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排序方式: 共有971条查询结果,搜索用时 15 毫秒
961.
962.
目的 分析65例慢性阻塞性肺疾病急性加重期(AECOPD)患者血清降钙素原变化及其指导意义.方法 本研究纳入65例AECOPD患者,随机分成A组(PCT指导组)、B组(一般治疗组).A组按患者血PCT高低及变化判断抗生素的使用时间;B组根据患者临床症状判断抗生素的使用时间.分别记录A、B两组抗生素的使用时间、住院天数、临床有效率,加重例数和死亡例数用于评估.结果 A组的抗生素使用时间多为7~10 d:B组大多数为2周以上,二者有明显差异(P<0.05);A、B两组住院时间也存在显著差异(P<0.05).结论 PCT在AECOPD患者治疗中,具有指导意义,能够有效缩短抗生素使用时间及缩短住院天数. 相似文献
963.
Steady-state binding of ADP to blood platelets and isolated membranes has not previously been obtained because of complications arising from metabolism of the ligand and dilution due to its secretion from storage granules. In the present studies, competition binding isotherms (n = 9) using paraformaldehyde-fixed platelets showed that [2-3 H]ADP bound to two sites with a small amount (approximately 5% of total) of nonspecific binding: 410,000 +/- 40,000 sites of low affinity (Kd 7.9 +/- 2.0 mumol/L) and 160,000 +/- 20,000 sites of high affinity (Kd 0.35 +/- 0.04 mumol/L) corresponding to the ADP concentration required for activation in fresh platelets (0.1-0.5 mumol/L). All agonists and antagonists examined were able to compete with ADP at the high-affinity site. The strong platelet agonists 2-methylthio ADP and 2-(3- aminopropylthio)ADP competed with ADP at the high-affinity site with dissociation constant values of 7 mumol/L and 200 mumol/L, respectively. The partial agonist 2',3'-dialdehyde ADP and the weak agonist GDP also competed at the high-affinity site with Kd values of 5 mumol/L and 49 mumol/L, respectively. The sequence of binding affinities of other adenine nucleotides at the high-affinity site corresponded to their relative activities as known antagonists of platelet activation by ADP; namely, ADP(Kd 0.35 mumol/L) approximately equal to ATP (Kd 0.45 mumol/L) much greater than AMP (Kd 360 mumol/L). Adenosine and 2-chloroadenosine did not compete with ADP. ADP binding to the high-affinity site was inhibited by p-mercuribenzene sulfonate (Ki 250 mumol/L) but only very weakly by 5'-p- fluorosulfonylbenzoyladenosine (Ki 1 mmol/L). All the above nucleotides also competed with ADP at the low-affinity sites but, because of the high concentrations of competing nucleotide required, dissociation constants at this site were obtained only for ATP (21 mumol/L), 2-MeS ADP (200 mumol/L) and 2',3'-dialdehyde ADP (270 mumol/L). 8-Bromo ADP competed strongly with ADP at the high-affinity site (Kd 0.40 mumol/L) but weakly if at all at the low-affinity site. 8-Bromo ADP inhibited platelet activation induced by ADP (EC50 approximately 100 mumol/L) but not by collagen, thrombin, or ionophore A23187.(ABSTRACT TRUNCATED AT 400 WORDS) 相似文献
964.
目的:研究唐古特红景天95%乙醇提取物对大鼠慢性低氧性肺动脉高压(HPH)的作用及其分子机制。方法:雄性Wistar大鼠随机分为对照组、低氧组、低氧+生理盐水组、低氧+低剂量药物组(1.25 g.kg-1.d-1)、低氧+高剂量药物组(2.5 g.kg-1.d-1)5组,每组15只。除对照组外,其余各组动物均置于低压氧舱内(模拟海拔4 500 m的高原环境),每24 h开舱0.5 h进行灌药等处理,连续30 d。检测各组大鼠的肺血流动力学变化、右心室肥厚指数;光镜观察直径50~100μm的肺动脉管壁厚度占外径的百分比(WT%);采用实时荧光定量PCR方法,检测各组动物肺组织内皮素-1(ET-1)和内皮细胞一氧化氮合酶(eNOS)mRNA的表达;采用ELISA法检测各组动物血清ET-1和eNOS蛋白的含量。结果:与低氧对照组和低氧生理盐水组相比,高剂量唐古特红景天干预,具有以下药理作用:①降低大鼠的平均肺动脉压(mPAP),右心室肥厚指数(RV/LV+S),血红蛋白含量(Hb),红细胞压积(Hct)(P<0.01);②减轻大鼠肺动脉的肌化程度(P<0.05);③降低大鼠肺组织ET-1 mRNA表达,上调大鼠肺组织内皮细胞(eNOS)mRNA表达(P<0.05);④降低大鼠血清ET-1蛋白的含量,上调大鼠血清内皮细胞eNOS蛋白的含量(P<0.05)。结论:唐古特红景天对于HPH的形成具有一定的防治作用,其药理作用机制与上调eNOS mRNA和蛋白表达、抑制ET-1 mRNA和蛋白表达有关。 相似文献
965.
With eukaryotic cells, butyrate is known to induce a series of morphological and biochemical changes that mimic cellular differentiation. With platelets, we have found that butyrate (10 mmol/L) caused an approximately threefold increase in sensitivity to calcium ionophore A23187 and arachidonate. Maximum aggregation was observed at agonist concentrations of 3 mumol/L and 170 mumol/L, respectively, as compared with required concentrations of 10 mumol/L and 400 mumol/L in the absence of butyrate. Similar effects were seen with isobutyric acid, and about one-half the effect was shown with valerate and caproate, but lower homologues showed no synergistic effect. No ultrastructural changes were observed in platelets incubated with butyrate, and the aggregation effects were reversible and returned to normal on removal of butyrate. Membrane fluidity was unchanged by butyrate as measured by changes in the fluorescence depolarization of diphenylhexatriene. Butyrate caused a 60% to 70% increase in the uptake of 3H-arachidonate. Butyrate also potentiated the inhibition of platelet function by prostaglandin E1 and forskolin and uptake of 3H- forskolin was increased approximately 20%. In contrast, platelet response to other agonists (ADP, epinephrine, collagen, thrombin, and platelet-activating factor) was essentially unaffected by butyrate. These results suggest that butyrate may increase the uptake of certain hydophobic agonists and antagonists by platelets. Similar mechanisms for uptake of endogenous effectors may explain the response of eukaryotic cells to butyrate in culture. 相似文献
966.
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968.
969.
Katherine S Ruth Purdey J Campbell Shelby Chew Ee Mun Lim Narelle Hadlow Bronwyn GA Stuckey Suzanne J Brown Bjarke Feenstra John Joseph Gabriela L Surdulescu Hou Feng Zheng J Brent Richards Anna Murray Tim D Spector Scott G Wilson John RB Perry 《European journal of human genetics : EJHG》2016,24(2):284-290
Genetic factors contribute strongly to sex hormone levels, yet knowledge of the regulatory mechanisms remains incomplete. Genome-wide association studies (GWAS) have identified only a small number of loci associated with sex hormone levels, with several reproductive hormones yet to be assessed. The aim of the study was to identify novel genetic variants contributing to the regulation of sex hormones. We performed GWAS using genotypes imputed from the 1000 Genomes reference panel. The study used genotype and phenotype data from a UK twin register. We included 2913 individuals (up to 294 males) from the Twins UK study, excluding individuals receiving hormone treatment. Phenotypes were standardised for age, sex, BMI, stage of menstrual cycle and menopausal status. We tested 7 879 351 autosomal SNPs for association with levels of dehydroepiandrosterone sulphate (DHEAS), oestradiol, free androgen index (FAI), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, progesterone, sex hormone-binding globulin and testosterone. Eight independent genetic variants reached genome-wide significance (P<5 × 10−8), with minor allele frequencies of 1.3–23.9%. Novel signals included variants for progesterone (P=7.68 × 10−12), oestradiol (P=1.63 × 10−8) and FAI (P=1.50 × 10−8). A genetic variant near the FSHB gene was identified which influenced both FSH (P=1.74 × 10−8) and LH (P=3.94 × 10−9) levels. A separate locus on chromosome 7 was associated with both DHEAS (P=1.82 × 10−14) and progesterone (P=6.09 × 10−14). This study highlights loci that are relevant to reproductive function and suggests overlap in the genetic basis of hormone regulation. 相似文献
970.
The gene responsible for Clouston hidrotic ectodermal dysplasia maps to the pericentromeric region of chromosome 13q 总被引:4,自引:0,他引:4
Kibar Z; Der Kaloustian VM; Brais B; Hani V; Fraser FC; Rouleau GA 《Human molecular genetics》1996,5(4):543-547
Hidrotic ectodermal dysplasia (HED), Clouston type, is an autosomal
dominant skin disorder which is most common in the French-Canadian
population and is characterized by hair defects, nail dystrophy and
palmoplantar hyperkeratosis. Biophysical and biochemical studies conducted
in HED suggested a molecular abnormality of keratins. We tested eight
French-Canadian families segregating HED for linkage to microsatellite
markers flanking the known keratin genes and were able to exclude linkage
to these loci. Therefore, a genome-wide search for the HED gene was
initiated. The first lod score above 3.00 was obtained with the marker
D13S175 located in the pericentromeric region of chromosome 13q (Zmax =
8.12 at zero recombination). The cumulative lod scores were above 3.00 for
six other markers in the region. A multipoint linkage analysis using the
markers D13S175, D13S141 and D13S143 gave a maximum lod score of 11.12 at
D13S141 with the one-lod- unit support interval spanning a 12.7 cM region
which includes D13S175 and D13S141. Haplotype analysis allowed us to
establish D13S143 as the telomeric flanking marker for the HED candidate
region.
相似文献