Description: This study investigates the behaviour of molybdenum (Mo) isotopes during magmatic differentiation. Molybdenum isotope compositions, as well as concentrations of rare earth elements and a selection of trace elements, have been determined for a well characterised sequence of lavas from Hekla volcano, Iceland, covering a compositional range from basalt to rhyolite (46-72wt.% SiO2), and thought to have developed by differentiation and mixing of melts derived from a cogenetic source. All samples have identical Mo isotopic compositions with an average δ98Mo of -0.15±0.05‰ (2 s.d.; n=23). There is therefore no resolvable Mo isotope fractionation during magmatic differentiation at Hekla. This finding is supported by the fact that Mo remains highly incompatible in Hekla lavas, increasing from 1.3 to 4.6μg/g from basalt to rhyolite, indicating that the crystallising phases are extracting only limited amounts of Mo from the magma and therefore that significant fractionation of Mo isotopes is unlikely. It has previously been proposed that cerium (Ce) and Mo have similar bulk distribution coefficients and are equally incompatible during mantle melting. While both Ce and Mo remain incompatible in Hekla lavas, the Ce/Mo ratio decreases from 50 to 36 during magmatic differentiation indicating that Mo is more incompatible than Ce. Comparison of Mo with other incompatible trace elements indicates that Mo is as incompatible as La and slightly less incompatible than K. Sulphur (S) decreases strongly from ~200 to as low as ~2μg/g from basalt to andesite and more evolved compositions, yet this has no effect on the Mo isotopes. Therefore, Mo does not exhibit significant chalcophile behaviour in Hekla magmas. The Mo isotopic signature therefore may be used as an indicator of parent magma composition and a potential discriminant of assimilation processes.

Description: Major depression is an important clinical factor in ventricular arrhythmia. Patients diagnosed with major depression overexpress N -methyl- d -aspartate receptors (NMDARs). Previous studies found that chronic NMDAR activation increases susceptibility to ventricular arrhythmias. We aimed to explore the mechanisms by which NMDAR activation may increase susceptibility to ventricular arrhythmias. Male rats were randomly assigned to either normal environments as control (CTL) group or 4 wk of chronic mild stress (CMS) to produce a major depression disorder (MDD) model group. After 4 wk of CMS, depression-like behaviors were measured in both groups. Varying doses (1–100 μM) of NMDA and 10 μM NMDA antagonist (MK-801) were perfused through ventricular myocytes isolated from MDD rats to measure the L-type calcium current ( I Ca-L ) and transient outward potassium current ( I to ). Structural remodeling was assessed using serial histopathology including Masson’s trichrome dye. Electrophysiological characteristics were evaluated using Langendorff perfusion. Depression-like behaviors were observed in MDD rats. MDD rats showed longer action potential durations at 90% repolarization and higher susceptibility to ventricular arrhythmias than CTL rats. MDD rats showed lower I Ca-L and I to current densities than CTL rats. Additionally, NMDA reduced both currents in a concentration-dependent manner, whereas there was no significant impact on the currents when perfused with MK-801. MDD rats exhibited significantly more fibrosis areas in heart tissue and reduced expression of Kv4.2, Kv4.3, and Cav1.2. We observed that acute NMDAR activation led to downregulation of potassium and L-type calcium currents in a rat model of depression, which may be the mechanism underlying ventricular arrhythmia promotion by depression.

Description: The alveolar epithelium is composed of type I cells covering most of the gas-blood exchange surface and type II cells secreting surfactant that lowers surface tension of alveoli to prevent alveolar collapse. Here, we have identified a subgroup of type II cells expressing a higher level of cell surface molecule CD44 (CD44 high type II cells) that composed ~3% of total type II cells in 5–10-wk-old mice. These cells were preferentially apposed to lung capillaries. They displayed a higher proliferation rate and augmented differentiation capacity into type I cells and the ability to form alveolar organoids compared with CD44 low type II cells. Moreover, in aged mice, 18–24 mo old, the percentage of CD44 high type II cells among all type II cells was increased, but these cells showed decreased progenitor properties. Thus CD44 high type II cells likely represent a type II cell subpopulation important for constitutive regulation of alveolar homeostasis.