Intergroup relations in organisations

The problem statement of this research is, "What is the· basis of the intergroup relations that potentially lead to ineffective work behaviour, and how does it manifest in groups within a specific consulting organisation, in terms of the premises of the Tavistock model of group relations?" The psychodynamic approach, psychoanalytic technique, open systems theory and object relations theory were used. The unstructured interview and hermeneutic approach were used for collection of data, and analysis and interpretation. The results of the research indicate that groups, in interaction with other groups, may install defences against anxieties which could undermine the success of their work efforts .. Issues of ' . ' nonclarity of task, group boundary and identity issues, authority issues and reactions of projection seemed prevalent. Various hypotheses were developed which could be used as a basis for further research.Industrial and Organisation PsychologyM.A. (Industrial Psychology

A Gene for Autosomal Recessive Limb-Girdle Muscular Dystrophy in Manitoba Hutterites Maps to Chromosome Region 9q31-q33: Evidence for Another Limb-Girdle Muscular Dystrophy Locus

SummaryCharacterized by proximal muscle weakness and wasting, limb-girdle muscular dystrophies (LGMDs) are a heterogeneous group of clinical disorders. Previous reports have documented either autosomal dominant or autosomal recessive modes of inheritance, with genetic linkage studies providing evidence for the existence of at least 12 distinct loci. Gene products have been identified for five genes responsible for autosomal recessive forms of the disorder. We performed a genome scan using pooled DNA from a large Hutterite kindred in which the affected members display a mild form of autosomal recessive LGMD. A total of 200 markers were used to screen pools of DNA from patients and their siblings. Linkage between the LGMD locus and D9S302 (maximum LOD score 5.99 at recombination fraction .03) was established. Since this marker resides within the chromosomal region known to harbor the gene causing Fukuyama congenital muscular dystrophy (FCMD), we expanded our investigations, to include additional markers in chromosome region 9q31-q34.1. Haplotype analysis revealed five recombinations that place the LGMD locus distal to the FCMD locus. The LGMD locus maps close to D9S934 (maximum multipoint LOD score 7.61) in a region that is estimated to be ∼4.4 Mb (Genetic Location Database composite map). On the basis of an inferred ancestral recombination, the gene may lie in a 300-kb region between D9S302 and D9S934. Our results provide compelling evidence that yet another gene is involved in LGMD; we suggest that it be named “LGMD2H.

Insights into Electrolytic Pre Lithiation A Thorough Analysis Using Silicon Thin Film Anodes

Pre lithiation via electrolysis, herein defined as electrolytic pre lithiation, using cost efficient electrolytes based on lithium chloride LiCl , is successfully demonstrated as a proof of concept for enabling lithium ion battery full cells with high silicon content negative electrodes. An electrolyte for pre lithiation based on amp; 947; butyrolactone and LiCl is optimized using boron containing additives lithium bis oxalato borate, lithium difluoro oxalate borate and CO2 with respect to the formation of a protective solid electrolyte interphase SEI on silicon thin films as model electrodes. Reversible lithiation in Si Li metal cells is demonstrated with Coulombic efficiencies CEff of 95 96 for optimized electrolytes comparable to 1 m LiPF6 EC EMC 3 7. Formation of an effective SEI is shown by cyclic voltammetry and X ray photoelectron spectroscopy XPS . electrolytic pre lithiation experiments show that notable amounts of the gaseous product Cl2 dissolve in the electrolyte leading to a self discharge Cl2 Cl amp; 8722; shuttle mechanism between the electrodes lowering pre lithiation efficiency and causing current collector corrosion. However, no significant degradation of the Si active material and the SEI due to contact with elemental chlorine is found by SEM, impedance, and XPS. In NCM111 Si full cells, the capacity retention in the 100th cycle can be significantly increased from 54 to 78 by electrolytic pre lithiation, compared to reference cells without pre lithiation of S

Photoperiodic regime influences onset of lens opacities in a non-human primate

Background Opacities of the lens are typical age-related phenomena which have a high influence on photoreception and consequently circadian rhythm. In mouse lemurs, a small bodied non-human primate, a high incidence (more than 50% when >seven years) of cataracts has been previously described during aging. Previous studies showed that photoperiodically induced accelerated annual rhythms alter some of mouse lemurs’ life history traits. Whether a modification of photoperiod also affects the onset of age dependent lens opacities has not been investigated so far. The aim of this study was therefore to characterise the type of opacity and the mouse lemurs’ age at its onset in two colonies with different photoperiodic regimen. Methods Two of the largest mouse lemur colonies in Europe were investigated: Colony 1 having a natural annual photoperiodic regime and Colony 2 with an induced accelerated annual cycle. A slit-lamp was used to determine opacities in the lens. Furthermore, a subset of all animals which showed no opacities in the lens nucleus in the first examination but developed first changes in the following examination were further examined to estimate the age at onset of opacities. In total, 387 animals were examined and 57 represented the subset for age at onset estimation. Results The first and most commonly observable opacity in the lens was nuclear sclerosis. Mouse lemurs from Colony 1 showed a delayed onset of nuclear sclerosis compared to mouse lemurs from Colony 2 (4.35 ± 1.50 years vs. 2.75 ± 0.99 years). For colony 1, the chronological age was equivalent to the number of seasonal cycles experienced by the mouse lemurs. For colony 2, in which seasonal cycles were accelerated by a factor of 1.5, mouse lemurs had experienced 4.13 ± 1.50 seasonal cycles in 2.75 ± 0.99 chronological years. Discussion Our study showed clear differences in age at the onset of nuclear sclerosis formation between lemurs kept under different photoperiodic regimes. Instead of measuring the chronological age, the number of seasonal cycles (N = four) experienced by a mouse lemur can be used to estimate the risk of beginning nuclear sclerosis formation. Ophthalmological examinations should be taken into account when animals older than 5–6 seasonal cycles are used for experiments in which unrestricted visual ability has to be ensured. This study is the first to assess and demonstrate the influence of annual photoperiod regime on the incidence of lens opacities in a non-human primate

TRIM32 Regulates Skeletal Muscle Stem Cell Differentiation and Is Necessary for Normal Adult Muscle Regeneration

Limb girdle muscular dystrophy type 2H (LGMD2H) is an inherited autosomal recessive disease of skeletal muscle caused by a mutation in the TRIM32 gene. Currently its pathogenesis is entirely unclear. Typically the regeneration process of adult skeletal muscle during growth or following injury is controlled by a tissue specific stem cell population termed satellite cells. Given that TRIM32 regulates the fate of mammalian neural progenitor cells through controlling their differentiation, we asked whether TRIM32 could also be essential for the regulation of myogenic stem cells. Here we demonstrate for the first time that TRIM32 is expressed in the skeletal muscle stem cell lineage of adult mice, and that in the absence of TRIM32, myogenic differentiation is disrupted. Moreover, we show that the ubiquitin ligase TRIM32 controls this process through the regulation of c-Myc, a similar mechanism to that previously observed in neural progenitors. Importantly we show that loss of TRIM32 function induces a LGMD2H-like phenotype and strongly affects muscle regeneration in vivo. Our studies implicate that the loss of TRIM32 results in dysfunctional muscle stem cells which could contribute to the development of LGMD2H

Erratum to: Mutation screening in 86 known X-linked mental retardation genes by droplet-based multiplex PCR and massive parallel sequencing

Item does not contain fulltext[This corrects the article DOI: 10.1007/s11568-010-9137-y.].1 december 200

Pathogenesis of myonecrosis induced by crude venom and a myotoxin of Bothrops asper.

The pathogenesis of skeletal muscle necrosis induced by crude Bothrops asper venom and isolated myotoxic phospholipase was studied using light and electron microscopy. White mice were injected intramuscularly with a dose of 2.5 micrograms/g and tissue samples were taken at 30 min and 1, 3, 6, 12, 24, and 48 hr. Toxin-injected muscle showed localized wedge-shaped lesions ("delta lesions") by 30 min, which included disrupted plasma membranes. At 1 and 3 hr the predominant type of necrotic cell contained clumped myofibrils in which individual myofilaments were indistinguishable. At later time periods there was a relaxation and redistribution of myofilaments resulting in a more homogeneous and hyaline appearance of necrotic cells. Some mitochondria were swollen and had flocculent densities, and most of them were disrupted, having only one membrane and vesiculated cristae. The basal lamina was intact at all time intervals. Phagocytosis of muscle cell debris started at 3 hr and was prominent by 24-48 hr. In crude venom-injected muscle many cells showed pathologic features identical to those observed after myotoxin injection. Crude venom also induced hemorrhage which was evident 30 min after injection, reaching its highest level by 12 hr. At 3, 6, and 12 hr some cells were undergoing different pathologic changes which appeared to be due to ischemia. Although these cells were irreversibly damaged, as indicated by ruptured plasma membrane, their myofibrillar structure was better preserved than that of toxin-affected cells. The Z line was absent, but A, I, H, and M bands were intact. As a result of Z line loss, sarcomeres were disoriented. It is proposed that the myotoxin induces myonecrosis by first altering the integrity of the plasma membrane, thereby increasing the permeability to calcium, other ions, and molecules which leads to death of the cell. Crude venom affects muscle cells in two ways: by direct action of myotoxin (s) and by ischemia due to hemorrhage.UCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP

Isolation of a myotoxin from Bothrops asper venom: Partial characterization and action on skeletal muscle

A myotoxic phospholipase has been isolated from Bothrops asper venom by ion-exchange chromatography on CM-Sephadex followed by gel filtration on Sephadex G-75. The toxin is a basic polypeptide with an estimated molecular weight of 10,700. It has both phospholipase A and indirect hemolytic activities, but is devoid of proteolytic, direct hemolytic and hemorrhagic effects. When injected i.m. into mice the toxin induces a rapid increase in plasma creatine kinase levels and a series of degenerative events in skeletal muscle which lead to myonecrosis. The toxin induces an increase in intracellular calcium levels and is able to hydrolyze muscle phospholipids in vivo. Pretreatment with the calcium antagonist verapamil failed to prevent the myotoxic activity. It is proposed that B. asper myotoxin causes cell injury by disrupting the integrity of skeletal muscle plasma membrane and that myotoxicity is at least partially due to the phospholipase A activity of the toxin.Universidad de Costa RicaUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP

Drug Discovery for Duchenne Muscular Dystrophy via Utrophin Promoter Activation Screening

Background: Duchenne muscular dystrophy (DMD) is a devastating muscle wasting disease caused by mutations in dystrophin, a muscle cytoskeletal protein. Utrophin is a homologue of dystrophin that can functionally compensate for its absence when expressed at increased levels in the myofibre, as shown by studies in dystrophin-deficient mice. Utrophin upregulation is therefore a promising therapeutic approach for DMD. The use of a small, drug-like molecule to achieve utrophin upregulation offers obvious advantages in terms of delivery and bioavailability. Furthermore, much of the time and expense involved in the development of a new drug can be eliminated by screening molecules that are already approved for clinical use. Methodology/Principal Findings: We developed and validated a cell-based, high-throughput screening assay for utrophin promoter activation, and used it to screen the Prestwick Chemical Library of marketed drugs and natural compounds. Initial screening produced 20 hit molecules, 14 of which exhibited dose-dependent activation of the utrophin promoter and were confirmed as hits. Independent validation demonstrated that one of these compounds, nabumetone, is able to upregulate endogenous utrophin mRNA and protein, in C2C12 muscle cells. Conclusions/Significance: We have developed a cell-based, high-throughput screening utrophin promoter assay. Using this assay, we identified and validated a utrophin promoter-activating drug, nabumetone, for which pharmacokinetics an