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Jun Lu

Bio: Jun Lu is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Medicine & Materials science. The author has an hindex of 135, co-authored 1526 publications receiving 99767 citations. Previous affiliations of Jun Lu include Drexel University & Argonne National Laboratory.


Papers
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Journal ArticleDOI
TL;DR: It is shown that expression signatures of as few as two miRNAs could accurately discriminate ALL from AML, and that epigenetic regulation might play an important role in the regulation of expression of miRNAAs in acute leukemias.
Abstract: Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, whereas acute myeloid leukemia (AML) is the most common acute leukemia in adults. In general, ALL has a better prognosis than AML. To understand the distinct mechanisms in leukemogenesis between ALL and AML and to identify markers for diagnosis and treatment, we performed a large-scale genome-wide microRNA (miRNA, miR) expression profiling assay and identified 27 miRNAs that are differentially expressed between ALL and AML. Among them, miR-128a and -128b are significantly overexpressed, whereas let-7b and miR-223 are significantly down-regulated in ALL compared with AML. They are the most discriminatory miRNAs between ALL and AML. Using the expression signatures of a minimum of two of these miRNAs resulted in an accuracy rate of >95% in the diagnosis of ALL and AML. The differential expression patterns of these four miRNAs were validated further through large-scale real-time PCR on 98 acute leukemia samples covering most of the common cytogenetic subtypes, along with 10 normal control samples. Furthermore, we found that overexpression of miR-128 in ALL was at least partly associated with promoter hypomethylation and not with an amplification of its genomic locus. Taken together, we showed that expression signatures of as few as two miRNAs could accurately discriminate ALL from AML, and that epigenetic regulation might play an important role in the regulation of expression of miRNAs in acute leukemias.

485 citations

Journal ArticleDOI
TL;DR: The established heterojunction between the interfaces of TiO2 nanoparticles and g-C3N4 nanosheets as well as introduced Ti(3+) led to the rapid electron transfer rate and improved photoinduced electron-hole pair's separation efficiency, resulting in the improved photocatalytic performance of the Ti( 3+) self-doped TiO 2/g-C 3N4 heterojunctions.
Abstract: A simple one-step calcination route was used to prepare Ti3+ self-doped TiO2/g-C3N4 heterojunctions by mixture of H2Ti3O7 and melamine. X-ray diffraction (XRD), transmission electron microscopy (TEM), high-resolution transmission electron microscopy (HRTEM), X-ray photoelectron spectroscopy (XPS), electron spin resonance (ESR) spectroscopy, and UV–Vis diffuse reflectance spectroscopy (UV–vis DRS) technologies were used to characterize the structure, crystallinity, morphology, and chemical state of the as-prepared samples. The absorption of the prepared Ti3+ self-doped TiO2/g-C3N4 heterojunctions shifted to a longer wavelength region in comparison with pristine TiO2 and g-C3N4. The photocatalytic activities of the heterojunctions were studied by degrading methylene blue under a 30 W visible-light-emitting diode irradiation source. The visible-light photocatalytic activities enhanced by the prepared Ti3+ self-doped TiO2/g-C3N4 heterojunctions were observed and proved to be better than that of pure TiO2 and ...

476 citations

Journal ArticleDOI
TL;DR: The results suggest that melanopsin expression defines a subset of RGCs that play a broad role in theregulation of nonvisual photoreception, providing collateralized projections that contribute to circadian entrainment, negative masking, the regulation of sleep-wake states, and the pupillary light reflex.
Abstract: The rod and cone photoreceptors that mediate visual phototransduction in mammals are not required for light-induced circadian entrainment, negative masking of locomotor activity, suppression of pineal melatonin, or the pupillary light reflex. The photopigment melanopsin has recently been identified in intrinsically photosensitive retinal ganglion cells (RGCs) that project to the suprachiasmatic nucleus (SCN), intergeniculate leaflet (IGL), and olivary pretectal nucleus, suggesting that melanopsin might influence a variety of irradiance-driven responses. We have found novel projections from RGCs that express melanopsin mRNA to the ventral subparaventricular zone (vSPZ), a region involved in circadian regulation and negative masking, and the sleep-active ventrolateral preoptic nucleus (VLPO) and determined the subsets of melanopsin-expressing RGCs that project to the SCN, the pretectal area (PTA), and the IGL division of the lateral geniculate nucleus (LGN). Melanopsin was expressed in the majority of RGCs that project to the SCN, vSPZ, and VLPO and in a subpopulation of RGCs that innervate the PTA and the IGL but not in RGCs projecting to the dorsal LGN or superior colliculus. Two-thirds of RGCs containing melanopsin transcript projected to each of the SCN and contralateral PTA, and one-fifth projected to the ipsilateral IGL. Double-retrograde tracing from the SCN and PTA demonstrated a subpopulation of RGCs projecting to both sites, most of which contained melanopsin mRNA. Our results suggest that melanopsin expression defines a subset of RGCs that play a broad role in the regulation of nonvisual photoreception, providing collateralized projections that contribute to circadian entrainment, negative masking, the regulation of sleep-wake states, and the pupillary light reflex.

461 citations

Journal ArticleDOI
TL;DR: This work designs a parent 3D atomic laminate, (Mo2/3Sc1/3)2AlC, with in-plane chemical ordering, and by selectively etching the Al and Sc atoms, shows evidence for 2D Mo1.33C sheets with ordered metal divacancies and high electrical conductivities.
Abstract: The exploration of two-dimensional solids is an active area of materials discovery. Research in this area has given us structures spanning graphene to dichalcogenides, and more recently 2D transition metal carbides (MXenes). One of the challenges now is to master ordering within the atomic sheets. Herein, we present a top-down, high-yield, facile route for the controlled introduction of ordered divacancies in MXenes. By designing a parent 3D atomic laminate, (Mo2/3Sc1/3)2AlC, with in-plane chemical ordering, and by selectively etching the Al and Sc atoms, we show evidence for 2D Mo1.33C sheets with ordered metal divacancies and high electrical conductivities. At ∼1,100 F cm−3, this 2D material exhibits a 65% higher volumetric capacitance than its counterpart, Mo2C, with no vacancies, and one of the highest volumetric capacitance values ever reported, to the best of our knowledge. This structural design on the atomic scale may alter and expand the concept of property-tailoring of 2D materials. Vacancies in 2D materials can influence their properties, however controlling their formation remains a challenge. Here the authors show that selective etching of a 3D laminate with in-plane chemical ordering results in formation of MXenes with ordered divacancies, as well as elevated conductance and supercapacitance.

461 citations

Journal ArticleDOI
TL;DR: Dicer1 may be an important haploinsufficient tumor suppressor gene and, furthermore, that other factors controlling miRNA biogenesis may also function in this manner.
Abstract: MicroRNAs (miRNAs) are short, noncoding RNAs that function to suppress post-transcriptionally the expression of target mRNAs, predominately via inhibition of translation. Such translational inhibition relies on imperfect base-pairing between the miRNA and the target transcript, with the interaction at nucleotides 2–8 (or the “seed” region) of the miRNA being required for translational repression. Computational prediction of miRNA targets based on seed regions and sequence conservation has revealed a widespread potential for miRNA-mediated transcript regulation, with hundreds of putative mRNA targets for an individual miRNA (Bartel 2004). In line with their broad-based effects, miRNAs have been proposed to function as oncogenes or tumor suppressor genes based on their inhibition of a variety of tumor-suppressive and oncogenic mRNAs, respectively (Plasterk 2006; Ventura and Jacks 2009). In particular, three distinct mechanisms have been posited. First, oncogenic miRNAs can undergo gain of function in tumors. This has been most clearly demonstrated for the miR-17∼92 cluster, whose amplification in B-cell lymphomas promotes their development, potentially through its control of B-cell differentiation (He et al. 2005; Koralov et al. 2008; Ventura et al. 2008). Furthermore, tumor-suppressive miRNAs could undergo loss of function in tumors. This has been shown for several miRNAs, including the let-7 family, whose expression can limit lung tumorigenesis through inhibition of oncogenes like the Ras family and HMGA2 (Esquela-Kerscher et al. 2008; Kumar et al. 2008). In particular, let-7 family members are in sites of frequent deletion in human tumors, and their processing is inhibited by the oncogenic Lin-28 proteins (Heo et al. 2008; Newman et al. 2008; Viswanathan et al. 2008; Chang et al. 2009). Finally, oncogenes can acquire mutations to remove miRNA-binding sites in tumors. This has been described for HMGA2, whose translocation promotes lipoma development by releasing the transcript from let-7-mediated tumor suppression (Mayr et al. 2007). We reported a global down-regulation of miRNAs in several types of human and murine cancer (Lu et al. 2005). From this initial study, it was unclear whether this widespread loss of miRNAs was merely a consequence of tumor development or was functionally related to the disease process. We demonstrated previously that this global loss of miRNAs was functionally relevant to oncogenesis, as impairment of miRNA maturation enhanced transformation in both cancer cells and a K-Ras-driven model of lung cancer (Kumar et al. 2007). While these studies provide a framework to explain inhibition of miRNA biogenesis in cancer, the genetic basis of impaired miRNA processing in human cancer has been largely undefined. For a subset of miRNAs, widespread silencing occurs at the transcriptional level via the c-Myc oncogene (Chang et al. 2008). However, it has also been shown that such broad reductions in miRNAs can occur post-transcriptionally, since changes in miRNA levels frequently occur without changes in the levels of the primary miRNA transcript (Thomson et al. 2006). Recently, it was shown that mutations in the miRNA processing component TARBP2 occur frequently in mismatch repair-deficient colon cancer, and that these mutations promote tumorigenesis by impaired processing of miRNAs (Melo et al. 2009). While interesting, these limited cases do not resolve the common global reduction of miRNAs in human cancers. Moreover, the precise genetics of such changes in tumors is poorly defined, especially as no components of the miRNA processing pathway have been reported to be completely deleted in human tumors. This is not surprising, since it has been shown that germline deletion of miRNA processing components Dicer1 and Dgcr8 in mice fails to produce viable progeny (Bernstein et al. 2003; Wang et al. 2007). Thus, conditional deletion of miRNA processing components provides a powerful means of examining the role of miRNAs in tumorigenesis.

455 citations


Cited by
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Journal ArticleDOI
04 Mar 2011-Cell
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.

51,099 citations

Journal ArticleDOI
TL;DR: The Gene Set Enrichment Analysis (GSEA) method as discussed by the authors focuses on gene sets, that is, groups of genes that share common biological function, chromosomal location, or regulation.
Abstract: Although genomewide RNA expression analysis has become a routine tool in biomedical research, extracting biological insight from such information remains a major challenge. Here, we describe a powerful analytical method called Gene Set Enrichment Analysis (GSEA) for interpreting gene expression data. The method derives its power by focusing on gene sets, that is, groups of genes that share common biological function, chromosomal location, or regulation. We demonstrate how GSEA yields insights into several cancer-related data sets, including leukemia and lung cancer. Notably, where single-gene analysis finds little similarity between two independent studies of patient survival in lung cancer, GSEA reveals many biological pathways in common. The GSEA method is embodied in a freely available software package, together with an initial database of 1,325 biologically defined gene sets.

34,830 citations

Journal ArticleDOI

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08 Dec 2001-BMJ
TL;DR: There is, I think, something ethereal about i —the square root of minus one, which seems an odd beast at that time—an intruder hovering on the edge of reality.
Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

33,785 citations

01 May 1993
TL;DR: Comparing the results to the fastest reported vectorized Cray Y-MP and C90 algorithm shows that the current generation of parallel machines is competitive with conventional vector supercomputers even for small problems.
Abstract: Three parallel algorithms for classical molecular dynamics are presented. The first assigns each processor a fixed subset of atoms; the second assigns each a fixed subset of inter-atomic forces to compute; the third assigns each a fixed spatial region. The algorithms are suitable for molecular dynamics models which can be difficult to parallelize efficiently—those with short-range forces where the neighbors of each atom change rapidly. They can be implemented on any distributed-memory parallel machine which allows for message-passing of data between independently executing processors. The algorithms are tested on a standard Lennard-Jones benchmark problem for system sizes ranging from 500 to 100,000,000 atoms on several parallel supercomputers--the nCUBE 2, Intel iPSC/860 and Paragon, and Cray T3D. Comparing the results to the fastest reported vectorized Cray Y-MP and C90 algorithm shows that the current generation of parallel machines is competitive with conventional vector supercomputers even for small problems. For large problems, the spatial algorithm achieves parallel efficiencies of 90% and a 1840-node Intel Paragon performs up to 165 faster than a single Cray C9O processor. Trade-offs between the three algorithms and guidelines for adapting them to more complex molecular dynamics simulations are also discussed.

29,323 citations