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Hassing Albert posted an update 6 months, 2 weeks ago
IL-9 is produced by Th9 cells and is classically known as a growth-promoting cytokine. Although protumorigenic functions of IL-9 are described in T cell lymphoma, recently, we and others have reported anti-tumor activities of IL-9 in melanoma mediated by mast cells and CD8+ T cells. However, involvement of IL-9 in invasive breast and cervical cancer remains unexplored. In this study, we demonstrate IL-9-dependent inhibition of metastasis of both human breast (MDA-MB-231 and MCF-7) and cervical (HeLa) tumor cells in physiological three-dimensional invasion assays. To dissect underlying mechanisms of IL-9-mediated suppression of invasion, we analyzed IL-9-dependent pathways of cancer cell metastasis, including proteolysis, contractility, and focal adhesion dynamics. IL-9 markedly blocked tumor cell-collagen degradation, highlighting the effects of IL-9 on extracellular matrix remodeling. Moreover, IL-9 significantly reduced phosphorylation of myosin L chain and resultant actomyosin contractility and also increased focal adhesion formation. Finally, IL-9 suppressed IL-17- and IFN-γ-induced metastasis of both human breast (MDA-MB-231) and cervical (HeLa) cancer cells. In conclusion, IL-9 inhibits the metastatic potential of breast and cervical cancer cells by controlling extracellular matrix remodeling and cellular contractility.We use publicly available data to show that published papers in top psychology, economics, and general interest journals that fail to replicate are cited more than those that replicate. This difference in citation does not change after the publication of the failure to replicate. #link# Only 12% of postreplication citations of nonreplicable findings acknowledge the replication failure. Existing evidence also shows that experts predict well which papers will be replicated. Given this prediction, why are nonreplicable papers accepted for publication in the first place? A possible answer is that the review team faces a trade-off. When the results are more “interesting,” they apply lower standards regarding their reproducibility.Subsoils below 20 cm are an important reservoir in the global carbon cycle, but little is known about their vulnerability under climate change. We measured a statistically significant loss of subsoil carbon (-33 ± 11%) in warmed plots of a conifer forest after 4.5 years of whole-soil warming (4°C). The loss of subsoil carbon was primarily from unprotected particulate organic matter. Warming also stimulated a sustained 30 ± 4% increase in soil CO2 efflux due to increased CO2 production through the whole-soil profile. The observed in situ decline in subsoil carbon stocks with warming is now definitive evidence of a positive soil carbon-climate feedback, which could not be concluded based on increases in CO2 effluxes alone. The high sensitivity of subsoil carbon and the different responses of soil organic matter pools suggest that models must represent these heterogeneous soil dynamics to accurately predict future feedbacks to warming.MRN-MDC1 plays a central role in the DNA damage response (DDR) and repair. Using proteomics of isolated chromatin fragments, we identified DDR factors, such as MDC1, among those highly associating with a genomic locus upon transcriptional activation. Purification of MDC1 in the absence of exogenous DNA damage revealed interactions with factors involved in gene expression and RNA processing, in addition to DDR factors. ChIP-seq showed that MRN subunits, MRE11 and NBS1, colocalized throughout the genome, notably at TSSs and bodies of actively transcribing genes, which was dependent on the RNAPII transcriptional complex rather than transcription per se. Depletion of MRN increased RNAPII abundance at MRE11/NBS1-bound genes. Prolonged MRE11 or NBS1 depletion induced single-nucleotide polymorphisms across actively transcribing MRN target genes. These data suggest that association of MRN with the transcriptional machinery constitutively scans active genes for transcription-induced DNA damage to preserve the integrity of the coding genome.
To examine presentation, management and long-term sequelae of ocular hypertension and uveitic glaucoma.
Retrospective observational study of all subjects with uveitic glaucoma or ocular hypertension seen in Auckland uveitis clinics over the last 10 years.
A total of 188 eyes of 139 subjects with uveitic glaucoma or ocular hypertension were included for analysis. Total follow-up was 1854.5 eye years (mean 9.9 years). The mean age at uveitis diagnosis was 49.3 years. 52.5% of subjects were male. The most common diagnoses were idiopathic uveitis (29.3%), sarcoidosis (13.3%), herpes zoster (6.9%), HLA-B27 uveitis (6.9%), tuberculosis (5.9%) and Posner-Schlossmann or cytomegalovirus (CMV) uveitis (5.3%). Median intraocular pressure (IOP) at diagnosis was 35 mm Hg (IQR 29-45). 144 eyes (77.0%) developed glaucoma during the follow-up period, of whom 41 lost some central vision due to glaucoma. Oral acetazolamide was required for IOP control in 64.5%, 50 eyes underwent trabeculectomy, 18 eyes required a tube and 6 underwent minimally invasive glaucoma surgery.
Rapid progression was observed from ocular hypertension to uveitic glaucoma. Uveitic glaucoma is aggressive, with high likelihood of requiring surgical management and high risk of central vision loss. Close collaboration between uveitis and glaucoma specialists is required to maximise outcomes for these patients.
Rapid progression was observed from ocular hypertension to uveitic glaucoma. Uveitic glaucoma is aggressive, with high likelihood of requiring surgical management and high risk of central vision loss. Close collaboration between uveitis and glaucoma specialists is required to maximise outcomes for these patients.The common cooccurrence of antibiotics and phages in both natural and engineered environments underscores the need to understand their interactions and implications for bacterial control and antibiotic resistance propagation. Here, aminoglycoside antibiotics that inhibit protein synthesis (e.g., kanamycin and neomycin) impeded the replication of coliphage T3 and Bacillus phage BSP, reducing their infection efficiency and mitigating their hindrance of bacterial growth, biofilm formation, and tolerance to antibiotics. For example, treatment with phage T3 reduced subsequent biofilm formation by Escherichia coli liquid cultures to 53% ± 5% of that of the no-phage control, but a smaller reduction of biofilm formation (89% ± 10%) was observed for combined exposure to phage T3 and kanamycin. Despite sharing a similar mode of action with aminoglycosides (i.e., inhibiting protein synthesis) and antagonizing phage replication, albeit to a lesser degree, tetracyclines did not inhibit bacterial control by phages. selleck chemicals combined with tetracycline showed higher suppression of biofilm formation than when combined with aminoglycosides (25% ± 6% of the no-phage control).
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