全文获取类型
收费全文 | 7365篇 |
免费 | 356篇 |
国内免费 | 154篇 |
专业分类
耳鼻咽喉 | 83篇 |
儿科学 | 80篇 |
妇产科学 | 29篇 |
基础医学 | 802篇 |
口腔科学 | 204篇 |
临床医学 | 400篇 |
内科学 | 721篇 |
皮肤病学 | 41篇 |
神经病学 | 492篇 |
特种医学 | 135篇 |
外科学 | 518篇 |
综合类 | 1129篇 |
预防医学 | 444篇 |
眼科学 | 59篇 |
药学 | 2325篇 |
3篇 | |
中国医学 | 266篇 |
肿瘤学 | 144篇 |
出版年
2024年 | 25篇 |
2023年 | 85篇 |
2022年 | 134篇 |
2021年 | 198篇 |
2020年 | 153篇 |
2019年 | 160篇 |
2018年 | 189篇 |
2017年 | 197篇 |
2016年 | 207篇 |
2015年 | 184篇 |
2014年 | 456篇 |
2013年 | 519篇 |
2012年 | 480篇 |
2011年 | 449篇 |
2010年 | 361篇 |
2009年 | 401篇 |
2008年 | 313篇 |
2007年 | 336篇 |
2006年 | 304篇 |
2005年 | 299篇 |
2004年 | 235篇 |
2003年 | 150篇 |
2002年 | 157篇 |
2001年 | 130篇 |
2000年 | 122篇 |
1999年 | 112篇 |
1998年 | 98篇 |
1997年 | 100篇 |
1996年 | 71篇 |
1995年 | 65篇 |
1994年 | 85篇 |
1993年 | 56篇 |
1992年 | 85篇 |
1991年 | 73篇 |
1990年 | 74篇 |
1989年 | 77篇 |
1988年 | 58篇 |
1987年 | 58篇 |
1986年 | 54篇 |
1985年 | 68篇 |
1984年 | 53篇 |
1983年 | 33篇 |
1982年 | 52篇 |
1981年 | 38篇 |
1980年 | 36篇 |
1979年 | 39篇 |
1977年 | 29篇 |
1976年 | 31篇 |
1974年 | 28篇 |
1973年 | 40篇 |
排序方式: 共有7875条查询结果,搜索用时 0 毫秒
21.
背根神经节Nav1.8磷酸化在大鼠糖尿病痛性周围神经病变中的作用 总被引:2,自引:0,他引:2
目的 本研究采用射频热凝毁损腰交感神经节,探讨背根神经节(DRG)Nav1.8磷酸化在大鼠糖尿病痛性周围神经病变中的作用。方法 采用腹腔注射链尿佐菌素诱导糖尿病痛性周围神经病变大鼠模型,取造模成功的大鼠20只,随机分为糖尿病对照组(D组)及交感神经节射频热凝组(R组),每组10只,另取10只同月龄大鼠为正常对照组(C组)。R组大鼠在X光机介导下行右侧L3,4椎旁腰交感神经节射频热凝毁损。分别于射频热凝前、射频热凝后1、2周时,采用von Frey纤维丝测定大鼠右侧后爪对机械性刺激缩足反应的阈值(PWT);射频热凝后2周,采用Western-blotting方法测定DRG细胞Nav1.8蛋白和苏氨酸磷酸化Nav1.8蛋白表达,并采用透射电镜观察大鼠腓肠神经超微病理结构。结果 与C组比较,射频热凝前D组和R组PWT降低(P<0.01)。射频热凝后1~2周,R组较D组PWT升高,但仍较C组降低(P<0.05)。C组髓鞘排列均匀,轴突内可见形态正常的线粒体;D组脱髓鞘明显,髓鞘板层排列紊乱、断裂、肿胀;R组脱髓鞘程度明显减轻,髓鞘板层局部排列紊乱、空泡形成。与C组比较,D组和R组Nav1.8蛋白表达降低(P<0.05),而苏氨酸磷酸化Nav1.8蛋白表达增高(P<0.01);R组苏氨酸磷酸化Nav1.8蛋白表达低于D组(P<0.05)。结论 DRG细胞Nav1.8的磷酸化可能是糖尿病痛性周围神经病变大鼠痛觉过敏形成的机制之一。 相似文献
22.
目的探讨硬膜外腔注射生理盐水对剖宫产术患者腰麻效果的影响。方法择期行子宫下段剖宫产术患者60例,年龄24~30岁,体重59~73 kg,随机分为2组,每组30例,A组蛛网膜下腔注射规定剂量的0.75%布比卡因后硬膜外腔注射生理盐水5 ml;B组蛛网膜下腔注射0.75%布比卡因。按序贯法进行试验,设定布比卡因的起始剂量为9 mg,剂量梯度为1.5 mg,若上一例有效,则下一例递减一个剂量梯度,若无效则下一例递增一个剂量梯度,蛛网膜下腔阻滞有效的标准为注射布比卡因后20 min内阻滞上平面达T5。采用概率单位法计算ED50。结果A组布比卡因的ED50(5.8 mg)低于B组(8.1 mg),两组比值为0.72,95%置信区间为0.27~0.98,区间范围不包括1,差异有统计学意义(P〈0.05)。结论硬膜外腔注射生理盐水可增强剖宫产术患者腰麻的效果。 相似文献
23.
Ion channel expression by white matter glia: I. Type 2 astrocytes and oligodendrocytes 总被引:12,自引:0,他引:12
White matter is a compact structure consisting primarily of neuronal axons and glial cells. As in other parts of the nervous system, the function of glial cells in white matter is poorly understood. We have explored the electrophysiological properties of two types of glial cells found predominantly in white matter: type 2 astrocytes and oligodendrocytes. Whole-cells and single-channel patch-clamp techniques were used to study these cell types in postnatal rat optic nerve cultures prepared according to the procedures of Raff et al. (Nature, 303:390-396, 1983b). Type 2 astrocytes in culture exhibit a "neuronal" channel phenotype, expressing at least six distinct ion channel types. With whole-cell recording we observed three inward currents: a voltage-sensitive sodium current qualitatively similar to that found in neurons and both transient and sustained calcium currents. In addition, type 2 astrocytes had two components of outward current: a delayed potassium current which activated at 0 mV and an inactivating calcium-dependent potassium current which activated at -30 mV. Type 2 astrocytes in culture could be induced to fire single regenerative potentials in response to injections of depolarizing current. Single-channel recording demonstrated the presence of an outwardly rectifying chloride channel in both type 2 astrocytes and oligodendrocytes, but this channel could only be observed in excised patches. Oligodendrocytes expressed only one other current: an inwardly rectifying potassium current that is mediated by 30- and 120-pS channels. Because these channels preferentially conduct potassium from outside to inside the cell, and because they are open at the resting potential of the cell, they would be appropriate for removing potassium from the extracellular space; thus it is proposed that oligodendrocytes, besides myelinating axons, play an important role in potassium regulation in white matter. The conductances present in oligodendrocytes suggest a "modulated Boyle and Conway mechanism" of potassium accumulation. 相似文献
24.
Miwa Baba Ryozo Oishi Kiyomi Saeki 《Naunyn-Schmiedeberg's archives of pharmacology》1988,337(4):423-428
Summary The effects of opioids on the permeability of the blood-brain barrier (BBB) were examined in mice with sodium fluorescein as an indicator of the permeability. The brain was perfused with saline 30 min after injection of sodium fluorescein (40 mg/kg, i. v.) and examined by fluorometry. Morphine hydrochloride (0.3–10 mg/kg, s. c.) markedly increased the brain level of sodium fluorescein dose-dependently without influencing the plasma level, when administered 20 min before sodium fluorescein injection. Intracerebroventricularly (i. c. v.) injected morphine hydrochloride (0.5 and 1.0 Erg) increased the brain sodium fluorescein level. Buprenorphine (0.1 and 0.5 mg/kg, s. c.) was also effective. However, pentazocine, ethylketazocine, U-50488H and SKF-10047 had no significant influence. The i.c.v. administration of [D-Ala2, McPhe4, Gly(ol)5]enkephalin (0.1 g) and [D-Ala2, D-Leu5]enkephalin (0.5 g) but not of [D-Thr2, Leu5]enkephalin-Thr increased the brain level of sodium fluorescein significantly. A small dose of naloxone (i. p.) significantly inhibited the effects of morphine, buprenorphine, [D-Ala2, McPhe4, Gly(ol)5]enkephalin and [D-Ala3, D-Leu5]enkephalin. ICI-174864 co-administered i. c. v. with [D-Ala2, D-Leu5]enkephalin was ineffective in antagonizing the effect of the latter. These findings suggest that the stimulation of µ opioid receptors results in an increase in BBB permeability to sodium fluorescein.
Send offprint requests to K. Saeki 相似文献
25.
Francisco Alvarado Edith Brot-Laroche Manuel L'Herminier Heini Murer Gertrude Stange 《Pflügers Archiv : European journal of physiology》1979,382(1):35-41
Harmaline inhibition of sodium uptake and of sodium-dependentd-glucose transport was investigated using brush-border membrane vesicles from frozen rabbit jejunum. Under sodium-gradient conditions, initiald-glucose uptake (20 s) was inhibited by harmaline at concentrations above 0.5 mM, but at lower harmaline concentrationsd-glucose uptake was stimulated by 10–15%. When a similar potassium gradient was used, harmaline had no effect. At concentrations upt to 2 mM, harmaline did not alter the equilibrium uptake ofd-glucose ord-mannitol. After pre-equlibration with sodium (25 mM),d-glucose uptake was inhibited at harmaline concentrations ranging from 0.1 to 2 mM. Sodium (10 mM) uptake was also inhibited by harmaline. Increasing the sodium concentration reduced the inhibitory effect of harmaline on tracer sodium uptake as well as on sodium-dependentd-glucose uptake. Similar to phlorizin, harmaline (1 mM) was able to prevent glucose-induced sodium influx across the brush-border membrane.Sodium uptake into brush-border membrane vesicles seems to be inhibited at lower harmaline concentrations than sodium-dependentd-glucose uptake. At high (2 mM) inhibitor concentrations, however, sodium-dependent glucose uptake is more strongly inhibited than sodium uptake. These results suggest that harmaline inhibits both sodium and sodium-dependent transport across intestinal brush-border membranes by interacting with specific sodium-binding sites. 相似文献
26.
Cellular dehydration induced by water deprivation or hypertonic saline injection reduces feeding in a variety of species. Normal feeding in rats is maintained during isotonic saline consumption by increasing the intake of saline compared to the usual intake of water. Hamsters do not show the spontaneous preference for isotonic saline noted in rats, even after adrenalectomy. In the present investigation, feeding by hamsters was depressed during both isotonic and hypertonic saline consumption compared to the usual feeding with water. Saline intakes did not exceed water intakes under similar conditions. When fluid intakes were elevated by prior fluid deprivation, feeding rates increased at all concentrations of saline after a delay proportional to the osmolality of the solution. Positive 24-hr sodium balances were always associated with saline consumption. Water and hypertonic saline injections reduced feeding, and the fluid loads were excreted very slowly. When hamsters were fluid deprived prior to injections, saline totally suppressed feeding, while water increased feeding compared to sham injected controls. It is concluded that cellular dehydration produces a reduction of feeding in hamsters drinking isotonic or hypertonic saline. Reduced feeding with isotonic saline consumption results from the failure of hamsters to increase their ad lib intake of that solution. The prolonged retention of both sodium and fluid after saline consumption or injection suggests that further saline intake may be inhibited by an expansion of the extracellular space. 相似文献
27.
Bernd Sutor Walter Zieglgänsberger 《Pflügers Archiv : European journal of physiology》1987,410(1-2):102-111
Intracellular recordings were obtained from rat neocortical neurons in vitro. The current-voltage-relationship of the neuronal membrane was investigated using current- and single-electrode-voltage-clamp techniques. Within the potential range up to 25 mV positive to the resting membrane potential (RMP: –75 to –80 mV) the steady state slope resistance increased with depolarization (i.e. steady state inward rectification in depolarizing direction). Replacement of extracellular NaCl with an equimolar amount of choline chloride resulted in the conversion of the steady state inward rectification to an outward rectification, suggesting the presence of a voltage-dependent, persistent sodium current which generated the steady state inward rectification of these neurons. Intracellularly injected outward current pulses with just subthreshold intensities elicited a transient depolarizing potential which invariably triggered the first action potential upon an increase in current strength. Single-electrode-voltage-clamp measurements reveled that this depolarizing potential was produced by a transient calcium current activated at membrane potentials 15–20 mV positive to the RMP and that this current was responsible for the time-dependent increase in the magnitude of the inward rectification in depolarizing direction in rat neocortical neurons. It may be that, together with the persistent sodium current, this calcium current regulates the excitability of these neurons via the adjustment of the action potential threshold. 相似文献
28.
Objective and design: Myeloperoxidase (MPO) and proinflammatory cytokines play an important role in the development of inflammation. These markers
are generally measured using tedious ELISA procedures. In this study, a novel technique utilizing antibody conjugated quantum
dot nanoparticles was developed to detect Myeloperoxidase, Interleukin-1α (IL-1α) and Tumor Necrosis Factor-α (TNF-α) in vivo in the dextran sodium sulfate (DSS) model of experimental colitis.
Materials and methods: Colitis was induced in animals (n = 8 animals/group) by feeding 4% DSS solution ad libitum for seven to eight days. Quantum Dots (QDs) exhibiting fluorescence at various wavelengths were conjugated to MPO, IL-1α
and TNF-α polyclonal antibodies and tested in vivo at various stages of colitis. Tissue sections obtained were imaged with confocal microscope. The image intensity obtained
from the tissue specimen was correlated with clinical activity measured as Disease Activity Index (DAI).
Results: Myeloperoxidase, IL-1α and TNF-α were visualized with quantum dots on various days of disease. The intensity of quantum dots
increased with the increase in inflammation. The increase in intensity showed an excellent correlation with the DAI based
on the clinical parameters.
Conclusion: The study demonstrated that multiple biomarkers can be detected simultaneously and their quantitative expression correlated
well with clinical disease severity. This novel technology should facilitate design of a novel optical platform for imaging
various biomarkers of inflammation, early detection of acute and chronic disease markers and inflammation-mediated cancer
markers. This detection may also facilitate determination of therapeutic success.
Received 14 March 2007; returned for revision 8 May 2007; accepted by M. Parnham 27 June 2007 相似文献
29.
Kamran Sardari 《Comparative clinical pathology》2007,16(2):97-102
Local injection of a mixture of beta-aminopropionitril fumarate (BAPN-f) and sodium hyaluronate (NaH+) together with controlled exercise were evaluated for treatment of superficial digital flexor tendon (SDFT) injuries in horses.
Fourteen mixed breed horses with subacute SDF tendon injuries in forelimbs were randomly assigned to two groups. One group
received BAPN-f (0.7 mg/ml) and the other received NaH+ (10 mg/ml) all by intratendinous injection. Controlled exercise started during the first week after intratendinous treatment
and continued for 12 weeks. Cross-sectional area (CSA) of the SDFT, diameter of the SDFT, and relative area of the lesion
(presence of CSA) were measured by ultrasonographic examination. Lesions were semiquantitatively graded for echogenicity on
a scale of 0 to 4. The lesion severity in CSA was significantly reduced by BAPN and NaH compared to those horses treated by
BAPN only (p < 0.05). Lesion echogenicity score was significantly higher in horses treated with BAPN and NaH+ at day 0 compared to horses treated with BAPN (p < 0.05). At the end of the study, lesion echogenicity score was significantly reduced in the horses treated with BAPN and
NaH+ compared to horses treated by BAPN only (p < 0.05). According to the results of the present study, a combination of BAPN-f and NaH+ has a greater beneficial effect on tendon healing and remodeling in horses, as assessed by sonographic examination, compared
to treatment with single drugs. 相似文献
30.
Drago F Frisina M Grech M Nicolosi A Micale V Nicosia A Medico M Foti F 《Neuroscience letters》2001,300(3):176-178
Melatonin affects the circadian sleep/wake cycle, but it is not clear whether it may influence drug-induced narcosis. Sodium thiopenthal was administered intraperitoneally into male rats pre-treated with melatonin (0.05, 0.5, 5 and 50 mg/kg). Melatonin pre-treatment affected in a dual manner barbiturate narcosis, however, no dose-effect correlation was found. In particular, low doses reduced the latency to and prolonged the duration of barbiturate narcosis. In contrast, the highest dose of melatonin (50 mg/kg) caused a paradoxical increase in the latency and produced a sustained reduction of the duration of narcosis, and a reduction in mortality rate. Melatonin 0.5 and 5 mg/kg influenced the duration but not the latency of ketamine- or diazepam-induced narcosis. Thus, the dual action of melatonin on pharmacological narcosis seems to be specific for the barbiturate mechanism of action. 相似文献