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T Udagawa

Publications and source records attributed to T Udagawa.

At least 37 records · Page 2Linked to original sources
PubMed1996

ADP-ribosylation of the G protein Rho inhibits integrin regulation of tumor cell growth.

Using a gastric derived tumor line, we investigated the involvement of beta 1 integrin and Rho in cell growth regulation in response to collagen. The addition of C3 exoenzyme from clostridium botulinum to specifically ribosylate and inhibit the function of the rho gene products inhibited cellular proliferation in a dose-dependent fashion. C3 exoenzyme exhibited broad cytostatic activity toward a number of tumor lines and induced G0/G1 accumulation, cyclin A inhibition, and pronounced alterations in cell morphology. Integrin-mediated adhesion to collagen led to the expression of the cyclin A gene whose expression could be blocked using anti-beta 1 integrin monoclonal antibodies. Phospholipid levels were induced upon beta 1 integrin-mediated adhesion to collagen, and the phospholipid induction was inhibited by either antibodies to beta 1 integrin or pretreatment of cells with C3 exoenzyme. Significant reduction in phospholipid levels correlated with proliferation for a panel of tumor lines deprived of adhesion to substrate. These results implicate a novel role for integrins and Rho in the regulation of tumour growth in response to matrix.

ADP Ribose Transferases↗
PubMed1995

Integrin-mediated entry into S phase of human gastric adenocarcinoma cells.

The integrins are a family of integral membrane receptors that participate in binding to various extracellular and cell surface proteins during adhesion, migration, and homing of normal and neoplastic cells. In this study, we characterized the involvement of integrins in mediating the growth of an adhesion-dependent gastric adenocarcinoma line, ST2. This line was distinguished and selected for study based on its inability to grow when suspended in soft agar or plated on poly(2-hydroxyethyl methacrylate)-coated dishes. ST2 cells arrested in G0/G1 of the cell cycle when deprived of adhesion to substrate. Using purified matrix components, collagen was found to be highly active in promoting beta 1 integrin-mediated cell attachment and spreading. Subsequent to spreading on collagen, the cells were released from G0/G1 block and progressed into S phase. Monoclonal antibodies to alpha 2 or beta 1 integrin blocked the reinduction of both cell spreading and entry into S phase. These studies suggest that during the metastatic process, integrin receptor interaction with the insoluble matrix may be an important step leading to proliferation of some tumors.

Adenocarcinoma↗
PubMed1993

[Anesthetic management of a patient with a history of right upper lobectomy for esophageal resection via left thoracotomy].

We anesthetized a patient for esophageal resection in a right lateral decubitus position, because of his right pleural adhesion after lobectomy for tuberculosis. Although hypoxemia was expected on left lung compression during the surgery, oxygenation was not compromised. A good ventilation/perfusion relationship might have been maintained in both the right and left lungs during the procedure.

Anesthesia, Epidural↗
PubMed1992

A VLA-4 alpha-chain specific monoclonal antibody enhances CD3-induced IL-2/IL-2 receptor-dependent T-cell proliferation.

Cross-linking the T-cell receptor-associated CD3 complex using the immobilized monoclonal antibody OKT3 can induce low levels of proliferation of purified resting T cells. The effect of coimmobilizing a monoclonal antibody 19H8 specific for the alpha-chain of the integrin VLA-4 on T-cell activation was evaluated. The level of proliferation induced by coimmobilization of the anti-VLA-4 with OKT3 was about 2- to 3-fold over proliferation induced by maximal OKT3 stimulation. The costimulatory activity of 19H8 was dependent on CD3 stimulation since immobilized 19H8 by itself did not induce proliferation. IL-2 secretion was found to be increased over 2-fold with 19H8 costimulation. Addition of exogenous IL-2 resulted in enhanced proliferation of both OKT3 and OKT3 plus 19H8-stimulated cells, but T cells coactivated with 19H8 exhibited a greater capacity to proliferate in response to exogenously supplied IL-2. Analysis of IL-2 receptor expression by flow cytometry revealed that the percentage of CD25-positive cells activated with either OKT3 or OKT3 plus 19H8 is comparable, but the mean fluorescence of cells coactivated with 19H8 is about 3-fold over cells stimulated with OKT3 alone. Dependency of the 19H8 enhanced proliferation on the IL-2/IL-2 receptor system was established by using IL-2-specific neutralizing antisera that reduced the proliferation of T cells activated with OKT3 alone or OKT3 plus 19H8 to comparable levels.2+hese results demonstrate that adhesion molecules may operate at the level of cytokine production and expression of its receptors to modulate the activation state of a cell.

Antibodies, Monoclonal↗
PubMed1991

[Diaphragmatic fatigue and its recovery are influenced by markedly decreased cardiac output: possible involvement of neuromuscular junction].

Effects of highly decreased cardiac output on the development and recovery of diaphragmatic fatigue were studied in dogs. The fatigue was induced by supramaximal electrical stimulation (20 Hz) of phrenic nerves for 30 minutes. Cardiac output was reduced during this period to 30% of control value by mechanically obstructing inferior vena cava with a balloon in animals with lowered cardiac output group (lowered Qt group). Cardiac output was maintained at normal value throughout the experiment in animals of the other group (control group). The animals were observed for recovery for 60 minutes after induction of the fatigue. The standardized transdiaphragmatic pressure (Pdi/Pdi 100) and integrated electromyographic activity (Edi/Edi 100) elicited by electrical test stimuli (20, 100 Hz) were significantly lower in lowered Qt group (P less than 0.01) during entire fatigue and recovery period. The decrease of Pdi/Pdi 100 and Edi/Edi 100 at high frequency test stimuli (100 Hz) was observed only in lowered Qt group. These results suggest that when cardiac output is severely decreased the diaphragm is more susceptible to fatigue, and that this may be caused by a failure of neuromuscular junction as well as by an impaired excitation-contraction coupling.

Animals↗
PubMed1990

Experimental cancer cachexia induced by transplantable colon 26 adenocarcinoma in mice.

The present study investigates a tumor model for cachectic mice. Among various murine transplantable tumors, used for assessing cytostatics, we identified colon 26 adenocarcinoma (colon 26) as capable of causing cachexia. Fifteen days after inoculation, the tumor grew to about 6% of the body weight causing substantial carcass weight loss of 3.4 g (14.5% of the carcass weight). When the tumor size was 2.7 g at 3 weeks after the inoculation, the carcass weight was 12 g less than the age-matched control. The tumor continued to grow while the mice maintained this weight, surviving for an average of 45 days. This extensive weight loss was essentially the wasting of adipose and muscle tissues. Hypoglycemia and hypercorticism occurred during the time of the weight loss. In addition, the colon 26 caused disorders of hepatic functions: the concentration of acute phase proteins in serum increased; the number of hepatic glucocorticoid-cytosol receptors decreased; and activities of hepatic catalase and drug-metabolizing enzymes decreased. On the other hand, noncachectic mice with Meth A fibrosarcoma gained weight, which was somewhat less than the control, and had neither hypoglycemia nor hypercorticism, although some mild disorders of hepatic functions were found. Mice bearing colon 26 is an appropriate model for elucidating the mechanism that causes cachexia.

Adenocarcinoma↗
PubMed1990

Transport of divalent cations with tetracycline as mediated by the transposon Tn10-encoded tetracycline resistance protein.

Tetracycline uptake into inverted membrane vesicles from Tn10-bearing Escherichia coli cells required divalent cations. The degree of the stimulation of tetracycline uptake by various divalent cations showed the following decreasing order: Co2+ greater than Mn2+ greater than Mg2+ greater than Cd2+ greater than Ca2+. This order is consistent with the increasing order of the dissociation constants for metal chelate complexes of tetracycline. The Hill constants for the tetracycline uptake rate with various divalent cation concentrations were one. These observations strongly suggested that a 1:1 complex of tetracycline and a divalent cation was transported by a tetracycline resistance protein. This notion was confirmed by our observations that 60Co2+ was actively taken up with tetracycline by the membrane vesicles prepared from resistant cells. In the absence of tetracycline, no uptake of 60Co2+ was observed. It is clear that the 60Co2+ uptake was mediated by the tetracycline resistance protein, because the membrane vesicles from tetracycline-sensitive cells did not show the uptake of 60Co2+ and tetracycline. The 60Co2+ uptake was inhibited in the presence of other divalent cations, without any significant effect on tetracycline uptake, indicating that these cations are also transported with tetracycline by the tetracycline resistance protein.

Biological Transport↗