Bibliotheca Latino-Hebraica Sive De Scriptoribus Latinis, Qui ex diversis nationibus contra Iudaeos, vel de re Hebraica utumque scripsere : additis Observationibus Criticis, Et Philologico-Historicis, quibus quae circa patriam, aetatem, vitse instititum, mortemq, auctorum consideranda veniunt, exponuntur

Auct. Et Vindice Carolo Ioseph Imbonato

Complectens reliquas post Y. duodecim Alphabeti literas K, L, M, N, S, ʿ, P, Ts, Ḳ, R, Sh, T

ed. Carolo Ioseph Imbonato

Die Vormauer Italiens. Zur kulturellen Repräsentation eines konfessionellen Grenzraums (17. und 18. Jahrhundert)

Im Spätherbst 1583 visitierte der Mailänder Erzbischof Carlo Borromeo trotz ausdrücklichem Verbot der Drei Bünde die südlichen Täler Graubündens. 1620 fielen spanische Truppen ins Veltlin ein, um die katholischen Untertanen im Kampf gegen ihre mehrheitlich protestantischen Herren aus Graubünden zu unterstützen. Kirchliche wie weltliche Akteure rechtfertigten ihr Eingreifen mit der konfessionellen Grenzsituation. Der Graubündner Alpenraum bilde eine «Vormauer Italiens» resp. das «Tor zu Italien», die es gegen die Protestanten zu verteidigen gelte. Sei dieser gemischtkonfessionelle Grenzraum (2/3 Protestanten; 1/3 Katholiken) einmal in die Hände der «Häretiker» gefallen, könne sich der Protestantismus ungehindert in ganz Italien ausbreiten. Dass die Denkfigur der konfessionellen Grenze handlungsanleitend und handlungslegitimierend wirkte, haben Untersuchungen zur Ereignisgeschichte und zur politischen Sprache ausführlich belegt. Weniger bekannt ist, dass sie sich tief einschrieb in die kulturelle und religiöse Praxis der Katholiken. Der Beitrag zeigt auf, wie sich im Verlaufe des 17. Jahrhunderts ein Set an kulturellen Repräsentationen ausbildete, das auf subtile Weise die konfessionelle Grenze anzeigte und sie längerfristig festigte. Festgestellt werden kann zunächst, dass in Graubünden und im Veltlin unter den Auspizien der römischen Missionskongregation de Propaganda Fide eine reiche Sakrallandschaft entstanden ist und die vielen Kirchen, Kapellen, Kreuzwege, Bildstöcke etc. die katholischen Gebiete ostentativ gegen die protestantischen Nachbarn abgrenzten. Volkskundliche Erhebungen haben sodann auf eine aussergewöhnlich hohe Zahl von Kirchen und Kapellen aufmerksam gemacht, in denen um eine Gnade gebeten oder mit Votivgaben für ein erfahrenes Wunder gedankt wurde. Das dichte Netz dieser Gnadenorte und die damit verbundenen Frömmigkeitspraktiken – so die These des Beitrages – waren Teil einer katholischen Symbolpolitik, die darauf ausgerichtet war, die katholischen Gebiete im konfessionellen Grenzraum augenfällig in das Gnadenterritorium der katholischen Kirche zu integrieren. Denn dort, wo sich Wunder ereigneten, war dies ein klarer Beweis für die gottgewollte Zugehörigkeit zur katholischen Universalkirche. Ebenfalls der Konsolidierung der konfessionellen Grenze dienten drittens die zahlreichen Bruderschaften, die über ihre Erzbruderschaften in Rom oder Mailand sowohl auf der institutionellen wie auch auf der symbolischen Ebene für eine stärkere Anbindung an das katholische Italien sorgten.

Johannis Buxtorfii Lexicon hebraicum et chaldaicum : complectens omnes voces, tam primas quam derivatas, quae in sacris bibliis, hebraeâ, [et] ex parte chaldaeâ linguâ scriptis, extant

interpretationis fide, exemplorum Biblicorum copiâ ... Accesit lexicon breve rabbinico-philosophicum ... cum indice ...

Das apologetische Schreiben des Josua Lorki an den Abtrünnigen Don Salomon ha-Lewi (Paulus de Santa Maria)

hrsg. nach drei Handschriften mit einer ausführlichen Einl.und deutscher Übers., nebst zwei Anhängen versehen von L. Landau

Comparative dendritic cell biology of veterinary mammals.

Dendritic cells (DC) have a main function in innate immunity in that they sense infections and environmental antigens at the skin and mucosal surfaces and thereby critically influence decisions about immune activation or tolerance. As professional antigen-presenting cells, they are essential for induction of adaptive immune responses. Consequently, knowledge on this cell type is required to understand the immune systems of veterinary mammals, including cattle, sheep, pigs, dogs, cats, and horses. Recent ontogenic studies define bona fide DC as an independent lineage of hematopoietic cells originating from a common precursor. Distinct transcription factors control the development into the two subsets of classical DC and plasmacytoid DC. These DC subsets express a distinguishable transcriptome, which differs from that of monocyte-derived DC. Using a comparative approach based on phenotype and function, this review attempts to classify DC of veterinary mammals and to describe important knowledge gaps.

Significant lethality following liver resection in A20 heterozygous knockout mice uncovers a key role for A20 in liver regeneration

Hepatic expression of A20, including in hepatocytes, increases in response to injury, inflammation and resection. This increase likely serves a hepatoprotective purpose. The characteristic unfettered liver inflammation and necrosis in A20 knockout mice established physiologic upregulation of A20 as integral to the anti-inflammatory and anti-apoptotic armamentarium of hepatocytes. However, the implication of physiologic upregulation of A20 in modulating hepatocytes' proliferative responses following liver resection remains controversial. To resolve the impact of A20 on hepatocyte proliferation and the liver's regenerative capacity, we examined whether decreased A20 expression, as in A20 heterozygous knockout mice, affects outcome following two-third partial hepatectomy. A20 heterozygous mice do not demonstrate a striking liver phenotype, indicating that their A20 expression levels are still sufficient to contain inflammation and cell death at baseline. However, usually benign partial hepatectomy provoked a staggering lethality (>40%) in these mice, uncovering an unsuspected phenotype. Heightened lethality in A20 heterozygous mice following partial hepatectomy resulted from impaired hepatocyte proliferation due to heightened levels of cyclin-dependent kinase inhibitor, p21, and deficient upregulation of cyclins D1, E and A, in the context of worsened liver steatosis. A20 heterozygous knockout minimally affected baseline liver transcriptome, mostly circadian rhythm genes. Nevertheless, this caused differential expression of >1000 genes post hepatectomy, hindering lipid metabolism, bile acid biosynthesis, insulin signaling and cell cycle, all critical cellular processes for liver regeneration. These results demonstrate that mere reduction of A20 levels causes worse outcome post hepatectomy than full knockout of bona fide liver pro-regenerative players such as IL-6, clearly ascertaining A20's primordial role in enabling liver regeneration. Clinical implications of these data are of utmost importance as they caution safety of extensive hepatectomy for donation or tumor in carriers of A20/TNFAIP3 single nucleotide polymorphisms alleles that decrease A20 expression or function, and prompt the development of A20-based liver pro-regenerative therapies.

Blocking the epithelial-to-mesenchymal transition pathway abrogates resistance to anti-folate chemotherapy in lung cancer.

Anticancer therapies currently used in the clinic often can neither eradicate the tumor nor prevent disease recurrence due to tumor resistance. In this study, we showed that chemoresistance to pemetrexed, a multi-target anti-folate (MTA) chemotherapeutic agent for non-small cell lung cancer (NSCLC), is associated with a stem cell-like phenotype characterized by an enriched stem cell gene signature, augmented aldehyde dehydrogenase activity and greater clonogenic potential. Mechanistically, chemoresistance to MTA requires activation of epithelial-to-mesenchymal transition (EMT) pathway in that an experimentally induced EMT per se promotes chemoresistance in NSCLC and inhibition of EMT signaling by kaempferol renders the otherwise chemoresistant cancer cells susceptible to MTA. Relevant to the clinical setting, human primary NSCLC cells with an elevated EMT signaling feature a significantly enhanced potential to resist MTA, whereas concomitant administration of kaempferol abrogates MTA chemoresistance, regardless of whether it is due to an intrinsic or induced activation of the EMT pathway. Collectively, our findings reveal that a bona fide activation of EMT pathway is required and sufficient for chemoresistance to MTA and that kaempferol potently regresses this chemotherapy refractory phenotype, highlighting the potential of EMT pathway inhibition to enhance chemotherapeutic response of lung cancer.

The enduring effects of psychodynamic treatments vis-à-vis alternative treatments: A multilevel longitudinal meta-analysis

Although evidence suggests that the benefits of psychodynamic treatments are sustained over time, presently it is unclear whether these sustained benefits are superior to non-psychodynamic treatments. Additionally, the extant literature comparing the sustained benefits of psychodynamic treatments compared to alternative treatments is limited with methodological shortcomings. The purpose of the current study was to conduct a rigorous test of the growth of the benefits of psychodynamic treatments relative to alternative treatments across distinct domains of change (i.e., all outcome measures, targeted outcome measures, non-targeted outcome measures, and personality outcome measures). To do so, the study employed strict inclusion criteria to identify randomized clinical trials that directly compared at least one bona fide psychodynamic treatment and one bona fide non-psychodynamic treatment. Hierarchical linear modeling (Raudenbush, Bryk, Cheong, Congdon, & du Toit, 2011) was used to longitudinally model the impact of psychodynamic treatments compared to non-psychodynamic treatments at post-treatment and to compare the growth (i.e., slope) of effects beyond treatment completion. Findings from the present meta-analysis indicated that psychodynamic treatments and non-psychodynamic treatments were equally efficacious at post-treatment and at follow-up for combined outcomes (k=20), targeted outcomes (k=19), non-targeted outcomes (k=17), and personality outcomes (k=6). Clinical implications, directions for future research, and limitations are discussed.

Bibliotheca Magna Rabbinica De Scriptoribus, et scriptis Hebraicis, ordine Alphabetico Hebraicè, et Latinè digestis

Auct. Ivlio Bartoloccio de Celleno

Identification and analysis of novel mitotic inhibitors of the Caenorhabditis elegans Aurora B kinase

Proper execution of mitosis requires the accurate segregation of replicated DNA into each daughter cell. The highly conserved mitotic kinase AIR-2/Aurora B is a dynamic protein that interacts with subsets of cofactors and substrates to coordinate chromosome segregation and cytokinesis in Caenorhabdiris elegans. To identify components of the AIR-2 regulatory pathway, a genome-wide RNAi-based screen for suppressors of air-2 temperature-sensitive mutant lethality was conducted. Here, I present evidence that two classes of suppressors identified in this screen are bona fide regulators of the AIR-2 kinase. The strongest suppressor cdc-48.3, encodes an Afg2/Spaf-related Cdc48-like AAA+ ATPase that regulates AIR-2 kinase activity and stability during C. elegans embryogenesis. Loss of CDC-48.3 suppresses the lethality of air-2 mutant embryos, marked by the restoration of the dynamic behavior of AIR-2 and rescue of chromosome segregation and cytokinesis defects. Loss of CDC-48.3 leads to mitotic delays and abnormal accumulation of AIR-2 during late telophase/mitotic exit. In addition, AIR-2 kinase activity is significantly upregulated from metaphase through mitotic exit in CDC-48.3 depleted embryos. Inhibition of the AIR-2 kinase is dependent on (1) a direct physical interaction between CDC-48.3 and AIR-2, and (2) CDC-48.3 ATPase activity. Importantly, the increase in AIR-2 kinase activity does not correlate with the stabilization of AIR-2 in late mitosis. Hence, CDC-48.3 is a bi-functional inhibitor of AIR-2 that is likely to act via distinct mechanisms. The second class of suppressors consists of psy-2/smk-1 and pph-4.1, which encode two components of the conserved PP4 phosphatase complex that is essential for spindle assembly, chromosome segregation, and overall mitotic progression. AIR-2 and its substrates are likely to be targets of this complex since mitotic AIR-2 kinase activity is significantly increased during mitosis when either PSY-2/SMK-1 or PPH-4.l is depleted. Altogether, this study demonstrates that during the C. elegans embryonic cell cycle, regulators including the CDC-48.3 ATPase and PP4 phosphatase complex interact with and control the kinase activity, targeting behavior and protein stability of the Aurora B kinase to ensure accurate and timely progression of mitosis. ^

Characterization of a Novel Role for the Tousled- like Kinase in Kinetochore Assembly and Function in Caenorhabditis elegans

Chromosome segregation is a critical step during cell division to avoid aneuploidy and promote proper organismal development. Correct sister chromatid positioning and separation during mitosis helps to achieve faithful transmission of genetic material to daughter cells. This prevents improper chromosome partitioning that can potentially result in extrachromosomal fragments, increasing the tumorigenic potential of the cells. The kinetochore is a protenaicious structure responsible for the initiation and orchestration of chromosome movement during mitosis. This highly conserved structure among eukaryotes is required for chromosome attachment to the mitotic spindle and failure to assemble the kinetochore results in aberrant chromosome segregation. Thus elucidating the mechanism of kinetochore assembly is important to have a better understanding of the regulation that controls chromosome segregation. Our previous work identified the C. elegans Tousled-like kinase (TLK-1) as a mitotic kinase and depletion of TLK-1 results in embryonic lethality, characterized by nuclei displaying poor mitotic chromosome alignment, lagging chromosome, and chromosome bridges during anaphase. Additionally, previous studies from our group revealed that TLK-1 is phosphorylated independently by Aurora B at serine 634, and by CHK-1 at threonine T610. The research presented herein reveals that both phosphorylated forms of TLK-1 associate with the kinetochore during mitosis. Moreover, by systematic depletion of kinetochore proteins, I uncovered that pTLK-1 is bona fide kinetochore component that is located at the outer kinetochore layer, influencing the microtubule-binding interface. I also demonstrated that TLK-1 is necessary for the kinetochore localization of the microtubule interacting proteins CLS-2 and LIS-1 and I show that embryos depleted of TLK-1 presented an aberrant twisted kinetochore pattern. Furthermore, I established that the inner kinetochore protein KNL-2 is an in vitro substrate of TLK-1 indicating a possible role of TLK-1 in regulating centromeric assembly. Collectively, these results suggest a novel role for the Tousled-like kinase in regulation of kinetochore assembly and microtubule dynamics and demonstrate the necessity of TLK-1 for proper chromosome segregation in C. elegans.

Aelii Antonii Nebrissensis Rerum a Fernando et Elisabe Hispaniar[um] felicissimis Regibus gestaru[m] Decades duae, Necno[n] belli Nauarie[n]sis libri duo.

Sign.: [], A-Z8, 2A-2F8

Sermones / domini petri hieremie ...

Lugares e imp. tomados de colofones en f2v y 3h4v y fecha tomada de colofón en V5v

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