The gut microbiome consists of a multi-kingdom microbial community. Whilst the role of bacteria as causal contributors governing host physiological development is well established, the role of fungi remains to be determined. Here, we use germ-free mice colonized with defined species of bacteria, fungi, or both to differentiate the causal role of fungi on microbiome assembly, immune development, susceptibility to colitis, and airway inflammation. Fungal colonization promotes major shifts in bacterial microbiome ecology, and has an independent effect on innate and adaptive immune development in young mice. While exclusive fungal colonization is insufficient to elicit overt dextran sulfate sodium-induced colitis, bacterial and fungal co-colonization increase colonic inflammation. Ovalbumin-induced airway inflammation reveals that bacterial, but not fungal colonization is necessary to decrease airway inflammation, yet fungi selectively promotes macrophage infiltration in the airway. Together, our findings demonstrate a causal role for fungi in microbial ecology and host immune functionality, and therefore prompt the inclusion of fungi in therapeutic approaches aimed at modulating early life microbiomes.

Telehealth-PR was an effective tool for increasing COPD PR services, and demonstrated improvements in quality of life and exercise capacity comparable with Standard-PR.

Key points• Sympathetic nervous system activity causes tonic vasoconstriction in resting and contracting skeletal muscle. Vasoactive molecules released from the active skeletal muscle and/or endothelium have been shown to inhibit sympathetic vasoconstriction, a phenomenon defined as functional sympatholysis.• A definitive mechanism responsible for functional sympatholysis has yet to be identified; however, nitric oxide (NO) appears to be involved.• It is unknown whether exercise training alters the inhibition of sympathetic vasoconstriction and NO-mediated sympatholysis in resting and contracting skeletal muscle.• The present findings demonstrate that short-term exercise training augments functional sympatholysis in a training-intensity-dependent manner through a NO-dependent mechanism. These novel findings advance our understanding of the effects of exercise training on the regulation of sympathetic vasoconstriction in resting and contracting skeletal muscle.Abstract We tested the hypothesis that short-term mild-(M) and heavy-intensity (H) exercise training would enhance sympatholysis through a nitric oxide (NO)-dependent mechanism. Sprague-Dawley rats (n = 36) were randomly assigned to sedentary (S) or to M (20 m min −1 5% gradient) or H exercise training groups (40 m min −1 5% gradient). Rats assigned to M and H groups trained on 5 days week −1 for 4 weeks, with the volume of training being matched between groups. Rats were anaesthetized and instrumented for stimulation of the lumbar sympathetic chain and the measurement of arterial blood pressure and femoral artery blood flow. The triceps surae muscle group was stimulated to contract rhythmically at 30 and 60% of maximal contractile force (MCF). The percentage change of femoral vascular conductance (%FVC) in response to sympathetic stimulation delivered at 2 and 5 Hz was determined at rest and during contraction at 30 and 60% MCF. The vascular response to sympathetic stimulation was reduced as a function of MCF in all rats (P < 0.05). At 30% MCF, the magnitude of sympatholysis (%FVC restcontraction; %FVC) was greater in H compared with M and S groups ( %FVC at 2 Hz, S, 9 ± 5; M, 11 ± 8; and H, 18 ± 7; and %FVC at 5 Hz, S, 6 ± 6; M, 12 ± 9; and H, 18 ± 7; P < 0.05) and was greater in H and M compared with S at 60% MCF ( %FVC at 2 Hz, S, 15 ± 5; M, 25 ± 3; and H, 36 ± 6; and %FVC at 5 Hz, S, 22 ± 6; M, 33 ± 9; and H, 39 ± 9; P < 0.05). Blockade of NO synthase did not alter the magnitude of sympatholysis in S during contraction at 30 or 60% MCF. In contrast, NO synthase inhibition diminished sympatholysis in H at 30% MCF and in M and H at 60% MCF (P < 0.05). The present findings indicate that short-term

After completing this course, the reader will be able to:1. Discuss cardiorespiratory fitness and cardiac functional reserve in postmenopausal women treated with chemoendocrine therapy.2. List the cardiovascular risk factors in this study that were found to be less favorable among patients than among controls.3. Explain the significance of peak aerobic power as a predictor of cardiovascular disease.Access and take the CME test online and receive 1 AMA PRA Category 1 Credit ™ at CME.TheOncologist.com CME CME ABSTRACTPurpose. To examine cardiovascular function and risk profile of postmenopausal women treated with chemoendocrine therapy (CET) for hormone receptorpositive operable breast cancer. Methods. Forty-seven breast cancer patients and 11 age-matched healthy controls were studied. Participants performed a cardiopulmonary exercise test with expired gas analysis and impedance cardiography to assess peak aerobic power (VO 2peak ) and cardiovascular function (stroke volume, cardiac output, cardiac power output, and cardiac reserve). Traditional (i.e., body mass index, lipid profile, and fasting insulin and glucose) and novel (i.e., C-reactive protein, brain natriuretic peptide) cardiovascular risk biochemical factors were also assessed.Results. Breast cancer patients had significantly lower peak exercise stroke volume (68 ؎ 9 versus 76 ؎ 11 ml/ beat), cardiac output (10.4 ؎ 1.5 versus 11.7 ؎ 2.4 l/minute), cardiac power output (3.0 ؎ 0.5 versus 3.5 ؎ 0.9 Watts), cardiac power output reserve (1.7 ؎ 0.6 versus 2.4 ؎ 0.8 Watts), and VO 2peak (1.3 ؎ 0.3 versus 1.6 ؎ 0.2 l⅐min ؊1 ) than control subjects (p-values < .05). Patients with the greatest impairment in VO 2peak had the worse cardiovascular risk profile. Exploratory analyses Conclusion. Breast cancer patients treated with adjuvant CET have a significantly and markedly lower cardiorespiratory fitness and cardiac functional reserve compared with age-and sex-matched controls. AI therapy may be associated with a more unfavorable cardiovascular risk profile than TAM. Prospective studies are required to further investigate the clinical value of these findings.