Advanced Photoshop Issue No. 119 [EXCLUSIVE]

I have the same issue with a 30 page document. I followed the instructions above-except there was not an option to save at the end. I have 30 individual pages saved : ( What did I do wrong and why did Adobe make this so hard!!!

I had this issue while trying to save some legal docs with lots of form fields. I tried a bunch of things and then got an error message that helped, so I did File -> Save a copy and that gave a warning but I was able to save what i needed which was a version of the form as submitted with form fields filled in.

In the only patient who did not respond, the FLT3-ITD+ clone was smallest in this cohort and only constituted a very minor fraction of the leukemia cells. This observation was consistent with the in vitro findings, which indicated that FLT3 inhibitors were less efficacious in leukemia cells with a low FLT3-ITD allele burden, compared with those obtained in advanced disease with high allele burden, which might be more dependent on FLT3 signaling.41

Previously, single-cell RNA sequencing (scRNA-seq) analyses of healthy individuals have revealed the tissue distribution of host receptors that are required for SARS-CoV-2 entry5,6,7, and examination of bronchoalveolar lavage fluid and blood from patients with COVID-19 of varying severity has identified the effects of SARS-CoV-2 infection on immune responses and cytokine dysregulation8,9,10,11,12. However, owing to the practical limitations of accessing patient tissues, the effects of SARS-CoV-2 at the level of the lung tissue remain unclear. A series of autopsy studies that examined formalin-fixed, paraffin-embedded (FFPE) tissue sections from individuals who died of COVID-19 extended our understanding of virus organotropism, but these studies were limited in their discovery potential by low-plex assays (for example, immunohistochemistry) and/or prolonged post-mortem intervals (PMIs), which adversely affect RNA quality13,14,15.

DATPs were more frequent in COVID-19 than control lungs (Fig. 3i). Immunofluorescence staining of corresponding tissues showed that the frequency of KRT8+ and CLDN4+ DATPs was higher in COVID-19 lungs (Fig. 3j, Extended Data Fig. 8r, s), and we observed progressive loss of AT1 cell abundance with increasing time from symptom onset to death (Extended Data Fig. 8t). Overall, these data suggest that, in addition to direct destruction of the alveolar epithelium by viral infection, lung-regenerative processes are impaired in individuals with COVID-19.

Although our study provides insight into host responses to lethal SARS-CoV-2 infection, it is limited by a small sample size. However, through coordinated efforts, our work will contribute to a collection of studies, including the companion paper by T. M. Delorey et al.32, with streamlined protocols and harmonized metadata to enable integration and combined analyses, and will help to account for important co-variables. Furthermore, because our analysis is focused on lung tissue from patients who died of COVID-19, we have examined only a subset of potential disease phenotypes. Nonetheless, several observations, such as the rapid development of pulmonary fibrosis (Supplementary Discussion), are likely to be relevant for patients who survive severe COVID-19, and may inform our understanding of the long-term complications seen in these individuals33.

In conclusion, we have generated a molecular single-cell lung atlas from short-PMI tissue specimens and identified pathological circuits of lethal COVID-19. This atlas establishes an important resource for investigating host responses to SARS-CoV-2 and understanding potential long-term pulmonary sequelae resulting from COVID-19, and provides a basis for therapeutic development for severe disease.

We are grateful to all donors and their families. This work is part of the Human Cell Atlas (www.humancellatlas.org/publications). We thank J. Bhattacharya, I. Tabas, A. Tall and S. Roth for discussions. B.I. is supported by National Institute of Health (NIH) National Cancer Institute (NCI) grants K08CA222663, R37CA258829 and U54CA225088, a FastGrant, the Burroughs Wellcome Fund Career Award for Medical Scientists and the Louis V. Gerstner, Jr. Scholars Program. J.Q. is supported by R01HL152293 and R01HL132996. H. Huang is supported by the Department of Defense (DoD) Discovery Award W81XWH-21-1-0196. A.R. is supported by an NCI T32CA203702 grant. O.E. is supported by Volastra, Janssen and Eli Lilly research grants, NIH grants UL1TR002384, R01CA194547, and Leukemia and Lymphoma Society SCOR 7012-16, SCOR 7021-20 and SCOR 180078-02 grants. R.E.S. is supported by NIH grants NCI R01CA234614, NIAID R01AI107301, NIDDK R01DK121072 and RO3DK117252, and is an Irma Hirschl Trust Research Award Scholar. D.S. is a Damon Runyon Fellow supported by the Damon Runyon Cancer Research Foundation (DRQ-03-20). This research was funded in part through the NIH Support Grant S10RR027050 for flow cytometry analysis and the NIH/NCI Cancer Center Support Grant P30CA013696 at Columbia University Genetically Modified Mouse Model Shared Resource, Molecular Pathology Shared Resource and its Tissue Bank.

B.I. provided overall supervision. J.C.M., H. Huang, J.Q. and B.I. conceived this project. J.C.M., H. Huang, A.D.A., A.F., Y.F., H.R., M.G.C., Y.B., X.V.G., M.R., S.W.C., P.H., A.E.K. and A.S.H performed experiments. J.C.M., J.B., H. Huang, Y.W., A.N., S.T., A.F.R., D.S., C.J.F., A.D.A., A.M.L. and G.A.A. performed analyses. I.K., A.B., J.H.L., C.M., S.M.L., A.D.P., E.Z., G.S.M., A.S. and H. Hibshoosh oversaw and performed tissue collection, and performed pathological review of tissues. E.J.T. facilitated rapid autopsy specimen collection. D.T.M., M.F.B., N.A., M.S.-F., S.F.B., R.E.S. and O.E. provided signatures, materials and data. R.F.S., R.E.S., O.E. and J.Q. performed coordination of specific analyses and experiments. R.F.S. oversaw fibroblast experiments and analyses. R.E.S. and O.E. oversaw tissue mass cytometry analysis. J.Q. oversaw in vivo studies. D.S., C.J.F. and A.M.L. contributed equally. J.C.M., H. Huang, A.D.A., J.Q. and B.I. wrote the manuscript. All authors reviewed and approved the final manuscript.

a, Heatmap of top differentially regulated genes (log-normalized and centred, see Methods) among indicated alveolar macrophages in COVID-19 and control samples. Top lane indicates cell type and group. Rows indicate expression of genes. b, Violin plot of AXL expression (log-normalized) in alveolar macrophages from controls and COVID-19 tissues. Wilcoxon rank-sum test with Bonferroni adjusted P value indicated on top. c, Expression of AXL (log-normalized) among major cell types. Expression of this gene was nearly exclusive to fibroblasts and myeloid and epithelial cells.

Restricted to Arts and Entertainment Technologies majors. An introduction to advanced visual coding for performance and production. Three lecture hours a week for one semester, with lab hours as required. Offered on the letter-grade basis only. Prerequisite: Arts and Entertainment Technologies 306.

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Restricted to Arts and Entertainment Technologies majors. Continued exploration of methods and procedures used in the professional production of 3-D modeling, animation, and visual effects, including advanced modeling techniques, advanced surfacing techniques, specularity, sequenced mapping, and 3-D digital printing. Three lecture hours a week for one semester, with studio hours as required. Prerequisite: Arts and Entertainment Technologies 326 or 326C.

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Restricted to Arts and Entertainment Technologies majors. In-depth investigation of live entertainment technology, including topics such as advanced media server programming, advanced lighting applications, and advanced 3D projection mapping. Six laboratory hours a week for one semester, with additional laboratory hours as required. May be repeated for credit when the topics vary. Offered on the letter-grade basis only. Prerequisite: Arts and Entertainment Technologies 316C.

Restricted to Arts and Entertainment Technologies majors. Introduction to historical approaches to video game design. Includes video game histories and archives, critical analysis of design, game development and contemporary social issues in gaming. Three lecture hours a week for one semester, with lab hours as required. Arts and Entertainment Technologies 333E and 339 (Topic: History of Game Design) may not both be counted. Offered on the letter-grade basis only. Prerequisite: Arts and Entertainment Technologies 310 and 318C.

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CSC 391 Advanced Topics in Computer ScienceA different topic is presented each semester. These topics include mobile programming, object-oriented methodologies, expert systems, artificial intelligence, advanced graphics concepts, database management, wireless research, algorithm analysis. It is designed to provide the serious student with a challenging course on a topic that might not usually be developed at the elementary or intermediate levels. The instructor provides a syllabus discussing the topics to be covered in the semester prior to the actual offering of the course. Prerequisite: Changes based on topic 2b1af7f3a8