One stage corrective surgery early in life for tetralogy of Fallot, with reference to postoperative cardiac function.
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Biomedical subjects
Publications and source records attributed to T Tamura.
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Isozymes of adenylate kinase (ATP:AMP phosphotransferase, EC 2.7.4.3) were purified from skeletal muscle and liver of rats to essentially homogeneous states by acrylamide gel electrophoresis and sodium dodecyl sulfate gel electrophoresis. The isozyme from muscle was purified by acidification to pH 5.0, and column chromatography on phosphocellulose, Sephadex G-75 and Blue Sepharose CL-6B, while that from liver was purified by column chromatography on Blue Sepharose CL-6B, Sephadex G-75 and carboxymethyl cellulose. By these procedures the muscle isozyme was purified about 530-fold in 29% yield, and the liver isozyme about 3600-fold in 27% yield from the respective tissue extracts. The molecular weights of the muscle and liver isozymes were estimated as about 23 500 and 30 500, respectively, by both sodium dodecyl sulfate gel electrophoresis and molecular sieve chromatography, and no subunit of either isozyme was detected. The isoelectric points of the muscle and liver isozymes were 7.0 and 8.1, respectively. The Km values of the respective enzymes for ATP and ADP were similar, but the Km(AMP) of the liver isozyme was about one-fifth of that of the muscle isozyme. Immunological studies with rabbit antiserum against the rat muscle isozyme showed that the muscle isozyme was abundant in muscle, heart and brain, while the liver isozyme was abundant in liver and kidney.
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Folate mono- and polyglutamate standards were assayed by a microbiological method and by four commercially available radioassay methods to evaluate the usefulness of radioassay techniques for the quantitation of naturally occurring folates. Folate monoglutamates exhibited different responses in the radioassay procedures, depending on the one-carbon constituent and oxidation state. Folate polyglutamates exhibited an increased response that varied depending on the folate concentration. The varied responses of folate mono- and polyglutamates in the radioassay procedures make this technique unsuitable for the determination of the mixture of folate derivatives that are normally encountered in biological extracts.
A case of congenital Letterer-Siwe disease associated with protein losing enteropathy is presented. The patient was born at term after an uneventful pregnancy, and generalized eczematous skin eruptions were observed at birth. Excessive protein loss from the intestine was recognized. A cutaneous biopsy from typical lesions revealed histiocytic infiltrations and Langerhans' cell granules in the cytoplasm of the histiocytes.
Multiple mutants of Escherichia coli defective in penicillin-binding proteins (PBPs) were constructed, and into these strains Co1E1 plasmids carrying the genes for PBP-1a, -1b, or -3 were introduced. From these plasmid-carrying strains, PBP-1a and -1b were purified by ampicillin-Sepharose affinity chromatography and PBP-3 by cephalexin-Sepharose affinity chromatography. Improved purification was achieved by differential elution with NH2OH. Purified PBP-1b synthesized murein when added to the membrane fraction of a PBP-1b-defective mutant, which by itself failed to support murein synthesis in vitro. The PBP-1b preparation was able to synthesize murein from the lipid intermediate extracted with chloroform/methanol but was unable to utilize UDP-linked precursors for murein synthesis. Murein synthesis was inhibited by vancomysin, ristocetin, moenomycin, and enduracidin, but not by beta-lactam antibiotics. The synthesized murein was shown to contain crosslinked muropeptides. Their crosslinking was abolished by action of beta-lactam antibiotics. The PBP-1a and -3 preparations showed substantially no activity for murein synthesis in the same reaction system. None of the three PBPs showed D-alanine carboxypeptidase activity with UDP-N-acetylmuramoyl-pentapeptide as substrate or endopeptidase activity with bis(disaccharide-peptide) as substrate.
Plasma and red blood cell folate levels of healthy, well-nourished lactating mothers were measured. Folate levels in their breast-fed infants were significantly higher than in the mothers. No abnormal hematological findings were observed in either mothers or infants. Folate levels in breast milk and in the infants' plasma were significantly correlated. The mean breast-milk folate level was 141.4 ng/ml. The total daily folate intake for breast-fed infants was assessed at 14 to 25 micrograms/kg body weight. The plasma and red blood cell folate levels of the lactating mothers were significantly increased after oral administration of 1 mg pteroylmonoglutamate daily for 4 weeks. However, milk folate level did not change.
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The role of specific cell-mediated immune responses in human cytomegalovirus (CMV) infections was studied by an in vitro lymphocyte transformation test, using a whole blood culture. CMV-induced in vitro lymphocyte proliferation was mainly dependent on the presence of sensitized T-cells. Three of five seronegative patients with B-cell deficiency showed positive lymphocyte responses to CMV antigen. In contrast, a patient with ataxia-telangiectasia who was shedding the virus in urine did not show a cellular response to either CMV or phytohemagglutinin. Age-related differences were found in the CMV lymphocyte transformation test. The responses were generally low (P less than 0.025) in infants and higher in older children and adults. CMV lymphocyte transformation responses were lower in 15 children who were excreting CMV in urine when tested than in 17 seropositive children who were not excreting the virus.
The local secretory immune mechanism in infants with cytomegalovirus infection was studied by a measurement of neutralizing antibody in saliva. Neutralizing antibodies were determined by the microculture plaque assay in 65 saliva specimens including 54 samples from cytomegalovirus-infected subjects and 11 from seronegative controls. In addition, cytomegalovirus isolation from saliva or urine or both and antibody determination in serum and saliva were simultaneously performed on seven infants with cytomegalovirus excretion over long periods. Results obtained were as follows. (i) Neutralizing antibodies were detected in 41 (76%) of 54 saliva specimens obtained from infected subjects but in none of the 11 seronegative controls. (ii) Neutralizing antibodies in saliva were of low titer but persistently detectable in all but one of the seven infants. No relationship was recognized between the cessation of virus excretion and the development of neutralizing antibodies in saliva. (iii) Virus-neutralizing activity was specifically found in the immunoglobulin A fraction of pooled saliva by diethylaminoethyl cellulose chromatography.
Antibodies to human cytomegalovirus (CMV)-specific antigens were determined in sera serially collected from 10 infants with primary CMV infection. Antibodies to pre-early nuclear antigens (PENA), which are detectable in human embryonic lung cells within 3 h of CMV infection by anticomplement immunofluorescence staining, developed in all the patients. However, in contrast to the early response of anti-early antigens (EA), anti-late antigens (LA), and immunoglobulin M antimembrane antigens (MA), seroconversion or the maximum antibody response to PENA was usually observed 1 or more months later. Immunoglobulin M antibody to MA became undetectable soon after recovery from illness, followed by a decrease in anti-EA, anti-PENA, and then anti-LA titers. Results indicated analogy of the clinical significance of anti-PENA in CMV infection to that of anti-Epstein-Barr nuclear antigen in infectious mononucleosis and support the idea that parallel determinations of anti-PENA and IgM anti-MA antibodies can be useful for identifying the acute or chronic phase of primary CMV infection.
A 2-month-old female infant with typical features of the 13q-syndrome was found to be a hitherto unreported mosaic consisting of 46,XX,del(13)(q22)-46,XX,r(13)(p13q22). Both of the 13q- and r(13) chromosomes were Ag N banding positive. Therefore, it was assumed that they had retained the satellite stalks. Two possible mechanisms were proposed for the genesis of the mosaicism. Firstly, the patients started with the 13q- chromosome, which then underwent breakage and reunion at both ends to form the r(13) chromosome. Secondly, the patients started with the r(13) chromosome, which reopened at or close to the joining point to form the 13q- chromosome.
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