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991.
Xiang Yang Zhang Dong Feng Zhou Ling Yan Qi Song Chen Lian Yuan Cao Da Chun Chen Mei Hong Xiu Fan Wang Gui Ying Wu Lin Lu Therese A. Kosten Thomas R. Kosten 《Psychopharmacology》2009,204(1):177-184
Objective Both schizophrenia and oxidative stress have been associated with immune system abnormalities in interleukin-2 and -6 (IL-2;
IL-6) and increases in superoxide dismutase (SOD) activity. These abnormalities may improve during antipsychotic drug treatment
that reduces symptoms in schizophrenic patients.
Materials and methods Subjects included 30 healthy controls (HC) and 78 schizophrenic (SCH) in-patients who were randomly assigned to 12 weeks of
double-blind treatment with risperidone 6 mg/day or haloperidol 20 mg/day. Ratings using the Positive and Negative Syndrome
Scale (PANSS) were correlated with blood SOD and serum IL-2 levels.
Results SCH patients who were medication-free for 2 weeks had greater SOD, IL-2, and IL-6 levels than HC. At baseline, these SOD elevations
were associated with higher PANSS total scores and the IL-2 elevations with lower PANSS positive symptom scores. The SOD and
IL-2 levels in the SCH were also positively correlated. After treatment, PANSS positive symptoms and both SOD and IL-2 showed
a significant decrease, but IL-6 showed no change. The SOD and IL-2 reductions were correlated with the reductions in PANSS
total score, and SOD reductions also correlated with positive subscore reductions. Females showed these associations more
strongly than males.
Conclusion Our results suggest that the dysregulation in the cytokine system and oxidative stress in patients with schizophrenia is implicated
in clinical symptoms and is improved at least partially with antipsychotic treatment. The stronger associations in females
deserve further study and confirmation. 相似文献
992.
Human amniotic fluid-derived stem cells are rejected after transplantation in the myocardium of normal, ischemic, immuno-suppressed or immuno-deficient rat 总被引:10,自引:0,他引:10
993.
Jing Y Gravenstein S Chaganty NR Chen N Lyerly KH Joyce S Deng Y 《Experimental gerontology》2007,42(8):719-732
NKT cells are important for initiating and regulating immune responses. We investigated the age-related changes in the CD1d-restricted semi-invariant NKT (iNKT) cells in peripheral blood of healthy adults. The iNKT cell frequency was 2.5- to 10.7-fold less in healthy elderly subjects (61 years and over) compared to the healthy young subjects (20-40 years, p<0.001). This age-related decline in iNKT cells was observed both in freshly isolated PBMC and in cultures where iNKT cells were enriched by alpha-GalCer stimulation using either the Valpha24/Vbeta11 TCR antibody pair or the CD1d-tetramer as the iNKT cell marker. The decline in frequency was associated with an alteration in the iNKT cell subset compositions: an increase in the proportion of CD4+ subset and a decrease in the proportion of CD4/CD8 double-negative (DN) subset. The age-related decline in iNKT cells and changes in subset composition were independent from the age-related changes of conventional T cells/T cell subsets. Additionally, there was a Th1 to Th2 shift in the cytokine response profile from iNKT cells with aging. We conclude that aging is associated with a significant decline in iNKT cell frequency in peripheral blood, accompanied with alterations in subset composition and cytokine response profile. 相似文献
994.
995.
The use of vinca alkaloids in preparation for splenectomy of corticosteroid refractory chronic immune thrombocytopenic purpura patients 总被引:1,自引:0,他引:1
Szczepanik AB Sikorska A Slomkowski M Konopka L 《International journal of laboratory hematology》2007,29(5):347-351
Administration of vinca alkaloids (VA) to chronic corticosteroid refractory immune thrombocytopenia (ITP) patients results in a temporary increase of platelet count. The aim of the study was to evaluate the efficacy of vinca alkaloids in preparing adult corticosteroid refractory chronic ITP patients for splenectomy as well as to compare the costs of this method with costs of applying intravenous immunoglobulins. The study included 12 chronic ITP patients refractory to corticosteroids applied for 3-144 months. The patients were prepared for splenectomy with average 3.0 (from 1 to 4) 2-h intravenous infusions of vinca alkaloids at 7 day intervals. In eight patients, vincristin was used in a total dose of 6 mg (2 mg per infusion), in two patients, vinblastin was used in total dose of 30 mg (10 mg per infusion), and in two patients, vincristin and vinblastin infusions were administered alternatively. In nine of the 12 treated patients (75%) the platelet count increased to > or = 80 x 10(9)/l, which allowed safe splenectomy. Three patients unreactive to VA treatment were prepared for splenectomy with intravenous gammaglobulin infusions. Splenectomy was performed in 12 patients, in eight with laparoscopic method, in four with classic method. No complications during surgical intervention were observed. In none of the VA treated patients was myelosupression or liver or/and kidney dysfunction observed. Splenectomy resulted in normalization of platelet count in all patients after operation and in six of nine patients followed up for 10 months (on the average). Matching of VA costs with treatment efficacy and comparison with similar costs for intravenous immunoglobulin treatment revealed many fold lower costs of the former method. 相似文献
996.
Hiraki S Ono S Kinoshita M Tsujimoto H Seki S Mochizuki H 《American journal of surgery》2007,193(6):676-680
BACKGROUND: We investigated cellular immune responses, in particular interferon gamma (IFN-gamma) production, by peripheral blood mononuclear cells (PBMCs) in patients with septic and nonseptic surgical stress, focusing on interleukin (IL)-18 and its receptor (IL-18R). METHODS: Thirty-two patients with alimentary tract carcinoma who underwent elective surgery (OP) and 26 septic patients (SP) with peritonitis were enrolled in this study. Blood was collected on the first postoperative day (POD1), POD5, POD10, and POD15 in the OP group and on the emergency admission in the SP group. Ten healthy volunteers served as controls. PBMCs were cultured in the presence of anti-CD3 antibody or IL-2 and IL-12, with or without additional IL-18 stimulation, to measure IFN-gamma production. IL-18R expression on CD56+ NK (natural killer) cells was evaluated by flow cytometry. RESULTS: IL-2- and IL-12-induced IFN-gamma production by PBMCs was suppressed significantly in both the OP (POD5) and SP groups compared with that in healthy controls. Interestingly, additional IL-18 stimulation up-regulated IFN-gamma production by PBMCs in the OP group as well as the control group, but not in the SP group. IL-18R expression on CD56+ NK cells was maintained consistently in the OP group as well as the control group, but decreased in the SP group. CONCLUSIONS: IFN-gamma production induced by cytokines (IL-2 and IL-12) was suppressed in PBMCs from both patients with sepsis and those who had undergone elective surgery. However, IL-18R expression on CD56+ NK cells was different between patients with sepsis and nonseptic surgical stress. Our results suggest that exogenous IL-18 administration may be effective in preventing immune suppression in patients with nonseptic elective surgery. 相似文献
997.
Louise Pontell Patricia Castelucci Mária Bagyánszki Tanja Jovic Michelle Thacker Kulmira Nurgali Romke Bron John B. Furness 《Virchows Archiv : an international journal of pathology》2009,455(1):55-65
An acute enteritis is commonly followed by intestinal neuromuscular dysfunction, including prolonged hyperexcitability of
enteric neurons. Such motility disorders are associated with maintained increases in immune cells adjacent to enteric ganglia
and in the mucosa. However, whether the commonly used animal model, trinitrobenzene sulphonate (TNBS)-induced enteritis, causes
histological and immune cell changes similar to human enteric neuropathies is not clear. We have made a detailed study of
the mucosal damage and repair and immune cell invasion following intralumenal administration of TNBS. Intestines from untreated,
sham-operated and TNBS-treated animals were examined at 3 h to 56 days. At 3 h, the mucosal surface was completely ablated,
by 6 h an epithelial covering was substantially restored and by 1 day there was full re-epithelialisation. The lumenal epithelium
developed from a squamous cell covering to a fully differentiated columnar epithelium with mature villi at about 7 days. Prominent
phagocytic activity of enterocytes occurred at 1–7 days. A surge of eosinophils and T lymphocytes associated with the enteric
nerve ganglia occurred at 3 h to 3 days. However, elevated immune cell numbers occurred in the lamina propria of the mucosa
until 56 days, when eosinophils were still three times normal. We conclude that the disruption of the mucosal surface that
causes TNBS-induced ileitis is brief, a little more than 6 h, and causes a transient immune cell surge adjacent to enteric
ganglia. This is much briefer than the enteric neuropathy that ensues. Ongoing mucosal inflammatory reaction may contribute
to the persistence of enteric neuropathy. 相似文献
998.
Fred W. Perrino Scott Harvey Nadine M. Shaban Thomas Hollis 《Journal of molecular medicine (Berlin, Germany)》2009,87(1):25-30
Mutations in the genes encoding the RNaseH2 and TREX1 nucleases have been identified in patients with Aicardi–Goutieres syndrome
(AGS). To determine if the AGS RNaseH2 mutations result in the loss of nuclease activity, the human wild-type RNaseH2 and
four mutant complexes that constitute the majority of mutations identified in AGS patients have been prepared and tested for
ribonuclease H activity. The heterotrimeric structures of the mutant RNaseH2 complexes are intact. Furthermore, the ribonuclease
H activities of the mutant complexes are indistinguishable from the wild-type enzyme with the exception of the RNaseH2 subunit
A (Gly37Ser) mutant, which exhibits some evidence of altered nuclease specificity. These data indicate that the mechanism
of RNaseH2 dysfunction in AGS cannot be simply explained by loss of ribonuclease H activity and points to a more complex mechanism
perhaps mediated through altered interactions with as yet identified nucleic acids or protein partners. 相似文献
999.
Hye Ryoun Jang Gang Jee Ko Barbara A. Wasowska Hamid Rabb 《Journal of molecular medicine (Berlin, Germany)》2009,87(9):859-864
Kidney ischemia–reperfusion injury (IRI) engages both the innate and adaptive immune responses. Cellular mediators of immunity,
such as dendritic cells, neutrophils, macrophages, natural killer T, T, and B cells, contribute to the pathogenesis of renal
injury after IRI. Postischemic kidneys express increased levels of adhesion molecules on endothelial cells and toll-like receptors
on tubular epithelial cells. Soluble components of the immune system, such as complement activation proteins and cytokines,
also participate in injury/repair of postischemic kidneys. Experimental studies on the immune response in kidney IRI have
resulted in better understanding of the mechanisms underlying IRI and led to the discovery of novel therapeutic and diagnostic
targets. 相似文献
1000.
Specificity and memory are the hallmarks of the adaptive immune system of vertebrates. However, phenomena of specificity upon priming of immunity have recently been demonstrated also in invertebrates, which rely exclusively on innate immune defence. It has been suggested that phagocytosis might represent a core candidate for such specificity in invertebrates. We here developed in vitro phagocytosis measurements for different bacteria in the woodlouse Porcellio scaber (Crustacea: Isopoda). After immune priming with heat-killed bacteria, hemocytes showed increased phagocytosis of a previously encountered bacterial strain compared to other bacteria. These data support the role of phagocytosis in invertebrate immunological specificity and suggest a high degree of specificity that even enables to differentiate between strains of the same bacterial species. 相似文献