Publications by authors named "S I Kleĭner"

Congenital heart disease (CHD) is the most common birth defect in newborns, often requiring cardiac surgery with concomitant thymectomy that is known to increase disease susceptibility later in life. Studies of γδ T cells, which are one of the dominant T cells in the early fetal human thymus, are rare. Here, we provide a comprehensive analysis of the γδ T cell compartment via flow cytometry and next-generation sequencing in children and infants with CHD, who underwent cardiac surgery shortly after birth.

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Background: This study aimed to assess the impact of dedicated cardiac protocol (DCP) on diagnostic accuracy of state-of-the-art digital [F]-FDG-PET/CT in infective endocarditis (IE) and the intra-individual comparison of the performance with that of conventional whole-body approach (WBA) and to analyze the effects of the expertise level of the investigators.

Methods: 44 patients suspected for IE underwent digital-FDG-PET/CT after overnight fasting. Each three consultants and trainees reread PET images blinded to the examination approach and clinical information.

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Hydrogels derived from fluorenylmethoxycarbonyl (Fmoc)-conjugated amino acids and peptides demonstrate remarkable potential in biomedical applications, including drug delivery, tissue regeneration, and tissue engineering. These hydrogels can be injectable, offering a minimally invasive approach to hydrogel implantation. Given their potential for prolonged application, there is a need for non-destructive evaluation of their properties over extended periods.

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Article Synopsis
  • Mutations in the COL1A1 and COL1A2 genes, which produce type I collagen, are found in 85%-90% of osteogenesis imperfecta (OI) patients, leading to weak bones and skeletal deformities.
  • The study used mouse models to explore the effects of monoclonal antibodies targeting activin A and myostatin on muscle and bone in both normal and OI-affected mice.
  • Results showed that while myostatin inhibition increased muscle mass in all mice, none of the treatments significantly improved bone structure, particularly in cortical bone, highlighting limitations in using these pathways for treating bone-related issues in OI.
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Asynchronous skeletal muscle degeneration/regeneration is a hallmark feature of Duchenne muscular dystrophy (DMD); however, traditional -omics technologies that lack spatial context make it difficult to study the biological mechanisms of how asynchronous regeneration contributes to disease progression. Here, using the severely dystrophic D2-mdx mouse model, we generated a high-resolution cellular and molecular spatial atlas of dystrophic muscle by integrating spatial transcriptomics and single-cell RNAseq datasets. Unbiased clustering revealed nonuniform distribution of unique cell populations throughout D2-mdx muscle that were associated with multiple regenerative timepoints, demonstrating that this model faithfully recapitulates the asynchronous regeneration observed in human DMD muscle.

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