La Gestalt

C'est un fait que comme théorie vivante, la Gestalt a été et reste ouverte aux influences de l'extérieur. De Freud, en passant par Reich, Jung et Rank, aux philosophies orientales autant qu'occidentales contemporaines, sans oublier Moreno ni les théories organismiques allemandes du début du siècle, la Gestalt est née et a été façonnée par son génial et original auteur, Frederick S. Perls. Comme ce dernier ne s'est jamais refermé sur ses vérités connues et découvertes une fois pour toutes, la Gestalt présente un système de concepts et d'instruments cohérents mais ouverts. Toutefois, il est important, pour laisser émerger graduellement les éléments qui composent ce tout complexe, de dire un mot des grands axes théoriques qui en composent les assises. Ils sont au nombre de quatre : 1) la psychanalyse, qui comprend elle-même le courant freudien et le courant jungien ; 2) l'analyse caractérielle de W. Reich ; 3) la théorie allemande gestaltiste et organismique sur la perception ; 4) le courant philosophique existentiel. On peut ajouter un cinquième courant, qui tout en étant moins fondamental que les quatre premiers est assez original pour qu'il vaille la peine d'en parler, il s'agit du courant des religions orientales, telles le Taoïsme et le Zen.The authors describe Gestalt Therapy. They retrace its fundamental theoretical axes. These are psychoanalysis, character analysis, the german Gestalt theory of perception, existentialism, and the Orient. Some principal concepts are then elaborated more fully such as the cycle of awareness, desensitization, excitation anxiety and the five defense mechanisms: retroflection, introjection, projection, deflection, and confluence. The nature and goals of the therapeutic process are also described before the presentation of some techniques specific to this approach such as enactment and role playing. Finally, certain basic Gestalt rules, which aim at facilitating and intensifying the communication process among group members, are enunciated

Gene Expression Profiling and Molecular Characterization of Antimony Resistance in Leishmania amazonensis

Leishmania are unicellular microorganisms that can be transmitted to humans by the bite of sandflies. They cause a spectrum of diseases called leishmaniasis, which are classified as neglected tropical diseases by the World Health Organization. The treatment of leishmaniasis is based on the administration of antimony-containing drugs. These drugs have been used since 1947 and still constitute the mainstay for leishmaniasis treatment in several countries. One of the problems with these compounds is the emergence of resistance. Our work seeks to understand how these parasites become resistant to the drug. We studied antimony-resistant Leishmania amazonensis mutants. We analyzed gene expression at the whole genome level in antimony-resistant parasites and identified mechanisms used by Leishmania for resistance. This work could help us in developing new strategies for treatment in endemic countries where people are unresponsive to antimony-based chemotherapy. The identification of common mechanisms among different species of resistant parasites may also contribute to the development of diagnostic kits to identify and monitor the spread of resistance

Genome sequencing of the lizard parasite Leishmania tarentolae reveals loss of genes associated to the intracellular stage of human pathogenic species

The Leishmania tarentolae Parrot-TarII strain genome sequence was resolved to an average 16-fold mean coverage by next-generation DNA sequencing technologies. This is the first non-pathogenic to humans kinetoplastid protozoan genome to be described thus providing an opportunity for comparison with the completed genomes of pathogenic Leishmania species. A high synteny was observed between all sequenced Leishmania species. A limited number of chromosomal regions diverged between L. tarentolae and L. infantum, while remaining syntenic to L. major. Globally, >90% of the L. tarentolae gene content was shared with the other Leishmania species. We identified 95 predicted coding sequences unique to L. tarentolae and 250 genes that were absent from L. tarentolae. Interestingly, many of the latter genes were expressed in the intracellular amastigote stage of pathogenic species. In addition, genes coding for products involved in antioxidant defence or participating in vesicular-mediated protein transport were underrepresented in L. tarentolae. In contrast to other Leishmania genomes, two gene families were expanded in L. tarentolae, namely the zinc metallo-peptidase surface glycoprotein GP63 and the promastigote surface antigen PSA31C. Overall, L. tarentolae's gene content appears better adapted to the promastigote insect stage rather than the amastigote mammalian stage

Claude Tousignant

Proposing a biographical survey, Corbeil describes Tousignant's activities in Montreal during the 1950s and 60s. Biographical notes. Circa 20 bibl. ref

Gene amplification and point mutations in pyrimidine metabolic genes in 5-fluorouracil resistant Leishmania infantum.

The human protozoan parasites Leishmania are prototrophic for pyrimidines with the ability of both de novo biosynthesis and uptake of pyrimidines.Five independent L. infantum mutants were selected for resistance to the pyrimidine analogue 5-fluorouracil (5-FU) in the hope to better understand the metabolism of pyrimidine in Leishmania. Analysis of the 5-FU mutants by comparative genomic hybridization and whole genome sequencing revealed in selected mutants the amplification of DHFR-TS and a deletion of part of chromosome 10. Point mutations in uracil phosphorybosyl transferase (UPRT), thymidine kinase (TK) and uridine phosphorylase (UP) were also observed in three individual resistant mutants. Transfection experiments confirmed that these point mutations were responsible for 5-FU resistance. Transport studies revealed that one resistant mutant was defective for uracil and 5-FU import.This study provided further insights in pyrimidine metabolism in Leishmania and confirmed that multiple mutations can co-exist and lead to resistance in Leishmania

Role of thymidine kinase (<i>LinJ21.1450</i>) in methotrexate susceptibility.

<p>Growth curves in the presence of methotrexate were determined for <i>L. infantum</i> wild-type cells (lines with circles) and the Lin5FU500.3 mutant (lines with squares), each transfected either with an empty vector (pSP72<i>αHYGα</i>) (black circles and black squares respectively) or with a thymidine kinase expression construct (pSP72<i>αHYGα</i>-<i>LinJ.21.1450</i>) (white circles and white squares respectively). Average of three independent biological replicates. Transfection of <i>TK</i> in the mutant led to MTX susceptibility that was statistically different than the mock control (p<0.05).</p

Resistance levels to 5-FU and MTX in <i>L. infantum</i> 263 WT and 5-FU resistant mutants.

*<p>Rev = revertant strain cultured without drug pressure over 30 passages;</p>**<p>(p<0,005).</p

<i>DHFR-TS</i> amplification and resistance to 5-fluorouracil.

<p>(<b>A</b>). Comparative genomic hybridization (CGH) experiments between wild-type and Lin5FU500.2 cells. Grey, equal amount of DNA between the two strains; black, increased copy number of DNA in the mutant Lin5FU500.2. (<b>B</b>). Southern blots of total digested DNAs isolated from WT and each mutant strains at 0 and 30 passages without drug were hybridized to a specific <i>DHFR-TS</i> probe. The DNA was digested to discriminate the chromosomal copy (C*) from the amplified copy (A*). (<b>C</b>). Role of <i>DHFR-TS</i> in 5-FU resistance. Growth curves of wild-type <i>L. infantum</i> parasites transfected with the expression construct pSP72<i>αHYGα- DHFR-TS</i> (black squares) or with the empty vector pSP72<i>αHYGα</i> (white squares) or the Lin5FU500.2 revertant transfected with pSP72<i>αHYGα- DHFR-TS</i> (black circles) or pSP72<i>αHYGα</i> (white circles). Average of at least three independent experiments. Transfection of <i>DHFR-TS</i> led to 5FU resistance that was statistically significant compared to mock transfectants (p<0.05).</p