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71.
The degree of heavy chain (H) editing, the types of Vkappa editors, and the pattern of Jkappa usage are correlated with a range of the affinity of anti-DNA. This range was determined by the number and location of arginine (R) residues in the VH. We, here, changed a key arginine residue in the VH of anti-DNA transgene to glycine, which sharply reduces the affinity for dsDNA. However, complete reversion of this anti-DNA to germline enhances the affinity for phosphatidylserine (PS). The B cells of this low-affinity anti-DNA and anti-PS transgenic mouse are tightly regulated by receptor editing. Thus, anti-PS B cells are another example of a constitutive self-antigen regulated in the bone marrow. 相似文献
72.
Ivana Horvat Ana Boban Renata Zadro Margareta Radic Antolic Ranka Serventi-Seiwerth Pavle Roncevic Ivo Radman Dubravka Sertic Marijo Vodanovic Drazen Pulanic Sandra Basic-Kinda Nadira Durakovic Silva Zupancic-Salek Radovan Vrhovac Igor Aurer Damir Nemet Boris Labar 《Clinical Lymphoma, Myeloma & Leukemia》2019,19(1):53-63
Introduction
Thrombosis is the most common complication in Philadelphia chromosome negative (Ph?) myeloproliferative neoplasms patients.Patients and Methods
In a cohort of 258 Ph? myeloproliferative neoplasm patients, the difference between patients with and without thrombosis was analyzed according to genetic thrombophilia factors, JAK2 V617F status and burden allele, blood count, cardiovascular risk factors and age. Patients were also divided in polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) subgroups as well as by the type of thrombosis.Results
Analysis of cardiovascular risk factors regarding arterial thrombosis showed that PV patients with thrombosis had higher incidence of diabetes (P = .030), ET patients more often had hypertension (P = .003) and hyperlipidemia (P = .005), while PMF patients had hyperlipidemia (P = .046) and at least one cardiovascular risk factor (P = .044). Moreover, leukocytes > 18 × 109/L and V617F burden allele > 25.7% were statistically significantly different in PV patients (P = .019 and borderline significant at P = .055, respectively), while in ET patients leukocytes > 9.2 × 109/L (P < .001) and age at diagnosis of > 55 years were statistically significantly different (P = .002). PMF patients with V617F burden allele ≤ 34.8% were more prone to thrombosis (P = .032). When comparing patients with and without venous thrombosis, cutoff value of V617F burden allele > 90.4% was significant for PV patients with thrombosis (P = .036), as was > 56.7% for PMF patients with thrombosis (P = .046). Platelets ≤ 536 × 109/L and age at diagnosis > 54 years showed statistically significant difference for ET patients with thrombosis (P = .015 and P = .041, respectively).Conclusion
On the basis of our results, a new scoring system for thrombosis risk in PV could be made, while PMF prognostic model may be expanded for better recognition of potential thrombotic risk factors. 相似文献73.
Leonela Luce Martín M. Abelleyro Micaela Carcione Chiara Mazzanti Liliana Rossetti Pamela Radic Irene Szijan Sebastián Menazzi Liliana Francipane Julián Nevado Pablo Lapunzina Carlos De Brasi Florencia Giliberto 《Neuromuscular disorders : NMD》2021,31(3):253-263
This work describes a family with Duchenne muscular dystrophy (DMD) with a rare case of a symptomatic pregnant woman. The main aim was to perform prenatal molecular diagnosis to provide genetic counseling. The secondary aim was to suggest the molecular mechanisms causing the complex structural variant (cxSV) identified. To accomplish this, we used a multi-technique algorithm including segregation analysis, Multiplex Ligation-dependent Probe Amplification, PCR, X-chromosome inactivation studies, microarrays, whole genome sequencing and bioinformatics. We identified a duplication of exons 38–43 in the DMD gene in all affected and obligate carrier members, proving that this was the DMD-causing mutation. We also observed a skewed X-chromosome inactivation in the symptomatic woman that explained her symptomatology. In addition, we identified a cxSV (duplication of exons 38–43 and deletion of exons 45–54) in the affected boy. The molecular characterization and bioinformatic analyses of the breakpoint junctions allowed us to identify Double Strand Breaks stimulator motifs and suggested the replication-dependent Fork Stalling and Template Switching as the most probable mechanisms leading to the duplication. In addition, the de novo deletion might have been the result of a germline inter-chromosome non-allelic recombination involving the Non-Homologous End Joining mechanism. In conclusion, the diagnostic strategy used allowed us to provide accurate molecular diagnosis and genetic counseling. In addition, the familial molecular diagnosis together with the in-depth characterization of the cxSV helped to determine the chronology of the molecular events, and propose and understand the molecular mechanisms involved in the generation of this complex rearrangement. 相似文献
74.
Nenad Filipovic Radun Vulovic Aleksandar Peulic Radivoje Radakovic Djordje Kosanic Branko Ristic 《Journal of Sports Science and Medicine》2009,8(4):584-590
The purpose of this investigation was to use a combination of image processing, force measurements and finite element modeling to calculate deformation of the knee cartilage during jumping. Professional athletes performed jumps analyzed using a force plate and high-speed video camera system. Image processing was performed on each frame of video using a color recognition algorithm. A simplified mass-spring-damper model was utilized for determination of global force and moment on the knee. Custom software for fitting the coupling characteristics was created. Simulated results were used as input data for the finite element calculation of cartilage deformation in the athlete’s knee. Computer simulation data was compared with the average experimental ground reaction forces. The results show the three-dimensional mechanical deformation distribution inside the cartilage volume. A combination of the image recognition technology, force plate measurements and the finite element cartilage deformation in the knee may be used in the future as an effective noninvasive tool for prediction of injury during jumping.
Key points
- Even there are many existing mathematical models of force distribution during running or jumping (Liu et al, 1998), to our knowledge there is no interdisciplinary approach where imaging processing, finite element modeling and experimental force plate system are employed.
- The aim is to explore noninvasive deformation in the knee cartilage during athlete’s jumping on the force plate.
- An original image algorithms and software were developed as well as complex mathematical models using high-performance computational power of finite element modeling together with one-dimensional dynamics model.
- The initial results showed cartilage deformation in the knee and future research will be focused on the methodology and more precisely determination of the stress and strain distribution in the knee cartilage during training phase of sportsman.
75.
Aleksandra Konic-Ristic Dejan Dodig Radmilo Krstic Svetislav Jelic Ivan Stankovic Aleksandra Ninkovic Jelena Radic Irina Besu Branka Bonaci-Nikolic Njegica Jojic Milica Djordjevic Dragan Popovic Zorica Juranic 《BMC immunology》2009,10(1):1-7
Background
Extensive allelic matching in the human leukocyte antigen (HLA) genes is regarded as a prerequisite for good clinical success of allogeneic haematopoietic stem cell transplantation (HSCT). Also other genetic factors can be assumed to play a role in preventing and controlling the complications associated with allogeneic HSCT, in particular graft-versus-host disease (GvHD). Interleukin-10 (IL-10) and its receptor (IL-10R), key regulators of the immune response, are among these candidates. We studied the association of IL-10 and IL-10Rβ gene polymorphisms with the occurrence of GvHD in 309 HLA-identical sibling donor and recipient pairs.Results
The difference in genotypic IL-10 production between patient and donor in combination with patient IL-10Rβ A/A genotype predisposed strongly to acute GvHD (OR = 7.15, p = 0.000023). On the other hand, a combination of same genotypic IL-10 production with patient IL-10Rβ A/A genotype protected from chronic GvHD (OR = 0.407, p = 0.0097).Conclusion
Our results suggest that IL-10 and IL-10Rβ genes have a synergistic effect on the risk of GvHD. 相似文献76.
77.
Stimac D Tomulic V Hauser G Jakljevic T Radic M 《Journal of clinical gastroenterology》2006,40(6):559; author reply 559-559; author reply 560
78.
Petković M Krstulja M Radic J Zamolo G Muhvić D Lovasic I Kujundzic M Franko A 《International journal of surgical pathology》2008,16(3):337-340
A case of rare tumor, Merkel cell carcinoma, located in the ear canal of a 25-year-old woman is presented. A polypoid tumor mass was extirpated, and tympanoplasty was done at the first operation, whereas at the second operation, all the bones of the ear canal were removed. Epitympanum and cavum were filled with tumor, and the tumor mass was removed in toto. The histopathology and immunohistochemical staining characteristics of tumor confirmed the presence of Merkel cell tumor. Postoperatively, radiation therapy to the tumor bed was completed. There was no clinical or radiographic evidence of recurrence or metastasis of Merkel cell tumor for 3 years. 相似文献
79.
80.
Bosma GC Kim J Urich T Fath DM Cotticelli MG Ruetsch NR Radic MZ Bosma MJ 《The Journal of experimental medicine》2002,196(11):1483-1495
Class switch recombination (CSR), similar to V(D)J recombination, is thought to involve DNA double strand breaks and repair by the nonhomologous end-joining pathway. A key component of this pathway is DNA-dependent protein kinase (DNA-PK), consisting of a catalytic subunit (DNA-PKcs) and a DNA-binding heterodimer (Ku70/80). To test whether DNA-PKcs activity is essential for CSR, we examined whether IgM(+) B cells from scid mice with site-directed H and L chain transgenes were able to undergo CSR. Although B cells from these mice were shown to lack DNA-PKcs activity, they were able to switch from IgM to IgG or IgA with close to the same efficiency as B cells from control transgenic and nontransgenic scid/+ mice, heterozygous for the scid mutation. We conclude that CSR, unlike V(D)J recombination, can readily occur in the absence of DNA-PKcs activity. We suggest nonhomologous end joining may not be the (primary or only) mechanism used to repair DNA breaks during CSR. 相似文献