Search PubMed⌕ Search

Biomedical subjects

T Hatakeyama

Publications and source records attributed to T Hatakeyama.

At least 37 records · Page 2Linked to original sources

Huge facial schwannoma extending into the middle cranial fossa and cerebellopontine angle without facial nerve palsy--case report.

A 46-year-old male presented with a huge facial schwannoma extending into both the middle cranial fossa and the cerebellopontine angle but without manifesting facial nerve palsy. Neurological examination on admission revealed no deficits except for speech disturbance. Computed tomography showed a multicystic tumor extending into the middle cranial fossa and the cerebellopontine angle, with destruction of the petrous bone. The tumor was totally grossly removed. Histological examination identified schwannoma. Total facial nerve palsy appeared postoperatively, but hearing acuity was preserved at a useful level. Facial nerve palsy is one of the most typical symptoms in patients with facial schwannoma, but is not always manifested even if the tumor extends into both the middle cranial fossa and the cerebellopontine angle.

Adult↗

Dream-recall frequency and waking imagery.

The purpose was to investigate the relationship between dream-recall frequency and waking imagery, so 323 undergraduates completed four imagery tests: (1) Sheehan's modified version of Betts' Questionnaire on Mental Imagery, (2) Marks' Vividness of Visual Imagery Questionnaire, (3) the Gordon Test of Visual Imagery Control, (4) Richardson's Verbalizer Visualizer Questionnaire, and a dream-recall questionnaire which contained a question about dream-recall frequency. When scores on the four imagery tests and the seven sensory subscales of the Questionnaire on Mental Imagery were compared for the n = 82 frequent and n = 80 infrequent dream recallers, higher recall was associated with more vivid voluntary images and more frequent use of visual imagery; however, control visual imagery as measured by the Test of Visual Imagery Control was not associated with dream-recall frequency. Scores for frequent use of visual imagery on dream-recall frequency might have been due to the two items of the Verbalizer-Visualizer Questionnaire which asked about dream experiences. The results for the seven sensory subscales of the Betts' questionnaire indicated that the frequency of dream recall was significantly related to scores on visual, cutaneous, and organic but not on auditory, gustatory, kinaesthetic, and olfactory subscales. No significant differences were found between males and females. Present findings indicated that forming vivid mental images in the waking state is related to frequency of dream recall and support Cohen's salience theory of dream recall, i.e., that evoking vivid waking mental images voluntarily may play an important role in retrieving dream images or saving them during wakefulness. All sensory modalities should be considered in study of dream recall.

Adult↗

Activation of Helicobacter pylori VacA toxin by alkaline or acid conditions increases its binding to a 250-kDa receptor protein-tyrosine phosphatase beta.

Helicobacter pylori, a Gram-negative gastric bacterium, secretes VacA, a cytotoxin that causes vacuolar degeneration of susceptible cells. Velocity sedimentation analysis showed that treatment of VacA at alkaline pH led to disassembly of VacA oligomers, an observation reported previously for acid-treated VacA. Exposure of VacA to acid or alkali increased its binding to AZ-521 cells, as shown by indirect immunofluorescence and flow cytometry. Moreover, immunoprecipitates with polyclonal antibodies against VacA from AZ-521 cells previously exposed to acid- or alkali-treated VacA had a 250-kDa glycoprotein containing galactose-beta(1-3)-N-acetylgalactosamine and galactose-beta(1-4)-N-acetylglucosamine. p250, purified by chromatography on peanut agglutinin affinity and Superose 6 columns, contained N-terminal and internal amino acid sequences of YRQQRKLVEEIGWSYT and LIIQDHILEATQDDY, respectively. These sequences are identical to those of a receptor protein-tyrosine phosphatase (RPTPbeta/PTPzeta); in agreement, p250 reacted with anti-human RPTPbeta monoclonal antibody. Immunoprecipitation with anti-human RPTPbeta antibody of solubilized membrane preparations previously incubated with VacA or heat-inactivated VacA demonstrated that RPTPbeta bound native, but not denatured, VacA. Acidic and alkaline treatments were associated with activation of VacA and increased binding to the cell surface RPTPbeta.

Amino Acid Sequence↗

Identification of the TCL1/MTCP1-like 1 (TML1) gene from the region next to the TCL1 locus.

The region on chromosome 14q32.1 is frequently involved in chromosomal translocations and inversions with one of the T-cell receptor loci in human T-cell leukemias and lymphomas. The breakpoints of the different rearrangements segregate into two clusters: inversion on the centromeric side and simple balanced translocations on the telomeric side. If the target gene activated by these different types of chromosomal rearrangements is the same, the gene must reside between the two clusters of breakpoints in a region of approximately 160 kb. By screening of a placenta cDNA library using genomic probes derived from the vicinity of TCL1 locus, we have identified a gene coding for a 1.7-kb transcript that is expressed in leukemic cells carrying a t(14;14)(q11;q32) chromosome translocation. The cognate cDNA sequence reveals an open reading frame of 384 nucleotides encoding a Mr 15,000 protein with approximately 30% of homology with both p14TCL1 and p13MTCP1 oncoproteins. The genomic organization of the TML1 locus was characterized, with three exons located 15 kb from and tail-to-tail in relation to TCL1 locus. Because of its location and sequence similarity with TCL1 and MTCP1 oncoproteins, this gene, named TML1 (TCL1/MTCP1-like 1) is a candidate gene that is potentially involved in leukemogenesis.

Amino Acid Sequence↗

Structural organization of the human Elk1 gene and its processed pseudogene Elk2.

In the ets gene family of transcription factors, ELK1 belongs to the subfamily of Ternary Complex Factors (TCFs) which bind to the Serum Response Element (SRE) in conjunction with a dimer of Serum Response Factors (SRFs). The primary structure of the human Elk1 gene was determined by genomic cloning. The gene structure of Elk1 spans 15.2 kb and consists of seven exons and six introns. The coding sequence resides on exons 3, 4, 5, 6 and 7. Sequencing of cDNA clones isolated from human hippocampus library revealed that the second exon was often skipped by an alternative splicing event. All introns commenced with nucleotides GT at the 5' boundary and ended with nucleotides AG at the 3' boundary, in agreement with the proposed consensus sequence for intron spliced donor and acceptance sites. Sequence inspection of the 5'-flanking region revealed the absence of a 'TATA' box and the presence of putative cis-acting regulatory elements such as Sp1, GATA-1, CCAAT, and c-Myb. Moreover, the sequence analysis of Elk2 locus on 14q32.3 confirmed that Elk2 gene corresponds to a processed pseudogene of Elk1 which has been reported between alpha 1 gene (IGHA1) and pseudo gamma gene (IGHGP) of immunoglobulin heavy chain. Furthermore, the results of Southern analysis using DNAs from human-mouse hybrid cell lines carrying a part of 14q32 region revealed that there is another locus hybridizing to Elk1 cDNA on 14q32.2 --> qter region in addition to Elk2 locus between IGHA1 and IGHGP loci.

Alternative Splicing↗

Isolation and mapping of a putative b subunit of human ATP synthase (ATP-BL) from human leukocytes.

From a human-leukocyte cDNA library, we cloned cDNA encoding a novel protein, which has a significant homology with the b subunit of ATP synthase (proton-transporting ATPase, F1F0-ATPase; EC3.6.1.34) derived from Anabaena sp. strain PCC 7120. The cDNA has an open reading frame of 1314 nucleotides corresponding to 438 amino acids. The coding sequence was 37.9% identical over 57 amino acid with b subunit of ATP synthase. The 34-amino-acid region of the predicted peptide sequence displays a coiled-coil motif that could form a complex with some other protein(s). We designated this novel gene as ATP-BL because of its homology to the b subunit of ATP synthase. The ATP-BL locus was mapped by fluorescence in situ hybridization (FISH) and radiation hybrid mapping to the q24 region of chromosome 16.

Amino Acid Sequence↗

Effect of amino acid substitution in amphiphilic alpha-helical peptides on peptide-phospholipid membrane interaction.

It was previously found that a cationic amphiphilic peptide, Ac-(Leu-Ala-Arg-Leu)3-NHCH3 (4(3)), caused the destabilization of a phospholipid membrane and showed strong antibacterial activity [Lee et al. Biochim. Biophys. Acta 1986; 862: 211-219]. In order to investigate the effect of changing alpha-helix propensity, hydrophobicity and basicity in 4(3) on the peptide conformation and activity, the 4(3) analogs, [Gly (or Val)6]4(3), [Gly (or Val)2,6]4(3), [Gly (or Val)2,6,10]4(3), [Gln3]4(3), [Gln3,7]4(3) and [Gln3,7,11]4(3) were synthesized. Except for [Val2,6]4(3) and [Val2,6,10]4(3), which mainly formed a beta-structure, other peptides formed an alpha-helix and showed moderate membrane-perturbing activity toward neutral and acidic lipid vesicles. All the peptides other than [Val2,6,10]4(3) and [Gln3,7,10]4(3) had the antibacterial activity comparable with that of 4(3). The relationship between the membrane-perturbing activity and the antibacterial activity was not always parallel. Conclusively, the Ala-->Val substitution in 4(3) causes the change of peptide conformation and the presence of a cationic amino acid residue is necessary for the antibacterial activity.

Amino Acid Sequence↗

Interaction of bundled Ser-rich amphiphilic peptides with phospholipid membranes.

To investigate properties of hydrophilic bundled peptides and their interactions with phospholipid membranes, bundled peptides named [Trp2]- and [Trp12]-4alpha-46S9, which are composed of four fragments of amphiphilic 24-mer peptide, were designed and synthesized. Tryptophan (Trp) was introduced at the 2nd position from the N-terminal or at the centre (12th) of the helix to monitor the peptide-lipid interaction. Circular dichroism measurements indicated that the peptides had low alpha-helicities in a buffer solution (pH 7.4) and also in the presence of dipalmitoyl-DL-3-phosphatidylcholine (DPPC) vesicles. In the presence of DPPC/dipalmitoyl-DL-3-phosphatidylglycerol (DPPG) (3:1) vesicles, the measurement could not be taken because of turbidity induced by vesicle aggregation. Both peptides had moderate perturbation activity for both the neutral and acidic vesicles at 25 degrees C. The perturbation patterns at 50 degrees C were much different from those at 25 degrees C and the maximum activity reached 100% at a low peptide concentration. The results of the measurement of membrane fusion activity of peptides showed a similar tendency to that found in the perturbation experiment. A quenching experiment indicated that the Trp2 and Trp12 residues in [Trp2]- and [Trp12]-4alpha-46S9 were scarcely embedded in neutral lipid membranes.

Amino Acid Sequence↗

Vacuolating cytotoxin purified from Helicobacter pylori causes mitochondrial damage in human gastric cells.

We investigated the effects of vacuolating cytotoxin (VacA) prepared from Helicobacter pylori on the metabolism of gastric epithelial cells, AZ-521. VacA caused the ATP levels to decrease in a time-dependent manner; by approximately 20% in 6 h, 35% in 12 h and 50% in 24 h, at a concentration of 120 nM. This decrease was also dependent on the concentration of VacA. To evaluate the impairment of mitochondria by VacA, mitochondrial membrane potential was estimated by flow cytometric analysis using 3, 3'-dihexyloxacarbocyanine iodide as a substrate. VacA decreased membrane potential with the relative fluorescence intensity of AZ-521 cells in 6 h from 52+/-3 to 24+/-1. Treatment of the cells with bafilomycin A1, a specific inhibitor of vacuolar ATPase proton pump, showed no apparent effect on these changes in the levels of ATP and the mitochondrial membrane potential. Secondly, we estimated the effect of VacA on oxygen consumption. VacA inhibited oxygen consumption in AZ-521 cells: the levels of PO 2 in the medium of control cells decreased by 73% in 3 h and 37% in 6 h, whereas those in VacA-treated cells were 84% in 3 h and 59% in 6 h. Flow cytometric analysis showed the number of cells in the G0/G1 phase was increased by VacA. Taken together, VacA induced an inactivation of energy metabolism followed by mitochondrial damage, leading to impairment of the cell cycle in gastric epithelial cells.

Adenocarcinoma↗

Isolation and mapping of a polymorphic CA repeat sequence at the human VRK1 locus.

VRK1 is a novel human putative serine/threonine kinase, and is located on chromosome 14 at band q32 where an autosomal recessive congenital microphthalmia (CMIC) is mapped. We isolated a polymorphic dinucleotide CA repeat marker from a genomic clone containing the human VRK1 gene. This polymorphism will be useful in genetic studies of disorders localized at the 14q32 region, such as CMIC.

Base Sequence↗

Assignment of the human poly(A) polymerase (PAP) gene to chromosome 14q32.1-q32.2 and isolation of a polymorphic CA repeat sequence.

We report the chromosomal localization of the gene for human poly(A) polymerase (PAP) and the characterization of a newly isolated CA repeat near the PAP locus. By fluorescence in situ hybridization and polymerase chain reaction (PCR)-based analysis with both a human/rodent monochromosomal hybrid cell panel and a radiation hybrid mapping panel, this gene was mapped on the q32.1-q32.2 region of chromosome 14. From a genomic clone containing the human PAP locus, we have isolated a polymorphic dinucleotide (CA) sequence. High heterozygosity (0.81) makes this polymorphism a useful marker in the genetic study of disorders localized at the 14q32 region, such as autosomal recessive congenital microphthalmia (CMIC).

Chromosome Mapping↗

Long-term evaluation of treatment for functional tricuspid regurgitation with regurgitant volume: characteristic differences based on primary cardiac lesion.

OBJECTIVES: The aim of this study was to characterize differences in the long-term effects of treatment for functional tricuspid regurgitation based on the primary cardiac lesion. METHODS: Ninety-six patients with valvular heart disease and 32 patients with atrial septal defects associated with tricuspid regurgitation were studied. The tricuspid annular diameter was associated with evidence of right heart failure. In valvular heart disease, a Kay annuloplasty was performed in 33 patients with a tricuspid annular diameter of >/=40 mm to 44 mm, a modified De Vega annuloplasty in 12 patients with a tricuspid annular diameter of >/=45 mm to 49 mm, and a modified De Vega annuloplasty, annuloplasty using a Carpentier ring, or tricuspid valve replacement in each of 4 patients with a tricuspid annular diameter of >/=50 mm. In atrial septal defects, a Kay annuloplasty was performed in 11 patients with a tricuspid annular diameter of >/=45 mm to 49 mm, and a modified De Vega annuloplasty was performed in 5 patients with a tricuspid annular diameter of >/=50 mm. A mean follow-up period was 79 months after operation. RESULTS: In the patients with a tricuspid annular diameter of <50 mm, the hemodynamic and clinical findings and tricuspid regurgitation remarkably improved. In the patients with valvular heart disease with a tricuspid annular diameter of >/=50 mm, however, the right heart parameters also showed improvement but less so when compared with those patients with a tricuspid annular diameter of <50 mm. In addition, 4 patients undergoing a modified De Vega annuloplasty have had a gradual increase in tricuspid regurgitation and clinical manifestations late after the operation. In contrast, all 5 patients with atrial septal defects with a tricuspid annular diameter of >/=50 mm have shown remarkable improvement, similar to those with a tricuspid annular diameter of <50 mm. Preoperative analyses revealed that the right heart function in atrial septal defects had not deteriorated to the same extent as in valvular heart disease. CONCLUSION: In the patients with a severely dilated tricuspid anulus (>/=50 mm), the postoperative change of tricuspid regurgitation differed between those patients with valvular heart disease and atrial septal defects.

Cardiac Output, Low↗

Characterization of the interaction of hemolytic lectin CEL-III from the marine invertebrate, Cucumaria echinata, with artificial lipid membranes: involvement of neutral sphingoglycolipids in the pore-forming process.

The hemolytic lectin, CEL-III, is a Ca2+-dependent, galactose/N-acetylgalactosamine-specific lectin purified from the marine invertebrate, Cucumaria echinata (Holothuroidea). After binding to specific carbohydrates on the erythrocyte surface, CEL-III forms ion-permeable pores by oligomerizing in the membrane, which leads to colloid osmotic rupture of the cells. When incubated with liposomes composed of total lipids from the human erythrocyte membrane, CEL-III efficiently induced the leakage of carboxyfluorescein (CF) trapped in the vesicles, suggesting the presence of its receptor in the membrane lipids. The rate of CF-leakage increased with increasing temperature, although the hemolytic activity of CEL-III had been found to be much higher at lower temperatures (around 10 degrees C). Identification of the receptor for CEL-III was performed by examining the ability of individual lipids from human erythrocytes to induce CF-leakage from DOPC-liposomes. As a result, the most effective receptor was found to be lactosyl ceramide (LacCer), while globoside (Gb4Cer) also showed slight induction of CF-leakage. On the other hand, a binding assay involving CEL-III-horseradish peroxidase conjugate indicated that CEL-III exhibits similar affinity for LacCer and Gb4Cer, suggesting that the structure or length of the carbohydrate portion of sphingoglycolipids is also relevant as to their ability to induce CF-leakage in addition to their affinity. Electron micrographs of CEL-III-treated liposomes revealed that CEL-III induced considerable morphological changes in the vesicles, while a clearly distinguishable oligomeric structure of the protein was not observed.

Animals↗

Effect of the hemolytic lectin CEL-III from Holothuroidea Cucumaria echinata on the ANS fluorescence responses in sensitive MDCK and resistant CHO cells.

The addition of CEL-III to sensitive MDCK cells preincubated with 8-anilino-1-naphthalenesulfonate (ANS) caused an increase in the fluorescence intensity of the probe. The increase in the ANS fluorescence caused by CEL-III was Ca2+-dependent and strongly inhibited by 0.1 M lactose, indicating that Ca2+-dependent binding of CEL-III to specific carbohydrate receptors on the plasma membrane is responsible for this phenomenon. In contrast, no significant effect of CEL-III on the ANS fluorescence was observed in CHO cells, which are highly resistant to CEL-III cytotoxicity. In MDCK cells, energy transfer from tryptophan residues to bound ANS molecules was observed in the presence of CEL-III, but not in CHO cells. Furthermore, the amount of ANS bound to MDCK cells increased as the concentration of CEL-III increased. Therefore, a simple interpretation is that the CEL-III-induced increase in ANS fluorescence is attributable to an increase of the hydrophobic region in the plasma membrane where ANS could bind. Immunoblotting analysis of proteins from cells treated with CEL-III indicated that CEL-III oligomers were irreversibly bound to the cells, and the amount of oligomer bound to MDCK cells was much greater than that bound to CHO cells under any conditions tested. The oligomerization may be accompanied by an enhancement of the hydrophobicity of CEL-III molecules, which in turn provides new ANS-binding sites. The difference in susceptibility of MDCK and CHO cells to CEL-III cytotoxicity may be due to a difference in oligomerization of bound CEL-III.

Anilino Naphthalenesulfonates↗

Prevention of reactive oxygen-induced endothelial cell injury by blocking its process.

Endothelial cell (EC) injury induced by reactive oxygen species (ROS) was investigated and effects of Ca(2+) channel blockers, agents which elevate intracellular cAMP levels ([cAMP](i)), and protein kinase inhibitors on H(2)O(2)-induced EC injury were analyzed using human umbilical vein EC cultures. Exposure to H(2)O(2) increased intracellular Ca(2+) levels and decreased [cAMP](i). Ca(2+) channel blockers, [cAMP](i)-elevating agents, and protein kinase inhibitors significantly inhibited H(2)O(2)-induced EC injury. Data suggest that H(2)O(2)-induced EC injury is mediated by extracellular Ca(2+) influx, intracellular cAMP efflux, and intracellular signaling, each of which is blocked by Ca(2+) channel blockers, [cAMP](i)-elevating agents, or protein kinase inhibitors. It is suggested that ischemia/reperfusion injury induced by ROS may be prevented by Ca(2+) channel blockers, [cAMP](i)-elevating agents, and protein kinase inhibitors.

1-Methyl-3-isobutylxanthine↗

Molecular mechanism for pore-formation in lipid membranes by the hemolytic lectin CEL-III from marine invertebrate Cucumaria echinata.

The pore-forming activity of CEL-III, a Gal/GalNAc specific lectin from the Holothuroidea Cucumaria echinata, was examined using artificial lipid membranes as a model system of erythrocyte membrane. The carboxyfluorescein (CF)-leakage studies clearly indicated that CEL-III induced the formation of pores in the dipalmitoyl phosphatidyl choline (DPPC)-lactosyl ceramide (LacCer) liposomes effectively but not in the DPPC-glucosyl ceramide (GlcCer) liposomes or DPPC liposomes. Such a leakage of CF was strongly inhibited by lactose, a potent inhibitor of CEL-III, suggesting that the leakage is mediated through the specific binding of CEL-III to the carbohydrate chains on the surface of the liposomes. The leakage of CF from the DPPC-lactosyl ceramide liposomes was pH-dependent, and it increased with increasing pH. The immunoblotting analysis and circular dichroism data indicated that upon interaction with liposomes, CEL-III associated to form an oligomer concomitantly with a marked conformational change. Furthermore, channel measurements showed that CEL-III has an ability to form small ion channels in the planar lipid bilayers consisting of diphytanoylphosphatidylcholine and human globoside (Gb4Cer)/LacCer.

Animals↗

Carbohydrate-dependent hemolytic activity of the conjugate composed of a C-type lectin, CEL-I, and an amphiphilic alpha-helical peptide, 4(3)-beta Ala2.

A lectin-cationic peptide conjugate, 4(3)-CEL-I, was prepared from an invertebrate C-type lectin, CEL-I, and an amphiphilic alpha-helical peptide, 4(3)-beta Ala2 [Ac-(Leu-Ala-Arg-Leu)3-beta Ala2]. When 4(3)-CEL-I was incubated with rabbit erythrocytes, hemolysis was observed, especially at basic pH. Inhibition experiment using some carbohydrates suggested that hemolytic activity of 4(3)-CEL-I was caused by the interaction between 4(3)-beta Ala2 portion in the conjugate and the lipid bilayer after binding to the carbohydrate chains on the cell surface by the lectin activity of CEL-I.

Animals↗

Pituitary metastasis from carcinoma of the urinary bladder mimicking pituitary apoplexy--case report.

A 70-year-old male presented with pituitary metastasis from transitional cell carcinoma of the urinary bladder manifesting as sudden headache, transient unconsciousness, and visual disturbance mimicking apoplexy of pituitary adenoma. Computed tomography showed a suprasellar tumor with intratumoral and intraventricular hemorrhage. Magnetic resonance imaging demonstrated an intra- and suprasellar mass lesion mimicking pituitary adenoma. Diabetes insipidus developed soon after. The tumor was subtotally removed. Histological examination revealed transitional cell carcinoma. An intratumoral hemorrhage may be associated with a pituitary metastasis if the patient presents with symptoms such as pituitary apoplexy.

Aged↗