Elastic substance in so-called myoepitheliomas of minor salivary gland origin.
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Biomedical subjects
Publications and source records attributed to K Katoh.
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The effects of substance P on fluid and amylase secretion were examined in the exocrine pancreas of the rat and the mouse in vivo and in vitro. In the anaesthetised rat, a single intravenous injection of substance P caused an atropine resistant increase in both the basal and caerulein stimulated flow of pancreatic juice and amylase output, but reduced the secretin stimulated pancreatic juice flow. In vitro experiments using superfused mouse pancreatic fragments supported the in vivo result showing that substance P enhanced caerulein stimulated amylase output.
The T cell hybridoma (#5104-2) which produces a suppressor factor to suppress the hen egg-white lysozyme (HEL) specific T cell proliferative response in an antigen specific manner was developed in our laboratories. Suppression by this suppressor factor require an I-J subregion matching between suppressor factor donor and donor of HEL-specific proliferative T cells. The Igh restriction between this suppressor factor donor and HEL-primed responder cell donor has not yet been observed in our experimental system. This suppressor factor has binding activity to HEL and is bound to anti-I-J antibody columns. It was also found to suppress the HEL specific delayed type hypersensitivity (DTH) responses when administered at the induction phase.
The suppressor T cell (Ts) function of old NZW, NZB, C57BL/6 and (NZB X NZW) F1 [B/W)F1), mice to the 2,4-dinitro-1-fluorobenzene (DNFB) hapten was studied. Intravenous administration of dinitrophenyl (DNP) coupled syngeneic lymphoid cells (which normally induce DNP specific suppression) did not result in suppression of DNFB-specific contact hypersensitivity (CS) responses in old NZB or (B/W) F1 mice. Nevertheless, when spleen cells from these old mice were injected into young mice (either (B/W)F1 or A/Sn), strong suppression of the induction phase of CS responses was observed. In addition, effector phase suppressor activity was also observed when splenic cells from tolerized old (B/W) F1 donors were transferred into young (B/W)F1 mice during the effector phase of the CS response. In both cases, the significant cells in the transfer were I-J+ T cells. Thus, the old mice retained functional Ts1 and Ts2 suppressor cells. However, the suppressive activity of the old mice could be reconstituted with spleen cells from primed young mice, suggesting that they have a defect in the Ts3 subset. This was further supported by the finding that the significant cells from the primed young mice were I-J positive and cyclophosphamide-sensitive.
A case of rhabdomyosarcoma of the embryonal alveolar type arising from the prostate in a 6-year-old boy was reported with a immunohistochemical survey. Tumor cells in the biopsied inguinal lymph node were weakly positive for myoglobin and CPK-mm and showed positive staining for neuron specific enolase (NSE). At autopsy, an immunohistochemical examination demonstrated that the tumor cells, especially differentiated elongated cells, were strongly positive for myoglobin, CPK-mm and NSE. An enzyme immunoassay for three distinct subunits of NSE revealed a 320 fold increase in the beta subunit of enolase which is specific for heart and skeletal muscle. The diagnostic significance of immunohistochemical methods for rhabdomyoblasts was discussed.
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The nucleotide sequences of cytoplasmic 5S rRNA from four bryophytes, Marchantia polymorpha, Lophocolea heterophylla, Plagiomnium trichomanes and Anthoceros punctatus have been determined. These RNAs are 119 nucleotides long except for the Anthoceros RNA that has 118 nucleotides. Their sequences are highly similar to each other (91-99% identity) and are more related to those from seed plants (78-83% identity) than to those from green algae (61-73% identity).
Polygalacturonase was isolated from cell suspension cultures of a thalloid liverwort, Marchantia polymorpha. The enzyme in the ;buffer-soluble' protein fraction was dialyzed at pH 5.2 and further purified 91-fold by a combination of chromatographic techniques including CM-Sephadex, Sephacryl S-200, DEAE-Sephadex, and Sephadex G-200. The purified enzyme had an optimum activity in the pH range at 3.6 to 3.8 and molecular weight of 76,000 daltons, and its activity was not stimulated by cations. The enzyme was identified as an exohydrolase from viscometric data and chromatographic analysis of the reaction products.The polysaccharides extracted from the Marchantia cell walls with 2% (w/v) Na hexametaphosphate solution were separated into two fractions, neutral polysaccharides (fraction P-N) and acidic polysaccharides (fraction P-A) by a DEAE-Sephadex column. The fraction P-N was not susceptible to the purified exopolygalacturonase, whereas fraction P-A was partially degraded. This resulted in hydrolysis of 19.5% of the glycosyl linkages of fraction P-A with the release of galacturonic acids. The specific activity of exopolygalacturonase increased during the growth cycle.
Genetic control of PQ prolongation of the electrocardiogram (ECG) in the mouse, immunized with killed group A streptococci, was studied by using various congenic mice. Mice of H-2a, H-2k and H-2f haplotypes showed high frequencies of PQ prolongation, while haplotypes of H-2b, H-2d and H-2s showed low frequencies of PQ prolongation. Studies using various recombinant mice revealed that at least one immune-associated (Ir) gene mapped in the left side of the I-B subregion. High responsiveness of F1 hybrids of H-2b and H-2d, as well as B10.A(5R) and B10.A(3R), suggests the existence of a complementing gene. In addition, the differences between C3H and CKB, as well as differences between C3H.SW and CWB, indicate that another Ir gene maps in the immunoglobulin heavy chain (Igh) coding loci. Repeated injections of anti-I-J or anti-I-A antisera also modified this PQ prolongation. These results suggested that both the major histocompatibility complex (MHC) and immunoglobulin (Igh) loci seem to be playing important roles in the pathogenesis of PQ prolongation.
In order to investigate the actions of acetylcholine (ACh), catecholamines and substance P on K transport in the submaxillary gland, measurements of net K flux to and from the gland tissue using flame photometry, Na efflux from the tissue using radioactive 22Na, and membrane potential and input resistance using micro-electrodes were carried out on isolated superfused segments of rat and mouse submaxillary glands. ACh (5.5 X 10(-8) to 5.5 X 10(-4) M), phenylephrine (5 X 10(-7) to 5 X 10(-4) M) or substance P (10(-9) to 10(-5) M) stimulation for 5 min induced a transient K release followed by a small K uptake after the cessation of stimulation. The K release was markedly enhanced by the simultaneous addition of ouabain (10(-3) M). On the other hand, isoprenaline (2.5 X 10(-9) to 2.5 X 10(-5) M) induced a transient K uptake without any preceding K release. The K uptake was completely blocked by the addition of ouabain. Noradrenaline induced only K uptake at a low concentration (3 X 10(-7) M), but induced transient K release followed by marked K uptake at higher concentrations (3 X 10(-6) to 3 X 10(-4) M). The K release induced by noradrenaline was suppressed by the addition of phentolamine (10(-5) M), while the K uptake was suppressed by propranolol (5 X 10(-6) M). The K release induced by ACh, phenylephrine, noradrenaline or substance P was severely reduced by Ca omission from the superfusing solution and restored by the re-admission of Ca. The isoprenaline- or noradrenaline-induced K uptake was, however, little affected by Ca omission. Application of isoprenaline (2.5 X 10(-6) M) induced an increase in 22 Na efflux. The increase in 22Na efflux was completely abolished in the presence of ouabain. Local application to the tissue bath of isoprenaline (4.7 X 10(-13) to 4.7 X 10(-12) mole) or noradrenaline (5.7 X 10(-12) to 5.7 X 10(-11) mole) in the presence of phentolamine (10(-5) M) induced membrane hyperpolarization without any appreciable change in input resistance. The hyperpolarization was abolished in the presence of ouabain (10(-3) M) or propranolol (5 X 10(-6) M) or in a K-free or low Na solution. Higher doses of both agonists, however, induced depolarization or biphasic responses (initial depolarization followed by hyperpolarization). The depolarizations were accompanied by a moderate reduction in input resistance. It is concluded that in the rat and mouse submaxillary gland acinar cells cholinergic, alpha-adrenergic or substance P stimulation causes K release (and perhaps Na uptake) resulting in activation of the Na-K pump, while beta-adrenergic receptor stimulation might directly activate the Na-K pump resulting in K uptake, or might cause Na uptake resulting in activation of the Na-K pump.
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Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells. It was found that these monoclonal anti-CB-20 antibodies detect the new allotypic determinants (distinct from the B cell Igh-C region determinant) expressed only on the augmenting or suppressor T cells. Genetic analysis of these antigenic determinants revealed these antibodies react with the gene products located on the telomeric side chromosome of the Igh variable region gene (Igh-V) cluster. These antibodies when given in vivo caused a modification of antibody production. The antibody activity was absorbed by Con A-stimulated B10.BR (H-2b, Igh-1b), C57BL/6 (H-2b, Igh-1b), CWB (H-2b, Igh-1b), CB-20 (H-2d, Igh-1b), and BAB-14 (H-2d, Igh-1b) spleen cells, but not by Con A-stimulated C3H.SW (H-2b, Igh-1j), BALB/c (H-2d, Igh-1a), A/Sn (H-2a, Igh-1e), and C.AL-20 (H-2d, Igh-1d) spleen cells. In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice. One monoclonal antibody reacted with 4-hydroxy-3-nitrophenyl acetyl- (NP) hapten-specific augmenting T cells, and the other two batches of monoclonal antibodies reacted with NP-specific suppressor T cells of NP-mediated cutaneous responses. A mapping study with these recombinants limits the gene coding for the T cell-specific determinants to a gene within the variable region to the telomeric side of NP-VH and to the centromeric side of prealbumin. This segment is inclusive of all immunoglobulin genes, the region Owen named IgT-C, and a histocompatibility gene (H-Ig).
An implant metastasis developed along the tract after percutaneous transhepatic cholecystoscopy 5 months after initial placement of the catheter into the gallbladder. Percutaneous transhepatic cholecystoscopy is conducted by insertion of choledochofiberscope into the gallbladder through the dilated sinus tract established around a catheter inserted into the gallbladder. The catheter had been placed for total of 15 days. Two days after the removal of the catheter, cholecystectomy supplemented by partial resection of the liver was carried out because of the extent of a gallbladder carcinoma. The choledochofiberscope used was Olympus CHF type 4B, with a thinner flexible part 5.0 mm in diameter. It is not surprising that carcinoma of the biliary tract or pancreas may seed along the tract of a biliary drainage catheter, but only few reports describing such incidence related to percutaneous transhepatic biliary drainage have previously been published. Physicians should be aware of this complication whenever a firm nodule develops at the site of previous entry of a biliary drainage catheter in a patient with malignant obstruction.
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