Inflammatory responses to acute exercise during pulmonary rehabilitation in patients with COPD

Objective Pulmonary rehabilitation is a cornerstone treatment in the management of chronic obstructive pulmonary disease (COPD). Acute bouts of exercise can lead to short bursts of inflammation in healthy individuals. However, it is unclear how COPD patients respond to acute bouts of exercise. This study assessed inflammatory responses to exercise in COPD patients at the start (phase 1) and end (phase 2) of pulmonary rehabilitation. Methods Blood samples were collected before and after an acute exercise bout at the start (phase 1, n = 40) and end (phase 2, n = 27) of pulmonary rehabilitation. The primary outcome was change in fibrinogen concentrations. Secondary outcomes were changes in CRP concentrations, total/differential leukocyte counts, markers of neutrophil activation (CD11b, CD62L and CD66b), and neutrophil subsets (mature, suppressive, immature, progenitor). Results Acute exercise (phase 1) did not induce significant changes in fibrinogen (p = 0.242) or CRP (p = 0.476). Total leukocyte count [mean difference (MD), 0.5 ± 1.1 (109 L−1); p = 0.004], neutrophil count [MD, 0.4 ± 0.8 (109 L−1); p < 0.001], and immature neutrophils (MD, 0.6 ± 0.8%; p < 0.001) increased post-exercise. Neutrophil activation markers, CD11b (p = 0.470), CD66b (p = 0.334), and CD62L (p = 0.352) were not significantly altered post-exercise. In comparison to the start of pulmonary rehabilitation (phase 2), acute exercise at the end of pulmonary rehabilitation led to a greater fibrinogen response (MD, 84 mg/dL (95% CI − 14, 182); p = 0.045). Conclusion An acute bout of exercise does not appear to induce significant alterations in the concentrations of inflammatory mediators but can increase white blood cell subsets post-exercise. A greater fibrinogen response to acute exercise is seen at the end of pulmonary rehabilitation when compared to the start. Further research is required to understand the clinical context of these acute inflammatory responses to exercise

The drivers and functions of rock juggling in otters

This is the final version. Available on open access from the Royal Society via the DOI in this recordData accessibility: Data and code for rock juggling frequency, hunger and food puzzles can be accessed through the Dryad Digital Repository: https://doi.org/10.5061/dryad.rn8pk0p64. Tables of post hoc test results for puzzle order have been uploaded as part of the electronic supplementary material.Object play refers to the seemingly non-functional manipulation of inanimate items when in a relaxed state. In juveniles, object play may help develop skills to aid survival. However, why adults show object play remains poorly understood. We studied potential drivers and functions of the well-known object play behaviour of rock juggling in Asian small-clawed (Aonyx cinereus) and smooth-coated (Lutrogale perspicillata) otters. These are closely related species, but Asian small-clawed otters perform extractive foraging movements to exploit crabs and shellfish while smooth-coated otters forage on fish. We thus predicted that frequent rock jugglers might be better at solving extractive foraging puzzles in the first species, but not the latter. We also assessed whether species, age, sex and hunger correlated with rock juggling frequency. We found that juvenile and senior otters juggled more than adults. However, rock juggling frequency did not differ between species or sexes. Otters juggled more when ‘hungry’, but frequent jugglers did not solve food puzzles faster. Our results suggest that rock juggling may be a misdirected behaviour when hungry and may facilitate juveniles’ motor development, but it appears unrelated to foraging skills. We suggest future studies to reveal the ontogeny, evolution and welfare implications of this object play behaviour.Royal Societ

Varieties of living things: Life at the intersection of lineage and metabolism

publication-status: Publishedtypes: Articl

Racial differences in human platelet PAR4 reactivity reflect expression of PCTP and miR-376c.

Racial differences in the pathophysiology of atherothrombosis are poorly understood. We explored the function and transcriptome of platelets in healthy black (n = 70) and white (n = 84) subjects. Platelet aggregation and calcium mobilization induced by the PAR4 thrombin receptor were significantly greater in black subjects. Numerous differentially expressed RNAs were associated with both race and PAR4 reactivity, including PCTP (encoding phosphatidylcholine transfer protein), and platelets from black subjects expressed higher levels of PC-TP protein. PC-TP inhibition or depletion blocked PAR4- but not PAR1-mediated activation of platelets and megakaryocytic cell lines. miR-376c levels were differentially expressed by race and PAR4 reactivity and were inversely correlated with PCTP mRNA levels, PC-TP protein levels and PAR4 reactivity. miR-376c regulated the expression of PC-TP in human megakaryocytes. A disproportionately high number of microRNAs that were differentially expressed by race and PAR4 reactivity, including miR-376c, are encoded in the DLK1-DIO3 locus and were expressed at lower levels in platelets from black subjects. These results suggest that PC-TP contributes to the racial difference in PAR4-mediated platelet activation, indicate a genomic contribution to platelet function that differs by race and emphasize a need to consider the effects of race when developing anti-thrombotic drugs

Chloramphenicol causes fusion of separated nucleoids in Escherichia coli K-12 cells and filaments.

Chloramphenicol is frequently used for better visualization of the Escherichia coli nucleoid. Here, we show that chloramphenicol causes not only rounding off of the nucleoid but also fusion of as many as four separated nucleoids. Nucleoid fusion occurred in fast-growing cells and in filaments obtained by dicF antisense RNA induction or in ftsZ84(Ts) and pbpB(Ts) mutants. Thus, treatment with chloramphenicol erroneously suggests that DNA segregation is inhibited