全文获取类型
收费全文 | 2229篇 |
免费 | 27篇 |
国内免费 | 32篇 |
专业分类
2288篇 |
出版年
2023年 | 23篇 |
2022年 | 14篇 |
2021年 | 21篇 |
2020年 | 40篇 |
2019年 | 17篇 |
2018年 | 39篇 |
2017年 | 16篇 |
2016年 | 18篇 |
2015年 | 65篇 |
2014年 | 81篇 |
2013年 | 129篇 |
2012年 | 61篇 |
2011年 | 132篇 |
2010年 | 99篇 |
2009年 | 149篇 |
2008年 | 143篇 |
2007年 | 151篇 |
2006年 | 99篇 |
2005年 | 93篇 |
2004年 | 83篇 |
2003年 | 61篇 |
2002年 | 52篇 |
2001年 | 27篇 |
2000年 | 36篇 |
1999年 | 40篇 |
1998年 | 44篇 |
1997年 | 42篇 |
1996年 | 43篇 |
1995年 | 45篇 |
1994年 | 39篇 |
1993年 | 32篇 |
1992年 | 31篇 |
1991年 | 42篇 |
1990年 | 35篇 |
1989年 | 22篇 |
1988年 | 23篇 |
1987年 | 19篇 |
1986年 | 11篇 |
1985年 | 19篇 |
1984年 | 28篇 |
1983年 | 17篇 |
1982年 | 34篇 |
1981年 | 19篇 |
1980年 | 20篇 |
1979年 | 22篇 |
1978年 | 3篇 |
1977年 | 5篇 |
1976年 | 1篇 |
1974年 | 2篇 |
1971年 | 1篇 |
排序方式: 共有2288条查询结果,搜索用时 15 毫秒
111.
Abstract: The relationship between iron-dependent fetal mouse spinal cord neuron injury and the generation of endogenous lipid hydroperoxides (LOOHs) has been investigated. Cultured spinal cord neurons were incubated with ferrous iron (3–200 µM). Cell viability was measured in terms of the uptake of α-[methyl-3H]aminoisobutyric acid ([3H]AIB). Both endogenously and iron-generated LOOH, i.e., free fatty acid hydroperoxide (FFAOOH), phosphatidylethanolamine hydroperoxide (PEOOH), and phosphatidylcholine hydroperoxide (PCOOH), were measured directly by an HPLC-chemiluminescence (HPLC-CL) assay. The FFAOOH, PEOOH, and PCOOH levels in neurons incubated with 200 µM Fe2+ for 40 min were, respectively, 22-, 158-, and sevenfold higher than those in non-iron-exposed cultures, demonstrating that phosphatidylethanolamine (PE) was most sensitive to peroxidation. The dose-response and time course of Fe2+-induced generation of these LOOHs were also established. In both experiments, the LOOH levels were correlated directly with loss of neuronal viability, suggesting strongly a direct relationship between lipid peroxidation and cell injury. On examination of the time course of the LOOH generation, an immediate increase in PEOOH and PCOOH levels with only 30 s of Fe2+ incubation was observed. In contrast, a lag phase in the increase in FFAOOH level (2 min after Fe2+ addition) suggested a delay in the activation of phospholipase A2 (PLA2) required for the hydrolysis and generation of FFAOOH. This culture system provides an excellent model for screening antioxidant neuroprotective compounds with regard to their ability to protect against iron-dependent peroxidative injury and the relationship of the neuroprotection to inhibition of lipid peroxidation and/or PLA2. 相似文献
112.
An electron-rich iron(III) porphyrin complex (meso-tetramesitylporphinato)iron(III) chloride [Fe(TMP)Cl], was found to catalyze the epoxidation of olefins by aqueous 30% H2O2 when the reaction was carried out in the presence of 5-chloro-1-methylimidazole (5-Cl-1-MeIm) in aprotic solvent. Epoxides were the predominant products with trace amounts of allylic oxidation products, indicating that Fenton-type oxidation reactions were not involved in the olefin epoxidation reactions. cis-Stilbene was stereospecifically oxidized to cis-stilbene oxide without giving isomerized trans-stilbene oxide product, demonstrating that neither hydroperoxy radical (HOO·) nor oxoiron(IV) porphyrin [(TMP)FeIV=O] was responsible for the olefin epoxidations. We also found that the reactivities of other iron(III) porphyrin complexes such as (meso-tetrakis(2,6-dichlorophenyl)porphinato)iron(III) chloride [Fe(TDCPP)Cl], (meso-tetrakis(2,6-difluorophenyl)porphinato)iron(III) chloride [Fe(TDFPP)Cl], and (meso-tetrakis(pentafluorophenyl)porphinato)iron(III) chloride [Fe(TPFPP)Cl] were significantly affected by the presence of the imidazole in the epoxidation of olefins by H2O2. These iron porphyrin complexes did not yield cyclohexene oxide in the epoxidation of cyclohexene by H2O2 in the absence of 5-Cl-1-MeIm in aprotic solvent; however, addition of 5-Cl-1-MeIm to the reaction solutions gave high yields of cyclohexene oxide with the formation of trace amounts of allylic oxidation products. We proposed, on the basis of the results of mechanistic studies, that the role of the imidazole is to decelerate the O–O bond cleavage of an iron(III) hydroperoxide porphyrin (or H2O2–iron(III) porphyrin adduct) and that the intermediate transfers its oxygen to olefins prior to the O–O bond cleavage. 相似文献
113.
Johanna Marin‐Carbonne Vincent Busigny Jennyfer Miot Claire Rollion‐Bard Elodie Muller Nadja Drabon Damien Jacob Sylvain Pont Martin Robyr Tomaso R. R. Bontognali Camille Franois Stephanie Reynaud Mark Van Zuilen Pascal Philippot 《Geobiology》2020,18(3):306-325
On the basis of phylogenetic studies and laboratory cultures, it has been proposed that the ability of microbes to metabolize iron has emerged prior to the Archaea/Bacteria split. However, no unambiguous geochemical data supporting this claim have been put forward in rocks older than 2.7–2.5 giga years (Gyr). In the present work, we report in situ Fe and S isotope composition of pyrite from 3.28‐ to 3.26‐Gyr‐old cherts from the upper Mendon Formation, South Africa. We identified three populations of microscopic pyrites showing a wide range of Fe isotope compositions, which cluster around two δ56Fe values of ?1.8‰ and +1‰. These three pyrite groups can also be distinguished based on the pyrite crystallinity and the S isotope mass‐independent signatures. One pyrite group displays poorly crystallized pyrite minerals with positive Δ33S values > +3‰, while the other groups display more variable and closer to 0‰ Δ33S values with recrystallized pyrite rims. It is worth to note that all the pyrite groups display positive Δ33S values in the pyrite core and similar trace element compositions. We therefore suggest that two of the pyrite groups have experienced late fluid circulations that have led to partial recrystallization and dilution of S isotope mass‐independent signature but not modification of the Fe isotope record. Considering the mineralogy and geochemistry of the pyrites and associated organic material, we conclude that this iron isotope systematic derives from microbial respiration of iron oxides during early diagenesis. Our data extend the geological record of dissimilatory iron reduction (DIR) back more than 560 million years (Myr) and confirm that micro‐organisms closely related to the last common ancestor had the ability to reduce Fe(III). 相似文献
114.
Summary Concentration of N, P, K, Ca, Mg and S in summer groundnut crop was higher than in kharif while Zn, Fe, Mn and Cu contents were higher in summer crop. Kernel's N, P and Zn; Leaflet's Ca and Mn; Stem's K and Fe; Root's S and Cu and Petiole's Mg contents were highest. Shell's N, P, K, Mg, S, Zn and Cu; Kernel's Ca, Fe and Mn contents were the least. N, P, K, S, Zn and Cu concentrations decreased linearly as the crop grew. Ca, Mg, Fe and Mn concentrations did not display any distinct pattern. Ca concentration was positively correlated with pod yield in both the seasons. 相似文献
115.
116.
The oxidation of thiocyanate by iron(V) (Fe(V)) was studied as a function of pH in alkaline solutions by a premix pulse radiolysis technique. The rates decrease with an increase in pH. The rate law for the oxidation of SCN− by Fe(V) was obtained as −d[Fe(V)]/dt = k10{[H+]2/([H+]2 + K2[H+] + K2K3)}[Fe(V)][SCN−], where k10 = 5.72 ± 0.19 × 106 M−1 s−1, pK2 = 7.2, and pK3 = 10.1. The reaction precedes via a two-electron oxidation, which converts Fe(V) to Fe(III). Thiocyanate reacts approximately 103× faster with iron(V) than does with iron(VI). 相似文献
117.
Background
Plant and animal ferritins stem from a common ancestor, but plant ferritins exhibit various features that are different from those of animal ferritins. Phytoferritin is observed in plastids (e.g., chloroplasts in leaves, amyloplasts in tubers and seeds), whereas animal ferritin is largely found in the cytoplasm. The main difference in structure between plant and animal ferritins is the two specific domains (TP and EP) at the N-terminal sequence of phytoferritin, which endow phytoferritin with specific iron chemistry. As a member of the nonheme iron group of dietary iron sources, phytoferritin consists of 24 subunits that assemble into a spherical shell storing up to ∼ 2000 Fe3 + in the form of an iron oxyhydroxide-phosphate mineral. This feature is distinct from small molecule nonheme iron existing in cereals, which has poor bioavailability.Scope of review
This review focuses on the relationship between structure and function of phytoferritin and the recent progress in the use of phytoferritin as iron supplement.Major conclusions
Phytoferritin, especially from legume seeds, represents a novel alternative dietary iron source.General significance
An understanding of the chemistry and biology of phytoferritin, its interaction with iron, and its stability against gastric digestion is beneficial to design diets that will be used for treatment of global iron deficiency. 相似文献118.
119.
Pyridoxal isonicotinoyl hydrazone (PIH) and many of its analogs are effective iron chelators in vivo and in vitro, and are of interest for the treatment of secondary iron overload. Because previous work has implicated the Fe(3+)-chelator complexes as a determinant of toxicity, the role of iron-based oxidative stress in the toxicity of PIH analogs was assessed. The Fe(3+) complexes of PIH analogs were reduced by K562 cells and the physiological reductant, ascorbate. Depletion of the antioxidant, glutathione, sensitized Jurkat T lymphocytes to the toxicity of PIH analogs and their Fe(3+) complexes, and toxicity of the chelators increased with oxygen tension. Fe(3+) complexes of pyridoxal benzoyl hydrazone (PBH) and salicyloyl isonicotinoyl hydrazone (SIH) caused lipid peroxidation and toxicity in K562 cells loaded with eicosapentenoic acid (EPA), a readily oxidized fatty acid, whereas Fe(PIH)(2) did not. The lipophilic antioxidant, vitamin E, completely prevented both the toxicity and lipid peroxidation caused by Fe(PBH)(2) in EPA-loaded cells, indicating a causal relationship between oxidative stress and toxicity. PBH also caused concomitant lipid peroxidation and toxicity in EPA-loaded cells, both of which were reversed as its concentration increased. In contrast, PIH was inactive, while SIH was equally toxic toward control and EPA-loaded cells, without causing lipid peroxidation, indicating a much smaller contribution of oxidative stress to the mechanism of toxicity of these analogs. In summary, PIH analogs and their Fe(3+) complexes are redox active in the intracellular environment. The contribution of oxidative stress to the overall mechanism of toxicity varies across the series. 相似文献
120.
An oxalate-bridged binuclear iron(III) complex, [(acac)2Fe(μ-ox)Fe(acac)2], (acac−=acetylacetonate anion and ox2−=oxalate anion) was prepared. The complex crystallized as two types of crystals under different conditions: one had 1,2-dichloroethane as a solvent molecule of crystallization 2, the other did not 1. Both compounds have been characterized by X-ray crystallography, infrared spectroscopy, and thermogravimetric analysis. Compound 1 has also been characterized by UV-Vis and 1H NMR spectroscopies, mass spectrometry, and electrochemistry. In both crystals, each iron(III) is coordinated in an octahedral arrangement by the oxygen atoms of an oxalate-bridging ligand and four oxygen atoms belonging to peripheral acac ligands in an octahedral arrangement. The intermetallic distance of Fe?Fe is 5.4368(9) Å in 1 and 5.438(2) Å in 2. Two iron(III) ions in each crystal are bridged by the oxalate and both lie in the oxalate-plane. The results of thermal analyses imply that the thermal stability of 2 is lower than that of 1. Cyclic voltammograms of 1 in acetonitrile and dichloromethane at low temperature showed two consecutive, quasi-Nernstian, one-electron reduction steps corresponding to the reduction of FeIII-FeIII to FeIII-FeII followed by the reduction of FeIII-FeII to FeII-FeII. The electrochemical comproportionation constants (Kc) of the equilibrium (FeIII-FeIII) + (FeII-FeII) ? 2(FeIII-FeII) are 108.9 in acetonitrile medium and 108.5 in dichloromethane, respectively. The considerably large Kc values indicate that the main factor contributing to the stabilization of the FeIII-FeII mixed-valence state is electronic delocalization through the oxalate-bridge. 相似文献