In this article, we present results on the identification and behavioral analysis of social bots in a sample of 542,584 Tweets, collected before and after Japan's 2014 general election. Typical forms of bot activity include massive Retweeting and repeated posting of (nearly) the same message, sometimes used in combination. We focus on the second method and present (1) a case study on several patterns of bot activity, (2) methodological considerations on the automatic identification of such patterns and the prerequisite near-duplicate detection, and (3) we give qualitative insights into the purposes behind the usage of social/political bots. We argue that it was in the latency of the semi-public sphere of social media—and not in the visible or manifest public sphere (official campaign platform, mass media)—where Shinzō Abe's hidden nationalist agenda interlocked and overlapped with the one propagated by organizations such as Nippon Kaigi and Internet right-wingers (netto uyo) during the election campaign, the latter potentially forming an enormous online support army of Abe's agenda.

Human jaw periosteum-derived cells (JPCs) represent an alternative cell source to bone marrow-derived mesenchymal stem cells for tissue engineering applications in the oral and maxillofacial surgery. In this study we investigated how far the presence or expression of human mesenchymal stem cell antigen-1/tissue non-specific alkaline phosphatase (MSCA-1/TNAP) and LNGFR (CD271) can be utilized to select and enrich the osteogenic progenitor cell fraction from the entire JPC population. Depending on their mineralization capacity, we classified the human isolated JPCs into mineralizing (mJPCs) and non-mineralizing JPCs (nmJPCs). Flow cytometric analyses revealed that undifferentiated mJPCs expressed MSCA-1/TNAP at significant higher levels than nmJPCs at day 5 and 10 of osteogenesis. Western blot analyses showed increased MSCA-1/TNAP expression levels in mJPCs during osteogenesis, whereas in nmJPCs MSCA-1/TNAP expression remained undetectable. Using the MSCA-1 and LNGFR specific antibodies, we separated the positive and negative fractions from the entire mJPC population. In order to analyse the mineralization capacity of the MSCA-1⁺ and LNGFR⁺ cell subsets, we quantified the calcium deposition in both subpopulations in comparison to the respective negative subpopulations. The MSCA-1⁺/TNAP⁺ cell fraction showed a significant higher osteogenic capacity compared to the MSCA-1-/TNAP- cell fraction whereas the LNGFR^+/- cell fractions did not differ in their osteogenic potential. Our findings suggest that MSCA-1 may represent a promising osteogenic marker for mJPC.

Isolated jaw periosteum-derived cells (JPCs) comprise a morphologically heterogeneous population. There are no known specific surface markers that are able to distinguish between progenitors and cells of other tissue types. The aim of our study was to identify differentiation markers as predictors of JPC mineralization capacity. JPCs underwent osteogenic differentiation after cultivation in osteogenic medium containing known activators. By FACS analysis, we found the low affinity nerve growth factor receptor (LNGFR–CD271) to be induced during the first five days of osteogenesis and that it was expressed at higher levels in mineralizing JPCs (mJPCs) in comparison to non-mineralizing JPCs (nmJPCs). Similar results were obtained by semi-quantitative immunohistochemical stainings and western blot analyses. Quantitative real-time PCR results showed significantly higher LNGFR and alkaline phosphatase transcript levels in mJPCs compared to nmJPCs. LNGFR is a differentiation marker that distinguishes between mineralizing JPCs and non-mineralizing JPCs during the first phase of osteogenesis and can therefore be considered an early surface marker of osteogenic capacity in vitro.

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Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and a post hoc analysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney. In vitro, murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550, https://clinicaltrials.gov/ct2/show/NCT02682550). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically, in vitro data suggested that IL-6 rather than C3 cleavage products