Search

The Cottingham formula expresses the leading contribution of the electromagnetic interaction to the proton-neutron mass difference as an integral over the forward Compton amplitude. Since quarks and gluons reggeize, the dispersive representation of this amplitude requires a subtraction. We assume that the asymptotic behaviour is dominated by Reggeon exchange. This leads to a sum rule that expresses the subtraction function in terms of measurable quantities. The evaluation of this sum rule leads to $m_{QED}^{p-n}=0.58\pm 0.16\,\mbox{MeV}$., Comment: 26 pages, 9 figures. Update, matches the version published in EPJC

The Cottingham formula expresses the electromagnetic part of the mass of a particle in terms of the virtual Compton scattering amplitude. At large photon momenta, this amplitude is dominated by short distance singularities associated with operators of spin 0 and spin 2. In the difference between proton and neutron, chiral symmetry suppresses the spin 0 term. Although the angular integration removes the spin 2 singularities altogether, the various pieces occurring in the standard decomposition of the Cottingham formula do pick up such contributions. These approach asymptotics extremely slowly because the relevant Wilson coefficients only fall off logarithmically. We rewrite the formula in such a way that the leading spin 2 contributions are avoided ab initio. Using a sum rule that follows from Reggeon dominance, the numerical evaluation of the e.m. part of the mass difference between proton and neutron yields $m_{QED}^{p-n}=0.58\pm 0.16\,$MeV. The result indicates that the inelastic contributions are small compared to the elastic ones., Comment: 11 pages. A typo in Eq. (21) corrected

BACKGROUND: Although evidence from psychosis patients demonstrates the adverse effects of cannabis use (CU) at a young age and that the rate of CU is high in subgroups of young violent patients with psychotic disorders, little is known about the possible effect of the age of onset of CU on later violent behaviors (VB). So, we aimed to explore the impact of age at onset of CU on the risk of displaying VB in a cohort of early psychosis patients. METHOD: Data were collected prospectively over a 36-month period in the context of an early psychosis cohort study. A total of 265 patients, aged 18-35 years, were included in the study. Logistic regression was performed to assess the link between age of onset of substance use and VB. RESULTS: Among the 265 patients, 72 had displayed VB and 193 had not. While violent patients began using cannabis on average at age 15.29 (0.45), nonviolent patients had started on average at age 16.97 (0.35) (p = 0.004). Early-onset CU (up to age 15) was a risk factor for VB (odds ratio = 4.47, confidence interval [CI]: 1.13-20.06) when the model was adjusted for age group, other types of substance use, being a user or a nonuser and various violence risk factors and covariates. History of violence and early CU (until 15) were the two main risk factors for VB. CONCLUSIONS: Our results suggest that early-onset CU may play a role in the emergence of VB in early psychosis.

The Cottingham formula expresses the electromagnetic part of the mass of a particle in terms of the virtual Compton scattering amplitude. At large photon momenta, this amplitude is dominated by short distance singularities associated with operators of spin 0 and spin 2. In the difference between proton and neutron, chiral symmetry suppresses the spin 0 term. Although the angular integration removes the spin 2 singularities altogether, the various pieces occurring in the standard decomposition of the Cottingham formula do pick up such contributions. These approach asymptotics extremely slowly because the relevant Wilson coefficients only fall off logarithmically. We rewrite the formula in such a way that the leading spin 2 contributions are avoided ab initio. Using a sum rule that follows from Reggeon dominance, the numerical evaluation of the e.m. part of the mass difference between proton and neutron yields $m_{QED}^{p-n}=0.58\pm 0.16\,$MeV. The result indicates that the inelastic contributions are small compared to the elastic ones., Comment: 11 pages. A typo in Eq. (21) corrected

The Cottingham formula expresses the leading contribution of the electromagnetic interaction to the proton-neutron mass difference as an integral over the forward Compton amplitude. Since quarks and gluons reggeize, the dispersive representation of this amplitude requires a subtraction. We assume that the asymptotic behaviour is dominated by Reggeon exchange. This leads to a sum rule that expresses the subtraction function in terms of measurable quantities. The evaluation of this sum rule leads to $m_{QED}^{p-n}=0.58\pm 0.16\,\mbox{MeV}$., Comment: 26 pages, 9 figures. Update, matches the version published in EPJC

The Cottingham formula expresses the electromagnetic part of the mass of a particle in terms of the virtual Compton scattering amplitude. At large photon momenta, this amplitude is dominated by short distance singularities associated with operators of spin 0 and spin 2. In the difference between proton and neutron, chiral symmetry suppresses the spin 0 term. Although the angular integration removes the spin 2 singularities altogether, the various pieces occurring in the standard decomposition of the Cottingham formula do pick up such contributions. These approach asymptotics extremely slowly because the relevant Wilson coefficients only fall off logarithmically. We rewrite the formula in such a way that the leading spin 2 contributions are avoided ab initio. Using a sum rule that follows from Reggeon dominance, the numerical evaluation of the e.m. part of the mass difference between proton and neutron yields $m_{QED}^{p-n}=0.58\pm 0.16\,$MeV. The result indicates that the inelastic contributions are small compared to the elastic ones., Comment: 11 pages. A typo in Eq. (21) corrected

The Cottingham formula expresses the leading contribution of the electromagnetic interaction to the proton-neutron mass difference as an integral over the forward Compton amplitude. Since quarks and gluons reggeize, the dispersive representation of this amplitude requires a subtraction. We assume that the asymptotic behaviour is dominated by Reggeon exchange. This leads to a sum rule that expresses the subtraction function in terms of measurable quantities. The evaluation of this sum rule leads to $m_{QED}^{p-n}=0.58\pm 0.16\,\mbox{MeV}$., Comment: 26 pages, 9 figures. Update, matches the version published in EPJC

Background: Previous literature suggests that prevalence of cannabis use in the early phase of psychosis is high, and that early psychosis patients are at high-risk for violent behavior. However, the link between cannabis use and violent behavior in early psychosis patients is unclear. We carried out a study on a sample of early psychosis patients, in order to explore the impact of cannabis use on the risk of violent behavior (VB), while taking into account (1) potential confounding factors and, (2) interactions with other dynamic risk factors of VB. Method: In a sample of 265 early psychosis patients, treated at the Treatment and Early Intervention in Psychosis Program (TIPP) in Lausanne, we used logistic regression models to explore the link between various dynamic risk factors of VB [positive symptoms, substance use disorder (drugs including cannabis, alcohol and others drugs), insight, impulsivity, affective instability, and treatment adherence], and VB occurring during treatment. In order to understand hierarchical effects attributable to the combinations of risk factors on VB we conducted a Classification and Regression Tree (CART). Results: Our results show that cannabis use disorder is a risk factor for VB. The associations among risk factors suggest the presence of two patient profiles with an increased rate of VB: the first is composed of patients with cannabis use disorder and impulsivity, and the second of patients combining cannabis use disorder, absence of insight and non-adherence to treatment. The results also show the moderating role of insight and adherence to treatment on the rate of VB in patients with cannabis use disorder. Conclusion: This study suggests that cannabis use disorder is a significant risk factor for VB amongst early psychosis patients, particularly when combined with either impulsivity, lack of insight and non-adherence to treatment. These results suggest that preventive strategies could be developed on the basis of such patient p

The difference between the electromagnetic self-energies of proton and neutron can be calculated with the Cottingham formula, which expresses the self-energies as an integral over the electroproduction cross sections---provided the nucleon matrix elements of the current commutator do not contain a fixed pole. We show that, under the same proviso, the subtraction function occurring in the dispersive representation of the virtual Compton forward scattering amplitude is determined by the cross sections. The representation in particular leads to a parameter-free sum rule for the nucleon polarizabilities. We evaluate the sum rule for the difference between the electric polarizabilities of proton and neutron by means of the available parameterizations of the data and compare the result with experiment., Comment: 30 pages, 7 figures; The typos in Eqs. (10), (27), (56), (57), (63) and (B.46) are corrected. None of the results of the paper is affected

The difference between the electromagnetic self-energies of proton and neutron can be calculated with the Cottingham formula, which expresses the self-energies as an integral over the electroproduction cross sections---provided the nucleon matrix elements of the current commutator do not contain a fixed pole. We show that, under the same proviso, the subtraction function occurring in the dispersive representation of the virtual Compton forward scattering amplitude is determined by the cross sections. The representation in particular leads to a parameter-free sum rule for the nucleon polarizabilities. We evaluate the sum rule for the difference between the electric polarizabilities of proton and neutron by means of the available parameterizations of the data and compare the result with experiment., Comment: 30 pages, 7 figures; The typos in Eqs. (10), (27), (56), (57), (63) and (B.46) are corrected. None of the results of the paper is affected

The difference between the electromagnetic self-energies of proton and neutron can be calculated with the Cottingham formula, which expresses the self-energies as an integral over the electroproduction cross sections---provided the nucleon matrix elements of the current commutator do not contain a fixed pole. We show that, under the same proviso, the subtraction function occurring in the dispersive representation of the virtual Compton forward scattering amplitude is determined by the cross sections. The representation in particular leads to a parameter-free sum rule for the nucleon polarizabilities. We evaluate the sum rule for the difference between the electric polarizabilities of proton and neutron by means of the available parameterizations of the data and compare the result with experiment., Comment: 30 pages, 7 figures; The typos in Eqs. (10), (27), (56), (57), (63) and (B.46) are corrected. None of the results of the paper is affected

1 januari 2010, Contains fulltext : 87970.pdf (publisher's version ) (Closed access), OBJECTIVES: Chronic inflammation is a major risk factor for systemic bone loss leading to osteoporotic fracture and substantial morbidity and mortality. Inflammatory cytokines, particularly tumour necrosis factor (TNF) and interleukin-1 (IL1), are thought to play a key role in the pathogenesis of inflammation-induced bone loss, but their exact roles are yet to be determined. METHODS: To determine whether TNF directly triggers bone loss or requires IL1, human TNFalpha mice (hTNFtg) were crossed with mice lacking IL1alpha and IL1beta (IL1(-/-)hTNFtg). Systemic bone architecture was evaluated using CT scanning, static and dynamic bone histomorphometry and serum markers of bone metabolism. RESULTS: hTNFtg mice developed severe bone loss accompanied by a severe distortion of bone microarchitecture. Bone trabeculae were thinner and decreased in numbers, resulting in increased trabecular separation. Histomorphometric analyses revealed strongly increased bone resorption in hTNFtg mice compared with wild-type mice. In contrast, IL1(-/-)hTNFtg mice were fully protected from systemic bone loss despite still developing inflammation in their joints. Lack of IL1 completely reversed increased osteoclast formation and bone resorption in hTNFtg mice and the increased levels of RANKL in these mice. Structural parameters and osteoclast and osteoblast numbers were indistinguishable from wild-type mice. CONCLUSIONS: These data indicate that IL1 is essential for TNF-mediated bone loss. Despite TNF-mediated inflammatory arthritis, systemic bone is fully protected by the absence of IL1, which suggests that IL1 is an essential mediator of inflammatory osteopenia.

01 januari 2010, Contains fulltext : 87970.pdf (publisher's version ) (Closed access), OBJECTIVES: Chronic inflammation is a major risk factor for systemic bone loss leading to osteoporotic fracture and substantial morbidity and mortality. Inflammatory cytokines, particularly tumour necrosis factor (TNF) and interleukin-1 (IL1), are thought to play a key role in the pathogenesis of inflammation-induced bone loss, but their exact roles are yet to be determined. METHODS: To determine whether TNF directly triggers bone loss or requires IL1, human TNFalpha mice (hTNFtg) were crossed with mice lacking IL1alpha and IL1beta (IL1(-/-)hTNFtg). Systemic bone architecture was evaluated using CT scanning, static and dynamic bone histomorphometry and serum markers of bone metabolism. RESULTS: hTNFtg mice developed severe bone loss accompanied by a severe distortion of bone microarchitecture. Bone trabeculae were thinner and decreased in numbers, resulting in increased trabecular separation. Histomorphometric analyses revealed strongly increased bone resorption in hTNFtg mice compared with wild-type mice. In contrast, IL1(-/-)hTNFtg mice were fully protected from systemic bone loss despite still developing inflammation in their joints. Lack of IL1 completely reversed increased osteoclast formation and bone resorption in hTNFtg mice and the increased levels of RANKL in these mice. Structural parameters and osteoclast and osteoblast numbers were indistinguishable from wild-type mice. CONCLUSIONS: These data indicate that IL1 is essential for TNF-mediated bone loss. Despite TNF-mediated inflammatory arthritis, systemic bone is fully protected by the absence of IL1, which suggests that IL1 is an essential mediator of inflammatory osteopenia.

01 januari 2010, Contains fulltext : 87970.pdf (publisher's version ) (Closed access), OBJECTIVES: Chronic inflammation is a major risk factor for systemic bone loss leading to osteoporotic fracture and substantial morbidity and mortality. Inflammatory cytokines, particularly tumour necrosis factor (TNF) and interleukin-1 (IL1), are thought to play a key role in the pathogenesis of inflammation-induced bone loss, but their exact roles are yet to be determined. METHODS: To determine whether TNF directly triggers bone loss or requires IL1, human TNFalpha mice (hTNFtg) were crossed with mice lacking IL1alpha and IL1beta (IL1(-/-)hTNFtg). Systemic bone architecture was evaluated using CT scanning, static and dynamic bone histomorphometry and serum markers of bone metabolism. RESULTS: hTNFtg mice developed severe bone loss accompanied by a severe distortion of bone microarchitecture. Bone trabeculae were thinner and decreased in numbers, resulting in increased trabecular separation. Histomorphometric analyses revealed strongly increased bone resorption in hTNFtg mice compared with wild-type mice. In contrast, IL1(-/-)hTNFtg mice were fully protected from systemic bone loss despite still developing inflammation in their joints. Lack of IL1 completely reversed increased osteoclast formation and bone resorption in hTNFtg mice and the increased levels of RANKL in these mice. Structural parameters and osteoclast and osteoblast numbers were indistinguishable from wild-type mice. CONCLUSIONS: These data indicate that IL1 is essential for TNF-mediated bone loss. Despite TNF-mediated inflammatory arthritis, systemic bone is fully protected by the absence of IL1, which suggests that IL1 is an essential mediator of inflammatory osteopenia.

The pion decay constant f_pi plays a crucial role in many areas of low energy particle physics. Its value may e.g. be deduced from experimental data on leptonic pion decays. Here, we provide comments on several aspects of this evaluation. In particular, we point out that at the present level of experimental accuracy, the value of f_pi is sensitive to the value of the pion mass chosen in its chiral expansion., Comment: 15 pages, 3 figures. Accepted for publication in Phys. Lett. B

We review the theory of hadronic atoms in QCD+QED. The non-relativistic effective Lagrangian approach, used to describe this type of bound states, is illustrated with the case of pi+pi- atoms. In addition, we discuss the evaluation of isospin-breaking corrections to hadronic atom observables by invoking chiral perturbation theory., Comment: Commissioned article for Ann. Rev. Nucl. Part. Sci., 34 pages, 5 figures, 3 references added

We investigate radiative corrections to K --> 3 pi decays. In particular, we extend the non-relativistic framework developed recently to include real and virtual photons and show that, in a well-defined power counting scheme, the results reproduce corrections obtained in the relativistic calculation. Real photons are included exactly, beyond the soft-photon approximation, and we compare the result with the latter. The singularities generated by pionium near threshold are investigated, and a region is identified where standard perturbation theory in the fine structure constant alpha may be applied. We expect that the formulae provided allow one to extract S-wave pi pi scattering lengths from the cusp effect in these decays with high precision., Comment: 57 pages, 17 figures

We investigate radiative corrections to K --> 3 pi decays. In particular, we extend the non-relativistic framework developed recently to include real and virtual photons and show that, in a well-defined power counting scheme, the results reproduce corrections obtained in the relativistic calculation. Real photons are included exactly, beyond the soft-photon approximation, and we compare the result with the latter. The singularities generated by pionium near threshold are investigated, and a region is identified where standard perturbation theory in the fine structure constant alpha may be applied. We expect that the formulae provided allow one to extract S-wave pi pi scattering lengths from the cusp effect in these decays with high precision., Comment: 57 pages, 17 figures

kein Abstract verfügbar

kein Abstract verfügbar

Objectives: Chronic myeloid leukemia (CML) is effectively treated by Imatinib (IM) via inhibition of the BCR-ABL tyrosine kinase. However, also related tyrosine kinases like abl, c-Kit, PDGF-R, and c-FMS are blocked by IM. As shown in adult humans and mice, abl-controlled protein folding as part of the endoplasmatic stress response in heart myoblasts as well as bone "remodeling" depending on PDGF-R and c-FMS is impaired under imatinib exposure (Dewar AL et al 2005, Kerkelä R et al 2006, Fitter S et al 2008). The influence of IM on the growing heart and skeleton of immature animals has not been studied so far. With respect to treatment of pediatric CML we report alterations in these organs of juvenile mice chronically exposed to IM during the growth period. Methods: From the age of 4–14 weeks (w) [development milestones of mice: weaning 3 w; puberty 7 w; epiphysial lines closure 18 w] C3H/Neu male and female wild-type mice were chronically exposed to IM via the drinking water at concentrations of 500 mg/l (group A), 750 mg/l (group B), and 1000mg/l (group C). Femur length and overall skeletal development was analysed by whole body X-ray analysis using a mammography device. Bone metabolic activity was assessed by total body Na18F PET and CT after 5w and 10w of exposure using dedicated small animal tomographs. Bone mineral density and microstructure of tibiae were analysed by pQCT and microCT (resolution 12.5µ m) while the number of osteoclasts and resorption lacunae in femora and vertebrae was assessed by histomorphometry. Plasma concentration of IM, osteocalcin, and activity of the tartrate resistant acid phosphatase (TRAP5b) was also determined. The heart was examined histologically and ultrastructurally by electron microscopy. Results: IM was tolerated well and mean uptake of 80 mg/kg/d A. 110 mg/kg/d B. and 150 mg/kg/d C. resulted in serum levels of 60–674 ng/ml, 36–242 ng/ml and 51–534 ng/ml, respectively. Body weight gain was delayed in groups B and C until the

We investigate radiative corrections to K --> 3 pi decays. In particular, we extend the non-relativistic framework developed recently to include real and virtual photons and show that, in a well-defined power counting scheme, the results reproduce corrections obtained in the relativistic calculation. Real photons are included exactly, beyond the soft-photon approximation, and we compare the result with the latter. The singularities generated by pionium near threshold are investigated, and a region is identified where standard perturbation theory in the fine structure constant alpha may be applied. We expect that the formulae provided allow one to extract S-wave pi pi scattering lengths from the cusp effect in these decays with high precision., Comment: 57 pages, 17 figures

Objectives: Chronic myeloid leukemia (CML) is effectively treated by Imatinib (IM) via inhibition of the BCR-ABL tyrosine kinase. However, also related tyrosine kinases like abl, c-Kit, PDGF-R, and c-FMS are blocked by IM. As shown in adult humans and mice, abl-controlled protein folding as part of the endoplasmatic stress response in heart myoblasts as well as bone "remodeling" depending on PDGF-R and c-FMS is impaired under imatinib exposure (Dewar AL et al 2005, Kerkelä R et al 2006, Fitter S et al 2008). The influence of IM on the growing heart and skeleton of immature animals has not been studied so far. With respect to treatment of pediatric CML we report alterations in these organs of juvenile mice chronically exposed to IM during the growth period. Methods: From the age of 4–14 weeks (w) [development milestones of mice: weaning 3 w; puberty 7 w; epiphysial lines closure 18 w] C3H/Neu male and female wild-type mice were chronically exposed to IM via the drinking water at concentrations of 500 mg/l (group A), 750 mg/l (group B), and 1000mg/l (group C). Femur length and overall skeletal development was analysed by whole body X-ray analysis using a mammography device. Bone metabolic activity was assessed by total body Na18F PET and CT after 5w and 10w of exposure using dedicated small animal tomographs. Bone mineral density and microstructure of tibiae were analysed by pQCT and microCT (resolution 12.5µ m) while the number of osteoclasts and resorption lacunae in femora and vertebrae was assessed by histomorphometry. Plasma concentration of IM, osteocalcin, and activity of the tartrate resistant acid phosphatase (TRAP5b) was also determined. The heart was examined histologically and ultrastructurally by electron microscopy. Results: IM was tolerated well and mean uptake of 80 mg/kg/d A. 110 mg/kg/d B. and 150 mg/kg/d C. resulted in serum levels of 60–674 ng/ml, 36–242 ng/ml and 51–534 ng/ml, respectively. Body weight gain was delayed in groups B and C until the

Contains fulltext : 52277.pdf (publisher's version ) (Closed access), Blocking TNF effectively inhibits inflammation and structural damage in human rheumatoid arthritis (RA). However, so far it is unclear whether the effect of TNF is a direct one or indirect on up-regulation of other mediators. IL-1 may be one of these candidates because it has a central role in animal models of arthritis, and inhibition of IL-1 is used as a therapy of human RA. We removed the effects of IL-1 from a TNF-mediated inflammatory joint disease by crossing IL-1alpha and beta-deficient mice (IL-1-/-) with arthritic human TNF-transgenic (hTNFtg) mice. Development of synovial inflammation was almost unaffected on IL-1 deficiency, but bone erosion and osteoclast formation were significantly reduced in IL-1-/-hTNFtg mice, compared with hTNFtg mice based on an intrinsic differentiation defect of IL-1-deficient monocytes. Most dramatically, however, cartilage damage was absent in IL-1-/-hTNFtg mice. Chimera studies revealed that protection of cartilage is based on the loss of IL-1 on hematopoietic, but not mesenchymal, cells, leading to decreased expression of ADAMTS-5 and MMP-3. These data show that TNF-mediated cartilage damage is completely and TNF-mediated bone damage is partially dependent on IL-1, suggesting that IL-1 is a crucial mediator for inflammatory cartilage and bone degradation.

Contains fulltext : 52277.pdf (publisher's version ) (Closed access), Blocking TNF effectively inhibits inflammation and structural damage in human rheumatoid arthritis (RA). However, so far it is unclear whether the effect of TNF is a direct one or indirect on up-regulation of other mediators. IL-1 may be one of these candidates because it has a central role in animal models of arthritis, and inhibition of IL-1 is used as a therapy of human RA. We removed the effects of IL-1 from a TNF-mediated inflammatory joint disease by crossing IL-1alpha and beta-deficient mice (IL-1-/-) with arthritic human TNF-transgenic (hTNFtg) mice. Development of synovial inflammation was almost unaffected on IL-1 deficiency, but bone erosion and osteoclast formation were significantly reduced in IL-1-/-hTNFtg mice, compared with hTNFtg mice based on an intrinsic differentiation defect of IL-1-deficient monocytes. Most dramatically, however, cartilage damage was absent in IL-1-/-hTNFtg mice. Chimera studies revealed that protection of cartilage is based on the loss of IL-1 on hematopoietic, but not mesenchymal, cells, leading to decreased expression of ADAMTS-5 and MMP-3. These data show that TNF-mediated cartilage damage is completely and TNF-mediated bone damage is partially dependent on IL-1, suggesting that IL-1 is a crucial mediator for inflammatory cartilage and bone degradation.

We review the theory of hadronic atoms in QCD + QED, based on a non-relativistic effective Lagrangian framework. We first provide an introduction to the theory, and then describe several applications: meson-meson, meson-nucleon atoms and meson-deuteron compounds. Finally, we compare the quantum field theory framework used here with the traditional approach, which is based on quantum-mechanical potential scattering., Comment: 140 pages, 19 postscript figures, the replaced version contains an additional reference

Contains fulltext : 52277.pdf (publisher's version ) (Closed access), Blocking TNF effectively inhibits inflammation and structural damage in human rheumatoid arthritis (RA). However, so far it is unclear whether the effect of TNF is a direct one or indirect on up-regulation of other mediators. IL-1 may be one of these candidates because it has a central role in animal models of arthritis, and inhibition of IL-1 is used as a therapy of human RA. We removed the effects of IL-1 from a TNF-mediated inflammatory joint disease by crossing IL-1alpha and beta-deficient mice (IL-1-/-) with arthritic human TNF-transgenic (hTNFtg) mice. Development of synovial inflammation was almost unaffected on IL-1 deficiency, but bone erosion and osteoclast formation were significantly reduced in IL-1-/-hTNFtg mice, compared with hTNFtg mice based on an intrinsic differentiation defect of IL-1-deficient monocytes. Most dramatically, however, cartilage damage was absent in IL-1-/-hTNFtg mice. Chimera studies revealed that protection of cartilage is based on the loss of IL-1 on hematopoietic, but not mesenchymal, cells, leading to decreased expression of ADAMTS-5 and MMP-3. These data show that TNF-mediated cartilage damage is completely and TNF-mediated bone damage is partially dependent on IL-1, suggesting that IL-1 is a crucial mediator for inflammatory cartilage and bone degradation.

We review the theory of hadronic atoms in QCD + QED, based on a non-relativistic effective Lagrangian framework. We first provide an introduction to the theory, and then describe several applications: meson-meson, meson-nucleon atoms and meson-deuteron compounds. Finally, we compare the quantum field theory framework used here with the traditional approach, which is based on quantum-mechanical potential scattering., Comment: 140 pages, 19 postscript figures, the replaced version contains an additional reference

The pion mass difference generates a pronounced cusp in K --> 3 pi decays, the strength of which is related to the pi pi S-wave scattering lengths. We apply an effective field theory framework developed earlier to evaluate the amplitudes for K_L --> 3 pi decays in a systematic manner, where the strictures imposed by analyticity and unitarity are respected automatically. The amplitudes for the decay eta --> 3 pi are also given., Comment: 15 pages, 3 figures, uses Elsevier style

The cusp effect in K \to 3\pi and data on K_e4 decays allow one to extract experimental information on the elastic \pi\pi scattering amplitude near threshold, and to confront the outcome of the analyses with predictions made in the framework of QCD. In my talk I pointed out that these predictions concern an isospin symmetric world, while experiments are carried out in the real world, where isospin breaking effects -- generated by electromagnetic interactions and by the mass difference of the up and down quarks -- are always present. I discussed the corrections required to account for these, so that a meaningful comparison with the predictions becomes possible. In particular, I pointed out that there is a spectacular isospin breaking effect in K_e4 decays, overlooked so far. Once it is taken into account, the previous discrepancy between NA48/2 data on K_e4 decays and the prediction of \pi\pi scattering lengths disappears., Comment: Plenary talk given at the International Conference KAON'07, Laboratori Nazionali di Frascati, Italy, May 21-25, 2007. To appear in the proceedings. 10 pages, 3 figures

We review the theory of hadronic atoms in QCD + QED, based on a non-relativistic effective Lagrangian framework. We first provide an introduction to the theory, and then describe several applications: meson-meson, meson-nucleon atoms and meson-deuteron compounds. Finally, we compare the quantum field theory framework used here with the traditional approach, which is based on quantum-mechanical potential scattering., Comment: 140 pages, 19 postscript figures, the replaced version contains an additional reference

In this talk, I comment on the theoretical and experimental status of kaonic atoms, in particular, \bar K\pi and \bar Kp bound states., Comment: Invited plenary talk at the International Conference "DAFNE 2004: Physics at meson factories" - Frascati (It), June 7-11, 2004. 9 pages (LaTex), 1 figure. To appear in the Proceedings

Motivated by recent experimental results and ongoing measurements, we review the chiral perturbation theory prediction for radiative Ke3 decays (neutral kaons). Special emphasis is given on the stability of the inner bremsstrahlung-dominated relative branching ratio vs. the Ke3 form factors, and on the separation of the structure dependent amplitude in differential distributions over the phase space. For the structure dependent terms, an assessment of the order p^6 corrections is given. In particular, a full next-to-leading order calculation of the axial component is performed. The experimental analysis of the photon energy spectrum is discussed, and other potentially useful distributions are introduced., Comment: Version published in Eur.Phys.J.C.: 23 pages (LaTeX), 10 figures. Minor changes in text, typos removed, references updated, Springer style file used

These are the proceedings of the workshop "HadAtom03," held at the European Centre for Theoretical Nuclear Physics and Related Studies (ECT*), Trento (Italy), October 13 - 17, 2003. The main topics discussed at the workshop were the physics of hadronic atoms and in this context recent results in experiment and theory. Included here are the list of participants, the scientific program and a short contribution from each speaker., Comment: 46 pages, 16 postscript figures, Proceedings of the workshop "HadAtom03," 13-17 October Trento, Italy

The scalar radius of the pion plays an important role in CHPT, because it is related to one of the basic effective coupling constants, viz. the one which controls the quark mass dependence of F_pi at one loop. In a recent paper, Yndurain derives a {\it robust lower bound} for this radius, which disagrees with earlier determinations. We show that such a bound does not exist: the "derivation" relies on an incorrect claim. Moreover, we discuss the physics of the form factors associated with the operators \ubar u, \dbar d and \sbar s and show that their structure in the vicinity of the K \Kbar threshold is quite different. Finally, we draw attention to the fact that the new data on the slope of the scalar K_l3 form factor confirm a recent, remarkably sharp theoretical prediction., Comment: 13 pages, 2 figures. v2: minor changes - version to appear on Phys. Lett. B. v3: Published version. Values of the measured K-pi radii corrected

In this talk, I comment on the theoretical and experimental status of kaonic atoms, in particular, \bar K\pi and \bar Kp bound states., Comment: Invited plenary talk at the International Conference "DAFNE 2004: Physics at meson factories" - Frascati (It), June 7-11, 2004. 9 pages (LaTex), 1 figure. To appear in the Proceedings

The scalar radius of the pion plays an important role in CHPT, because it is related to one of the basic effective coupling constants, viz. the one which controls the quark mass dependence of F_pi at one loop. In a recent paper, Yndurain derives a {\it robust lower bound} for this radius, which disagrees with earlier determinations. We show that such a bound does not exist: the "derivation" relies on an incorrect claim. Moreover, we discuss the physics of the form factors associated with the operators \ubar u, \dbar d and \sbar s and show that their structure in the vicinity of the K \Kbar threshold is quite different. Finally, we draw attention to the fact that the new data on the slope of the scalar K_l3 form factor confirm a recent, remarkably sharp theoretical prediction., Comment: 13 pages, 2 figures. v2: minor changes - version to appear on Phys. Lett. B. v3: Published version. Values of the measured K-pi radii corrected

Motivated by recent experimental results and ongoing measurements, we review the chiral perturbation theory prediction for radiative Ke3 decays (neutral kaons). Special emphasis is given on the stability of the inner bremsstrahlung-dominated relative branching ratio vs. the Ke3 form factors, and on the separation of the structure dependent amplitude in differential distributions over the phase space. For the structure dependent terms, an assessment of the order p^6 corrections is given. In particular, a full next-to-leading order calculation of the axial component is performed. The experimental analysis of the photon energy spectrum is discussed, and other potentially useful distributions are introduced., Comment: Version published in Eur.Phys.J.C.: 23 pages (LaTeX), 10 figures. Minor changes in text, typos removed, references updated, Springer style file used

These are the proceedings of the workshop "HadAtom03," held at the European Centre for Theoretical Nuclear Physics and Related Studies (ECT*), Trento (Italy), October 13 - 17, 2003. The main topics discussed at the workshop were the physics of hadronic atoms and in this context recent results in experiment and theory. Included here are the list of participants, the scientific program and a short contribution from each speaker., Comment: 46 pages, 16 postscript figures, Proceedings of the workshop "HadAtom03," 13-17 October Trento, Italy

I present introductory lectures on the use of effective field theory methods in QCD at low energies., Comment: 37 pages (LaTex), 15 figures. Lectures given at the 41. Internationale Universit\"atswochen f\"ur Theoretische Physik, Schladming, Styria, Austria, February 22-28, 2003. To appear in the Proceedings

In a recent paper, Pelaez and Yndurain evaluate some of the low energy observables of pi pi scattering and obtain flat disagreement with our earlier results. The authors work with unsubtracted dispersion relations, so that their results are very sensitive to the poorly known high energy behaviour of the scattering amplitude. They claim that the asymptotic representation we used is incorrect and propose an alternative one. We repeat their calculations on the basis of the standard, subtracted fixed-t dispersion relations, using their asymptotics. The outcome fully confirms our earlier findings. Moreover, we show that the Regge parametrization proposed by these authors for the region above 1.4 GeV violates crossing symmetry: Their ansatz is not consistent with the behaviour observed at low energies., Comment: Added more material, mostly in Sects. 7, 8 and 9, in support of the same conclusions. Latex, 28 pages, 3 figures

In quantum field theory, the splitting of the Hamiltonian into a strong and an electromagnetic part cannot be performed in a unique manner. We propose a convention for disentangling these two effects: one matches the parameters of two theories -- with and without electromagnetic interactions -- at a given scale mu_1, referred to as the matching scale. This procedure enables one to analyze the separation of strong and electromagnetic contributions in a transparent manner. We illustrate the method -- in the framework of the loop expansion -- in a Yukawa model, as well as in the linear sigma model, where we also investigate the corresponding low-energy effective theory., Comment: 19 pages (LaTex), 5 figures, published version. References in the introduction added, discussion shortened, 1 figure removed, conclusions unchanged

I present introductory lectures on the use of effective field theory methods in QCD at low energies., Comment: 37 pages (LaTex), 15 figures. Lectures given at the 41. Internationale Universit\"atswochen f\"ur Theoretische Physik, Schladming, Styria, Austria, February 22-28, 2003. To appear in the Proceedings

In a recent paper, Pelaez and Yndurain evaluate some of the low energy observables of pi pi scattering and obtain flat disagreement with our earlier results. The authors work with unsubtracted dispersion relations, so that their results are very sensitive to the poorly known high energy behaviour of the scattering amplitude. They claim that the asymptotic representation we used is incorrect and propose an alternative one. We repeat their calculations on the basis of the standard, subtracted fixed-t dispersion relations, using their asymptotics. The outcome fully confirms our earlier findings. Moreover, we show that the Regge parametrization proposed by these authors for the region above 1.4 GeV violates crossing symmetry: Their ansatz is not consistent with the behaviour observed at low energies., Comment: Added more material, mostly in Sects. 7, 8 and 9, in support of the same conclusions. Latex, 28 pages, 3 figures

In quantum field theory, the splitting of the Hamiltonian into a strong and an electromagnetic part cannot be performed in a unique manner. We propose a convention for disentangling these two effects: one matches the parameters of two theories -- with and without electromagnetic interactions -- at a given scale mu_1, referred to as the matching scale. This procedure enables one to analyze the separation of strong and electromagnetic contributions in a transparent manner. We illustrate the method -- in the framework of the loop expansion -- in a Yukawa model, as well as in the linear sigma model, where we also investigate the corresponding low-energy effective theory., Comment: 19 pages (LaTex), 5 figures, published version. References in the introduction added, discussion shortened, 1 figure removed, conclusions unchanged