Stress studies on Ti and TiN interlayer in (100) silicon wafers

Ti is used to improve wettability between Al and Si. TiN is used as a diffusion barrier to prevent diffusion of Al into Si during annealing. In this study, stress from Ti and TiN thin-films on (100) Silicon wafers are studied using Stoney’s equation. [1st Award

Motivations and deterrents of Asian small and medium-sized enterprises’ willingness to adopt green electricity

10.1016/j.jclepro.2022.133233Journal of Cleaner Production370133233-13323

A Spot-Area Method to Evaluate the Incidence Angle Modifier of Photovoltaic Devices-Part 1: Cells

10.1109/JPHOTOV.2023.3236187IEEE JOURNAL OF PHOTOVOLTAIC

Impact of urban block typology on building solar potential and energy use efficiency in tropical high-density city

10.1016/j.apenergy.2019.02.033APPLIED ENERGY240513-53

Targeting Treg cells with GITR activation alleviates resistance to immunotherapy in murine glioblastomas

International audienceAbstract Immune checkpoint blockers (ICBs) have failed in all phase III glioblastoma (GBM) trials. Here, we show that regulatory T (Treg) cells play a key role in GBM resistance to ICBs in experimental gliomas. Targeting glucocorticoid-induced TNFR-related receptor (GITR) in Treg cells using an agonistic antibody (αGITR) promotes CD4 Treg cell differentiation into CD4 effector T cells, alleviates Treg cell-mediated suppression of anti-tumor immune response, and induces potent anti-tumor effector cells in GBM. The reprogrammed GBM-infiltrating Treg cells express genes associated with a Th1 response signature, produce IFNγ, and acquire cytotoxic activity against GBM tumor cells while losing their suppressive function. αGITR and αPD1 antibodies increase survival benefit in three experimental GBM models, with a fraction of cohorts exhibiting complete tumor eradication and immune memory upon tumor re-challenge. Moreover, αGITR and αPD1 synergize with the standard of care treatment for newly-diagnosed GBM, enhancing the cure rates in these GBM models

A bacterial cell-cell communication signal with cross-kingdom structural analogues

10.1046/j.1365-2958.2003.03883.xMolecular Microbiology513903-912MOMI

Head and Body/Tail Pancreatic Carcinomas Are Not the Same Tumors

International audienceThe association between pancreatic ductal adenocarcinoma (PDAC) location (head vs. Body/Tail (B/T)) and clinical outcome remains controversial. We collected clinicopathological and gene expression data from 249 resected PDAC samples from public data sets, and we compared data between 208 head and 41 B/T samples. The 2-year overall survival (OS) was better for the head than for the B/T PDACs (44 vs. 27%, p = 0.043), especially when comparing tumors with similar TNM classification (T3/4N0M0: 67% vs. 17%, p = 0.002) or from the same molecular class (squamous subtype: 31% vs. 0%, p < 0.0001). Bailey’s molecular subtypes were differentially distributed within the two groups, with the immunogenic subtype being underrepresented in the “B/T” group (p = 0.005). Uni- and multivariate analyses indicated that PDAC anatomic location was an independent prognostic factor. Finally, the supervised analysis identified 334 genes differentially expressed. Genes upregulated in the “head” group suggested lymphocyte activation and pancreas exocrine functions. Genes upregulated in the “B/T” group were related to keratinocyte differentiation, in line with the enrichment for squamous phenotype. We identified a robust gene expression signature (GES) associated with B/T PDAC location, suggesting that head and B/T PDAC are different. This GES could serve as an indicator for differential therapeutic management based on PDAC location