Ethnisierung und Differenzerfahrung: Fremdheit als alltägliches und als methodologisches Problem

"Auf der Grundlage einer umfangreicheren empirischen Analyse der Erfahrungen jugendlicher Migranten und Migrantinnen haben wir zwei Arten bzw. Dimensionen alltäglicher, d.h. existentieller Fremdheit von grundsätzlicher Bedeutung unterschieden: zum einen die Erfahrungen der Ethnisierung, welche die (Fremd-) Konstruktion von Identität betreffen, die das zentrale Thema gegenwärtiger Migrationsforschung darstellt. Die andere – zumeist vernachlässigte - Dimension der Fremdheit ist diejenige der Differenzerfahrungen, welche die alltägliche Praxis habituellen Handelns, also die Habitusformation der Jugendlichen, betreffen. Insbesondere diese Differenzerfahrungen werden auf der Grundlage empirischer Belege erläutert. In einer Selbstreflexion auf unsere eigene Analyseeinstellung als Sozialforscher unterscheiden wir – mit Bezug auf die Forschungstraditionen der Mannheimschen Wissenssoziologie und der Chicagoer Schule – diese existentiellen Probleme der Fremdheit von der Fremdheit als methodischem Prinzip. Dabei wird das Zusammenspiel von Vertrautheit und Fremdheit im Verhältnis der Forschenden zu ihrem Feld methodologisch begründet." (Autorenreferat)"On base of a larger empirical research about young migrants we could differentiate two manners or dimensions of strangeness which are of principle importance: One dimension is that of experiences of ethnization which concerns the construction of social identity by others and which is the central topic of actual migration research. The other – mostly neglected – dimension concerns the experiences of difference in the everyday habitualized action, in the formation of the habitus of the young people. Especially these eyperiences of difference are explained on base of empirical evidence. In self-reflection on our own analytical stance as social researchers these existential problems of strangeness are differentiated from strangeness as a methodical principle – with references to the sociology of knowledge (Karl Mannheim) and the tradition of Chicago School. Finally the interplay between familiarity and strangeness of the researchers in relation to the field is methodologically substantiated." (author's abstract

Assessing Coral Reef Fish Population and Community Changes in Response to Marine Reserves in the Dry Tortugas, Florida, USA

The efficacy of no-take marine reserves (NTMRs) to enhance and sustain regional coral reef fisheries was assessed in Dry Tortugas, Florida, through 9 annual fishery-independent research surveys spanning 2 years before and 10 years after NTMR implementation. A probabilistic sampling design produced precise estimates of population metrics of more than 250 exploited and non-target reef fishes. During the survey period more than 8100 research dives utilizing SCUBA Nitrox were optimally allocated using stratified random sampling. The survey domain covered 326 km2, comprised of eight reef habitats in four management areas that offered different levels of resource protection: the Tortugas North Ecological Reserve (a NTMR), Dry Tortugas National Park (recreational angling only), Dry Tortugas National Park Research Natural Area (a NTMR), and southern Tortugas Bank (open to all types of fishing). Surveys detected significant changes in population occupancy, density, and abundance within management zones for a suite of exploited and non-target species. Increases in size, adult abundance, and occupancy rates were detected for many principal exploited species in protected areas, which harbored a disproportionately greater number of adult spawning fishes. In contrast, density and occupancy rates for aquaria and non-target reef fishes fluctuated above and below baseline levels in each management zone. Observed decreases in density of exploited species below baseline levels only occurred at the Tortugas Bank area open to all fishing. Our findings indicate that these NTMRs, in conjunction with traditional fishery management control strategies, are helping to build sustainable fisheries while protecting the fundamental ecological dynamics of the Florida Keys coral-reef ecosystem

Population gene introgression and high genome plasticity for the zoonotic pathogen Streptococcus agalactiae

The influence that bacterial adaptation (or niche partitioning) within species has on gene spillover and transmission among bacteria populations occupying different niches is not well understood. Streptococcus agalactiae is an important bacterial pathogen that has a taxonomically diverse host range making it an excellent model system to study these processes. Here we analyze a global set of 901 genome sequences from nine diverse host species to advance our understanding of these processes. Bayesian clustering analysis delineated twelve major populations that closely aligned with niches. Comparative genomics revealed extensive gene gain/loss among populations and a large pan-genome of 9,527 genes, which remained open and was strongly partitioned among niches. As a result, the biochemical characteristics of eleven populations were highly distinctive (significantly enriched). Positive selection was detected and biochemical characteristics of the dispensable genes under selection were enriched in ten populations. Despite the strong gene partitioning, phylogenomics detected gene spillover. In particular, tetracycline resistance (which likely evolved in the human-associated population) from humans to bovine, canines, seals, and fish, demonstrating how a gene selected in one host can ultimately be transmitted into another, and biased transmission from humans to bovines was confirmed with a Bayesian migration analysis. Our findings show high bacterial genome plasticity acting in balance with selection pressure from distinct functional requirements of niches that is associated with an extensive and highly partitioned dispensable genome, likely facilitating continued and expansive adaptation

Less invasive Achilles tendon reconstruction

<p>Abstract</p> <p>Background</p> <p>The optimal management of chronic ruptures of the Achilles tendon is surgical reconstruction. Reconstruction of the Achilles tendon using peroneus brevis has been widely reported. Classically, these procedures involve relatively long surgical wounds in a relatively hypovascular area which is susceptible to wound breakdown.</p> <p>Results</p> <p>We describe our current method of peroneus brevis reconstruction for the Achilles tendon using two para-midline incisions.</p> <p>Conclusion</p> <p>This technique allows reconstruction of the Achilles tendon using peroneus brevis preserving skin integrity over the site most prone to wound breakdown, and can be especially used to reconstruct the Achilles tendon in the presence of previous surgery.</p

Genetic architecture distinguishes systemic juvenile idiopathic arthritis from other forms of juvenile idiopathic arthritis: Clinical and therapeutic implications

Objectives Juvenile idiopathic arthritis (JIA) is a heterogeneous group of conditions unified by the presence of chronic childhood arthritis without an identifiable cause. Systemic JIA (sJIA) is a rare form of JIA characterised by systemic inflammation. sJIA is distinguished from other forms of JIA by unique clinical features and treatment responses that are similar to autoinflammatory diseases. However, approximately half of children with sJIA develop destructive, long-standing arthritis that appears similar to other forms of JIA. Using genomic approaches, we sought to gain novel insights into the pathophysiology of sJIA and its relationship with other forms of JIA. Methods We performed a genome-wide association study of 770 children with sJIA collected in nine countries by the International Childhood Arthritis Genetics Consortium. Single nucleotide polymorphisms were tested for association with sJIA. Weighted genetic risk scores were used to compare the genetic architecture of sJIA with other JIA subtypes. Results The major histocompatibility complex locus and a locus on chromosome 1 each showed association with sJIA exceeding the threshold for genome-wide significance, while 23 other novel loci were suggestive of association with sJIA. Using a combination of genetic and statistical approaches, we found no evidence of shared genetic architecture between sJIA and other common JIA subtypes. Conclusions The lack of shared genetic risk factors between sJIA and other JIA subtypes supports the hypothesis that sJIA is a unique disease process and argues for a different classification framework. Research to improve sJIA therapy should target its unique genetics and specific pathophysiological pathways

The Bowen–Conradi syndrome protein Nep1 (Emg1) has a dual role in eukaryotic ribosome biogenesis, as an essential assembly factor and in the methylation of Ψ1191 in yeast 18S rRNA

The Nep1 (Emg1) SPOUT-class methyltransferase is an essential ribosome assembly factor and the human Bowen–Conradi syndrome (BCS) is caused by a specific Nep1D86G mutation. We recently showed in vitro that Methanocaldococcus jannaschii Nep1 is a sequence-specific pseudouridine-N1-methyltransferase. Here, we show that in yeast the in vivo target site for Nep1-catalyzed methylation is located within loop 35 of the 18S rRNA that contains the unique hypermodification of U1191 to 1-methyl-3-(3-amino-3-carboxypropyl)-pseudouri-dine (m1acp3Ψ). Specific 14C-methionine labelling of 18S rRNA in yeast mutants showed that Nep1 is not required for acp-modification but suggested a function in Ψ1191 methylation. ESI MS analysis of acp-modified Ψ-nucleosides in a Δnep1-mutant showed that Nep1 catalyzes the Ψ1191 methylation in vivo. Remarkably, the restored growth of a nep1-1ts mutant upon addition of S-adenosylmethionine was even observed after preventing U1191 methylation in a Δsnr35 mutant. This strongly suggests a dual Nep1 function, as Ψ1191-methyltransferase and ribosome assembly factor. Interestingly, the Nep1 methyltransferase activity is not affected upon introduction of the BCS mutation. Instead, the mutated protein shows enhanced dimerization propensity and increased affinity for its RNA-target in vitro. Furthermore, the BCS mutation prevents nucleolar accumulation of Nep1, which could be the reason for reduced growth in yeast and the Bowen-Conradi syndrome

Expanded RNA-binding activities of mammalian Argonaute 2

Mammalian Argonaute 2 (Ago2) protein associates with microRNAs (miRNAs) or small interfering RNAs (siRNAs) forming RNA-induced silencing complexes (RISCs/miRNPs). In the present work, we characterize the RNA-binding and nucleolytic activity of recombinant mouse Ago2. Our studies show that recombinant mouse Ago2 binds efficiently to miRNAs forming active RISC. Surprisingly, we find that recombinant mouse Ago2 forms active RISC using pre-miRNAs or long unstructured single stranded RNAs as guides. Furthermore, we demonstrate that, in vivo, endogenous human Ago2 binds directly to pre-miRNAs independently of Dicer, and that Ago2:pre-miRNA complexes are found both in the cytoplasm and in the nucleus of human cells

MicroRNAs in cell proliferation, cell death, and tumorigenesis

MicroRNAs (miRNAs) are a recently discovered class of ∼18–24 nucleotide RNA molecules that negatively regulate target mRNAs. All studied multicellular eukaryotes utilise miRNAs to regulate basic cellular functions including proliferation, differentiation, and death. It is now apparent that abnormal miRNA expression is a common feature of human malignancies. In this review, we will discuss how miRNAs influence tumorigenesis by acting as oncogenes and tumour suppressors

The DEAH-box RNA helicase RHAU binds an intramolecular RNA G-quadruplex in TERC and associates with telomerase holoenzyme

Guanine-quadruplexes (G4) consist of non-canonical four-stranded helical arrangements of guanine-rich nucleic acid sequences. The bulky and thermodynamically stable features of G4 structures have been shown in many respects to affect normal nucleic acid metabolism. In vivo conversion of G4 structures to single-stranded nucleic acid requires specialized proteins with G4 destabilizing/unwinding activity. RHAU is a human DEAH-box RNA helicase that exhibits G4-RNA binding and resolving activity. In this study, we employed RIP-chip analysis to identify en masse RNAs associated with RHAU in vivo. Approximately 100 RNAs were found to be associated with RHAU and bioinformatics analysis revealed that the majority contained potential G4-forming sequences. Among the most abundant RNAs selectively enriched with RHAU, we identified the human telomerase RNA template TERC as a true target of RHAU. Remarkably, binding of RHAU to TERC depended on the presence of a stable G4 structure in the 5′-region of TERC, both in vivo and in vitro. RHAU was further found to associate with the telomerase holoenzyme via the 5′-region of TERC. Collectively, these results provide the first evidence that intramolecular G4-RNAs serve as physiologically relevant targets for RHAU. Furthermore, our results suggest the existence of alternatively folded forms of TERC in the fully assembled telomerase holoenyzme