Microchimerism and graft acceptance: cardiac allograft acceptance following antiadhesion molecules antibody therapy.
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Animals↗
Biomedical subjects
Y Koga
Publications and source records attributed to Y Koga.
[Apoptosis induction and its mechanism in HIV infection].
Evidence is accumulating that apoptotic pathways account for the depletion of CD4 T cells in HIV-1 infected individuals. These pathways may be mediated, either directly by a virus infection or indirectly, through the priming of uninfected cells to apoptosis, when triggered by different agents. The participation of apoptosis in the cytopathic effect of CD4 T cells infected with HIV, in vitro, has already been shown. In our study using human CD4 cell clones expressing gp160 of HIV-1 under the control of inducible promoter, cell killing due to apoptosis was induced in the cells when gp160 was synthesized and a complex formed with gp160 in the cell. Non-infected CD4 T cells present in the vicinity of an infected cell may be killed through several mechanisms that involve gp120-CD4 interactions. Gp120 shed from infected cells can interact with CD4 on non-infected cells. Cross-linking of CD4 by such gp120 or by further binding of anti-gp120 antibody to gp120 may prime CD4 T cells for apoptosis following antigen-driven activation.
Apoptosis↗
Microchimerism and graft acceptance: IV. Cardiac allograft acceptance following anti-adhesion molecule antibody therapy.
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Animals↗
[Prolonged antinociceptive effect after epidural injection of polyethylene glycol-morphine composites in rats].
Epidurally administered morphine is useful in the management of postoperative or cancer pain, and a reliable method which can produce prolongation of analgesia with a single dose may be very useful. We synthesized a polyethylene glycol-morphine (PEG-morphine) composites and examined the duration of analgesia after a single epidural administration dose of this agent in the rat. The molecular weight of PEG was functionally evaluated. PEG-morphine was injected surgically along the epidural space. Morphine in doses of 2.5, 5.0 and 7.5 mg and PEG only were administered. A second group of animals received intramuscular injections of PEG-morphine (5.0mg). Animals were then tested for analgesia using the tail-flick test. The antinociceptive effect of 7.5mg was significantly longer than that of 2.5mg or 5.0mg. Neither PEG alone nor intramuscular administration of PEG-morphine induced antinociceptive effect. Sensory blockade was reversible and the animal appeared to have normal sensory perception. We conclude that the antinociceptive effect of morphine is dose-dependent and its duration can be prolonged when administered as a PEG-morphine composite in the epidural space.
Analgesics, Opioid↗
Construction of the plasmid PMEX8-HAK1 and random site-directed mutagenesis of human cytosolic adenylate kinase.
The pMEX8-hAK1 vector was devised from the pAK plasmid (Kim J. H. et al., 1989, Protein Engineering 5, 379-386), which could directly express human adenylate kinase proteins without recombination and its single strand DNA could be withdrawn with helper phage for random site-directed mutagenesis. The conserved key residues at Lys21, Lys27, and Thr39 were engineered to obtain mutants for kinetic analysis. Three mutants were obtained as K21P, K27R, and T39S, their specific activities were strikingly reduced compared to those of wild type adenylate kinase. This pMEX8-hAK1 will be a powerful tool for site-directed mutagenesis to detect the substrate-enzyme interaction for human adenylate kinase including various other enzymes.
Adenylate Kinase↗
[Plausibility in selecting the method of mitral valve replacement preserving the posterior subvalvular tissue].
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Female↗
Prognostic factors for short-term survival in alcoholic hepatitis in Japan: analysis by logistic regression.
Prognostic factors for the outcome of patients with alcoholic hepatitis were identified by logistic regression analysis. To predict the outcome immediately after admission, clinical data from 97 patients with alcoholic hepatitis on admission were introduced to multivariate analysis. Independent prognostic factors for favorable outcome were hepaplastin time, peripheral white blood cell count, age (40 to 60 years), and serum creatinine level (below 1.4 mg/dl). Sensitivity, specificity, positive predictive value, negative predictive value, and predictive accuracy were 0.78, 0.89, 0.78, 0.89, and 0.86, respectively. The resultant equation for the death rate was applied to another set of patients with alcoholic hepatitis as a validation study. Predictive accuracy estimated 0.95 in validation. The prognostic index derived was simple, accurate, and useful in the prediction of the outcome in patients with alcoholic hepatitis. Furthermore, it provides the clinician with an indication of the necessity for the intensive care of patients in a critical condition.
Adult↗
Two survival cases of alcoholic lactic acidosis complicated with diabetes mellitus and alcoholic liver disease.
We have experienced two patients with alcoholic lactic acidosis complicated with liver disease and diabetes mellitus who were successfully treated. They developed hypoglycemia, dehydration, lactic acidosis, and renal failure after drinking a large volume of alcohol without eating for 1 week before onset. Acidosis was thought to be directly related to excessive alcoholic intake, because it was no associated with severe liver failure and rhabdomyolysis. During monitoring of respiratory and circulatory functions, a rapid infusion of fluids adjusting to water and electrolyte imbalance was performed. A mixture of physiological saline and 5% glucose solution was thought to be effective in these cases. Patients recovered from renal failure and lactic acidosis without hemodialysis. Our experience will hopefully provide a key to successful treatment of fatal alcoholic lactic acidosis.
Acidosis, Lactic↗
Molecular cloning of mouse intestinal trefoil factor and its expression during goblet cell changes.
A cDNA encoding mouse intestinal trefoil factor (mITF) was successfully cloned and sequenced from the small intestine of C57BL/6 mouse by using the combination of reverse transcription-PCR and rapid amplification of cDNA ends methods. The gene was, similar to rat and human ITFs, mainly expressed in the small and large intestine. The mITF expression was up-regulated during the recovery phase after depletion of goblet cells in acetic acid-induced colitis. On the other hand, the expression in the jejunum was not altered, while goblet cell hyperplasia was induced by Nippostrongylus brasiliensis infection. These results suggest that the mITF expression did not simply correlate with the number of goblet cells. The mITF may play an important role in the maintenance and repair of mucosal function of the rectum. Additionally, the mITF in the jejunum may play a role in alteration of the physicochemical nature of goblet cell mucins, thereby affecting the establishment of intestinal helminths.
Acetates↗
A myosin missense mutation, not a null allele, causes familial hypertrophic cardiomyopathy.
BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by myocardial hypertrophy of unknown etiology. Missense mutations of the cardiac beta-myosin-heavy-chain (beta-MHC) gene that may be responsible for cardiac hypertrophy have been detected in patients with HCM. On the other hand, gross structural abnormalities in the cardiac beta-MHC gene, ie, an alpha/beta hybrid gene and partial deletion of the gene, have also been reported. The direct correlation between gross abnormalities and development of HCM is not well understood. METHODS AND RESULTS: We analyzed the structure of the cardiac beta-MHC gene from patients with HCM by using polymerase chain reaction-DNA conformation polymorphism analysis and found two sequence variations in exons 3 and 22 in one patient. These sequence variations at codon 54 (exon 3; nonsense mutation) and codon 870 (exon 22; Arg-to-His mutation) were identified by direct sequencing and dot-blot hybridization with allele-specific oligonucleotide probes. Relatives of this patient were examined for the mutations. It was revealed that the missense mutation was inherited from the affected father and the nonsense mutation from the unaffected grandmother through the unaffected mother. In addition, the missense mutation was also found in seven other patients from two other unrelated multiplex HCM families. CONCLUSIONS: The Arg870His mutation was suggested to cause HCM. In contrast, the gene with the nonsense mutation would encode for a cardiac beta-MHC protein of only 53 amino acid residues, which may be too short to be incorporated into the thick filament assembly of cardiac myosin chains and showed no dominant phenotype of heart disease. This is the first report of a nonsense mutation in the human cardiac beta-MHC gene.
Base Sequence↗
Two new phospholipids, hydroxyarchaetidylglycerol and hydroxyarchaetidylethanolamine, from the Archaea Methanosarcina barkeri.
The structures of two new ether phospholipids of the methanogenic Archaea, Methanosarcina barkeri, were determined as hydroxyarchaetidylglycerol and hydroxyarchaetidylethanolamine by means of chemical, chromatographic and enzymatic analyses, and fast atom bombardment-mass spectrometry. These lipids are hydroxy diether analogs of phosphatidylglycerol and phosphatidylethanolamine, respectively, with beta-hydroxyarachaeol (2-O-(3'-hydroxy)phytanyl-3-O-phytanyl-sn-glycerol) as a core lipid. In addition, two other ether phospholipids, usual archaetidylglycerol and archaetidylethanolamine, were also identified in the organism. The stereochemical structure of the unalkylated glycerophosphate of hydroxyarchaetidylglycerol and archaetidylglycerol was determined as sn-glycerol-3-phosphate by use of sn-glycerol-3-phosphate dehydrogenase. The stereochemical configuration of the glycerophosphoglycerol backbone of these lipids was a mirror image of that of diacylphosphatidylglycerol from the organisms of the domains Bacteria and Eucarya, and it was shared with extremely halophilic Archaea. These four phospholipids, in addition to five lipids that had already been reported, accounted for 88% of the total polar lipids of this organism.
Chromatography, Gas↗
Evidence of redox-linked signaling for producing a giant signal complex.
Previously we showed that a thiol-reactive heavy metal, HgCl2, crosslinked multiple cell surface receptors through a ligand-independent pathway, which produced massive aggregates of phosphotyrosine (PTYR)-containing proteins beneath plasma membrane [Nakashima et al. (1994): J Immunol 152: 1064-1071]. In this study we characterized these unique aggregates at the molecular level. The lysates in Brij 96 of thymocytes treated with HgCl2 were separated into the supernatant and pellet fractions by simple centrifugation. Selected PTYR-containing proteins and p56lck appeared in the pellet fraction as quickly as 5 s after exposure to HgCl2, and were further increased in amount by 5 min. Although the mechanism of triggering these events was redox-linked, the majority of proteins in the Brij 96-insoluble aggregates were dissociated in SDS-PAGE under nonreducing condition. This suggested that PTYR-containing proteins and p56lck themselves do not form dimer or polymer directly by thiol-mediated bond. The pellet fraction was further found to include some other signal delivery elements, such as GTPase activating protein, phosphatidylinositol 3 kinase, and mitogen-activated protein kinase. Finally, all of these signal elements and selected PTYR-containing proteins were collected in the same fraction by the sucrose density gradient centrifugation. These results suggest a unique redox-linked pathway of formation of a giant signal complex.
Animals↗
Analysis of cybrids harboring MELAS mutations in the mitochondrial tRNA(Leu(UUR)) gene.
MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes), a maternally inherited mitochondrial disorder, has been associated with an A-->G transition at nucleotide 3243 and a T-->C transition at nucleotide 3271, both in the mitochondrial tRNA(Leu(UUR)) gene. We transferred mitochondria harboring these mutations into human cells lacking endogenous mtDNA (rho o cells), and analyzed the resulting transmitochondrial cytoplasmic hybrid (cybrid) cell lines for the relationship of genotype to phenotype. Cybrids containing high levels of mutated genomes showed decreased rates of synthesis of mitochondrial translation products, reduced respiratory chain function, and increased amounts of a novel unprocessed RNA species (RNA 19). Overall effects on mitochondrial functions were more severe for the MELAS 3243 cybrids as compared to the MELAS 3271 cybrids. These data, combined with our previous observations, suggest that RNA 19 may play an important, but as yet uncharacterized, role in the pathogenesis of this mitochondrial disorder.
Genes↗
Molecular mass measurement of polymerase chain reaction products amplified from human blood DNA by electrospray ionization mass spectrometry.
We report here on the first analysis of polymerase chain reaction (PCR) products amplified from a small amount of human blood DNA by electrospray ionization mass spectrometry (ESI-MS). Adenomatous polyposis coli (APC) gene fragment of about 50 base pairs (bp) with a relative molecular mass (M(r)) of approximately 15,000 u was amplified from human blood DNA by PCR. The accurate molecular mass of the PCR products was determined with an accuracy of approximately 0.005% by ESI-MS. The amount of DNA used was only 100 ng (approximately 50 zmol; the theoretically required amount of blood is therefore less than 1 microliter for PCR). The ESI-MS measurement of the PCR products proved to be a new accurate, sensitive and fast tool for gene diagnosis.
Base Sequence↗
Esophagoaortic fistula caused by esophageal tuberculosis: report of a case.
We report herein the case of a 73-year-old woman who was urgently admitted to hospital with severe hematemesis. An emergency endoscopy revealed a protruding lesion 36 cm from the incisors; however, respiratory insufficiency precluded surgery and despite aggressive medical treatment, the patient's respiratory status continued to deteriorate, leading to death on the 36th hospital day. An autopsy revealed the source of the hemorrhage to be a fistula connecting the esophagus and the descending aorta. Histopathologic studies showed that this fistula was caused by esophageal tuberculosis.
Aged↗
Aneurysm of the transverse cervical artery occurring in association with a cavernous hemangioma as a complication of Klippel-Trénaunay syndrome: report of a case.
We report herein the case of a 14-year-old girl with Klippel-Trénaunay syndrome who developed an aneurysm of the transverse cervical artery. Because it was continuing to increase in size, with an associated risk of rupture, an aneurysmectomy was performed. Pathological examination of the resected specimen revealed a cavernous hemangioma located near the aneurysm. To our knowledge no other case of an aneurysm occurring in association with a cavernous hemangioma as a complication of Klippel-Trénaunay syndrome has ever been reported.
Adolescent↗
Microcephaly and early-onset nephrotic syndrome--confusion in Galloway-Mowat syndrome.
We report a 2-year-old girl with nephrotic syndrome, microcephaly, seizures and psychomotor retardation. Histological studies of a renal biopsy revealed focal glomerular sclerosis with mesangiolysis and capillary microaneurysms. Dysmorphic features were remarkable: abnormal-shaped skull, coarse hair, narrow forehead, large low-set ears, almond-shaped eyes, low nasal bridge, pinched nose, thin lips and micrognathia. Cases with this rare combination of microcephaly and early onset of nephrotic syndrome with various neurological abnormalities have been reported. However, clinical manifestations and histological findings showed a wide variation, and there is a lot of confusion in this syndrome. We therefore reviewed the previous reports and propose a new classification of this syndrome.
Child, Preschool↗
Analysis of target organs for the latency of murine cytomegalovirus DNA using specific pathogen free and germfree mice.
Cytomegalovirus (CMV) establishes a latent infection in its host; however, the organ sites of viral latency and its mechanism still remain to be fully clarified. To elucidate this issue, a latent infection with murine (M) CMV was attempted to induce in mice and the organ sites of the latent viral genome were examined for more than one year by a polymerase chain reaction (PCR). As a result, latent MCMV DNA was detectable in both the lung and the spleen as late as 59 weeks after infection. The heart was also observed to be a target organ of latent MCMV DNA, though the amount of viral DNA was much less than that seen in the lung and spleen. In germfree (GF) mice, on the other hand, no such latent viral DNA was observed in the spleens, while it was seen, but to a significantly smaller degree, in the lungs and the hearts than in the same organs of specific pathogen-free (SPF) mice. The amount of infectious virions generated in the host appeared to be almost equal between the GF and SPF mice. The above findings therefore suggest that the spleen, lung and heart are target organs for MCMV latency and the indigenous bacterial flora, which are not colonizing in GF mice, play an important role in the establishment of such viral latency in SPF mice.
Amino Acid Sequence↗