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881.
Procalcitonin and C-reactive protein levels in neonatal infections 总被引:17,自引:0,他引:17
G Monneret JM Labaune C Isaac F Bienvenu G Putet J Bienvenu 《Acta paediatrica (Oslo, Norway : 1992)》1997,86(2):209-212
In order to assess the potential of procalcitonin measurement in the management of neonatal sepsis, daily variations in serum procalcitonin (measured by an immunoluminometric assay) were evaluated in 94 control and infected newborn infants in comparison to C-reactive protein (measured by an immunonephelometric method). High levels of procalcitonin correlated with bacterial invasion and showed no discrepancies with C-reactive protein. Procalcitonin increased (up to 400 μg 1-1 ) and returned to the normal range (< 0.1 g1-1 ) more quickly than C-reactive protein, suggesting that procalcitonin may be an early marker of favourable outcome. Another finding is a significant procalcitonin peak on the first day of life in the control group, independent of any infectious stimulus. In conclusion, procalcitonin seems to be an interesting marker of neonatal sepsis but additional investigations are needed to understand better its mechanism of synthesis in order to determine its clinical usefulness. 相似文献
882.
ML Harries JM Walker DM Williams S Hawkins IA Hughes 《Archives of disease in childhood》1997,77(5):445-447
The changes in the male voice in relation to the biological characteristics of puberty were assessed longitudinally in 26 boys. Speaking and singing fundamental frequencies were analysed in relation to the Tanner staging of puberty, saliva testosterone levels, and the Cooksey classification of voice analysis. There were abrupt changes in voice characteristics between Tanner stages G3 and G4 and more gradually from stages C3 to C5 of Cooksey. Although testosterone concentrations were not predictive of the changes, there was a correlation with testis volume. Voice fundamental frequencies were seen to change abruptly in late puberty, in contrast with previous studies. There is a good correlation between the Tanner and Cooksey methods of classification during male puberty. 相似文献
883.
M Shrinath JH Walter M Haeney JM Couriel MA Lewis AL Herrick 《Archives of disease in childhood》1997,76(5):441-444
The case is reported of an infant with hyperammonaemia secondary to severe distal renal tubular acidosis. A clinical association between increased concentrations of ammonia in serum and renal tubular acidosis has not previously been described. In response to acidosis the infant's kidneys presumably increased ammonia synthesis but did not excrete ammonia, resulting in hyperammonaemia. The patient showed poor feeding, frequent vomiting, and failure to thrive, but did not have an inborn error of metabolism. This case report should alert doctors to consider renal tubular acidosis in the differential diagnosis of severely ill infants with metabolic acidosis and hyperammonaemia. 相似文献
884.
OBJECTIVES: To identify problems in managing asthmatic children in school, which if dealt with would help reduce absenteeism and improve participation in school activities. DESIGN: A survey by questionnaire to headteachers. SETTING: Schools in Merthyr and Rhondda Cynon Taff, South Wales. SUBJECT: Asthmatic schoolchildren in areas studied. MAIN OUTCOME MEASURES: Facilities in schools to manage asthma, headteachers' perceptions of knowledge of asthma management by teachers, possession of written policies, and desire for further training. RESULTS: There are 216 schools in the area studied, with 55,166 schoolchildren. A total of 191 (88%) headteachers returned the completed questionnaire. Five hundred and twenty seven (17%) children were reported absent from school during one term because of asthma, with an average of nine days of schooling lost per asthmatic child per term (range 2-16 days). Only 76 (40%) schools allowed children to be responsible for their inhalers, and 12 (6%) schools required parents to administer inhalers. In 115 (60%) schools, headteachers believed their staff were familiar with the management of asthma. A total of 174 (91%) headteachers expressed interest in further training. CONCLUSION: This study highlights the need to train teachers and provide an agreed joint education and health policy on managing asthma in school. 相似文献
885.
JM Davis WN Rosenfeld SE Richter MR Parad IH Gewolb AR Spitzer WA Carlo RJ Couser A Price E Flaster N Kassem L Edwards J Tierney S Horowitz 《Pediatrics》1997,100(1):24-30
OBJECTIVES: To examine the safety and pharmacokinetics of multiple intratracheal (IT) doses of recombinant human CuZn superoxide dismutase (rhSOD) in premature infants with respiratory distress syndrome who are at risk for developing bronchopulmonary dysplasia (BPD). Methods. Thirty-three infants (700 to 1300 g) were randomized and blindly received saline, 2.5 mg/kg or 5 mg/kg rhSOD IT within 2 hours of surfactant administration. Infants were treated every 48 hours (as long as endotracheal intubation was required) up to 7 doses. Serial blood and urine studies, chest radiographs, neurosonograms, SOD concentration and activity measurements, and tracheal aspirate (TA) inflammatory markers were assessed throughout the 28-day study. RESULTS: SOD concentrations in serum (0.1 [0.05/0.15] microg/mL-geometric mean with lower/upper confidence intervals), tracheal aspirates (TA) (0.2 [0.1/0.3] microg/mL) and urine (0.3 [0.2/0.4] microg/mL) were similar at baseline in all 3 groups and did not change significantly in the placebo group. In the rhSOD treatment groups, SOD concentrations were increased on day 3 and did not change significantly thereafter over the 14-day dosing period (also measured on days 5, 7, and 13). SOD concentrations averaged 0.4 [0.3/0.5] microg/mL in serum, 0.8 [0.6/1.2] microg/mL in TA and 1.1 [1.0/1.3] microg/mL in urine for the low-dose group and 0.6 [0.5/0.7] microg/mL in serum, 1.1 [0.9/1.5] microg/mL in TA, and 2.2 [1.6/2.9] microg/mL in urine for the high-dose group over the 14-day dosing period. Enzyme activity directly correlated with SOD concentration and rhSOD was active even when excreted in urine. TA markers of acute lung injury (neutrophil chemotactic activity, albumin concentration) were lower in the rhSOD agroups compared with placebo. No significant differences in any clinical outcome variable were noted between groups. CONCLUSIONS: These data indicate that multiple IT doses of rhSOD increase the concentration and activity of the enzyme in serum, TA and urine, reduce TA lung injury markers and are well-tolerated. Further clinical trials examining the efficacy of rhSOD in the prevention of BPD are warranted. 相似文献
886.
Verghis SB; Essigmann JM; Kadlubar FF; Morningstar ML; Lasko DD 《Carcinogenesis》1997,18(12):2403-2414
Mutagenesis by the human bladder carcinogen 4-aminobiphenyl (ABP) was
studied in single-stranded DNA from a bacteriophage M13 cloning vector. In
comparison to ABP lesions in double-stranded DNA, lesions in single-
stranded DNA were approximately 70-fold more mutagenic and 50-fold more
genotoxic. Sequencing analysis of ABP-induced mutations in the lacZ gene
revealed exclusively base-pair substitutions, with over 80% of the
mutations occurring at G sites; the G at position 6310 accounted for 25% of
the observed mutations. Among the sequence changes at G sites, G- ->T
transversions predominated, followed by G-->C transversions and G--
>A transitions. In order to further elucidate the mutagenic mechanism of
ABP, an oligonucleotide containing the major DNA adduct, N-
(deoxyguanosin-8-yl)-4-aminobiphenyl (dG(8-ABP)), was situated within the
PstI site of a single-stranded M13 genome. After in vivo replication of the
adduct containing ABP-modified and control (unadducted) genomes, the
mutational frequency and mutational specificity of the dG(8-ABP) lesion
were determined. The targeted mutational efficiency was approximately
0.01%, and the primary mutation observed was the G-->C transversion.
Thus dG(8-ABP), albeit weakly mutagenic at the PstI site, can contribute to
the mutational spectrum of ABP lesions.
相似文献
887.
A series of promoting and non-promoting barbiturates and hydantoins were
examined for their ability to sustain the growth of a phenobarbital
(PB)-dependent hepatocyte line in cell culture. The effective liver tumor
promoters, pentobarbital, allobarbital and 5- ethyl-5-phenylhydantoin,
replaced PB and supported 6/27C1 hepatocyte colony formation in vitro at
52-87% of the level induced by PB. The weak promoters secobarbital and
amobarbital supported colony formation at only 11-19% of the PB control. A
significant correlation was observed for in vivo and in vitro promotion
activities of barbiturates and hydantoins, indicating that clonal expansion
by 6/27C1 hepatocytes was promoter-dependent. Cell density also appeared to
influence hepatocyte growth in vitro. Hepatocyte colonies acquired the
ability to grow in the absence of PB, such that after 10 days incubation
with PB, approximately 50% of colonies continued to grow in the absence of
promoter. This phenomenon of clone-size-dependent hepatocyte growth
suggested the operation of an autocrine growth factor pathway. Addition of
the hepatocyte mitogen and autocrine growth factor, transforming growth
factor-alpha (TGF-alpha), to culture medium lacking PB induced a
dose-dependent increase in 6/27C1 hepatocyte colony formation. At the
optimal concentration of 3 ng/ml, TGF-alpha sustained hepatocyte clonal
expansion at 84% of the level induced by 2 mM PB. Individual 6/27C1
colonies that grew from single cells in the presence of TGF-alpha were
tested for promoter-dependent colony formation. Either PB or TGF-alpha
supported colony formation by these cells at similar levels and when
combined at optimal concentrations, the response appeared to be saturated.
When these factors were tested in combination at suboptimal concentrations,
the two compounds were additive for supporting colony formation by the
parental 6/27C1 line. The ability of TGF-alpha to replace PB and sustain
hepatocyte clonal expansion was confirmed with the tumorigenic 6/15
hepatocyte line. These results suggest that TGF- alpha and PB may promote
hepatocarcinogenesis by stimulating a common signal transduction pathway.
相似文献
888.
Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) polymorphisms and lung cancer risk among Northwestern Mediterraneans 总被引:7,自引:1,他引:7
To-Figueras J; Gene M; Gomez-Catalan J; Galan MC; Fuentes M; Ramon JM; Rodamilans M; Huguet E; Corbella J 《Carcinogenesis》1997,18(8):1529-1533
Several polymorphic genes including those encoding for glutathione S-
transferases (GST) have been reported to be involved in modifying lung
cancer risk in smokers. The gene GSTM1 is frequently deleted in humans and
a possible association between the null genotype and lung cancer risk is
controversial. Another polymorphic gene of the same supergene family,
GSTT1, is also involved in the detoxification of some environmental
carcinogens. Both genes were genotyped in (a) a group of lung cancer
patients (n = 160); (b) a group of healthy smokers (n = 120); (c) a group
of blood donors from the general population (n = 192). All patients and
controls were Northwestern Mediterranean Caucasians. The results show that
the GSTM1 null genotype (GSTM1*0/GSTM1*0) was slightly over represented in
the lung cancer patients (frequency of 58%; OR: 1.40, 95% CI: 0.74-2.61,
referred to healthy smokers). The histological type most clearly modified
was small cell carcinoma (frequency of 62.2%, OR: 1.91, CI: 0.78-4.69). The
subdivision of the patients with one or two copies of the GSTM1 gene
according to a GSTM1*A, GSTM1*B or GSTM1*A/B genotype (frequencies of
28.2%, 11.2%, 2.5% respectively) revealed no significant differences
between the cases and both control groups. The frequency of the deleted
GSTT1 genotype among the lung cancer patients (24%) was not significantly
increased (OR: 1.08, CI: 0.57-2.05, referred to healthy smokers). The
results showed that 14.4% of the patients presented homozygous deletion of
both GSTT1 and GSTM1 (12.5% among healthy smokers) suggesting no
potentiation between null genotypes for lung cancer risk.
相似文献
889.
Influence of diets containing high and low risk factors for colon cancer on early stages of carcinogenesis in human flora-associated (HFA) rats 总被引:3,自引:2,他引:3
Hambly RJ; Rumney CJ; Cunninghame M; Fletcher JM; Rijken PJ; Rowland IR 《Carcinogenesis》1997,18(8):1535-1539
Germ-free rats colonised with a human intestinal flora were fed diets
containing high risk (HR) or low risk (LR) factors for colorectal cancer,
and putative biomarkers were evaluated in the colonic mucosa; (i)
proliferation, (ii) 1,2-dimethylhydrazine (DMH)-induced aberrant crypt foci
and (iii) DMH-induced DNA damage. The HR diet was high in fat (45% of
calories) and low in calcium and fibre, reflecting levels characteristic of
typical western diets. The LR diet was low in fat (<5% of calories), and
high in calcium and fibre. The nutrient/energy ratio of the two diets were
similar. Mucosal crypt cell proliferation, assessed after microdissection,
was higher on the LR diet (mean number of mitoses per crypt was 2.65 on the
LR diet, and 1.62 on the HR diet; P < 0.05). Aberrant crypt foci (ACF)
were assessed in the mucosa 12 weeks after DMH treatment. On the HR diet
there were significantly more small ACF with 1 and 2 crypts per focus, but
fewer ACF with 3, 5 and 7 or more crypts per focus. There was no
significant difference in total ACF or the total number of crypts. The
effect of diet on DNA damage in the colon was assessed in vivo by the comet
assay. Animals were fed a HR or LR diet for 12 weeks before treatment with
DMH or saline. For carcinogen-treated animals, DNA damage was significantly
higher in colon cells from animals on the HR diet. On the LR diet both DNA
damage and the induction of small ACF were reduced despite an increase in
cell proliferation. The increase in large ACF on the LR diet may be
attributable to elevated crypt cell proliferation possibly increasing crypt
fission rates.
相似文献
890.
Welters MJ; Maliepaard M; Jacobs-Bergmans AJ; Baan RA; Schellens JH; Ma J; van der Vijgh WJ; Braakhuis JM; Fichtinger-Schepman AM 《Carcinogenesis》1997,18(9):1767-1774
For the improvement of chemotherapy with platinum (Pt)-containing drugs a
sensitive assay to detect the induced Pt-DNA adducts is needed. Therefore,
the 32P-postlabelling assay, described by Blommaert and Saris (Nucleic
Acids Res., 1995, 23, 1300-1306), to detect the major adducts Pt-GG and
Pt-AG has substantially been improved and compared with ELISA and AAS. For
the quantification of the adducts, TpT was added as an internal standard
immediately after isolation of the Pt- adducts from digested DNA samples.
It was found that 32P-labelling of both GpG and ApG, the dinucleotides
obtained after deplatination of the adducts, was equally efficient as that
of TpT. To isolate the Pt- adducts on basis of a positive charge, the pH of
DNA digests was adjusted to approximately 3 prior to separation by strong
cation- exchange chromatography. For the subsequent deplatination a volume
of only 12 microl of 0.2 M NaCN was used, which did not interfere with the
following labelling step. The quantification of the 32P-labelled
dinucleotides was performed by phosphorimaging of spots after separation on
TLC as well as by 32P-counting of fractions collected after separation by
HPLC. The method was used to determine adduct levels in in vitro
cisplatin-treated DNA and in DNA isolated from cisplatin-treated cultured
cells, tumor xenografts from cisplatin- treated mice, and from white blood
cells and (tumor) tissues from cisplatin-treated patients. The results show
a significant correlation with the adduct levels as determined with atomic
absorption spectroscopy (high levels) or with specific antibodies (low
levels). This assay appears to be useful for the determination of low
levels of Pt-adducts in small DNA samples as present in clinical specimens
such as blood and tumor tissue, but also in buccal mucosal cells and fine
needle aspirates.
相似文献