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It has been argued in forensic science that the empirical validation of a forensic inference system or methodology should be performed by replicating the conditions of the case under investigation and using data relevant to the case. This study demonstrates that the above requirement for validation is also critical in forensic text comparison (FTC); otherwise, the trier-of-fact may be misled for their final decision. Two sets of simulated experiments are performed: one fulfilling the above validation requirement and the other overlooking it, using mismatch in topics as a case study. Likelihood ratios (LRs) are calculated via a Dirichlet-multinomial model, followed by logistic-regression calibration. The derived LRs are assessed by means of the log-likelihood-ratio cost, and they are visualized using Tippett plots. Following the experimental results, this paper also attempts to describe some of the essential research required in FTC by highlighting some central issues and challenges unique to textual evidence. Any deliberations on these issues and challenges will contribute to making a scientifically defensible and demonstrably reliable FTC available.

In Germany, forensic linguistics is regularly made use of for law enforcement purposes. Since the 1980s, it is part of a federal forensic science institute and has developed with other, more widely-known forensic sciences side by side. Its contributions are fully accepted by the German police and the courts. To illustrate the processes surrounding expert evidence in German jurisprudence, the forensic linguistic expert work on a homicide case will be outlined at its various stages, i.e. from investigation up to the confirmation of the judgement after an appeal to the Federal Court of Justice. Tracing the course of the case, general provisions (legal or otherwise) concerning each stage of law enforcement are outlined and it will be described how they apply to forensic linguistics. Special attention is paid to the role of the expert, the expert’s rights and responsibilities, and what can be learned from the feedback of court proceedings.

Lurid tales of kickbacks, slush funds and sex-for-favours at the Wolfsburg-based automaker made front pages across Germany for weeks in summer of 2005, prompting the resignations of [Klaus Volkert] and VW personnel boss Peter Hartz. \"This is a crass example of a two-tier judiciary,\" Volkert's lawyer Johann Schwenn said of the verdict. The same judge last year gave Hartz a two-year suspended sentence and fined him about half a million euros.

\"I did not concern myself with this,\" [Ferdinand Piech] told the corruption trial of VW's former works council head, Klaus Volkert, and Volkert's former management contact. \"I was at no point during my time on the executive board aware of the abuse of expenses by the works council,\" he said.

The preprophase band (PPB) is a faithful but transient predictor of the division plane in somatic cell divisions. Throughout mitosis the PPBs positional information is preserved by factors that continuously mark the division plane at the cell cortex, the cortical division zone, by their distinct spatio-temporal localization patterns. However, the mechanism maintaining these identity factors at the plasma membrane after PPB disassembly remains obscure. The pair of kinesin-12 class proteins PHRAGMOPLAST ORIENTING KINESIN1 (POK1) and POK2 are key players in division plane maintenance. Here, we show that POK1 is continuously present at the cell cortex, providing a spatial reference for the site formerly occupied by the PPB. Fluorescence recovery after photobleaching analysis combined with microtubule destabilization revealed dynamic microtubule-dependent recruitment of POK1 to the PPB during prophase, while POK1 retention at the cortical division zone in the absence of cortical microtubules appeared static. POK1 function is strictly required to maintain the division plane identity factor TANGLED (TAN) after PPB disassembly, although POK1 and TAN recruitment to the PPB occur independently during prophase. Together, our data suggest that POKs represent fundamental early anchoring components of the cortical division zone, translating and preserving the positional information of the PPB by maintaining downstream identity markers.

Increased anthropogenic inputs of nitrogen (N) to the biosphere during the last few decades have resulted in increased groundwater and surface water concentrations of N (primarily as nitrate), posing a global problem. Although measures have been implemented to reduce N inputs, they have not always led to decreasing riverine nitrate concentrations and loads. This limited response to the measures can either be caused by the accumulation of organic N in the soils (biogeochemical legacy) – or by long travel times (TTs) of inorganic N to the streams (hydrological legacy). Here, we compare atmospheric and agricultural N inputs with long-term observations (1970–2016) of riverine nitrate concentrations and loads in a central German mesoscale catchment with three nested subcatchments of increasing agricultural land use. Based on a data-driven approach, we assess jointly the N budget and the effective TTs of N through the soil and groundwater compartments. In combination with long-term trajectories of the C–Q relationships, we evaluate the potential for and the characteristics of an N legacy. We show that in the 40-year-long observation period, the catchment (270 km2) with 60 % agricultural area received an N input of 53 437 t, while it exported 6592 t, indicating an overall retention of 88 %. Removal of N by denitrification could not sufficiently explain this imbalance. Log-normal travel time distributions (TTDs) that link the N input history to the riverine export differed seasonally, with modes spanning 7–22 years and the mean TTs being systematically shorter during the high-flow season as compared to low-flow conditions. Systematic shifts in the C–Q relationships were noticed over time that could be attributed to strong changes in N inputs resulting from agricultural intensification before 1989, the break-down of East German agriculture after 1989 and the seasonal differences in TTs. A chemostatic export regime of nitrate was only found after several years of stabilized N inputs. The changes in C–Q relationships suggest a dominance of the hydrological N legacy over the biogeochemical N fixation in the soils, as we expected to observe a stronger and even increasing dampening of the riverine N concentrations after sustained high N inputs. Our analyses reveal an imbalance between N input and output, long time-lags and a lack of significant denitrification in the catchment. All these suggest that catchment management needs to address both a longer-term reduction of N inputs and shorter-term mitigation of today's high N loads. The latter may be covered by interventions triggering denitrification, such as hedgerows around agricultural fields, riparian buffers zones or constructed wetlands. Further joint analyses of N budgets and TTs covering a higher variety of catchments will provide a deeper insight into N trajectories and their controlling parameters.

Nearly nothing is known about the consequences of ultra-long-distance running on knee cartilage. In this mobile MRI field study, we analysed the biochemical effects of a 4,486 km transcontinental multistage ultra-marathon on femorotibial joint (FTJ) cartilage. Serial MRI data were acquired from 22 subjects (20 male, 18 finisher) using a 1.5 T MR scanner mounted on a 38-ton trailer, travelling with the participants of the TransEurope FootRace (TEFR) day by day over 64 stages. The statistical analyses focused on intrachondral T2* behaviour during the course of the TEFR as the main outcome variable of interest. T2* mapping (sagittal FLASH T2* weighted gradient echo) is a validated and highly accurate method for quantitative compositional cartilage analysis of specific weightbearing areas of the FTJ. T2* mapping is sensitive to changes in the equilibrium of free intrachondral water, which depends on the content and orientation of collagen and the proteoglycan content in the extracellular cartilage matrix. Within the first 1,100 km, a significant running load-induced T2* increase occurred in all joint regions: 44.0% femoral-lateral, 42.9% tibial-lateral, 34.9% femoral-medial, and 25.1% tibial-medial. Osteochondral lesions showed no relevant changes or new occurrence during the TEFR. The reasons for stopping the race were not associated with knee problems. As no further T2* elevation was found in the second half of the TEFR but a decreasing T2* trend (recovery) was observed after the 3,500 km run, we assume that no further softening of the cartilage occurs with ongoing running burden over ultra-long distances extending 4,500 km. Instead, we assume the ability of the FTJ cartilage matrix to reorganize and adapt to the load.

The application of multiple omics technologies in biomedical cohorts has the potential to reveal patient-level disease characteristics and individualized response to treatment. However, the scale and heterogeneous nature of multi-modal data makes integration and inference a non-trivial task. We developed a deep-learning-based framework, multi-omics variational autoencoders (MOVE), to integrate such data and applied it to a cohort of 789 people with newly diagnosed type 2 diabetes with deep multi-omics phenotyping from the DIRECT consortium. Using in silico perturbations, we identified drug–omics associations across the multi-modal datasets for the 20 most prevalent drugs given to people with type 2 diabetes with substantially higher sensitivity than univariate statistical tests. From these, we among others, identified novel associations between metformin and the gut microbiota as well as opposite molecular responses for the two statins, simvastatin and atorvastatin. We used the associations to quantify drug–drug similarities, assess the degree of polypharmacy and conclude that drug effects are distributed across the multi-omics modalities. Clinical multi-omics data are integrated and analyzed using a generative deep-learning model.

Intra-amniotic infection (IAI) is one major driver for preterm birth and has been demonstrated by clinical studies to exert both beneficial and injurious effects on the premature lung, possibly due to heterogeneity in the microbial type, timing, and severity of IAI. Due to the inaccessibility of the intra-amniotic cavity during pregnancies, preclinical animal models investigating pulmonary consequences of IAI are indispensable to elucidate the pathogenesis of bronchopulmonary dysplasia (BPD). It is postulated that on one hand imbalanced inflammation, orchestrated by lung immune cells such as macrophages, may impact on airway epithelium, vascular endothelium, and interstitial mesenchyme, resulting in abnormal lung development. On the other hand, excessive suppression of inflammation may as well cause pulmonary injury and a certain degree of inflammation is beneficial. So far, effective strategies to prevent and treat BPD are scarce. Therapeutic options targeting single mediators in signaling cascades and mesenchymal stromal cells (MSCs)-based therapies with global regulatory capacities have demonstrated efficacy in preclinical animal models and warrant further validation in patient populations. Ante-, peri- and postnatal exposome analysis and therapeutic investigations using multiple omics will fundamentally dissect the black box of IAI and its effect on the premature lung, contributing to precisely tailored and individualized therapies.

Infection with influenza A viruses (IAV) provokes activation of cellular defence mechanisms contributing to the innate immune and inflammatory response. In this process the cyclooxygenase-2 (COX-2) plays an important role in the induction of prostaglandin-dependent inflammation. While it has been reported that COX-2 is induced upon IAV infection, in the present study we observed a down-regulation at later stages of infection suggesting a tight regulation of COX-2 by IAV. Our data indicate the pattern-recognition receptor RIG-I as mediator of the initial IAV-induced COX-2 synthesis. Nonetheless, during on-going IAV replication substantial suppression of COX-2 mRNA and protein synthesis could be detected, accompanied by a decrease in mRNA half-life. Interestingly, COX-2 mRNA stability was not only imbalanced by IAV replication but also by stimulation of cells with viral RNA. Our results reveal tristetraprolin (TTP), which is known to bind COX-2 mRNA and promote its rapid degradation, as regulator of COX-2 expression in IAV infection. During IAV replication and viral RNA accumulation TTP mRNA synthesis was induced, resulting in reduced COX-2 levels. Accordingly, the down-regulation of TTP resulted in increased COX-2 protein expression after IAV infection. These findings indicate a novel IAV-regulated cellular mechanism, contributing to the repression of host defence and therefore facilitating viral replication.