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81.
82.
The right mid-lung window 总被引:1,自引:0,他引:1
Goodman LR; Golkow RS; Steiner RM; Teplick SK; Haskin ME; Himmelstein E; Teplick JG 《Radiology》1982,143(1):135
83.
6q deletions define distinct clinico-pathologic subsets of non- Hodgkin's lymphoma 总被引:11,自引:1,他引:11
Offit K; Parsa NZ; Gaidano G; Filippa DA; Louie D; Pan D; Jhanwar SC; Dalla- Favera R; Chaganti RS 《Blood》1993,82(7):2157-2162
Commonly observed in lymphoid neoplasms, deletions of 6q have been correlated with histologic and clinical subsets of non-Hodgkin's lymphoma (NHL). Our recent analysis of loss of heterozygosity of 6q loci in NHL showed two regions of minimal molecular deletion (RMD), an RMD1 at 6q25-27 and an RMD2 at 6q21-23. To establish correlations between these RMDs and regions of minimal cytogenetic deletions (RCDs) on 6q, and to define associations between RCDs and clinico-pathologic features, we have analyzed chromosome 6 abnormalities in 459 consecutively ascertained, karyotypically abnormal cases of NHL. Among these, 126 (27.5%) cases had structural abnormalities of chromosome 6, of which 94 were deletions. Analysis of these deletions identified three RCDs. An RCD1 encompassing 6q25-27 was seen in 45 intermediate- grade NHL. An RCD2 at 6q21 was observed in 11 high-grade NHL, 9 of which were of the immunoblastic subtype. An RCD3 at 6q23 was noted in 18 low-grade NHL lacking a t(14;18) translocation. Of these 18 cases, 12 were small lymphocytic NHL and, in 2 of these, del(6q) was the sole karyotypic abnormality. In 20 cases of low-grade NHL with t(14;18), the deletions spanned both RCD1 and RCD3. These data suggested the presence of at least 3 tumor suppressor genes on 6q within RCD1, RCD2, and RCD3; they also showed associations between RCDs in 6q and subsets of NHL, including a specific association between a group of well-differentiated lymphoid neoplasms and RCD3. The apparent heterogeneity of breakpoints when all NHLs are considered together explains the inability of previous studies to reliably establish correlations between recurring 6q deletions and histologic and clinical features of NHL. 相似文献
84.
A gradient in the duration of the G1 phase in the murine neocortical proliferative epithelium 总被引:2,自引:6,他引:2
Miyama S; Takahashi T; Nowakowski RS; Caviness VS Jr 《Cerebral cortex (New York, N.Y. : 1991)》1997,7(7):678-689
Neuronogenesis in the neocortical pseudostratified ventricular epithelium
(PVE) is initiated rostrolaterally and progresses caudo- medially as
development progresses. Here we have measured the cytokinetic parameters
and the fractional neuronal output parameter, Q, of laterally located
early-maturing regions over the principal embryonic days (E12-E15) of
neocortical neuronogenesis in the mouse. These measures are compared with
ones previously made of a medial, late- maturing portion of the PVE.
Laterally, as medially, the duration of the neuronogenetic interval is 6
days and comprises 11 integer cell cycles. Also, in both lateral and medial
areas the length of G1 phase (TG1) increases nearly 4-fold and is the only
cell cycle parameter to change. Q progresses essentially identically
laterally and medially with respect to the succession of integer cell
cycles. Most importantly, from E12 to E13 there is a steeply declining
lateral to medial gradient in TG1. The gradient is due both to the lateral
to medial graded stage of neuronogenesis and to the stepwise increase in
TG1 with each integer cycle during the neuronogenetic interval. To our
knowledge this gradient in TG1 of the cerebral PVE is the first cell
biological gradient to be demonstrated experimentally in such an extensive
proliferative epithelial sheet. We suggest that this gradient in TG1 is the
cellular mechanism for positionally encoding a protomap of the neocortex
within the PVE.
相似文献
85.
Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate 总被引:3,自引:2,他引:3
We observed that pretreatment of male F344 rats with benzyl selenocyanate,
a versatile organoselenium chemopreventive agent in several animal model
systems, decreases the levels of DNA and RNA modifications produced in the
liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms
involved, we pretreated male F344 rats with either benzyl selenocyanate,
its sulfur analog benzyl thiocyanate, phenobarbital or cobalt
protoporphyrin IX; the latter is a depletor of P450. We then determined (1)
the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on
2-nitropropane- induced liver DNA and RNA modifications and (3) amount of
nitrate excreted in rat urine following administration of the carcinogen.
Pretreatment with benzyl selenocyanate or phenobarbital increased the
denitrification activity of liver microsomes by 217 and 765%, respectively,
increased liver P4502B1 by 31- and 435-fold, respectively, decreased the
levels of 2-nitropropane-induced modifications in liver DNA (29-70% and
17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and
increased the 24-h urinary excretion of nitrate by 157 and 209%,
respectively. Pretreatment with benzyl thiocyanate had no significant
effect on any of these parameters. Pretreatment with cobalt protoporphyrin
IX decreased liver P4502B 1 by 87%, decreased the denitrification activity
of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate
by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic
acid modifications by 17-67%. These results indicate that the metabolic
sequence from 2-nitropropane to the reactive species causing DNA and RNA
modifications does not involve the removal of the nitro group. Moreover,
they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic
acid modifications in part by increasing its detoxication through induction
of denitrification, although it is evident that other mechanisms must also
be involved.
相似文献
86.
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90.
Zusammenfassung Die Behandungsstrategien und Operationstechniken urologischer Erkrankungen unterliegen einer ständigen Fortentwicklung. Die Therapieschemata und operativen Eingriffe werden zunehmend differenzierter und komplexer. Für den uro-radiologisch tätigen Radiologen ist es deshalb unerläßlich, sich mit Therapie und OP-Techniken zu befassen, um postoperative Befunde werten und einordnen zu können. Im ersten Teil der Übersicht werden aktuelle Therapie und postoperative Bildgebung bei Nephrolithiasis, bei Nierentumoren und bei Erkrankungen der Ureteren abgehandelt. Die Auswahl der geeigneten Untersuchungsmodalität und der sinnvolle Einsatz der Bildgebung im zeitlichen Zusammenhang mit dem Eingriff werden dargelegt. Besonderer Wert wird auf die Darstellung jeweils typischer postoperativer Befunde gelegt. Die Abklärung eingiffsspezifischer Komplikationen und ihr radiologisches Bild werden geschildert.
相似文献
相似文献