Ena-DATASET-KULVIB-23-04-2019-13:34:17:693-212 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001004969 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Three vaccines are recommended by the Advisory Committee on Immunization Practices (ACIP) for routine vaccination of adolescents aged 11-12 years to protect against 1) pertussis; 2) meningococcal disease caused by types A, C, W, and Y; and 3) human papillomavirus (HPV)-associated cancers (1). At age 16 years, a booster dose of quadrivalent meningococcal conjugate vaccine (MenACWY) is recommended. Persons aged 16-23 years can receive serogroup B meningococcal vaccine (MenB), if determined to be appropriate through shared clinical decision-making. CDC analyzed data from the 2019 National Immunization Survey-Teen (NIS-Teen) to estimate vaccination coverage among adolescents aged 13-17 years in the United States.* Coverage with ?1 dose of HPV vaccine increased from 68.1% in 2018 to 71.5% in 2019, and the percentage of adolescents who were up to date† with the HPV vaccination series (HPV UTD) increased from 51.1% in 2018 to 54.2% in 2019. Both HPV vaccination coverage measures improved among females and males. An increase in adolescent coverage with ?1 dose of MenACWY (from 86.6% in 2018 to 88.9% in 2019) also was observed. Among adolescents aged 17 years, 53.7% received the booster dose of MenACWY in 2019, not statistically different from 50.8% in 2018; 21.8% received ?1 dose of MenB, a 4.6 percentage point increase from 17.2% in 2018. Among adolescents living at or above the poverty level,§ those living outside a metropolitan statistical area (MSA)¶ had lower coverage with ?1 dose of MenACWY and with ?1 HPV vaccine dose, and a lower percentage were HPV UTD, compared with those living in MSA principal cities. In early 2020, the coronavirus disease 2019 (COVID-19) pandemic changed the way health care providers operate and provide routine and essential services. An examination of Vaccines for Children (VFC) provider ordering data showed that vaccine orders for HPV vaccine; tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap); and MenACWY decreased in mid-March when COVID-19 was declared a national emergency (Supplementary Figure 1, https://stacks.cdc.gov/view/cdc/91795). Ensuring that routine immunization services for adolescents are maintained or reinitiated is essential to continuing progress in protecting persons and communities from vaccine-preventable diseases and outbreaks.
| S-EPMC7439984 | biostudies-literature
Project description:Streptococcus mitis 17/34 Genome sequencing and assembly
| PRJNA206048 | ENA
Project description:Alzheimer's disease is the most common neurodegenerative disorder in the world. Its most significant symptoms are memory loss and decrease in cognition. Alzheimer's disease is characterized by aggregation of two proteins in the brain namely A? (amyloid ?) and tau. Recent evidence suggests that the interaction of soluble A? with nAChR (nicotinic acetylcholine receptors) contributes to disease progression. In this study, we determine the NMR structure of an A?17-34 peptide solubilized by the addition of two glutamic acids at each terminus. Our results indicate that the A? peptide adopts an ?-helical structure for residues 19-26 and 28-33. The ?-helical structure is broken around residues S26, N27 and K28, which form a kink in the helical conformation. This ?-helix was not described earlier in an aqueous solution without organic solvents, and at physiological conditions (pH 7). These data are in agreement with A? adopting an ?-helical conformation in the membrane before polymerizing into amyloid ?-sheets and provide insight into the intermediate state of A? in Alzheimer's disease.
| S-EPMC4242080 | biostudies-literature
Project description:PURPOSE OF REVIEW:To inform readers of recent advances in our understanding of the development and function of Th17 T cells and emerging data suggesting that the interleukin-23/interleukin-17 axis may be involved in the pathogenesis of spondyloarthritis. RECENT FINDINGS:The discovery of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existing paradigms and the role of Th1 T cells in many autoimmune diseases. The development and cytokine profile of Th17 T cells differs in mice and humans. In humans, interleukin-23 synergizes with interleukin-6 and interleukin-1 to promote Th17 development. In mice, transforming growth factor-beta and interleukin-6 are critical, whereas interleukin-23 is more important at later stages promoting interleukin-17 production. In mice, CD4+ cells producing interferon-gamma appear to be distinct from interleukin-17-producing cells, while in humans cells secreting both cytokines have been observed. Growing evidence from animal models, cytokine analyses of patient fluids, and whole-genome association studies suggest that the interleukin-23/interleukin-17 axis plays an important role in spondyloarthritis pathogenesis. Possible links between an HLA-B27-induced unfolded protein response and activation of the interleukin-23/interleukin-17 axis have been observed in animal models and may contribute to the development of the spondyloarthritis phenotype. SUMMARY:Activation of the interleukin-23/interleukin-17 axis in spondyloarthritis has important therapeutic implications.
| S-EPMC3494971 | biostudies-literature
Project description: Not available
| S-EPMC6630869 | biostudies-literature
Project description:This article highlights and emphasizes how new knowledge of mechanisms linked to the interleukin-23 (IL-23)/IL-17 pathway is relevant to the pathophysiology of axial spondyloarthritis (axSpA) and demonstrates how molecules in IL-23/IL-17 pathway provide novel therapeutic targets for axSpA patients.Similarly to ankylosing spondylitis (AS), the increased frequency of Th17 cells in nr-axSpA patients underscores the concept that these disorders can be viewed on a spectrum. Recent findings suggest that the contribution of IL-23/IL-17 signaling pathways possibly differs in male and female AS patients. The finding that IL-17 and IL-22 secreting-type 3 innate lymphoid cells are increased in AS patients point to their potential role in the pathogenesis of axSpA. Reports of dysbiosis in the gut microbiome of AS patients support previous work indicating a possible causal relationship between altered gut flora, ileocolonic inflammation and axSpA. Of important clinical relevance are results from clinical trials supporting the efficacy and safety of agents that block IL-12/23 (ustekinumab) and IL-17 (secukinumab and ixekizumab) in AS patients.Recent studies further establish the central position of the IL-23/IL-17 pathway in the pathogenesis of axSpA. Targeting the IL-23/IL-17 pathway appears to be a safe and effective strategy for treatment of axSpA patients.
| S-EPMC5777167 | biostudies-literature
Project description:In inflammatory rheumatic disorders, the immune system attacks and damages the connective tissues and invariably internal organs. During the past decade, remarkable advances having been made towards our understanding on the cellular and molecular mechanisms involved in rheumatic diseases. The discovery of IL-23/IL-17 axis and the delineation of its important role in the inflammation led to the introduction of many needed new therapeutic tools. We will present an overview of the rationale for targeting therapeutically the IL-23/IL-17 axis in rheumatic diseases and the clinical benefit which has been realized so far. Finally, we will discuss the complex interrelationship between IL-23 and IL-17 and the possible uncoupling in certain disease settings.
| S-EPMC8018566 | biostudies-literature
Project description:Interleukin-23 (IL-23) is known to play a crucial role in the development and maintenance of T helper 17 cells. It has been previously demonstrated that IL-17 is involved in experimental Lyme arthritis, caused by Borrelia burgdorferi bacteria. However, the precise role of the IL-23 receptor (IL-23R) for the B. burgdorferi-induced IL-17 responses or human Lyme disease has not yet been elucidated. IL-23R single nucleotide polymorphism (SNP) rs11209026 was genotyped using the TaqMan assay. Functional studies were performed using peripheral blood mononuclear cells, and cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Dose-dependent production of IL-23 and IL-17 by B. burgdorferi could be observed. Interestingly, when IL-23 bioactivity was inhibited by a specific antibody against IL-23p19, IL-17 production was significantly downregulated. In contrast, production of gamma interferon (IFN-?) was not affected after the blockade of IL-23 activity. Moreover, individuals bearing a single nucleotide polymorphism in the IL-23R gene (Arg381Gln) produced significantly less IL-17 after B. burgdorferi stimulation compared with that of the individuals bearing the wild type. Despite lower IL-17 production, the IL-23R gene polymorphism did not influence the development of chronic Lyme disease in a cohort of patients with Lyme disease. This study demonstrates that IL-23R signaling is needed for B. burgdorferi-induced IL-17 production in vitro and that an IL-23R gene SNP leads to impaired IL-17 production. However, the IL-23R gene polymorphism is not crucial for the pathogenesis of chronic Lyme.
| S-EPMC3257938 | biostudies-literature
Project description:The misfolding and self-assembly of the amyloid-beta (Aβ) peptide into aggregates is a molecular signature of the development of Alzheimer's disease, but molecular mechanisms of the peptide aggregation remain unknown. Here, we combined Atomic Force Microscopy (AFM) and Molecular Dynamics (MD) simulations to characterize the misfolding process of an Aβ peptide. Dynamic force spectroscopy AFM analysis showed that the peptide forms stable dimers with a lifetime of ∼1 s. During MD simulations, isolated monomers gradually adopt essentially similar nonstructured conformations independent from the initial structure. However, when two monomers approach their structure changes dramatically, and the conformational space for the two monomers become restricted. The arrangement of monomers in antiparallel orientation leads to the cooperative formation of β-sheet conformation. Interactions, including hydrogen bonds, salt bridges, and weakly polar interactions of side chains stabilize the structure of the dimer. Under the applied force, the dimer, as during the AFM experiments, dissociates in a cooperative manner. Thus, misfolding of the Aβ peptide proceeds via the loss of conformational flexibility and formation of stable dimers suggesting their key role in the subsequent Aβ aggregation process.
| S-EPMC3695694 | biostudies-literature
Project description:Description not provided
| EGAD00001005088 | EGA