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Metamaterial has been captivated a popular notion, offering photonic functionalities beyond the capabilities of natural materials. Its desirable functionality primarily relies on well-controlled conditions such as structural resonance, dispersion, geometry, filling fraction, external actuation, etc. However, its fundamental building blocks--meta-atoms--still rely on naturally occurring substances. Here, we propose and validate the concept of gradient and reversible atomic-engineered metamaterials (GRAM), which represents a platform for continuously tunable solid metaphotonics by atomic manipulation. GRAM consists of an atomic heterogenous interface of amorphous host and noble metals at the bottom, and the top interface was designed to facilitate the reversible movement of foreign atoms. Continuous and reversible changes in GRAM's refractive index and atomic structures are observed in the presence of a thermal field. We achieve multiple optical states of GRAM at varying temperature and time and demonstrate GRAM-based tunable nanophotonic devices in the visible spectrum. Further, high-efficiency and programmable laser raster-scanning patterns can be locally controlled by adjusting power and speed, without any mask-assisted or complex nanofabrication. Our approach casts a distinct, multilevel, and reversible postfabrication recipe to modify a solid material's properties at the atomic scale, opening avenues for optical materials engineering, information storage, display, and encryption, as well as advanced thermal optics and photonics. [ABSTRACT FROM AUTHOR]

The attainment of both high strength and toughness is the ultimate goal for most structural materials. Although ceramic material has been considered for use as a structural material due to its high strength and good chemical stability, it suffers from the limitation of low toughness. For instance, although Y2O3- stabilized tetragonal ZrO2 polycrystals (Y- TZPs) exhibit remarkable toughness among ceramics due to their phase transformation toughening mechanism, this toughness is still much weaker than that of metals. Here, we report Y- TZP- based ceramic materials with toughnesses exceeding 20 MPa m1/2, which is comparable to those of metals, while maintaining strengths over 1,200 MPa. The superior mechanical properties are realized by reducing the phase stability of tetragonal zirconia by tailoring the microstructure and chemistry of the Y- TZP. The proposed ceramic materials can further advance the design and application of ceramic- based structural materials. [ABSTRACT FROM AUTHOR]

Airborne bacteria are an influential component of the Earth’s microbiomes, but their community structure and biogeographic distribution patterns have yet to be understood. We analyzed the bacterial communities of 370 air particulate samples collected from 63 sites around the world and constructed an airborne bacterial reference catalog with more than 27 million nonredundant 16S ribosomal RNA (rRNA) gene sequences. We present their biogeographic pattern and decipher the interlacing of the microbiome co-occurrence network with surface environments of the Earth. While the total abundance of global airborne bacteria in the troposphere (1.72 × 1024 cells) is 1 to 3 orders of magnitude lower than that of other habitats, the number of bacterial taxa (i.e., richness) in the atmosphere (4.71 × 108 to 3.08 × 109) is comparable to that in the hydrosphere, and its maximum occurs in midlatitude regions, as is also observed in other ecosystems. The airborne bacterial community harbors a unique set of dominant taxa (24 species); however, its structure appears to be more easily perturbed, due to the more prominent role of stochastic processes in shaping community assembly. This is corroborated by the major contribution of surface microbiomes to airborne bacteria (averaging 46.3%), while atmospheric conditions such as meteorological factors and air quality also play a role. Particularly in urban areas, human impacts weaken the relative importance of plant sources of airborne bacteria and elevate the occurrence of potential pathogens from anthropogenic sources. These findings serve as a key reference for predicting planetary microbiome responses and the health impacts of inhalable microbiomes with future changes in the environment. [ABSTRACT FROM AUTHOR]

Pancreas ductal adenocarcinoma (PDAC) is a highly lethal cancer that typically presents as advanced. unresectable disease. This invasive tendency, coupled with intrinsic resistance to standard therapies and genome instability, are major contributors to poor long-term survival. The genetic elements governing the invasive propensity of PDAC have not been well elucidated. Here, in the course of validating resident genes in highly recurrent and focal amplifications in PDAC, we have identified Rio Kinase 3 (RIOK3) as an amplified gene that alters cytoskeletal architecture as well as promotes pancreatic ductal cell migration and invasion. We determined that RIOK3 promotes its invasive activities through activation of the small G protein, Rac. This genomic and functional link to Rac signaling prompted a genome wide survey of other components of the Rho family network, revealing p21 Activated Kinase 4 (PAK4) as another amplified gene in PDAC tumors and cell lines. Like RIOK3, PAK4 promotes pancreas ductal cell motility and invasion. Together, the genomic and functional profiles establish the Rho family GTP-binding proteins as integral to the hallmark invasive nature of this lethal disease. [ABSTRACT FROM AUTHOR]

Activating KRAS mutations and p16Ink4a inactivation are near universal events in human pancreatic ductal adenocarcinoma (PDAC). In mouse models, KrasG12D initiates formation of premalignant pancreatic ductal lesions, and loss of either Ink4a/Arf (p16Ink4a/p19Arf) or p53 enables their malignant progression. As recent mouse modeling studies have suggested a less prominent role for p16Ink4a in constraining malignant progression, we sought to assess the pathological and genomic impact of inactivation of p16Ink4a, p9Arf, and/or p53 in the KrasG12D model. Rapidly progressive PDAC was observed in the setting of homozygous deletion of either p53 or p16Ink4a, the latter with intact germ-line p53 and p19Arf sequences. Additionally, KrasG12D in the context of heterozygosity either for p53 plus p16Ink4a or for p16Ink4a/p19Arf produced PDAC with longer latency and greater propensity for distant metastases relative to mice with homozygous deletion of p53 or p16Ink4a/p19Arf. Tumors from the double-heterozygous cohorts showed frequent p16Ink4a inactivation and loss of either p53 or p19Arf. Different genotypes were associated with specific histopathologic characteristics, most notably a trend toward less differentiated features in the homozygous p16Ink4a/p19Arf mutant model. High-resolution genomic analysis revealed that the tumor suppressor genotype influenced the specific genomic patterns of these tumors and showed overlap in regional chromosomal alterations between murine and human PDAC. Collectively, our results establish that disruptions of p16Ink4a and the p19Arf-p53 circuit play critical and cooperative roles in PDAC progression, with specific tumor suppressor genotypes provocatively influencing the tumor biological phenotypes and genomic profiles of the resultant tumors. [ABSTRACT FROM AUTHOR]

Lung cancer is the leading cause of cancer mortality worldwide, yet there exists a limited view of the genetic lesions driving this disease. In this study, an integrated high-resolution survey of regional amplifications and deletions, coupled with gene-expression profiling of non-small-cell lung cancer subtypes, adenocarcinoma and squamous-cell carcinoma (SCC), identified 93 focal copy- number alterations, of which 21 span <0.5 megabases and contain a median of five genes. Whereas all known lung cancer genes/loci are contained in the dataset, most of these recurrent copy-number alterations are previously uncharacterized and include high-amplitude amplifications and homozygous deletions. Notably, despite their distinct histopathological phenotypes, adenocarcinoma and SCC genomic profiles showed a nearly complete overlap, with only one clear SCC-specific amplicon. Among the few genes residing within this amplicon and showing consistent overexpression in SCC is p63, a known regulator of squamous-cell differentiation. Furthermore, intersection with the published pancreatic cancer comparative genomic hybridization dataset yielded, among others, two focal amplicons on 8p12 and 20q11 common to both cancer types. Integrated DNA-RNA analyses identified WHSC1LI and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer. [ABSTRACT FROM AUTHOR]