The impact of income shocks on children education: the 1987-1989 locust plague in Mali.

This paper estimates the long run impact of a large income shock, by exploiting the regional variation of the 1987-1989 locust invasion in Mali. Using exhaustive Population Census data, we construct birth cohorts of individuals and compare those born and living in the years and villages a ected by locust plagues with other cohorts. We assert that in-utero and early childhood exposure to income shock had a larger negative effects on the probability to go to school than later childhood exposure. Indeed, the proportion of boys born during the shock and who later enrolled at school is reduced by 4.9% if they lived in a community invaded by locusts, and by 3.5% for girls. This impact goes up to 6% for boys and 5% for girls living in rural areas. Concerning the number of years of education and the probability to achieve primary school, no real impact is found for boys while girls who lived in a community a ected by locusts have completed between 0.25 and 0.67 lower grades than if they had lived in another community. Finally, we nd that children living in rural localities and belonging to farmer households appear to have been much more affected than other children, living in urban localities or belonging to cattle breeder or shopkeeper households.Locust.; Education; Shocks; Mali;

Modélisation de la combustion turbulente des mélanges hétérogènes en richesse. Application au calcul d'une flamme stabilisée par l'élargissement brusque d'un canal bidimensionnel

International audienc

t(12;13)(p13;q12) ETV6/FLT3

Review on t(12;13)(p13;q12) ETV6/FLT3 , with data on DNA, on the protein encoded, and where the gene is implicated

Using Bacterial Artificial Chromosomes in Leukemia Research: The Experience at the University Cytogenetics Laboratory in Brest, France

The development of the bacterial artificial chromosome (BAC) system was driven in part by the human genome project in order to construct genomic DNA libraries and physical maps for genomic sequencing. The availability of BAC clones has become a valuable tool for identifying cancer genes. We report here our experience in identifying genes located at breakpoints of chromosomal rearrangements and in defining the size and boundaries of deletions in hematological diseases. The methodology used in our laboratory consists of a three-step approach using conventional cytogenetics followed by FISH with commercial probes, then BAC clones. One limitation to the BAC system is that it can only accommodate inserts of up to 300 kb. As a consequence, analyzing the extent of deletions requires a large amount of material. Array comparative genomic hybridization (array-CGH) using a BAC/PAC system can be an alternative. However, this technique has limitations also, and it cannot be used to identify candidate genes at breakpoints of chromosomal rearrangements such as translocations, insertions, and inversions

t(11;22)(q13;q13) HRASLS5/PHF21B

Review on t(11;22)(q13;q13), with data on clinics, and the genes involved

inv(3)(q21q26) RPN1/MECOM

review on inv(3)(q21q26) RPN1/MECO

ETV6-RUNX1 and RUNX1 directly regulate RAG1 expression: one more step in the understanding of childhood B-cell acute lymphoblastic leukemia leukemogenesis.

Funder: Société Française de Biochimie et Biologie Moléculaire ; French Research MinistryFunder: Cancéropole Grand Ouest ; Région Bretagne ; Société Française d’HématologieFunder: Ligue Régionale contre le cancer ;ETV6-RUNX1 and RUNX1 directly promote RAG1 expression. ETV6-RUNX1 and RUNX1 preferentially bind to the −1200 bp enhancer of RAG1 and the −80 bp promoter of RAG1 gene respectively, and compete for these bindings. ETV6-RUNX1 and RUNX1 induce an excessive RAG recombinase activity. ETV6-RUNX1 participates directly in two events of the multi-hit ALL leukemogenesis: as an initiating event and as an activator of RAG1 expression

Expression of TRPC6 channels in human epithelial breast cancer cells

<p>Abstract</p> <p>Background</p> <p>TRP channels have been shown to be involved in tumour generation and malignant growth. However, the expression of these channels in breast cancer remains unclear. Here we studied the expression and function of endogenous TRPC6 channels in a breast cancer cell line (MCF-7), a human breast cancer epithelial primary culture (hBCE) and in normal and tumour breast tissues.</p> <p>Methods</p> <p>Molecular (Western blot and RT-PCR), and immunohistochemical techniques were used to investigate TRPC6 expression. To investigate the channel activity in both MCF-7 cells and hBCE we used electrophysiological technique (whole cell patch clamp configuration).</p> <p>Results</p> <p>A non selective cationic current was activated by the oleoyl-2-acetyl-sn-glycerol (OAG) in both hBCE and MCF-7 cells. OAG-inward current was inhibited by 2-APB, SK&F 96365 and La³⁺. TRPC6, but not TRPC7, was expressed both in hBCE and in MCF-7 cells. TRPC3 was only expressed in hBCE. Clinically, TRPC6 mRNA and protein were elevated in breast carcinoma specimens in comparison to normal breast tissue. Furthermore, we found that the overexpression of TRPC6 protein levels were not correlated with tumour grades, estrogen receptor expression or lymph node positive tumours.</p> <p>Conclusion</p> <p>Our results indicate that TRPC6 channels are strongly expressed and functional in breast cancer epithelial cells. Moreover, the overexpression of these channels appears without any correlation with tumour grade, ER expression and lymph node metastasis. Our findings support the idea that TRPC6 may have a role in breast carcinogenesis.</p