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排序方式: 共有1322条查询结果,搜索用时 810 毫秒
1.
旨在探究宿主蛋白程序性细胞死亡因子10(programmed cell death factor 10,PDCD10)通过抑制Ⅰ型干扰素表达进而促进口蹄疫病毒(foot-and-mouth disease virus,FMDV)的复制。首先,本研究验证了过表达和沉默PDCD10对FMDV复制的影响,接着利用双荧光素酶报告系统探究PDCD10对Ⅰ型干扰素信号通路活化的影响,最后,利用实时荧光定量PCR探究PDCD10对Ⅰ型干扰素通路下游刺激基因(IFN-stimulated genes,ISGs)转录的影响。结果表明,过表达PDCD10显著促进FMDV的复制,沉默PDCD10显著抑制FMDV的复制。与对照相比,过表达PDCD10后感染仙台病毒(Sendai virus,SeV)的细胞培养液上清液显著促进FMDV复制,进一步,PDCD10显著抑制SeV诱导的IFN-β启动子以及NF-κB的激活且呈剂量依赖性,并且PDCD10负调控Ⅰ型干扰素通路信号分子转录,最后还发现PDCD10负调控Ⅰ型干扰素下游ISGs转录。本研究结果为深入探究PDCD10在抗病毒天然免疫中的作用积累了资料。  相似文献   
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AIM: To observe the changes of Notch1 expression and autophagy in the renal tissues of diabetic mice, and to explore the regulatory effect of Notch1 on tubulointerstitial fibrosis by inhibiting autophagy in diabetic nephro-pathy. METHODS: The mice were randomly divided into normal control group (db/m mice) and diabetes group (db/db mice), with 8 rats in each group. After 12 weeks of feeding, the mice were sacrificed and the corresponding biochemical indexes were measured. The protein expression of Notch1 in the renal tubular epithelial cells was observed by immunohistochemical staining. The protein levels of Notch1, PTEN, p-Akt (Thr308), Akt, p-mTOR (Ser2448), mTOR, LC3, P62, collagen type Ⅰ (Col-Ⅰ) and collagen type Ⅲ (Col-Ⅲ) were determined by Western blot. RESULTS: Compared with the db/m mice, the blood glucose, glycosylated hemoglobin, serum creatinine, triglyceride and total cholesterol were increased in the db/db mice (P<0.01). Renal tubular epithelial cell vacuolar degeneration, renal tubular expansion and interstitial inflammatory cell infiltration in db/db mouse renal tissues with HE staining were observed. The images of Masson staining showed collagenous fiber-like substance deposition in the glomerular capillaries and renal interstitium, and disarrangement of tubular structure in the renal tissues of db/db mice. The protein expression levels of PTEN and LC3-Ⅱ were decreased (P<0.01 or P<0.05), while the protein levels of Notch1, P62, p-mTOR (Ser2448), p-Akt (Thr308), Col-I and Col-III were increased in the db/db mice as compared with the db/m mice (P<0.01). However, no significant change of total mTOR and Akt proteins between the 2 groups was found. CONCLUSION: Notch1 protein expression was increased, PTEN expression was significantly reduced, Akt/mTOR pathway was activated, autophagy was inhibited, and fibrosis was aggravated in the renal tissues of the diabetic mice.  相似文献   
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CAO Rui-ping  WANG Jiao  WANG Ce 《园艺学报》2018,34(6):1061-1066
AIM: To investigate the role of zerumbone (ZER) in 1-methyl-4-phenylpyridinium (MPP+)-induced cytotoxicity of human neuroblastoma SH-SY5Y cells. METHODS: Human neuroblastoma SH-SY5Y cells were cultured in vitro and the protective effect of ZER against MPP+-induced cytotoxicity was measured by CCK-8 assay. Flow cytometry was used to determine the apoptosis and reactive oxygen species (ROS). The expression of Parkinson disease protein 7 (PARK7) was knocked-down by using PARK7-specific short hairpin RNA (shRNA). The protein levels of PARK7, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were determined by Western blot. RESULTS: MMP+ remarkably reduced the cell viability in a dose-dependent and time-dependent manner. The SH-SY5Y cell injury model was established by treatment with MPP+ at 600 μmol/L for 24 h. ZER up-regulated the protein levels of PARK7 and Nrf2 (P<0.05), alleviated apoptosis (P<0.05), and reduced ROS production (P<0.05) in the SH-SY5Y cell injury model. Meanwhile, N-acetyl-L-cysteine (NAC) had the similar functions. Moreover, significant reductions in the protein levels of Nrf2 and HO-1 (P<0.05), and obvious increases in apoptosis (P<0.05) and ROS level (P<0.05) were demonstrated in PARK7-knockdown cells. CONCLUSION: ZER protects SH-SY5Y cells against MPP+-induced cytotoxi-city, which may be related to activation of PARK7/Nrf2/HO-1 pathway, and subsequent attenuation of oxidative stress and apoptosis.  相似文献   
5.
AIM: To explore the effect of tanshinone ⅡA on human osteosarcoma HOS cells and the underlying mechanism.METHODS: The cell viability and the appropriate dose of tanshinone ⅡA were determined by CCK-8 assay. Colony formation assay and Transwell assay were used to investigate the proliferation and migration abilities of the HOS cells treated with tanshinone ⅡA. The apoptosis of the HOS cells was monitored by Hoechst 33258 staining, transmission electron microscopy and flow cytometry. The protein levels of apoptosis-related molecules and JNK signaling-associated proteins were determined by Western blot. Meanwhile, a JNK inhibitor was added for confirming the relationship between the pathway and apoptosis mentioned above.RESULTS: Tanshinone ⅡA inhibited both HOS cell proliferation and migration in a dose-and time-dependent manner. Exposure of the HOS cells to tanshinone ⅡA resulted in the activation of apoptosis. Tanshinone ⅡA treatment increased the protein levels of cleaved caspase-3, Bax and JNK signaling-associated proteins, and decreased the protein level of Bcl-2, which were reversed by JNK inhibitor SP600125. Moreover, the result of CCK-8 assay revealed that tanshinone ⅡA-induced cell death was alleviated by JNK inhibitor.CONCLUSION: Tanshinone ⅡA induces cell growth inhibition and the activation of apoptosis via JNK signaling pathway in human osteosarcoma HOS cells.  相似文献   
6.
The prognosis of liver cancer was inferior among tumors. New medicine treatments are urgently needed. In this study, a novel exopolysaccharide EPS364 was purified from Vibrio alginolyticus 364, which was isolated from a deep-sea cold seep of the South China Sea. Further research showed that EPS364 consisted of mannose, glucosamine, gluconic acid, galactosamine and arabinose with a molar ratio of 5:9:3.4:0.5:0.8. The relative molecular weight of EPS364 was 14.8 kDa. Our results further revealed that EPS364 was a β-linked and phosphorylated polysaccharide. Notably, EPS364 exhibited a significant antitumor activity, with inducing apoptosis, dissipation of the mitochondrial membrane potential (MMP) and generation of reactive oxygen species (ROS) in Huh7.5 liver cancer cells. Proteomic and quantitative real-time PCR analyses indicated that EPS364 inhibited cancer cell growth and adhesion via targeting the FGF19-FGFR4 signaling pathway. These findings suggest that EPS364 is a promising antitumor agent for pharmacotherapy.  相似文献   
7.
AIM: To investigate the autophagy of human ovarian cancer SKOV3 cells induced by cepharanthine and to explore its mechanism. METHODS: The effect of cepharanthine on the viability of ovarian cancer SKOV3 cells was measured by CCK-8 assay. The SKOV3 cells were treated with cepharanthine, and then the formation of autophagosome was observed with acridine orange staining under fluorescence microscope. The protein levels of LC3, AKT, p-AKT, mTOR, p-mTOR and GAPDH in the SKOV3 cells treated with cepharanthine were determined by Western blot.RESULTS: Cepharanthine significantly inhibited the viability of ovarian cancer SKOV3 cells in a dose-dependent manner (P<0.05). The number of the intracellular acidic autophagosomes with bright red fluorescence was significantly increased after cepharanthine treatment in the SKOV3 cells. The expression of LC3-Ⅱ in SKOV3 cells was significantly enhanced after cepharanthine treatment. Furthermore, treatment with cepharanthine in the SKOV3 cells also resulted in a significant down-regulation of phosphorylated form of AKT and mTOR (P<0.01), while the total protein level was not changed. Combination of cepharanthine and 3-methyladenine resulted in a substantial decrease in the cell viability compared with using cepharanthine alone.CONCLUSION: Cepharanthine significantly inhibits the growth of human ovarian cancer SKOV3 cells and induces the autophagy, which may be correlated with down-regulation of PI3K/AKT/mTOR signaling pathway.  相似文献   
8.
AIM:To investigate the effect of Kechuanning on airway remodeling and the protein level of p-ERK1/2 in lung tissues of asthmatic rats induced by virus. METHODS:The asthmatic rat model induced by respiratory syncytial virus was established. The experimental rats were divided into normal group, asthma model group, low dose (0.33 mL/kg), middle dose (3.0 mL/kg) and high dose (10 mL/kg) of Kechuanning groups, and PD98059 (3 mg/kg) group. The airway responsiveness of the rats was measured by animal ventilator. The pathological changes of the lung tissues were observed by HE staining. PAS staining and Masson staining were used to observe goblet epithelial cells metaplasia and airway collagen deposition. The expression of matrix metalloproteinases-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in the lung tissues of the rats was detected by immunohistochemical staining. The protein levels of ERK1/2 and p-ERK1/2 were determined by Western blot. RESULTS:Compared with model group, the airway responsiveness of the rats in middle dose and high dose of Kechuanning groups was significantly decreased (P<0.01), the injury of lung tissues was significantly decreased, the goblet epithelial cells metaplasia and airway collagen deposition were significantly reduced (P<0.01), and the expression of MMP-9 and TIMP-1 in the lung tissues was also significantly decreased (P<0.01). In addition, the protein level of p-ERK1/2 in high dose of Kechuanning group was significantly decreased compared with model group (P<0.01). CONCLUSION:Kechuanning may treat asthma by regulating the expression of p-ERK1/2 in the lung tissues and improving the airway remodeling symptoms of asthmatic rats induced by virus.  相似文献   
9.
Polyethers is one of the main components of water-glycol-base non-inflammble hydraulic fluid. This paper describes an optimized technique synthesizing polyether from ethylene oxide and epoxypropane. The synthetic polyethers meets the technical requirement  相似文献   
10.
The induction of a hypersensitive reaction in Samsun NN tobacco by tobacco mosaic virus (TMV) at 20°C leads to the development of both localized and systemic acquired resistance, and is associated with the appearance of pathogenesis-related proteins (PR's) and large increases in peroxidase activity and ethylene production. Salicylic acid (SA) induced a similar resistance in treated plant parts and occasionally also in untreated upper leaves of plants of which three lower leaves had been injected. SA also induced the same four PR's, but these were confined to the treated leaves. Thus, the connection between the presence of PR's and the reduction of TMV multiplication and spread may not be direct.In contrast to TMV, SA did not stimulate ethylene production and hardly increased peroxidase activity. Induction of acquired resistance and PR's by SA developed equally well at 20°C and at 32°C. However, pricking leaves with needles moistened with the ethylene-releasing compound ethephon mimicked TMV infection in inducing acquired resistance and PR's in both treated and untreated leaves at 20°C, but not at 32°C. Ethephon increased peroxidase activity at both temperatures, but only at 20°C dit it induce changes in both the anodic and the cathodic isoenzymes that were similar to those induced as a result of TMV infection. SA induced PR's and reduced TMV multiplication in Samsun tobacco, and inhibited virus spread in Samsun NN at 32°C.These observation indicate that neither the induction of PR's, nor the development of acquired resistance is temperature-sensitive. On the other hand, the effects of ethephon are temperature-sensitive in the same way as the hypersensitive response to TMV. It can thus be hypothesized that ethylene, produced naturally during the hypersensitive reaction of tobacco to TMV, leads to the temperature-sensitive synthesis or release of a presumably benzoic acid-type compound that functions as the natural inducer of PR's and acquired resistance. Although vanillic acid has been shown to accumulate in hypersensitively reacting tobacco leaves, it produced none of the effects of SA, and thus cannot be the natural inducer.Samenvatting Inductie van een overgevoeligheidsreactie in Samsun NN-tabak door tabaksmozaïekvirus (TMV) bij 20°C leidt tot de ontwikkeling van een verworven resistentie die zowel lokaal als systemisch werkzaam is, en gaat samen met het verschijnen van pathogenesis-related proteins (PR's) en sterke toename in de activitieit van peroxidase en de produktie van ethyleen. Salicylzuur (SA) induceerde een vergelijkbare resistentie in behandelde plantedelen en af en toe ook in niet behandelde bovenbladeren van planten waarvan drie onderbladeren waren ingespoten. SA induceerde ook dezelfde vier PR's, maar deze waren beperkt tot de behandelde bladeren. Er bestaat dus geen directe samenhang tussen de aanwezigheid van PR's en de remming van de vermeerdering en uitbreiding van TMV in de plant.In tegenstelling tot TMV stimuleerde SA de ethyleenproduktie niet en verhoogde het de peroxidaseactiviteit nauwelijks. Inductie van verworven resistentie en PR's door SA trad even goed op bij 32°C als bij 20°C. Net als infectie met TMV leidde aanprikken van bladeren met naalden die gedoopt waren in een oplossing van ethefon — waaruit in het blad ethyleen vrijkomt — echter tot inductie van verworven resistentie en PR's in zowel behandelde als onbehandelde bladeren bij 20°C, maar niet bij 32°C. Ethefon verhoogde de peroxidaseactiviteit bij beide temperaturen, maar alleen bij 20°C induceerde het veranderingen in zowel de anodische als de kathodische isoënzymen die vergelijkbaar waren met die welke geïnduceerd werden als gevolg van infectie met TMV. SA induceerde PR's en verminderde de vermenigvuldiging van TMV in Samsun tabak, en remde de uitbreiding van het virus in Samsun NN bij 32°C.Deze waarnemingen tonen dat noch de inductie van PR's, noch de ontwikkeling van verworven resistentie een temperatuurgevoelig proces is. Daarentegen zijn de effecten van ethefon op dezelfde wijze temperatuurgevoelig als de overgevoeligheidsreactie op TMV. Men kan daarom veronderstellen dat ethyleen, dat op natuurlijke wijze geproduceerd wordt tijdens de overgevoeligheidsreactie van tabak op TMV, aanleiding geeft tot een temperatuurgevoelig proces, namelijk de synthese of het vrijkomen van een verbinding, vermoedelijk een benzoëzuurderivaat, dat fungeert als de natuurlijke inductor van PR's en verworven resistentie. Hoewel is aangetoond dat vanillinezuur zich ophoopt in overgevoelig reagerende tabaksbladeren, veroorzaakte deze verbinding geen enkel van de effecten van SA. Vanillinezuur kan dus niet de natuurlijke inductor zijn.  相似文献   
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