L’organisation de la frontière arabo-byzantine en Cappadoce (VIIIe-IXe siècle)

International audienceLa genèse de la frontière entre l’empire byzantin et le califat a été analysée d’abord et avant tout comme un processus conduit à l’instigation des Arabes, responsables, dans la seconde moitié du VIIIe siècle, sous les premiers califes abbassides, de la mise en placedu système frontalier des ‛awāṣim et des thughūr en Cilicie, en Syrie du Nord et en Mésopotamie. Quant aux Byzantins, soucieux de protéger le plateau central de l’Anatolie, ils auraient contribué dans un premier temps à la formation d’un no man’s land, avant de procéder, à la fin du VIIIe et dans la première moitié du IXe siècle, à la création de verrous frontaliers dans les régions du taurus et de l’Antitaurus, les clisures de Séleucie, de Cappadoce et de Charsianon, élevées ultérieurement au rang de thèmes. l’ensemble de ces mesures font, à cette date, des anciennes provinces de Cappadoce (Cappadoce I et Cappadoce II) avec celles d’Arménie et l’Isaurie la zone de frontière par excellence entre les deux puissances, du moins jusqu’au début de la reconquête byzantine, dans la seconde moitié du IXe siècle

Les Maurozômai, Byzance et le sultanat de Rūm. Note sur le sceau de Jean Comnène Maurozômès

International audienceÉtude de la famille des Maurozômai dans l'Empire byzantin et le sultanat de Rum aux xiie et xiiie siècles

Sceaux des musées de Kayseri et de Niğde (Cappadoce byzantine)

International audiencePublication des sceaux byzantins des musées de Kayseri et Niğde (Turquie)

Byzantium in question in 13th-century Seljuk Anatolia

International audienceÉtude des rapports entre l’Empire byzantin, le sultanat seldjoukide et les communautés chrétiennes et hellénophones d’Anatolie centrale au xiiie siècle

La circulation monétaire dans la Cappadoce byzantine d'après les collections des musées de Kayseri et de Niğde

International audienceL'analyse des monnaies byzantines des collections des deux musées de Cappadoce, Kayseri et Niğde (près de 1500, échelonnées du début du VIe au XIIe siècle) a établi les liens privilégiés de la Cappadoce avec la Syrie et la faiblesse de son intégration économique à l'échelle de l'empire au VIe siècle, la précocité et l'ampleur de la déprise monétaire caractéristique des VIIe et VIIIe siècles, les effets de l'action politique et administrative dans la région. En l'absence de presque toute donnée économique et au vu de la faiblesse des connaissances proprement archéologiques, ces données éclairent avec assez de précision l'insertion de l'Anatolie centrale dans l'économie et les échanges de l'empire en même temps que l'impact, direct et indirect, de la confrontation avec le califat, des conclusions d'autant plus importantes que l'Anatolie centrale est alors la matrice d'une aristocratie militaire et foncière qui s'impose dans le gouvernement de l'Empire à partir du IXe siècle

La Cappadoce et les provinces d’Orient dans l’Antiquité tardive (4e-7e siècle pC)

Although Cappadocia did not become a border province of the Byzantine Empire until the 8th century, it did occupy, particularly its southernmost region, a pivotal position between Anatolia and the Eastern provinces.This location provided a strategic position in the Empire, before weakening after Syria and Mesopotamia passed under Islamic rule. This paper aims at 1) highlighting the close cultural, religious and economic ties that united Cappadocia with Syria and Palestine, precisely when the Eastern Roman Empire began to develop around Constantinople; and 2) analyzing the impact of these links in the very history of Cappadocia. To what extent southern Cappadocia which, for many years, was a contact region, has become a margin

Longitudinal liver stiffness assessment in patient with chronic hepatitis C undergoing antiviral therapy.

BACKGROUND/AIMS:Liver stiffness (LS) measurement by means of transient elastography (TE) is accurate to predict fibrosis stage. The effect of antiviral treatment and virologic response on LS was assessed and compared with untreated patients with chronic hepatitis C (CHC). METHODS: TE was performed at baseline, and at weeks 24, 48, and 72 in 515 patients with CHC. RESULTS: 323 treated (62.7%) and 192 untreated patients (37.3%) were assessed. LS experienced a significant decline in treated patients and remained stable in untreated patients at the end of study (P<0.0001). The decline was significant for patients with baseline LS ≥ 7.1 kPa (P<0.0001 and P 0.03, for LS ≥ 9.5 and ≥ 7.1 kPa vs lower values, respectively). Sustained virological responders and relapsers had a significant LS improvement whereas a trend was observed in nonresponders (mean percent change -16%, -10% and -2%, for SVR, RR and NR, respectively, P 0.03 for SVR vs NR). In multivariate analysis, high baseline LS (P<0.0001) and ALT levels, antiviral therapy and non-1 genotype were independent predictors of LS improvement. CONCLUSIONS: LS decreases during and after antiviral treatment in patients with CHC. The decrease is significant in sustained responders and relapsers (particularly in those with high baseline LS) and suggests an improvement in liver damage

Sustained proliferation in cancer: mechanisms and novel therapeutic targets

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression

Control of Mitochondrial Membrane Permeabilization by Adenine Nucleotide Translocator Interacting with HIV-1 Viral Protein R and Bcl-2

Viral protein R (Vpr), an apoptogenic accessory protein encoded by HIV-1, induces mitochondrial membrane permeabilization (MMP) via a specific interaction with the permeability transition pore complex, which comprises the voltage-dependent anion channel (VDAC) in the outer membrane (OM) and the adenine nucleotide translocator (ANT) in the inner membrane. Here, we demonstrate that a synthetic Vpr-derived peptide (Vpr52-96) specifically binds to the intermembrane face of the ANT with an affinity in the nanomolar range. Taking advantage of this specific interaction, we determined the role of ANT in the control of MMP. In planar lipid bilayers, Vpr52-96 and purified ANT cooperatively form large conductance channels. This cooperative channel formation relies on a direct protein–protein interaction since it is abolished by the addition of a peptide corresponding to the Vpr binding site of ANT. When added to isolated mitochondria, Vpr52-96 uncouples the respiratory chain and induces a rapid inner MMP to protons and NADH. This inner MMP precedes outer MMP to cytochrome c. Vpr52-96–induced matrix swelling and inner MMP both are prevented by preincubation of purified mitochondria with recombinant Bcl-2 protein. In contrast to König's polyanion (PA10), a specific inhibitor of the VDAC, Bcl-2 fails to prevent Vpr52-96 from crossing the mitochondrial OM. Rather, Bcl-2 reduces the ANT–Vpr interaction, as determined by affinity purification and plasmon resonance studies. Concomitantly, Bcl-2 suppresses channel formation by the ANT–Vpr complex in synthetic membranes. In conclusion, both Vpr and Bcl-2 modulate MMP through a direct interaction with ANT