Vokalschwächung im peruanischen Spanisch

Diese Studie befasst sich mit der wenig untersuchten Vokalschwächung im peruanischen Spanisch, die als ein singuläres Merkmal der Hochlandgebiete Hispanoamerikas (tierras altas) gilt und üblicherweise auf den Sprachkontakt mit indigenen Sprachen zurückgeführt wird. Die Beschreibung des Merkmals im hispanoamerikanischen Spanischen im Allgemeinen und im peruanischen Spanisch im Speziellen verdeutlicht jedoch, dass die Sprachkontakthypothese aus mehreren Gründen problematisch ist. Es könnte sich möglicherweise sogar um ein altspanisches Merkmal handeln, das sich durch die Prozesse der Kolonisierung in abgelegenen Gebieten Hispanoamerikas erhalten hat. Die Analyse von Sprachdaten im Umfang von 13 489 Vokal-Tokens aus dem Hochland (tierras altas) und dem Küstentiefland (tierras bajas) des Departments Arequipa liefert weitere unerwartete Ergebnisse: Zum einen ist die Vokalschwächung in Peru nicht nur im Hochland, sondern auch an der Küste verbreitet. Dort kann sie nicht mit Sprachkontakt in Verbindung gebracht werden. Zum anderen besteht sie nicht nur – wie bisher angenommen – aus Entstimmungen und Elisionen, sondern auch aus Kürzungen und Zentralisierungen. Dies bedeutet eine bemerkenswerte Übereinstimmung mit der Vokalschwächung in Mexiko, wo sie bisher am besten erforscht worden ist.Este estudio trata de la debilitación vocálica en el español peruano, un fenómeno muy poco estudiado que se considera un rasgo singular de los altiplanos hispanoamericanos (las llamadas tierras altas) y que se explica, por lo general, como consecuencia del contacto con lenguas indígenas. Sin embargo, la descripción de este rasgo en el español hispanoamericano en general, y en el español peruano en particular, muestra que la hipótesis del contacto de lenguas es problemática por varias razones. Incluso podría tratarse de un rasgo del español medieval que se ha mantenido en regiones alejadas de Hispanoamérica debido a la dinámica propia de la colonización, como muestran los procesos de debilitación vocálica en el español medieval. El análisis de 13 489 tokens vocálicos del altiplano (tierras altas) y de la costa (tierras bajas) del departamento de Arequipa arroja aún más resultados inesperados. Por un lado, la debilitación vocálica no sólo se encuentra difundida en el altiplano, sino también en la costa; y esto no se puede explicar a través del contacto con lenguas indígenas. Por otro lado, la debilitación vocálica no sólo comprende vocales ensordecidas y elididas, como se suponía previamente, sino que también se pueden observar realizaciones abreviadas y centralizadas. Esto significa que se da una notable coincidencia con la debilitación vocálica de México, que es donde el fenómeno ha sido estudiado hasta ahora con mayor exhaustividad.This work focuses on the little-studied process of vowel weakening in Peruvian Spanish, a process considered to be a unique feature of the highlands of Hispanic America (tierras altas) and usually attributed to contact with indigenous languages. An analysis of this feature in Latin American Spanish in general and in Peruvian Spanish in particular reveals that the language-contact hypothesis is problematic for several reasons. As a review of vowel weakening processes in Old Spanish shows, this might even be a feature of Old Spanish which has survived in remote areas of Hispanic America due to the dynamics of colonization. The analysis of linguistic data comprising 13 489 vowel tokens from the highlands (tierras altas) and the lowland coastal areas (tierras bajas) of the department of Arequipa produces further unexpected results. On the one hand, it shows that vowel weakening is not only a linguistic feature of the Peruvian highlands, but also of the lowland coastal areas where it could not have arisen through contact with indigenous languages. On the other hand, it reveals that this process does not only involve devoicing and elision as previously thought, but also shortening and centralization. This indicates a remarkably close correspondence to vowel weakening in Mexico, where this process has previously been studied in the greatest depth

Español costeño vs. español andino en Perú: reexamen de la cuestión

This paper deals with the origin of the theory of español costeño and español andino, focusing on yeísmo and lleísmo, on the basis of which the theory was developed at the turn of the 19th century. I argue that the early conception of español costeño and español andino has strongly influenced the kind of research we have been conducting about the geographic varieties to this day. The aim of this study therefore, is to sharpen our understanding of the former zeitgeist of research and to stimulate further ‘big data’-based studies on español costeño, español andino and español amazónico, the third Peruvian geographic variety, traditionally neglected by linguistic research.Este artículo analiza cómo comenzaron a desarrollarse a finales del siglo XIX los conceptos diatópicos de español costeño y de español andino en relación con los rasgos de pronunciación ‘yeísmo’ y ‘lleísmo’. Sostengo que la investigación lingüística actual sigue influenciada por estos conceptos diatópicos de los inicios de la lingüística hispánica peruana. El objetivo de este estudio, por lo tanto, es situar las primeras observaciones sobre las variedades diatópicas del español costeño y del español andino en su zeitgeist científico y estimular más estudios basados en big data sobre el español costeño, el español andino y el español amazónico, la tercera variedad diatópica peruana, que tradicionalmente ha recibido poca atención por parte de la investigación lingüística

HIV-1 Induces Apoptosis in Primary Osteoblasts and HOBIT Cells through TNF-alfa Activation

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Gefährdete Sprachen – Einleitung

Diese Einleitung gibt einen kurzen Überblick über das Thema "Gefährdete Sprachen" und stellt die in dieser Ausgabe enthaltenen Beiträge vor

The Effect of Steel Industrial Residue-Enriched Soil on the Initial Growth and Heavy Metal Profiles of Elephantgrass

Heavy metal contamination of industrial sites are becoming a matter of growing concern. In spite of the substantial progress in the assessment of the influence of steel industrial plant waste on soil and water (Adamo et al., 2002), studies on the immediate responses of cultivated plants are still scarce. The objective of this experiment was to verify the short-term effects of soil added phosphate mud (P mud) or metallurgical scale (M scale), which are trace element-rich steel industry residues, on the initial uptake and heavy metal profiles of elephantgrass (Pennisetum purpureum

Development of C-TILDA: A modified TILDA method for reservoir quantification in long term treated patients infected with subtype C HIV-1

A better characterization of the HIV reservoir is pivotal for the development of effective eradication strategies. Accurate quantification of the latent reservoir remains challenging. Starting from a regular blood draw, the Tat/Rev induced limiting dilution assay (TILDA) combines serial dilution of CD4+ T cells with a PCR-based detection of HIV-1 spliced mRNA produced upon cell stimulation. Here we adapted the original protocol for HIV-1 subtype B to detect tat/rev mRNAs transcribed from reactivated latently infected cells in long term suppressed patients infected with HIV-1 subtype C. Given the heterogeneity of global HIV epidemiology, it is pivotal to develop assays with optimal performances also in patients infected with non-B subtypes. We observed that, in these patients infected with subtype C virus, the HIV reservoir quantified by TILDA correlates with both the time of virological suppression and CD4/CD8 ratio

A Two-Color Haploid Genetic Screen Identifies Novel Host Factors Involved in HIV-1 Latency

To identify novel host factors as putative targets to reverse HIV-1 latency, we performed an insertional mutagenesis genetic screen in a latent HIV-1 infected pseudohaploid KBM7 cell line (Hap-Lat). Following mutagenesis, insertions were mapped to the genome, and bioinformatic analysis resulted in the identification of 69 candidate host genes involved in maintaining HIV-1 latency. A select set of candidate genes was functionally validated using short hairpin RNA (shRNA)-mediated depletion in latent HIV-1 infected J-Lat A2 and 11.1 T cell lines. We confirmed ADK, CHD9, CMSS1, EVI2B, EXOSC8, FAM19A, GRIK5, IRF2BP2, NF1, and USP15 as novel host factors involved in the maintenance of HIV-1 latency. Chromatin immunoprecipitation assays indicated that CHD9, a chromodomain helicase DNA-binding protein, maintains HIV-1 latency via direct association with the HIV-1 5′ long terminal repeat (LTR), and its depletion results in increased histone acetylation at the HIV-1 promoter, concomitant with HIV-1 latency reversal. FDA-approved inhibitors 5-iodotubercidin, trametinib, and topiramate, targeting ADK, NF1, and GRIK5, respectively, were characterized for their latency reversal potential. While 5-iodotubercidin exhibited significant cytotoxicity in both J-Lat and primary CD4(+) T cells, trametinib reversed latency in J-Lat cells but not in latent HIV-1 infected primary CD4(+) T cells. Importantly, topiramate reversed latency in cell line models, in latently infected primary CD4(+) T cells, and crucially in CD4(+) T cells from three people living with HIV-1 (PLWH) under suppressive antiretroviral therapy, without inducing T cell activation or significant toxicity. Thus, using an adaptation of a haploid forward genetic screen, we identified novel and druggable host factors contributing to HIV-1 latency

Allele-specific long-distance regulation dictates IL-32 isoform switching and mediates susceptibility to HIV-1

We integrated data obtained from HIV-1 genome-wide association studies with T cell-derived epigenome data and found that the noncoding intergenic variant rs4349147, which is statistically associated with HIV-1 acquisition, is located in a CD4+ T cell-specific deoxyribonuclease I hypersensitive region, suggesting regulatory potential for this variant. Deletion of the rs4349147 element in Jurkat cells strongly reduced expression of interleukin-32 (IL-32), approximately 10-kb upstream, and chromosome conformation capture assays identified a chromatin loop between rs4349147 and the IL-32 promoter validating its function as a long-distance enhancer. We generated single rs4349147-A or rs4349147-G allele clones and demonstrated that IL-32 enhancer activity and interaction with the IL-32 promoter are strongly allele dependent; rs4349147 -/A cells display reduced IL-32 expression and altered chromatin conformation as compared to rs4349147 G/- cells. Moreover, RNA sequencing demonstrated that rs4349147 G/- cells express a lower relative ratio of IL-32α to non-a isoforms than rs4349147 -/A cells and display increased expression of lymphocyte activation factors rendering them more prone to infection with HIV-1. In agreement, in primary CD4+ T cells, both treatment with recombinant IL-32γ (rIL-32γ) but not rIL-32α, and exogenous lentiviral overexpression of IL-32γ or IL-32β but not IL-32α resulted in a proinflammatory T cell cytokine environment concomitant with increased susceptibility to HIV infection. Our data demonstrate that rs4349147-G promotes transcription of non-IL-32α isoforms, generating a proinflammatory e

Detection of antisense protein (ASP) RNA transcripts in individuals infected with human immunodeficiency virus type 1 (HIV-1).

The detection of antisense RNA is hampered by reverse transcription (RT) non-specific priming, due to the ability of RNA secondary structures to prime RT in the absence of specific primers. The detection of antisense RNA by conventional RT-PCR does not allow assessment of the polarity of the initial RNA template, causing the amplification of non-specific cDNAs. In this study we have developed a modified protocol for the detection of human immunodeficiency virus type 1 (HIV-1) antisense protein (ASP) RNA. Using this approach, we have identified ASP transcripts in CD4+ T cells isolated from five HIV-infected individuals, either untreated or under suppressive therapy. We show that ASP RNA can be detected in stimulated CD4+ T cells from both groups of patients, but not in unstimulated cells. We also show that in untreated patients, the patterns of expression of ASP and env are very similar, with the levels of ASP RNA being markedly lower than those of env. Treatment of cells from one viraemic patient with α-amanitin greatly reduces the rate of ASP RNA synthesis, suggesting that it is associated with RNA polymerase II, the central enzyme in the transcription of protein-coding genes. Our data represent the first nucleotide sequences obtained in patients for ASP, demonstrating that its transcription indeed occurs in those HIV-1 lineages in which the ASP open reading frame is present

HIV eradication: Combinatorial approaches to activate latent viruses

The concept of eradication of the Human Immune Deficiency Virus (HIV) from infected patients has gained much attention in the last few years. While combination Anti-Retroviral Therapy (c-ART) has been extremely effective in suppressing viral replication, it is not curative. This is due to the presence of a reservoir of latent HIV infected cells, which persist in the presence of c-ART. Recently, pharmaceutical approaches have focused on the development of molecules able to induce HIV-1 replication from latently infected cells in order to render them susceptible to viral cytopathic effects and host immune responses. Alternative pathways and transcription complexes function to regulate the activity of the HIV promoter and might serve as molecular targets for compounds to activate latent HIV. A combined therapy coupling various depressors and activators will likely be the most effective in promoting HIV replication while avoiding pleiotropic effects at the cellular level. Moreover, in light of differences among HIV subtypes and variability in integration sites, the combination of multiple agents targeting multiple pathways will increase likelihood of therapeutic effectiveness and prevent mutational escape. This review provides an overview of the mechanisms that can be targeted to induce HIV activation focusing on potential combinatorial approaches