Polarized XAFS study of the atomic displacements and phase transitions in KNbO3.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
K Yagi
Publications and source records attributed to K Yagi.
Induction of apoptosis in cultured colon cancer cells by transfection with human interferon beta gene.
The growth of SW480 colon cancer cells following the transfection with the human interferon beta (hIFNbeta) gene entrapped in cationic multilamellar liposomes was effectively inhibited, but not that of the cells transfected with the gene from which the secretion signal sequence of hIFNbeta had been deleted. The amount of hIFNbeta secreted in the medium from SW480 cells transfected with hIFNbeta gradually increased and became maximum 3 days after the transfection, but no hIFNbeta was detected in the medium of the cells transfected with the secretion signal-deleted hIFNbeta. These findings indicate that the growth inhibition of SW480 cells after the transfection with hIFNbeta was caused by hIFNbeta secreted from the transfected cells. At that time, SW480 cells were induced to undergo apoptosis, which was identified by morphological aspects, viz., chromatin condensation, nuclear segmentation, and nucleosomal DNA fragmentation. The hIFNbeta-induced apoptosis was found to be linked to the activation of caspases 3 and 8 as evidenced by immunoblot, enzymological, and cell death inhibition analyses.
Apoptosis↗
Does the pineal gland play a role in neuroendocrine fear responses?
The pineal gland secretes melatonin under an influence of suprachiasmatic nucleus neurones. Pinealectomy or melatonin administration affects behavioural responses to novel stimuli. Fear or novel stimuli inhibit vasopressin (VP) and facilitate oxytocin (OT) or prolactin (PRL) release from the pituitary. Thus the suprachiasmatic nucleus-pineal gland system may modulate VP, OT and PRL responses to conditioned fear stimuli. In the present experiments with male rats, pinealectomy or melatonin administration did not significantly change VP, OT or PRL responses to conditioned fear stimuli. Electrolytic lesions of the suprachiasmatic nuclei impaired VP but not OT or PRL responses. The results show that the pineal gland is not involved in neuroendocrine responses to conditioned fear stimuli and suggest that the suprachiasmatic nucleus is necessary for the VP response to fear stimuli.
Animals↗
Appropriately spaced nuclear localizing signals are necessary for efficient nuclear import of nonnuclear proteins.
To deliver nonnuclear proteins into the nucleus, we have examined the locations and number of nuclear localizing signals by use of simian virus 40 large T-antigen (SV40Ta) and yeast enhanced green fluorescent protein (yEGFP) in Saccharomyces cerevisiae as a model system. When only one SV40Ta was added to either the N- or C-terminus of yEGFP, the fluorescence of yEGFP was detected in both the nucleus and the cytoplasm. When two SV40Ta signals were added, one to the N-terminus and one to the C-terminus of yEGFP (SV40Ta-yEGFP-SV40Ta), the fluorescence of yEGFP was localized in only the nucleus. When the presequence of cytochrome oxidase subunit IV (pCOXIV) was inserted between the SV40Ta and the N-terminus of yEGFP (SV40Ta-pCOXIV-yEGFP-SV40Ta) in this construct, the fluorescence was located in both the nucleus and the cytoplasm, suggesting that the increased distance between the two SV40Ta signals decreased the efficiency of transport into the nucleus. When an additional SV40Ta signal was inserted between pCOXIV and yEGFP (SV40Ta-pCOXIV-SV40Ta-yEGFP), the fluorescence was localized only in the nucleus, indicating that two SV40Ta signals spaced by pCOXIV of 28 amino acid residues forming an alpha-helix are potent in transporting yEGFP into the nucleus. These results indicate that two SV40Ta signals spaced appropriately are essential for the efficient transport of the nonnuclear protein into the nucleus.
Amino Acid Sequence↗
Repression of nitrogenase by ethanol in nitrogen-deprived cultures of Rhodovulum sulfidophilum.
Light-dependent H2 evolution did not occur in nitrogen-deprived cultures of Rhodovulum sulfidophilum in the presence of ethanol. When ethanol was added to cells which had been grown with ammonia, derepression of the nitrogen fixation genes (nifHD) was inhibited at an ethanol concentration of 1 mM. On the other hand, when cells had nitrogenase-catalyzed proton-reducing activity prior to ethanol addition, reduction of the nifHD transcript level did not occur after the addition. In cells grown with ammonia, concomitant addition of an auxiliary oxidant such as dimethylsulfoxide or sodium bicarbonate resulted in derepression of nitrogenase activity in the presence of ethanol. These results suggest that the electron-accepting process is necessary for derepression of nif genes in cultures which use ethanol as the electron donor.
Ammonia↗
Alternatively spliced variant of Smad2 lacking exon 3. Comparison with wild-type Smad2 and Smad3.
An alternatively spliced variant of Smad2 with a deletion of exon 3 (Smad2Deltaexon3) is found in various cell types. Here, we studied the function of Smad2Deltaexon3 and compared it with those of wild-type Smad2 containing exon 3 (Smad2(wt)) and Smad3. When transcriptional activity was measured using the p3TP-lux construct, Smad2Deltaexon3 was more potent than Smad2(wt), and had activity similar to Smad3. Transcriptional activation of the activin-responsive element (ARE) of Mix.2 gene promoter by Smad2Deltaexon3 was also similar to that by Smad3, and slightly less potent than that by Smad2(wt). Phosphorylation by the activated transforming growth factor-beta type I receptor and heteromer formation with Smad4 occurred to similar extents in Smad2Deltaexon3, Smad2(wt), and Smad3. However, DNA binding to the activating protein-1 sites of p3TP-lux was observed in Smad2Deltaexon3 as well as in Smad3, but not in Smad2(wt). In contrast, Smad2(wt), Smad2Deltaexon3, and Smad3 efficiently formed ARE-binding complexes with Smad4 and FAST1, although Smad2(wt) did not directly bind to ARE. These results suggest that exon 3 of Smad2 interferes with the direct DNA binding of Smad2, and modifies the function of Smad2 in transcription of certain target genes.
Alternative Splicing↗
Formation of lens aldose reductase mixed disulfides with GSH by UV irradiation and its proteolysis by lens calpain.
Explore the source record for details and available documents.
Aldehyde Reductase↗
Clinical relevance of antibiotic-induced endotoxin release in patients undergoing hepatic resection.
It has been proved that antibiotics binding to penicillin-binding protein 3 (PBP3) are associated with the greater release of endotoxin than those that bind to PBP2 in both in vitro and animal models. The aim of this study is to evaluate the potential clinical implications of antibiotic-induced endotoxin release after hepatic resection. Forty-five patients who underwent hepatic resection in our clinic were enrolled. The patients were divided into two groups. Group A (n = 26): antibiotics that bind primarily to PBP3, including cefmetazole (CMZ), latamoxef (LMOX), flomoxef (FMOX), were used. Group B (n = 19); antibiotics that bind to both PBP2 and PBP3, including cefazolin (CEZ), cefoperazone (CPZ), cefotiam (CTM). Postoperative complications, liver functional tests, and chemical mediators [endotoxin, interleukins (IL-6, IL-8), tumor necrosis factor alpha (TNFalpha), granulocyte colony-stimulating factor (G-CSF), hepatotrophic growth factor (HGF) were examined after hepatic resection. There were no significant differences in the backgrounds of the two groups. Eight patients in each group developed postoperative complications; in particular, 9 of 13 patients with biliary tract carcinoma developed postoperative complications. No significant elevation of peripheral blood endotoxin was noted by the endospecy method, in any of the patients, although six died following sepsis. Pre- and postoperative levels of cytokines showed no significant difference between the two groups. Our data suggest that clinical antibiotic-induced endotoxin release would not occur after hepatic resection regardless of the antibiotic, probably owing to continuous scavenging of endotoxin from peripheral blood.
Analysis of Variance↗
Ictal paraphasia induced by language activity.
Four patients with ictal speech disturbance were studied. Their seizures featured isolated, or series of, brief episodes of fluent paraphasia, paragraphia, and comprehension deficit. These episodes were often induced by language activity. Six patients with ictal paraphasia or paragraphia, as a recurrent habitual seizure, are reported in the literature. All ten cases, including the four cases described here and the six cases reported in the literature, featured patients who uttered meaningless speech fluently or displayed paragraphia. The syllables uttered during seizures contained many neologisms and resembled the neologistic jargon of patients with fluent aphasias of the Wernicke type. Nine patients had clusters or status of brief seizures and four patients had auditory hallucination as an ictal event. The seizures in six patients were easily induced by the use of language. Seizure focus was on the left side in all patients mentioned. The possibility of another type of language-induced seizures than those seen in reading epilepsy or language-induced epilepsy is suggested in which myoclonias of the jaw and face, or upper extremities are the main seizure types.
Adult↗
Effectiveness of polyamidoamine dendrimers modified with tripeptide growth factor, glycyl-L-histidyl-L-lysine, for enhancement of function of hepatoma cells.
Cationic polyamidoamine dendrimers are known to be highly branched cascade polymers. Tripeptide growth factor, glycyl-L-histidyl-L-lysine (GHK), was employed as a ligand for activation or attachment of cells from a rat hepatoma cell line, H4-H-E-C3, and immobilized at the terminus of the dendrimer (GHK-dendrimer) to develop a suitable surface for use as a culture substratum in the bioartificial liver support system (BAL). The growth of cells was inhibited by increasing the number of generations of GHK-dendrimers. On the other hand, urea synthesis and lidocaine clearance of the cells adhered on fifth generation GHK-dendrimers were enhanced much more than on first generation GHK-dendrimers. GHK was shown to act as a growth inhibitor and an activator of hepatoma cells. These properties of GHK are advantageous for the utilization of hepatoma cells in BAL. Ligand-modified dendrimers are very promising for the creation of a high-performance substratum for cell culture and high performance bioartificial organs, as well as for high-performance bioartificial liver systems. GHK may have the potential to be a highly useful ligand.
Journal Article↗
Clinical features and treatment of children with hemolytic uremic syndrome caused by enterohemorrhagic Escherichia coli O157:H7 infection: experience of an outbreak in Sakai City, 1996.
Presented is a study of 15 patients (seven males and eight females ranging between 5 and 10 years of age) with hemolytic uremic syndrome (HUS) associated with hemorrhagic colitis that was caused by enterohemorrhagic Escherichia coli (EHEC) O157:H7, encountered during the outbreak in Sakai City in July, 1996. The complete form of HUS, which includes the three characteristics hemolytic anemia, thrombocytopenia and acute renal dysfunction, was noted in eight patients, while an incomplete form of HUS, which did not include all three characteristics, was noted in seven patients. Regarding treatment, intravenous gamma-globulin was administered in nine patients and dialysis was performed in five patients (two males and three females) with the complete form of HUS. In three of these five patients, plasma exchange was also performed. Weaning from dialysis was accomplished by the 15th day of disease in all patients. Some patients developed pancreatitis, central nervous system symptoms, fundal hemorrhage and elevation of transaminase, although these abnormalities subsided uneventfully. Renal biopsy, which was performed in two patients who recovered from acute renal failure but still had mild proteinuria and a decrease in creatinine clearance, showed moderate changes in the glomeruli and tubulointerstitium. One year after onset of disease, hematological and urological findings were within normal limits in all patients except one with the complete form of HUS, who still had slightly decreased creatinine clearance.
Child↗
Amyloid beta protein (25-35) phosphorylates MARCKS through tyrosine kinase-activated protein kinase C signaling pathway in microglia.
Myristoylated alanine-rich C kinase substrate (MARCKS) is a widely distributed specific protein kinase C (PKC) substrate and has been implicated in membrane trafficking, cell motility, secretion, cell cycle, and transformation. We found that amyloid beta protein (A beta) (25-35) and A beta (1-40) phosphorylate MARCKS in primary cultured rat microglia. Treatment of microglia with A beta (25-35) at 10 nM or 12-O-tetradecanoylphorbol 13-acetate (1.6 nM) led to phosphorylation of MARCKS, an event inhibited by PKC inhibitors, staurosporine, calphostin C, and chelerythrine. The A beta (25-35)-induced phosphorylation of MARCKS was inhibited by pretreatment with the tyrosine kinase inhibitors genistein and herbimycin A, but not with pertussis toxin. PKC isoforms alpha, delta, and epsilon were identified in microglia by immunocytochemistry and western blots using isoform-specific antibodies. PKC-delta was tyrosine-phosphorylated by the treatment of microglia for 10 min with A beta (25-35) at 10 nM. Other PKC isoforms alpha and epsilon were tyrosine-phosphorylated by A beta (25-35), but only to a small extent. We propose that a tyrosine kinase-activated PKC pathway is involved in the A beta (25-35)-induced phosphorylation of MARCKS in rat microglia.
Amyloid beta-Peptides↗
Expression of two dead box genes (DDX1 and DDX6) is independent of that of MYCN in human neuroblastoma cell lines.
To examine whether two DEAD box genes, DDX1 and DDX6, would have some roles in the progression of tumors, we investigated the correlation of the expression of these genes with that of MYCN in neuroblastomas either with or without MYCN amplification. The mRNA of MYCN was observed only in the cell lines with amplification of MYCN. The mRNAs of DDX1 and DDX6 were found in all the cell lines examined, but the correlation between the mRNA levels of DDX1 or DDX6 and MYCN was poor. These findings suggest that the expression of neither DEAD box gene is correlated with the gene expression of MYCN.
DEAD-box RNA Helicases↗
Disposable gloves in the treatment of pressure sores.
Explore the source record for details and available documents.
Adolescent↗
Plasma homocysteine level and development of coronary artery disease.
BACKGROUND: The plasma level of homocysteine is an independent risk factor for atherosclerotic vascular disease. The relationship between plasma homocysteine level and the onset of coronary artery disease (CAD) has not been established. OBJECTIVE: To investigate the relationship between plasma homocysteine level and the age at which CAD was diagnosed. METHODS: Fifty-seven male patients aged < or = 65 years (mean age 53 years) with angiographically proven symptomatic CAD seen consecutively and 138 age-matched male control subjects (mean age 52 years) free from atherosclerotic vascular disease were studied. They were divided into two subgroups, a group of younger subjects (aged < or = 55 years) and a group of older subjects (aged 56-65 years). RESULTS: Plasma homocysteine levels in CAD patients significantly exceeded those of control subjects (means 13.4 versus 10.6 nmol/ml, P = 0.0002). Plasma homocysteine level of subjects in younger CAD group was significantly higher than that of subjects in older CAD group (15.0 versus 11.3 nmol/ml, P = 0.03), and age and logarithmically transformed plasma homocysteine level exhibited a significant negative correlation (r = -0.28, P = 0.03) for subjects in CAD group. Among control subjects, members of our two age subgroups had similar plasma homocysteine levels. Younger CAD patients had significantly higher plasma homocysteine levels than did younger controls (15.0 versus 10.4 nmol/ml, P < 0.0001). However, for older groups there was no significant difference between plasma homocysteine levels in CAD patients and controls (11.3 versus 10.9 nmol/ml). Multiple regression analysis showed that only logarithmically transformed plasma homocysteine level was a significant predictor for age of onset of CAD. CONCLUSION: An elevated level of plasma homocysteine is more important in the development of premature CAD than it is in that of late-onset CAD among men.
Adult↗
Wavelength dependence of photoparoxysmal responses in photosensitive patients with epilepsy.
PURPOSE: We tried to specify the relation between the photoparoxysmal response (PPR) and the wavelength spectra of flashing light in various photosensitive epileptic syndromes in the physiologic state. METHODS: Intermittent photic stimulation (IPS) by a Grass PS22 photic stimulator was performed with wavelength-specific optical filters in photosensitive patients with epilepsy (idiopathic generalized epilepsy, IGE; hereditary dentatorubral-pallidoluysian atrophy, DRPLA) and photosensitive subjects without epilepsy. RESULTS: Five of 19 normal trichromat patients with IGE and an IGE patient with deuteranomaly showed wavelength-dependent PPRs. The wavelength-dependent PPRs were elicited only by IPS containing wavelength spectra approximately 700 nm in the normal trichromat patients. Two of four patients with DRPLA showed wavelength-dependent PPRs, and two other DRPLA patients showed quantity-of-light-dependent PPRs. Quantity-of-light-dependent PPRs are elicited by IPS containing more than a certain quantity of light, independent of the wavelength composition of the flashing light. Two of five subjects without epilepsy showed wavelength-dependent PPRs. CONCLUSIONS: There are wavelength-dependent and quantity-of-light-dependent pathophysiologic mechanisms for eliciting PPRs by low-luminance IPS. Consideration of the quantity and wavelength composition of light from electronic screens will lead to the prevention of photosensitive seizures induced by electronic screen games.
Cerebral Cortex↗
Intracellular signaling of the TGF-beta superfamily by Smad proteins.
TGF-beta is a potent inhibitor of cell growth, and accumulating evidence suggests that perturbation of the TGF-beta signaling pathway leads to tumorigenesis. Smads are recently identified proteins that mediate intracellular signaling of the TGF-beta superfamily. Smads 2 and 3 are phosphorylated by the TGF-beta type I receptor. Smad4 was originally identified as a candidate tumor suppressor gene in pancreatic cancers. Smads 2 and 3 form complexes with Smad4 upon TGF-beta stimulation. The heteromeric Smad complexes translocate into the nucleus, where they activate expression of target genes. Our recent study demonstrated that Smads exist as monomers in the absence of TGF-beta. Smads 2 and 3 form homo- as well as hetero-oligomers with Smad4 upon ligand stimulation. Both homo-oligomers and hetero-oligomers directly bind to DNA, suggesting that the signaling pathway of Smads may be multiplex. Smads 2 and 3 associate with transcriptional coactivators such as p300 in a ligand-dependent manner, p300 enhances transactivation by TGF-beta, suggesting that coactivators link Smads to the basal transcriptional machinery. A missense mutation of Smad2 identified in colorectal and lung cancers was introduced to Smad3. The mutant, Smad3(DE), blocked the activation of wild-type Smad2 and Smad3. Thus, the missense mutation not only disrupts the function of the wild-type Smad but also creates a dominant-negative Smad, which could actively contribute to oncogenesis.
Animals↗
Abetalipoproteinemia caused by maternal isodisomy of chromosome 4q containing an intron 9 splice acceptor mutation in the microsomal triglyceride transfer protein gene.
Uniparental disomy (UPD), a rare inheritance of 2 copies of a single chromosome homolog or a region of a chromosome from one parent, can result in various autosomal recessive diseases. Abetalipoproteinemia (ABL) is a rare autosomal recessive deficiency of apoB-containing lipoproteins caused by a microsomal triglyceride transfer protein (MTP) deficiency. In this study, we describe a patient with ABL inherited as a homozygous intron 9 splice acceptor G(-1)-to-A mutation of the transfer protein gene. This mutation alters the splicing of the mRNA, resulting in a 36 amino acids, in-frame deletion of sequence encoded by exon 10. We analyzed chromosome 4, including MTP gene (4q22-24), using short tandem repeat markers. The proband has only his mother's genes in chromosome 4q spanning a 150-centimorgan region; ie, segmental maternal isodisomy 4q21-35, probably due to mitotic recombination. Nonpaternity between the proband and his father was excluded using 6 polymorphic markers from different chromosomes (paternity probability, 0.999). Maternal isodisomy (maternal UPD 4q) was the basis for homozygosity of the MTP gene mutation in this patient.
Abetalipoproteinemia↗