Molecular anchoring to oxide surfaces in ultrahigh vacuum and in aqueous electrolytes: phosphonic acids on atomically-defined cobalt oxide.

In this work, we investigated the interaction of phenylphosphonic acid (PPA, C6H5PO3H2) with atomically-defined Co3O4(111) thin films, grown on Ir(100), under ultrahigh vacuum (UHV) conditions and in the electrochemical environment. In the first step, we employed infrared reflection absorption spectroscopy (IRAS) and followed the formation of a saturated monolayer (380 K) in UHV. We observed that the binding motif changes from a chelating tridentate in the sub-monolayer regime to a chelating bidentate at full monolayer coverages. In the electrochemical environment, we analyzed the interaction of PPA with the same Co3O4(111) surface by electrochemical infrared reflection absorption spectroscopy (EC-IRRAS) (0.3 VRHE-1.3 VRHE). When adsorbed at pH 10 from an ammonia buffered aqueous solution, PPA binds to the surface in form of a fully deprotonated chelating bidentate. With increasing electrode potential, we observed two fully reversible processes. At low buffer concentration, protons are released upon oxidation of surface Co2+ ions and lead to protonation of the anchored phosphonates. At high buffer concentration, most of the protons released are accepted by NH3. Simultaneously, the surface phosphonate changes its adsorption motif from bidentate to tridentate while adopting a more upright geometry.

Pleuroparenchymal Fibroelastosis: A Review of Histopathologic Features and the Relationship Between Histologic Parameters and Survival.

Pleuroparenchymal fibroelastosis (PPFE) is now a defined clinicopathologic entity in the updated 2013 ATS/ERS classification of idiopathic interstitial pneumonias (IIPs), which has led to a significant increase in cases being diagnosed at our institution. We have therefore reviewed 43 PPFE cases (58 biopsies in total) to assess whether any clinical or histopathologic features provide prognostic information. A semiquantatitive grading system was used to assess extent of fibroblastic foci, intra-alveolar fibroelastosis, visceral pleural fibrosis, chronic inflammation in areas of fibrosis, vascular fibrointimal thickening, and presence of granulomas. Other patterns of interstitial lung disease were also noted, if present. All biopsies showed intra-alveolar fibroelastosis, fibroblastic foci at the leading edge of fibrosis and chronic inflammation within areas of fibrosis, 91% showed vascular fibrointimal thickening of vessels, 73% showed pleural fibrosis, and 35% showed granulomas. Ten cases showed a coexistent IIP (5 showed usual interstitial pneumonia, 5 showed features of hypersensitivity pneumonitis). There was no significant correlation with mortality and severity of histologic parameters, other than a significant decrease in mortality in PPFE with coexistent granulomas, after adjusting for age and gender (hazard ratio, 0.27; P=0.049). Male gender was also associated with an increased risk of mortality, after adjusting for age (hazard ratio, 4.8; P=0.045). PPFE is more common than previously thought, not infrequently showing coexistent pathology, specifically usual interstitial pneumonia and granulomatous lung disease, our data suggesting the latter may have prognostic significance.

Restrictive allograft syndrome and idiopathic pleuroparenchymal fibroelastosis: do they really have the same histology?

AIMS: Restrictive allograft syndrome (RAS) and idiopathic pleuroparenchymal fibroelastosis (IPPFE) are two different diseases reported to share the same histology. RAS relates to chronic allograft dysfunction in lung transplantation, with IPPFE being a rare condition in native lungs. Our aim is to compare their histologies alongside biopsies of usual interstitial pneumonia (UIP), to determine if there are differences that might help to elucidate the pathogenesis. METHODS AND RESULTS: We selected four postmortem allograft lungs from patients who developed a clear clinical RAS pattern, five biopsies diagnosed as IPPFE, five UIP biopsies and five sections of normal lung. Histopathological features were described without knowledge of clinical and radiological features. Both RAS allografts and IPPFE biopsies showed intra-alveolar fibrosis and elastosis (IAFE), but RAS allografts also showed concomitant obliterative bronchiolitis, vascular lymphoplasmacytic inflammation within fibrointimal thickening, less fibroblastic foci (FF) at the advancing edge of the fibrosis (one against 14.4 FF in 2 mm2 ) and a slight reduction of the capillary network compared to UIP (P = 0.07) and controls (P = 0.06). The main differences seen in UIP were the lack of IAFE and the presence of honeycomb change. CONCLUSIONS: RAS and PPFE histopathology both show IAFE, but display various differences, particularly in their vascular morphology that may allow further understanding of pathogenesis.

[Electrophysiological and clinical characterization of left atrial macroreentrant tachycardia]. / Caracterización electrofisiológica y clínica de la taquicardia macrorreentrante auricular izquierda.

BACKGROUND AND OBJECTIVE: We are reporting the characteristics of 9 patients with left atrial macroreentrant tachycardia, an arrhythmia not well studied in man. PATIENTS AND METHOD: Mean age was 60 years and 7 were men. Tachycardia was spontaneous in 6 and induced in 3. Two had no heart disease, 2 sick sinus syndrome, 3 aortic prosthesis, 2 hypertension, 1 cardiomyopathy and 1 chronic bronchitis. Simultaneous recordings from right atrial, coronary sinus and right pulmonary artery were obtained at baseline and with atrial pacing. Macroreentrant tachycardia was diagnosed when entrainment with fusion was documented. RESULTS: Cycle length was 230-440 ms (287 67). The ECG showed atypical flutter in 3 patients and P waves with flat baseline in 6. Coronary sinus activation was distal to proximal in 7. Right atrial activation was circular in 3 with previous typical flutter ablation. Entrainment from the right atrium produced long return cycles in the right atrial recordings, but equal to basal tachycardic cycle in coronary sinus recordings. Entrainment from the coronary sinus produced local return cycles equal to basal cycle in 8 and prolonged in 1. After stimulation, 4 recovered sinus rhythm, 4 went to atrial fibrillation and 1 had no change. After a follow-up of 9-19 months 5 remain in sinus rhythm treated with antiarrhythmic drugs and/or atrial pacing. CONCLUSIONS: Left atrial macroreentrant tachycardia is associated with organic heart disease. The ECG most frequent pattern tends to show P waves with flat baseline at a relatively slow rate. Most circuits turn clockwise in anterior view. Atrial stimulation is not very effective for cardioversion to sinus rhythm. The prognosis of long term rhythm is uncertain.