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51.
AIM: The research was to investigate the effects of the Tian ma gou teng decoction on the electric physiology feature of L-type calcium channels in the vascular smooth muscle cells in spontaneously hypertensive rats (SHR), and to further explain the mechanism of the Tian ma gou teng decoction in the intervention of blood pressure.METHODS: 12-week-old SHRs were assigned randomly into five groups:group A (treated with Tian ma gou teng decoction), group B (treated with Tian ma gou teng decoction with subtraction concha haliotidis), group C (treated with nifedipine), group D (treated with concha haliotidis), group E (treated with normal saline as control), each group consisted of 9 rats. After treatments were conducted for 4 weeks, the free calcium concentration in serum was measured. The electric physiology feature of L-type calcium channels in the vascular smooth muscle cells was analyzed by patch clamp technique (PCT).RESULTS: No significant difference between group A and group C was observed in the serum free calcium concentration (P>0.05). There were significant differences among group B, group D and group E (P<0.05), compared to before treatment, the change in group E was the most obvious. A decrease in the L-type calcium channel current of vascular smooth muscle cells was observed in group A and group C. The function of group D was feeble, no decrease in the L-type calcium channels current of vascular smooth muscle cells was observed in group B and group E.CONCLUSION: Tian ma gou teng decoction can increase the serum free calcium concentration and block the L-type calcium channel current in vascular smooth muscle cells, indicating one of the mechanism of intervention of blood pressure.  相似文献   
52.
AIM:To investigate the effects of apelin on ventricular arrythmias and cardiac functions in rat Langendorff perfusion-simulated myocardial ischemia model by observing the changes of transient sodium currents (INa) in normal cells and the simulated ischemic cells in rat left ventricle. METHODS:Ventricular cells were enzymatically isolated by the Langendorff perfusion system. INa was recorded by the technique of whole-cell patch-clamp. Some elements in the extracellular fluid were changed to simulate the normal or ischemic status. Forty Wistar rats were divided into 4 groups:normal group, ischemic group, normal with apelin group and ischemic with apelin group. The effect of apelin-13 on INa was observed. The method of rat Langendorff perfusion was used to simulate the ischemic heart model. The ventricular arrhythmia scores and heart functional parameters were compared. The expression level of sodium channel protein,type V,alpha subunit (SCN5A) in ventricular ischemic cells was measured by Western blotting. RESULTS: Apelin-13 increased INa amplitude in both normal myocardial cells [(-86±13) pA/pF] and ischemic myocardial cells [(-52±15) pA/pF]. The results of current-voltage curve analysis indicated that apelin-13 did not change the conduction velocity of INa in the 4 groups [(3.2±0.2) pS/pF, (3.1±0.3) pS/pF,(2.9±0.1)pS/pF and (2.8±0.4) pS/pF,respectively, P>0.05]. The membrane potentials at 50% maximal activation in the 4 groups were (-21.9±0.6) mV, (-28.7±0.3) mV, (-30.5±0.7) mV and (-36.8±0.2) mV, respectively, and the slope of activation curves was 5.6±0.3, 5.1±0.4, 4.3±0.3 and 4.9±0.6 (P>0.05), respectively. No difference of ventricular arrhythmia scores between normal group and normal with apelin group, as well as between ischemic group and ischemic with apelin group was observed. LVEDP in normal with apelin group was lower than that in normal group.The dp/dtmax and dp/dtmin in normal with apelin group were higher than those in normal group. Apelin improved cardiac function parameters in the ischemic hearts. The expression of SCN5A was not affected by apelin (28.8±3.6, 29.4±4.1, 30.1±2.9 and 31.3±3.8,respectively,P>0.05). CONCLUSION:Apelin-13 changes the gating properties of sodium channel, enhances the peak INa and facilitates the opening of sodium channel without inducing ventricular arrhythmias. Apelin-13 has a positive inotropic effect on both normal and ischemic hearts.  相似文献   
53.
探究社会资本对农户投资效率的影响与机制对提高农户种粮收益、提升粮食综合生产能力具有重要意义。基于2021年江苏省6县(区)401户农户调查数据,运用数据包络分析方法测算水稻种植户的投资效率,采用Tobit模型实证分析社会资本对水稻种植户投资效率的影响,并检验其作用机制。研究结果表明:样本水稻种植户投资效率整体偏低,平均产出效率和收入效率分别为0.66和0.50。不同类型社会资本对水稻种植户投资效率均有显著正向影响。其中,亲友型和身份型社会资本通过促进生产性借贷资金投入提高投资效率;组织型和企业型社会资本则通过拓展销售渠道发挥作用。异质性分析表明,社会资本对不同效率水平的种植户以及不同劳动力流动水平下的影响存在显著差异。据此,建议应充分发挥社会资本的积极作用,通过大力扶持新型农业经营主体、推行多方联动贷款模式、加快农业全产业链建设等途径促进农户投资效率稳步提升。  相似文献   
54.
AIM: To investigate the mechanism of quercetin improving rat coronary artery myogenic response under high glucose (HG) by measuring muscle tension of coronary arterial ring and recording voltage-gated K+ channel (Kv) current of coronary artery smooth muscle cells by whole cell patch clamp. METHODS: The coronary rings from the normal SD rats were acutely isolated, and then divided into 6 groups: (1) control group; (2) HG group; (3) HG+low dose (3 μmol/L) of quercetin group; (4) HG+moderate dose (10 μmol/L) of quercetin group; (5) HG+high dose (30 μmol/L) of quercetin group; (6) HG+C6303 (PKC inhibitor)+high dose of quercetin group. Determinations of coronary artery response to vasoconstrictor (60 mmol/L KCl or 0.1 mmol/L U46619) or vasodilator (ACh at 10-9~10-5 mol/L) were performed, and the percentage of coronary ring tension was calculated using the contraction as 100% caused by 60 mmol/L KCl. The rat coronary artery smooth muscle cells were acutely isolated for recording the Kv current using whole cell patch clamp. RESULTS: Compared with control group, the contraction amplitudes to 60 mmol/L KCl or 0.1 mmol/L U46619 were significantly increased under HG incubation. Quercetin intervention concentration-dependently reduced the coronary artery contraction amplitude. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. Compared with control group, the diastolic amplitude to ACh decreased significantly in HG group, and quercetin intervention concentration-dependently increased the coronary artery diastolic amplitude. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. Compared with control group, HG incubation inhibited Kv current of coronary artery vascular smooth muscle cells significantly, and quercetin intervention attenuated the inhibitory effect of HG on Kv current intensity. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. CONCLUSION: Quercetin has a protective effect on myogenic response of coronary artery under HG and the effects is related to the increase in Kv current and the activation of PKC in vascular smooth muscle cells.  相似文献   
55.
为了探究迷宫流道齿间角对灌水器水力性能的影响,应用CFD流场和速度场的数值分析方法,研究齿间角度分别为50°,60°,70°和80°时正齿型和斜齿型迷宫灌水器的流场和速度场随齿间角的变化规律.研究结果表明:相比于RNG k-ε模型和SST模型,标准k-ε模型的计算结果与试验结果更加接近;正齿型和斜齿型迷宫灌水器通道内主要存在2处低速回流区,即齿型的左上侧低速回流区和右下侧低速回流区;相比于正齿型迷宫灌水器,斜齿型迷宫灌水器左上侧的低速区域较多,而右下侧的低速区域较少;随着齿间角度不断增加,灌水器内的流量不断增大,斜齿型迷宫灌水器内的流量增加受齿间角度的影响更为明显;正齿型迷宫灌水器的流量系数较大,但流态指数较小,齿间角度为70°的正齿型迷宫灌水器的流态指数在所有灌水器中最小,其水力性能最好.  相似文献   
56.
AIM:To investigate the effects of voltage-dependent K+ channel 1.5 (Kv1.5) on the proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia+hypercapnia condition and the relationship with mitogen-activated protein kinase(MAPK) signal pathway. METHODS:The PASMCs isolated from the male SD rat were cultured under hypoxia+hypercapnia condition, and randomly divided into normal group (N group), hypoxia+hypercapnia group (HH group), hypoxia+hypercapnia+DMSO incubation group (HD group), hypoxia+hypercapnia+U0126 (an extracellular signal-regulated kinase 1/2 inhibitor) incubation group (HU group), hypoxia+hypercapnia+SB203580 (a p38 mitogen-activated protein kinase inhibitor) incubation group (HS group), and hypoxia+hypercapnia+anisomycin (an agonist of MAPK) incubation group (HA group). Cell Counting Kit-8 was used to detect the cell viability. The protein expression of Kv1.5, PCNA and Bax was detected by Western blotting. RESULTS:Compared with N group, the cell viability and PCNA protein expression in HH group and HD group were significantly raised (P<001), but Kv1.5 and Bax proteins were significantly decreased (P<0.01). No difference between HH group and HD group was observed (P>005). Compared with HD group, the cell viability and PCNA protein expression in HU group, HS group and HA group were decreased (P<0.05 or P<0.01), but Kv1.5 protein and Bax protein were raised (P<0.01), with the most significant changes in HA group. CONCLUSION:The regulation of Kv1.5 to the proliferation and apoptosis of PASMCs under hypoxia+hypercapnia condition might have a relationship with the activation of MAPK signal pathway.  相似文献   
57.
AIM: To investigate the role of potassium channels in the regulation of intracellular free calcium concentration ( [Ca2+]i) of pulmonary artery smooth muscle cells (PASMCs) in rats. METHODS: The fluorescence Ca2+ indicator Fura-2/AM was used to observe [Ca2+]i of rat PASMCs in normal and chronic hypoxic condition. The influences of potassium channels on PASMCs proliferation were assessed by MTT assay. RESULTS: 1. In normoxic condition, [Ca2+]i was (156.91±8.60) nmol/L, and in hypoxic condition, [Ca2+]i was (294.01±16.81) nmol/L. 2. In normoxic condition, the voltage-dependent K+-channel antagonist 4-aminopyridine (4AP), but not the Ca2+-activated K+-channel antagonist tetraethylammonium (TEA) and the ATP-sensitive K+-channel antagonist glibenclamide (Glib) increased [Ca2+]i. 3. In hypoxic condition, 4AP and TEA caused the rise in [Ca2+]i , but Glib had no effect on [Ca2+]i. 4. MTT assay showed that 4AP increased the value of absorbing light degree (A value) in normoxic and hypoxic condition (0.582±0.062,0.873±0.043,respectively, P<0.01), TEA increased A value only in hypoxic condition, and Glib had no effect on the proliferation of PASMCs. CONCLUSIONS: KV plays an important role in the regulation of [Ca2+]i and proliferation of PASMCs. KCa serves as distinct responsive roles in the regulation of proliferation of PASMCs in hypoxic condition. KATP has no effect on [Ca2+]i and proliferation of PASMCs in normoxic and hypoxic conditions.  相似文献   
58.
59.
AIM:To study the effect of farrerol (Far) on nicotine-induced proliferation of rat pulmonary smooth muscle cells (PASMCs), and further to explore its relationship with voltage-dependent potassium channels (Kv) 1.5 and Kv2.1. METHODS:Firstly, the effect of nicotine on the proliferation of PASMCs was detected by cell counting method, and the optimal concentration of nicotine was selected. Primary cultured PASMCs were randomly divided into 5 groups:normal control group, nicotine (1 μmol/L)group, nicotine (1 μmol/L) + Far (10-6 mol/L, 10-5 mol/L and 10-4 mol/L) Far group. The activity of caspase-3 was measured by apoptosis kit, the cell viability was measured by CCK-8 assay, the apoptotic rate was analyzed by flow cytometry. The expression of Kv1.5 and Kv2.1, and apoptosis-related factors Bcl-2 and Bax at mRNA and protein levels was determined by RT-qPCR and Western blot respectively. RESULTS:Nicotine at 1 μmol/L increased the number of PASMCs to the maximum extent (P<0.01). Nicotine at 1 μmol/L significantly reduced the caspase-3 activity and enhanced the cell viability of the PASMCs (P<0.01). Farrerol at 10-6~10-4 mol/L eliminated the effect of PASMCs induced by nicotine in a concentration dependent manner. Compared with control group, nicotine at 1 μmol/L significantly increased the proliferation and inhibited the apoptotic rate of rat PASMCs (P<0.01). The apoptotic rate of PASMCs in farrerol intervention group was significantly higher than that in nicotine group (P<0.01). Nicotine at 1 μmol/L significantly inhibited the expression of Kv1.5, Kv2.1 and Bax but increased the expression of Bcl-2 in PASMCs (P<0.01). Farrerol at 10-5 mol/L obviously inhibited the effect of PASMCs induced by nicotine. CONCLUSION:Farrerol eliminates nicotine-induced inhibition of caspase-3 and Bax, and enhancement of Bcl-2 in PASMCs by enhancing Kv1.5 and Kv2.1 expression.  相似文献   
60.
【目的】寻求半立方抛物线形明渠共轭水深的迭代计算方法。【方法】根据半立方抛物线形明渠断面的几何形态及棱柱体水平明渠水跃方程,推求得到半立方抛物线形明渠共轭水深的迭代计算公式,并从理论上证明其收敛性;通过对工程中不同流量Q与不同断面形状参数p多种组合情况下的共轭水深进行计算和趋势线拟合,建立计算共轭水深迭代初值的直接计算式。【结果】推导出半立方抛物线形渠道断面的水跃方程,并进而得到跃前水深、跃后水深的迭代计算公式,运用迭代初值直接计算式求出迭代初值,将该值代入共轭水深迭代计算公式,经过几步迭代便可收敛得到精度很高的共轭水深值。【结论】推求的半立方抛物线形明渠共轭水深迭代计算公式物理概念明确、计算简捷、精度高、适用范围广,可以满足工程实践要求。  相似文献   
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