Adsorption of pyrolysate mutagens by vegetable fibers.
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Adsorption↗
Biomedical subjects
T Kada
Publications and source records attributed to T Kada.
The SOS-function-inducing activity of chemical mutagens in Escherichia coli.
The SOS-function-inducing activities of 42 chemical mutagens were investigated in Escherichia coli K12. The induction of the SOS function was assayed by monitoring the beta-galactosidase activity in the sulA::lacZ fusion strain PQ37 . To correct for the inhibitory effects of test chemicals on mRNA or protein synthesis, the level of the constitutive alkaline phosphatase was assayed in parallel. Most of the mutagens reported to be mutagenic to the Ames' Salmonella tester strains showed the SOS-function-inducing activity. The inducible SOS repair may be responsible for not only base-change mutations but also frameshift mutations. However, 9-aminoacridine, ethidium bromide and 4-nitro-o-phenylenediamine did not induce the SOS function, suggesting that the mutagenesis induced by these mutagens may occur independently of SOS repair. Present results support the SOS mutagenesis model that error-prone SOS repair plays an important role in mutagenesis induced by most chemical mutagens.
Alkaline Phosphatase↗
CT of acquired abnormalities of the portal venous system.
Computed tomography (CT), including biphasic contrast material-enhanced helical dynamic scanning and three-dimensional CT angiography, is useful in evaluating acquired abnormalities of the portal venous system. At contrast-enhanced CT, portal venous thrombus usually manifests as low-attenuation intraluminal lesions combined with enlargement of the affected portal vein. Cavernous transformation, a masslike network of intertwined veins that provides an alternative pathway for a stenosed or occluded portal vein, is depicted as multiple, periportal vascular structures. At helical dynamic CT, arterioportal shunts manifest as early enhancement of the affected portal vein, transient hyperperfusion abnormalities with lobar or segmental distribution, or transient wedge-shaped enhancement peripheral to the tumor. In patients with portosplenic venous invasion by malignant neoplasms, peripancreatic or perigastric veins may dilate if they function as hepatopetal collateral veins. In patients with portal hypertension, a variety of hepatofugal collateral pathways can develop, including esophageal, paraesophageal, coronary gastric, inferior phrenic, paraumbilical, abdominal wall, splenorenal, gastrorenal, retrocaval, and mesocaval collateral pathways. An understanding of the varied CT appearances of acquired abnormalities of the portal venous system will allow more definitive diagnosis and help avoid false diagnosis of disease.
Collateral Circulation↗