University of Cyprus

Amid intensifying great-power rivalry and the growing geo-economic centrality of energy corridors, the Eastern Mediterranean has re-emerged as a pivotal arena of strategic contestation in the post-Cold War order. Against this backdrop, this study asks: How has U.S. policy shaped the evolving energy and security dynamics of the Eastern Mediterranean since the 2000s, and what has this meant for regional alignments—particularly with regard to Türkiye—and for competition with Russia and China? By addressing this question, the study seeks to assess not only Washington’s strategic objectives and policy instruments, but also the broader implications of its engagement for regional order and great-power rivalry, using strategic landscape analysis as the guiding methodological framework along with case study and secondary resources. The findings indicate that U.S. policy has reshaped the Eastern Mediterranean’s energy and security landscape primarily through security partnerships, legislative initiatives, and calibrated military engagement rather than direct energy dependence. By strengthening ties with Greece, the Republic of Cyprus, Israel, and Egypt, Washington has contributed to the consolidation of new regional alignments, while its strained relations with Türkiye—amid maritime disputes, defense tensions, and Syria policy divergences—have encouraged Ankara’s more autonomous and at times Russia-leaning posture. Simultaneously, U.S. efforts to counter Russian military entrenchment and limit China’s infrastructural and technological expansion have embedded the region more deeply within broader patterns of great-power competition, transforming the regional, if not global, energy security order.

The Cyprus Genome Project characterizes the genetic landscape of the Cypriot population to address the lack of population-specific data in global repositories. We employed a serial independent pool-sequencing (pool-seq) strategy to sequence DNA from 10,000 healthy bone marrow donors, randomized into 10 independent biological replicates. This study design was selected to leverage specific operational and statistical advantages. Operationally, the method enables the processing of a large cohort that would be cost-prohibitive using individual sequencing. Statistically, the use of 10 independent biological replicates allowed for the differentiation of true low-frequency variants from sequencing artifacts. Furthermore, this design enabled the calculation of empirical confidence intervals for variant frequencies. We utilized both Whole Exome Sequencing and a targeted gene panel (813 genes) to maximize read depth and sensitivity. The study identified over 4 million variants, including > 100,000 variants absent from the gnomAD v4.1 and ClinVar databases. Validation against published clinical cohorts confirmed high concordance (r > 0.92). The results highlight significant differences between local and global allele frequencies, including pathogenic variants that are common in Cyprus but rare globally. The results, including an interactive genome map with full annotations from gnomAD v4.1 and ClinVar, are publicly accessible at www.cyprusgenome.org, with the aim of advancing healthcare and facilitating future clinical research.

Inherited kidney diseases represent a genetically and clinically heterogeneous group of disorders affecting both pediatric and adult populations. Advances in next-generation sequencing (NGS) have improved diagnostic precision; however, genotype-phenotype correlations and diagnostic yield vary substantially across disease entities. We retrospectively evaluated 165 patients referred for genetic testing due to suspected inherited kidney disease. Patients were classified into three clinical groups: polycystic kidney disease, Alport syndrome, and other syndromic patients with inherited kidney diseases. Genetic analysis was performed using NGS with Human Phenotype Ontology-based gene filtering and included evaluation of both single-nucleotide variants and copy number variations. Overall diagnostic yield differed markedly between groups. A molecular diagnosis was achieved in 71.4% of Alport patients, 41.0% of PKD patients, and 70.2% of patients in the Other syndromic group. In the Alport group, variants were identified exclusively in COL4A3, COL4A4, and COL4A5, with pathogenicity and gene involvement correlating with disease severity and the presence of extrarenal manifestations. The PKD group showed predominant involvement of PKD1, followed by PKHD1 and PKD2, while a substantial proportion of patients remained genetically negative, reflecting technical and biological complexity. The Other group exhibited pronounced genetic heterogeneity, with variants distributed across multiple genes involved in tubular, glomerular, metabolic, and ciliopathy-related pathways. Computational assessments demonstrated that several variants of uncertain significance (VUS) were located in functionally critical domains and were predicted to disrupt protein stability, intermolecular interactions, or conserved structural motifs, thereby supporting the biological plausibility of their potential pathogenic impact. Phenotype-driven NGS enables effective molecular diagnosis across diverse inherited kidney diseases while revealing disease-specific differences in diagnostic yield and genotype-phenotype correlations. Systematic inclusion of variants of uncertain significance and careful integration of genetic and clinical data are essential for accurate interpretation and long-term patient management. Collectively, this study enhances understanding of inherited kidney diseases and underscores the value of integrating comprehensive genomic and computational approaches into routine nephrogenetic practice.

Spatial heterogeneity in water and energy fluxes drives patterns of vegetation productivity and soil carbon and nutrient cycling across landscapes. However, most ecohydrological models either neglect lateral transfers or treat biogeochemical processes in a spatially decoupled manner, limiting their ability to reproduce observed catchment-scale patterns. We address this gap by extending the mechanistic ecohydrological model Tethys–Chloris–Biogeochemistry (T&C-BG) to a fully distributed configuration (T&C-BG-2D) that explicitly represents lateral routing of soil carbon and nutrients. The model is evaluated against long-term hydrological and biogeochemical observations from the Hafren catchment (UK) and the Erlenbach catchment (Swiss pre-Alps), where it successfully reproduces observed dynamics of several river solutes, including dissolved organic carbon, ammonia, and nitrate. To overcome the computational bottleneck of distributed model initialization, we further introduce a hybrid spin-up framework combining flux-tracking one-dimensional simulations with a random forest–based spatial extrapolation. This approach efficiently generates spatially heterogeneous and topography-informed initial conditions while reducing computational costs by up to 90%. Together, these advances enable efficient, spatially explicit ecohydrological–biogeochemical modeling across complex landscapes.

Suzuki–Miyaura coupling of 3-chloro-5-[(2-ethylhexyl)amino]-4H-1,2,6-thiadiazin-4-one with phenylboronic acid, at ca. 100 °C, gave 3-[(2-ethylhexyl)amino]-5-phenyl-4H-1,2,6-thiadiazin-4-one in 69% yield. Another nucleophilic substitution reaction of 3-chloro-5-[(4-oxo-5-phenyl-4H-1,2,6-thiadiazin-3-yl)amino]-4H-1,2,6-thiadiazin-4-one with 2-ethylhexan-1-amine at ca. 100 °C gave 3-[(2-ethylhexyl)amino]-5-[(4-oxo-5-phenyl-4H-1,2,6-thiadiazin-3-yl)amino]-4H-1,2,6-thiadiazin-4-one in 93% yield.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host immune response to an infection. Sepsis is often associated with significant hemostatic disorders that may lead to extensive intravascular thrombosis, disseminated intravascular coagulation (DIC), multi-organ dysfunction syndrome (MODS), and increased mortality. Sepsis-induced coagulopathy (SIC) is currently recognized as an early distinct phase of hemostatic derangement caused by sepsis, and a prodrome of overt DIC. SIC is characterized by endovascular clotting activation, hypercoagulability, and consumption of clotting factors and platelets. DIC, traditionally considered the final stage of this process, is now recognized as a part of a continuum of pathophysiological dysregulation with a distinct clinical significance. Despite being extensively studied in the adult population, SIC remains poorly defined in neonates. The distinct characteristics of neonatal hemostasis, coupled with immunological immaturity, pose significant challenges to the direct application of adult diagnostic approaches of SIC in this population. This review focuses on the pathophysiological mechanisms of SIC and the unique characteristics of neonatal hemostasis, summarizes current knowledge regarding the underlying mechanisms of neonatal SIC, and explores the developmental interplay between inflammation and hemostasis. By integrating current evidence, the review aims to establish a conceptual framework that will guide future experimental and clinical studies directed toward improving the management and outcomes of neonates who develop coagulopathy during sepsis.