A NEW BROADBAND MICROSTRIP QUADRATURE HYBRID WITH VERY FLAT PHASE RESPONSE

A new broadband microstrip branch-line quadrature hybrid with very flat phase response is presented. The device is made by cascading four branch-line couplers with arbitrary power division. The novel design is based on the microstrip transposition of a broadband waveguide polariser [4]. Across a 32% bandwidth centred at 9.3 GHz, the RL and the IL are respectively -15 dB and -3 dB/-4 dB; the phase difference is very flat, i.e. 90°±1.5°

Nonischemic left ventricular scar and cardiac sudden death in the young

Nonischemic left ventricular scar (NLVS) is a pattern of myocardial injury characterized by midventricular and/or subepicardial gadolinium hyperenhancement at cardiac magnetic resonance, in absence of significant coronary artery disease. We aimed to evaluate the prevalence of NLVS in juvenile sudden cardiac death and to ascertain its etiology at autopsy. We examined 281 consecutive cases of sudden death of subjects aged 1 to 35 years. NLVS was defined as a thin, gray rim of subepicardial and/or midmyocardial scar in the left ventricular free wall and/or the septum, in absence of significant stenosis of coronary arteries. NLVS was the most frequent finding (25%) in sudden deaths occurring during sports. Myocardial scar was localized most frequently within the left ventricular posterior wall and affected the subepicardial myocardium, often extending to the midventricular layer. On histology, it consisted of fibrous or fibroadipose tissue. Right ventricular involvement was always present. Patchy lymphocytic infiltrates were frequent. Genetic and molecular analyses clarified the etiology of NLVS in a subset of cases. Electrocardiographic (ECG) recordings were available in more than half of subjects. The most frequent abnormality was the presence of low QRS voltages (<0.5 mV) in limb leads. In serial ECG tracings, the decrease in QRS voltages appeared, in some way, progressive. NLVS is the most frequent morphologic substrate of juvenile cardiac sudden death in sports. It can be suspected based on ECG findings. Autopsy study and clinical screening of family members are required to differentiate between arrhythmogenic right ventricular cardiomyopathy/dysplasia and chronic acquired myocarditis

Btk regulation in human and mouse B cells via protein kinase C phosphorylation of IBtk {gamma

The inhibitor of Bruton tyrosine kinase (IBtk) is a negative regulator of the Bruton tyrosine kinase (Btk), which plays a major role in B-cell differentiation; however, the mechanisms of IBtk-mediated regulation of Btk are unknown. Here we report that B-cell receptor (BCR) triggering caused serine-phosphorylation of IBtk at protein kinase C consensus sites and dissociation from Btk. By liquid chromatography and mass-mass spectrometry and functional analysis, we identified IBtk-S87 and -S90 as the critical amino acid residues that regulate the IBtk binding affinity to Btk. Consistently, the mutants IBtk carrying S87A and S90A mutations bound constitutively to Btk and down-regulated Ca2 fluxes and NF-B activation on BCR triggering. Accordingly, spleen B cells from Ibtk/ mice showed an increased activation of Btk, as evaluated by Y551-phosphorylation and sustained Ca2 mobilization on BCR engagement. These findings identify a novel pathway of Btk regulation via protein kinase C phosphorylation of IBtk. (Blood. 2011;117(24):6520-6531