[An expression of tumor-associated antigen which was recognized by a monoclonal antibody KM-93 in oral tumor--comparison between tissue antigen and serum antigen].
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Biomedical subjects
Publications and source records attributed to T Tsuji.
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The carbohydrate-binding specificities of lectins purified from Agaricus bisporus (ABA-I), Arachis hypogaea (PNA), Bauhinia purpurea (BPA), Glycine max (SBA), and Vicia villosa (VVA-B4) have been studied by affinity chromatography on columns of the immobilized lectins, and quantitatively analyzed by frontal affinity chromatography. These five lectins could be classified into two groups with respect to their reactivities with typical mucin-type glycopeptides, beta-D-Galp-(1----3)-alpha-D-GalpNAc-(1----3)-Ser/Thr (2) and alpha-D-GalpNAc-(1----3)-Ser/Thr (3). One group, which consists of ABA-I, PNA, and BPA, preferentially binds to 2, and the other, which consists of SBA and VVA-B4, shows higher affinity for 3 than for 2. Among the lectins tested, only ABA-I was found to bind to a sialylated glycopeptide, whic which was prepared from human erythrocyte glycophorin A and contains three three tetrasaccharide chains having the structure of alpha-NeuAc-(2----3)-beta-D-GAlp-(1----3)-NeuAC-(2----6)]-alpha-D-Galp NAc-(1----, with an association constant of 15 microM, whereas the association constants of the other four lectins for this sialylated glycopeptide were less than 3.5 mM. On the other hand, removal of the beta-D-galactopyranosyl group from a glycopeptide containing sequence 2 resulted in decreased association constants for the three lectins of the first group, especially ABA-I and PNA. The two lectins of the second group showed a high affinity for 3, but SBA preferentially interacted with oligosaccharides containing the alpha-D-GalpNAc-(1----3)-beta-D-Galp-(1----3)-D-GlapNAc sequence, prepared from a blood group A-active oligosaccharide.
Human-type blood group activities on the red blood cells (RBCs) of three chimpanzees were individually examined with commercial mouse monoclonal antibodies (anti-A, -B, -H, -M, -N, -Lea, and -Leb) as well as lectins (UEA-I and VGA) and conventional polyclonal antisera for the systems ABO, MN, Lewis, Rh-Hr, P, Kell, Kidd, Duffy, and Lutheran. For further analysis of the MN antigens, treatment of the RBCs with sialidase, trypsin, and chymotrypsin were employed. The activities recognized among the three chimpanzees were A, H, M, N, Leb, c, S, k, and Jka. The RBCs of the three individuals possessed the A antigen which showed the same serologic activity as the human A1. Those chimpanzee RBCs showed higher H-activity than the human A1 RBCs. The Lewis b activity was revealed by the absorption-elution method. The RBCs of the three individuals showed a reactivity to the polyclonal anti-M reagents, which was affected by both the sialidase and trypsin treatment. The RBCs of two individuals were agglutinated with the monoclonal anti-N. The receptor was sensitive to sialidase and chymotrypsin. The RBCs of the three individuals, however, did not react with the monoclonal anti-M or with one of the polyclonal anti-N. These results indicate structural differences in the glycophorins and MN antigens between the human and chimpanzee.
The CT findings in 5 patients with cerebral paragonimiasis in the chronic state are presented. The findings were: 1) multiple, densely calcified areas with a variety of round or nodular shapes in the brain, 2) a large low density area surrounding or connecting with the calcified areas, and 3) cortical atrophy and ventricular dilatation. The relation between the CT findings and the previously reported plain skull X-ray findings or neuropathological findings are discussed.
Alpha-fetoprotein (AFP) synthesis in non-malignant liver tissue of 34 patients with chronic hepatitis or liver cirrhosis, some of whom also had hepatocellular carcinoma (HCC), was studied by light and ultrastructural immunohistochemistry using peroxidase-labeled anti-human AFP. Simultaneously, the serum level of AFP was measured in these patients by radioimmunoassay. AFP-positive cells were identified in non-malignant liver tissue of 7 patients with elevation of serum AFP. AFP was demonstrated in several hepatocytes which were clustered in hepatic lobules, and also in some bile ductular cells which were distributed in the periphery of portal tracts. In an immunoelectron microscopic study of AFP-positive hepatocytes, dense reaction products of anti-AFP were localized in the membranes and cisternae of rough endoplasmic reticulum (r-ER), perinuclear space (PNS) and Golgi apparatus. The prominent feature of AFP-positive hepatocytes was abundant r-ER encompassing many mitochondria. As to AFP-positive bile ductular cells, they had scanty cytoplasm and few intracytoplasmic organelles and were surrounded by basement membrane. AFP was focally localized in the r-ER of such bile ductular cells. These observations suggest that AFP can be produced by malignant and non-malignant liver cells and that in non-malignant liver tissues, AFP can be produced by two distinct cell types; bile ductular cells and hepatocytes themselves.
Fulminant hepatic failure (FHF) was produced in rats with intraperitoneal injection of D-galactosamine. 15NH4Cl (50 mg/kg of body weight) was injected into the rats via the tail vein. Arterial blood was drawn before and 5, 15, 30, 60 min after the injection of 15NH4Cl. 15N-ammonia, -urea, and -glutamine (amide and amino) were determined by gas chromatography and mass spectrometry. The plasma 15N-ammonia level was higher but decreased more rapidly in the FHF rats than in the control rats. This suggests that in FHF rats, the systemic vascular pool of ammonia is enlarged and ammonia clearance from blood is increased. The incorporation of 15N into urea was significantly different between the two groups. In FHF rats, the plasma urea-15N level rose 5 min after the injection, decreased at 15 min and was elevated again up to 60 min after injection. This biphasic change suggests that in FHF rats the incorporation of 15N into the extrahepatic glutamine pool is accelerated up to 15 min and that after 30 min a larger volume of glutamine-amide-15N is transferred to the urea cycle.
Histochemical evaluation of lectins was performed to examine the carbohydrate residues of oval cells induced by administration of alpha-naphthylisothiocyanate (ANIT), 2-acetylaminofluorene (2-AAF) and 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) in comparison with those of normal bile ducts and proliferated bile ductules induced by bile duct ligation. The normal bile ducts showed intense binding of Ricinus communis agglutinin, concanavalin A and wheat germ agglutinin, and weak binding of Ulex europaeus agglutinin I (UEA I). A few cells in the portal bile ducts showed binding of peanut agglutinin (PNA). Two different binding patterns were observed in oval cells and proliferated bile ductules. One group showed increased binding of PNA, while the other showed intense binding of UEA I. In both groups, binding of other lectins was similar to those of the normal bile duct. The first group included oval cells induced by 2-AAF and 3'-Me-DAB, and the second included both oval cells induced by ANIT and proliferated bile ductules induced by ligation. These results suggest that oval cells and proliferated bile ductules have their own specific carbohydrate residues and that oval cells induced by the carcinogens might be a cell population different from those induced by non-carcinogens and proliferated bile ductules by ligation.
To clarify molecular fluctuations during ocular development, we prepared monoclonal antibodies named MAb 111 and MAb 23 which bound differentially to the neural retina, pigmented epithelium, iris and ciliary body. In newborn mice, MAb 111 bound to the pigmented epithelium including the retinal pigmented epithelium, the pigmented layer of the ciliary epithelium and the outer layer of the iris epithelium. MAb 111 also bound to the non-pigmented layer of the ciliary epithelium and the inner layer of the iris epithelium. MAb 23 bound to the neural retina, the pigmented layer of the ciliary epithelium and the outer layer of the iris epithelium. Using these two monoclonal antibodies, we performed immunohistochemical analyses on developing mouse eyes and reached the conclusion that the optic cup has already been determined to differentiate into the retina, ciliary body and iris, on the 15th day of gestation, when the ciliary body and iris are not morphologically demarcated.
Two elderly patients with dural arteriovenous malformations in the anterior cranial fossa are reported. These patients experienced rupture of the malformations at the age of 73 and 87 years. Surgical excision of the malformation was carried out on the younger patient. In the other case megavoltage x-ray therapy was applied because radical operation was not prudent. A search of the literature provided 26 other cases of this malformation involving the anterior cranial fossa. These are the first cases of rupture of arteriovenous malformation in the anterior fossa in patients over the age of 70.
Ammonia contents in the brain stem and prosencephalon markedly increased in a rat model of acute hepatic failure induced by partial hepatectomy following CCl4 intoxication. In hepatic failure rats, synaptosomal glutamic acid (excitatory amino acid neurotransmitter) contents decreased significantly in the prosencephalon, and GABA (inhibitory amino acid neurotransmitter) contents decreased significantly in the brain stem. The molar ratio of glutamic acid to glutamine significantly diminished in the brain stem. Glutamic acid decarboxylase activity in the synaptosomes and the binding of [3H]glutamic acid and [3H]GABA to synaptosomal membrane preparations were unchanged in acute hepatic failure rats. These results indicate than an insufficiency of both excitatory and inhibitory neurotransmitter amino acids is induced by high ammonia contents in the synaptosomes of the brain stem during acute hepatic failure.
The distribution of six blood group-related antigens, A, B, H, Lea, Leb and sialylated Lea antigens, in the intrahepatic biliary tree was studied. These carbohydrate antigens in fixed normal liver tissues were immunostained with the use of highly specific monoclonal antibodies in an avidin-biotin-peroxidase complex method. Bile ducts expressed both ABH and Lewis blood group antigens. However, only Lewis blood group antigens could be detected in the bile ductules. Canaliculo-ductular junctions could be clearly delineated with the anti-Lewis blood group antibodies, especially with anti-Lea antibody. Small Lewis antigen-positive cells were scattered intralobularly. They were adjacent to parenchymal liver cells, mainly in Rappaport zone 1, and apparently in continuity with the portal biliary tree. Sialylated Lea antigen was found in some septal bile ducts. No blood group antigen could be detected in the bile canaliculi. These results indicate that (1) biliary tract of a given size has its own pattern of blood group antigen expression, and (2) biliary epithelial cells are not identical with regard to the phenotypic expression of their structural carbohydrates. In future, it will be possible to classify biliary epithelial cells by their blood group antigen expression.
Bone scintigraphy was performed in 17 patients with previously known lung metastases of osteosarcoma. 99Tcm-MDP uptake was observed in all primary bone lesions but lung metastatic lesions were positive in only six patients (35%). 99Tcm-MDP uptake by lung metastases was significantly correlated with bone and osteoid formation in the metastatic lesions and preoperative serum ALPase values. These clinical observations were confirmed by using nude mice transplanted with human lung metastatic osteosarcoma. 99Tcm-MDP scintigraphy appears to be useful for detecting lung metastases of osteosarcoma only in a selected group of patients.
We have studied a new component of the elastic fibre system in the human dermis, which we call 'elastic sheet', using scanning and transmission electron microscopy. The structure is long, broad and flat with some holes, and may be the base of the elastic fibre system from which elastic fibres originate.
Seventy-two patients with HBsAg-positive chronic hepatitis were studied for serum antibody to delta antigen (anti-HD) by radioimmunoassay. Delta antigen (HDAg) in liver of the 72 patients was also studied immunohistochemically using peroxidase-labeled anti-HD. In one of the 72 patients, high titers of anti-HD and intrahepatic HDAg were detected. In this patient, HDAg was localized mainly in nuclei and occasionally in the cytoplasm of hepatocytes. By immunoelectron microscopy, HDAg was observed diffusely in some hepatocytic nuclei, but their nucleoli, perichromatin and heterochromatin were devoid of HDAg. Occasionally, inclusion body-like ring-shaped or irregularly shaped aggregates of HDAg were observed in nuclei. At higher magnification, these aggregates consisted of an HDAg-positive amorphous substance and microtubular structures. In their vicinity, scattered HDAg-positive granules were also present. By conventional electron microscopy, similar inclusion bodies composed of a clustered amorphous substance and microtubular structures 10-20 nm in diameter, together with 20-30 nm irregular granules were observed in hepatocyte nuclei, but no core of Dane particles were found. These novel intranuclear structures were not observed in other patients with chronic hepatitis B. It is suggested that they may represent the characteristic ultrastructure associated with delta infection.
Three patients are reported, each with a reddish macule or plaque (7-10 mm) induced by trauma. The histology of these lesions showed hyperkeratosis, acanthosis and marked dilation of vessels in the papillary to deep dermis. The electron microscopic study revealed a layer of endothelial cells surrounding the dilated vessels, suggestive of telangiectasia. The relationship between this entity and solitary angiokeratoma is discussed.
Eight cases with striae distensae associated with obesity or prolonged corticosteroid intake were examined by light and scanning electron microscopy. Fine elastic fibers predominated in early lesions, while thick elastic fibers predominated in older lesions. In early lesions the periphery showed thick and tortuous elastic fibers, but in older lesions it was of normal appearance. It is suggested the elastic fibers in striae were newly synthesized and gradually increased and thickened with age.
The ADP-ribosyltransferase activity of polypeptide A1 of cholera toxin and that of Escherichia coli heat-labile enterotoxin (LT) are primarily responsible for the toxic activities of these toxins. Since the amino acid sequences of the two A1 polypeptides are very similar, their functional mechanisms are considered to be the same. Arg-146 of polypeptide A1 is thought to be involved in the active site, because this amino acid of cholera toxin has been identified as the site of self-ADP-ribosylation. However, the exact role of Arg-146 and the significance of self-ADP-ribosylation in toxicity remain unclear. We substituted Arg-146 of polypeptide A1 of LT with Gly by oligonucleotide-directed mutagenesis and examined the biological property of the resultant mutant LT. The substitution changed the mobility of subunit A on sodium dodecyl sulfate-polyacrylamide gel but did not reduce the vascular permeability activity of LT. This result indicates that Arg-146 is not absolutely required for toxic activity and that LT can express its toxic activity without self-ADP-ribosylation at Arg-146.