Inhomogeneity of the intrinsic magnetic field in superconducting YBa2Cu3OX compounds as revealed by rare-earth EPR-probe

X-band electron paramagnetic resonance on doped Er3+ and Yb3+ ions in Y0.99(Yb,Er)0.01Ba2Cu3OX compounds with different oxygen contents in the wide temperature range (4-120)K have been made. In the superconducting species, the strong dependencies of the linewidth and resonance line position from the sweep direction of the applied magnetic field are revealed at the temperatures significantly below TC. The possible origins of the observed hysteresis are analyzed. Applicability of the presented EPR approach to extract information about the dynamics of the flux-line lattice and critical state parameters (critical current density, magnetic penetration depth, and characteristic spatial scale of the inhomogeneity) is discussedComment: 17 pages, 5 Figures. Renewed versio

Climate trends and glacier retreat in the Cordillera Blanca, Peru, revisited

The total glacial area of the Cordillera Blanca, Peru, has shrunk by more than 30% in the period of 1930 to the present with a marked glacier retreat also in the recent decades. The aim of this paper is to assess local air temperature and precipitation changes in the Cordillera Blanca and to discuss how these variables could have affected the observed glacier retreat between the 1980s and present. A unique data set from a large number of stations in the region of the Cordillera Blanca shows that after a strong air temperature rise of about 0.31 °C per decade between 1969 and 1998, a slowdown in the warming to about 0.13 °C per decade occurred for the 30 years from 1983 to 2012. Additionally, based on data from a long-term meteorological station, it was found that the freezing line altitude during precipitation days has probably not increased significantly in the last 30 years. We documented a cooling trend for maximum daily air temperatures and an increase in precipitation of about 60 mm/decade since the early 1980s. The strong increase in precipitation in the last 30 years probably did not balance the increase of temperature before the 1980s. It is suggested that recent changes in temperature and precipitation alone may not explain the glacial recession within the thirty years from the early 1980s to 2012. Glaciers in the Cordillera Blanca may be still reacting to the positive air temperature rise before 1980. Especially small and low-lying glaciers are characterised by a serious imbalance and may disappear in the near future

Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice

Galanin is a neuropeptide with a wide distribution in the central and peripheral nervous systems and whose physiological effects are mediated through three G protein-coupled receptor subtypes, GalR1, GalR2, and GalR3. Several lines of evidence indicate that galanin, as well as activation of the GalR1 receptor, is a potent and effective modulator of neuronal excitability in the hippocampus.In order to test more formally the potential influence of GalR1 on seizure-induced excitotoxic cell death, we conducted functional complementation tests in which transgenic mice that exhibit decreased expression of the GalR1 candidate mRNA underwent kainate-induced status epilepticus to determine if the quantitative trait of susceptibility to seizure-induced cell death is determined by the activity of GalR1. In the present study, we report that reduction of GalR1 mRNA via null mutation or injection of the GalR1 antagonist, galantide, prior to kainate-induced status epilepticus induces hippocampal damage in a mouse strain known to be highly resistant to kainate-induced neuronal injury. Wild-type and GalR1 knockout mice were subjected to systemic kainate administration. Seven days later, Nissl and NeuN immune- staining demonstrated that hippocampal cell death was significantly increased in GalR1 knockout strains and in animals injected with the GalR1 antagonist. Compared to GalR1-expressing mice, GalR1-deficient mice had significantly larger hippocampal lesions after status epilepticus.Our results suggest that a reduction of GalR1 expression in the C57BL/6J mouse strain renders them susceptible to excitotoxic injury following systemic kainate administration. From these results, GalR1 protein emerges as a new molecular target that may have a potential therapeutic value in modulating seizure-induced cell death

Different Human Copper-Zinc Superoxide Dismutase Mutants, SOD1G93A and SOD1H46R, Exert Distinct Harmful Effects on Gross Phenotype in Mice

Amyotrophic lateral sclerosis (ALS) is a heterogeneous group of fatal neurodegenerative diseases characterized by a selective loss of motor neurons in the brain and spinal cord. Creation of transgenic mice expressing mutant Cu/Zn superoxide dismutase (SOD1), as ALS models, has made an enormous impact on progress of the ALS studies. Recently, it has been recognized that genetic background and gender affect many physiological and pathological phenotypes. However, no systematic studies focusing on such effects using ALS models other than SOD1G93A mice have been conducted. To clarify the effects of genetic background and gender on gross phenotypes among different ALS models, we here conducted a comparative analysis of growth curves and lifespans using congenic lines of SOD1G93A and SOD1H46R mice on two different genetic backgrounds; C57BL/6N (B6) and FVB/N (FVB). Copy number of the transgene and their expression between SOD1G93A and SOD1H46R lines were comparable. B6 congenic mutant SOD1 transgenic lines irrespective of their mutation and gender differences lived longer than corresponding FVB lines. Notably, the G93A mutation caused severer disease phenotypes than did the H46R mutation, where SOD1G93A mice, particularly on a FVB background, showed more extensive body weight loss and earlier death. Gender effect on survival also solely emerged in FVB congenic SOD1G93A mice. Conversely, consistent with our previous study using B6 lines, lack of Als2, a murine homolog for the recessive juvenile ALS causative gene, in FVB congenic SOD1H46R, but not SOD1G93A, mice resulted in an earlier death, implying a genetic background-independent but mutation-dependent phenotypic modification. These results indicate that SOD1G93A- and SOD1H46R-mediated toxicity and their associated pathogenic pathways are not identical. Further, distinctive injurious effects resulted from different SOD1 mutations, which are associated with genetic background and/or gender, suggests the presence of several genetic modifiers of disease expression in the mouse genome

Recurrence of Diabetic Pedal Ulcerations Following Tendo-Achilles Lengthening

Foot and ankle surgeons are frequently challenged by the devastating systemic consequences of diabetes mellitus manifested through neuropathy, integumentary and joint breakdown, delayed healing, decreased ability to fight infection, and fragile tendon/ligaments. Diabetic neuropathic pedal ulcerations lead to amputations at an alarming rate and also carry a high mortality rate. This article will discuss causes of diabetic pedal ulcerations that persist or recur after tendo-Achilles lengthening and will highlight areas that need to be addressed by the practitioner such as infection, vascular and nutritional status, glucose control, off-loading, biomechanics, and patient compliance

Snow and ice in the desert: reflections from a decade of connecting cryospheric science with communities in the semiarid Chilean Andes

Citizen science and related engagement programmes have proliferated in recent years throughout the sciences but have been reasonably limited in the cryospheric sciences. In the semiarid Andes we at the Centro de Estudios Avanzados en Zonas Áridas have developed a range of initiatives together with the wider community and stakeholder institutions to improve our understanding of the role snow and ice play in headwater catchments. In this paper we reflect on ongoing engagement with communities living and working in and near study sites of cryospheric science in northern Chile as a strategy that can both strengthen the research being done and empower local communities

Outcome of experimental stroke in C57Bl/6 and Sv/129 mice assessed by multimodal ultra-high field MRI

Transgenic mice bred on C57Bl/6 or Sv/129 genetic background are frequently used in stroke research. It is well established that variations in cerebrovascular anatomy and hemodynamics can influence stroke outcome in different inbred mouse lines. We compared stroke development in C57Bl/6 and Sv/129 mice in the widely used model of transient middle cerebral artery occlusion (tMCAO) by multimodal ultra-high field magnetic resonance imaging (MRI)

MicroRNA-34a upregulation during seizure-induced neuronal death

MicroRNAs (miRNAs) are short, noncoding RNAs that function as posttranscriptional regulators of gene expression by controlling translation of mRNAs. A subset of miRNAs may be critical for the control of cell death, including the p53-regulated miRNA, miR-34a. Because seizures activate p53, and p53-deficient mice are reportedly resistant to damage caused by prolonged seizures, we investigated the role of miR-34a in seizure-induced neuronal death in vivo. Status epilepticus was induced by intra-amygdala microinjection of kainic acid in mice. This led to an early (2 h) multifold upregulation of miR-34a in the CA3 and CA1 hippocampal subfields and lower protein levels of mitogen-activated kinase kinase kinase 9, a validated miR-34a target. Immunoprecipitation of the RNA-induced silencing complex component, Argonaute-2, eluted significantly higher levels of miR-34a after seizures. Injection of mice with pifithrin-α, a putative p53 inhibitor, prevented miR-34a upregulation after seizures. Intracerebroventricular injection of antagomirs targeting miR-34a reduced hippocampal miR-34a levels and had a small modulatory effect on apoptosis-associated signaling, but did not prevent hippocampal neuronal death in models of either severe or moderate severity status epilepticus. Thus, prolonged seizures cause subfield-specific, temporally restricted upregulation of miR-34a, which may be p53 dependent, but miR-34a is probably not important for seizure-induced neuronal death in this model