The objective of the study is to examine the effects of age and gender on finger coordination. Twelve young (24 +/- 8 yr; 6 men and 6 women) and 12 elderly (75 +/- 5 yr; 6 men and 6 women) subjects performed single-finger maximal contraction [maximal voluntary contraction (MVC)], four-finger MVC, and four-finger ramp force production tasks by pressing on individual force transducers. A drop in the force of individual fingers during four-finger MVC tasks compared with single-finger MVC tasks (force deficit) was larger, whereas unintended force production by other fingers during single-finger MVC tasks (enslaving) was smaller, in elderly than in young subjects and in women than in men. Force deficit was smaller and enslaving was larger in subjects with higher peak force. During the ramp task, the difference between the variance of total force and the sum of variances of individual forces showed a logarithmic relation to the level of total force, across all subject groups. These findings suggest that indexes of finger coordination scale with force-generating capabilities across gender and age groups.

The diagnostic and prognostic criteria of acute-on-chronic liver failure (ACLF) were developed in patients with no Hepatitis B virus (HBV) cirrhosis (CANONIC study). The aims of this study were to evaluate whether the diagnostic (CLIF-C organ failure score; CLIF-C OFs) criteria can be used to classify patients; and the prognostic score (CLIF-C ACLF score) could be used to provide prognostic information in HBV cirrhotic patients with ACLF. 890 HBV associated cirrhotic patients with acute decompensation (AD) were enrolled. Using the CLIF-C OFs, 33.7% (300 patients) were diagnosed as ACLF. ACLF was more common in the younger patients and in those with no previous history of decompensation. The most common organ failures were ‘hepatic’ and ‘coagulation’. As in the CANONIC study, 90-day mortality was extremely low in the non-ACLF patients compared with ACLF patients (4.6% vs 50%, p < 0.0001). ACLF grade and white cell count, were independent predictors of mortality. CLIF-C ACLFs accurately predicted short-term mortality, significantly better than the MELDs and a disease specific score generated for the HBV patients. Current study indicates that ACLF is a clinically and pathophysiology distinct even in HBV patients. Consequently, diagnostic criteria, prognostic scores and probably the management of ACLF should base on similar principles.

In the present study, we tested the hypothesis that 17␤-estradiol (␤E2) is a neuroprotectant in the retina, using two experimental approaches: 1) hydrogen peroxide (H 2 O 2 )-induced retinal neuron degeneration in vitro, and 2) light-induced photoreceptor degeneration in vivo. We demonstrated that both ␤E2 and 17␣-estradiol (␣E2) significantly protected against H 2 O 2 -induced retinal neuron degeneration; however, progesterone had no effect. ␤E2 transiently increased the phosphoinositide 3-kinase (PI3K) activity, when phosphoinositide 4,5-bisphosphate and [32 ␥ATP] were used as substrate. Phospho-Akt levels were also transiently increased by ␤E2 treatment. Addition of the estrogen receptor antagonist tamoxifen did not reverse the protective effect of ␤E2, whereas the PI3K inhibitor LY294002 inhibited the protective effect of ␤E2, suggesting that ␤E2 mediates its effect through some PI3K-dependent pathway, independent of the estrogen receptor. Pull-down experiments with glutathione S-transferase fused to the N-Src homology 2 domain of p85, the regulatory subunit of PI3K, indicated that ␤E2 and ␣E2, but not progesterone, identified phosphorylated insulin receptor ␤-subunit (IR␤) as a binding partner. Pretreatment with insulin receptor inhibitor, HNMPA, inhibited IR␤ activation of PI3K. Systemic administration of ␤E2 significantly protected the structure and function of rat retinas against light-induced photoreceptor cell degeneration and inhibited photoreceptor apoptosis. In addition, systemic administration of ␤E2 activated retinal IR␤, but not the insulin-like growth factor receptor-1, and produced a transient increase in PI3K activity and phosphorylation of Akt in rat retinas. The results show that estrogen has retinal neuroprotective properties in vivo and in vitro and suggest that the insulin receptor/PI3K/Akt signaling pathway is involved in estrogen-mediated retinal neuroprotection.

Duchenne muscular dystrophy (DMD) is a fatal disease characterized by deterioration of striated muscle, affecting skeletal and cardiac muscles. Recently, several therapeutic approaches have shown promise for repairing dystrophic skeletal muscles. However, these methods often leave the dystrophic heart untreated. Here we show that, in comparison to fully dystrophin-deficient animals, targeted transgenic repair of skeletal muscle, but not cardiac muscle, in otherwise dystrophin-deficient (mdx) mice paradoxically elicited a fivefold increase in cardiac injury and dilated cardiomyopathy in these animals in vivo. Skeletal muscle repair was shown to increase the voluntary activity of the mdx mice as quantified by voluntary running on the exercise wheel. Because the dystrophin-deficient heart is highly sensitive to increased stress, we hypothesize that increased activity (enabled by the repaired skeletal muscle) provided the stimulus for heightened cardiac injury and heart remodeling. In support of this hypothesis, the primary cellular compliance defect in dystrophin-deficient cardiac myocytes was found to be unchanged by skeletal muscle repair in the mdx mice. These findings provide new information on the evolution of cardiac disease in dystrophin-deficient animals and underscore the importance of implementing global striated muscle therapies for muscular dystrophy.

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These data show the correlation between some of the parameters of serum lipids and arterial stiffness. LDL-C was independently associated with aortic stiffness, and HDL-C was independently inversely associated with aortic stiffness and peripheral stiffness.

In this article, we discuss techniques for sense through wall human detection for different types of walls. We have focused on detection of stationary human target behind wall based on breathing movements. In detecting the breathing motion, a Doppler based method is used. Also a new approach based on short time Fourier transform is discussed and an already proposed clutter reduction technique based on singular value decomposition is applied to different measurements.

Dysregulation of long non-coding RNAs (LncRNAs) participated into the initiation and progression of different diseases via direct regulation of proteins or indirect regulation of microRNA (miRNA)-target genes. LINC00473 is a novel carcinoma-related LncRNA and up-regulated in many cancers for tumor growth and metastasis, but its role in chemotherapy resistance is unclear. We here investigated the function of LINC00473 in colorectal cancer (CRC) in vitro and in vivo. The CRC tissues (n=20) and relative normal tissues were collected and found that LINC00473 was overexpressed in CRC tissues when compared with which in normal tissues. Highly expressed LINC00473 predicted large tumor size, high TNM stage of CRC patients. Interestingly, the tumor suppressor miR-15a was down-regulated and negatively correlated with LINC00473 levels in CRC. LINC00473 harbored the binding sites for miR-15a and reduced its availability in CRC cell line HCT116. Knockdown of LINC00473 elevated the expression of miR-15a. Moreover, in the Taxol-resistant HCT116, the LINC00473 level was further increased than that in HCT116. Knockdown of LINC00473 restored the Taxol-induced cytotoxicity, inhibited the cell vitality, colony formation and induced apoptosis, impaired the ability of migration or invasion, but these effects could be abrogated by the inhibition of miR-15a. Mechanistically, the BCL-2-related anti-apoptosis pathway was activated and the multidrug-resistant (MDR) genes LRP, MDR1 were up-regulated by LINC00473. Furthermore, inhibition of LINC00473 in vivo could overcome the Taxol resistance of CRC cells, could recover the expression of tumor suppressor miR-15a and chemotherapy-induced tumor regression, indicating that LINC00473 functioned as oncogene in CRC via miR-15a.