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Der Beitrag analysiert Ungleichheitseffekte des 2007 eingeführten Elterngelds. Wir zeigen, dass die familienpolitische Einführung der Ressource Elterngeld die Einkommensungleichheiten der Produktions- bzw. Erwerbssphäre auf die Reproduktions- bzw. Familiensphäre übertragen hat. Das Elterngeld trägt damit aber zumindest bislang nicht (wie angedacht) zur Aufhebung der asymmetrischen Aufteilung von (entlohnter) Erwerbsarbeit und (nicht-entlohnter) Sorgearbeit zwischen Elternteilen bei. Stattdessen verdeutlicht unsere räumlich orientierte Untersuchung des Elterngeldbezugs ungleiche Muster in den Bewältigungsmöglichkeiten kinderbezogener Sorgearbeiten. Die an der ungleichen Geographie des Elterngelds deutlich werdende Ausdifferenzierung von Bearbeitungschancen von Elternschaft interpretieren wir als Ausdruck von sozialen Spaltungstendenzen auf dem Gebiet der Reproduktion, die von der familienpolitischen Einführung des Elterngelds forciert worden sind.
Carcinogenesis is a multistep process. Besides somatic mutations in tumor cells, stroma-associated immunity is a major regulator of tumor growth. Tumor cells produce and secrete diverse mediators to create a local microenvironment that supports their own survival and growth. It is becoming apparent that iron acquisition, storage, and release in tumor cells is different from healthy counterparts. It is also appreciated that macrophages in the tumor microenvironment acquire a tumor-supportive, anti-inflammatory phenotype that promotes tumor cell proliferation, angiogenesis, and metastasis. Apparently, this behavior is attributed, at least in part, to the ability of macrophages to support tumor cells with iron. Polarization of macrophages by apoptotic tumor cells shifts the profile of genes involved in iron metabolism from an iron sequestering to an iron-release phenotype. Iron release from macrophages is supposed to be facilitated by ferroportin. However, lipid mediators such as sphingosine-1-phosphate, released form apoptotic tumor cells, upregulate lipocalin-2 (Lcn-2) in macrophages. This protein is known to bind siderophore-complexed iron and thus, may participate in iron transport in the tumor microenvironment. We describe how macrophages handle iron in the tumor microenvironment, discuss the relevance of an iron-release macrophage phenotype for tumor progression, and propose a new role for Lcn-2 in tumor-associated macrophages.
Objective: About 2% of all pregnancies are complicated by the implantation of the zygote outside the uterine cavity and termed ectopic pregnancy. Whereas a multitude of guidelines exists and related research is constantly growing, no thorough assessment of the global research architecture has been performed yet. Hence, we aim to assess the associated scientific activities in relation to geographical and chronological developments, existing research networks and socioeconomic parameters.
Design: Retrospective, descriptive study.
Setting: On the basis of the NewQIS platform, scientometric methods were combined with novel visualising techniques such as density-equalising mapping to assess the scientific output on ectopic pregnancy. Using the Web of Science, we identified all related entries from 1900 to 2012.
Results: 8040 publications were analysed. The USA and the UK were dominating the field in regard to overall research activity (2612 and 723 publications), overall citation numbers and country-specific H-Indices (US: 80, UK: 42). Comparison to economic power of the most productive countries demonstrated that Israel invested more resources in ectopic pregnancy-related research than other nations (853.41 ectopic pregnancy-specific publications per 1000 billlion US$ gross domestic product (GDP)), followed by the UK (269.97). Relation to the GDP per capita index revealed 49.3 ectopic pregnancy-specific publications per US$1000 GDP per capita for the USA in contrast to 17.31 for the UK. Semiqualitative indices such as country-specific citation rates ranked Switzerland first (24.7 citations per ectopic pregnancy-specific publication), followed by the Scandinavian countries Finland and Sweden. Low-income countries did not exhibit significant research activities.
Conclusions: This is the first in-depth analysis of global ectopic pregnancy research since 1900. It offers unique insights into the global scientific landscape. Besides the USA and the UK, Scandinavian countries and Switzerland can also be regarded as leading nations with regard to their relative socioeconomic input.
Being the most aggressive type of brain tumor, glioblastoma is estimated to be diagnosed in about 12,400 new cases in 2017. The diagnosis is dramatic to patients and relatives and leaves open many unanswered questions for them. One is the big question why there is no cure as in other tumors. This review illustrates the US and global research efforts that have been made over the past century. It demonstrates the great magnitude of energy invested by US clinicians and scientists but undoubtedly, more research is needed and funding by NIH and other sources should be continued on the same level.
The human MET receptor tyrosine kinase contributes to vertebrate development and cell proliferation. As a proto‐oncogene, it is a target in cancer therapies. MET is also relevant for bacterial infection by Listeria monocytogenes and is activated by the bacterial protein internalin B. The processes of ligand binding, receptor activation, and the diffusion behavior of MET within the plasma membrane as well as its interconnections with various cell components are not fully understood. We investigated the receptor diffusion dynamics using single‐particle tracking and imaging fluorescence correlation spectroscopy and elucidated mobility states of resting and internalin B‐bound MET. We show that internalin B‐bound MET exhibits lower diffusion coefficients and diffuses in a more confined area in the membrane. We report that the fraction of immobile receptors is larger for internalin B‐bound receptors than for resting MET. Results of single‐particle tracking in cells treated with various cytotoxins depleting cholesterol from the membrane and disrupting the actin cytoskeleton and microtubules suggest that cholesterol and actin influence MET diffusion dynamics, while microtubules do not have any effect.
The description of quantized collective excitations stands as a landmark in the quantum theory of condensed matter. A prominent example occurs in conventional magnets, which support bosonic magnons—quantized harmonic fluctuations of the ordered spins. In striking contrast is the recent discovery that strongly spin-orbital-coupled magnets, such as α-RuCl3, may display a broad excitation continuum inconsistent with conventional magnons. Due to incomplete knowledge of the underlying interactions unraveling the nature of this continuum remains challenging. The most discussed explanation refers to a coherent continuum of fractional excitations analogous to the celebrated Kitaev spin liquid. Here, we present a more general scenario. We propose that the observed continuum represents incoherent excitations originating from strong magnetic anharmonicity that naturally occurs in such materials. This scenario fully explains the observed inelastic magnetic response of α-RuCl3 and reveals the presence of nontrivial excitations in such materials extending well beyond the Kitaev state.
Cytokine regulation of high-output nitric oxide (NO) derived from inducible NO synthase (iNOS) is critically involved in inflammation biology and host defense. Herein, we set out to characterize the role of type I interferon (IFN) as potential regulator of hepatic iNOS in vitro and in vivo. In this regard, we identified in murine Hepa1-6 hepatoma cells a potent synergism between pro-inflammatory interleukin-β/tumor necrosis factor-α and immunoregulatory IFNβ as detected by analysis of iNOS expression and nitrite release. Upregulation of iNOS by IFNβ coincided with enhanced binding of signal transducer and activator of transcription-1 to a regulatory region at the murine iNOS promoter known to support target gene expression in response to this signaling pathway. Synergistic iNOS induction under the influence of IFNβ was confirmed in alternate murine Hepa56.1D hepatoma cells and primary hepatocytes. To assess iNOS regulation by type I IFN in vivo, murine acetaminophen (APAP)-induced sterile liver inflammation was investigated. In this model of acute liver injury, excessive necroinflammation drives iNOS expression in diverse liver cell types, among others hepatocytes. Herein, we demonstrate impaired iNOS expression in type I IFN receptor-deficient mice which associated with diminished APAP-induced liver damage. Data presented indicate a vital role of type I IFN within the inflamed liver for fine-tuning pathological processes such as overt iNOS expression.
Background: How a dentist works, such as the patterns of movements performed daily, is also largely affected by the workstation Dental tasks are often executed in awkward body positions, thereby causing a very high degree of strain on the corresponding muscles. The objective of this study is to detect those dental tasks, during which awkward postures occur most frequently. The isolated analysis of static postures will examine the duration for which these postures are maintained during the corresponding dental, respectively non-dental, activities.
Methods: 21 (11f/10 m) dentists (age: 40.1 ± 10.4 years) participated in this study. An average dental workday was collected for every subject. To collect kinematic data of all activities, the CUELA system was used. Parallel to the kinematic examination, a detailed computer-based task analysis was conducted. Afterwards, both data sets were synchronized based on the chronological order of the postures assumed in the trunk and the head region. All tasks performed were assigned to the categories "treatment" (I), "office" (II) and "other activities" (III). The angle values of each body region (evaluation parameter) were examined and assessed corresponding to ergonomic standards. Moreover, this study placed a particular focus on static positions, which are held statically for 4 s and longer.
Results: For "treatment" (I), the entire head and trunk area is anteriorly tilted while the back is twisted to the right, in (II) and (III) the back is anteriorly tilted and twisted to the right (non-neutral position). Static positions in (I) last for 4–10s, static postures (approx. 60%) can be observed while in (II) and (III) in the back area static positions for more than 30 s are most common. Moreover, in (II) the back is twisted to the right for more than 60 s in 26.8%.
Conclusion: Awkward positions are a major part of a dentists’ work. This mainly pertains to static positions of the trunk and head in contrast to "office work." These insights facilitate the quantitative description of the dentist profession with regard to the related physical load along with the health hazards to the musculoskeletal system. Moreover, the results allow for a selective extraction of the most unfavorable static body positions that dentists assume for each of the activities performed.
The sphingolipid sphingosine-1-phosphate (S1P) emerges as an important regulator of immunity, mainly by signaling through a family of five specific G protein-coupled receptors (S1PR1–5). While S1P signaling generally has the potential to affect not only trafficking but also differentiation, activation, and survival of a diverse range of immune cells, the specific outcome depends on the S1P receptor repertoire expressed on a given cell. Among the S1PRs, S1PR4 is specifically abundant in immune cells, suggesting a major role of the S1P/S1PR4 axis in immunity. Recent studies indeed highlight its role in activation of immune cells, differentiation, and, potentially, trafficking. In this review, we summarize the emerging data that support a major role of S1PR4 in modulating immunity in humans and mice and discuss therapeutic implications.
S1P provokes tumor lymphangiogenesis via macrophage-derived mediators such as IL-1β or lipocalin-2
(2017)
A pleiotropic signaling lipid, sphingosine-1-phosphate (S1P), has been implicated in various pathophysiological processes supporting tumor growth and metastasis. However, there are only a few descriptive studies suggesting a role of S1P in tumor lymphangiogenesis, which is critical for tumor growth and dissemination. Corroborating own data, the literature suggests that apoptotic tumor cell-derived S1P alters the phenotype of tumor-associated macrophages (TAMs) to gain protumor functions. However, mechanistically, the role of TAM-induced lymphangiogenesis has only been poorly described, mostly linked to the production of lymphangiogenic factors such as vascular endothelial growth factor C (VEGF-C) and VEGF-D, or transdifferentiation into lymphatic endothelial cells. Recent findings highlight a rather underappreciated role of S1P in tumor lymphangiogenesis, referring to the production of interleukin-1β (IL-1β) and lipocalin-2 (LCN2) by a tumor-promoting macrophage phenotype. In this review, we aim to provide to the readers with the current understanding of the molecular mechanism how apoptotic cell-derived S1P triggers TAMs to promote lymphangiogenesis.