Exacerbations of Chronic Obstructive Pulmonary Disease (COPD): An Ecological Study in the Basque Country,Spain (2000–2011)

Chronic obstructive pulmonary disease (COPD) is a prevalent condition in adults aged ≥40 years characterized by progressive airflow limitation associated with chronic inflammatory response to noxious particles in the airways and lungs. Smoking, genetics, air pollution, nutrition and other factors may influence COPD development. Most hospitalizations and deaths for COPD are caused by its acute exacerbations, which greatly affect the health and quality of life of COPD patients and pose a high burden on health services. The aims of this project were to identify trends, geographic patterns and risk factors for COPD exacerbations, as revealed by hospitalizations and deaths, in the Basque Country, Spain, over a period of 12 years (2000–2011). Hospitalization and mortality rates for COPD were 262 and 18 per 100,000 population, respectively, with clusters around the biggest cities. Hospital mortality was 7.4%. Most hospitalized patients were male (77.4%) and accounted for 72.1% of hospital mortality. Hospitalizations decreased during the study period, except for 50–64 year-old women, peaking significantly. Using a multivariate modeling approach it was shown that hospitalizations were positively correlated with increased atmospheric concentrations of NO₂, CO, PM₁₀, and SO₂, and increased influenza incidence, but were negatively associated with increased temperatures and atmospheric O₃ concentration. COPD exacerbations decreased in the Basque Country during 2000–2011, but not among 50–64-year-old women, reflecting the high smoking prevalence among Spanish women during the 1970–1990s. The main metropolitan areas were those with the highest risk for COPD exacerbations, calling attention to the role of heavy car traffic. Influenza virus, cold temperatures, and increased atmospheric NO₂, CO, PM₁₀, and SO₂ (but decreased O₃) concentrations were identified as potential contributors to the burden of COPD exacerbations in the community. These findings are important for both the understanding of the disease process and in providing potential targets for COPD-reducing initiatives and new avenues for research.     

Multiple Coronary Artery Aneurysms of the Right Coronary Artery in Neonate with Pulmonary Atresia with Intact Ventricular Septum

Pulmonary atresia with intact ventricular septum (PA/IVS) with right ventricular‐dependent coronaries is a rare congenital cardiac anomaly. It has been associated with wide range of considerable anomalies including sinusoids, fistulae, coronary stenosis, or complete atresia. Coronary artery aneurysms in a neonate with PA/IVS have not been described. We report a case of neonate with pulmonary atresia with intact ventricular septum with giant coronary artery aneurysms.     

Early pregnancy induced expression of prostaglandin E2 receptors EP2 and EP4 in the ovine endometrium and regulated by interferon tau through multiple cell signaling pathways

Prostaglandin E2 (PGE₂) plays pleiotropic roles at fetal-maternal interface during establishment of pregnancy. The objectives of the study were to: (i) determine regulation of PGE2 receptors EP1, EP2, EP3, and EP4 in the endometrium during the estrous cycle and early pregnancy; and (ii) understand endometrial epithelial and stromal cell-specific hormonal regulation of EP2 and EP4 in sheep. Results indicate that: (i) early pregnancy induces expression of EP2 and EP4 but not EP1 and EP3 proteins in the endometrium on days 12-16 compared to that of estrous cycle; (ii) intrauterine infusion of interferon tau (IFNT) increases expression of EP2 and EP4 proteins in endometrium; and (iii) IFNT activates distinct epithelial and stromal cell-specific JAK, EGFR, ERK1/2, AKT, or JNK signaling module to regulate expression of EP2 and EP4 proteins in the ovine endometrium. Our results indicate a role for EP2 and EP4-mediated PGE₂ signaling in endometrial functions and establishment of pregnancy in ruminants.     

Crystallization Behavior and Mechanical Properties of Poly(ε-caprolactone) Reinforced with Barium Sulfate Submicron Particles

Poly(ε-caprolactone) (PCL) was mixed with submicron particles of barium sulfate to obtain biodegradable radiopaque composites. X-ray images comparing with aluminum samples show that 15 wt.% barium sulfate (BaSO₄) is sufficient to present radiopacity. Thermal studies by differential scanning calorimetry (DSC) show a statistically significant increase in PCL degree of crystallinity from 46% to 52% for 25 wt.% BaSO₄. Non-isothermal crystallization tests were performed at different cooling rates to evaluate crystallization kinetics. The nucleation effect of BaSO₄ was found to change the morphology and quantity of the primary crystals of PCL, which was also corroborated by the use of a polarized light optical microscope (PLOM). These results fit well with Avrami–Ozawa–Jeziorny model and show a secondary crystallization that contributes to an increase in crystal fraction with internal structure reorganization. The addition of barium sulfate particles in composite formulations with PCL improves stiffness but not strength for all compositions due to possible cavitation effects induced by debonding of reinforcement interphase.     

Analysis of KCNH2 and CACNA1C schizophrenia risk genes on EEG functional network modulation during an auditory odd-ball task

European Archives of Psychiatry and Clinical Neuroscience - A deficit in task-related functional connectivity modulation from electroencephalogram (EEG) has been described in schizophrenia. The use...     

Tricuspid Atresia Associated with Truncus Arteriosus versus Aortopulmonary Window: Combining Fetal and Postnatal Echocardiography to Make the Diagnosis

The coincident occurrence of tricuspid atresia and aortopulmonary window (APW) is exceedingly rare, with one previous case reported in the literature. We present a patient with tricuspid atresia, pulmonary atresia, and APW. Postnatal echocardiograms demonstrated no visible pulmonary valve, and additional defects including a bicuspid aortic valve, right aortic arch and anomalous coronary arteries raised suspicion for tricuspid atresia with persistent truncus arteriosus. However, fetal echocardiography and direct visualization of the anatomy confirmed the alternate diagnosis. The patient underwent successful palliation consisting of APW repair, atrial septectomy and a 3.5 mm modified Blalock–Taussig shunt, followed by a bidirectional cavopulmonary connection.     

Antibodies to factor XII are distinct from antibodies to prothrombin in patients with the anti-phospholipid syndrome

Patients with the anti-phospholipid syndrome (APS) have antiphospholipid antibodies (aPA) which are often targeted towards phospholipid binding proteins such as beta2-glycoprotein I and prothrombin. Antibodies to factor XII (FXIIabs) have also been identified in some patients with APS. Factor XII (FXII) is a member of the kringle family of proteins which include plasminogen and prothrombin. Antibodies to prothrombin have been associated with myocardial infarction and have been shown to cross react with plasminogen. Sixteen patients with APS and FXIIabs were investigated for the presence of antibodies to prothrombin, by enzyme linked immunosorbent assay in a calcium (Ca++) independent assay. All sixteen showed different antibody binding patterns than those observed for antibodies to FXII. Eight patients were further investigated using surface plasmon resonance (SPR) for antibody binding to covalently bound FXII and to covalently bound prothrombin in both Ca++ dependent and independent systems. Of three patients demonstrating antibody binding to FXII by SPR, none demonstrated antibody binding to prothrombin in a Ca++ independent system with one demonstrating antibody binding to prothrombin that was Ca++ dependent. Of five patients who did not bind FXII by SPR, one demonstrated antibody binding to prothrombin in a Ca++ independent system while two demonstrated antibody binding to prothrombin in a Ca++ dependent system. Antibodies to FXII in patients with APS appear to be distinct from antibodies to prothrombin.