-> NEW!!! Give your feedback about the seminars via your smartphone or laptop by Friday 3pm! : https://wwwfbm.unil.ch/sondage/index.php/528578?newtest=Y&lang=en
Cell & Molecular Biology 3-6 months paid internship in Heidelberg Germany (with possibility of fulltime position offer thereafter).
WMT AG is a biotech company developing new anti-cancer drugs for clinical development.
More info: https://www.wm-therapeutics.com/
If interested, please send your letter of motivation to jobs@wm-therapeutics.com, along with clear and concise application documents and an indication of your availability.
Finding easily all pictures of CIG events at the same place and being able to share yours too would be great, wouldn’t it ?
It’s now possible via the new page “Pictures of the events” on the CIG’s intranet (wiki) : https://wiki.unil.ch/fbm-cig/books/socialize-at-the-cig (UNIL login)
Remember there is also a slack at your disposal to chat with other members and look for a shared room / company for a coffee / running partner… etc
J Clin Invest. 2022 Jul 1;132(13):e162359. doi: 10.1172/JCI162359.
Sylviane Lagarrigue, Isabel C Lopez-Mejia, Pierre-Damien Denechaud, Xavier Escoté, Judit Castillo-Armengol, Veronica Jimenez, Carine Chavey, Albert Giralt, Qiuwen Lai, Lianjun Zhang, Laia Martinez-Carreres, Brigitte Delacuisine, Jean-Sébastien Annicotte, Emilie Blanchet, Sébastien Huré, Anna Abella, Francisco J Tinahones, Joan Vendrell, Pierre Dubus, Fatima Bosch, C Ronald Kahn, Lluis Fajas
Hello!
I am Nermin Abolnaga. I am a SUR participant in UNIL, currently working in Dr. Maria Gambetta’s Lab at the CIG.
I’ll be helping Ms. Anastasia Semanova tackle a couple of question marks surrounding insulator gene sequences.
I have found Switzerland to be welcoming and found Gambetta’s lab even more so. I come from Cairo, Egypt, and will be starting my senior year at the University of Science and Technology in Zewail City once I get back. During my sophomore and junior years, I worked with Dr. Mohamed Elhadidy at the Center For Genomics in Zewail City. I was in charge of hunting down integrons in bacterial isolates and characterizing them once captured.
Excited to meet everyone at the CIG!
Mol Psychiatry. 2022 Jun 29. doi: 10.1038/s41380-022-01674-9. Online ahead of print.
Maris Alver 1 2 3, Valentina Mancini 4, Kristi Läll 5, Maude Schneider 4 6, Luciana Romano 7, Estonian Biobank Research Team; Reedik Mägi 5, Emmanouil T Dermitzakis 7, Stephan Eliez 7 4, Alexandre Reymond 8
While the recurrent 22q11.2 deletion is one of the strongest genetic risk factors for schizophrenia (SCZ), variability of its associated neuropsychiatric endophenotypes reflects its incomplete penetrance for psychosis development. To assess whether this phenotypic variability is linked to common variants associated with SCZ, we studied the association between SCZ polygenic risk score (PRS) and longitudinally acquired phenotypic information of the Swiss 22q11.2DS cohort (n = 97, 50% females, mean age 17.7 yr, mean visit interval 3.8 yr). The SCZ PRS with the best predictive performance was ascertained in the Estonian Biobank (n = 201,146) with LDpred. The infinitesimal SCZ PRS model showed the strongest capacity in discriminating SCZ cases from controls with one SD difference in SCZ PRS corresponding to an odds ratio (OR) of 1.73 (95% CI 1.57-1.90, P = 1.47 × 10-29). In 22q11.2 patients, random-effects ordinal regression modelling using longitudinal data showed SCZ PRS to have the strongest effect on social anhedonia (OR = 2.09, P = 0.0002), and occupational functioning (OR = 1.82, P = 0.0003) within the negative symptoms course, and dysphoric mood (OR = 2.00, P = 0.002) and stress intolerance (OR = 1.76, P = 0.0002) within the general symptoms course. Genetic liability for SCZ was additionally associated with full scale cognitive decline (β = -0.25, P = 0.02) and with longitudinal volumetric reduction of the right and left hippocampi (β = -0.28, P = 0.005; β = -0.23, P = 0.02, respectively). Our results indicate that the polygenic contribution to SCZ acts upon the threshold-lowering first hit (i.e., the deletion). It modifies the endophenotypes of 22q11.2DS and augments the derailment of developmental trajectories of negative and general symptoms, cognition, and hippocampal volume.
