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111.
Fanjie Meng Mathias M.J. Bellaiche Jae-Yeol Kim Gül H. Zerze Robert B. Best Hoi Sung Chung 《Biophysical journal》2018,114(4):870-884
Monomers of amyloid-β (Aβ) protein are known to be disordered, but there is considerable controversy over the existence of residual or transient conformations that can potentially promote oligomerization and fibril formation. We employed single-molecule Förster resonance energy transfer (FRET) spectroscopy with site-specific dye labeling using an unnatural amino acid and molecular dynamics simulations to investigate conformations and dynamics of Aβ isoforms with 40 (Aβ40) and 42 residues (Aβ42). The FRET efficiency distributions of both proteins measured in phosphate-buffered saline at room temperature show a single peak with very similar FRET efficiencies, indicating there is apparently only one state. 2D FRET efficiency-donor lifetime analysis reveals, however, that there is a broad distribution of rapidly interconverting conformations. Using nanosecond fluorescence correlation spectroscopy, we measured the timescale of the fluctuations between these conformations to be ~35 ns, similar to that of disordered proteins. These results suggest that both Aβ40 and Aβ42 populate an ensemble of rapidly reconfiguring unfolded states, with no long-lived conformational state distinguishable from that of the disordered ensemble. To gain molecular-level insights into these observations, we performed molecular dynamics simulations with a force field optimized to describe disordered proteins. We find, as in experiments, that both peptides populate configurations consistent with random polymer chains, with the vast majority of conformations lacking significant secondary structure, giving rise to very similar ensemble-averaged FRET efficiencies. 相似文献
112.
Invasive species increasingly threaten global biodiversity with faunal homogenization, and are of specific concern in the highly diverse aquatic systems of the Southeast United States. However, patterns of invasion and variables influencing invasion success remain poorly understood. This study followed the introduction, establishment, and invasion processes of nonindigenous Weed Shiner (Notropis texanus, Family: Cyprinidae), and examined environmental correlates of their persistence. Potential shifts in the native fish assemblage in Bear Creek, Alabama and Mississippi, USA, due to Weed Shiner presence were also investigated. Assemblage shifts were evaluated using Jaccard and Morisita similarity indices and nonmetric multidimensional scaling (NMDS) ordination. Weed Shiner exhibited an initial rapid expansion in range and abundance, followed by a range contraction in 2012, and range and abundance decline in 2013 and 2014. Weed Shiner persists at the most human-impacted, downstream sites in Bear Creek. Similarity indices and NMDS indicated that despite rapid initial proliferation of Weed Shiner, native fish assemblage did not significantly change. Rather, the native fish assemblage structure in Bear Creek is temporally variable and influenced by watershed area, land-use, high intensity development, mixed-hardwood forest and evergreen forest (pine monoculture). Limiting future Weed Shiner impacts in the system and successful conservation of the Bear Creek fish assemblage will rely on managing land use changes and mitigating development effects in the watershed. 相似文献
113.
Rebecca M. Broeckel Friederike Feldmann Kristin L. McNally Abhilash I. Chiramel Gail L. Sturdevant Jacqueline M. Leung Patrick W. Hanley Jamie Lovaglio Rebecca Rosenke Dana P. Scott Greg Saturday Fadila Bouamr Angela L. Rasmussen Shelly J. Robertson Sonja M. Best 《PLoS pathogens》2021,17(12)
Kyasanur Forest disease virus (KFDV) and the closely related Alkhurma hemorrhagic disease virus (AHFV) are emerging flaviviruses that cause severe viral hemorrhagic fevers in humans. Increasing geographical expansion and case numbers, particularly of KFDV in southwest India, class these viruses as a public health threat. Viral pathogenesis is not well understood and additional vaccines and antivirals are needed to effectively counter the impact of these viruses. However, current animal models of KFDV pathogenesis do not accurately reproduce viral tissue tropism or clinical outcomes observed in humans. Here, we show that pigtailed macaques (Macaca nemestrina) infected with KFDV or AHFV develop viremia that peaks 2 to 4 days following inoculation. Over the course of infection, animals developed lymphocytopenia, thrombocytopenia, and elevated liver enzymes. Infected animals exhibited hallmark signs of human disease characterized by a flushed appearance, piloerection, dehydration, loss of appetite, weakness, and hemorrhagic signs including epistaxis. Virus was commonly present in the gastrointestinal tract, consistent with human disease caused by KFDV and AHFV where gastrointestinal symptoms (hemorrhage, vomiting, diarrhea) are common. Importantly, RNAseq of whole blood revealed that KFDV downregulated gene expression of key clotting factors that was not observed during AHFV infection, consistent with increased severity of KFDV disease observed in this model. This work characterizes a nonhuman primate model for KFDV and AHFV that closely resembles human disease for further utilization in understanding host immunity and development of antiviral countermeasures. 相似文献
114.
Stoichiometric traits of stickleback: Effects of genetic background,rearing environment,and ontogeny
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Miguel Costa Leal Rebecca J. Best Dan Durston Rana W. El‐Sabaawi Blake Matthews 《Ecology and evolution》2017,7(8):2617-2625
Phenotypes can both evolve in response to, and affect, ecosystem change, but few examples of diverging ecosystem‐effect traits have been investigated. Bony armor traits of fish are good candidates for this because they evolve rapidly in some freshwater fish populations, and bone is phosphorus rich and likely to affect nutrient recycling in aquatic ecosystems. Here, we explore how ontogeny, rearing environment, and bone allocation among body parts affect the stoichiometric phenotype (i.e., stoichiometric composition of bodies and excretion) of threespine stickleback. We use two populations from distinct freshwater lineages with contrasting lateral plating phenotypes (full vs. low plating) and their hybrids, which are mostly fully plated. We found that ontogeny, rearing environment, and body condition were the most important predictors of organismal stoichiometry. Although elemental composition was similar between both populations and their hybrids, we found significant divergence in phosphorus allocation among body parts and in phosphorus excretion rates. Overall, body armor differences did not explain variation in whole body phosphorus, phosphorus allocation, or phosphorus excretion. Evolutionary divergence between these lineages in both allocation and excretion is likely to have important direct consequences for ecosystems, but may be mediated by evolution of multiple morphological or physiological traits beyond plating phenotype. 相似文献
115.
116.
Guofeng Wu Jan de Leeuw Andrew K. Skidmore Herbert H. T. Prins Elly P. H. Best Yaolin Liu 《Hydrobiologia》2009,623(1):213-222
Almost 95% of the entire population of the Siberian crane (Grus leucogeranus) winter in Poyang Lake, China, where they forage on the tubers of the submerged aquatic macrophyte Vallisneria spiralis. The Three Gorges Dam on the Yangtze River may possibly affect this food source of the Siberian crane by affecting the light
intensity reaching the top of the V. spiralis canopy. In this study, the photosynthetically active radiation at the top of the V. spiralis canopy (PARtc) in Lake Dahuchi was modeled from 1998 to 2006, and the potential impacts of changes in water level and turbidity on the
underwater light climate of V. spiralis were analyzed. PARtc was calculated from incident irradiance while the losses due to reflection at the water surface, absorption, and scattering
within the water column were taken into consideration. The results indicated significant differences in PARtc between years. Six years of water level and Secchi disk depth records revealed a seasonal switching of the lake from a turbid
state at low water levels in autumn, winter, and spring to a clear state at high water levels during the monsoon in summer.
The highest PARtc occurred at intermediate water levels, which were reached when the Yangtze River forces Lake Dahuchi out of its turbid state
in early summer and the water becomes clear. The intended operation of the Three Gorges Dam, which will increase water levels
in May and June, may advance the moment when Lake Dahuchi switches from turbid to clear. We suggest that this might increase
production of V. spiralis and possibly improve the food habitat conditions for wintering Siberian crane in Poyang Lake.
相似文献
Guofeng WuEmail: |
117.
Brian P. Delisle Heather A. S. Underkofler Brooke M. Moungey Jessica K. Slind Jennifer A. Kilby Jabe M. Best Jason D. Foell Ravi C. Balijepalli Timothy J. Kamp Craig T. January 《The Journal of biological chemistry》2009,284(5):2844-2853
The pro-arrhythmic Long QT syndrome (LQT) is linked to 10 different genes
(LQT1–10). Approximately 40% of genotype-positive LQT patients
have LQT2, which is characterized by mutations in the human ether-a-go-go
related gene (hERG). hERG encodes the voltage-gated
K+ channel α-subunits that form the pore of the rapidly
activating delayed rectifier K+ current in the heart. The purpose
of this study was to elucidate the mechanisms that regulate the intracellular
transport or trafficking of hERG, because trafficking is impaired for about
90% of LQT2 missense mutations. Protein trafficking is regulated by small
GTPases. To identify the small GTPases that are critical for hERG trafficking,
we coexpressed hERG and dominant negative (DN) GTPase mutations in HEK293
cells. The GTPases Sar1 and ARF1 regulate the endoplasmic reticulum (ER)
export of proteins in COPII and COPI vesicles, respectively. Expression of DN
Sar1 inhibited the Golgi processing of hERG, decreased hERG current
(IhERG) by 85% (n ≥ 8 cells per group, *, p
< 0.01), and reduced the plasmalemmal staining of hERG. The coexpression of
DN ARF1 had relatively small effects on hERG trafficking. Surprisingly, the
coexpression of DN Rab11B, which regulates the endosomal recycling, inhibited
the Golgi processing of hERG, decreased IhERG by 79% (n
≥ 8 cells per group; *, p < 0.01), and reduced the plasmalemmal
staining of hERG. These data suggest that hERG undergoes ER export in COPII
vesicles and endosomal recycling prior to being processed in the Golgi. We
conclude that hERG trafficking involves a pathway between the ER and endosomal
compartments that influences expression in the plasmalemma.The human KCNH2 or ether-a-go-go related gene
(hERG)3
encodes the voltage-gated K+ channel α-subunits that
oligomerize to form the pore of the rapidly activating delayed rectifier
K+ current (IKr) in cardiac myocytes
(1–3).
Hundreds of hERG mutations are linked to the congenital
pro-arrhythmic Type 2 Long QT syndrome (LQT2) and functional studies suggest
that these mutations result in a loss of normal hERG K+ channel
(hERG) function (4,
5). In LQT2, missense mutations
are the dominant abnormality and many LQT2 missense mutations reduce hERG
K+ current (IhERG) by decreasing the intracellular
transport or trafficking of hERG to the Golgi apparatus (Golgi) and the cell
surface membrane (plasmalemma)
(6). Therefore, disruption of
hERG K+ channel trafficking appears to be a principal mechanism for
disease.Movement of proteins between membrane-bound intracellular compartments is
mediated by small transport vesicles, which bud from a donor compartment to
fuse with an appropriate acceptor compartment. The trafficking of many
transmembrane and secretory proteins between the ER and Golgi compartments is
dependent on the small GTPases ADP-ribosylation factor 1 (ARF1) and Sar1,
which regulate the formation of coat-associated protein complex I (COPI) and
II (COPII) vesicles, respectively
(7–19).
These small GTPases facilitate the polymerization of transport vesicle protein
coats on the donor membrane. Vesicular cargo selection, docking, and fusion to
the target membrane are regulated by adaptor proteins, SNARE proteins, and Rab
GTPases. To rationally develop novel therapeutic targets that may increase the
expression of trafficking-deficient LQT2 mutant channels, the molecular
mechanisms that regulate the trafficking of hERG need to be explored. The
purpose of this study is to identify transport proteins that regulate the
trafficking of wild type (WT) hERG. We used a strategy of testing specific WT
GTPases or ones containing dominant negative (DN) mutations to interfere with
their function. 相似文献
118.
Dipankar Bhattacharya Mayuri S. M. Best R. Perera R. J. Kuhn Rob Striker 《Journal of virology》2009,83(18):9195-9205
Serine/threonine phosphorylation of the nonstructural protein 5 (NS5) is a conserved feature of flaviviruses, but the kinase(s) responsible and function(s) remain unknown. Mass spectrometry was used to compare the phosphorylation sites of the NS5 proteins of yellow fever virus (YFV) and dengue virus (DENV), two flaviviruses transmitted by mosquitoes. Seven DENV phosphopeptides were identified, but only one conserved phosphoacceptor site (threonine 449 in DENV) was identified in both viruses. This site is predicted to be a protein kinase G (PKG) recognition site and is a strictly conserved serine/threonine phosphoacceptor site in mosquito-borne flaviviruses. In contrast, in tick-borne flaviviruses, this residue is typically a histidine. A DENV replicon engineered to have the tick-specific histidine residue at this position is replication defective. We show that DENV NS5 purified from Escherichia coli is a substrate for PKG in vitro and facilitates the autophosphorylation of PKG as seen with cellular substrates. Phosphorylation in vitro by PKG also occurs at threonine 449. Activators and inhibitors of PKG modulate DENV replication in cell culture but not replication of the tick-borne langat virus. Collectively, these data argue that PKG mediates a conserved serine/threonine phosphorylation event specifically for flaviviruses spread by mosquitoes.The flavivirus genus contains many medically important species, including dengue virus (DENV), yellow fever virus (YFV), West Nile virus (WNV), and tick-borne encephalitis virus (TBEV). More than 2 billion people are at risk of infection by DENV alone, leading to an estimated 50 million cases annually, which may increase further as the range of the mosquito vector expands with urbanization (24). While disease from mosquito-borne flaviviruses is particularly common, there are other flaviviral human pathogens that exist with transmission cycles that do not involve mosquitoes. Tick-borne transmission is the other well-described route, but non-arthropod-borne routes also exist (for example, bats). It is likely that each transmission route has genetic adaptations that facilitate that route, but such changes are not yet understood (7).Serine/threonine phosphorylation is a conserved feature across all three genera of the family Flaviviridae, including the genus flavivirus (the others genera being pestivirus and hepacivirus). Among the features of Flaviviridae, the most-studied examples are the multiple phosphorylations of nonstructural protein 5A (NS5A) of hepatitis C virus, which exists in both basal (termed p56) and hyperphosphorylated (termed p58) states mediated by multiple kinases that both are necessary for and limit replication (14, 18, 23). Phosphorylation of NS5B, the RNA-dependent RNA polymerase (RdRP), has also been shown to affect replicon activity (10). In the genus flavivirus, several mosquito-borne viruses (DENV, WNV, and YFV) and at least one tick-borne encephalitis virus are known to have phosphorylated forms of nonstructural protein NS5 (2, 9, 11, 13, 19). In the genus flavivirus, NS5 is central to viral replication, as it possesses both RdRP and methyltransferase activities. DENV phosphorylation of NS5 correlates with the loss of NS5 interactions with the viral helicase NS3. A hyperphosphorylated form of NS5 was found to localize to the nucleus, away from the cytoplasmic sites of viral replication (6, 9). A nuclear localization sequence is present in DENV NS5 and is phosphorylated in vitro by host CKII, but the relationship between phosphorylation and nuclear localization has yet to be fully elucidated (17). Multiple different serine/threonine phosphorylation events likely occur in the flaviviral life cycle, potentially affecting various functions of NS5 (2), but the role of these events and identity of the kinase(s) responsible are largely unknown.In this report, we used mass spectrometry to identify serine/threonine phosphorylation sites in DENV. A single phosphoacceptor site, previously identified in YFV, is conserved specifically in the mosquito-borne flaviviruses but not the tick-borne flaviviruses. Furthermore, in vitro studies reveal that this site is phosphorylated by a cyclic-nucleotide-dependent kinase, protein kinase G (PKG), and a phosphoacceptor threonine/serine is required for replication. Taken together, these data implicate the PKG pathway in flaviviral replication for the first time and suggest a host cell pathway that could be targeted by antiviral therapy. 相似文献
119.
Fredrik I. Andersson Anders Tryggvesson Michal Sharon Alexander V. Diemand Mirjam Classen Christoph Best Ronny Schmidt Jenny Schelin Tara M. Stanne Bernd Bukau Carol V. Robinson Susanne Witt Axel Mogk Adrian K. Clarke 《The Journal of biological chemistry》2009,284(20):13519-13532
The Clp protease is conserved among eubacteria and most eukaryotes, and
uses ATP to drive protein substrate unfolding and translocation into a chamber
of sequestered proteolytic active sites. The main constitutive Clp protease in
photosynthetic organisms has evolved into a functionally essential and
structurally intricate enzyme. The model Clp protease from the cyanobacterium
Synechococcus consists of the HSP100 molecular chaperone ClpC and a
mixed proteolytic core comprised of two distinct subunits, ClpP3 and ClpR. We
have purified the ClpP3/R complex, the first for a Clp proteolytic core
comprised of heterologous subunits. The ClpP3/R complex has unique functional
and structural features, consisting of twin heptameric rings each with an
identical ClpP33ClpR4 configuration. As predicted by its
lack of an obvious catalytic triad, the ClpR subunit is shown to be
proteolytically inactive. Interestingly, extensive modification to ClpR to
restore proteolytic activity to this subunit showed that its presence in the
core complex is not rate-limiting for the overall proteolytic activity of the
ClpCP3/R protease. Altogether, the ClpP3/R complex shows remarkable
similarities to the 20 S core of the proteasome, revealing a far greater
degree of convergent evolution than previously thought between the development
of the Clp protease in photosynthetic organisms and that of the eukaryotic 26
S proteasome.Proteases perform numerous tasks vital for cellular homeostasis in all
organisms. Much of the selective proteolysis within living cells is performed
by multisubunit chaperone-protease complexes. These proteases all share a
common two-component architecture and mode of action, with one of the best
known examples being the proteasome in archaebacteria, certain eubacteria, and
eukaryotes (1).The 20 S proteasome is a highly conserved cylindrical structure composed of
two distinct types of subunits, α and β. These are organized in
four stacked heptameric rings, with two central β-rings sandwiched
between two outer α-rings. Although the α- and β-protein
sequences are similar, it is only the latter that is proteolytic active, with
a single Thr active site at the N terminus. The barrel-shaped complex is
traversed by a central channel that widens up into three cavities. The
catalytic sites are positioned in the central chamber formed by the
β-rings, adjacent to which are two antechambers conjointly built up by
β- and α-subunits. In general, substrate entry into the core
complex is essentially blocked by the α-rings, and thus relies on the
associating regulatory partner, PAN and 19 S complexes in archaea and
eukaryotes, respectively (1).
Typically, the archaeal core structure is assembled from only one type of
α- and β-subunit, so that the central proteolytic chamber contains
14 catalytic active sites (2).
In contrast, each ring of the eukaryotic 20 S complex has seven distinct
α- and β-subunits. Moreover, only three of the seven
β-subunits in each ring are proteolytically active
(3). Having a strictly
conserved architecture, the main difference between the 20 S proteasomes is
one of complexity. In mammalian cells, the three constitutive active subunits
can even be replaced with related subunits upon induction by
γ-interferon to generate antigenic peptides presented by the class 1
major histocompatibility complex
(4).Two chambered proteases architecturally similar to the proteasome also
exist in eubacteria, HslV and ClpP. HslV is commonly thought to be the
prokaryotic counterpart to the 20 S proteasome mainly because both are Thr
proteases. A single type of HslV protein, however, forms a proteolytic chamber
consisting of twin hexameric rather than heptameric rings
(5). Also displaying structural
similarities to the proteasome is the unrelated ClpP protease. The model Clp
protease from Escherichia coli consists of a proteolytic ClpP core
flanked on one or both sides by the ATP-dependent chaperones ClpA or ClpX
(6). The ClpP proteolytic
chamber is comprised of two opposing homo-heptameric rings with the catalytic
sites harbored within (7). ClpP
alone displays only limited peptidase activity toward short unstructured
peptides (8). Larger native
protein substrates need to be recognized by ClpA or ClpX and then translocated
in an unfolded state into the ClpP proteolytic chamber
(9,
10). Inside, the unfolded
substrate is bound in an extended manner to the catalytic triads (Ser-97,
His-122, and Asp-171) and degraded into small peptide fragments that can
readily diffuse out (11).
Several adaptor proteins broaden the array of substrates degraded by a Clp
protease by binding to the associated HSP100 partner and modifying its protein
substrate specificity (12,
13). One example is the
adaptor ClpS that interacts with ClpA (EcClpA) and targets N-end rule
substrates for degradation by the ClpAP protease
(14).Like the proteasome, the Clp protease is found in a wide variety of
organisms. Besides in all eubacteria, the Clp protease also exist in mammalian
and plant mitochondria, as well as in various plastids of algae and plants. It
also occurs in the unusual plastid in Apicomplexan protozoan
(15), a family of parasites
responsible for many important medical and veterinary diseases such as
malaria. Of all these organisms, photobionts have by far the most diverse
array of Clp proteins. This was first apparent in cyanobacteria, with the
model species Synechococcus elongatus having 10 distinct Clp
proteins, four HSP100 chaperones (ClpB1–2, ClpC, and ClpX), three ClpP
proteins (ClpP1–3), a ClpP-like protein termed ClpR, and two adaptor
proteins (ClpS1–2) (16).
Of particular interest is the ClpR variant, which has protein sequence
similarity to ClpP but appears to lack the catalytic triad of Ser-type
proteases (17). This diversity
of Clp proteins is even more extreme in photosynthetic eukaryotes, with at
least 23 different Clp proteins in the higher plant Arabidopsis
thaliana, most of which are plastid-localized
(18).We have recently shown that two distinct Clp proteases exist in
Synechococcus, both of which contain mixed proteolytic cores. The
first consists of ClpP1 and ClpP2 subunits, and associates with ClpX, whereas
the other has a proteolytic core consisting of ClpP3 and ClpR that binds to
ClpC, as do the two ClpS adaptors
(19). Of these proteases, it
is the more constitutively abundant ClpCP3/R that is essential for cell
viability and growth (20,
21). It is also the ClpP3/R
complex that is homologous to the single type in eukaryotic plastids, all of
which also have ClpC as the chaperone partner
(16). In algae and plants,
however, the complexity of the plastidic Clp proteolytic core has evolved
dramatically. In Arabidopsis, the core complex consists of five ClpP
and four ClpR paralogs, along with two unrelated Clp proteins unique to higher
plants (22). Like ClpP3/R, the
plastid Clp protease in Arabidopsis is essential for normal growth
and development, and appears to function primarily as a housekeeping protease
(23,
24).One of the most striking developments in the Clp protease in photosynthetic
organisms and Apicomplexan parasites is the inclusion of ClpR within the
central proteolytic core. Although this type of Clp protease has evolved into
a vital enzyme, little is known about its activity or the exact role of ClpR
within the core complex. To address these points we have purified the intact
Synechococcus ClpP3/R proteolytic core by co-expression in E.
coli. The recombinant ClpP3/R forms a double heptameric ring complex,
with each ring having a specific ClpP3/R stoichiometry and arrangement.
Together with ClpC, the ClpP3/R complex degrades several polypeptide
substrates, but at a rate considerably slower than that by the E.
coli ClpAP protease. Interestingly, although ClpR is shown to be
proteolytically inactive, its inclusion in the core complex is not
rate-limiting to the overall activity of the ClpCP3/R protease. In general,
the results reveal remarkable similarities between the evolutionary
development of the Clp protease in photosynthetic organisms and the eukaryotic
proteasome relative to their simpler prokaryotic counterparts. 相似文献
120.