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N00.00069: Nanoscale Velcro-like Effect: Synthesis and Rheological Properties of Polymer Loop-Grafted Nanoparticles N00.00328: Accumulating mutations lead to frequent adaptation of non-genic loci and de novo gene birth N00.00353: Analysis of the dynamics of the growing and branching network of filamentous fungus Podospora anserina.

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N00.00304: Targeted insertion of large genetic payloads using cas directed LINE-1 reverse transcriptase Wang, X. et al. Non-invasive detection of biliary tract cancer by low-coverage whole genome sequencing from plasma cell-free DNA: A prospective cohort study. Transl. Oncol. 14, 100908 (2021). N00.00057: Comparison of Various Methods to Analyze Aperiodic Percolated Nanostructures in Molecular Dynamics simulations N00.00020: Simulating the co-assembly of cellulose nanocrystals and gold nanorods-effect of size distribution and densityTian Y, Gu G, Johnson P, Rao T, Tsang T, Wang E (2018) Topological insulators for the generation of electron beams. Applied Physics Letters 113:233504. doi: 10.1063/1.5052415 N00.00062: Electrospun polyampholyte nanofibers with different hydrophobic and ionic chain densities N00.00117: Controlling Ensemble Chain Conformations with Precise Sequence Patterning of Polypeptoids

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N00.00170: Linear and quadratic electromechanical effects of a room temperature ferroelectric nematic liquid crystal N00.00077: Impact of polymer molecular weight on droplet coalescence and the properties of parts printed via powder bed fusion Yamagiwa, H. & Tomiyama, H. Intestinal metaplasia-dysplasia-carcinoma sequence of the gallbladder. Acta Pathol. Jpn. 36, 989–997 (1986). Macro01 was preferentially enriched in metastatic lesions (Fig. 4c; Supplementary Fig. S11a) and was mapped to tumor-associated macrophages (TAMs) (Fig. 4g; Supplementary Table S10), with extensive upregulation of ISGs (e.g., ISG15, GPNMB, IFI6) and lipid metabolism genes (e.g., APOC1, CTSD, PLA2G7) (Fig. 4b, f; Supplementary Table S9), conceivably implying its immunosuppressive role conferred by IFN-stimulated lipid reprogramming 29, 30. The S100A8 + THBS1 + Macro02 subset, rich in S100A family genes ( S100A8, S100A9, S100A12, VCAN, and FCN1), typically mapped to myeloid-derived suppressor cell-like (MDSC-like) macrophages (Fig. 4f, g) 31, 32, 33. Apart from its affluence in inflamed gallbladders akin to other chronic infections (Fig. 4c) 34, several GBC patients, especially one advanced case (GBC9), showed pronounced enrichment (Supplementary Fig. S11a), whereby this subset conceivably induced an immunocompromised state through regulating cytokine production and leukocyte chemotaxis (Fig. 4i). Macro03 ( FCGBP + CX3CR1 + C3 +) was enriched in GBCs (Fig. 4c), especially in two early cases (GBC1-2) (Supplementary Fig. S11a), typically expressing the tumor-promoting marker TREM2 (Fig. 4b, e, f) 35. It behaved as an immunosuppressive TAM subset by regulating leukocyte migration, differentiation, and chemotaxis (Fig. 4i). With marked patient occupancy (GBC6) (Fig. 4c; Supplementary Fig. S11a), Macro04 exhibited versatile tumor-promoting roles, including cytokine production (e.g., TNFAIP3, CXCL3), pro-angiogenesis (e.g., VEGFA), and ECM remodeling (e.g., SPP1) (Fig. 4e–g, j) 28, 36, 37. Macro05 displayed prominently active proliferation features ( MKI67 + STMN1 +) (Fig. 4b, f), likely serving as self-renewal gallbladder-resident macrophages 38. This subcluster was frequently found within GBCs (Supplementary Fig. S11a); however, a benign outlier (CC6 with XGC) was noted, whereby proliferating macrophages probably contributed to the shaping of ‘foamy’ macrophage milieu in XGC-related destructive inflammation. Predominantly residing in PTs (Fig. 4c), Macro06 synchronously behaved as M2-like TAMs (e.g., LYVE1, SEPP1, MRC1, FOLR2) 39, as well as perivascular TAMs (e.g., MRC1, VCAM1, SLC40A1) (Fig. 4f, g), which probably facilitated vascular development and cancer cell intravasation (Fig. 4c–g) 32, 40. Collectively, tumor-derived macrophages displayed more prominent M2- and TAM-like traits, together with boosted angiogenesis and phagocytosis processes. In contrast, their benign counterparts behaved more like M1- or MDSC-like macrophages (Fig. 4h). As for different epithelial subtypes, subtype II exhibited more active crosstalk with macrophages (Supplementary Fig. S11b). Cancer cell-derived MIF or COPA potentially dictated the crosstalk with macrophages through CD74-related signaling pathways and, reciprocally, macrophage-secreted granulin (GRN) might send tumor-promoting signals to cancer cells via TNF receptors (Supplementary Fig. S11c, d).These results together revealed three subtypes of gallbladder cancer cells relevant to patient prognosis, which displayed distinct transcriptomic and genomic signatures, providing potential markers and targets for GBC diagnosis and treatment. Identification of myeloid cell subsets nurturing the immunosuppressive TME Leticia Galera-Laporta, Kaito Kikuchi, Colleen Weatherwax, Jamie Y Lam, Eun Chae Moon, Emmanuel A Theodorakis, Jordi Garcia-Ojalvo, Gürol M Süel