves spreading from the left frontal region. Interictal EEG showed slowing of background activity and high-amplitude paroxysmal discharges on the left frontal and central regions. Postmortem examination of the brain revealed tissue defects in the superior and middle frontal gyri caused by resection at the time of gyrectory and old cysts in the deep frontal white matter as late sequelae of the psychosurgery. There was fibrillary gliosis in the surrounding cerebral convolutions and the deep white matter. We considered that the glial scar in the frontal lobes, on the left side in particular, had developed the epileptogenic focus. The pathophysiological mechanism by which the intractable epileptic seizures appeared 41 years after psychosurgery is discussed.

Aged↗
PubMed1995

[The efficacy of intravenous lidocaine on various types of neuropathic pain].

We examined the efficacy of systemic local anesthetics on various types of neuropathic pain in 89 patients. Lidocaine 1.5 mg.kg-1 was infused intravenously for one minute. Pain score (PS) by visual analogue scale (VAS, 0-10) was measured 1, 5, 15 and 35 min after the infusion. The efficacy of intravenous lidocaine was evaluated by PS which was lowest after infusion. PS decreased to less than 50 percent of pre-infusion value in more than 75 percent of cases of cancer pain, postherpetic neuralgia, trigeminal neuralgia, low back pain with signs of root pain or spinal canal stenosis, peripheral nerve injury and thalamic pain, in 50-75 percent of cases of herpetic neuralgia, and in less than 50 percent of cases of cervical spondylosis, spinal cord injury, reflex sympathetic dystrophy, causalgia and psychogenic pain. This study suggests that systemic local anesthetics is effective in neuropathy due to cancer pain, postherpetic neuralgia, trigeminal neuralgia, low back pain with signs of root pain or spinal canal stenosis, peripheral nerve injury and thalamic pain.

Aged↗
PubMed1995

[Neutropenia in patient with X-linked hyper-IgM syndrome].

The X-linked form of hyper-IgM syndrome (HIGM1) is a rare disorder characterized by the inability of B cells to undergo isotype switch by a deficiency of CD40 ligand (CD40L) on activated T lymphocytes. The patients suffer from recurrent infections not only due to a lack of B lymphocyte activation but also due to defect of T lymphocyte functions. In addition, neutropenia is frequently accompanied by these symptoms. A patient with HIGM1, we experienced, suffered from recurrent infections and neutropenia. But he had a normal number of hematopoietic stem cell by the in vitro colony forming assay. CD34+ myeloid stem cell has been known to express CD40. We speculated by these facts that myeloid cell numbers are regulated by CD40-CD40L interaction.

Adolescent↗
PubMed1994

Mutant isolation of mouse DNA topoisomerase II alpha in yeast.

For characterizing in vivo functions of a mammalian protein, it is informative to obtain conditional mutations and apply them to the mouse genetic system. However, the isolation of conditional mutations has been quite difficult in cultured cells. We report here that functional expression of a heterologous mammalian gene in the yeast Saccharomyces cerevisiae provides a system for isolating mutated genes. We found that the cloned mouse TOP2 alpha cDNA, which encodes mouse DNA topoisomerase II (topo II) alpha, could rescue the lethal phenotype caused by yeast top2 null mutation. In order to generate and select temperature-sensitive mouse topo II alpha, an expression plasmid was mutagenized in vitro and was transformed, using the plasmid shuffling method, into the yeast strain, in which the endogenous TOP2 gene had been disrupted. We observed that one of such clone of yeast cells harboring a mutagenized mouse TOP2 alpha showed temperature-sensitive growth. Enzymatic assays and sequencing analysis revealed that this phenotype was caused by the thermosensitive nature of the mutant mouse protein, which has isoleucine at amino acid 961 instead of threonine. Therefore we have isolated the first conditional mutation in the mouse TOP2 alpha.

Amino Acid Sequence↗
PubMed1994

Lidocaine protects hippocampal neurons against ischemic damage by preventing increase of extracellular excitatory amino acids: a microdialysis study in Mongolian gerbils.

Extracellular levels of amino acids in the hippocampal CA1 region of the gerbil were analyzed by a microdialysis-HPLC procedure. Transient forebrain ischemia produced significant increase in aspartate, glutamate, glycine and taurine (760%, 1070%, 190% and 1210%, respectively), and neuronal blockade by perfusion with a lidocaine (4 mM)-containing medium resulted in 67%, 79%, 58% and 59% reduction in the peak values of each amino acid, respectively. On the other hand, an intracerebroventricular administration of lidocaine, 0.8 mumol or more, produced a protective effect against delayed damage of hippocampal CA1 pyramidal cells, which was caused by bilateral carotid artery occlusion for 4 min. The results suggest that lidocaine may protect neurons against ischemic damage, by preventing the ischemia-induced rise of extracellular concentration of excitatory amino acid.

Animals↗