Final State Interactions and the Transverse Structure of the Pion

In the factorized picture of semi-inclusive deep inelastic scattering the naive time reversal-odd parton distributions exist by virtue of the gauge link which is intrinsic to their definition. The link structure describes initial/final-state interactions of the active parton due to soft gluon exchanges with the target remnant. Though these interactions are non-perturbative, calculations of final-state interaction have been performed in a perturbative one-gluon approximation. We include higher-order contributions by applying non-perturbative eikonal methods to calculate the Boer-Mulders function of the pion. Using this framework we explore under what conditions the Boer-Mulders function can be described in terms of factorization of final state interactions and a spatial distortion.Comment: 13 pages, 5 figures; Proceedings of the workshop, "Recent Advances in Perturbative QCD and Hadronic Physics" ECT*, Trento (Italy), in Honor of Anatoli V. Efremov on the occasion of his 75th Birthday, to appear in Mod. Phys. Lett.

What can we learn from the breaking of the Wandzura-Wilczek relation?

We review the study the Wandzura-Wilczek relation for the structure function g_2, with a particular attention on the connection with the framework of Transverse Momentum Dependent factorization. We emphasize that the relation is broken by two distinct twist-3 terms. In the light of these findings, we clarify what can be deduced from the available experimental data on g_2, which indicate a breaking of the order 20-40%, and how to individually measure the twist-3 terms.Comment: Talk given by Alberto Accardi at "Spin structure at long distances," Jefferson Lab, March 12-13 200

Generalized parton correlation functions for a spin-1/2 hadron

The fully unintegrated, off-diagonal quark-quark correlator for a spin-1/2 hadron is parameterized in terms of so-called generalized parton correlation functions. Such objects, in particular, can be considered as mother distributions of generalized parton distributions on the one hand and transverse momentum dependent parton distributions on the other. Therefore, our study provides new, model-independent insights into the recently proposed nontrivial relations between generalized and transverse momentum dependent parton distributions. We find that none of these relations can be promoted to a model-independent status. As a by-product we obtain the first complete classification of generalized parton distributions beyond leading twist. The present paper is a natural extension of our previous corresponding analysis for spin-0 hadrons.Comment: 41 pages, 3 figures; v2: added referenc

Final state interactions and the transverse structure of the pion using non-perturbative eikonal methods

In the factorized picture of semi-inclusive hadronic processes the naive time reversal-odd parton distributions exist by virtue of the gauge link which renders it color gauge invariant. The link characterizes the dynamical effect of initial/final-state interactions of the active parton due soft gluon exchanges with the target remnant. Though these interactions are non-perturbative, studies of final-state interaction have been approximated by perturbative one-gluon approximation in Abelian models. We include higher-order contributions by applying non-perturbative eikonal methods incorporating color degrees of freedom in a calculation of the Boer-Mulders function of the pion. Using this framework we explore under what conditions the Boer Mulders function can be described in terms of factorization of final state interactions and a spatial distribution in impact parameter space.Comment: To appear in Phys.Lett.B, 9 pages, 5 figures, added refs. and discussio

Corrigendum to "Cytostatic drugs differentially affect phenotypic features of porcine coronary artery smooth muscle cell populations" [FEBS Lett. 581 (2007) 5847–5851]

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The use of a tailored surgical technique for minimally invasive esophagectomy

ObjectiveUncertainty exists among surgeons as to whether minimally invasive esophagectomy (MIE) is a comparable operation to open esophagectomy (OE). The surgical technique and oncologic dissection should not be degraded when using a minimally invasive approach.MethodsWe reviewed a single hospital’s experience with both OE and MIE. From 2000 to 2010, 257 patients underwent esophagectomy by 1 of 3 surgical techniques: transhiatal, Ivor Lewis, or 3-hole.ResultsOf the 257 patients (median age, 67 years; range, 58–74), 92 underwent MIE. Both groups were comparable in terms of gender, age, comorbidities, surgical technique, and induction chemotherapy and radiotherapy. The overall median follow-up was 29.5 months (range, 9.9–61.5). The MIE group had a significantly shorter operative time (MIE vs OE, 330 vs 365 minutes, P = .04), length of stay (MIE vs OE, 9 vs 12 days, P < .01), intensive care unit admission rate (MIE vs OE, 55% vs 81%, P < .01), intensive care unit length of stay (MIE vs OE, 1 vs 2 days, P < .01), and estimated blood loss (MIE vs OE, 100 vs 400 mL, P < .01). More lymph nodes were harvested in the MIE group than in the OE group (17 vs 11 nodes, P < .01). There were insignificant differences in 30-day mortality (MIE vs OE, 2.2% vs 3.0%; P = .93) and overall survival (P = .19), as well as in the rates of all complications, except pneumonia (MIE vs OE, 2% vs 13%; P = .01).ConclusionsA thoracic surgeon can safely tailor the MIE to a patient’s anatomy and oncologic demands while maintaining equivalent survival

An Expert Perspective on Phosphate Dysregulation With a Focus on Chronic Hypophosphatemia

Because of their rarity, diseases characterized by chronic hypophosphatemia can be underrecognized and suboptimally managed, resulting in poor clinical outcomes. Moreover, serum phosphate may not be measured routinely in primary care practice. Authors participated in several working sessions to advance the understanding of phosphate homeostasis and the causes, consequences, and clinical implications of chronic hypophosphatemia. Phosphate levels are regulated from birth to adulthood. Dysregulation of phosphate homeostasis can result in hypophosphatemia, which becomes chronic if phosphate levels cannot be normalized. Chronic hypophosphatemia may be underrecognized as serum phosphate measurement is not always part of routine analysis in the primary care setting and results might be misinterpreted, for instance, due to age-specific differences not being accounted for and circadian variations. Clinical consequences of chronic hypophosphatemia involve disordered endocrine regulation, affect multiple organ systems, and vary depending on patient age and the underlying disorder. Signs and symptoms of chronic hypophosphatemic diseases that manifest during childhood or adolescence persist into adulthood if the disease is inadequately managed, resulting in an accumulation of clinical deficits and a progressive, debilitating impact on quality of life. Early identification and diagnosis of patients with chronic hypophosphatemia is crucial, and clinical management should be started as soon as possible to maximize the likelihood of improving health outcomes. Furthermore, in the absence of a universally accepted description for "chronic hypophosphatemia," a definition is proposed here that aims to raise awareness of these diseases, facilitate diagnosis, and guide optimal phosphate management strategies by improving monitoring and assessment of patient response to treatment. (c) 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).Peer reviewe

Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome:an international cross-sectional study

Background:Small cohort studies have reported high parathyroid hormone (PTH) levels in patients with Bartter syndrome and lower serum phosphate levels have anecdotally been reported in patients with Gitelman syndrome. In this cross-sectional study, we assessed PTH and phosphate homeostasis in a large cohort of patients with salt-losing tubulopathies. Methods:Clinical and laboratory data of 589 patients with Bartter and Gitelman syndrome were provided by members of the European Rare Kidney Diseases Reference Network (ERKNet) and the European Society for Paediatric Nephrology (ESPN). Results:A total of 285 patients with Bartter syndrome and 304 patients with Gitelman syndrome were included for analysis. Patients with Bartter syndrome type I and II had the highest median PTH level (7.5 pmol/L) and 56% had hyperparathyroidism (PTH &gt;7.0 pmol/L). Serum calcium was slightly lower in Bartter syndrome type I and II patients with hyperparathyroidism (2.42 versus 2.49 mmol/L; P = .038) compared to those with normal PTH levels and correlated inversely with PTH (rs −0.253; P = .009). Serum phosphate and urinary phosphate excretion did not correlate with PTH. Overall, 22% of patients had low serum phosphate levels (phosphate—standard deviation score &lt; −2), with the highest prevalence in patients with Bartter syndrome type III (32%). Serum phosphate correlated with tubular maximum reabsorption of phosphate/glomerular filtration rate (TmP/GFR) (rs 0.699; P &lt; .001), suggesting renal phosphate wasting. Conclusions:Hyperparathyroidism is frequent in patients with Bartter syndrome type I and II. Low serum phosphate is observed in a significant number of patients with Bartter and Gitelman syndrome and appears associated with renal phosphate wasting.</p