With regard to standardization of measurements, seven studies, used a private, non-observed clinical setting, one instructed to measure at home, and three studies did not describe the setting in which measurements took place. The following factors of influence were accounted for: circadian rhythm in three studies, time since last ejaculation in none and time since last defecation in one of the studies, intra-abdominal pressure in six studies, and the accustomed position in two studies. With regard to outcome assessment, of eight studies which measured PVR only two measured total bladder capacity. All studies defined their methods for the other urodynamic measurements. This study aims to determine the influence of body position during voiding on urodynamic parameters for both healthy males and men with LUTS by summarizing the scientific evidence for either the sitting or standing position. We found that in patients with LUTS the sitting position is associated with a trend towards a more favorable urodynamic profile: Qmax is increased, PVR is lowered and time spent urinating is shorter than in the standing position. In healthy males however, the results of our meta-analysis show no posture-related differences in any of the measured urodynamic parameters. We therefore conclude that for healthy men the debate on the standing versus sitting voiding posture cannot be settled by urodynamic arguments alone. To our knowledge, this is the first systematic review and metaanalysis to assess urodynamics and posture-related changes. Three articles provided a summarization in the form of a literature review, however a meta-analysis is of greater value in evidence-based clinical decision making. Apart from demonstrating a trend towards an improved urodynamic profile in LUTS patients, we unfortunately proved the accompanying heterogeneity as well. Consequently, some care should be taken in the interpretation of the results. Statistical analysis in order to identify the exact cause of the heterogeneity remains difficult in such a small number of studies. An arbitrary minimum number of ten studies is needed to perform funnel plot analysis and Egger tests to objectify publication bias.

Therefore, the detection and prevention of CKD are important issues in health care. Increasing evidence supports a significant correlation between serum uric acid levels and the development of CKD. A recently published paper reviewed the relationship between hyperuricemia and CKD based on longitudinal observational and interventional studies and raised the possibility of uric acid as a potential therapeutic target to prevent the onset of CKD. As elevated serum uric acid is a proposed risk factor for cardiovascular disease and other established cardiovascular risk factors, such as diabetes, hypertension, and metabolic syndrome, whether serum uric acid is an independent risk factor for the development of CKD or is merely an incidental finding related to the severity of CKD remains unknow. Although one previous meta-analysis reported a positive association between serum uric acid levels and an increased risk of CKD, the evidence was limited due to unexplained, moderate heterogeneity across the included studies. Additionally, possible confounding by other factors needs to be explored to firmly establish the potential role of uric acid in CKD. Therefore, given the recent accumulation of evidence and intervention studies, we conducted a metaanalysis of longitudinal cohort studies to quantify the nature and magnitude of the association between serum uric acid levels and incident CKD and to measure this association according to the study design and population characteristics. Fifteen independent cohort studies reporting 99,205 participants and 3,492 incident cases were identified. Four studies were conducted in Western countries, and 11 studies were conducted in Asian countries. The selected studies were published from 2005 through 2013, and the number of subjects per study ranged from 519 to 18,778. Six studies recruited participants from population registries. Seven study populations were from healthy checkup population, and two study population included factory employees. The mean serum uric acid level for the subjects ranged from 4.0 to 6.9 mg/dL, and their mean age ranged from 40.5 to 74.5 years. Two studies exclusively included men, and four studies included women and men.

A close interaction between mitochondria and the cytoskeleton is essential to ensure the proper distribution of mitochondria within a cell. Recent studies have highlighted interactions between intermediate filaments, notably NFL or Vimentin and the key molecules necessary for the maintenance of organelle integrity and mitochondrial motility. The NFL-TBS.40-63 peptide is able to alter microtubule formation when it is internalized by T98G glioblastoma cells and inhibits their proliferation. In this study, we have evaluated the effect of NFL-TBS.40-63 peptide internalization on mitochondrial biogenesis and function. Our observations revealed a negative impact on T98G cell respiration after 6 hours of NFL-TBS.40-63 peptide treatment. This action on mitochondrial function, at lower concentrations than those necessary to disturb the cytoskeleton, could be related to a primary modification of the mitochondrial motility. It has been shown that peptides derived from the N-terminal domain of intermediate filaments, like desmin, vimentin and keratin, can interact with the unpolymerized tubulin. A recent study demonstrated that the N-terminal domain of vimentin can also directly bind mitochondria and serve as an adaptor between actin microfilaments and mitochondria. We suggest that the primary action of NFL-TBS.40-63 leads to sequential organization of the peptide, which disturbs the cytoskeleton and reorganizes the mitochondrial network. This should be related to the conserved FIS1/MFN2 ratio we observed at higher peptide concentrations. At a 10 mM peptide treatment, we also revealed a colocalization of NFLTBS. 40-63 with mitochondria and a specific accumulation at the microtubules’ extremities, which may limit membrane ruffling, as previously reported. This study revealed that the NFL-TBS.40-63 peptide provokes a redistribution of mitochondria throughout the cytoplasm.