Measurement of the Deuteron Structure Function F₂ in the Resonance Region and Evaluation of its Moments

Inclusive electron scattering off the deuteron has been measured to extract the deuteron structure function F2 with the CEBAF Large Acceptance Spectrometer (CLAS) at the Thomas Jefferson National Accelerator Facility. The measurement covers the entire resonance region from the quasielastic peak up to the invariant mass of the final-state hadronic system W similar or equal to 2.7 GeV with four-momentum transfers Q2 from 0.4 to 6 (GeV/c)2. These data are complementary to previous measurements of the proton structure function F2 and cover a similar two-dimensional region of Q2 and Bjorken variable x. Determination of the deuteron F2 over a large x interval including the quasielastic peak as a function of Q2, together with the other world data, permit a direct evaluation of the structure function moments for the first time. By fitting the Q2 evolution of these moments with an OPE-based twist expansion we have obtained a separation of the leading twist and higher twist terms. The observed Q2 behavior of the higher twist contribution suggests a partial cancelation of different higher twists entering into the expansion with opposite signs. This cancelation, found also in the proton moments, is a manifestation of the duality phenomenon in the F2 structure function

Differential Cross Sections for + p → K⁺ + Y for Λ and Σ⁰ Hyperons

High-statistics cross sections for the reactions + p → K⁺ + Λ and + p → K⁺ + Σ⁰ have been measured using CLAS at Jefferson Lab for center-of-mass energies W between 1.6 and 2.53 GeV, and for -0.85 \u3c cos θ Kc.m. \u3c +0.95. In the K⁺ + Λ channel we confirm a resonance-like structure near W=1.9 GeV at backward kaon angles. The position and width of this structure change with angle, indicating that more than one resonance is likely playing a role. The K⁺ + Λ channel at forward angles and all energies is well described by a t-channel scaling characteristic of Regge exchange, whereas the same scaling applied to the K⁺ + Σ⁰ channel is less successful. Several existing theoretical models are compared to the data, but none provide a good representation of the results

Beam-Helicity Asymmetries in Double-Charged-Pion Photoproduction on the Proton

Beam-helicity asymmetries for the two-pion-photoproduction reaction ⃗p → p π+π- have been studied for the first time in the resonance region for center-of-mass energies between 1.35 and 2.30 GeV. The experiment was performed at Jefferson Lab with the CEBAF Large Acceptance Spectrometer using circularly polarized tagged photons incident on an unpolarized hydrogen target. Beam-helicity-dependent angular distributions of the final-state particles were measured. The large cross-section asymmetries exhibit strong sensitivity to the kinematics and dynamics of the reaction. The data are compared with the results of various phenomenological model calculations, and show that these models currently do not provide an adequate description for the behavior of this new observable

η’ Photoproduction on the Proton for Photon Energies from 1.527 to 2.227 GeV

Differential cross sections for the reaction γp→η′p have been measured with the CLAS spectrometer and a tagged photon beam with energies from 1.527 to 2.227 GeV. The results reported here possess much greater accuracy than previous measurements. Analyses of these data suggest for the first time the coupling of the η′N channel to both the S11(1535) and P11(1710) resonances, known to couple strongly to the ηN channel in photoproduction on the proton, and the importance of J=3/2 resonances in the process

“Am I my genes?”: Questions of identity among individuals confronting genetic disease

Purpose: To explore many questions raised by genetics concerning personal identities that have not been fully investigated. Methods: We interviewed in depth, for 2 hours each, 64 individuals who had or were at risk for Huntington disease, breast cancer, or alpha-1 antitrypsin deficiency. Results: These individuals struggled with several difficult issues of identity. They drew on a range of genotypes and phenotypes (e.g., family history alone; mutations, but no symptoms; or symptoms). They often felt that their predicament did not fit preexisting categories well (e.g., “sick,” “healthy,” “disabled,” “predisposed”), due in part to uncertainties involved (e.g., unclear prognoses, since mutations may not produce symptoms). Hence, individuals varied in how much genetics affected their identity, in what ways, and how negatively. Factors emerged related to disease, family history, and other sources of identity. These identities may, in turn, shape disclosure, coping, and other health decisions. Conclusions: Individuals struggle to construct a genetic identity. They view genetic information in highly subjective ways, varying widely in what aspects of genetic information they focus on and how. These data have important implications for education of providers (to assist patients with these issues), patients, and family members; and for research, to understand these issues more fully

Malignant hyperthermia

Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle that presents as a hypermetabolic response to potent volatile anesthetic gases such as halothane, sevoflurane, desflurane and the depolarizing muscle relaxant succinylcholine, and rarely, in humans, to stresses such as vigorous exercise and heat. The incidence of MH reactions ranges from 1:5,000 to 1:50,000–100,000 anesthesias. However, the prevalence of the genetic abnormalities may be as great as one in 3,000 individuals. MH affects humans, certain pig breeds, dogs, horses, and probably other animals. The classic signs of MH include hyperthermia to marked degree, tachycardia, tachypnea, increased carbon dioxide production, increased oxygen consumption, acidosis, muscle rigidity, and rhabdomyolysis, all related to a hypermetabolic response. The syndrome is likely to be fatal if untreated. Early recognition of the signs of MH, specifically elevation of end-expired carbon dioxide, provides the clinical diagnostic clues. In humans the syndrome is inherited in autosomal dominant pattern, while in pigs in autosomal recessive. The pathophysiologic changes of MH are due to uncontrolled rise of myoplasmic calcium, which activates biochemical processes related to muscle activation. Due to ATP depletion, the muscle membrane integrity is compromised leading to hyperkalemia and rhabdomyolysis. In most cases, the syndrome is caused by a defect in the ryanodine receptor. Over 90 mutations have been identified in the RYR-1 gene located on chromosome 19q13.1, and at least 25 are causal for MH. Diagnostic testing relies on assessing the in vitro contracture response of biopsied muscle to halothane, caffeine, and other drugs. Elucidation of the genetic changes has led to the introduction, on a limited basis so far, of genetic testing for susceptibility to MH. As the sensitivity of genetic testing increases, molecular genetics will be used for identifying those at risk with greater frequency. Dantrolene sodium is a specific antagonist of the pathophysiologic changes of MH and should be available wherever general anesthesia is administered. Thanks to the dramatic progress in understanding the clinical manifestation and pathophysiology of the syndrome, the mortality from MH has dropped from over 80% thirty years ago to less than 5%