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71.
72.
Cell cycle arrest, apoptosis and p53 expression in nickel(II) acetate- treated Chinese hamster ovary cells 总被引:5,自引:1,他引:4
Nickel(II) compounds are known human and animal carcinogens. In this study,
the effects of nickel(II) acetate on cell cycle, apoptosis and p53
expression were investigated in order to unveil the elements of early
cellular responses to the metal. Chinese hamster ovary (CHO) cells were
grown for 72 h in Ham's F-12 medium containing 0, 40, 80, 160, 240, 320,
480 or 640 microM nickel(II) acetate. DNA fragmentation, representative of
apoptosis, was examined by agarose gel electrophoresis. The distribution of
cells among various phases of cell cycle was determined by DNA flow
cytometry. Expression of p53 protein was measured by the Western blotting
technique. DNA fragmentation was detectable in cells treated with > or =
160 microM nickel(II) and its intensity increased with increasing
nickel(II) concentration. The proportion of cells at S phase declined in a
nickel(II) concentration- dependent manner. The decline was accompanied by
an increase of cell proportion in G2/M phase and the increase became
statistically significant in cells exposed to at least 480 microM
nickel(II). Expression of p53 protein was not different from that in the
control among samples treated with < or = 480 microM nickel(II).
However, an extra fraction that migrated close to the p53 protein fraction
was detected in cells treated with 640 microM nickel(II). Our findings
suggest that nickel(II) modulates cellular response through effectors
involved in both G2/M arrest and apoptosis regulatory pathways. The
proportion of cells arrested at G2/M phase or undergoing apoptosis depends
directly on nickel(II) concentration. High concentration of nickel(II)
appears to up-regulate protein(s) other than the common form of p53
protein.
相似文献
73.
74.
Liu JM; Chu HC; Chin YH; Chen YM; Hsieh RK; Chiou TJ; Whang-Peng J 《Japanese journal of clinical oncology》1997,27(1):37-41
The aim of this study was to ascertain the prevalence of alternative
medicine consumption in Chinese cancer patients on active conventional
treatment. A cross sectional survey of 100 consecutive advanced cancer
patients admitted to a cancer clinical trial referral unit were personally
interviewed by their assigned oncology research nurse using a specially
designed questionnaire. The results showed that 64% of our patients used
indigenous Chinese medication. In all age groups except the over-70s (P =
0.043), > 50% took such medication, more female (76%) than male (57.6%)
patients (P = 0.323). Patients of all educational levels (P = 0.062) and
religious backgrounds (P = 0.08) consumed alternative medicines. Duration
of alternative medication consumption was less than three months in 50% of
patients, with costs between US$40 and 2000/month for 70% of patients.
Reasons cited for alternative medication consumption was hope that it might
be of some benefit to their well being or disease control, and maybe even
result in a miracle cure. Sources of advice on medication were mostly from
strangers (by word of mouth), family, friends, the media, and infrequently
from qualified professional Chinese doctors. Reasons for discontinuing such
treatment were mostly given as lack of positive effect. In conclusion,
Chinese cancer patients, willingly, rampantly and non-selectively seek out
and consume alternative medications, with almost total ignorance of the
medication consumed, oblivious to any potential side effects, and with
little subjective benefit.
相似文献
75.
The E6 and E7 genes of HPV-16 or HPV-18 both are necessary for effective
immortalization of primary human genital keratinocytes. To analyse the
individual role of E6 and E7 genes in dysregulating cell growth, we cloned
the HPV-16 E6, E7 and E6/E7 genes into retroviruses. Primary human
keratinocytes (PHK) were then infected with these retroviruses and selected
in differentiation-inducing medium (high calcium and serum). The E6/E7
retroviruses were the most effective at inducing differentiation-resistant
colonies. Intermediate numbers of colonies were induced by E6 and low
numbers by E7. Interestingly, only cultures infected with E7 and E6/E7
retroviruses showed a significant proportion of cells progressing into the
S phase, consistent with our earlier studies showing that E7 is required
for the efficient immortalization of genital keratinocytes. Accompanying
this entry into S phase, the E7 or E6/E7 transduced cells expressed high
levels of cyclins A, B and E, but lower levels of cyclin D. In addition,
cdc-2, cdk-2 and cdk-4 were also increased. No significant differences were
detected in the expression of c-myc and c-fos between the vector and any of
the transduced cells. Keratinocytes infected with the E7 retrovirus
exhibited decreased levels of Rb protein and increased levels of p53,
whereas cells infected with E6-expressing retroviruses displayed normal
levels of Rb protein and decreased levels of p53. Finally, E7 induced a
three-fold increase in bcl-2 expression. Our results indicate that the
HPV-16 E7 gene alone is sufficient to bypass keratinoctye growth arrest
induced by serum and calcium exposure and that the discordant expression of
several cell regulatory proteins accompanies this unregulated
proliferation.
相似文献
76.
77.
目的:观察烧成温度对多孔生物陶瓷制品孔结构、显气孔率与容重、水渗透率、收缩率以及压缩强度的影响。方法:实验于2002-09/2005-09在武汉理工大学生物中心和重庆邮电大学生物实验中心完成。采用可控多孔生物陶瓷制备技术,改变烧成温度,其他因素(如成型工艺、升温速度和保温时间等)不变,分别制得不同的样品;用电子扫描显微镜观察孔道和表面形貌;根据GB/T1964~1967-1996和GB/T1969~1970-1996测量显气孔率、容重;用自制水渗透率测定仪测定水渗透率;用体积法测定收缩率。用ASTM材料强度测试机测定压缩强度。结果:①烧成温度对孔结构的影响:在900℃以内时烧成温度的变化对大孔的影响不明显,仍然在500μm左右,但当烧成温度增加到1000℃,大孔变小到400μm左右。烧成温度的变化对小孔的影响比较明显,小孔明显增大,当烧成温度800℃增加到1000℃时,小孔从10μm左右增大到20~30μm左右。烧成温度的变化对微孔的影响也比较明显,小孔明显增大,当烧成温度800℃增加到1000℃时,小孔从4μm左右增大到6μm左右。②烧成温度对显气孔率及容重的影响:随着烧成温度的提高,样品的显气孔率下降幅度增大,容重的增加幅度增大。③烧成温度对水渗透率的影响:随着烧成温度的提高,样品的水渗透率下降幅度增大,容重的增加幅度增大。④不同烧成温度对收缩率的影响:随着烧成温度的提高,样品的收缩率增大。⑤烧成温度对压缩强度的影响:随着烧成温度的提高,压缩强度增大。而在800℃以后继续升温,压缩强度急剧增大。结论:烧成温度对孔结构、显气孔率与容重、水渗透率、收缩率以及压缩强度有着重要的影响,为了保证成品有较好的孔结构、较高的显气孔率的同时具有一定的机械强度,烧成温度选择在850℃左右较佳。 相似文献
78.
79.
Anatomy of the minor fissure: evaluation with thin-section CT 总被引:2,自引:0,他引:2
80.
目的:观察局灶性脑缺血大鼠脑内生长相关蛋白43表达与滋补肝肾中药合剂干预效果的关系。方法:实验于2004-06/2005-06在山东大学医学院药理实验室、山东中医药大学中西医结合肿瘤防治中心实验室完成。雄性Wistar大鼠49只按随机数字表法随机分为假手术组、模型组(分设1,2,3周时间点)、中药组(分设1,2,3周时间点),每组7只。模型组与中药组进行右侧近端大脑中动脉电凝术造成大鼠局灶性脑缺血模型,假手术组行同样开颅术,但不凝闭大脑中动脉,其余操作同模型组。于造模成功后第6天起中药组灌胃给予滋补肝肾中药复方,剂量为9g/(kg·d),余2组分别灌胃给予同等量生理盐水,1次/d。假手术组大鼠于术后1周时麻醉下断头处死,模型组与中药组分别于给药1,2,3周时处死,取材后用免疫组化法观察局灶性脑缺血大鼠脑内生长相关蛋白的表达。结果:纳入大鼠49只,造模不成功或死亡14只,最后每组5只共35只大鼠进入结果分析。模型组生长相关蛋白阳性信号密度值在给药1周、2周及3周组与假手术组比较差异均无显著性意义[(15.7±1.4)%,(15.3±1.3)%,(15.4±1.1)%,(15.1±1.3)%,P>0.05];中药组在治疗1周后生长相关蛋白阳性信号密度值较假手术组及模型组差异尚无显著性,但2周及3周组表达显著增强,与模型组和假手术组比较,差异有显著性意义[(23.4±1.3)%,(24.1±1.4)%,P<0.01]。结论:滋补肝肾中药复健片能增强局灶性脑缺血大鼠脑内生长相关蛋白43的表达,从而促进缺血性脑卒中后的神经功能重塑。 相似文献