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R Kessler

Publications and source records attributed to R Kessler.

At least 19 recordsLinked to original sources
PubMed2003

Measurements of the Decay KL-->e+ e- mu+ mu-.

The KTeV experiment at Fermilab has isolated a total of 132 events from the rare decay K(L)-->e+ e- mu+ mu-, with an estimated background of 0.8 events. The branching ratio of this mode is determined to be [2.69+/-0.24(stat)+/-0.12(syst)]x10(-9), with a radiative cutoff of M(2)(ee mu mu)/M(2)(K)>0.95. The first measurement using this mode of the parameter alpha from the D'Ambrosio-Isidori-Portolès (DIP) model of the K(L)gamma*gamma* vertex yields a result of -1.59+/-0.37, consistent with values obtained from other decay modes. Because of the limited statistics, no sensitivity is found to the DIP parameter beta. We use this decay mode to set limits on CP and lepton violation.

Journal Article↗
PubMed2002

Search for the KL-->pi 0 pi 0 e+e- decay in the KTeV experiment.

The recent discovery of a large CP violating asymmetry in KL-->pi+pi-e+e- mode has prompted us to seach for the associated KL-->pi 0 pi 0 e+e- decay mode in the KTeV-E799 experiment at Fermilab. In 2.7 x 10(11) K(L) decays, one candidate event has been observed with an expected background of 0.3 event, resulting in an upper limit for the KL-->pi 0 pi 0 e+e- branching ratio of 6.6 x 10(-9) at the 90% C.L.

Journal Article↗
PubMed2002

Radiative decay width measurements of neutral kaon excitations using the primakoff effect.

We use K(L)'s in the 100-200 GeV energy range to produce 147 candidate events of the axial vector pair K1(1270)-K1(1400) in the nuclear Coulomb field of a Pb target and determine the radiative widths Gamma(K1(1400)-->K0+gamma)=280.8+/-23.2(stat)+/-40.4(syst) keV and Gamma(K1(1270)-->K0+gamma)=73.2+/-6.1(stat)+/-28.3(syst) keV. These first measurements appear to be lower than the quark-model predictions. We also place upper limits on the radiative widths for K(*)(1410) and K(*)(2)(1430) and find that the latter is vanishingly small in accord with SU(3) invariance in the naive quark model.

Journal Article↗
PubMed2002

Measurement of the K(L) charge asymmetry.

We present a measurement of the charge asymmetry delta(L) in the mode K(L)-->pi(+/-)e(-/+)nu based on 298 x 10(6) analyzed decays. We measure a value of delta(L) = [3322+/-58(stat)+/-47(syst)]x10(-6), in good agreement with previous measurements and 2.4 times more precise than the current best published result. The result is used to place more stringent limits on CPT and DeltaS = DeltaQ violation in the neutral kaon system.

Journal Article↗
PubMed2002

[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome].

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.

Hemodynamics↗
PubMed2002

[Long-term oxygen therapy for chronic respiratory failure. Rationale, indications, modalities].

Long-term oxygen therapy (LOT) has become quite popular over the last 20 years due to better knowledge of the beneficial effect (improved life expectancy, improved quality of life, stabilization of the pulmonary hypertension) and to technological progress (concentrators, liquid oxygen). Ambulatory techniques have greatly contributed to the widespread use of oxygen therapy as has the decision of the French National Health Insurance System to reimburse this costly treatment. Almost all the studies devoted to the clinical and functional aspects of LOT have concerned patients with chronic obstructive pulmonary disease (COPD). By extension, it is generally accepted that LOT is warranted in other forms of respiratory failure (diffuse fibrosis, cyphoscoliosis, cystic fibrosis, etc.) when blood gas criteria similar to those retained for COPD are present: PaO(2)<=55 mmHg during stable periods with control measurements at lest 3 weeks apart; PaO(2) between 56 and 60 mmHg if there is also an elevated red cell count or pulmonary hypertension, signs of cor pulmonale ou frank hypoxemia during sleep. These consensus indications are widely accepted but other indications remain controversial: should LOT be prescribed for moderate hypoexmia (PaO(2) >=60 mmHg), exercise-induced hyoxemia alone, sleep hypoxemia alone? Appropriate studies are lacking so systematic prescription of LOT cannot be recommended in these three situations. The duration of LOT should be >=16 h/d, and if possible >=18 h/d. It has been established that objective results (life expectancy, improvement in pulmonary hypertension) are better for longer daily treatment. Patient compliance is however often insufficient. In addition to education, the best way to improve patient participation is to strive for improved quality of life with oxygen therapy (portable device, liquid oxygen) in these patients.

Home Care Services↗
PubMed2001

Phosphorylation and inactivation of yeast 6-phosphofructo-2-kinase contribute to the regulation of glycolysis under hypotonic stress.

Phosphorylation of yeast 6-phosphofructo-2-kinase and its role for the regulation of glycolysis under hypoosmotic conditions were investigated. 6-Phosphofructo-2-kinase was found to be phosphorylated in vitro by protein kinase C at serine 652 and thereby inactivated. Protein phosphatase 2A reversed the phosphorylative inhibition of the enzyme. When yeast cells were shifted to hypotonic media, 6-phosphofructo-2-kinase was found to be phosphorylated and inactivated. Under in vivo conditions, two phosphate residues were incorporated into the enzyme. One of them is bound to serine 652, indicating that this modification was probably caused by yeast protein kinase C1. The second phosphate is bound to Ser8 within the N-terminal peptide T(1-41) which contains several serine residues but no protein kinase C recognition sequence. Site-directed mutagenesis confirmed that the phosphorylation of serine 652 but not the N-terminal modification is responsible for the in vivo inactivation of 6-phosphofructo-2-kinase. The obtained results suggest that the phosphorylation of 6-phosphofructo-2-kinase mediates a response of the cells to an activation of the hypoosmolarity MAP kinase pathway. Via a suppression of glycolysis, the inactivation of 6-phosphofructo-2-kinase is expected to be responsible for the observed accumulation of glucose 6-phosphate, an essential precursor of the cell wall glucans, and the decrease of glycerol, an important osmolyte.

Amino Acid Sequence↗
PubMed2001

First measurement of form factors of the decay Xi(0) --> Sigma(+)e(-)nu macro(e).

We present the first measurement of the form factor ratios g(1)/f(1) (direct axial vector to vector), g(2)/f(1) (second class current), and f(2)/f(1) (weak magnetism) for the decay Xi(0)-->Sigma(+)e(-)nu macro(e) using the KTeV (E799) beam line and detector at Fermilab. From the Sigma(+) polarization measured with the decay Sigma(+)-->p pi(0) and the e(-)-nu; correlation, we measure g(1)/f(1) to be 1.32+/-(0.21)(0.17)(stat)+/-0.05(syst), assuming the SU(3)(f) (flavor) values for g(2)/f(1) and f(2)/f(1). Our results are all consistent with exact SU(3)(f) symmetry.

Journal Article↗
PubMed2001

Branching ratio measurement of the decay K(L) --> e(+)e(-)mu(+)mu(-).

We have collected a 43 event sample of the decay K(L)-->e(+)e(-)mu(+)mu(-) with negligible backgrounds and measured its branching ratio to be (2.62+/-0.40+/-0.17)x10(-9). We see no evidence for CP violation in this decay. In addition, we set the 90% confidence upper limit on the combined branching ratios for the lepton flavor violating decays K(L)-->e(+/-)e(+/-)mu(-/+)mu(-/+) at B(K(L)-->e(+/-)e(+/-)mu(-/+)mu(-/+))< or =1.23x10(-10), assuming a uniform phase space distribution.

Journal Article↗
PubMed2001

Measurement of the branching ratio and form factor of K(L)-->mu(+)mu(-)gamma.

We report on the analysis of the rare decay K(L)-->mu(+)mu(-)gamma the 1997 data from the KTeV experiment at Fermilab. A total of 9327 candidate events are observed with 2.4% background, representing a factor of 40 increase in statistics over the current world sample. We find that B(K(L)-->mu(+)mu(-)gamma) = (3.62 +/- 0.04(stat) +/- 0.08(syst)) x 10(-7). The form factor parameter alpha(K*) is measured to be alpha(K*) = -0.160(+0.026)(-0.028). In addition, we make the first measurement of the parameter alpha from the D'Ambrosio-Isidori-Portolés form factor, finding alpha = -1.54 +/- 0.10. In that model, this alpha measurement limits the Cabibbo-Kobayashi-Maskawa parameter rho>-0.2.

Journal Article↗
PubMed2001

"Natural history" of pulmonary hypertension in a series of 131 patients with chronic obstructive lung disease.

The prognostic value and the evolution of pulmonary hypertension (PH) in patients with markedly hypoxemic chronic obstructive pulmonary disease (COPD), treated or not with long-term oxygen therapy (LTOT), has been extensively investigated. However, little is known in patients with mildly or moderately hypoxemic COPD not requiring LTOT. Therefore, we assessed the evolution of pulmonary hemodynamics in 131 patients with stable COPD by performing two right heart catheterizations at a mean (+/- SD) time interval of 6.8 +/- 2.9 yr. At inclusion (T0), no patient had PH (i.e., the mean pulmonary artery pressure [Ppa] at rest was < 20 mm Hg). Group 1 included 55 patients without exercising PH and group 2 included 76 patients with exercising PH, defined by a pulmonary arterial pressure (Ppa) > 30 mm Hg during a steady-state 40-W exercise. Group 2 patients compared with group 1 patients had a significantly higher resting Ppa (16 +/- 3 mm Hg versus 14 +/- 2 mm Hg, p = 0.001). At the second catheterization, 33 (25%) patients (9 of 55 in group 1, 24 of 76 in group 2, p = 0.048) showed a resting Ppa > 20 mm Hg, but PH was generally mild, ranging from 20 to 42.5 mm Hg. The mean Ppa at second evaluation was 16 +/- 5 mm Hg in group 1 and 19 +/- 7 mm Hg in group 2 (p = 0.01). The patients who developed resting PH at the second catheterization (T1) had higher resting and exercising Ppa (p = 0.001 and p = 0.002, respectively), and significantly lower resting and exercising Pa(O(2)) (p = 0.005 and p = 0.012, respectively) at T0. Logistic regression analysis showed that resting and exercising Ppa were independent predictors (at T0) for the subsequent development of PH (p = 0.029 and p = 0.027, respectively). The patients who developed resting PH (T1) had a significantly worsening of Pa(O(2)) (from 63.5 mm Hg at T0 to 60 mm Hg at T1, p = 0.047), whereas the Pa(O(2)) as a mean was stable in the remainder (69.5 mm Hg at T0 and T1). These results show the following. The progression of Ppa over time in patients with COPD with mild to moderate hypoxemia is rather slow, the average change for the group as a whole being of + 0.4 mm Hg/yr. Only about 25% of patients with COPD with mild to moderate hypoxemia and without resting PH at the onset will develop PH during a 6-yr follow-up. The patients with exercising PH at the onset have a significantly increased risk of developing PH over time. Only resting and exercising Ppa at the onset are independently related to the subsequent development of PH. However, in individual cases, the models of linear or logistic regression do not allow a pertinent prediction of the level of Ppa or the presence of PH at the second right heart catheterization.

Blood Pressure↗
PubMed2001

Measurements of the rare decay K(L) --> e(+)e(-)e(+)e(-).

We observe 441 K(L)-->e(+)e(-)e(+)e(-) candidate events with a background of 4.2 events and measure B(K(L)-->e(+)e(-)e(+)e(-)) = [3.72+/-0.18(stat)+/-0.23(syst)]x10(-8) in the KTeV/E799II experiment at Fermilab. Using the distribution of the angle between the planes of the e(+)e(-) pairs, we measure the CP parameters beta(CP) = -0.23+/-0.09(stat)+/-0.02(syst) and gamma(CP) = -0.09+/-0.09(stat)+/-0.02(syst). We also present the first detailed study of the e(+)e(-) invariant mass spectrum in this decay mode.

Journal Article↗
PubMed2001

Measurement of the branching ratio and asymmetry of the decay Xi degrees -->Sigma degrees gamma.

We have studied the rare weak radiative hyperon decay Xi degrees -->Sigma degrees gamma in the KTeV experiment at Fermilab. We have identified 4045 signal events over a background of 804 events. The dominant Xi degrees -->Lambdapi degrees decay, which was used for normalization, is the only important background source. An analysis of the acceptance of both modes yields a branching ratio of B(Xi degrees -->Sigma degrees gamma)/B(Xi degrees -->Lambdapi degrees ) = (3.34+/-0.05+/-0.09)x10(-3). By analyzing the final state decay distributions, we have also determined that the Sigma degrees emission asymmetry parameter for this decay is alpha(XiSigma) = -0.63+/-0.09.

Journal Article↗
PubMed2001

Splice isoforms of ubiquitous 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase in human brain.

In human brain we were able to demonstrate sequence diversity of the ubiquitous 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2/FBPase-2). Six different isoforms of PFK-2/FBPase-2, two of which are identical with the ubiquitous PFK-2/FBPase-2 and the inducible PFK-2, respectively, could be identified. The heterogeneity of human brain PFK-2/FBPase-2 isoforms is generated by alternative splicing. Three hitherto unrecognized exons were detected. The multiple PFK-2/FBPase-2 transcripts encode proteins which differ with respect to their length and to the amino acid composition of the carboxyl-termini. The isoform pattern of ubiquitous PFK-2/FBPase-2 is more complex in human brain than in skeletal muscle and liver.

Alternative Splicing↗
PubMed2001

Study of the K(0)(L) --> pi(+)pi(-)gamma Direct Emission Vertex.

We have performed studies of the K(0)(L)-->pi(+)pi(-)gamma direct emission ( DE) and inner Bremsstrahlung ( IB) vertices, based on data collected by KTeV during the 1996 Fermilab fixed target run. We find a(1)/a(2) = -0.737+/-0.034 GeV2 for the DE form-factor parameter in the rho-propagator parametrization, and report on fits of the form factor to linear and quadratic functions as well. We concurrently measure gamma(K(0)(L)-->pi(+)pi(-)gamma,E(*)(gamma)>20 MeV)/gamma(K(0)(L)-->pi(+)pi(-)) = (20.8+/-0.3)x10(-3), and a K(0)(L)-->pi(+)pi(-)gamma DE/(DE+IB) branching ratio of 0.683+/-0.011.

Journal Article↗
PubMed2001

Search for the decay KL --> pi(0)e+e-.

We report on a search for the decay KL-->pi(0)e+e- carried out by the KTeV/E799 experiment at Fermilab. This decay is expected to have a significant CP violating contribution and the measurement of its branching ratio could support the Cabibbo-Kobayashi-Maskawa mechanism for CP violation or could point to new physics. Two events were observed in the 1997 data with an expected background of 1.06+/-0.41 events, and we set an upper limit B(KL-->pi(0)e+e-)<5.1 x 10(-10) at the 90% confidence level.

Journal Article↗
PubMed2001

Nicotine dependence in the United States: prevalence, trends, and smoking persistence.

BACKGROUND: The prevalence of smoking in the United States has been closely monitored. However, little is known about the epidemiology of nicotine dependence. We studied DSM-III-R nicotine dependence in the United States, trends across cohorts, and the role of nicotine dependence in smoking persistence. METHODS: The Tobacco Supplement to the National Comorbidity Survey was administered to a representative subset of 4414 persons aged 15 to 54 years. The World Health Organization's Composite International Diagnostic Interview was used to assess nicotine dependence. RESULTS: Lifetime prevalence of nicotine dependence was 24%, nearly half of those who had ever smoked daily for a month or more. The highest risk for nicotine dependence occurred in the first 16 years after daily smoking began, at which point the rate declined and continued at a slower pace for several years. Nicotine dependence increased the risk of smoking persistence, with an odds ratio (OR) of 2.2 (95% confidence interval [CI], 1.6-3.0). Members of the most recent cohort, who were 15 to 24 years of age at the time of the survey, were the least likely to smoke daily, but those who smoked had the highest risk of dependence: OR for daily smoking in the most recent vs earliest cohort was 0.7 (95% CI, 0.5-0.9), and for dependence among smokers, 7.2 (95% CI, 5.0-10.4). CONCLUSIONS: Despite evidence that nicotine dependence is the leading preventable cause of death and morbidity, it remains a common psychiatric disorder. Smoking cessation and the decline in uptake in recent years varied across subgroups of the population.

Adolescent↗