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). Karnoub, A. E. et al. Mesenchymal stem cells within tumour stroma promote breast cancer metastasis. Nature 449, 557–563 (2007). Cheng, S. et al. A pan-cancer single-cell transcriptional atlas of tumor infiltrating myeloid cells. Cell 184, 792–809.e23 (2021). Yang L, Fang J, Wang J, Hui S, Zhou L, Xu B, Chen Y, Zhang Y, Lai C, Jiao G, Sheng Z, Wei X, Shao G, Xie L, Wang L, Chen Y, Zhao F, Hu S, Hu P, Tang S. Yang L, et al. Front Plant Sci. 2023 Jul 24;14:1222288. doi: 10.3389/fpls.2023.1222288. eCollection 2023. Front Plant Sci. 2023. PMID: 37554558 Free PMC article.

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Van Lidth de Jeude, J. F., Vermeulen, J. L., Montenegro-Miranda, P. S., Van den Brink, G. R. & Heijmans, J. A protocol for lentiviral transduction and downstream analysis of intestinal organoids. J. Vis. Exp. 98, e52531 (2015). Fawkner-Corbett, D. et al. Spatiotemporal analysis of human intestinal development at single-cell resolution. Cell 184, 810–826.e23 (2021). The association between subtype-specific markers and prognosis was explored in another independent GBC cohort from our hospital based on tissue microarray data ( n = 49; Fig. 3f–h; Supplementary Table S8). Increased expression of MUC2 (subtype I marker) was markedly associated with better overall survival ( P = 0.041; Fig. 3i). By contrast, overexpression of CTSD (subtype II marker), MSLN (subtype III marker), or SPP1 (subtype III marker) likely predicted decreased overall survival ( P = 0.008, P = 0.040, and P = 0.039, respectively; Fig. 3j, k). We further jointly used these markers to distinguish GBC subtypes: MUC2 high CTSD low MSLN low subtype_I, CTSD high MUC2 low MSLN low subtype_II, and MSLN high MUC2 low CTSD low subtype_III. Compared with subtype_I, both subtype_II and subtype_III GBCs had substantially decreased overall survival (Supplementary Fig. S6d). Taken together, inflammatory and mesenchymal signatures of mEPCs were more closely associated with GBC aggressiveness.

Wang E, Ben-Zvi I, Rao T, Dimitrov DA, Chang X, Wu Q, Xin T (2011) Secondary-electron emission from hydrogen-terminated diamond: Experiments and model. Physical Review Special Topics - Accelerators and Beams. doi: 10.1103/physrevstab.14.111301

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The probability distribution of the electrons in the band structure of the crystal. The solid parabola is the electron energy probability distribution in the valence band, while the dashed parabola curve is the electron energy probability distribution after being excited to the conduction band. σ is the width of the band below the maximum of the valence band. Reuse & Permissions Li H, Liu D, Dai Y, Luan T, Yu S (2018) Personalized search over encrypted data with efficient and secure updates in mobile clouds. IEEE Trans Emerg Top Comput 6(1):97–109 We unexpectedly identified a small fraction of mEPCs ( n = 12) with substantial CNV in a benign sample (CC1, the peritumoral tissue of GBC11). Despite some genomic nuances (e.g., fewer copy number gains involving chr8; fewer copy number losses involving chr19), this squad of mEPCs largely shared analogous CNV signatures with the main herd of malignant cells in the matched tumor sample (Fig. 2f). CC1-residing nEPCs showed top-ranking DEGs associated with metabolic process (e.g., DUOXA2), gallbladder homeostasis (e.g., TFF2), mucosal healing (e.g., SERPING1), and inflammatory response (e.g., PIGR) (Fig. 2g, h). In contrast, mEPCs from CC1 and GBC11 displayed upregulation of multiple tumor-specific genes (e.g., S100P, TSPAN1, CEACAM5). Putative mEPCs in CC1 and GBC11 shared vivid mRNA translation processes. Dissimilar to enriched pathways in CC1-derived mEPCs (e.g., tissue remodeling, neutrophil activation), mEPCs in GBC11 displayed ectopic expression of IGHA1 (Fig. 2g), presumably mediating aberrant tumor immunity and promoting tumor aggressiveness (Fig. 2h) 21. Putative mEPCs in CC1 strikingly showed the highest expression of PLA2G2A (log 2FC = 3.72, P = 7.5 × 10 −13) (Fig. 2g), a typical gastrointestinal mucosal marker 22. We next interrogated IHC data of our GBC cohort and transcriptomic data of external European Genome-Phenome Archive (EGA) GBC cohort 9, consistently revealing pronounced overexpression of PLA2G2A among early-stage GBCs. A trend was observed towards reduced PLA2G2A expression among advanced GBCs versus early cases, despite without statistical significance (Fig. 2i; Supplementary Fig. S4c). Moreover, PLA2G2A expression did not seem to correlate well with GBC etiology or overall survival (Supplementary Fig. S4a, b, d). We next established PLA2G2A-overexpressing GBC cell lines (NOZ and GBC-SD cells; Supplementary Fig. S4e). PLA2G2A overexpression potentiated proliferation, inhibited apoptosis, and significantly facilitated stemness of GBC cells, whereas unexpectedly retarding tumor migration and invasion (Supplementary Fig. S4f–j). Therefore, PLA2G2A likely served a stage-dependent role, more actively engaged in early carcinogenesis than in tumor progression. Identification of diverse subtypes of mEPCs associated with GBC prognosis

York, A. G. et al. Limiting cholesterol biosynthetic flux spontaneously engages type I IFN signaling. Cell 163, 1716–1729 (2015). Wang, K., Li, M. & Hakonarson, H. ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data. Nucleic Acids Res. 38, e164 (2010). Jahrsdorfer, B. et al. Granzyme B produced by human plasmacytoid dendritic cells suppresses T-cell expansion. Blood 115, 1156–1165 (2010).

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Sugihara R, Gupta RK (2011) Sensor localization with deterministic accuracy guarantee. In: INFOCOM, pp 1772–1780 Faget, D. V., Ren, Q. & Stewart, S. A. Unmasking senescence: context-dependent effects of SASP in cancer. Nat. Rev. Cancer 19, 439–453 (2019).Carpino, G. et al. Evidence for multipotent endodermal stem/progenitor cell populations in human gallbladder. J. Hepatol. 60, 1194–1202 (2014).

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Tian 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 Simulated spectral response of the bialkali photocathode at room temperature (297 K), 166 K, and liquid-nitrogen temperature (solid lines) and experimental data at room temperature (297 K) and 166 K (dots). Reuse & Permissions Fresh gallbladder tissues were obtained with informed consent from patients who underwent surgery at EHBH. Briefly, the tumor tissues were washed with PBS for 1–2 times, minced into 1 mm 3 with scissors, and incubated at 37 °C in digestion solution (Dulbecco’s Modified Eagle Medium (DMEM)) with 4 mg/mL collagenase D (Roche), 10 μM Y27632 (Sigma-Aldrich), and 1× Primocin (InvivoGen) on an orbital shaker for 1–2 h until no visible cell mass could be seen. Then, digestion was stopped by adding the cold termination medium (DMEM medium with 1% penicillin/streptomycin, 1× primocin, 10 μM Y27632, 10% FBS). The cell suspension was filtered through a 70 μm Nylon cell strainer and washed with cold Advanced DMEM/F12 twice before spinning at 300–400× g for 5 min. Re-suspension of the cells in cold human liver organoid medium mixed with Matrigel and was seeded into a 6/24-multiwell plate at 37 °C for 1 h. After polymerization of matrix, the human liver organoid medium was added to each well. The culture was generally changed every 3–4 days. After 1–2 weeks, the organoids were repeatedly blown with a gun tip to disperse the cells and then replanted into Matrigel at a ratio of 1: 2.Ge, Y. et al. Stem cell lineage infidelity drives wound repair and cancer. Cell 169, 636–650.e14 (2017).