Electromyographic patterns of upper extremity muscles during sitting pivot transfers performed by individuals with spinal cord injury

Although substantial upper extremity (U/E) muscular efforts are required when individuals with spinal cord injury (SCI) perform sitting pivot transfers, little is known about the electromyographic (EMG) activation patterns of key shoulder and elbow muscles solicited during the performance of this functional task. The aims of this study were to examine the EMG activation patterns of U/E muscles in 10 males with SCI, and to compare them across sitting pivot transfers performed toward seats of different heights (low, same, high). EMG data from the biceps, triceps, deltoid, pectoralis major and latissimus dorsi were recorded bilaterally. Transfers were divided into pre-lift, lift, and post-lift phases. Each phase was time- and amplitude-normalized using a mean dynamic EMG approach. Similar EMG activation patterns were found across the different transfers for all muscles (r_mean = 0.942–0.991), whereas moderate to high inter-subject variability (CV: 20.9–70.6%) was reported for the different muscles and transfers. Peak EMG occurred earlier at the trailing U/E compared to the leading one, and was observed around seat-off for most of the muscles. When transfer to a high target seat was compared to transfer to one of the same height, significantly higher relative EMG values were observed at the biceps (mean: 1.64 vs. 1.00) of the leading U/E as well as the deltoid (mean: 1.20 vs. 1.00) and pectoralis major (mean: 1.20 vs. 1.00; peak: 2.27 vs. 1.79) of the trailing U/E. Transferring to a low target seat did not lead to lower muscular demand than transferring to one of the same height (P > 0.05). These results indicate that coordinated and higher muscular efforts were generated at the trailing deltoid and pectoralis major when transferring to a high target seat compared to one of similar height. Higher muscular efforts were also developed at the leading biceps when transferring to a high target seat compared to a leveled one. Lowering the target seat with respect to the initial seat had no favorable effect on muscular demand.     

Decomposition of Bt transgenic rice residues and response of soil microbial community in rapeseed–rice cropping system

In this study, Bt transgenic rice (KMD rice) residue decomposition and the associated microbial community in a rapeseed–rice cropping system were assessed in comparison with its parental non-Bt rice variety (XiuShui 11). Decomposition was measured as mass loss by straw and root decay in litterbags over two consecutive years. Bacterial and fungal community compositions associated with residue decomposition were detected by terminal restriction fragment length polymorphism (T-RFLP) and the additive main effects multiplicative interaction (AMMI) analysis model. Decomposition dynamics and bacterial and fungal communities associated with decomposition were strongly affected by surface and incorporated placements, and by temporal factors. However, no significant differences were observed between Bt and non-Bt rice variety in either decomposition dynamics or in the soil microbial communities associated with residue decay. Our field study indicated that the insertion of the cry1Ab gene into Xiushui 11 rice genome had no significant effect on the residual decay and decomposition-associated microbial community compositions in the rapeseed-rice cropping system.     

Evolution of the CD163 family and its relationship to the bovine gamma delta T cell co-receptor WC1

Background  

The scavenger receptor cysteine rich (SRCR) domain is an ancient and conserved protein domain. CD163 and WC1 molecules are classed together as group B SRCR superfamily members, along with Spα, CD5 and CD6, all of which are expressed by immune system cells. There are three known types of CD163 molecules in mammals, CD163A (M130, coded for by CD163), CD163b (M160, coded for by CD163L1) and CD163c-α (CD163L1 or SCART), while their nearest relative, WC1, is encoded by a multigene family so far identified in the artiodactyl species of cattle, sheep, and pigs.     

Cortical Mechanics and Meiosis II Completion in Mammalian Oocytes Are Mediated by Myosin-II and Ezrin-Radixin-Moesin (ERM) Proteins

Cell division is inherently mechanical, with cell mechanics being a critical determinant governing the cell shape changes that accompany progression through the cell cycle. The mechanical properties of symmetrically dividing mitotic cells have been well characterized, whereas the contribution of cellular mechanics to the strikingly asymmetric divisions of female meiosis is very poorly understood. Progression of the mammalian oocyte through meiosis involves remodeling of the cortex and proper orientation of the meiotic spindle, and thus we hypothesized that cortical tension and stiffness would change through meiotic maturation and fertilization to facilitate and/or direct cellular remodeling. This work shows that tension in mouse oocytes drops about sixfold during meiotic maturation from prophase I to metaphase II and then increases ∼1.6-fold upon fertilization. The metaphase II egg is polarized, with tension differing ∼2.5-fold between the cortex over the meiotic spindle and the opposite cortex, suggesting that meiotic maturation is accompanied by assembly of a cortical domain with stiffer mechanics as part of the process to achieve asymmetric cytokinesis. We further demonstrate that actin, myosin-II, and the ERM (Ezrin/Radixin/Moesin) family of proteins are enriched in complementary cortical domains and mediate cellular mechanics in mammalian eggs. Manipulation of actin, myosin-II, and ERM function alters tension levels and also is associated with dramatic spindle abnormalities with completion of meiosis II after fertilization. Thus, myosin-II and ERM proteins modulate mechanical properties in oocytes, contributing to cell polarity and to completion of meiosis.     

Alpha-tocopherol induces calnexin in renal tubular cells: another protective mechanism against free radical-induced cellular damage

Pre-administration of alpha-tocopherol is protective against oxidative renal tubular damage and subsequent carcinogenesis by ferric nitrilotriacetate (Fe-NTA) in rats. We searched for mechanisms other than the scavenging effect of alpha-tocopherol with microarray analyses, which implicated calnexin, a chaperone for glycoproteins. Renal mRNA levels of calnexin significantly increased 3h after an injection of Fe-NTA in rats fed a standard diet whereas those fed an alpha-tocopherol-supplemented diet showed an increase prior to injection, but after injection showed a decrease in renal calnexin mRNA levels, with unaltered protein levels. In experiments using LLC-PK1 cells, addition of alpha-tocopherol was protective against oxidative stress by H2O2, concomitant with calnexin induction. Knockdown of calnexin by siRNA significantly reduced this protection. Furthermore, COS-7 cells transfected with the calnexin gene were more resistant to H2O2. Together with the fact that alpha-tocopherol induced N-acetylglucosaminyltransferase 3, our data suggest that alpha-tocopherol modifies glycoprotein metabolism partially by conferring mild ER stress. This adds another molecular mechanism of alpha-tocopherol toward cancer prevention.     

Growth factor-dependent AKT activation and cell migration requires the function of c-K(B)-Ras versus other cellular ras isoforms

K-Ras-negative fibroblasts are defective in their steady-state expression of MMP-2. This occurs through c-K(B)-Ras dependent regulation of basal levels of AKT activity. In this report, we have extended those studies to demonstrate that in the absence of K-Ras expression, PDGF-BB fails to induce significant AKT activation, although this was not the case in N-Ras-negative cells. This phenotype was directly linked to PDGF-dependent cell migration. All of the independently immortalized K-Ras-negative cells failed to migrate upon the addition of PDGF. Only ectopic expression of c-K(B)-Ras, not c-K(A)-Ras nor oncogenic N-Ras, could restore both PDGF-dependent AKT activation and cell migration. Since most Ras binding partners can interact with all Ras isoforms, the specificity of PDGF-dependent activation of AKT and enhanced cell migration suggests that these outcomes are likely to be regulated through a c-K(B)-Ras-specific binding partner. Others have published that of the four Ras isoforms, only K(B)-Ras can form a stable complex with calmodulin (CaM). Along those lines, we provide evidence that 1) PDGF addition results in increased levels of a complex between c-K(B)-Ras and CaM and 2) the biological outcomes that are strictly dependent on c-K(B)-Ras (AKT activation and cell migration) are blocked by CaM antagonists. The PDGF-dependent activation of ERK is unaffected by the absence of K(B)-Ras and presence of CaM antagonists. This is the first example of a linkage between a specific biological outcome, cell migration, and the activity of a single Ras isoform, c-K(B)-Ras.     

Freshwater sponge spicules: a new agent of ocular pathology

In a recent outbreak of human ocular injuries that occurred in the town of Araguatins, at the right bank of Araguaia river, state of Tocantins, Brazil, along the low water period of 2005, two patients (8 and 12-year-old boys) presented inferior adherent leukoma in the left eye (OS), and peripherical uveites, with snowbanking in the inferior pars plana. The third one (13-year-old girl) showed posterior uveites in OS, also with snowbanking. Histopathological analysis of lensectomy material from the three patients and vitrectomy from the last one revealed several silicious spicules (gemmoscleres) of the freshwater sponges Drulia uruguayensis and D. ctenosclera. This work brings material evidences, for the first time in the literature, that freshwater sponge spicules may be a surprising new etiological agent of ocular pathology.