bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between total thyroxine, thyroid palpation and a clinical index in hyperthyroid and healthy cats and cats with other diseases
Authors: Wehner Astrid , Koehler Ines , Ramspott Sabine , Hartmann Katrin 
Published: October 2018

Objectives Present-day diagnosis of hyperthyroidism is often established in the early stages where clinical signs and physical examination findings typically associated with the disease may not yet be present. The purpose of this study was to investigate thyroid palpation score (TPS), total thyroxine (T4), body weight, body condition score and a clinical scoring index, which assesses severity of illness and quality of life, in untreated hyperthyroid cats, healthy cats and cats with non-thyroidal illness. Methods Fifty-five cats with hyperthyroidism, 45 healthy cats and 327 euthyroid cats with non-thyroidal disease were prospectively enrolled. A Kruskal–Wallis test was used to determine any differences between metric data. A χ2 test was applied to compare nominal data between the three subgroups. Correlation between two variables was analysed using Spearman’s correlation coefficient. Results Almost 80% of the hyperthyroid cats and up to 20% of the healthy cats and cats with non-thyroidal illness had a palpable thyroid gland. Median TPS in hyperthyroid cats was 2, which was significantly higher compared with the other groups. Although there was a significant correlation between TPS and T4 when evaluating all cats, this could not be demonstrated in the three subgroups. Hyperthyroid cats with larger thyroid glands (TPS >3) did not have higher T4 levels. Hyperthyroid cats with lower clinical scores had significantly higher T4 levels compared with hyperthyroid cats with higher scores. Hyperthyroid cats were older and had lower body weights and body condition scores than other cats. Conclusions and relevance Hyperthyroid cats were commonly found to have palpable thyroid glands, but they were smaller than previously reported.
Reliability and Validity of Rowland Universal Dementia Assessment Scale in Turkish Population
Authors: Ayan Gizem , Afacan Ceyda , Poyraz Burc Cagrı , Bilgic Onur , Avci Suna , Yavuzer Hakan , Yuruyen Mehmet , Erdincler Deniz Suna , Ayan Burak , Doventas Alper 
Published: October 2018

Background: The aim is to validate Turkish version Rowland Universal Dementia Assessment Scale (RUDAS). Methods: One hundred forty patients (>65 years) were included. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition -V was used in all patients. Rowland Universal Dementia Assessment Scale was applied for 2 days. Results were compared with Mini-Mental State Examination; reliability, validity, and statistical values were determined. Results: Time validity was verified. Mini-mental state examination was correlated 45.3% in control and 73% in dementia group. Factor weights varied between 0.44 and 0.81; factor construct was verified as 6-item scoring. When 25 was cutoff point, sensitivity was 92.86% and specificity was 92.86%. Content validity index was found to be 100% by 7 specialists. Cronbach α (0.692) and test–retest reliability (intraclass correlation = 0.987) were determined. Conclusion: Rowland Universal Dementia Assessment Scale (Turkish) is validated and verified as reliable. Test could be applied for 5 minutes approximately; results are not affected by educational status, immigrant status, and language used; however, age and gender have significant effect on results.
Outcomes of early and reversible renal impairment in patients with ST segment elevation myocardial infarction undergoing percutaneous coronary intervention
Authors: Khoury Shafik , Margolis Gilad , Ravid Dor , Rozenbaum Zach , Keren Gad , Shacham Yacov 
Published: October 2018

Objective:
Acute kidney injury (AKI) is a frequent complication in patients with ST segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). While AKI occurring post-PCI has been well studied, the incidence and clinical significance of early renal impairment evident on hospital admission prior to PCI and which resolves towards discharge has not been investigated.

Methods:
We retrospectively studied 2339 STEMI patients treated with primary PCI. The incidence of renal impairment and in-hospital complications as well as short and long-term mortality were compared between patients who did not develop renal impairment, patients who developed post-PCI AKI and those who presented with renal impairment on admission but improved their renal function during hospitalization (improved renal function). Improved renal function was defined as continuous and gradual decrease of ⩾ 0.3 mg/dL in serum creatinine levels obtained at hospital admission.

Results:
One hundred and nineteen patients (5%) had improved renal function and 230 patients (10%) developed post-PCI AKI. When compared with patients with no renal impairment, improved renal function and post-PCI AKI were associated with more complications and adverse events during hospitalization as well as higher 30-day mortality. Long-term mortality was significantly higher among those with post-PCI AKI (63/230, 27%) following STEMI than those without renal impairment (104/1990, 5%; p&lt;0.001), but there was no significant difference in long term mortality between patients with no renal impairment and those with improved renal function (5% vs. 7.5%, p=0.17).

Conclusion:
In STEMI patients undergoing primary PCI, the presence of renal impairment prior to PCI which resolves towards discharge is not uncommon and is associated with adverse short-term outcomes but better long-term outcomes compared with post-PCI AKI.
Murine myeloproliferative disorder as a consequence of impaired collaboration between dendritic cells and CD4 T cells
Authors: Humblet-Baron Stéphanie , Barber John S. , Roca Carlos P. , Lenaerts Aurelie , Koni Pandelakis A. , Liston Adrian 
Published: October 2018

AbstractDendritic cells (DCs) are a key cell type in the initiation of the adaptive immune response. Recently, an additional role for DCs in suppressing myeloproliferation was discovered. Myeloproliferative disorder (MPD) was observed in murine studies with constitutive depletion of DCs, as well as in patients with congenital deficiency in DCs caused by mutations in GATA2 or IRF8. The mechanistic link between DC deficiency and MPD was not predicted through the known biology and has remained an enigma. Prevailing models suggest numerical DC deficiency leads to MPD through compensatory myeloid differentiation. Here, we formally tested whether MPD can also arise through a loss of DC function without numerical deficiency. Using mice whose DCs are deficient in antigen presentation, we find spontaneous MPD that is characterized by splenomegaly, neutrophilia, and extramedullary hematopoiesis, despite normal numbers of DCs. Disease development was dependent on loss of the MHC class II (MHCII) antigen-presenting complex on DCs and was eliminated in mice deficient in total lymphocytes. Mice lacking MHCII and CD4 T cells did not develop disease. Thus, MPD was paradoxically contingent on the presence of CD4 T cells and on a failure of DCs to activate CD4 T cells, trapping the cells in a naive Flt3 ligand–expressing state. These results identify a novel requirement for intercellular collaboration between DCs and CD4 T cells to regulate myeloid differentiation. Our findings support a new conceptual framework of DC biology in preventing MPD in mice and humans.
The platelet NLRP3 inflammasome is upregulated in sickle cell disease via HMGB1/TLR4 and Bruton tyrosine kinase
Authors: Vogel Sebastian , Arora Taruna , Wang Xunde , Mendelsohn Laurel , Nichols James , Allen Darlene , Shet Arun S. , Combs Christian A. , Quezado Zenaide M. N. , Thein Swee Lay 
Published: October 2018

AbstractA key inflammatory mechanism recently identified in platelets involves the Nod-like receptor nucleotide-binding domain leucine-rich repeat containing protein 3 (NLRP3) and Bruton tyrosine kinase (BTK), which control activation of caspase-1 within inflammasome complexes. We investigated platelet caspase-1 activity in the context of sickle cell disease (SCD) directly in platelets isolated from SCD patients (n = 24) and indirectly by incubating platelets from healthy subjects with plasma obtained from SCD patients (n = 20), both in steady state and during an acute pain crisis (paired samples). The platelet NLRP3 inflammasome was upregulated in SCD patients under steady state conditions compared with healthy controls, and it was further upregulated when patients experienced an acute pain crisis. The results were consistent with indirect platelet assays, in which SCD plasma increased caspase-1 activity of platelets from healthy subjects in an NLRP3-dependent fashion. The damage-associated molecular pattern molecule high-mobility group box 1 (HMGB1) was elevated in plasma of SCD subjects compared with healthy controls and correlated with caspase-1 activity in platelets. Pharmacological or antibody-mediated inhibition of HMGB1, Toll-like receptor 4, and BTK interfered with sickle plasma–induced platelet caspase-1 activation. In Townes SCD mice, caspase-1 activity and aggregation of circulating platelets were elevated, which was suppressed by IV injection of an NLRP3 inhibitor and the BTK inhibitor ibrutinib. Activation of the platelet NLRP3 inflammasome in SCD may have diagnostic and therapeutic implications.
Formal and computational modeling of anticipation mechanisms of resilience in the complex sociotechnical air transport system
Authors: Blok Anne-Nynke , Sharpanskykh Alexei , Vert Matthieu 
Published: October 2018

AbstractWith ever-growing numbers of passengers and complexity of the air transport system, it becomes more and more of a challenge to manage the system in an effective, safe, and resilient manner. This is especially evident when disruptions occur. Understanding and improving resilience of the air transport system and its adaptive capacity to disruptions is essential for the system’s uninterrupted successful performance. Using theoretical findings from behavioral sciences, this paper makes the first steps towards formalization of the adaptive capacity of resilience of the air transport system with a particular focus on its ability to anticipate. To this end, an expressive logic-based language called Temporal Trace Language is used. The proposed approach is illustrated by a case study, in which anticipatory mechanisms are implemented in an agent-based airport terminal operations model, to deal with a disruptive scenario of unplanned and challenging passenger demand at the security checkpoint. Results showed that the timing of an adaptive action could have a significant influence on reducing the risk of saturation of the system, where saturation implies performance loss. Additionally, trade-off relations were obtained between cost, corresponding to the extra resources mobilized, and the benefits, such as a decrease in risk of saturation of the passenger queue.
Making up symptoms: psychic indeterminacy and the construction of psychotic phenomena
Authors: Green Huw 
Published: October 2018

SummaryPsychotic phenomena include a far wider range of experiences than is captured by the brief descriptions offered in contemporary diagnostic guides. Given the richness of historical clinical phenomenology, what can account for the recent ascendancy of relatively impoverished descriptions of psychosis? One possible explanation is provided by Hacking's notion of dynamic nominalism, where human categories change over time in tandem with those who they classify. But although dynamic nominalism makes sense of changes in behaviour, it fails to account for change at the level of subjective experience. In this paper, psychotic symptoms are addressed in the light of the indeterminacy of subjective mental content. A naïve-introspectionist approach to mental symptoms assumes that, notwithstanding practical difficulties, such symptoms are reliably describable in principle. Contemporary philosophy of mind challenges this assumption. Lighting upon a verbal description for ineffable phenomena changes their nature, resolving them into new forms.Declaration of interestNone.
Single-Cell RNA Sequencing Reveals Novel Markers of Male Pituitary Stem Cells and Hormone-Producing Cell Types
Authors: Cheung Leonard Y M , George Akima S , McGee Stacey R , Daly Alexandre Z , Brinkmeier Michelle L , Ellsworth Buffy S , Camper Sally A 
Published: October 2018

Abstract
Transcription factors and signaling pathways that regulate stem cells and specialized hormone-producing cells in the pituitary gland have been the subject of intense study and have yielded a mechanistic understanding of pituitary organogenesis and disease. However, the regulation of stem cell proliferation and differentiation, the heterogeneity among specialized hormone-producing cells, and the role of nonendocrine cells in the gland remain important, unanswered questions. Recent advances in single-cell RNA sequencing (scRNAseq) technologies provide new avenues to address these questions. We performed scRNAseq on ∼13,663 cells pooled from six whole pituitary glands of 7-week-old C57BL/6 male mice. We identified pituitary endocrine and stem cells in silico, as well as other support cell types such as endothelia, connective tissue, and red and white blood cells. Differential gene expression analyses identify known and novel markers of pituitary endocrine and stem cell populations. We demonstrate the value of scRNAseq by in vivo validation of a novel gonadotrope-enriched marker, Foxp2. We present novel scRNAseq data of in vivo pituitary tissue, including data from agnostic clustering algorithms that suggest the presence of a somatotrope subpopulation enriched in sterol/cholesterol synthesis genes. Additionally, we show that incomplete transcriptome annotation can cause false negatives on some scRNAseq platforms that only generate 3′ transcript end sequences, and we use in vivo data to recover reads of the pituitary transcription factor Prop1. Ultimately, scRNAseq technologies represent a significant opportunity to address long-standing questions regarding the development and function of the different populations of the pituitary gland throughout life.
Secret Signals from Another World
Authors: Charles Matthew 
Published: October 2018

Abstract
Walter Benjamin refers to the “idea of revolution as an innervation of the technical organs of the collective” as one article of his politics. Drawing on some of the debates and tensions generated by the work of Miriam Bratu Hansen, the article analyzes lesser-known intellectual sources that influenced Benjamin’s theory of innervation. Rather than reconcile or integrate these sources with dominant philosophical reconstructions of what is sometimes characterized as Benjamin’s “Western Marxism” and elaborated, in the more familiar context of surrealist innervation, as a synthesis of Sigmund Freud and Karl Marx, the article attempts to reveal an alternative constellation of Soviet biomechanics and reactionary anticapitalist Lebensphilosophie, united in their shared rejection of Freudian psychoanalysis.
Heidegger in Hebrew
Authors: Herskowitz Daniel 
Published: October 2018

Abstract
This article deals with the largely neglected topic of Martin Heidegger’s Jewish reception by examining the translation of The Origin of the Work of Art into Hebrew by Shlomo Zemach in 1968. The various challenges confronting the coming-into-being of this translation are outlined by drawing on previously unknown archival material, including correspondence between Zemach and Vittorio Klostermann (Heidegger’s German publisher), as well as between Zemach and Heidegger himself. With a look at Heidegger’s reception in post-Holocaust Israel as reflected in the debates over his work provoked by Zemach’s translation, the article examines the question of the implied ties between translation and reconciliation and the particular political, moral, and religious challenges raised by putting Heidegger’s philosophy into Hebrew, the holy language.
Anticapitalist Affect
Authors: Norberg Jakob 
Published: October 2018

Abstract
In his writings on satire, the Marxist literary critic Georg Lukács argued that hatred could function as an anticapitalist affect. Hatred, he believed, equips the committed author with a set of traits—certainty, lucidity, endurance, and pitilessness—that are eminently useful for exposing and destroying a fundamentally criminal socioeconomic system. Contrary to the contemporary anxiety about hatred (hate speech, hate crimes), Lukács wanted to mobilize the affect for revolutionary ends. Yet he also admitted that hatred tends to grow in conditions of powerlessness, dependence, and frustration. As a consequence, Lukács could not unite the cool passion of hatred with the position of a confident revolutionary.
Spectator and Society
Authors: Westerman Richard 
Published: October 2018

Abstract
Interpretations of Georg Lukács’s theory of reification and consciousness have typically assumed that Lukács relies on an essentialized notion of subjectivity that can be restored by dereification. This article argues instead that he treats subjectivity as a formally defined position within the totality of consciousness, an account of consciousness that closely parallels Alois Riegl’s theory of the spectator as a formally defined component of works of art. Both Lukács and Riegl incorporate notions of agency and active involvement in the forms of representation into these accounts of subjectivity: what Riegl finds in the Kunstwollen of different works of art, Lukács finds in the formal structures of social reality. The article thus reinterprets reification as the formal definition of the subject as an isolated individual playing no active part in the structure of social forms. Finally, the article draws on Riegl’s idea that Dutch group portraits incorporate spectators as active constitutors of artistic form to offer some suggestions about Lukács’s theory of the revolutionary party.
Axonal degeneration induced by glutamate excitotoxicity is mediated by necroptosis
Authors: Hernández Diego E. , Salvadores Natalia A. , Moya-Alvarado Guillermo , Catalán Romina J. , Bronfman Francisca C. , Court Felipe A. 
Published: October 2018

ABSTRACT
Neuronal excitotoxicity induced by glutamate leads to cell death and functional impairment in a variety of central nervous system pathologies. Glutamate-mediated excitotoxicity triggers neuronal apoptosis in the cell soma as well as degeneration of axons and dendrites by a process associated with Ca2+ increase and mitochondrial dysfunction. Importantly, degeneration of axons initiated by diverse stimuli, including excitotoxicity, has been proposed as an important pathological event leading to functional impairment in neurodegenerative conditions. Here, we demonstrate that excitotoxicity-induced axonal degeneration proceeds by a mechanism dependent on the necroptotic kinases RIPK1 and RIPK3, and the necroptotic mediator MLKL. Inhibition of RIPK1, RIPK3 or MLKL prevents key steps in the axonal degeneration cascade, including mitochondrial depolarization, the opening of the permeability transition pore and Ca2+ dysregulation in the axon. Interestingly, the same excitotoxic stimuli lead to apoptosis in the cell soma, demonstrating the co-activation of two independent degenerative mechanisms in different compartments of the same cell. The identification of necroptosis as a key mechanism of axonal degeneration after excitotoxicity is an important initial step in the development of novel therapeutic strategies for nervous system disorders.
The topology of the lymphotoxin β receptor that accumulates upon endolysosomal dysfunction dictates the NF-κB signaling outcome
Authors: Banach-Orłowska Magdalena , Jastrzębski Kamil , Cendrowski Jarosław , Maksymowicz Małgorzata , Wojciechowska Karolina , Korostyński Michał , Moreau Dimitri , Gruenberg Jean , Miaczynska Marta 
Published: October 2018

ABSTRACT
Cytokine receptors, such as tumor necrosis factor receptor I (TNFRI, also known as TNFRSF1A) and lymphotoxin β receptor (LTβR), activate inflammatory nuclear factor (NF)-κB signaling upon stimulation. We have previously demonstrated that depletion of ESCRT components leads to endosomal accumulation of TNFRI and LTβR, and their ligand-independent signaling to NF-κB. Here, we studied whether other perturbations of the endolysosomal system could trigger intracellular accumulation and signaling of ligand-free LTβR. While depletion of the CORVET components had no effect, knockdown of Rab7a or HOPS components, or pharmacological inhibition of lysosomal degradation, caused endosomal accumulation of LTβR and increased its interaction with the TRAF2 and TRAF3 signaling adaptors. However, the NF-κB pathway was not activated under these conditions. We found that knockdown of Rab7a or HOPS components led to sequestration of LTβR in intraluminal vesicles of endosomes, thus precluding NF-κB signaling. This was in contrast to the LTβR localization on the outer endosomal membrane that was seen after ESCRT depletion and was permissive for signaling. We propose that the inflammatory response induced by intracellular accumulation of endocytosed cytokine receptors critically depends on the precise receptor topology within endosomal compartments.
Nuclear entry and export of FIH are mediated by HIF1α and exportin1, respectively
Authors: Wang Yihua , Zhong Shan , Schofield Christopher J. , Ratcliffe Peter J. , Lu Xin 
Published: October 2018

ABSTRACT
Hypoxia plays a crucial role at cellular and physiological levels in all animals. The responses to chronic hypoxia are, at least substantially, orchestrated by activation of the hypoxia inducible transcription factors (HIFs), whose stability and subsequent transcriptional activation are regulated by HIF hydroxylases. Factor inhibiting HIF (FIH), initially isolated as a HIFα interacting protein following a yeast two-hybrid screen, is an asparaginyl hydroxylase that negatively regulates transcriptional activation by HIF. This study aimed to define the mechanisms that govern transitions of FIH between the nucleus and cytoplasm. We report that FIH accumulates in the nucleus within a short time window during hypoxia treatment. We provide evidence, based on the application of genetic interventions and small molecule inhibition of the HIF hydroxylases, that the nuclear localization of FIH is governed by two opposing processes: nuclear entry by ‘coupling’ with HIF1α for importin β1-mediated nuclear import and active export via a Leptomycin B-sensitive exportin1-dependent pathway.
This article has an associated First Person interview with the first author of the paper.
Hepatocyte-like cells reveal novel role of SERPINA1 in transthyretin amyloidosis
Authors: Niemietz Christoph , Fleischhauer Lutz , Sandfort Vanessa , Guttmann Sarah , Zibert Andree , Schmidt Hartmut H.-J. 
Published: October 2018

ABSTRACT
Transthyretin (TTR)-related familial amyloid polyneuropathy (ATTR) results from aggregation and extracellular disposition of misfolded TTR mutants. Growing evidence suggests the importance of hepatic chaperones for the modulation of pathogenesis. We took advantage of induced pluripotent stem cell (iPSC)-derived hepatocyte-like cells (HLCs) from ATTR patients (ATTR-HLCs) to compare chaperone gene expression to that in HLCs from healthy individuals (H-HLCs). From the set of genes analyzed, chaperones that are predominantly located extracellularly were differently expressed. Expression of the chaperones showed a high correlation with TTR in both ATTR-HLCs and H-HLCs. In contrast, after TTR knockdown, the correlation was mainly affected in ATTR-HLCs suggesting that differences in TTR expression triggers aberrant chaperone expression. Serpin family A member 1 (SERPINA1) was the only extracellular chaperone that was markedly upregulated after TTR knockdown in ATTR-HLCs. Co-immunoprecipitation revealed that SERPINA1 physically interacts with TTR. In vitro assays indicated that SERPINA1 can interfere with TTR aggregation. Taken together, our results suggest that extracellular chaperones play a crucial role in ATTR pathogenesis, in particular SERPINA1, which may affect amyloid formation.