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To cite this article: Int J Dent Hygiene DOI: 10.1111/j.1601‐5037.2009.00398.xAl‐Haddad KA, Al‐Hebshi NN, Al‐Ak’hali MS. Oral health status and treatment needs among school children in Sana’a City, Yemen. Abstract: Data on the oral health status and treatment needs among Yemeni children are lacking. Objectives: To assess caries prevalence, treatment needs and gingival health status among school children in Sana’a City and to examine how these are affected by age, gender and khat chewing. Methods: 1489 children (6‐ to 14‐year old) were randomly selected from 27 schools representing all nine districts of Sana’a City. Dental caries and treatment needs were evaluated using standard WHO oral survey methods. The plaque index (PI), calculus index (CI) and the gingival index (GI), recorded at the six Ramfjord’s teeth, were used to assess gingival health status. Results: 4.1% of the study subjects were caries‐free. Prevalence of these was significantly higher among the males. Overall, mean dmfs, dmft, DMFS and DMFT scores were 8.45, 4.16, 3.59 and 2.25 respectively. The decayed component accounted for >85% of the scores. The highest dmfs/dmft means were found among the 6–8 years age group, while the highest DMFS/DMFT means were scored by the 12–14 years age group. The need for restorative treatment and extractions was high; the former was significantly higher among the females. All subjects had gingivitis; the mean PI, CI and GI were 1.25, 0.3 and 1.36 respectively. Khat chewing did not affect caries experience; however, it was significantly associated with higher PI, CI and GI scores. Conclusions: The prevalence of caries, gingivitis and treatment needs among children in Sana’a city is high. More surveys in other Yemeni cities to generate comprehensive data are required. 相似文献
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The human autosomal gene DAZLA: testis specificity and a candidate for male infertility 总被引:5,自引:1,他引:5
The DAZ (Deleted in AZoospermia) and DAZLA (DAZ-like autosomal) genes may
be determinants of male infertility. The DAZ gene on the long arm of the
human Y chromosome is a strong candidate for the 'azoospermia factor'
(AZF). Its role in spermatogenesis is supported by its exclusive expression
in testis, its deletion in a high percentage of males with azoospermia or
severe oligospermia, and its homology with a Drosophila male infertility
gene boule. No DAZ homologous sequences have been found on the mouse Y
chromosome. Instead, a Dazla gene was isolated from mouse chromosome 17 and
has been considered to be a murine homologue of DAZ. However, the homology
between human DAZ and mouse Dazla is not strong, and Dazla contains only
one of the seven DAZ repeats found in DAZ. We report the isolation of the
human DAZLA gene by screening a human testis cDNA library with a DAZ cDNA
clone. DAZLA encodes only one DAZ repeat and shares high homology with the
mouse Dazla, indicating that these two genes are homologues. Using a panel
of rodent-human somatic cell lines and fluorescence in situ hybridization,
the DAZLA gene was mapped to 3p24, a region not known to share homology
with mouse chromosome 17. The DAZLA gene may be involved in some familial
cases of autosomal recessive male infertility.
相似文献
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Amplification of EIF3S3 Gene Is Associated with Advanced Stage in Prostate Cancer 总被引:6,自引:0,他引:6 下载免费PDF全文
Outi Saramki Niels Willi Ola Bratt Thomas C. Gasser Pasi Koivisto Nina N. Nupponen Lukas Bubendorf Tapio Visakorpi 《The American journal of pathology》2001,159(6):2089-2094
Gain of the long arm of chromosome 8 (8q) is one of the most common gains found in the advanced prostate cancer by comparative genomic hybridization. We have previously identified a putative target gene for the 8q gain, EIF3S3, that encodes a p40 subunit of eukaryotic translation initiation factor 3 (eIF3). Here, we studied the frequency of the EIF3S3 amplification in different stages of prostate cancer and co-amplification of EIF3S3 and oncogene MYC. In addition, prognostic utility of the EIF3S3 copy number alteration was evaluated. The analyses were done with fluorescence in situ hybridization and tissue microarray technology. High-level amplification of EIF3S3 was found in 11 of 125 (9%) of pT1/pT2 tumors, 12 of 44 (27%) of pT3/pT4 tumors, and 8 of 37 (22%) of lymph node metastases as well as in 26 of 78 (33%) and 15 of 30 (50%) of hormone refractory locally recurrent tumors and metastases, respectively. The amplification was associated with high Gleason score (P < 0.001). One of the 79 tumors with EIF3S3 amplification had only two copies of MYC, whereas all tumors with amplification of MYC had also amplification of EIF3S3 indicating common co-amplification of the genes. Gain of EIF3S3 was associated with poor cancer-specific survival in incidentally found prostate carcinomas (P = 0.023). In the analyses of prostatectomy-treated patients, the amplification was not statistically significantly associated with progression-free time. In conclusion, amplification of EIF3S3 gene is common in late-stage prostate cancer suggesting that it may be functionally involved in the progression of the disease. 相似文献
76.
Genetic Aberrations in Hypodiploid Breast Cancer : Frequent Loss of Chromosome 4 and Amplification of Cyclin D1 Oncogene 总被引:1,自引:2,他引:1 下载免费PDF全文
Minna M. Tanner Ritva A. Karhu Nina N. Nupponen ke Borg Bo Baldetorp Tanja Pejovic Mrten Fern Dick Killander Jorma J. Isola 《The American journal of pathology》1998,153(1):191-199
The evolution of somatic genetic aberrations in breast cancer has remained poorly understood. The most common chromosomal abnormality is hyperdiploidy, which is thought to arise via a transient hypodiploid state. However, hypodiploidy persists in 1 to 2% of breast tumors, which are characterized by a poor prognosis. We studied the genetic aberrations in 15 flow cytometrically hypodiploid breast cancers by comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). Surprisingly, numerous copy number gains were detected in addition to the copy number losses. The number of gains per tumor was 4.3 ± 3.2 and that of losses was 4.5 ± 3.3 (mean ± SD), which is similar to that previously observed in hyperdiploid breast cancers. Gains at chromosomes or chromosomal regions at 11q13, 1q, 19, and 16p and losses of 2q, 4, 6q, 9p, 13, and 18 were most commonly observed. Compared with unselected breast carcinomas, hypodiploid tumors showed certain differences. Loss of chromosome 4 (53%) and gain of 11q13 (60%) were significantly more common in hypodiploid tumors. The gain at 11q13 was found by FISH to harbor amplification of the Cyclin D1 oncogene, which is therefore three to four times more common in hypodiploid than in unselected breast cancers (15 to 20%). Structural chromosomal aberrations (such as Cyclin D1 amplification) were present both in diploid and hypodiploid tumor cell populations, as assessed by FISH and CGH after flow cytometric sorting. Together these results indicate that hypodiploid tumors form a distinct genetic entity of invasive breast cancer, although they probably share a common genetic evolution pathway where structural chromosomal aberrations precede gross DNA ploidy changes. 相似文献
77.
Conway GS; Payne NN; Webb J; Murray A; Jacobs PA 《Human reproduction (Oxford, England)》1998,13(5):1184-1187
We have screened 132 women with premature ovarian failure for fragile X
(FRAXA) premutations. Three out of 23 (13%) pedigrees with the familial
premature ovarian failure and 3/106 (3%) of women with the sporadic form of
premature ovarian failure have FRAXA premutations compared with an expected
prevalence of 1:590 (P=0.02). The mechanism of the association between
FRAXA premutations and premature ovarian failure is unknown but as a
genetic marker, FRAXA screening will be particularly valuable in predicting
premature ovarian failure in some pedigrees and in the identification of
families at risk of transmitting fragile X syndrome.
相似文献
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