Pneumococcus meningitis varandossag soran.

Bacterial meningitis is a life-threatening disease. The incidence of meningitis is about 2.6-6 cases per 100.000 adults per year in developed countries. The most common causative microorganisms are Sreptococcus pneumoniae and Neisseria meningitidis. A 33-year-old multigravida, at 24 week of gestation was admitted to the hospital because of ear pain, haedache, fever and confusion. Lumbal puncture was performed and cerebrospinal fluid analysis showed signs of bacterial meningitis. Latex agglutination test was positive for S. pneumoniae, Gram-positive diplococci have seen under microscope and later cultivation verified S. pneumoniae as the causative agent. After ceftriaxon, dexamethasone administration and treatment in intensive care unit, left side mastoidectomy was performed since cranial computed tomography showed acut exacerbation of chronic mastoiditis on the left side. After extubation, mobilisation and 14 days antibiotic treatment the patient, who had residual hearing loss on the left side, was discharged from the hospital. During the treatment the foetal parameters were normal. The patient at 39 week of gestation gave birth to a healthy infant. Forty-eight case reports have been published in this topic around the world until April, 2012. The most common causative agents were S. pneumoniae and Listeria monocytogenes. Because of the little amount of data, it is hard to appreciate the actual incidence and prognosis of this life-threatening illness both for mother and infant. As far as we know this is the first published case report of meningitis during pregnancy in Hungary. By this article we would like to draw attention to the importance of teamwork, of prevention of brain abscess formation and of the removal of the infection's focus

Spatially Resolved Mapping of Local Polarization Dynamics in an Ergodic Phase of Ferroelectric Relaxor

Spatial variability of polarization relaxation kinetics in relaxor ferroelectric 0.9Pb(Mg1/3Nb2/3)O3-0.1PbTiO3 is studied using time-resolved Piezoresponse Force Microscopy. Local relaxation attributed to the reorientation of polar nanoregions is shown to follow stretched exponential dependence, exp(-(t/tau)^beta), with beta~~0.4, much larger than the macroscopic value determined from dielectric spectra (beta~~0.09). The spatial inhomogeneity of relaxation time distributions with the presence of 100-200 nm "fast" and "slow" regions is observed. The results are analyzed to map the Vogel-Fulcher temperatures on the nanoscale.Comment: 23 pages, 4 figures, supplementary materials attached; to be submitted to Phys. Rev. Let

The transcription factor STAT6 mediates direct repression of inflammatory enhancers and limits activation of alternatively polarized macrophages

The molecular basis of signal-dependent transcriptional activation has been extensively studied in macrophage polarization, but our understanding remains limited regarding the molecular determinants of repression. Here we show that IL-4-activated STAT6 transcription factor is required for the direct transcriptional repression of a large number of genes during in vitro and in vivo alternative macrophage polarization. Repression results in decreased lineage-determining transcription factor, p300, and RNA polymerase II binding followed by reduced enhancer RNA expression, H3K27 acetylation, and chromatin accessibility. The repressor function of STAT6 is HDAC3 dependent on a subset of IL-4-repressed genes. In addition, STAT6-repressed enhancers show extensive overlap with the NF-κB p65 cistrome and exhibit decreased responsiveness to lipopolysaccharide after IL-4 stimulus on a subset of genes. As a consequence, macrophages exhibit diminished inflammasome activation, decreased IL-1β production, and pyroptosis. Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli

Strain and Texture in Al-Interconnect Wires Measured by X-Ray Microbeam Diffraction

The local strain and texture in Al interconnect wires have been investigated using white and monochromatic x-ray microbeams on the MHATTCAT undulator beam line at the Advanced Photon Source. Intergrain and intragrain orientations were obtained with ~0.01 degree sensitivity using white beam measurements on wide Al pads (~100 Mu-m) and thin (2 Mu-m) Al wires. Orientation changes of up to 1 degree were found within individual grains of the (111) textured Al interconnects. Deviatoric strain measurements indicate small intragranular strain variations, but intergranular strain variations were found to be quite large

Anti-calmodulins and Tricyclic Adjuvants in Pain Therapy Block the TRPV1 Channel

Ca2+-loaded calmodulin normally inhibits multiple Ca2+-channels upon dangerous elevation of intracellular Ca2+ and protects cells from Ca2+-cytotoxicity, so blocking of calmodulin should theoretically lead to uncontrolled elevation of intracellular Ca2+. Paradoxically, classical anti-psychotic, anti-calmodulin drugs were noted here to inhibit Ca2+-uptake via the vanilloid inducible Ca2+-channel/inflamatory pain receptor 1 (TRPV1), which suggests that calmodulin inhibitors may block pore formation and Ca2+ entry. Functional assays on TRPV1 expressing cells support direct, dose-dependent inhibition of vanilloid-induced 45Ca2+-uptake at µM concentrations: calmidazolium (broad range)≥trifluoperazine (narrow range)>chlorpromazine/amitriptyline>fluphenazine>>W-7 and W-13 (only partially). Most likely a short acidic domain at the pore loop of the channel orifice functions as binding site either for Ca2+ or anti-calmodulin drugs. Camstatin, a selective peptide blocker of calmodulin, inhibits vanilloid-induced Ca2+-uptake in intact TRPV1+ cells, and suggests an extracellular site of inhibition. TRPV1+, inflammatory pain-conferring nociceptive neurons from sensory ganglia, were blocked by various anti-psychotic and anti-calmodulin drugs. Among them, calmidazolium, the most effective calmodulin agonist, blocked Ca2+-entry by a non-competitive kinetics, affecting the TRPV1 at a different site than the vanilloid binding pocket. Data suggest that various calmodulin antagonists dock to an extracellular site, not found in other Ca2+-channels. Calmodulin antagonist-evoked inhibition of TRPV1 and NMDA receptors/Ca2+-channels was validated by microiontophoresis of calmidazolium to laminectomised rat monitored with extracellular single unit recordings in vivo. These unexpected findings may explain empirically noted efficacy of clinical pain adjuvant therapy that justify efforts to develop hits into painkillers, selective to sensory Ca2+-channels but not affecting motoneurons