Magnetic excitations and anomalous spin wave broadening in multiferroic FeV2O4

We report on the different roles of two orbital-active Fe$^{2+}$ at the A site and V$^{3+}$ at the B site in the magnetic excitations and on the anomalous spin wave broadening in FeV$_{2}$O$_{4}$. FeV$_{2}$O$_{4}$ exhibits three structural transitions and successive paramagnetic (PM)-collinear ferrimagnetic (CFI)-noncollinear ferrimagnetic (NCFI) transitions. The high-temperature tetragonal/PM -orthorhombic/CFI transition is accompanied by the appearance of an energy gap with a high magnitude in the magnetic excitations due to strong spin-orbit coupling induced anisotropy at the Fe$^{2+}$ site. While there is no measurable increase in the energy gap from the orbital ordering of V$^{3+}$ at the orthorhombic/CFI-tetragonal/NCFI transition, anomalous spin wave broadening is observed in the orthorhombic/CFI state due to V$^{3+}$ spin fluctuations at the B site. The spin wave broadening is also observed at the zone boundary without softening, which is discussed in terms of magnon-phonon coupling.Comment: 4 pages, 3 figures, including one supplemental materia

Two-dimensional magnetic interactions in LaFeAsO

Inelastic neutron scattering measurements demonstrate that the magnetic interactions in antiferromagnetic LaFeAsO are two dimensional. Spin-wave velocities within the Fe layer and the magnitude of the spin gap are similar to the AFe2As2 based materials. However, the ratio of interlayer and intralayer exchange is found to be less than ∼10−4 in LaFeAsO, very similar to the cuprates, and ∼100 times smaller than that found in AFe2As2 compounds. The results suggest that the effective dimensionality of the magnetic system is highly variable in the parent compounds of the iron arsenides and weak three-dimensional interactions may limit the maximum attainable superconducting Tc

Epidemiology of intra-abdominal infection and sepsis in critically ill patients: “AbSeS”, a multinational observational cohort study and ESICM Trials Group Project

Purpose: To describe the epidemiology of intra-abdominal infection in an international cohort of ICU patients according to a new system that classifies cases according to setting of infection acquisition (community-acquired, early onset hospital-acquired, and late-onset hospital-acquired), anatomical disruption (absent or present with localized or diffuse peritonitis), and severity of disease expression (infection, sepsis, and septic shock). Methods: We performed a multicenter (n = 309), observational, epidemiological study including adult ICU patients diagnosed with intra-abdominal infection. Risk factors for mortality were assessed by logistic regression analysis. Results: The cohort included 2621 patients. Setting of infection acquisition was community-acquired in 31.6%, early onset hospital-acquired in 25%, and late-onset hospital-acquired in 43.4% of patients. Overall prevalence of antimicrobial resistance was 26.3% and difficult-to-treat resistant Gram-negative bacteria 4.3%, with great variation according to geographic region. No difference in prevalence of antimicrobial resistance was observed according to setting of infection acquisition. Overall mortality was 29.1%. Independent risk factors for mortality included late-onset hospital-acquired infection, diffuse peritonitis, sepsis, septic shock, older age, malnutrition, liver failure, congestive heart failure, antimicrobial resistance (either methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, extended-spectrum beta-lactamase-producing Gram-negative bacteria, or carbapenem-resistant Gram-negative bacteria) and source control failure evidenced by either the need for surgical revision or persistent inflammation. Conclusion: This multinational, heterogeneous cohort of ICU patients with intra-abdominal infection revealed that setting of infection acquisition, anatomical disruption, and severity of disease expression are disease-specific phenotypic characteristics associated with outcome, irrespective of the type of infection. Antimicrobial resistance is equally common in community-acquired as in hospital-acquired infection

Messgerät und Verfahren zum Betimmen einer maximalen Inhalationsleistung einer Person

Es wird ein Messgerät zum Bestimmen einer maximalen Inhalationsleistung einer Person, insbesondere für die Auswahl eines für die Person geeigneten Trockenpulverinhalationsgerätes, offenbart mit - einem Adapterstück (2) zum strömungstechnischen Koppeln des Messgerätes mit dem Atemsystem der Person, - einem mit dem Adapterstück (2) verbundenen, zu einer Atemluftquelle offenen Strömungskanal (11), und - einem in dem Strömungskanal (11) angeordneten Strömungswiderstand (4). Dieses Messgerät zeichnet sich erfindungsgemäß aus durch einen in dem Strömungskanal (11) zwischen dem Adapterstück (2) und dem Strömungswiderstand angeordneten Druckmesser (10) zum Bestimmen eines bei einem Inspirationsvorgang der Person in dem Strömungskanal (11) erzeugten Unterdruckes. Mit einem solchen Messgerät kann das Atemvermögen einer Person (insbesondere eines Patienten in der Trockenpulverinhalation) einfach, kostengünstig und zuverlässig bestimmt bzw. klassifiziert werden. Weiterhin wird ein Verfahren zum Bestimmen einer maximalen Inhalationsleistung einer Person beschrieben

Rational Roots of Sympathetic Overactivity by Neurogenic Pulmonary Edema Modeling Arising from Sympathyco-Vagal Imbalance in Subarachnoid Hemorrhage: An Experimental Study

Kanat, Ayhan/0000-0002-8189-2877WOS: 000384160300063PubMed: 27132179BACKGROUND: Autonomous innervations of the lungs are maintained by cervical sympathetic and vagal nerves. Sympathetic overactivity-induced neurogenic pulmonary edema (NPE) is known as a serious complication of subarachnoid hemorrhage, but the rational neuronal mechanism of that overactivity has not yet been clarified fully. the aim of this study was to examine whether there is a relationship between vagal nerve ischemia related sympathetic overactivity and neurogenic pulmonary edema in subarachnoid hemorrhage. METHODS: This study was conducted on 27 rabbits. A control group was formed of 5 animals, a sham group of 7 to which saline was administered, and a study group of 15 animals that were injected with homologous arterial blood into the cisterna magna. Electrocardiography and respiratory rhythm parameters were monitored for 3 weeks and the animals were then decapitated. Statistical analysis was made of the numbers of degenerated axons in the pulmonary branches of the vagal nerves, the neuron density of stellate ganglions and the vasospasm index of the pulmonary arteries. RESULTS: in the control group, the normal respiration rate was 34 +/- 6 bpm, total axon number was 1600 +/- 270/mm(2), degenerated axon number was 10 +/- 3/mm(2), and vasospasm index was 1.34 +/- 0.25. the sham group values were 30 +/- 3 bpm, 163 +/- 47/mm(2), and 1.95 +/- 0.45 and the study group values were 45 +/- 8 bpm, 530 +/- 92/mm(2), and 2.76 +/- 0.83. the mean stellate ganglion neuron density was evaluated as 8.112 +/- 1.230/mm(3) in all animals, as 7.420 +/- 4.10/mm(3) in animals with slight NPE, and as 12.512 +/- 1.236/mm(3) in animals that developed severe NPE. CONCLUSION: High neuron density of stellate ganglion may have important roots in sympathetic overactivity-related NPE development in subarachnoid hemorrhage

Spinal Subarachnoid Hemorrhage Induced Intractable Miotic Pupil. A Reminder of Ciliospinal Sympathetic Center Ischemia Based Miosis: An Experimental Study

AIM: To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). MATERIAL and METHODS: Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. RESULTS: The mean pupil diameter was 5180 ± 370 µm and the mean degenerated neuron density of the ciliospinal center was 4 ± 1/mm3 in animals of the control group (GI). These values were 9850 ± 610 µm, 10 ± 3/mm3 in sham (GII), and 7.010 ± 440 µm and 98 ± 21/mm3 in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. CONCLUSION: We showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH