[Studies on the serum levels of a carbohydrate antigen 19-9 (CA 19-9) in patients with ovarian cancer].
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Biomedical subjects
Publications and source records attributed to H Nishimura.
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We report a case of chronic myelogenous leukemia (CML) associated with pronounced peripheral lymphadenopathy, with the cells having the philadelphia (Phl) chromosome and T-cell features. A 23-year-old man who was diagnosed as having CML and treated with busulfan was admitted to our hospital because of increasing hepatosplenomegaly and pronounced lymphadenopathy. An axillary lymph node biopsy disclosed that the malignant cells formed rosettes with neuraminidase-treated sheep red blood cells (En) (95.0%) and were positive for Leu 1 (91.8%). Of the cytochemical reactions, peroxidase was negative and periodic acid-Shiff, acid alpha-naphthyl acetate esterase and beta-glucuronidase were all positive. The karyotype of the bone marrow cells was 46 XY Phl positive (22q-), and that of the lymph node cells was 51 XY Phl positive +8, +9, +18, +19, +21, 22q-. He was treated with various anti-leukemic agents and irradiation. Despite such treatments, he died of pneumonia. This is a report of a CML patients with blast crisis and tumor formation characterized by T-cell features.
In order to arrive at a final diagnosis of early cervical cancer by colposcopy alone, a colposcopic scoring system was applied to 172 patients with the disease. Each colposcopic pattern was scored from one point (for white epithelium) to 9 (for invasive cancer). The results obtained were as follows; 1) With these scoring criteria, stage 0 cancers were restricted to below 10 points and were characterized colposcopically by white epithelia with gland openings 2) In stage I-a lesion, atypical vessels, punctuation by irregular arrangement of the dots and concentration of abnormal gland openings were usually observed, and these findings were combined with each other to show a more complicated colposcopic pattern reflected in 11 to 18 points of the score 3) Frank invasions were indicated by 19 points or more, and punctuations or mosaics were seldom found in this stage, although the early "I-b" cancer was difficult to distinguish from I-a with this method 4) The diagnoses from this scoring system were identical with the final diagnoses confirmed by surgical methods in 66.7% of stage 0, 59.4% of I-a and 76.5% of I-b.
P-enolpyruvate carboxykinase protein was measured by radioimmunoassay in liver, kidney, and adipose tissue extracts from alloxan- and streptozotocin-diabetic rats, in liver extracts from C57BL/KsJ-db+/db+ "diabetic" mice and in liver extracts from normal mice subjected to different dietary or hormonal states. The radioimmunoassay method measured tissue enzyme concentration (nanomoles/g) and total organ enzyme content (nanomoles/liver) independently of assayable activity (units/g). The "apparent" specific activity (units/nmol) was calculated from the maximum velocity and enzyme concentration data. Extracts of rat liver mitochondria and of skeletal muscle cytosol were also analyzed for P-enolpyruvate carboxykinase by the radioimmunoassay. In "chemical" diabetes, P-enolpyruvate carboxykinase by the radioimmunoassay. In "chemical" diabetes, P-enolpyruvate carboxykinase concentration increased approximately 3-fold over the fed, normal liver value of 0.89 microM, approximately 1.6-fold over the normal kidney value of 1.9 microM and approximately 2.9-fold over the normal adipose tissue value of 0.030 microM. Chemical diabetes caused the specific activity to decrease from 0.38 to approximately 0.27 units/nmol in liver and from 0.48 to approximately 0.32 units/nmol in kidney. Insulin replacement by in vivo injection not only promptly lowered the abnormally high enzyme concentration in both tissues but, paradoxically, decreased the apparent specific activities further to approximately 0.16 in liver and to 0.23 in kidney. In the db+/db+ diabetic mouse the liver enzyme increased from 0.22 microM at 5 weeks of age to 0.44 microM at 18 weeks when serum glucagon concentration is known to be highest and the pancreatic beta cells to be depleted of insulin. While the enzyme protein concentration increased 2-fold in the 18-week-old db+/db+ mouse, total liver enzyme content had actually increased 5-fold due to liver enlargement. In fasted normal mice, glucagon-treated normal mice, and alloxan/streptozotocin-treated mice, the concentration of liver enzyme increased significantly compared to the values in fed control mice. Pharmacological doses of dexamethasone did not induce the mouse enzyme. Rat liver mitochondria contained only trace quantities of immunoassayable enzyme which can be explained by contamination with cytosolic proteins. Rat skeletal muscle also contained only insignificant quantities of the enzyme or perhaps another cross-reacting, immunoassayable protein. The data obtained in diabetes before and after treatment show that complex mechanisms of control by insulin and glucagon do operate to regulate P-enolpyruvate carboxykinase in liver, kidney, and adipose tissue.
Amino groups of batroxobin (Bothrops atrox thrombic protease) were modified with 2,4-bis(O-methoxypolyethylene glycol)-6-chloro-s-triazine (activated PEG2). The modified batroxobin had the reduced binding ability towards anti-batroxobin antibody but retained its enzymic activity in vitro and in vivo. Administration of modified batroxobin in which 29% of the total amino groups in the molecule had been modified, to beagle dogs preimmunized with native batroxobin gave rise to a marked reduction of the fibrinogen level in plasma, accompanied with an increased level of fibrinogen (fibrin) degradation products, FDP. On the other hand, no reduction of fibrinogen level was observed when native batroxobin instead of modified batroxobin was injected to immunized dogs.
The uptake of dimethialium, a thiamine analog having a methyl group in place of the hydroxyethyl group in the thiazole moiety, was studied in freshly isolated rat hepatocytes. In an Na+-medium, dimethialium at 10 microM was accumulated rapidly by the cells and an almost steady intra- to extracellular distribution ratio of 4.2 was attained in 5 min of incubation. The Kt and the Vmax for the saturable component were estimated to be 27 microM and 19 pmol/10(5) cells per min, respectively. In a K+ medium, the uptake of dimethialium was decreased to 58% of that of control. Ouabain and 2,4-dinitrophenol significantly lowered the rate of dimethialium uptake. Both phenylthiazinothiamine and oxythiamine were inhibitory on the uptake of dimethialium, which uptake was also inhibited by choline. These data indicate that dimethialium transport in liver cells proceeds via a carrier-mediated active process dependent on Na+ and biological energy. Furthermore, these results also suggest that thiamine transport in liver is dissociable from thiamine phosphorylation.
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Saline washed red blood cells of the toadfish convert [1-14C] arachidonic acid to products that cochromatograph with prostaglandin E2 and prostaglandin F2 alpha. This synthesis is inhibited by indomethacin (10 micrograms/ml). Conversion of arachidonic acid to prostaglandin E2 was confirmed by mass spectrometry. When saline washed toadfish red blood cells were incubated with a mixture of [1-14C]-arachidonic acid and [5,6,8,9,11,12,14,15,-3H]-arachidonic acid, comparison of the isotope ratios of the radioactive products indicated that prostaglandin F2 alpha was produced by reduction of prostaglandin E2. The capacity of toadfish red blood cells to reduce prostaglandin E2 to prostaglandin F2 alpha was confirmed by incubation of the cells with [1-14C] prostaglandin E2.
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A series of [(heteroarylamino)phenyl]alkanoic acids having pyridine, quinoline, or pyrimidine as the heteroaryl moiety was prepared as potential antiinflammatory agents. Among them, 2-[4-(2-pyridylamino)phenyl]propionic acid (14b) showed excellent antiinflammatory and analgesic activities with less tendency to cause gastric side effects. Structure-activity relationships are discussed.
Isolated segments of the renal tubules from the freshwater trout, Salmo gairdneri, were perfused in vitro to characterize ion and water transport. The distal tubule showed a transepithelial voltage (Vt) positive in the lumen (+17.8 +/- 1.4 mV). Furosemide added to the lumen and Na cyanide and ouabain added to the bath reduced the lumen-positive Vt of the distal tubule. Removal of either Cl- or Na+ from both perfusate and bathing medium abolished the lumen-positive Vt. When the distal tubule was perfused and bathed with isosmotic solution, net water flux (Jv) was nearly zero. Jv and hydraulic conductivity remained low when the osmolality of the bathing fluid was increased with raffinose. Neurohypophysial hormones added to the bath showed no effect. Chloride efflux (lumen to bath, 171.1 +/- 17.1 peq x mm-1. min-1) was significantly higher than chloride influx (bath to lumen, 105.6 +/- 12.3 peq x mm-1 x min-1), suggesting that net chloride reabsorption exists. These results suggest that in the freshwater trout, which lack the loop of Henle, the distal tubule acts as a diluting segment. The presence of sodium, in addition to chloride, is required to generate the lumen-positive Vt in the distal tubule.
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We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly, but flared up after several years. Skin lesions appeared in the form of erythema, papules, or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was 0%-2%. The serum lactate dehydrogenase (LDH) value was within normal range and was not associated with hypercalcemia; lymphadenopathy, hepatosplenomegaly, and bone marrow infiltration were very slight. In most cases, hypergammaglobulinemia was seen, and in one case, monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their anti-ATLA antibodies were positive; none had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness and died of cryptococcus meningitis. Based on clinical and pathologic differences, we believe that these cases should be distinguished from typical ATL cases for the purposes of prognosis and treatment.
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We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly but flared up after several years. Skin lesions appeared in the form of erythema, papules or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was from 0% to 2%. The serum lactic dehydrogenase value was within normal range, and was not associated with hypercalcemia, lymphadenopathy, or hepatosplenomegaly, and bone marrow infiltration was very slight. In most cases, hypergammaglobulinemia was seen, and in one case monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their sera were positive for anti-ATL-associated antigen antibodies. None of them had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness, and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness, and died or cryptococcus meningitis. These cases were clinically and pathologically different from typical ATL cases already reported, and we feel it necessary to make distinctions from the viewpoints of prognosis and treatment. In discussing these cases, we compared smoldering ATL with typical ATL, and deliberated upon the causes of both.