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Liver detection

Manganese(II)-A/, A/r -dipyridoxylethylenediamine-A/r, AT-diacetate 5,5 -bis(phosphate) 75 (DPDP) is clinically used for enhancing contrast in the liver (detection of hepatocellular carcinomas) (312). Some dissociation of Mn(II) appears to occur in the liver, and enhancement can also be obtained in functional adrenal tissues (313). Manganese(II)-tetrasulfonated phthalocyanine also shows tumor localization properties and is a more efficient relaxation agent than the analogous Gd(III) complexes (314). [Pg.238]

High Pressure Liquid Chromatography. In postmortem blood or liver detection limit 50 ng/ml and 100 ng/g respectively, UV detection— E. A. Queree et al, J. analyt. Toxicol, 1985, 9, 10-14. In urine paraquat and diquat, detection limit < 1 ig/ml, UV detection—R. G lWet al, J. Chromat., 1983, 255, 483-490. [Pg.853]

Isolated perfused liver Liver detecting DNA damage Hepatotoxicity/metabolism... [Pg.146]

Acetylation of mucin-bound and membrane-bound sialic acids makes them more resistant towards sialidase action [8,33,245,853,854]. This may be one of the reasons why intestinal mucins, especially of the colon, are often O-acetylated (ref. [245], and section 8.4.2). The high level of 0-acetylation of sialic acids observed in the endothelia of blood vessels, e.g, in liver, detected by histochemical methods using influenza C virus hemagglutinin, is assumed to have a similar function [234,235,730]. [Pg.343]

Yamamoto H, Yamashita Y, Takahashi M (1996) Development of hepatomas in hyperplastic nodules induced in the rat liver detection with superparamagnetic iron oxide-enhanced magnetic resonance imaging. Acad Radiol 3 330-335... [Pg.28]

La, Ce, Human liver, Detection of REE bond- Enriched stable IT About 12 REE-bonding 12... [Pg.58]

Oxyphenbutazone (712), y-hydroxyphenylbutazone and kebuzone (715) are metabolites of phenylbutazone in liver. The first cited is an equally potent antiinflammatory agent but slightly less toxic. Compounds (711) and (712) are rarely used as analgesics and antipyretics because of their toxicities. The first one is used in therapy of rheumatoid disorders characterized by a lack of detectable antiglobulin and antinuclear antibodies in the serum. The y-hydroxyphenylbutazone has marked uricosuric activity but little antirheumatic effect. Kebuzone (715) is an antiinflammatory agent still widely used in Europe. [Pg.296]

The hazards of chemicals are commonly detected in the workplace first, because exposure levels there are higher than in the general environment. In addition, the exposed population is well known, which allows early detection of the association between deleterious health effects and the exposure. The toxic effects of some chemicals, such as mercury compounds and soot, have been known already for centuries. Already at the end of the eighteenth century, small boys who were employed to climb up the inside of chimneys to clean them suffered from a cancer of the scrotum due to exposure to soot. This was the first occupational cancer ever identified. In the viscose industry, exposure to carbon disulfide was already known to cause psychoses among exposed workers during the nineteenth century. As late as the 1970s, vinyl chloride was found to induce angiosarcoma of the liver, a tumor that was practically unknown in ocher instances. ... [Pg.250]

In a study by Stresser and co-workers, the effect on tumor modulation by 227 has been investigated. HPLC on liver extracts from Fisher 344 rats revealed two major compounds, 3,3 -bisindolylmefliane (133) and a linear trimer, together with a < l(KX)-fold lower content of 4 in comparison with the two major substances. The HPLC isolate was derivatized with /V-methyl-/V-bis(trifluoroacetamide) that, upon MS detection, gave a compound identical to /V,W -ditrifluoroacetylindolo-[3,2-()]carbazole. The content of 4 in this system was estimated to be 0.(XKX)13% of the total dose of 227 given. Thus, it was concluded that the beneficial effect of oral distribution of 227 is due to the total content of derivatives formed (95MI5). [Pg.51]

The drug is metabolized rapidly in the liver, kidney, intestinal mucosa, and even red blood cells. Therefore it has a plasma half-life of only 10 min after bolus intravenous application. The major metabolite, uracil arabinoside (ara-U), can be detected in the blood shortly after cytarabine administration. About 80% of the dose is excreted in the urine within 24 h, with less than 10% appearing as cytarabine the remainder is ara-U. After continuous infusion, cytarabine levels in the liquor (cerebro-spinal fluid) approach 40% of that in plasma. Continuous infusion schedules allow maximal efficiency, with uptake peaks of 5-7 pM. It can be administered intrathecally as an alternative to methotrexate. [Pg.151]

HBV infection remains a major worldwide public health problem. The World Health Organization estimates that there are still 350 million chronic carriers of the vims, who are at risk of developing chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The success of IFN-a treatment - mainly performed as combined treatment with adenine-arabinoside - has been measured by the normalization of liver enzymes, loss of HBe antigen and of detectable viral DNA in the serum of patients. It has been estimated from several clinical trials that as many as 40% of treated HBV patients would respond to therapy with IFN-a or combined treatment with nucleoside analogues and IFN-a. [Pg.645]

Liver Gadolinium EOB DTPA Primovist MRI product, not approved for CT phase I, II clinical trials Uptake into hepatocytes Schmitz SA et al (1997) Detection of focal liver lesions CT of the hepatobiliary system with gadoxetic acid disodium, or Gd-EOB-DTPA. Radiology 2002 399-405... [Pg.1327]

Watmough, N.J.. Turnbull, D.M., Sherratt. H.S.A. Bartlett. K. (1989). Measurement of the acyl-CoA intermediates of p-oxidation by hplc with on-line radiochemical and photodiode-array detection. Application to the study of [U- C]hexadecanoate by intact rat liver mitochondria. Biochem. J. 262,261-269. [Pg.154]

No changes in GTP and y-GT activity were recorded after repeated administration of the above compounds. Also, histopathological examination did not point to liver necrosis. Similar phenomenon detected earlier after repeated administration of monobromobenzene, was interpreted as a result of damage of the microsomal enzymatic system responsible for the appearance of active metabolites (ref. 22). [Pg.397]

Administration of dibutyltin dichloride intraperito-neally to rats led to the formation of butyl(3-hydroxy-butyl)tm, butyl(4-hydroxybutyl)tin, and monobutyltin. The major metabolite (buty 1(3-hydroxybutyl)tin) was distributed to the kidney at a relatively high concentration compared with the other metabolites, and its concentration increased with time. Butyl(4-hydroxybutyl)tin was found in urine only. The parent compound and other metabolites were detected in the brain (Ishizaka et al., 1989). Dibutyltin diacetate was destarmylated by 14% within 90 h following a single oral dose in mice at 1.1 mg/kg body weight, with several butyltin derivatives found in the liver or faeces (Boyer, 1989). [Pg.21]


See other pages where Liver detection is mentioned: [Pg.459]    [Pg.172]    [Pg.172]    [Pg.585]    [Pg.362]    [Pg.459]    [Pg.172]    [Pg.172]    [Pg.585]    [Pg.362]    [Pg.44]    [Pg.111]    [Pg.116]    [Pg.139]    [Pg.47]    [Pg.241]    [Pg.317]    [Pg.103]    [Pg.799]    [Pg.270]    [Pg.200]    [Pg.203]    [Pg.501]    [Pg.523]    [Pg.551]    [Pg.625]    [Pg.1148]    [Pg.1219]    [Pg.1327]    [Pg.502]    [Pg.595]    [Pg.273]    [Pg.81]    [Pg.402]    [Pg.393]    [Pg.256]    [Pg.87]    [Pg.90]    [Pg.94]    [Pg.94]   
See also in sourсe #XX -- [ Pg.201 ]

See also in sourсe #XX -- [ Pg.185 ]




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