[Expression of soluble c-erbB-2 protein in serum of gastric cancer patients: preliminary report].
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Humans↗
Biomedical subjects
M Nakai
Publications and source records attributed to M Nakai.
[PMUE therapy (CDDP, MMC, UFT, etoposide) for advanced gastric cancer--a case report].
CDDP, MMC, UFT and Etoposide (PMUE)-combined therapy was given to a 62-year-old man with advanced gastric carcinoma. PMUE therapy consists of i.v. injection of CDDP 75 mg/m2 and MMC 10 mg/body on day 1, i.v. injection of Etoposide 50 mg/body on days 3, 4 and 5 and consecutive daily administration of UFT 400 mg/body, with 3 weeks as one course. He was admitted for Borrmann type 3 gastric carcinoma with multiple liver metastasis, lymph node metastases and peritoneal dissemination, the underwent total gastrectomy with R2 lymph node dissection. He was treated four times with this therapy after sensitivity test for carcinostatic agents (SDI test), which resulted in complete remission, as confirmed by CT scan and second-look operation. The patient has currently been free of disease, and we conclude that this PMUE therapy is extremely effective for advanced gastric carcinoma.
Antineoplastic Combined Chemotherapy Protocols↗
Identification of an ectopic developmental antigen that appears in malignant ascitic fluid.
A tumor-associated antigen that shares antigenicity with a pregnancy-associated protein has been detected in ascitic fluid of patients with advanced ovarian cancer. The protein, prepared from malignant ascitic fluid by the combination of poly(ethylene glycol) 4000 fractionation, DEAE-Sepharose column chromatography and preparative polyacrylamide gel electrophoresis (PAGE), was subsequently separated on sodium dodecyl sulfate-PAGE, as a single band corresponding to an approximate molecular mass of 91 kDa. Immunological analysis showed that this protein was a circulating species of an ectopic developmental antigen that markedly increases in biological fluids in tumor-bearing statuses.
Antigens, Neoplasm↗
Chemical stimulation of the rostral ventrolateral medullary pressor area decreases cerebral blood flow in anesthetized rats.
In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressor area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In one group of rats (n = 11), unilateral chemical stimulation of the VLPA produced a significant (P less than 0.01) increase in arterial blood pressure (ABP), a significant (P less than 0.05) decrease in CBF, and a significant (P less than 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 +/- 3 (mean +/- S.E.M.) and 48 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLPA; the CVR was 1.9 +/- 0.1 and 2.6 +/- 0.3 mmHg per ml.min-1.(100 g)-1 before and during the stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats (n = 8). Unilateral chemical stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly (P less than 0.05) from 57 +/- 14 to 41 +/- 9 and from 50 +/- 12 to 39 +/- 9 ml.min-1.(100 g)-1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly (P less than 0.05) from 2.6 +/- 0.6 to 3.5 +/- 0.8 and from 2.7 +/- 0.5 to 3.5 +/- 0.8 mmHg/[ml.min-1.(100 g)-1], respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Purification and characterization of three forms of differently glycosylated recombinant human granulocyte-macrophage colony-stimulating factor.
We have purified recombinant human granulocyte-macrophage colony-stimulating factor (hGM-CSF) produced in human lymphoblastoid Namalwa cells. From the results of tunicamycin treatment and N-glycosidase F digestion, it was demonstrated that Namalwa-derived hGM-CSF was highly glycosylated at two potential N-glycosylation sites and several O-glycosylation sites as previously shown for naturally occurring hGM-CSF. We classified the hGM-CSF molecules into three groups according to the molecular weight corresponding to the degree of N-glycosylation: the molecules with two N-glycosylation sites occupied (designated 2N), the molecules with either site glycosylated (1N), and the molecules lacking N-glycosylation (0N). Despite such varied degrees of N-glycosylation, almost all molecules were O-glycosylated. To investigate the role of carbohydrate moieties of hGM-CSF, we isolated each form of hGM-CSF and examined its biological properties. The 2N-type showed 200-fold less in vitro specific activity compared with unglycosylated Escherichia coli-derived hGM-CSF, although the activity of the 0N-type was equivalent to that of the E. coli-derived material. The 1N-type showed an intermediate level of activity. However, in terms of clearance from blood circulation in the rat, the 2N-type showed a half-life five times longer than that of the 0N-type and E. coli-derived hGM-CSF. From these findings, we concluded that N-linked carbohydrate moieties of hGM-CSF play conflicting physiological roles in the efficacy of the protein in vivo but that O-linked carbohydrate moieties do not have such effects.
Animals↗
Intrapulmonary bronchial blood flow of rats as studied by the microsphere method.
The intrapulmonary bronchial blood flow of the left lung (systemic arterial blood flow to the left lung via the bronchial artery) was determined in 45 anesthetized and artificially ventilated male Wistar rats, weighing 263 +/- 5 g (mean +/- SEM). The microsphere method was employed and designed so that recirculating microspheres across the peripheral arteriovenous anastomoses were prevented from lodging in the left lung, and disturbances of the isovolemic state of the animals became minimal. Under normal conditions with a mean arterial pressure of 115 +/- 2 mmHg (n = 40), the bronchial blood flow of the left lung was found to be 0.307 +/- 0.033 ml/min on average, and amounted to 0.52 +/- 0.06% of the cardiac output. The flow (ml/min) normalized per kg body weight, 100 g wet lung, or 100 g dry lung was 1.14 +/- 0.12, 76 +/- 8, or 368 +/- 39, respectively. The total intrapulmonary bronchial blood flow of the left and right lungs could be estimated by multiplying the intrapulmonary bronchial flow of the left lung by the weight ratio (total:left) of 2.9. The variability of the flow data was small, as confirmed in a study with simultaneous injection of two differently radiolabeled microspheres. The reproducibility of duplicate measurements was excellent.
Animals↗
Intrapulmonary bronchial circulation during hemorrhage.
Experiments were conducted on 119 anesthetized and artificially ventilated rats to evaluate effects of a physiological stimulus (hemorrhage) to the sympothoadrenal system on the bronchial circulation. In the presence of a sufficient dose of a vasopressin V1-receptor antagonist, moderate (81 mmHg on average, 33 rats) or severe hypotension (69 mmHg, 28 rats) was produced by controlled hemorrhage (11 or 9 rats, respectively), or by treatment with phenoxybenzamine (0.1 mg/kg, i.v., 12 rats, or 1.0 mg/kg, 10 rats), or the highly selective alpha 1-adrenoceptor antagonist, bunazosin (0.01 mg/kg i.v., 10 rats, or 0.1 mg/kg, 9 rats). During hypotension, the intrapulmonary bronchial blood flow (microsphere method) was decreased in a dose-dependent manner in the two antagonist-treated groups. However, these decreases were only of a moderate degree compared to the severe decrease in the hemorrhage group. Although the bronchovascular resistance was not significantly changed after treatment with either antagonist, this variable was greatly elevated during severe hemorrhagic hypotension, reaching 240 +/- 51% (P less than 0.001 with either antagonist study) of its baseline level. Changes in the pulmonary arterial and left atrial pressures, plasma vasopressin concentration, and renin activity were found to be less influential on these responses in 58 rats. Overall, we concluded that the sympathoadrenal mechanism powerfully increased the resistance and decreased the blood flow of the intrapulmonary bronchial circulation.
Animals↗
Hyperperfusion of the rat brain during reflex hypertension induced by sudden lowering of the cutaneous temperature.
In anesthetized and artificially ventilated rats, passive or reflex hypertension was produced by ligation of the abdominal aorta (12 rats), or sudden lowering of the cutaneous temperature to 25-30 degrees C achieved by exposure to cold water (26 rats), respectively. Cold exposure increased the blood flow (microsphere method) in all of the brain regions studied by 54-174% in the face of a reflex increment in the arterial pressure by 40% on average. The vascular resistance was changed by 0-(-)32%. Such hemodynamic alterations were greater in almost all of the brain regions than would be anticipated from the autoregulatory function of the brain circulation, as evidenced by a comparison with those observed during passive hypertension. Exposure to thermoneutral water resulted in the minimal changes in the hemodynamic states of the systemic as well as brain circulations (5 rats). The sympathetic nerves innervating the cranial vessels were strongly activated during the cold exposure, as confirmed by the observation of a large increase in flow in the temporalis muscle after acute surgical sympathectomy. However, sympathetic denervation did not alter the degree of hemodynamic changes occurring in the brain regions during cold exposure. We conclude that, in the face of reflex hypertension induced by cold exposure, the powerfully activated sympathetic nerves failed to exert their well-known effect on the brain blood flow which prevents it from rising to an excessively high level.
Animals↗
Hyperperfusion and enhanced metabolic state of the brain during sudden lowering of the cutaneous temperature in rats.
Forty-eight anesthetized and artificially ventilated rats were pretreated with the ganglion blocking agent, pentolinium (5 mg/kg, i.v.), followed by continuous phenylephrine infusion for maintenance of normotension. The rats were subjected to mock treatment (16 rats), to sudden exposure to thermoneutral water (34-36 degrees C, 16 rats), or to cold water (16 degrees C, 16 rats). The latter treatment lowered the cutaneous temperature to 25-30 degrees C. Neither one of these treatments produced any significant changes in arterial pressure or heart rate. Exposure to cold elicited hyperperfusion (microsphere method) in each of the brain regions studied. The increase in cerebral cortical blood flow (by 59 +/- 8%, mean +/- SEM) was most significant. The cerebral cortical metabolic rate for oxygen was increased by 46 +/- 10%. During the cold exposure, excellent tight coupling between the metabolic rate and blood flow was observed in the cerebral cortex. Mock treatment and exposure to thermoneutral water resulted in only trivial increases in blood flow and in metabolic rate. Thus, during cold exposure, an enhanced metabolic state of the brain represented the primary determinant increasing the brain blood flow, provided that normotension was maintained.
Animals↗
Complete nucleotide sequence of the gene for a surface protein antigen of Streptococcus sobrinus.
The complete nucleotide sequence of the gene for a cell surface protein antigen (SpaA) of Streptococcus sobrinus MT3791 (serotype g) was determined. The spaA gene consisted of 4,698 bp and coded for a protein of 170,202 Da. A putative signal peptide was found in the amino-terminal end of the protein. A potential promoter sequence and a putative Shine-Dalgarno sequence preceded the open reading frame. Two internal repeating amino acid sequences were present in SpaA. One repeating region, located in the amino-terminal region, was rich in alanine, and the other, located in the central region, was rich in proline. The molecular structure of SpaA was very similar to that of the surface protein antigen of Streptococcus mutans.
Amino Acid Sequence↗
Fastidious human adenovirus type 40 can propagate efficiently and produce plaques on a human cell line, A549, derived from lung carcinoma.
Human adenovirus type 40 (Ad40) cannot propagate in conventional established human cell lines such as KB or HeLa cells. However, it has been shown that Ad40 DNA replicates in KB18 cells which express Ad2 E1B genes, suggesting that Ad40 is defective in the E1B gene function in KB or HeLa cells. We show here that Ad40 can propagate and produce plaques on A549 cells which do not contain Ad E1B genes. Our experiments show that the levels of replication of Ad40 DNA and production of infectious Ad40 virus in A549 cells are the same as or higher than those in 293 or KB18 cells. Dot blot analysis shows that the levels of Ad40 E1A and E1B mRNAs expressed in A549 cells at early to intermediate times postinfection are at least 10-fold higher than those in KB or KB18 cells. Northern (RNA) blot analysis shows that large E1B mRNA species (approximately 24S to 26S) are synthesized prior to the onset of DNA replication in A549 cells. No E1B mRNA species are synthesized in KB or KB18 cells at early times postinfection, and no differences in the expression of E1B mRNAs are seen between KB and KB18 cells. The experiment suggests that A549 cells have a cellular factor(s) which activates Ad40 E1B mRNA synthesis and that the E1B mRNA synthesis helps Ad40 propagation. In contrast, Ad40 can propagate in KB18 cells by using Ad2 E1B gene products that are constitutively expressed in this cell line. Furthermore, this result shows that Ad40 cannot propagate in KB cells because of the failure in the expression of E1B genes at early times postinfection.
Adenovirus Early Proteins↗
Ultrastructural study on junctional complexes of the excurrent duct epithelia in the epididymal region in the fowl.
Junctional complexes of the epithelia lining the rete testis, efferent ductules, connecting ductules and epididymal duct in the fowl were examined by transmission electron microscopy and by a tracer method using lanthanum nitrate. The junctional complexes were composed of tight junctions, adhering junctions and desmosomes. In the rete testis, one or two points of membrane fusion were observed at the tight junctions. In the efferent and connecting ductules and epididymal duct, the tight junctions consisted of a series of punctate membrane fusions. The adhering junctions and desmosomes showed no remarkable structural differences among these excurrent ducts. Vascularly infused lanthanum nitrate penetrated into the tight junctions of individual epithelia for variable distances, but was prevented from entering the lumen at the site of membrane fusion. These results suggest that the tight junctions can restrict the diffusion of materials via the paracellular route, and that they play an important role in maintaining a suitable fluid environment within the excurrent ducts.
Animals↗
Macrophages in the rete testis of pubertal male fowl.
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Animals↗
[Ultrastructural analysis of morphogenesis of immunodeficiency viruses].
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CD4 Antigens↗
Insulin responsiveness to glucose and tissue responsiveness to insulin in lactating, pregnant, and nonpregnant, nonlactating beef cows.
Insulin responsiveness to glucose and tissue responsiveness to insulin, using the hyperglycemic clamp and the hyperinsulinemic euglycemic clamp techniques, were measured in lactating, late pregnant, and nonpregnant, nonlactating (NPNL) beef cows. The glucose infusion rate (GIR) in the hyperglycemic clamp technique was higher (P less than .05). in lactating cows than in NPNL cows. The plateau in plasma insulin concentration (insulin responsiveness) was higher (P less than .05) in lactating cows than in late pregnant and NPNL cows. Pregnant cows tended to have higher GIR and lower plateau in plasma insulin concentration than NPNL cows. In the hyperinsulinemic euglycemic clamp technique, GIR (tissue responsiveness to insulin) was higher (P less than .05) in lactating cows than in late pregnant cows; values for NPNL cows were intermediate. We conclude that insulin responsiveness to glucose and tissue responsiveness to insulin were enhanced during lactation but tended to be decreased during late pregnancy in beef cows.
Animals↗
Noninfectious doughnut-shaped human immunodeficiency virus type 1 can induce syncytia mediated by fusion of the particles with CD4-positive cells.
A defective doughnut-shaped human immunodeficiency virus type 1 (HIV-1)-producing cell clone (designated as L-2) was isolated from persistently HIV-1-infected MT-4 cells. The syncytium-forming capacity of the cell and virus particle fractions was examined in human CD4-positive T cells. Several cell lines producing infectious HIV-1 particles, such as persistently HIV-1-infected MOLT-4 (MOLT-4/HIV-1) cells, were used as controls. Syncytia were formed within 20 h by the cell fraction of both L-2 and MOLT-4/HIV-1 and the virus particle fraction of L-2, but not MOLT-4/HIV-1. These formations were not affected by 3'-azido-3'-deoxythymidine (ZDV). In contrast, similar syncytium formation was first observed 2 days after the incubation of the virus particle fraction of MOLT-4/LAV-1 and this syncytium formation mediated by the cell fractions of MOLT-4/HIV-1 and L-2 or the virus particle fraction of L-2 differently.
Antibodies, Monoclonal↗
[Methods for studying protein import into isolated mitochondria].
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Membranes↗
An increase in regional brain blood flow during hypertension induced by chemical inhibition of the nucleus tractus solitarius in rats.
Passive or neurogenic hypertension was produced by ligation of the aorta or microinjection of glutamate diethyl ester (GDEE) into the intermediate one-third of the nucleus tractus solitarius (NTS), respectively, in 44 anesthetized, artificially ventilated rats. After bilateral sympathectomy, the blood flow (microsphere method) was increased in the cerebral cortex, thalamus, and mesencephalon in a pressure-dependent manner in the face of neurogenic hypertension, as compared with the flow during passive hypertension. We speculate that some neurogenic mechanism tends to impair cerebrovascular autoregulation when afferents arising from cardiovascular receptors were blocked by GDEE within the NTS.
Animals↗