Relation between cardiac dimensions and peak oxygen uptake

<p>Abstract</p> <p>Background</p> <p>Long term endurance training is known to increase peak oxygen uptake (<inline-formula><graphic file="1532-429X-12-8-i1.gif"/></inline-formula>) and induce morphological changes of the heart such as increased left ventricular mass (LVM). However, the relationship between <inline-formula><graphic file="1532-429X-12-8-i1.gif"/></inline-formula> and the total heart volume (THV), considering both the left and right ventricular dimensions in both males and females, is not completely described. Therefore, the aim of this study was to test the hypothesis that THV is an independent predictor of <inline-formula><graphic file="1532-429X-12-8-i1.gif"/></inline-formula> and to determine if the left and right ventricles enlarge in the same order of magnitude in males and females with a presumed wide range of THV.</p> <p>Methods and Results</p> <p>The study population consisted of 131 subjects of whom 71 were athletes (30 female) and 60 healthy controls (20 female). All subjects underwent cardiovascular MR and maximal incremental exercise test. Total heart volume, LVM and left- and right ventricular end-diastolic volumes (LVEDV, RVEDV) were calculated from short-axis images. <inline-formula><graphic file="1532-429X-12-8-i1.gif"/></inline-formula> was significantly correlated to THV, LVM, LVEDV and RVEDV in both males and females. Multivariable analysis showed that THV was a strong, independent predictor of <inline-formula><graphic file="1532-429X-12-8-i1.gif"/></inline-formula> (R²= 0.74, p < 0.001). As LVEDV increased, RVEDV increased in the same order of magnitude in both males and females (R²= 0.87, p < 0.001).</p> <p>Conclusion</p> <p>Total heart volume is a strong, independent predictor of maximal work capacity for both males and females. Long term endurance training is associated with a physiologically enlarged heart with a balance between the left and right ventricular dimensions in both genders.</p

HuR/ELAVL1 drives malignant peripheral nerve sheath tumor growth and metastasis

Cancer cells can develop a strong addiction to discrete molecular regulators, which control the aberrant gene expression programs that drive and maintain the cancer phenotype. Here, we report the identification of the RNA-binding protein HuR/ELAVL1 as a central oncogenic driver for malignant peripheral nerve sheath tumors (MPNSTs), which are highly aggressive sarcomas that originate from cells of the Schwann cell lineage. HuR was found to be highly elevated and bound to a multitude of cancer-associated transcripts in human MPNST samples. Accordingly, genetic and pharmacological inhibition of HuR had potent cytostatic and cytotoxic effects on tumor growth, and strongly suppressed metastatic capacity in vivo. Importantly, we linked the profound tumorigenic function of HuR to its ability to simultaneously regulate multiple essential oncogenic pathways in MPNST cells, including the Wnt/β-catenin, YAP/TAZ, RB/E2F, and BET pathways, which converge on key transcriptional networks. Given the exceptional dependency of MPNST cells on HuR for survival, proliferation, and dissemination, we propose that HuR represents a promising therapeutic target for MPNST treatment

Didymodon rigidulus

Bryophyte

Cardiac output and cardiac index measured with cardiovascular magnetic resonance in healthy subjects, elite athletes and patients with congestive heart failure

<p>Abstract</p> <p>Background</p> <p>Cardiovascular Magnetic Resonance (CMR) enables non-invasive quantification of cardiac output (CO) and thereby cardiac index (CI, CO indexed to body surface area). The aim of this study was to establish if CI decreases with age and compare the values to CI for athletes and for patients with congestive heart failure (CHF).</p> <p>Methods</p> <p>CI was measured in 144 healthy volunteers (39 ± 16 years, range 21–81 years, 68 females), in 60 athletes (29 ± 6 years, 30 females) and in 157 CHF patients with ejection fraction (EF) below 40% (60 ± 13 years, 33 females). CI was calculated using aortic flow by velocity-encoded CMR and is presented as mean ± SD. Flow was validated in vitro using a flow phantom and in 25 subjects with aorta and pulmonary flow measurements.</p> <p>Results</p> <p>There was a slight decrease of CI with age in healthy subjects (8 ml/min/m² per year, r² = 0.07, p = 0.001). CI in males (3.2 ± 0.5 l/min/m²) and females (3.1 ± 0.4 l/min/m²) did not differ (p = 0.64). The mean ± SD of CI in healthy subjects in the age range of 20–29 was 3.3 ± 0.4 l/min/m², in 30–39 years 3.3 ± 0.5 l/min/m², in 40–49 years 3.1 ± 0.5 l/min/m², 50–59 years 3.0 ± 0.4 l/min/m² and >60 years 3.0 ± 0.4 l/min/m². There was no difference in CI between athletes and age-controlled healthy subjects but HR was lower and indexed SV higher in athletes. CI in CHF patients (2.3 ± 0.6 l/min/m²) was lower compared to the healthy population (p < 0.001). There was a weak correlation between CI and EF in CHF patients (r² = 0.07, p < 0.001) but CI did not differ between patients with NYHA-classes I-II compared to III-IV (n = 97, p = 0.16) or patients with or without hospitalization in the previous year (n = 100, p = 0.72). In vitro phantom validation showed low bias (−0.8 ± 19.8 ml/s) and in vivo validation in 25 subjects also showed low bias (0.26 ± 0.61 l/min, QP/QS 1.04 ± 0.09) between pulmonary and aortic flow.</p> <p>Conclusions</p> <p>CI decreases in healthy subjects with age but does not differ between males and females. We found no difference in CI between athletes and healthy subjects at rest but CI was lower in patients with congestive heart failure. The presented values can be used as reference values for flow velocity mapping CMR.</p