Towards next-to-next-to-leading-log accuracy for the width difference in the Bs−BˉsB_s-\bar{B}_s system: fermionic contributions to order (mc/mb)0(m_c/m_b)^0 and (mc/mb)1(m_c/m_b)^1

We calculate a class of three-loop Feynman diagrams which contribute to the next-to-next-to-leading logarithmic approximation for the width difference $\Delta\Gamma_{s}$ in the $B_s-\bar{B}_s$ system. The considered diagrams contain a closed fermion loop in a gluon propagator and constitute the order $\alpha_s^2 N_f$, where $N_f$ is the number of light quarks. Our results entail a considerable correction in that order, if $\Delta\Gamma_{s}$ is expressed in terms of the pole mass of the bottom quark. If the $\overline{MS}$ scheme is used instead, the correction is much smaller. As a result, we find a decrease of the scheme dependence. Our result also indicates that the usually quoted value of the NLO renormalization scale dependence underestimates the perturbative error.Comment: We corrected a typographical mistake in Eq. (4.18), made larger axis labels in Fig.2. Version accepted by JHE

Birth asphyxia as the major complication in newborns: Moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

Perinatal Asphyxia—oxygen deficit at delivery—can lead to severe hypoxic ischaemic organ damage in newborns followed by a fatal outcome or severe life-long pathologies. The severe insults often cause neurodegenerative diseases, mental retardation and epilepsies. The mild insults lead to so-called “minimal brain-damage disorders” such as attention deficits and hyperactivity, but can also be associated with the development of schizophrenia and life-long functional psychotic syndromes. Asphyxia followed by re-oxygenation can potentially lead to development of several neurodegenerative pathologies, diabetes type 2 and cancer. The task of individual prediction, targeted prevention and personalised treatments before a manifestation of the life-long chronic pathologies usually developed by newborns with asphyxic deficits, should be given the extraordinary priority in neonatology and paediatrics. Socio-economical impacts of educational measures and advanced strategies in development of robust diagnostic approaches targeted at effected molecular pathways, biomarker-candidates and potential drug-targets for tailored treatments are reviewed in the pap

Towards next-to-next-to-leading-log accuracy for the width difference in the Bs−B¯s system: fermionic contributions to order (mc/mb)⁰ and (mc/mb)¹

We calculate a class of three-loop Feynman diagrams which contribute to the next-to-next-to-leading logarithmic approximation for the width difference ΔΓs in the B s −B ¯ s system. The considered diagrams contain a closed fermion loop in a gluon propagator and constitute the order αs2Nf, where Nf is the number of light quarks. Our results entail a considerable correction in that order, if ΔΓs is expressed in terms of the pole mass of the bottom quark. If the MS ¯ scheme is used instead, the correction is much smaller. As a result, we find a decrease of the scheme dependence. Our result also indicates that the usually quoted value of the NLO renormalization scale dependence underestimates the perturbative error

Galloway-Mowat syndrome : an early-onset progressive encephalopathy with intractable epilepsy associated to renal impairment : two novel cases and review of literature

Galloway-Mowat Syndrome (GMS) is an autosomal recessively inherited condition which manifests with severe encephalopathy, featuring microcephaly, developmental delay, and early-onset intractable epilepsy. Patients typically show also renal involvement from the onset. We report two siblings with GMS presenting with early-onset, intractable epilepsy and neurological deterioration, later followed by renal impairment. In both patients intractable epilepsy started during the first months of life and included a combination of spasms, focal and myoclonic/atonic seizures, along with psychomotor retardation and dysmorphic features. One of the patient died from fulminating renal failure at age 6 years. The other patient developed only isolated proteinuria from the age 3 years. Our cases differ from 'classic' GMS, as manifested the clinical and laboratory features of renal involvement only some years later the onset of epilepsy and neurological symptoms. Therefore, the diagnosis of GMS should be considered in infants with intractable epilepsy, encephalopathy, and multiple neurological deficits, also in absence of renal manifestations. The literature data about the electroclinical features of epilepsy in GMS are also reviewed

Fine-structural distribution of MMP-2 and MMP-9 activities in the rat skeletal muscle upon training: a study by high-resolution in situ zymography

Matrix metalloproteinases (MMPs) are key regulators of extracellular matrix remodeling, but have also important intracellular targets. The purpose of this study was to examine the activity and subcellular localization of the gelatinases MMP-2 and MMP-9 in skeletal muscle of control and physically trained rats. In control hind limb muscle, the activity of the gelatinases was barely detectable. In contrast, after 5 days of intense exercise, in Soleus (Sol), but not Extensor digitorum longus (EDL) muscle, significant upregulation of gelatinolytic activity in myofibers was observed mainly in the nuclei, as assessed by high resolution in situ zymography. The nuclei of quiescent satellite cells did not contain the activity. Within the myonuclei, the gelatinolytic activity colocalized with an activated RNA Polymerase II. Also in Sol, but not in EDL, there were few foci of mononuclear cells with strongly positive cytoplasm, associated with apparent necrotic myofibers. These cells were identified as activated satellite cells/myoblasts. No extracellular gelatinase activity was observed. Gel zymography combined with subcellular fractionation revealed training-related upregulation of active MMP-2 in the nuclear fraction, and increase of active MMP-9 in the cytoplasmic fraction of Sol. Using RT-PCR, selective increase in MMP-9 mRNA was observed. We conclude that training activates nuclear MMP-2, and increases expression and activity of cytoplasmic MMP-9 in Sol, but not in EDL. Our results suggest that the gelatinases are involved in muscle adaptation to training, and that MMP-2 may play a novel role in myonuclear functions