[Gastric cancer and sigmoid colon cancer in a patient with chronic B-cell leukemia].
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Biomedical subjects
Publications and source records attributed to H Murakami.
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Bone morphogenetic protein (BMP) is known to induce cartilage from mesenchymal cells in organ culture. The purpose of the present study was to determine whether spinal ligaments differentiate into cartilage when cultured with BMP. Implantation of BMP into the yellow ligament was also done to make a model of the ossification of yellow ligament. The rabbit was employed as an experimental animal. In organ culture, BMP induced new cartilage from the posterior longitudinal ligament, the yellow ligament and the supraspinous ligament. This indicates that spinal ligaments have the potential to ossify, and bone or periosteum may not have a direct relationship with spinal ligament ossification. Ossification of the yellow ligament was produced by implantation of BMP. Blood vessels are thought to have some role in the ossification of spinal ligaments. The spinal cord was compressed posteriorly by the ossified yellow ligament. This ossification of the yellow ligament resembled that of human beings and may be regarded as a useful experimental model.
This report describes very rare siblings who had a left ventricular muscular diverticulum and hypertrophic cardiomyopathy. The first case is a 16-year-old male. On two-dimensional echocardiography, a left ventricular muscular diverticulum in the posterior wall and mitral valve prolapse were detected. The former was verified by left ventriculography. Endomyocardial biopsy showed findings compatible with hypertrophic cardiomyopathy. The second case is a 13-year-old female. Two-dimensional echocardiography revealed a left ventricular muscular diverticulum in the same location as that of the first case, and mitral valve prolapse as well. The former was confirmed by left ventriculography. The endomyocardial biopsy findings were compatible with hypertrophic cardiomyopathy. The coronary angiograms were normal in both cases. To our knowledge, familial appearance of a left ventricular diverticulum has not yet been reported, and a left ventricular diverticulum at the posterior wall in cases with hypertrophic cardiomyopathy is very rare.
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Macroscopic collateral vessels are widely regarded as the primary source of blood flow to collateral-dependent myocardium. Microscopic coronary collateral vessels have also been described, but their functional significance is controversial. Experiments were conducted in 18 anesthetized dogs with chronic coronary artery occlusions. Indices of collateral function demonstrated that all hearts were well-collateralized. The previously occluded coronary artery was cannulated distal to the obstruction for measuring retrograde flow before and after injection of either 13 microns or 84 microns emboli. Mean arterial pressure and heart rate were not altered by coronary embolization. Embolization with 13 micron spheres caused retrograde flow to increase by 43% (n = 11), whereas embolization with 84 micron spheres had no effect on retrograde flow (n = 7). Retrograde flow dislodged occlusive 84 micron spheres, since these spheres were found in the retrograde flow, and since antegrade flow increased by 250% after retrograde flow diversion. These findings demonstrate that collateral vessels less than 84 micron diameter contribute significantly to perfusion of chronically collateral-dependent myocardium.
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Oral administration of cepharanthin (bisbenzylisoquinoline alkaloid) to mice was effective in the organ-associated immune responses. Cepharanthin, as a biological response modifier (BRM), augmented natural killer (NK) activity of leukocytes isolated from the spleen, lymph node, lung, and liver. The degree of NK augmentation was almost the same in these organs without lymph node, and reached to the maximum levels 3 days after cepharanthin administration. In addition, adherent leukocytes (greater than 95% macrophages) isolated from the lung or liver following cepharanthin administration also exhibited an augmented macrophage-mediated cytotoxicity. These results suggest that such organ-associated immune responses may play an important role in the antitumor and/or antimetastatic effects mediated by cepharanthin.
A full-length cDNA clone (pADR) for adrenodoxin reductase was isolated by means of immunological screening from a bovine adrenal poly(A)+ mRNA library. A cDNA insert of 1,973 base pairs in length encoded the entire amino acid sequence of the adrenodoxin reductase precursor protein, which consists of 492 amino acids including an extrapeptide of 32 amino acids at the NH2-terminus. The cloned cDNA contained the complete 3'-noncoding region of 443 nucleotides including 59 nucleotides of poly(A) and 51 nucleotides in the 5'-noncoding region. The amino acid sequences from the 33rd to 70th, the 117th to 123rd, the 207th to 225th, the 247th to 323rd, the 385th to 426th, the 444th to 461st, and the 487th to 492nd in the predicted structure were identical with those of the purified adrenodoxin reductase and its digested peptides, with only four exceptions.
The behavior of benzo[a]pyrene (B[a]P) during peroxidation of phosphatidylcholine (PC) liposomes initiated by an azo compound was investigated to examine the mechanism of quinone formation from carcinogenic B[a]P mediated by nonenzymatic lipid peroxidation occurring in vivo. B[a]P had a retarding effect on the peroxidation of polyunsaturated fatty acid moiety of PC. The major oxidation products which accumulated in the peroxidized liposomes were B[a]P 1,6-, 3,6-, and 6,12-quinone. Antioxidants acting as scavengers of chain-propagating lipid peroxy radicals effectively prevented not only lipid peroxidation but also B[a]P oxidation in the liposomal suspension. PC hydroperoxides, the primary products of PC oxidation, did not react with B[a]P in the absence of the azo compound, indicating that lipid peroxy radicals, not lipid hydroperoxides, are responsible for the formation of these quinones. The experiments using 18O2 gas and 18O-labeled methyl linoleate hydroperoxides demonstrated that B[a]P quinones are formed by incorporating molecular oxygen and their origin is partly due to the lipid peroxy radical. The mechanism proposed for the formation of B[a]P quinones mediated by peroxidation of membrane lipids involves a direct attack of the lipid peroxy radical on B[a]P and subsequent autocatalytic oxidation. Weak carcinogenic and noncarcinogenic pentacyclic aromatic hydrocarbons showed little reactivity to the lipid peroxy radical in the liposomes. Thus, the facility of the peroxidative attack on B[a]P may be related to the powerful carcinogenic activity of this substance.
A novel carbonic anhydrase was purified from human saliva with inhibitor affinity chromatography followed by ion-exchange chromatography. The molecular weight was determined to be 42,000 on sodium dodecyl sulfate polyacrylamide gel electrophoresis, indicating that the human salivary enzyme is larger than the cytosolic isoenzymes CA I, CA II, and CA III (Mr 29,000) from human tissue sources. Each molecule of the salivary enzyme had two N-linked oligosaccharide chains which were cleaved by endo-beta-N-acetylglucosaminidase F but not by endo-beta-N-acetylglucosaminidase H, indicating that the oligosaccharides are complex type. The isoelectric point was determined to be 6.4, but significant charge heterogeneity was found in different preparations. The human salivary isozyme has lower specific activity than the rat salivary isozyme and the human red blood cell isozyme II in the CO2 hydratase reaction. The inhibitory properties of the salivary isozyme resemble those of CA II with iodide, sulfanilamide, and bromopyruvic acid, but the salivary enzyme is less sensitive to acetazolamide and methazolamide than CA II. Antiserum raised in a rabbit against the salivary enzyme cross-reacted with CA II from human erythrocytes, indicating that human salivary carbonic anhydrase and CA II must share at least one antigenic site. CA I and CA III did not crossreact with this antiserum. The amount of salivary carbonic anhydrase in the saliva of the CA II-deficient patients was greatly reduced, indicating that the CA II deficiency mutation directly or indirectly affects the expression of the salivary carbonic anhydrase isozyme. From these results we conclude that the salivary carbonic anhydrase is immunologically and genetically related to CA II, but that it is a novel and distinct isozyme which we tentatively designate CA VI.
The purpose of the present study was to contrive a new practical method for estimating total O2 uptake during exercise from total heart beats after individual evaluation of aerobic fitness levels. Twenty healthy male subjects participated in cycle ergometer tests, maximal O2 uptake (VO2max) tests and various simple tests including simple endurance tests. From the cycle ergometer results, the following formula for estimating total O2 uptake in exercise was determined: TVO2 (ml X kg-1) = SR125 X (45.8 X mean HR + 4268) X THB X 10(-4) where TVO2, THB, and mean HR are total O2 uptake, total heart beats, and mean heart rate (beats X min-1) in exercise, respectively, and SR125 is the slope of the regression line between accumulated heart beats and accumulated O2 uptake during exercise at 125 beats X min-1 of mean HR. SR125 had a significant correlation not only with VO2max but also with each score (X) in any simple endurance tests such as, for example, a step test for 2 min. In this case, accordingly, SR125 can be found as; SR125 = -0.00118X + 0.3478. These formulae indicate that the total O2 uptake of any exercising subject can be estimated from his total heart beats regardless of intensities of exercise when his aerobic fitness level is evaluated by the simple endurance test. The total O2 uptake estimated by our method was compared to that measured by the Douglas bag method, and the discrepancy between the two results was less than the errors of values estimated by traditional methods.
Nine human-human hybridoma clones, secreting monoclonal antibodies reactive with nucleic acids, were generated by fusing with lymphocytes of lung cancer or systemic lupus erythematosus patients. These hybridoma antibodies were classified into 5 types, in terms of reactivities with DNA, RNA, various synthetic nucleic acids and cardiolipin. Hybridoma clone SU-1 secreted antibody reacting with dsDNA, ssDNA and RNA (type I). Clone HL-321 did not react with these, but with poly (dT), poly (I) and poly (G) (type II). Clone HL-349 was reactive with almost all nucleic acids tested and also with cardiolipin (type III). Clones HF-4, HF-7, HB-7 and HL-259 reacted with ssDNA, poly (A), poly (G) and cardiolipin, but not with RNA (type IV). HB-5 and SH-9 antibodies were reactive only with poly (dT) (type V).
Mammary prolaction (PRL) receptors in 3-[(3-cholamidopropyl)dimethylammonio]propanesulfonic acid (Chaps) extract were immobilized on a nitrocellulose (NC) filter, and a binding assay using the filter-bound receptors was carried out in the absence of detergent. PRL binding to the receptors was dependent on the quantity of the receptors and the PRL added to the filters. The filter-bound receptors retained the specificity of binding to peptide hormones. Scatchard analysis showed that the number of PRL receptors and the dissociation constant for PRL binding are essentially unchanged after immobilization on a NC filter, indicating that the PRL binding site does not participate in the binding to the NC filter and is equally available for PRL binding. The monoclonal antibody (MAb) against the PRL receptor was able to bind specifically to the Chaps-solubilized and filter-bound PRL receptors, as shown by curvilinear Scatchard plots. Immobilization on NC filters permits direct detection and characterization of the soluble PRL receptor using labeled PRL or MAb.