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J Volk

Publications and source records attributed to J Volk.

At least 19 recordsLinked to original sources
PubMed2006

Measurement of the asymmetry in the decay Omega+-->LamdaKappa+-->rhopi+Kappa+.

The asymmetry in the rho angular distribution in the sequential decay Omega+-->LamdaKappa+-->rhopi+Kappa+. has been measured to be alphaOmegaalphaLamda=[+1.16+/-0.18(stat)+/-0.17(syst)]x10(-2) using 1.89x10(6) unpolarized Omega+ decays recorded by the HyperCP (E871) experiment at Fermilab. Using the known value of alphaLamda, and assuming that alphaLamda=-alphaLamda, alphaOmega=[-1.81+/-0.28(stat)+/-0.26(syst)]x10(-2). A comparison between this measurement of alphaOmegaalphaLamda and recent measurements of alphaOmegaalphaLamda made by HyperCP shows no evidence of a violation of CP symmetry.

Journal Article↗
PubMed2005

Effects of three resin monomers on the cellular glutathione concentration of cultured human gingival fibroblasts.

OBJECTIVES: Oral and systemic cells are permanently exposed to various types of xenobiotics, such as dental restorative materials, which may subsequently cause adverse effects. Objective of the present investigation was to analyze the effects of three important resin monomers on the glutathione metabolism of human gingival fibroblasts after an incubation period of 4h. METHODS: Cells were exposed to various concentrations of 2-hydroxyethyl methacrylate (HEMA; 0.1-10 mM), triethylene-glycol dimethacrylate (TEGDMA; 0.05-2.5 mM), and urethane dimethacrylate (UDMA; 0.005-0.25 mM). Subsequently, cellular glutathione (GSH) concentrations were determined after a treatment period of 4h using the monobromobimane assay. Data were statistically evaluated using Tukey ANOVA with p<0.05. RESULTS: GSH depletion was dependent on the type of the resin monomer: UDMA>TEGDMA>HEMA. The concentrations for a 50%-reduction of cellular GSH varied between 0.1 mM (0.05 mM) (UDMA), 0.33 mM (0.09 mM) (TEGDMA), and 1.6 mM (0.8 mM) (HEMA). Simultaneously, no decrease of cell numbers was found at any tested concentration. SIGNIFICANCE: These data indicate that the investigated resins may cause cell damage due to depletion of intracellular GSH level even at low concentrations within a short period of time. The decrease of GSH is an early reaction, which is triggered prior to other cytotoxic alterations.

Bridged Bicyclo Compounds↗
PubMed2005

Search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-).

A sensitive search for the lepton-number-violating decay Xi(-)-->pmu(-)mu(-) has been performed using a sample of approximately 10(9) Xi(-) hyperons produced in 800 GeV/c p-Cu collisions. We obtain B(Xi(-)-->pmu(-)mu(-))<4.0x10(-8) at 90% confidence, improving on the best previous limit by 4 orders of magnitude.

Journal Article↗
PubMed2005

Search for DeltaS = 2 nonleptonic hyperon decays.

A sensitive search for the rare decays Omega(-)--> Lambdapi(-) and Xi(0)--> ppi(-) has been performed using data from the 1997 run of the HyperCP (Fermilab E871) experiment. Limits on other such processes do not exclude the possibility of observable rates for |DeltaS| = 2 nonleptonic hyperon decays, provided the decays occur through parity-odd operators. We obtain the branching-fraction limits B(Omega(-)-->Lambdapi(-)) < 2.9 x 10(-6) and B(Xi(0)--> ppi(-)) < 8.2 x 10(-6), both at 90% confidence level.

Journal Article↗
PubMed2005

Evidence for the decay sigma+ --> pmu+ mu-.

We report the first evidence for the decay Sigma(+)-->pmu(+)mu(-) from data taken by the HyperCP (E871) experiment at Fermilab. Based on three observed events, the branching ratio is B(Sigma(+)-->pmu(+)mu(-))=[8.6(+6.6)(-5.4)(stat)+/-5.5(syst)]x10(-8). The narrow range of dimuon masses may indicate that the decay proceeds via a neutral intermediate state, Sigma(+)-->pP(0),P0-->mu(+)mu(-) with a P0 mass of 214.3+/-0.5 MeV/c(2) and branching ratio B(Sigma(+)-->pP(0),P0-->mu(+)mu(-))=[3.1(+2.4)(-1.9)(stat)+/-1.5(syst)]x10(-8).

Journal Article↗
PubMed2005

ROS formation and glutathione levels in human oral fibroblasts exposed to TEGDMA and camphorquinone.

Glutathione (GSH) is important for the self-protection of cells against oxidative stress and toxic xenobiotics, whereas reactive oxygen species (ROS) at elevated concentrations may cause detrimental alterations of cell membranes, DNA, and other cellular structures. The present investigation addressed the effects of triethylene-glycoldimethacrylate (TEGDMA) and camphorquinone (CQ) on glutathione metabolism and the formation of ROS in oral cells. Primary human pulp fibroblasts were exposed to various concentrations of TEGDMA and CQ (0.1-5 mM). Subsequently, GSH concentration and ROS formation were analyzed with the use of the monobromobimane assay (GSH) and 2',7'-dichlorofluorescein diacetate (DCFH-DA) (ROS). The endogenous ROS hydrogen peroxide (H2O2) was used as a positive control (0.02-2 mM). TEGDMA significantly decreased GSH at concentrations between 0.5 and 5 mM (p<0.05), but did not elevate ROS levels. Contrary, CQ increased ROS formation at concentrations>or=1 mM, but had only a moderate effect on GSH at the highest test concentration. Hydrogen peroxide increased ROS and simultaneously decreased GSH at concentrations of >or=0.2 mM. These data show that the investigated substances may cause cell damage due to various mechanisms, GSH decrease and/or ROS increase. As a consequence, TEGDMA and CQ released into an aqueous environment from resinous materials might interact, thus generating significant cytotoxic effects even at low concentrations.

Cells, Cultured↗
PubMed2004

Search for CP violation in charged-Xi and Lambda hyperon decays.

We have compared the p and p angular distributions in 117 x 10(6) Xi- -->Lambdapi- -->ppi-pi- and 41 x 10(6) Xi+ -->Lambda pi+ -->p pi+pi+ decays using a subset of the data from the HyperCP experiment (E871) at Fermilab. We find no evidence of CP violation, with the direct-CP-violating parameter AXiLambda identical with (alphaXialphaLambda-alpha Xialpha Lambda)/(alphaXialphaLambda+alphaXialphaLambda)=[0.0+/-5.1(stat)+/-4.4(syst)] x 10(-4).

Journal Article↗
PubMed2002

Observation of the decay K- --> pi(-)mu(+)mu(-) and measurements of the branching ratios for K+/- --> pi(+/-)mu(+)mu(-).

Using data collected with the HyperCP (E871) spectrometer during the 1997 fixed-target run at Fermilab, we report the first observation of the decay K--->pi(-)mu(+)mu(-) and new measurements of the branching ratios for K+/--->pi(+/-)mu(+)mu(-). By combining the branching ratios for the decays K+-->pi(+)mu(+)mu(-) and K--->pi(-)mu(+)mu(-), we measure Gamma(K+/--->pi(+/-)mu(+)mu(-))/Gamma(K+/--->all) = (9.8+/-1.0+/-0.5)x10(-8). The CP asymmetry between the rates of the two decay modes is [Gamma(K+-->pi(+)mu(+)mu(-))-Gamma(K--->pi(-)mu(+)mu(-))]/[Gamma(K+-->pi(+)mu(+)mu(-))+Gamma(K--->pi(-)mu(+)mu(-))] = -0.02+/-0.11+/-0.04.

Journal Article↗
PubMed2002

Clinical phase II study and pharmacological evaluation of rubitecan in non-pretreated patients with metastatic colorectal cancer-significant effect of food intake on the bioavailability of the oral camptothecin analogue.

A randomised, open label phase II study was performed in patients with advanced colorectal cancer to evaluate the safety, toxicity and antineoplastic activity of the topoisomerase I-inhibitor rubitecan. A cross-over design was chosen to determine the intrapatient variation of the bioavailability and pharmacokinetics of the anticancer agent depending on the timing of food intake in relation to the oral drug administration. Patients with previously untreated metastatic disease received two single oral doses of rubitecan 1.5 mg/m2 for assessment of the pharmacokinetics. They were randomised to have the first administration either after an overnight fasting period or immediately after a high calorie breakfast, and crossed over to the alternative schedule after a one-week washout period. After completion of the pharmacokinetic sampling, treatment continued with rubitecan given orally at a dose of 1.5 mg/m2/day, to be increased up to 2.0 mg/m2/day, under fasting conditions for 5 consecutive days per week until disease progression. 19 patients entered the trial after informed consent was obtained. A total number of 35 treatment cycles (median 2, range 1-4) were administered. All patients were evaluable for safety. The toxicity profile of rubitecan was generally mild to moderate, with sporadic cases of grade 4 toxicities (Common Toxicity Criteria (CTC) version 2.0) diarrhoea, leucopenia and neutropenia. None of 15 evaluable patients achieved an objective response. The majority had early disease progression. 14 patients were evaluable for pharmacokinetic analysis. The bioavailability of rubitecan was found to be strongly dependent on the timing of food intake with a fasted-to-fed ratio for C(max) of 1.98 (two-tailed P<0.001; ANOVA), T(max) 0.49 (P<0.001), AUC(0-8 h) 2.52 (P<0.001) and AUC(0-24 h) 1.64 (P=0.003). Rubitecan is well tolerated, but clinically inactive in colorectal cancer at the currently recommended dose and schedule. The bioavailability is strongly dependent on the timing of food intake in relation to the oral administration of the drug. The topoisomerase I-inhibitor should be administered under fasting conditions to achieve adequate drug exposure in future prospective trials in other tumour types.

Administration, Oral↗
PubMed2001

Safe administration of irinotecan, oxaliplatin and raltitrexed in a DPD-deficient patient with metastatic colon cancer.

Dihydropyrimidine dehydrogenase deficiency is diagnosed more frequently and is now generally accepted as a potentially life-threatening condition. It predisposes patients receiving treatment with fluoropyrimidines such as 5-fluorouracil (5-FU) to severe and, in case of complete dihydropyrimidine dehydrogenase deficiency, often fatal toxicity. A patient who had severe side effects following standard dose adjuvant 5-FU exposure was diagnosed of having hereditary partial dihydropyrimidine dehydrogenase deficiency. When the patient relapsed with liver metastases, we treated him with the non-fluoropyrimidine cytotoxic agents irinotecan, oxaliplatin and raltitrexed in sequential manner, and were able to show that these drugs can be safely applied in patients with this metabolic defect.

Adenocarcinoma↗
PubMed2000

Transmission of the haplosporidian parasite MSX Haplosporidium nelsoni to the eastern oyster Crassostrea virginica in an upweller system.

The haplosporidian oyster parasite MSX (Multinucleated Sphere X) Haplosporidium nelsoni was transmitted to eastern oysters Crassostrea virginica. Hatchery-raised, MSX-free juvenile oysters were placed in upweller tanks. Water to the tanks was filtered through a screen with 1 mm2 openings and originated from the water column overlaying naturally infected oysters beds (MSX prevalence 17 to 57%). MSX was diagnosed by histopathological analysis. MSX-disease (57% prevalence) with increased mortality (19%) was observed 11 wk after the beginning of the exposure and mortality of 80% after 16 wk. The study demonstrates transmission of MSX via water-borne infectious agents capable of passing through a 1 mm filter.

Animals↗
PubMed2000

Oxidative burst measurement in patients treated with cytostatics: influence of G-CSF and role as a prognostic factor.

The ability to generate reactive oxygen species, the so-called oxidative burst, is essential for neutrophils to kill infectious micro-organisms. Flow cytometry was used to study oxidative burst prior to, during, and after cytostatic therapy. Seven patients were treated according to the DexaBEAM regimen with 12 cycles monitored. Four patients were treated according to the B-NHL regimen in which nine cycles were monitored. Ten healthy volunteers were chosen as a control group without any treatment. Neutrophils were collected from heparinized peripheral blood and were stimulated by phorbol-12-myristate-13-acetate (PMA), N-formyl-methionyl-leucyl-phenylalanine (FMLP), and Escherichia coli. The oxidative burst was estimated by the amount of nonfluorescent dihydrorhodamine 123 converted to green fluorescent rhodamine 123. Measurements were done daily. The FMLP-induced burst was enhanced in patients before therapy as compared with the control group, whereas PMA-induced burst was decreased slightly. E. coli-, FMLP-, and PMA-induced oxidative burst decreased in both groups during cytostatic therapy. E. coli-induced burst increased again within 2 days of G-CSF treatment in vivo. FMLP-induced burst increased in the B-NHL group but decreased in the DexaBEAM group. In patients who have recovered from leukopenia the oxidative burst is still partly suppressed. PMA-induced oxidative burst measured at the start of therapy correlates with infectious complications. Thus, PMA-induced burst may be used as a simple method for evaluating the individual risk of infections during therapy. The results demonstrate the modulating effect of cytostatic drugs on the oxidative burst and may explain why some patients suffer from severe bacterial infections although the total number of granulocytes is normal.

Adult↗
PubMed1996

[Intrastromal keratectomy in high myopia. 1 year results].

Photorefractive keratectomy (PRK) by excimer laser is now a scientifically established treatment method in low and moderate myopia. In high and very high myopia, however, the formation of severe corneal haze or scars and a considerable regression of refraction remain obstacles to the use of PRK. One approach to these two problems is to perform an intrastromal keratectomy. PATIENTS AND METHOD. Between September 1992 and September 1994 intrastromal keratectomy was carried out in 42 eyes with myopia between -8.625 and -36 D. Twenty-one eyes (spherical equivalent of pre-operative refraction between -12.12 and -36 D) were treated by keratomileusis in situ, and 21 eyes (spherical equivalent of pre-operative refraction between -8.625 and -29.25 D) by intrastromal excimer laser keratectomy. Thirty-two eyes were followed up for at least 12 months. RESULTS. The post-operative refraction (spherical equivalent) ranged between +1.375 D and -5.0 D in the keratomileusis in situ group and between +1.5 D and -3.0 D in the intrastromal excimer laser keratectomy group. Nearly all patients regained their pre-operative visual acuity quickly. In the long-term follow-up (1 year) no significant regression of refraction occurred; the pre-operative visual acuity was regained in both groups after 1 year. Significant astigmatism was not induced. CONCLUSIONS. Intrastromal keratectomy is able to correct even very high myopias quite precisely and without regression of the refractive outcome. In addition, considerable haze can be avoided. For these reasons, in high and very high myopia intrastromal keratectomy seems to be superior to conventional anterior photorefractive keratectomy (PRK) by excimer laser.

Adult↗
PubMed1992

Suicides and parasuicides in a high-risk patient group on and off lithium long-term medication.

68 patients with affective disorders, and receiving lithium prophylaxis in a specialized lithium clinic were followed up for 8 years on average. Patients were selected for this study according to 2 criteria: They had been given lithium for at least 12 months, and they had attempted suicide at least once before onset of lithium prophylaxis. Outcome was analysed in terms of suicidal and parasuicidal behaviour. 55 patients took their lithium regularly, 13 discontinued or dropped the medication. One third of those patients having discontinued the medication died from suicide. Only one suicide occurred in patients with regular lithium intake and proven compliance during the last check before death. An impressive drop of parasuicides was observed in responders as well as in apparent non-responders. In total, 11 of 13 patients showed suicidal or parasuicidal behaviour 2 weeks-44 months after lithium discontinuation, which in about half of these cases took place on advice or with consent of the treating psychiatrist. It is concluded that lithium may have specific anti-suicidal properties, possibly related to its anti-aggressive effect, and that patients apparently not responding satisfactorily in terms of reduced number of episodes may still be protected against suicide or parasuicide.

Adult↗
PubMed1992

The effect of long-term lithium treatment on the mortality of patients with manic-depressive and schizoaffective illness.

Clinical research centers in Aarhus, Berlin, Hamilton and Vienna collected mortality data for 827 manic-depressive and schizoaffective patients given lithium treatment for more than 6 months. The average duration of the treatment was 81 months and the total time on lithium 5600 patient-years. For each patient, the mortality risk was calculated by entering the appropriate national life tables for the general population. The number of observed deaths was 44; the number of expected deaths was 49.7. The standardized mortality ratio, 0.89, did not differ significantly from 1.0. The mortality of manic-depressive patients is 2-3 times that of the general population. Our data show that the mortality of manic-depressive and schizoaffective patients given long-term lithium treatment does not differ significantly from that of the general population.

Adult↗