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Pancreatic cancer is a highly lethal disease, for which mortality closely parallels incidence. Most patients with pancreatic cancer remain asymptomatic until the disease reaches an advanced stage. There is no standard programme for screening patients at high risk of pancreatic cancer (eg, those with a family history of pancreatic cancer and chronic pancreatitis). Most pancreatic cancers arise from microscopic non-invasive epithelial proliferations within the pancreatic ducts, referred to as pancreatic intraepithelial neoplasias. There are four major driver genes for pancreatic cancer: KRAS, CDKN2A, TP53, and SMAD4. KRAS mutation and alterations in CDKN2A are early events in pancreatic tumorigenesis. Endoscopic ultrasonography and endoscopic ultrasonography-guided fine-needle aspiration offer high diagnostic ability for pancreatic cancer. Surgical resection is regarded as the only potentially curative treatment, and adjuvant chemotherapy with gemcitabine or S-1, an oral fluoropyrimidine derivative, is given after surgery. FOLFIRINOX (fluorouracil, folinic acid [leucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nanoparticle albumin-bound paclitaxel (nab-paclitaxel) are the treatments of choice for patients who are not surgical candidates but have good performance status.

\"What started as an inquiry into how executives can adopt AI to harness the best of human and machine capabilities turned into a much more profound rumination on the future of humanity and enterprise. This is a wake up call for business leaders across all sectors of the economy. Not only should you implement AI regardless of your industry, but once you do, you should fight to stay true to your purpose, your ethical convictions, indeed your humanity, even as our organizations continue to evolve. While not holding any punches about the dangers posed by AI, this book uniquely surveys where technology is limited, and where the true opportunities lie amidst all the disruptive change currently underway. As such, it is distinctively more optimistic than many of the competing titles on Big Technology. This is a compelling book that weaves together philosophical, psychological, and legal insights; organizational governance, operations, and strategy; and technological breakthroughs and limitations. The authors set out to identify where humans and machines can best complement one another to create an enterprise greater than the sum total of its parts: the Humachine. Combining the business and predictive acumen of Professor Nada R. Sanders, PhD (Distinguished Professor at Northeastern University) with the legal and philosophical perspective of John D. Wood, Esq. (Attorney and Member of the New York State Bar) the authors combine their strengths as internationally recognized experts in forecasting and sustainable business to bring us this profound yet accessible book. This is a \"must read\" for everyone interested in the future of human enterprise\"-- Provided by publisher.

Due to its poor prognosis and the late stage at which it is typically diagnosed, early detection of pancreatic cancer is a pressing clinical problem. Advances in genomic analysis of human pancreatic tissue and other biospecimens such as pancreatic cyst fluid, pancreatic juice and blood have opened the possibility of DNA-based molecular approaches for early detection of pancreatic cancer. In this Review, we discuss and focus on the pathological and molecular features of precancerous lesions of the pancreas, including pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm and mucinous cystic neoplasm, which are target lesions of early detection approaches. We also discuss the most prevalent genetic alterations in these precancerous lesions, including somatic mutations in the oncogenes KRAS and GNAS as well as tumour suppressor genes CDKN2A , TP53 and SMAD4 . We highlight the latest discoveries related to genetic heterogeneity and multifocal neoplasia in precancerous lesions. In addition, we review specific approaches, challenges and clinically available assays for early detection of pancreatic cancer using DNA-based molecular techniques. Although detection and risk stratification of precancerous pancreatic neoplasms are difficult problems, progress in this field highlights the promise of molecular approaches for improving survival of patients with this disease. Pancreatic cancer is typically diagnosed at a late stage and early detection is a priority. This Review focuses on precancerous lesions of the pancreas, describing their pathological and molecular features and highlighting different DNA-based molecular approaches for early detection and their clinical utility. Key points The target lesions for pancreatic cancer screening are high-grade precancerous lesions and early-stage invasive cancers. Precancerous lesions can be microscopic (pancreatic intraepithelial neoplasia (PanIN)) or macroscopic (intraductal papillary mucinous neoplasm (IPMN) and mucinous cystic neoplasm (MCN)), and these lesions are classified as low-grade or high-grade based on the morphological grade of dysplasia of their lining epithelium; although low-grade lesions share early oncogene mutations such as KRAS , mutations in other genes ( CDKN2A , TP53 and SMAD4 ) are limited to more advanced lesions. Studies have highlighted genetic heterogeneity in precancerous lesions and multifocal neoplasia in the pancreas, which should be considered when designing early detection approaches. The evolving understanding of the genetics of precancerous lesions has led to the development of clinically available assays for pancreatic cyst classification and detection of high-grade dysplasia and early-stage pancreatic cancers. Mutations in KRAS and/or GNAS are highly specific for mucinous cysts, such as IPMNs, while alterations in CDKN2A , TP53 and/or SMAD4 are almost exclusively seen in the setting of advanced lesions. The assessment of genetic alterations using a non-invasive method, such as from a patient’s blood specimen, holds promise not only for early detection of pancreatic cancer but also for the identification of precancerous lesions.

يسلط هذا الكتاب الضوء على تلك السبل المتباينة التي بنى الاستعمار من خلالها ما نعتقد أننا نعرفه عن العالم، بل كيف نتعرف عليه، ويكشف الدور الذي لعبه الاستعمار الأوروبي في اكتساب وبناء طرق المعرفة المختلفة في الآونة الأخيرة، بدأ العديد من الباحثين والعلماء والناشطين يتساءلون : هل هناك من طرق يمكن من خلالها الخلاص من استعمار المعرفة أو نقضه؟ يفحص كتاب نقض الاستعمار المعرفي مجموعة متنوعة من هذه المشاريع من منظور نقدي وفلسفي، ويقدم للقارئ مجموعة واسعة من المقاربات النقدية والأمثلة لمعالجة الموضوع. يبحث الكتاب أيضا في الإسهام السياسي والعلمي لفرانز فانون وأميلكار كابرال، فضلا عن المعالجات البحثية المعاصرة، موضحا كيف يمكن لتلك المعالجات الفلسفية والنقدية أن تساعد في الخروج من الأزمة التي تمخضت عن القضايا العملية والنظرية الراهنة في موضوع الاستعمار المعرفي. يصف مؤلف الكتاب كيف تؤثر علاقات القوة القائمة في الأمة والطبقة والعرق، كما أنه يدعو إلى نظرية تحررية للمعرفة تعترف بإمكان تطبيق الأساليب العلمية لحل المشكلات الاجتماعية.

Quantifying gross primary production (GPP) remains a major challenge in global carbon cycle research. Spaceborne monitoring of solar-induced chlorophyll fluorescence (SIF), an integrative photosynthetic signal of molecular origin, can assist in terrestrial GPP monitoring. However, the extent to which SIF tracks spatiotemporal variations in GPP remains unresolved. Orbiting Carbon Observatory-2 (OCO-2)’s SIF data acquisition and fine spatial resolution permit direct validation against ground and airborne observations. Empirical orthogonal function analysis shows consistent spatiotemporal correspondence between OCO-2 SIF and GPP globally. A linear SIF-GPP relationship is also obtained at eddy-flux sites covering diverse biomes, setting the stage for future investigations of the robustness of such a relationship across more biomes. Our findings support the central importance of high-quality satellite SIF for studying terrestrial carbon cycle dynamics.

At the atomic-cluster scale, pure boron is markedly similar to carbon, forming simple planar molecules and cage-like fullerenes. Theoretical studies predict that two-dimensional (2D) boron sheets will adopt an atomic configuration similar to that of boron atomic clusters. We synthesized atomically thin, crystalline 2D boron sheets (i.e., borophene) on silver surfaces under ultrahigh-vacuum conditions. Atomic-scale characterization, supported by theoretical calculations, revealed structures reminiscent of fused boron clusters with multiple scales of anisotropic, out-of-plane buckling. Unlike bulk boron allotropes, borophene shows metallic characteristics that are consistent with predictions of a highly anisotropic, 2D metal.

Microorganisms employ quorum sensing (QS) mechanisms to communicate with each other within microbial ecosystems. Emerging evidence suggests that intraspecies and interspecies QS plays an important role in antimicrobial resistance in microbial communities. However, the relationship between interkingdom QS and antimicrobial resistance is largely unknown. Here, we demonstrate that interkingdom QS interactions between a bacterium, Pseudomonas aeruginosa and a yeast, Candida albicans , induce the resistance of the latter to a widely used antifungal fluconazole. Phenotypic, transcriptomic, and proteomic analyses reveal that P. aeruginosa’s main QS molecule, N-(3-Oxododecanoyl)-L-homoserine lactone, induces candidal resistance to fluconazole by reversing the antifungal’s effect on the ergosterol biosynthesis pathway. Accessory resistance mechanisms including upregulation of C. albicans drug-efflux, regulation of oxidative stress response, and maintenance of cell membrane integrity, further confirm this phenomenon. These findings demonstrate that P. aeruginosa QS molecules may confer protection to neighboring yeasts against azoles, in turn strengthening their co-existence in hostile polymicrobial infection sites.

Pancreatic ductal adenocarcinoma (PDAC) is known to progress from one of two main precursor lesions: pancreatic intraepithelial neoplasia (PanIN) or intraductal papillary mucinous neoplasm (IPMN). The poor survival rates for patients with PDAC, even those diagnosed with localized disease, highlight the need for pancreatic cancer interception at the precursor stage. Although their basic biological drivers are well characterized, practical strategies for PanIN and IPMN interception remain elusive due to difficulties with detection, risk stratification, and low-morbidity intervention. Recently, advances in liquid biopsy, spatial multiomics analysis, and machine learning technology have provided deeper understanding of the molecular landscapes underlying pancreatic precursor development and progression. In this Review, we outline the different histologic phenotypes, clinical characteristics, and neoplastic cell-intrinsic and -extrinsic drivers of PanINs and IPMNs, with particular focus on current and potential future opportunities for pancreatic precancer interception.