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OBJECTIVE: The aim of this study was to characterize the clinical and morphologic features of neuronal ceroid lipofuscinosis (NCL) in the Polish Owczarek Nizinny (PON) breed of dog. ANIMALS: Nine Swedish PON dogs of both sexes were included in the study. PROCEDURE: All dogs underwent a detailed clinical evaluation, with emphasis on ophthalmic exams. Histopathology and electron microscopy were performed on the eyes, brain and various internal organs. Immunohistochemical staining for detection of sphingolipid activator proteins (SAPs) and mitochondrial ATP synthase (SCMAS) was performed on the eyes and brain. RESULTS: The dogs showed behavioral abnormalities, motor disturbances and visual impairment or blindness. Pupillary responses were abnormal while fundus changes varied from normal to severe retinal atrophy. Electroretinography (ERG) showed variable changes, from slight alterations in the process of dark adaptation to severely reduced or nonrecordable ERG a- and b-wave amplitudes. Histopathology revealed intracytoplasmic storage bodies within neurons of the brain and in retinal cells, especially the retinal pigment epithelium (RPE). Round to oval granular type of inclusion bodies, known as granular osmiophilic dense deposits (GRODS), were found in neuronal cells in the brain and in the retina. Immunohistochemistry identified the storage material in the brain and retina as consisting of SAPs. CONCLUSION: The presently described NCL disease in PON dogs shows similarities to previously recorded cases in the Miniature Schnauzer. The closest human equivalent to this disease is infantile NCL (CLN1), in which the major stored proteins are SAPs and the ultrastructure of the inclusion bodies of neuronal cells is granular. 相似文献
84.
甘肃省“121”雨水集流工程经济 总被引:1,自引:0,他引:1
李莉 《中国农村水利水电》2007,(9):50-52
甘肃中东部地区地处黄土高原,气候干旱,水资源缺乏,农村人畜饮水困难。“121”雨水集流工程的实施,有效地解决了这些地区的人畜饮水困难。为了客观评价“121”雨水集流工程的经济效益和作用,利用建设项目后评价理论与方法,对工程的经济效益进行了科学评价,国民经济评价结果可行,其结果可用于指导全省雨水利用工程的规划、设计,加强雨水利用工作的决策、管理。 相似文献
85.
通过对蒙古沙棘亚种优良品种与中国沙棘亚种优良类型F1代雄株的变异特性分析,建立了选择优 良单株的标准,为叶用型沙棘选择育种提供了科学依据。 相似文献
86.
AIM To analyze the regulatory effect of quercetin (QUE) on PTEN-induced putative kinase 1 (PINK1)/parkin mitochondrial autophagy pathway, and to explore the mechanism of quercetin in relieving cerebral ischemia/reperfusion (I/R) injury. METHODS Sixty SD male rats were randomly divided into sham operation group, model group (I/R group), QUE group,3-methyladenine (3-MA) group and QUE+3-MA group. Administration started in each group 3 days before modeling, once a day, at 30 min after the last administration,except sham group, the other groups used 4-vessel blockage method to establish the whole brain I/R model. On the day after modeling, the neural function was evaluated by neuropathy disability score (NDS). The volume of cerebral infarction was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The morphological changes of mitochondria in hippocampus were observed by transmission electron microscopy. The contents of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in hippocampus were measured by ELISA. The activity of superoxide dismutase (SOD) and contents of malondialdehyde (MDA) in hippocampus were detected by xanthine oxidase method, thiobarbituric acid condensation method. Western blot was used to detect the proteinex pression of PINK1, parkin and LC3-II in brain tissue. RESULTS Compared with sham group, the hippocampus of the rats in I/R group and QUE+3-MA group showed swelling of mitochondria, destruction or disappearance of internal crista and other pathological damage,also the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA, the protein expression levels of PINK1, parkin and LC3-II were increased (P <0.05), while NDS score and activity of SOD were decreased (P <0.05). Compared with I/R group and QUE+3-MA group, the pathological damage degree of hippocampus in QUE group was reduced, the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA were decreased (P <0.05), the proteinexpression levels of PINK1, parkin and LC3-II, and NDS score and activity of SOD were increased (P <0.05).The above indexes in 3-MA group were opposite to QUE group. No significant difference in the above indexes between I/R group and QUE+3-MA group was observed (P >0.05). CONCLUSION Quercetin activates mitochondrial autophagy and reduces cerebral I/R by regulating the expression of PINK1/parkin pathway proteins. 相似文献
87.
88.
HUANG Zeng-yan HUANG Man-ping PENG Chun-li LIU Yong-yuan LI Chun-yan LIANG Dong-hui 《园艺学报》2021,37(1):34-40
AIM To observe effects of emotional stimulation on expression of stromal cell-derived factor-1(SDF-1) and CXC chemokine receptor 4 (CXCR4) in plasma, platelets, aortas, hippocampus and bone marrow of apolipoprotein E gene knockout (ApoE -/-) mice, and to reveal the possible mechanism of the aggravated atherosclerotic plaque vulnerability by emotional stimulation. METHODS Thirty 8-week-old male ApoE -/- mice were randomly divided into normal control group, high fat group, and emotional stimulation group. Ten 8-week-old inbred C57BL/6J mice served as blank control group. After 12 weeks of intervention, the serum levels of SDF-1 and CXCR4 were investigated by ELISA. The protein levels of SDF-1 and CXCR4 in platelets, aortas, hippocampus and bone marrow were determined by Western blot. The pathological damage of aortas was observed by oil red O staining. RESULTS Compared with blank control group, normal control group and high fat group, the mice subjected to emotional stimulation showed more serious atherosclerosis in aortas detected by oil red O staining, and increased levels of SDF-1 and CXCR4 in the plasma and aortas were also observed (P <0.05). The results of Western blot showed that the protein levels of SDF-1 and CXCR4 in platelets, aortas and hippocampus were increased in the mice subjected emotional stimulation, but the expression of SDF-1 and CXCR4 in the bone marrow was decreased (P <0.05). CONCLUSION Imbalance of SDF-1/CXCR4 may be the key target by which emotional stimulation accelerates the progression of atherosclerosis. 相似文献
89.
ZHANG Qiong WAN Chang-wu YU Yan-ni XIA-Bing LIU Jiang-jin ZHANG Qiao-jun LI Zhu WANG Cheng-fei DAI Jia-lin WANG Jie 《园艺学报》2021,36(12):2133-2138
AIM To explore the possible mechanism of cathepsin C (CTSC) and tumor necrosis factor-α (TNF-α) in coronary heart disease (CHD) by detecting the protein expression of CTSC and TNF-α in human coronary artery tissue. METHODS The coronary artery tissues from 52 cases of CHD and 25 cases of accidental death without any heart disease in the Forensic Judicial Expertise Center of Guizhou Medical University from October 2018 to December 2019 were collected as CHD group and control group, respectively. The coronary artery stenosis and intimal plaque formation were examined by histopathology, the protein expression of CTSC and TNF-α was determined by Western blot, and the intracellular expression of CTSC and TNF-α was analyzed by immunohistochemical staining. RESULTS The results of HE staining showed that the intima of coronary artery in control group was smooth, and no thickening or stenosis was observed. In CHD group, the intima thickened irregularly, atherosclerotic plaques formed, the intima became thinner and the lumen showed eccentric stenosis in varying degrees (P <0.05). The results of Western blot showed that the expression of CTSC and TNF-α in CHD group was significantly higher than that in control group (P <0.05). Immunohistochemical staining showed that both CTSC and TNF-α were expressed in the cytoplasm of foam cells, and their positive expression was significantly higher than that in control group (P <0.05). The results of Pearson moment correlation analysis showed that there was positive correlation between the expression of CTSC and TNF-α in CHD (r2 =0.743, P <0.05). CONCLUSION The up-regulated expression of CTSC in coronary artery tissue may promote the expression of TNF-α and affect the occurrence and development of CHD. 相似文献
90.
Hiroshi UENO Osamu YAMATO Takeshi SUGIURA Moeko KOHYAMA Akira YABUKI Kenjiro MIYOSHI Kazuya MATSUDA Tsuyoshi UCHIDE 《The Journal of veterinary medical science / the Japanese Society of Veterinary Science》2016,78(1):91-95
A male Japanese domestic cat with retarded growth in Hokkaido, Japan, showed
progressive motor dysfunction, such as ataxia starting at 3 months of age and tremors,
visual disorder and seizure after 4 months of age. Finally, the cat died of neurological
deterioration at 9 months of age. Approximately half of the peripheral blood lymphocytes
had multiple abnormal vacuoles. Magnetic resonance imaging showed bisymmetrical
hyperintensity in the white matter of the parietal and occipital lobes in the forebrain on
T2-weighted and fluid-attenuated inversion recovery images, and mild encephalatrophy of
the olfactory bulbs and temporal lobes. The activity of lysosomal acid β-galactosidase in
leukocytes was negligible, resulting in the biochemical diagnosis of GM1 gangliosidosis.
Histologically, swollen neurons characterized by accumulation of pale, slightly granular
cytoplasmic materials were observed throughout the central nervous system. Dysmyelination
or demyelination and gemistocytic astrocytosis were observed in the white matter.
Ultrastructually, membranous cytoplasmic bodies were detected in the lysosomes of neurons.
However, genetic analysis did not identify the c.1448G>C mutation, which is the single
known mutation of feline GM1 gangliosidosis, suggesting that the cat was affected with a
new variant of the feline disease. 相似文献