New thermodynamic data for CoTiO3, NiTiO3 and CoCO3 based on low-temperature calorimetric measurements

The low-temperature heat capacities of nickel titanate (NiTiO3), cobalt titanate (CoTiO3), and cobalt carbonate (CoCO3) were measured between 2 and 300 K, and thermochemical functions were derived from the results. Our new data show previously unknown low-temperature lambda-shaped heat capacity anomalies peaking at 37 K for CoTiO3 and 26 K for NiTiO3. From our data we calculate standard molar entropies (298.15 K) for NiTiO3 of 90.9 ± 0.7 J mol-1 K-1 and for CoTiO3 of 94.4 ± 0.8 J mol-1 K-1. For CoCO3, we find only a small broad heat capacity anomaly, peaking at about 31 K. From our data, we suggest a new standard entropy (298.15 K) for CoCO3 of 88.9 ± 0.7 J mol-1 K-1

Intensivtransport Neugeborener mit respiratorischem Versagen

<jats:title>Zusammenfassung</jats:title><jats:sec> <jats:title>Hintergrund und Ziel der Studie</jats:title> <jats:p>Der Transport von Früh und Neugeborenen mit respiratorischem Versagen ist mit einem hohen Transportrisiko assoziiert und stellt höchste Anforderungen an medizinisches Personal und technische Ausrüstung. Eine kontinuierliche Überprüfung der Qualität ist daher unumgänglich. Ziel dieser monozentrischen retrospektiven Analyse ist es, die Mortalität transportierter Neugeborener mit respiratorischem Versagen mithilfe eines Outcomescores, Transport Risk index of Physiologic Stability, Version II, (TRIPS-II-Score) und im Vergleich zu bereits publizierter Literatur zu analysieren.</jats:p> </jats:sec><jats:sec> <jats:title>Methodik</jats:title> <jats:p>Es wurden 79 Intensivtransporte von Früh- und Neugeborenen mit hochgradigem respiratorischem Versagen retrospektiv analysiert. Zur Einschätzung des Transportrisikos und der Transportqualität wurde der TRIPS-II-Score erhoben und mit der Literatur verglichen.</jats:p> </jats:sec><jats:sec> <jats:title>Ergebnisse</jats:title> <jats:p>Insgesamt wurden 77 Patienten luft- (<jats:italic>n</jats:italic> = 56, 73 %) oder bodengebunden (<jats:italic>n</jats:italic> = 21, 27 %) transportiert. Zwei Patienten verstarben vor dem Transport. Kein Patient verstarb während des Transports. Alle Patienten mussten invasiv beatmet werden, davon 22 (29 %) mit Hochfrequenzoszillation (HFOV) und 55 (71 %) erhielten inhalatives Stickoxid (iNO). Der mittlere Oxygenierungsindex (OI) betrug 33 [4-100, min.-max.] Insgesamt mussten 24 Patienten (31 %) nach Aufnahme einer ECMO-Therapie unterzogen werden. Insgesamt verstarben 20 (26 %) Neugeborene, 7 davon in der ECMO-Therapie-Gruppe.</jats:p> </jats:sec><jats:sec> <jats:title>Schlussfolgerung</jats:title> <jats:p>Transporte von Neugeborenen mit schwerem Lungenversagen können durch den Einsatz eines spezialisierten Teams mit Sonderequipment meist komplikationslos durchgeführt werden. Die scheinbar sehr hohe Mortalität ist mit Daten der internationalen Literatur vergleichbar.</jats:p> </jats:sec&gt

Synthesis of trace element bearing single crystals of Chlor-Apatite (Ca5(PO4)3Cl) using the flux growth method

We present a new strategy on how to synthesize trace-element bearing (REE, Sr) chlorapatites Ca5(PO4)3Cl using the flux growth method. Synthetic apatites were up to several mm long, light blue in colour. The apatites were characterized using XRD, electron microprobe and laser ablation ICP-MS (LA-ICPMS) techniques and contained several hundred μg/g La, Ce, Pr, Sm, Gd and Lu and about 1700 μg/g Sr. The analyses indicate that apatites were homogenous (within the uncertainties) for major and trace elements

Lung disease caused by ABCA3 mutations

Background Knowledge about the clinical spectrum of lung disease caused by variations in the ATP binding cassette subfamily A member 3 (ABCA3) gene is limited. Here we describe genotype-phenotype correlations in a European cohort. Methods We retrospectively analysed baseline and outcome characteristics of 40 patients with two disease-causing ABCA3 mutations collected between 2001 and 2015. Results Of 22 homozygous (15 male) and 18 compound heterozygous patients (3 male), 37 presented with neonatal respiratory distress syndrome as term babies. At follow-up, two major phenotypes are documented: patients with (1) early lethal mutations subdivided into (1a) dying within the first 6 months or (1b) before the age of 5 years, and (2) patients with prolonged survival into childhood, adolescence or adulthood. Patients with null/null mutations predicting complete ABCA3 deficiency died within the 1st weeks to months of life, while those with null/other or other/other mutations had a more variable presentation and outcome. Treatment with exogenous surfactant, systemic steroids, hydroxychloroquine and whole lung lavages had apparent but many times transient effects in individual subjects. Conclusions Overall long-term (>5 years) survival of subjects with two disease-causing ABCA3 mutations was <20%. Response to therapies needs to be ascertained in randomised controlled trials

Lung disease caused by ABCA3 mutations

Background Knowledge about the clinical spectrum of lung disease caused by variations in the ATP binding cassette subfamily A member 3 (ABCA3) gene is limited. Here we describe genotype-phenotype correlations in a European cohort. Methods We retrospectively analysed baseline and outcome characteristics of 40 patients with two disease-causing ABCA3 mutations collected between 2001 and 2015. Results Of 22 homozygous (15 male) and 18 compound heterozygous patients (3 male), 37 presented with neonatal respiratory distress syndrome as term babies. At follow-up, two major phenotypes are documented: patients with (1) early lethal mutations subdivided into (1a) dying within the first 6 months or (1b) before the age of 5 years, and (2) patients with prolonged survival into childhood, adolescence or adulthood. Patients with null/null mutations predicting complete ABCA3 deficiency died within the 1st weeks to months of life, while those with null/other or other/other mutations had a more variable presentation and outcome. Treatment with exogenous surfactant, systemic steroids, hydroxychloroquine and whole lung lavages had apparent but many times transient effects in individual subjects. Conclusions Overall long-term (>5 years) survival of subjects with two disease-causing ABCA3 mutations was <20\%. Response to therapies needs to be ascertained in randomised controlled trials