Essai d'information sur les drogues en milieu scolaire genevois

Summary This compulsory information is given to students of 12 th grade (14 – 15 years). A film is shown which is followed by a discussion between the students of each class and a doctor of the Health Department who is specialized in drug prevention.Teachers and parents are also informed in the same way.The efficiency of this method will have to be proved in the future.

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Unterrichtsversuch über Drogen in Sekundarschulen in Genf

Zusammenfassung Dieser obligatorische Unterricht findet für Schüler vom 12. Schuljahr (14 – 15 Jahre alt) statt.Ein Film und eine nachfolgende Diskussion zwischen Schülern und Spezialistärzten der Jugend-und Gesundheitsabteilung sind dafür gebraucht werden. Die Lehrer der Sekundarschulen und die Eltern sind gleichfalls unterrichtet.Die Wirksamkeit dieser Präventiverziehung wird noch zu bestimmen sein.

     

A retrospective analysis of autotransplanted teeth including an evaluation of a novel surgical technique

Clinical Oral Investigations - To assess survival rates and frequency of complications for immature and mature autotransplanted teeth after at least 1 year in function. All consecutive patients who...     

Estudio epidemiológico de la tinea capitis en una población de Santiago de Chile. La aparición de Trichophyton tonsurans como agente etiológico

Introduction

Tinea capitis (TC) is a dermatophytosis that affects the hair and scalp. The epidemiology of TC depends on the different geographical areas and is variable over time. Direct microscopic examination and fungal culture are essential to confirm the diagnostic suspicion and to identify the germ involved.

IRC‐083864, a novel bis quinone inhibitor of CDC25 phosphatases active against human cancer cells

CDC25 phosphatases are key actors in cyclin‐dependent kinases activation whose role is essential at various stages of the cell cycle. CDC25 expression is upregulated in a number of human cancers. CDC25 phosphatases are therefore thought to represent promising novel targets in cancer therapy. Here, we report the identification and the characterization of IRC‐083864, an original bis‐quinone moiety that is a potent and selective inhibitor of CDC25 phosphatases in the low nanomolar range. IRC‐083864 inhibits cell proliferation of a number of cell lines, regardless of their resistance to other drugs. It irreversibly inhibits cell proliferation and cell cycle progression and prevents entry into mitosis. In addition, it inhibits the growth of HCT‐116 tumor spheroids with induction of p21 and apoptosis. Finally, IRC‐083864 reduced tumor growth in mice with established human prostatic and pancreatic tumor xenografts. This study describes a novel compound, which merits further study as a potential anticancer agent. © 2008 Wiley‐Liss, Inc.     

Pharmacologic inhibition of CDC25 phosphatases impairs interphase microtubule dynamics and mitotic spindle assembly

The CDC25 cell cycle regulators are promising targets for new pharmacologic approaches in cancer therapy. Inhibitory compounds such as BN82685 have proven to be effective in specifically targeting CDC25 in cultured cells and in inhibiting tumor cell growth. Here, we report that BN82685 impairs microtubule dynamic instability and alters microtubule organization and assembly at the centrosome in interphase cells. Treatment of mitotic cells with BN82685 delays mitotic spindle assembly, chromosome capture, and metaphase plate formation. Furthermore, we show that combining low concentrations of both BN82685 and paclitaxel inhibits the proliferation of HT29 human colon cancer cells. Our results show a role for CDC25 phosphatases in regulating microtubule dynamics throughout the cell cycle and suggest that combinations of CDC25 inhibitors with microtubule-targeting agents may be of therapeutic value.     

Differential mitotic degradation of the CDC25B phosphatase variants

CDC25 phosphatases control cell-cycle progression by dephosphorylating and activating cyclin-dependent kinases. CDC25B, one of the three members of this family in human cells, is thought to regulate initial mitotic events. CDC25B is an unstable protein whose proteasomal degradation is proposed to be controlled by beta-TrCP. Here, we have investigated the regulation of CDC25B during mitosis, using time-lapse video microscopy. We found that CDC25B expression is high during early mitosis, and that its degradation occurs after the metaphase-anaphase transition and cyclin B1 destruction. We also show that CDC25B degradation after metaphase is dependent on the integrity of the KEN-box and RRKSE motifs that are located within the alternatively spliced B domain, and that the CDC25B2 splice variant, that lacks this domain, is stable during mitosis. Furthermore, we show that the N-terminal region of CDC25B, encompassing the B domain, undergoes major conformational changes during mitosis that can be monitored by intramolecular fluorescence resonance energy transfer variation of specific CDC25B biosensors. This study demonstrates that CDC25B splice variants have differential mitotic stabilities, a feature that is likely to have major consequences on the local control of cyclin-dependent kinase-cyclin activities during mitotic progression.