Ferromagnetism or slow paramagnetic relaxation in Fe-doped Li3_3N?

We report on isothermal magnetization, M\"ossbauer spectroscopy, and magnetostriction as well as temperature-dependent alternating-current (ac) susceptibility, specific heat, and thermal expansion of single crystalline and polycrstalline Li$_2$(Li$_{1-x}$Fe$_x$)N with $x = 0$ and $x \approx 0.30$. Magnetic hysteresis emerges at temperatures below $T \approx 50\,$K with coercivity fields of up to $\mu_0H = 11.6\,$T at $T = 2\,$K and magnetic anisotropy energies of $310\,$K ($27\,$meV). The ac susceptibility is strongly frequency dependent ($f\,=\,10$--$10,000\,$Hz) and reveals an effective energy barrier for spin reversal of $\Delta E \approx 1100\,$K. The relaxation times follow Arrhenius behavior for $T > 25\,$K. For $T < 10\,$K, however, the relaxation times of $\tau \approx 10^{10}\,$s are only weakly temperature-dependent indicating the relevance of a quantum tunneling process instead of thermal excitations. The magnetic entropy amounts to more than $25\,$J mol$^{-1}_{\rm Fe}\,$K$^{-1}$ which significantly exceeds $R$ln2, the value expected for the entropy of a ground state doublet. Thermal expansion and magnetostriction indicate a weak magneto-elastic coupling in accordance with slow relaxation of the magnetization. The classification of Li$_2$(Li$_{1-x}$Fe$_x$)N as ferromagnet is stressed and contrasted with highly anisotropic and slowly relaxing paramagnetic behavior.Comment: 12 pages, 10 figure

Change in Terrestrial Human Footprint Drives Continued Loss of Intact Ecosystems

Human pressure mapping is important for understanding humanity's role in shaping Earth's patterns and processes. We provide the latest maps of the terrestrial human footprint and provide an assessment of change in human pressure across Earth. Between 2000 and 2013, 1.9 million km2 of land relatively free of human disturbance became highly modified. Our results show that humanity's footprint is eroding Earth's last intact ecosystems and that greater efforts are urgently needed to retain them

Modification of forests by people means only 40% of remaining forests have high ecosystem integrity

Many global environmental agendas, including halting biodiversity loss, reversing land degradation, and limiting climate change, depend upon retaining forests with high ecological integrity, yet the scale and degree of forest modification remain poorly quantified and mapped. By integrating data on observed and inferred human pressures and an index of lost connectivity, we generate a globally consistent, continuous index of forest condition as determined by the degree of anthropogenic modification. Globally, only 17.4 million km2 of forest (40.5%) has high landscape-level integrity (mostly found in Canada, Russia, the Amazon, Central Africa, and New Guinea) and only 27% of this area is found in nationally designated protected areas. Of the forest inside protected areas, only 56% has high landscape-level integrity. Ambitious policies that prioritize the retention of forest integrity, especially in the most intact areas, are now urgently needed alongside current efforts aimed at halting deforestation and restoring the integrity of forests globally

Life-threatening hypersensitivity pneumonitis induced by docetaxel (taxotere)

4 patients with advanced non-small-cell lung cancer (NSCLC) treated with docetaxel developed life-threatening pneumonitis requiring mechanical ventilation. Docetaxel (30–60 mg m−2, according to a different protocol) was infused within one hour with standard premedications. One patient's pneumonitis occurred 5 days after the first dose of docetaxel, and that of the other 3 between the 2nd and 6th cycles. Based on the clinical course, radiological findings of an interstitial pneumonitis, and exclusion of other possible resultant causes, including metastatic cancer, radiation pulmonary injury, infection, or connective tissue disease, hypersensitivity pneumonitis was diagnosed. The patients were treated with hydrocortisone at 1200 mg per day or methylprednisolone at 240 mg per day. Although 3 of the 4 had a partial improvement in lung oxygenation, all patients’ conditions of hypersensitivity pneumonitis persisted and were complicated by other events, such as hospital-acquired infection and tension pneumothorax. The presence of this unusual hypersensitivity pneumonitis, which was so severe as to be life-threatening and refractory to high-dose corticosteroid therapy, should be taken into account during docetaxel treatment. © 2001 Cancer Research Campaig

Strategy implementation: what is the failure rate?

It is often claimed that 50–90% of strategic initiatives fail. Although these claims have had a significant impact on management theory and practice, they are controversial. We aim to clarify why this is the case. Towards this end, an extensive review of the literature is presented, assessed, compared and discussed. We conclude that while it is widely acknowledged that the implementation of a new strategy can be a difficult task, the true rate of implementation failure remains to be determined. Most of the estimates presented in the literature are based on evidence that is outdated, fragmentary, fragile or just absent. Careful consideration is advised before using current estimates to justify changes in the theory and practice. A set of guiding principles is presented for assisting researchers to produce better estimates of the rates of failure

Challenges in Whole Exome Sequencing: An Example from Hereditary Deafness

Whole exome sequencing provides unprecedented opportunities to identify causative DNA variants in rare Mendelian disorders. Finding the responsible mutation via traditional methods in families with hearing loss is difficult due to a high degree of genetic heterogeneity. In this study we combined autozygosity mapping and whole exome sequencing in a family with 3 affected children having nonsyndromic hearing loss born to consanguineous parents. Two novel missense homozygous variants, c.508C>A (p.H170N) in GIPC3 and c.1328C>T (p.T443M) in ZNF57, were identified in the same ∼6 Mb autozygous region on chromosome 19 in affected members of the family. Both variants co-segregated with the phenotype and were absent in 335 ethnicity-matched controls. Biallelic GIPC3 mutations have recently been reported to cause autosomal recessive nonsyndromic sensorineural hearing loss. Thus we conclude that the hearing loss in the family described in this report is caused by a novel missense mutation in GIPC3. Identified variant in GIPC3 had a low read depth, which was initially filtered out during the analysis leaving ZNF57 as the only potential causative gene. This study highlights some of the challenges in the analyses of whole exome data in the bid to establish the true causative variant in Mendelian disease

Differentiation and Recruitment of Th9 Cells Stimulated by Pleural Mesothelial Cells in Human Mycobacterium tuberculosis Infection

Newly discovered IL-9–producing CD4+ helper T cells (Th9 cells) have been reported to contribute to tissue inflammation and immune responses, however, differentiation and immune regulation of Th9 cells in tuberculosis remain unknown. In the present study, our data showed that increased Th9 cells with the phenotype of effector memory cells were found to be in tuberculous pleural effusion as compared with blood. TGF-β was essential for Th9 cell differentiation from naïve CD4+ T cells stimulated with PMA and ionomycin in vitro for 5 h, and addition of IL-1β, IL-4 or IL-6 further augmented Th9 cell differentiation. Tuberculous pleural effusion and supernatants of cultured pleural mesothelial cells were chemotactic for Th9 cells, and this activity was partly blocked by anti-CCL20 antibody. IL-9 promoted the pleural mesothelial cell repairing and inhibited IFN-γ-induced pleural mesothelial cell apoptosis. Moreover, pleural mesothelial cells promoted Th9 cell differentiation by presenting antigen. Collectively, these data provide new information concerning Th9 cells, in particular the collaborative immune regulation between Th9 cells and pleural mesothelial cells in human M. tuberculosis infection. In particular, pleural mesothelial cells were able to function as antigen-presenting cells to stimulate Th9 cell differentiation