Measurement of the D(s)+ lifetime.

A high statistics measurement of the D(s)+ lifetime from the Fermilab fixed-target FOCUS photoproduction experiment is presented. We describe the analysis of the two decay modes, D(s)+ --> phi(1020)pi+ and D(s)+ -->K*(892)0K+, used for the measurement. The measured lifetime is 507.

A high statistics measurement of the Lambda(+)(c) lifetime.

A high statistics measurement of the Lambda(+)(c) lifetime from the Fermilab fixed-target FOCUS photoproduction experiment is presented. We describe the analysis technique with particular attention to the determination of the systematic uncertainty. The measured value of 204.

Search for CP violation in the decays D+--> K(S)pi+ and D+-->K(S)K+.

A high-statistics sample of photoproduced charm from the FOCUS experiment has been used to search for direct CP violation in the decay rates for D+-->K(S)pi+ and D+-->K(S)K+. We have measured the following asymmetry parameters relative to D+-->K-pi+pi+: A(CP)(K(S)pi+) = (-1.6+/-1.

Measurement of the branching ratios of D(+) and D(+)(s) hadronic decays to four-body final states containing a K(S).

We have studied hadronic four-body decays of D(+) and D(+)(s) mesons with a K(S) in the final state using data recorded during the 1996-1997 fixed-target run of the Fermilab high energy photoproduction experiment FOCUS. We report a new branching ratio measurement of gamma(D(+)-->K(S)K-pi(+)pi(+))/gamma(D(+)-->K(S)pi(+)pi(+)pi(-)) = 0.0768+/-0.

The induction and persistence of altered sphingolipid biosynthesis in rats treated with fumonisin B1.

The fumonisins produced by Fusarium spp. are carcinogenic in rodents and possibly carcinogenic to humans. One action of fumonisins is to inhibit the enzyme ceramide synthase and as a consequence disrupt de novo sphingolipid biosynthesis.

Study of the decay D0 --> K+pi-.

Using a large sample of photoproduced charm mesons from the FOCUS experiment at Fermilab (FNAL-E831), we observe the decay D0-->K+pi- with a signal yield of 149+/-31 events compared to a similarly cut sample consisting of 36 760+/-195 D0-->K-pi+ events. We use the observed ratio of D0-->K+pi- to D0-->K-pi+ (0.404+/-0.

Activation of mitogen-activated protein kinase by fumonisin B(1) stimulates cPLA(2) phosphorylation, the arachidonic acid cascade and cAMP production.

Activation of mitogen-activated protein kinase (MAPK) results in pleiotropic effects such as modulation of the transcription and activation of enzymes involved in signal transduction. One such enzyme is the cytoplasmic phospholipase A(2) (cPLA(2)), which releases arachidonic acid (AA). AA is the precursor of prostaglandins and leukotrienes, two inflammatory mediators, which regulate gene expression and protein kinase (PK) activity.

Analytical method for the determination of sphinganine and sphingosine in serum as a potential biomarker for fumonisin exposure.

The toxins produced by Fusarium moniliforme, which include fumonisins, are possible human carcinogens. Fumonisins are inhibitors of de novo sphingolipid biosynthesis. Alterations of the ratio of sphinganine (Sa) to sphingosine (So) in urine and serum has been proposed as a possible biomarker of exposure to this toxin.

Chemical degradation of wastes of antineoplastic agents. 2: Six anthracyclines: idarubicin, doxorubicin, epirubicin, pirarubicin, aclarubicin, and daunorubicin.

Object: Handling of genotoxic compounds commonly used in cancer chemotherapy generates contaminated wastes that require decontamination before disposal. Chemical methods are an alternative and/or a complement to incineration for the treatment of wastes and spills.

Methods: As part of a program initiated by the International Agency for Research on Cancer (IARC), 3 chemical methods readily available in the hospital environment--sodium hypochlorite (NaOCl, 5.

Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat.

Fumonisins and N-nitrosamines (NNO) are suggested risk factors in the development of human oesophageal cancer; exposure to both occurs in high risk populations in Africa and People's Republic of China. The hypothesis that the two would interact in oesophageal carcinogenesis was therefore tested by treating male rats with the known oesophageal carcinogen N-methylbenzylnitrosamine (NMBA), and fumonisin B1 (FB1). The treatment groups were: Group 1, NMBA (2.

Development of a new method for the analysis of sphinganine and sphingosine in urine and tissues.

The fumonisins are inhibitors of de novo sphingolipid biosynthesis in vitro and in vivo and thus possibly interfere with the regulation of cell growth, differentiation, and neoplastic transformation. In addition, the ratio of free sphinganine (Sa) to free sphingosine (So) has been proposed as a marker of exposure for animals or humans consuming feed or food contaminated by these toxins. A method to analyze these sphingolipid bases has been proposed [Merrill et al.

Validation in rats of two biomarkers of exposure to the food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP): PhIP-DNA adducts and urinary PhIP.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-DNA adducts in white blood cells and tissues and unmetabolized PhIP in urine were validated as biomarkers of exposure in male Fischer-344 rats treated with daily PhIP doses ranging from 1 to 0.0001 mg/kg. At the end of the 23 day treatment period all rats were killed and their blood and 10 tissues were collected for isolation of DNA and analysis of PhIP-DNA adducts by 32P-postlabeling and alkaline hydrolysis with GC/MS.

Analysis of DNA adducts of 2-amino-1-methyl-6-phenylimidazo[4,5- b]pyridine in rat and human tissues by alkaline hydrolysis and gas chromatography/electron capture mass spectrometry: validation by comparison with 32P-postlabeling.

A sensitive and specific method has been developed to measure levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) adducted to DNA in tissues. The method is based on alkaline hydrolysis of PhIP from DNA, followed by organic solvent extraction, derivatization to form the electron-capturing bis(pentafluorobenzyl) derivative, and analysis by gas chromatography/electron capture mass spectrometry (GC/MS) using a deuterium-labeled internal standard. The method can detect PhIP-DNA adducts at levels down to 0.

Gas chromatography-mass spectrometry analysis of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in urine and feces.

A method has been developed to measure levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) excreted in urine and feces. The method involves organic solvent extraction, derivatization to form electron-capturing bis-pentafluorobenzyl derivatives, and analysis by gas chromatography-negative ion chemical ionization mass spectrometry using a deuterium-labeled internal standard. The method can detect PhIP at levels of less than 1 ng/g in rat urine (5 ng/24 hr) and 5 ng/g (wet weight) in rat feces (50 ng/24 hr).

32P Postlabelling analysis of urinary mutagens from smokers of black tobacco implicates 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) as a major DNA-damaging agent.

When mutagens extracted from the urine of two smokers of black tobacco were reacted with DNA in vitro in the presence of a metabolic activation system, several DNA adducts were detected by 32P-postlabelling analysis. Some of these adducts were also visible, but only faintly, on the autoradiogram for a non-smoker's urine. DNA adducts produced in vitro by 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline or 2-amino-1-methyl-6-phenylimidazo[3,5-b]pyridine could not account for the adduct pattern produced by the urinary mutagens.