De la Rémunération du Personnel dans les Structures Professionnelles des Eglises à Bukavu

Le présent article porte sur la rémunération dans les structures professionnelles des Eglises à Bukavu. L’étude vise à (1) déterminer les masses salariales allouées aux agents par les structures professionnelles des Eglises ; (2) jauger le degré de satisfaction et de motivation des agents face à la rémunération qu’ils reçoivent et (3) à identifier les lignes des dépenses couvertes par ces salaires dans la Ville de Bukavu. Pour la collecte des données, 401 sujets issus de 42 structures professionnelles des Eglises de Bukavu ont été enquêtés à l’aide de l’outil questionnaire. La méthode structuro-fonctionnelle, l’analyse de contenu et le test chi carré ont soutenu le dépouillement et le traitement des données. Il ressort des résultats de la recherche que le salaire est un aspect important dans le fonctionnement harmonieux de toute structure professionnelle. Les masses salariales allouées aux agents varient selon les tailles, les productivités, l’accessibilité à la main d’œuvre et la bonne volonté des structures professionnelles des Eglises. Le salaire alloué aux agents oscille entre 0 et 2000 dollars par mois et par individu. Ce salaire ne suffit pas pour couvrir les besoins d’épargne et d’investissement. En dépit, de sa faiblesse à satisfaire aux besoins des agents, la rémunération est relativement bien payée par les structures professionnelles des Eglises protestantes plutôt que celles de l’Eglise catholique. Les agents sont ainsi démotivés et restent à la recherche permanente d’un travail qui procurerait la bonne rémunération. This paper focuses on determining the amount of wages allocated to employees in the Church organizations and enterprises. It assesses the extent to which employees are satisfied and motivated based on the wages they are paid, and it also examines how Church employees allocate their wages to meet the needs of their households. Data was collected in Bukavu through a selfadministered questionnaire on a sample of 401 Church employees. The data was processed and analyzed in SPSS and Excel through the structural functional method, together with content analysis and Chi-Square test. The findings indicate that salary is an important driver of smooth relationships and it is very important for the functioning of any Church organization or enterprise. The total amount of wages allocated to employees varies among Church organizations and enterprises. This is dependent on the organizational size, productivity, location of majority of the workforce, and the policy of the Church enterprise. On average, the salary per individual worker ranges from 0 to 2,000 dollars per month. The salary is not enough to cover savings and investment needs of employees, rather it only serves for subsistence needs such as food, school fees of children, and rent. The remuneration is higher for employees who work for protestant organizations and enterprises compared to Catholic Church. The employees therefore are unsatisfied, not motivated, and are in a continuous search for a better job

Somatic expansion of premutation alleles and the role of the mismatch repair and base excision repair proteins on repeat expansion in a mouse model of the fragile X-related disorders

The Fragile X-related disorders arise from an unusual mutation in the X-linked FMR1 gene. The mutation involves expansion, or an increase in the number of repeats, in a CGG•CCG repeat tract located in its 5' untranslated region. FMR1 alleles carrying 55-200 repeats are called Premutation (PM) alleles, and cause Fragile X associated tremor/ataxia syndrome (FXTAS) and Fragile X-associated primary ovarian insufficiency (FXPOI). FMR1 alleles having more than 200 repeats are referred to as full mutation (FM) alleles and cause Fragile X syndrome (FXS). These different alleles arise by intergenerational expansion of the repeat tract from smaller unstable alleles by a mechanism that is unknown. We have shown that in addition to germ line expansion, somatic expansion also occurs in a human cell line in vivo and in a FX PM mouse model. In the mouse model, we found that the extent of somatic instability is dependent on age, gender and tissue. Specifically, organs such as brain, liver and gonads are susceptible to expand more than heart and kidney and expansion is much more frequent in males than in females. No differences were found between male and female mice in the levels of the DNA repair proteins that had already been implicated in repeat expansion in model systems of other disorders thought to arise via a similar mechanism. Neither were there any differences between males and females in the amounts of proteins produced from X-linked DNA repair genes. We also showed that estrogen did not protect against expansion. However, we found that PM alleles expanded exclusively when they were located on the active X chromosome. Thus some of the differences between males and xii females in the level of somatic expansion might be due to the fact that females undergo X inactivation and thus have the PM allele on the inactive X chromosome in half (~50%) of their cells. It also indicates that transcription and/or an open chromatin configuration is required for expansion in the FX PM mouse

Heterozygosity for a hypomorphic polβ mutation reduces the expansion frequency in a mouse model of the fragile x-related disorders

Author Summary Unstable microsatellites are responsible for a number of debilitating human diseases known as the Repeat Expansion Diseases. The unstable microsatellites, which consist of tandem arrays of short repeat units, are prone to increase in length (expand) on intergenerational transmission and during the lifetime of the individual. Unlike the typical microsatellite instability seen in disorders like Lynch syndrome that arise from mutations in mismatch repair (MMR) genes, expansions of these microsatellites are abolished when MMR is lost. However, how MMR, which normally protects the genome against microsatellite instability, actually promotes microsatellite expansions in these diseases is unknown. There is evidence to suggest that a second DNA repair process, base excision repair (BER), may be involved, but whether the nicks generated early in the BER-process are subverted by an MMR-dependent pathway that generates expansions or whether some MMR proteins contribute to a BER-based expansion process is unclear. Here we show that a mutation that reduces the activity of Polβ, an essential BER enzyme, also reduces the expansion frequency. Since Polβ is essential for key events in BER downstream of the generation of nicks, our data favor a model in which expansions occur via a BER-dependent pathway in which MMR participates

Somatic alpha-synuclein mutations in Parkinson's disease: Hypothesis and preliminary data.

Alpha-synuclein (SNCA) is crucial in the pathogenesis of Parkinson's disease (PD), yet mutations in the SNCA gene are rare. Evidence for somatic genetic variation in normal humans, also involving the brain, is increasing, but its role in disease is unknown. Somatic SNCA mutations, arising in early development and leading to mosaicism, could contribute to PD pathogenesis and yet be absent or undetectable in DNA derived from peripheral lymphocytes. Such mutations could underlie the widespread pathology in PD, with the precise clinical outcome dependent on their type and the timing and location of their occurrence. We recently reported a novel SNCA mutation (c.150T>G, p.H50Q) in PD brain-derived DNA. To determine if there was mosaicism for this, a PCR and cloning strategy was used to take advantage of a nearby heterozygous intronic polymorphism. No evidence of mosaicism was found. High-resolution melting curve analysis of SNCA coding exons, which was shown to be sensitive enough to detect low proportions of 2 known mutations, did not reveal any further mutations in DNA from 28 PD brain-derived samples. We outline the grounds that make the somatic SNCA mutation hypothesis consistent with genetic, embryological, and pathological data. Further studies of brain-derived DNA are warranted and should include DNA from multiple regions and methods for detecting other types of genomic variation. © 2013 Movement Disorder Society

A MutSβ-Dependent Contribution of MutSα to Repeat Expansions in Fragile X Premutation Mice?

Author Summary: The repeat expansion diseases are a group of human genetic disorders that are caused by expansion of a specific microsatellite in a single affected gene. How this expansion occurs is unknown, but previous work in various models for different diseases in the group, including the fragile X-related disorders (FXDs), has implicated the mismatch repair complex MutSβ in the process. With the exception of somatic expansion in Friedreich ataxia, MutSα has not been reported to contribute to generation of expansions in other disease models. Here we show that MutSα does in fact play a role in both germ line and somatic expansions in a mouse model of the FXDs since the expansion frequency is significantly reduced in Msh6 -/- mice. However, since we have previously shown that loss of MutSβ eliminates almost all expansions, MutSα is apparently not able to fully substitute for MutSβ in the expansion process. We also show here that MutSα increases the stability of the structures formed by the fragile X repeats that are thought to be the substrates for expansion and promotes binding of MutSβ to the repeats. This, together with our genetic data, suggests possible models for how MutSα and MutSβ, could co-operate to generate repeat expansions in the FXDs

The fragile X locus is prone to spontaneous DNA damage that is preferentially repaired by nonhomologous end-joining to preserve genome integrity

Summary: A long CGG-repeat tract in the FMR1 gene induces the epigenetic silencing that causes fragile X syndrome (FXS). Epigenetic changes include H4K20 trimethylation, a heterochromatic modification frequently implicated in transcriptional silencing. Here, we report that treatment with A-196, an inhibitor of SUV420H1/H2, the enzymes responsible for H4K20 di-/trimethylation, does not affect FMR1 transcription, but does result in increased chromosomal duplications. Increased duplications were also seen in FXS cells treated with SCR7, an inhibitor of Lig4, a ligase essential for NHEJ. Our study suggests that the fragile X (FX) locus is prone to spontaneous DNA damage that is normally repaired by NHEJ. We suggest that heterochromatinization of the FX allele may be triggered, at least in part, in response to this DNA damage

Expression of various BER proteins in different mouse organs.

<p>Total protein was extracted from different organs of 3 different FXD mice as described in the Materials and Methods. Since in our experience proteins used as “normalizing controls” including β-actin and α-tubulin and GAPDH differ significantly in different organs, we took care to analyze equal amounts of protein as assessed by the Bradford Assay. Ten micrograms of protein from the organs of each animal were pooled and loaded onto 3–8% Tris-Acetate gels, resolved by gel electrophoresis and subjected to Western blotting as described in the Materials and Methods.</p