Proper Motion of Pulsar B1800-21

We report high angular resolution, multi-epoch radio observations of the young pulsar PSR B1800-21. Using two pairs of data sets, each pair spanning approximately a ten year period, we calculate the proper motion of the pulsar. We obtain a proper motion of mu_alpha=11.6 +- 1.8 mas/yr, mu_delta=14.8 +- 2.3 mas/yr, which clearly indicates a birth position at the extreme edge of the W30 supernova remnant. Although this does not definitively rule out an association of W30 and PSR B1800-21, it does not support an association.Comment: 13 pages, 1 color figure. Replaced with version accepted for publication in Astrophysical Journa

Clinical utility of genomic signatures in young breast cancer patients: a systematic review

Risk stratification by genomic signatures has been shown to improve prognostication and guide treatment decisions among patients with hormone-sensitive breast cancer. However, their role in young women has not been fully elucidated. In this review, a systematic search was conducted for published articles and abstracts from major congresses that evaluated the use of genomic signatures in young breast cancer patients. A total of 71 studies were analyzed, including 561,188 patients of whom 27,748 (4.9%) were young. Women aged 6440 years were subjected to genomic testing at a similar rate to older women but had a higher proportion of intermediate- to high-risk tumors when classified by EndoPredict (p = 0.04), MammaPrint (p < 0.01), and Oncotype DX (p < 0.01). In young women with low genomic risk, 6-year distant recurrence-free survival was 94%, while 5-year overall survival was nearly 100%. Nonetheless, young patients classified as low-risk had a higher tendency to receive chemotherapy compared to their older counterparts. In conclusion, genomic tests are useful tools for identifying young patients in whom chemotherapy omission is appropriate

Population structure of the Atlantic spotted dolphin (Stenella frontalis) inferred through ecological markers

Population structure studies play an increasingly integral role in conservation and management of marine mammal species. Genetic markers are commonly used; however, ecological markers (i.e. chemical compounds) are a fairly recent and useful tool to investigate ecological management units. The objective of this study is to investigate the population structure of the Atlantic spotted dolphin (Stenella frontalis) within its distribution in the Atlantic Ocean using data from stable isotopes of delta C-13 and delta N-15 and persistent organic pollutants as ecological markers. Based on previous studies that addressed distribution, morphometric analyses and molecular and ecological markers, we hypothesize that there are several ecological management units within the Atlantic Ocean. Our results confirmed population differentiation previously detected using genetic markers. Additionally, dolphins from the south-eastern coast of Brazil do not show complete ecological segregation from the Caribbean ones, while molecular analyses suggested genetic differentiation between the two regions. In the light of these results, we propose that at least two ecological management units should be considered, east and west of the Atlantic Ocean; however, the presence of one or two management units along the Atlantic coast of Central and South America needs further investigation

Glioma-induced inhibition of caspase-3 in microglia promotes a tumor-supportive phenotype

Glioma cells recruit and exploit microglia (the resident immune cells of the brain) for their proliferation and invasion ability. The underlying molecular mechanism used by glioma cells to transform microglia into a tumor-supporting phenotype has remained elusive. We found that glioma-induced microglia conversion was coupled to a reduction in the basal activity of microglial caspase-3 and increased S-nitrosylation of mitochondria-associated caspase-3 through inhibition of thioredoxin-2 activity, and that inhibition of caspase-3 regulated microglial tumor-supporting function. Furthermore, we identified the activity of nitric oxide synthase 2 (NOS2, also known as iNOS) originating from the glioma cells as a driving stimulus in the control of microglial caspase-3 activity. Repression of glioma NOS2 expression $\textit{in vivo}$ led to a reduction in both microglia recruitment and tumor expansion, whereas depletion of microglial caspase-3 gene promoted tumor growth. Our results provide evidence that inhibition of the denitrosylation of S-nitrosylated procaspase-3 mediated by the redox protein Trx2 is a part of the microglial pro-tumoral activation pathway initiated by glioma cancer cells.Supported by the Karolinska Institutet Foundation (X.S. and B.J.), the Swedish Childhood Cancer Foundation (A.M.O., B.J. and K.B.), the Swedish Research Council (M.A.B. and B.J.), the Strategic Research Programme in Cancer (B.J.), the Strategic Research Programme in Neuroscience (K.B.), the Swedish Cancer Foundation (B.J.), Spanish MINECO/FEDER/UE (J.L.V.), the Swedish Cancer Society (B.J.), the Swedish Brain Foundation (B.J.) and Swedish governmental grants for researchers working in healthcare (K.B.)

Correction: Viral burden is associated with age, vaccination, and viral variant in a population-representative study of SARS-CoV-2 that accounts for time-since-infection-related sampling bias.

[This corrects the article DOI: 10.1371/journal.ppat.1011461.]

Viral burden is associated with age, vaccination, and viral variant in a population-representative study of SARS-CoV-2 that accounts for time-since-infection-related sampling bias.

In this study, we evaluated the impact of viral variant, in addition to other variables, on within-host viral burden, by analysing cycle threshold (Ct) values derived from nose and throat swabs, collected as part of the UK COVID-19 Infection Survey. Because viral burden distributions determined from community survey data can be biased due to the impact of variant epidemiology on the time-since-infection of samples, we developed a method to explicitly adjust observed Ct value distributions to account for the expected bias. By analysing the adjusted Ct values using partial least squares regression, we found that among unvaccinated individuals with no known prior exposure, viral burden was 44% lower among Alpha variant infections, compared to those with the predecessor strain, B.1.177. Vaccination reduced viral burden by 67%, and among vaccinated individuals, viral burden was 286% higher among Delta variant, compared to Alpha variant, infections. In addition, viral burden increased by 17% for every 10-year age increment of the infected individual. In summary, within-host viral burden increases with age, is reduced by vaccination, and is influenced by the interplay of vaccination status and viral variant