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排序方式: 共有324条查询结果,搜索用时 15 毫秒
101.
TR Villa AR Correa Moutran LA Sobirai Diaz MM Pereira Pinto FA Carvalho AA Gabbai & D de Souza Carvalho 《Cephalalgia : an international journal of headache》2009,29(6):631-634
The aim of this study was to evaluate the visual attention of children with migraine and compare it with a control group. Thirty migrainous children and 30 controls without headache were subjected to a visual attention assessment with Trail Making Tests (TMT) A/B, Letter Cancellation Test, and the Brazilian computerized test Visual Attention Test, third edition. The migraine group was evaluated after 2 days without headache. The migraine group had an inferior performance compared with the control group on TMT A ( P = 0.03) and B ( P = 0.001), and more errors on tasks 1 ( P = 0.032) and 2 ( P = 0.015) of the Visual Attention Test, presenting difficulty with selective and alternate attention. Attention is a neurological function that depends on structures such as the brainstem, cerebral cortex and the limbic system and on neurotransmitters such as dopamine and noradrenaline. The neurochemical aspects involved in the physiopathology of migraine and attention mechanisms probably predispose these children to visual attention deficits. 相似文献
102.
103.
Lipoplatin, a liposomal formulation of cisplatin, was developed with almost negligible nephrotoxicity, ototoxicity and neurotoxicity, as demonstrated in preclinical and Phase I human studies. A polyethylene-glycol coating of the liposome nanoparticles is supposed to result in tumor accumulation of the drug by extravasation through the altered tumor vasculature. We explored the hypothesis that intravenous infusion of Lipoplatin results in tumor targeting in four independent patient cases (one with hepatocellular adenocarcinoma, two with gastric cancer and one with colon cancer) who underwent Lipoplatin infusion followed by a prescheduled surgery approximately 20 h later. Direct measurement of the platinum levels in specimens from the excised tumors and normal tissues showed that the total platinum levels were on average 10-50 times higher in malignant tissue compared to the adjacent normal tissue specimens; most effective targeting was observed in colon cancer, with an accumulation up to 200-fold higher in colon tumors compared to normal colon tissue. Of the several surgical specimens, gastric tumors displayed the highest levels of total platinum suggesting Lipoplatin as a candidate anticancer agent for gastric tumors; gastric tumor specimens had up to 260 micrograms platinum /g tissue, that was higher than any tissue level in animals treated at much higher doses. Fat tissue displayed a high accumulation of total platinum in surgical specimens in three different patients, correlating to the lipid capsule of cisplatin in its Lipoplatin formulation. It was also inferred that normal tissue had more platinum trapped in the tissue but not reacted with macromolecules, whereas tumor tissue displayed platinum that reacted with cellular macromolecules; the data were consistent with a model where Lipoplatin damages more tumor compared to normal cells. In conclusion, Lipoplatin has the ability to preferentially concentrate in malignant tissue both of primary and metastatic origin following intravenous infusion to patients. In this respect, Lipoplatin emerges as a very promising drug in the arsenal of chemotherapeutics. 相似文献
104.
Tenière P Songne K Frebourg T Moguelet P Foulatier O Michot F Le Pessot F Le Blanc I Scotte M 《Gastroentérologie clinique et biologique》2002,26(11):1047-1050
We report two cases of familial juvenile polyposis coli. SMAD4 gene mutation was found in our two patients, leading to the definite diagnosis. Colonic cancer occurred in the first patient. Long-term outcome was favorable after colectomy. In the second patient, prophylactic total colectomy was performed. Rectal bleeding, diarrhea, stomach obstruction and vomiting developed during the follow-up. Proctectomy, distal partial gastrectomy and total gastrectomy were successively performed. 相似文献
105.
Comparison of pulmonary and pleural responses of rats and hamsters to inhaled refractory ceramic fibers 总被引:1,自引:1,他引:0
Gelzleichter TR; Bermudez E; Mangum JB; Wong BA; Janszen DB; Moss OR; Everitt JI 《Toxicological sciences》1999,49(1):93-101
The present study was designed to determine whether pleural fiber burdens
or subchronic pleural fibroproliferative and inflammatory changes can help
explain the marked interspecies differences in pleural fibrosis and
mesothelioma that are observed following long-term inhalation of RCF-1
ceramic fibers by rats and hamsters. Fischer 344 rats and Syrian golden
hamsters were exposed to RCF-1 for 4 h per day, 5 days per week, for 12
consecutive weeks. Lung and pleural fiber burdens were characterized during
and after exposure. For all time points, approximately 67% of fibers
associated with lung tissues from both rats and hamsters were longer than 5
microns in length. In comparison, fibers longer than 5 microns recovered
from the pleural compartment, following a 12-week exposure and 12 weeks of
recovery, accounted for 13% (hamsters) and 4% (rats) of the distribution.
In the 12 weeks after the cessation of exposure, the number of fibers
longer than 5 microns in length remained constant in the hamster at
approximately 150 fibers per cm2 pleura. This was 2 to 3 times the
corresponding fiber surface density in the rat. Significant pulmonary and
pleural inflammation was detected at all time points and for both species.
DNA synthesis by pleural mesothelial cells was quantified by
bromodeoxyuridine uptake following 3 days of labeling. Labeling indices
were higher in hamsters than in rats, both for RCF-1-exposed and filtered
air-control animals and was highest for the parietal surface of the pleura.
Significantly greater collagen deposition was measured in the visceral
pleura of hamsters 12 weeks post-exposure but was not significantly
elevated in rats. These findings demonstrate that subchronic inhalation
exposure to RCF-1 induces pleural inflammation, mesothelial-cell turnover,
pleural fibrosis, and an accumulation of fibers with a length greater than
5 microns in the hamster. The accumulation of long fibers in the pleural
space may contribute to the pathology observed in the hamster following
chronic inhalation of RCF- 1, whereas the presence of short, thin fibers
may play a role in the acute-phase biological response seen in both
species.
相似文献
106.
Metabolism of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) by human cytochrome P4501B1 总被引:1,自引:1,他引:1
Cytochrome P4501B1 (CYP1B1) is the most recently identified member of the
dioxin-inducible CYP1 family. CYP1B1 is constitutively expressed in most
human tissues, including colon and breast, and can activate numerous
chemically diverse carcinogens. We evaluated the metabolism of the dietary
heterocyclic amine carcinogen 2-amino-1-methyl-6-
phenylimidazo[4,5-b]pyridine (PhIP) by microsomes from yeast expressing the
human CYP1B1 protein. PhIP metabolites were analysed by HPLC with
fluorescence and absorbance detection. We found that human CYP1B1
metabolizes PhIP to three products: N2-OH-PhIP, a mutagenic activation
product; 4'-OH-PhIP, a detoxification product; and 2-OH-PhIP, the mutagenic
potential of which is unknown. Metabolite identity was confirmed by
co-elution with authentic standards and synchronous fluorescence
spectroscopy. The identity of the 2-OH-PhIP standard was additionally
confirmed by mass spectrometry. Kinetic studies of the formation of
N2-OH-PhIP, 4'-OH-PhIP and 2-OH-PhIP by CYP1B1 indicated apparent Km values
of 5.7 +/- 1.3, 2.2 +/- 0.5 and 1.3 +/- 0.2 microM, respectively. Apparent
turnover rates were 0.40 +/- 0.03, 0.93 +/- 0.02 and 0.04 +/- 0.00 nmol
product/min nmol P450, respectively. At saturating levels of substrate,
CYP1B1-mediated formation of the non- mutagenic metabolite 4'-OH-PhIP was
favored two-fold over that of the mutagenic metabolite, N2-OH-PhIP and
>10-fold over that of 2-OH-PhIP. The formation of N2-OH-PhIP, a potent
mutagen implicated in the etiology of human colon and breast cancer,
indicates that CYP1B1 may play an important role in PhIP-mediated
carcinogenesis.
相似文献
107.
108.
McCormick DL; Ryan BM; Findlay JC; Gauger JR; Johnson TR; Morrissey RL; Boorman GA 《Carcinogenesis》1998,19(9):1649-1653
The results of a number of epidemiology studies suggest that exposure to
power frequency (50 and 60 Hz) magnetic fields may be a risk factor for
hematopoietic neoplasia. To generate experimental data to test this
hypothesis, the influence of magnetic field exposure on lymphoma induction
was determined in two strains of mice that are genetically predisposed to
the disease. PIM mice, which carry the pim-1 oncogene, are highly sensitive
to lymphoma induction by N-ethyl-N-nitrosourea (ENU); ENU-treated PIM mice
were studied as a 'high incidence' lymphoma model. TSG-p53 (p53 knockout)
mice, in which the p53 tumor suppressor gene has been deleted from the germ
line, develop lymphoma as an age- related change; hemizygous TSG-p53 mice
were studied as a 'low incidence' lymphoma model. Beginning 1 day after a
single i.p. injection of 25 mg ENU/kg body wt, groups of 30 PIM mice/sex
were exposed for 18.5 h/day to pure, linearly polarized, transient-free 60
Hz magnetic fields at field strengths of 0 (sham control), 0.02, 2.0 or
10.0 Gauss (G). An additional group of 30 PIM mice/sex was exposed
intermittently (1 h on, 1 h off) to 10.0 G fields. Groups of 30 TSG-p53
mice/sex were exposed continuously to magnetic field strengths of 0 (sham
control) or 10.0 G; TSG-p53 mice received no ENU. Studies were terminated
after 23 weeks of magnetic field exposure. Lymphoma incidence in male PIM
mice exposed continuously to 10.0 G magnetic fields was significantly
reduced from that seen in sex-matched sham controls; survival, lymphoma
incidence and lymphoma latency in other groups of PIM mice did not differ
from sham controls. Survival and lymphoma incidence in all groups of
TSG-p53 mice was 7% or less, regardless of magnetic field exposure regimen.
These data do not support the hypothesis that exposure to magnetic fields
is a significant risk factor for lymphoid neoplasia in mice with a genetic
predisposition to the disease.
相似文献
109.
Deletion/insertion mutation that causes biotinidase deficiency may result from the formation of a quasipalindromic structure 总被引:2,自引:0,他引:2
Pomponio RJ; Narasimhan V; Reynolds TR; Buck GA; Povirk LF; Wolf B 《Human molecular genetics》1996,5(10):1657-1661
Biotinidase is responsible for recycling the vitamin biotin from biocytin
that is formed after the proteolytic degradation of the biotin- dependent
carboxylases. We have identified a deletion/insertion mutation within exon
D of the human biotinidase gene in a child with biotinidase deficiency. The
mutation causes a frame shift and premature termination which are predicted
to result in a truncated protein. We propose that the mutation occurred
during DNA replication by either of two mechanisms. Both mechanisms involve
formation of a quasipalindromic hairpin loop in the template and
dissociation of DNA polymerase alpha. This mutation supports the formation
of palindromic structures as a possible cause of deletions in eukaryotes,
and supports the proposal, derived from in vitro studies, that polymerase
alpha may preferentially arrest or dissociate at specific template
sequences.
相似文献
110.