The Impact of Transcatheter Atrial Septal Defect Closure in the Older Population A Prospective Study

ObjectivesWe sought to prove that device closure of atrial septal defect (ASD) in older patients not only improves cardiac function but also results in symptomatic relief by improving functional class.BackgroundAtrial septal defect accounts for approximately 10% of all congenital cardiac defects. It is possible that ASD closure in older patients may derive benefits, though this is not well established. We therefore aim to prospectively assess the clinical status and functional class of older patients after transcatheter ASD closure.MethodsThis was a prospective study of all patients age 40 years or more who underwent device closure of a secundum ASD between April 2004 and August 2006. Investigations including atrial and brain natriuretic peptide levels, electrocardiography, chest X-ray, transthoracic echocardiogram, 6-min walk test, and quality of life questionnaire were performed before and at 6 weeks and 1 year after the procedure.ResultsTwenty-three patients (median age 70 years, 13 women) had transcatheter device closure of ASD. Median ASD size was 18 mm (range 9 to 30 mm). Median pulmonary artery pressure was 22 mm Hg (range 12 to 27 mm Hg). At 1 year, New York Heart Association functional class improved (p = 0.004) in 16 patients with significant improvement in 6-min walk-test distance (p = 0.004) and physical (p = 0.002) as well as mental health score (p = 0.03). There were no major complications. One year following closure there was a significant change in left ventricular end-diastolic (p = 0.001) and end-systolic dimensions (p = 0.001) and also significant reduction in right ventricular end-diastolic dimension (p < 0.001).ConclusionsOur data demonstrated that ASD closure at advanced age results in favorable cardiac remodeling and improvement of functional class

Dysregulation of Chemokine/Chemokine Receptor Axes and NK Cell Tissue Localization during Diseases.

Chemokines are small chemotactic molecules that play key roles in physiological and pathological conditions. Upon signaling via their specific receptors, chemokines regulate tissue mobilization and trafficking of a wide array of immune cells, including natural killer (NK) cells. Current research is focused on analyzing changes in chemokine/chemokine receptor expression during various diseases to interfere with pathological trafficking of cells or to recruit selected cell types to specific tissues. NK cells are a heterogeneous lymphocyte population comprising several subsets endowed with distinct functional properties and mainly representing distinct stages of a linear development process. Because of their different functional potential, the type of subset that accumulates in a tissue drives the final outcome of NK cell-regulated immune response, leading to either protection or pathology. Correspondingly, chemokine receptors, including CXCR4, CXCR3, and CX3CR1, are differentially expressed by NK cell subsets, and their expression levels can be modulated during NK cell activation. At first, this review will summarize the current knowledge on the contribution of chemokines to the localization and generation of NK cell subsets in homeostasis. How an inappropriate chemotactic response can lead to pathology and how chemokine targeting can therapeutically affect tissue recruitment/localization of distinct NK cell subsets will also be discussed

Density Functional Study of Structures and Electron Affinities of BrO4F/BrO4F−

The structures, electron affinities and bond dissociation energies of BrO4F/BrO4F− species have been investigated with five density functional theory (DFT) methods with DZP++ basis sets. The planar F-Br…O2…O2 complexes possess 3A′ electronic state for neutral molecule and 4A′ state for the corresponding anion. Three types of the neutral-anion energy separations are the adiabatic electron affinity (EAad), the vertical electron affinity (EAvert), and the vertical detachment energy (VDE). The EAad value predicted by B3LYP method is 4.52 eV. The bond dissociation energies De (BrO4F → BrO4-mF + Om) (m = 1–4) and De− (BrO4F− → BrO4-mF− + Om and BrO4F− → BrO4-mF + Om−) are predicted. The adiabatic electron affinities (EAad) were predicted to be 4.52 eV for F-Br…O2…O2 (3A′←4A′) (B3LYP method)

Heart Rate Acceleration of a Subsidiary Pacemaker by β-Adrenergic Stimulation

BACKGROUND AND OBJECTIVES: Recent evidence indicates that the membrane voltage and Ca(2+) clocks jointly regulate sinoatrial node (SAN) automaticity. However, the mechanism of heart rhythm acceleration of the subsidiary pacemaker (SP) during β-adrenergic stimulation is still unknown. Here we tested the hypothesis that the heart rate acceleration of the SP by β-adrenergic stimulation involves synergistic interactions between both clock mechanisms. SUBJECTS AND METHODS: We performed optical mapping and pharmacological interventions in 15 isolated Langendorff-perfused canine right atriums (RA). The SP model was produced by ligation of the SAN artery at the mid portion of the sulcus terminalis. RESULTS: In the 6 RAs with an intact SAN, 1 µmol/L isoproterenol infusion increased the heart rate from 82±9 to 166±18 bpm (102%) with late diastolic Ca(i) elevation (LDCAE) at the superior SAN. However, in the 6 SP models, the heart rate increased from 55±10 bpm to 106±11 bpm (92%, p=0.005) without LDCAE at the earliest activation site. The isoproterenol induced heart rate increase was reversed to 74±5 bpm (33% from baseline) by administering an infusion of the funny current blocker ZD 7288 (3 µmol/L, n=3), whereas, it was suppressed to 69±7 bpm (24% from baseline) by sarcoplasmic reticulum (SR) Ca(2+) emptying with administering ryanodine (10 µmol/L) plus thapsigargin (200 nmol/L, n=3). The isoproterenol induced heart rate increase was completely abolished by combined treatment with funny current blocker and SR Ca(2+) emptying (n=3). CONCLUSION: Acceleration of the Ca(2+) clock in the SP plays an important role in the heart rate acceleration during β-adrenergic stimulation, and this interacts synergistically with the voltage clock to increase the heart rate.ope

Compressed Magnetic Field in the Magnetically Regulated Global Collapsing Clump of G9.62+0.19

How stellar feedback from high-mass stars (e.g., H II regions) influences the surrounding interstellar medium and regulates new star formation is still unclear. To address this question, we observed the G9.62+0.19 complex in 850 mu m continuum with the James Clerk Maxwell Telescope/POL-2 polarimeter. An ordered magnetic field has been discovered in its youngest clump, the G9.62 clump. The magnetic field strength is determined to be similar to 1 mG. Magnetic field plays a larger role than turbulence in supporting the clump. However, the G9.62 clump is still unstable against gravitational collapse even if thermal, turbulent, and magnetic field support are taken into account together. The magnetic field segments in the outskirts of the G9.62 clump seem to point toward the clump center, resembling a dragged-in morphology, indicating that the clump is likely undergoing magnetically regulated global collapse. However, the magnetic field in its central region is aligned with the shells of the photodissociation regions and is approximately parallel to the ionization (or shock) front, indicating that the magnetic field therein is likely compressed by the expanding H II regions that formed in the same complex.Peer reviewe

ВЫЯВЛЕНИЕ МАРКЁРОВ H. PYLORI У БОЛЬНЫХ ОСТРЫМИ ВИРУСНЫМИ ГЕПАТИТАМИ

O-antigenes of H. рylori have been revealed аt patients with acute viral hepatitis (AVH) (57,7%), more often at patients with a cholestasis, than without cholestasis (in feces – 48,6% and 35,4%, in CIC – 14,8% and 4,5%, accord., and VacA (43,5%) and a high-molecular fibers complex (70,6%). In aggregate with high indicators of LII and smaller linkage of toxins in the CIC in cholestasis, this data testifies to important pathogenetic role of H. рylori in development of cholestasis, induced by an inflammation.У больных острыми вирусными гепатитами выявлены О-антигены H. рylori (57,7%), чаще у больных ссиндромом холестаза, чем без холестаза (в кале – 48,6% и 35,4%, в ЦИК – 14,8% и 4,5% соответственно, также VacA (43,5%) и комплекс высокомолекулярных белков (70,6%). В совокупности с высокими показателями лейкоцитарного индекса интоксикации и меньшим связыванием токсинов в ЦИК при холестазе эти данные свидетельствуют о важной патогенетической роли H. рylori в развитии холестаза, индуцированного воспалением