Obesity is associated with early cardiovascular dysfunction and reduced muscle strength. Whole-body vibration (WBV) training may improve arterial function and muscle strength. The effects of WBV training on arterial stiffness (brachial-ankle pulse wave velocity, baPWV), wave reflection (augmentation index, AIx), brachial systolic blood pressure (bSBP), aortic systolic blood pressure (aSBP), heart rate variability, and muscle strength (one-repetition maximum, 1RM) were examined in 10 young (21 ± 2 year) overweight/obese women (body mass index, BMI¼29.9 ± 0.8 kg m -2 ). Participants were randomized to a 6-week WBV training or non-exercising control (CON) period in a crossover design. WBV training (3 daysÂweek) consisted of static and dynamic squats and calf raises with vibration intensity at 25-30 Hz and 1-2 mm amplitude (2.83-4.86 G). There were significant (Po0.05) decreases in baPWV (À0.9±0.3 m s -1 ), AIx (À8.0±2.2 %), bSBP (À5.3±1.5 mm Hg), aSBP (À5.2 ± 2.1 mm Hg), low-frequency power (À0.13 ± 0.05 nu) and sympathovagal balance (LF/HF, À0.42 ± 0.16) after WBV training compared with CON. Significant (Po0.05) increases in high-frequency power (HF, 0.19 ± 0.04 nu) and leg extension 1RM (8.2±2.3 kg) occurred after WBV training compared with CON. Six weeks of WBV training decreased systemic arterial stiffness and aSBP via improvements in wave reflection and sympathovagal balance in young overweight/obese normotensive women. WBV training may benefit arterial function and muscle strength in deconditioned individuals who cannot perform conventional exercise.

Acute kidney injury (AKI) is a severe and frequent condition in hospitalized patients. Currently, no efficient therapy of AKI is available. Therefore, efforts focus on early prevention and potentially early initiation of renal replacement therapy to improve the outcome in AKI. The detection of AKI in hospitalized patients implies the need for early, accurate, robust, and easily accessible biomarkers of AKI evolution and outcome prediction because only a narrow window exists to implement the earlier-described measures. Even more challenging is the multifactorial origin of AKI and the fact that the changes of molecular expression induced by AKI are difficult to distinguish from those of the diseases associated or causing AKI as shock or sepsis. During the past decade, a considerable number of protein biomarkers for AKI have been described and we expect from recent advances in the field of omics technologies that this number will increase further in the future and be extended to other sorts of biomolecules, such as RNAs, lipids, and metabolites. However, most of these biomarkers are poorly defined by their AKI-associated molecular context. In this review, we describe the state-of-the-art tissue and biofluid proteomic and metabolomic technologies and new bioinformatics approaches for proteomic and metabolomic pathway and molecular interaction analysis. In the second part of the review, we focus on AKI-associated proteomic and metabolomic biomarkers and briefly outline their pathophysiological context in AKI.

Renal organic osmolytes, betaine and myo-inositol play a critical role in protecting renal cells from hyperosmotic stress. Kidney tissue transcriptomics of murine preclinical experimentation identified decreased expression of Slc6a12 and Slc5a11 mRNA in renal tissue consistent with defective tubular transport of these osmolytes. Imbalances in renal osmolyte regulation lead to increased renal cell damage and thus more progressive forms of CKD. Increases in renal osmolytes in urine could provide clinical diagnostic and prognostic information on CKD outcomes.

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RationaleDeterioration of ventricular fibrillation (VF) into asystole or severe bradycardia (electrical failure) heralds a fatal outcome of cardiac arrest. The role of metabolism in the timing of electrical failure remains unknown.ObjectiveTo determine metabolic factors of early electrical failure in an Ex-vivo canine model of cardiac arrest (VF+global ischemia).Methods and ResultsMetabolomic screening was performed in left ventricular biopsies collected before and after 0.3, 2, 5, 10 and 20 min of VF and global ischemia. Electrical activity was monitored via plunge needle electrodes and pseudo-ECG. Four out of nine hearts exhibited electrical failure at 10.1±0.9 min (early-asys), while 5/9 hearts maintained VF for at least 19.7 min (late-asys). As compared to late-asys, early-asys hearts had more ADP, less phosphocreatine, and higher levels of lactate at some time points during VF/ischemia (all comparisons p<0.05). Pre-ischemic samples from late-asys hearts contained ∼25 times more inorganic pyrophosphate (PPi) than early-asys hearts. A mechanistic role of PPi in cardioprotection was then tested by monitoring mitochondrial membrane potential (ΔΨ) during 20 min of simulated-demand ischemia using potentiometric probe TMRM in rabbit adult ventricular myocytes incubated with PPi versus control group. Untreated myocytes experienced significant loss of ΔΨ while in the PPi-treated myocytes ΔΨ was relatively maintained throughout 20 min of simulated-demand ischemia as compared to control (p<0.05).ConclusionsHigh tissue level of PPi may prevent ΔΨm loss and electrical failure at the early phase of ischemic stress. The link between the two protective effects may involve decreased rates of mitochondrial ATP hydrolysis and lactate accumulation.