The Quark Beam Function at NNLL

In hard collisions at a hadron collider the most appropriate description of the initial state depends on what is measured in the final state. Parton distribution functions (PDFs) evolved to the hard collision scale Q are appropriate for inclusive observables, but not for measurements with a specific number of hard jets, leptons, and photons. Here the incoming protons are probed and lose their identity to an incoming jet at a scale \mu_B << Q, and the initial state is described by universal beam functions. We discuss the field-theoretic treatment of beam functions, and show that the beam function has the same RG evolution as the jet function to all orders in perturbation theory. In contrast to PDF evolution, the beam function evolution does not mix quarks and gluons and changes the virtuality of the colliding parton at fixed momentum fraction. At \mu_B, the incoming jet can be described perturbatively, and we give a detailed derivation of the one-loop matching of the quark beam function onto quark and gluon PDFs. We compute the associated NLO Wilson coefficients and explicitly verify the cancellation of IR singularities. As an application, we give an expression for the next-to-next-to-leading logarithmic order (NNLL) resummed Drell-Yan beam thrust cross section.Comment: 54 pages, 9 figures; v2: notation simplified in a few places, typos fixed; v3: journal versio

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

Detrusor response to outlet obstruction

Bladder responses to outlet obstruction are thought to involve muscular hyperplasia, increased pressure, and finally, decompensation. While these things probably do occur, the process of bladder response to obstruction also includes loss of reflex control and deposition of collagen.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47058/1/345_2004_Article_BF00327002.pd

Overactive bladder – 18 years – Part II

ABSTRACT Traditionally, the treatment of overactive bladder syndrome has been based on the use of oral medications with the purpose of reestablishing the detrusor stability. The recent better understanding of the urothelial physiology fostered conceptual changes, and the oral anticholinergics – pillars of the overactive bladder pharmacotherapy – started to be not only recognized for their properties of inhibiting the detrusor contractile activity, but also their action on the bladder afference, and therefore, on the reduction of the symptoms that constitute the syndrome. Beta-adrenergic agonists, which were recently added to the list of drugs for the treatment of overactive bladder, still wait for a definitive positioning – as either a second-line therapy or an adjuvant to oral anticholinergics. Conservative treatment failure, whether due to unsatisfactory results or the presence of adverse side effects, define it as refractory overactive bladder. In this context, the intravesical injection of botulinum toxin type A emerged as an effective option for the existing gap between the primary measures and more complex procedures such as bladder augmentation. Sacral neuromodulation, described three decades ago, had its indication reinforced in this overactive bladder era. Likewise, the electric stimulation of the tibial nerve is now a minimally invasive alternative to treat those with refractory overactive bladder. The results of the systematic literature review on the oral pharmacological treatment and the treatment of refractory overactive bladder gave rise to this second part of the review article Overactive Bladder – 18 years, prepared during the 1st Latin-American Consultation on Overactive Bladder