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Mary F. Barbe Brendan A. Hilliard Mamta Amin Michele Y. Harris Lucas J. Hobson Geneva E. Cruz Jocelynne T. Dorotan Ryan W. Paul David M. Klyne Steven N. Popoff 《Journal of orthopaedic research》2020,38(11):2396-2408
Encapsulation of median nerves is a hallmark of overuse-induced median mononeuropathy and contributes to functional declines. We tested if an antibody against CTGF/CCN2 (termed FG-3019 or Pamrevlumab) reduces established neural fibrosis and sensorimotor declines in a clinically relevant rodent model of overuse in which median mononeuropathy develops. Young adult female rats performed a high repetition high force (HRHF) lever-pulling task for 18 weeks. Rats were then euthanised at 18 weeks (HRHF untreated), or rested and systemically treated for 6 weeks with either an anti-CCN2 monoclonal antibody (HRHF-Rest/FG-3019) or IgG (HRHF-Rest/IgG), with results compared with nontask control rats. Neuropathology was evident in HRHF-untreated and HRHF-Rest/IgG rats as increased perineural collagen deposition and degraded myelin basic protein (dMBP) in median nerves, and increased substance P in lower cervical dorsal root ganglia (DRG), compared with controls. Both groups showed functional declines, specifically, decreased sensory conduction velocity in median nerves, noxious cold temperature hypersensitivity, and grip strength declines, compared with controls. There were also increases of ATF3-immunopositive nuclei in ventral horn neurons in HRHF-untreated rats, compared with controls (which showed none). FG-3019-treated rats showed no increase above control levels of perineural collagen or dMBP in median nerves, Substance P in lower cervical DRGs, or ATF3-immunopositive nuclei in ventral horns, and similar median nerve conduction velocities and thermal sensitivity, compared with controls. We hypothesize that neural fibrotic processes underpin the sensorimotor declines by compressing or impeding median nerves during movement, and that inhibiting fibrosis using an anti-CCN2 treatment reverses these effects. 相似文献
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Douglas E. Holt Susan M. Hiniker John A. Kalapurakal John C. Breneman Jay C. Shiao Nicole Boik Benjamin T. Cooper Paige L. Dorn Matthew D. Hall Natalie Logie John T. Lucas Iain J. MacEwan Adam C. Olson Joshua D. Palmer Samir Patel Luke E. Pater Stephanie Surgener Derek S. Tsang Sarah A. Milgrom 《International journal of radiation oncology, biology, physics》2021,109(2):505-514
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Alcohol and hepatitis C mortality among males and females in the United States: a life table analysis 总被引:3,自引:0,他引:3
OBJECTIVE: Evidence from previous studies suggests that heavy alcohol use (HAU) exacerbates the rate of fibrosis progression in the liver and results in increased probability for premature death among patients with hepatitis C virus (HCV) infection. The current study uses population-based mortality data to investigate whether heavy drinking affects the age of death among individuals with HCV and, if so, whether this effect differs between men and women. METHODS: A total of 7,263,163 death records in the United States between 2000 and 2002 were drawn from the Multiple Cause of Death (MCD) public-use data files compiled by the National Center for Health Statistics (NCHS). International Classification of Diseases, Tenth Revision (ICD-10) codes were used to identify the presence of HCV (B17.1 and B18.2) and HAU (as indicated by alcohol-induced medical conditions, F10 and K70) either as the underlying cause or as one of the contributing causes of death. The deaths were divided into 4 distinctive cause-of-death categories: HCV without HAU, HAU without HCV, HCV plus HAU, and all others. The mean ages of death and the cumulative probabilities of death derived from multiple-cause life table were compared across these categories. RESULTS: Hepatitis C virus deaths showed an excessive prevalence of HAU when compared with non-HCV deaths. Compared with deaths of HCV without HAU, the mean age of death was shortened for deaths of HCV plus HAU (from 55.1 to 50.0 years among males, and from 61.0 to 49.1 years among females). The cumulative probability of death before age 65 was much higher for the latter than the former group (0.91 vs 0.68 among males, and 0.88 vs 0.47 among females). While HCV alone showed a disproportionate effect on premature death in males, HAU presented a stronger effect in females, resulting in a "catching-up" effect that diminished the gender difference in age of HCV death. CONCLUSIONS: This study provides mortality-based evidence to further establish heavy alcohol consumption as one of the key risk factors contributing to premature deaths from HCV in the United States. More importantly, this study, for the first time, presents empirical evidence that alcohol consumption affects men and women differently in HCV mortality. 相似文献
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The purpose of this study was to develop a Reference Data Set for Dental Age Assessment at the 13 year old threshold in Caucasian children.
Patients, Materials and Methods
The Reference Data Set comprised 5187 re-used Dental Panoramic Tomographs (DPTs) between the ages of 11-15 years, from both the Eastman Dental Hospital and King’s College Dental Hospital archives. Tooth Development Stages were recorded for the left maxillary and mandibular teeth and all four permanent third molars (Demirjian et al., 1973, Demirjian 1978). A separate Study Sample of DPTs, comprising 50 males and 50 females aged between 10 and 16 years was collected to test the accuracy of the method. Summary Data was generated for the individual Tooth Development Stages which consisted of the number (n-tds), mean (x), standard deviation (sd) and the standard error (se). By using the mathematical techniques of meta-analysis, this data was used to estimate the age of each subject in the Study Sample. The estimated Dental Age derived was compared to the gold standard of Chronological Age.Results
The mean difference between the Chronological Age and Dental Age was determined to be −0.1 years (−1.2 months) for males and 0.05 years (−0.6 months) for females.Conclusion
Dental Age was reliably estimated at the 13 year threshold. 相似文献59.
A rare event of a fall causing delayed intrathyroidal hematoma and respiratory distress is reported here. A 75-year-old woman with symptoms of vertigo causing syncope and fall 24 h earlier was seen and discharged from our emergency department after an unremarkable physical exam and 6-h observation period. Within 3 h of discharge, the patient was transported back by Emergency Medical Services with an enlarging neck mass and subjective respiratory distress. CT scan demonstrated a large, expanding hematoma, and the patient underwent an emergency hemithyroidectomy. Hürtle cell adenoma was found on pathologic specimen examination. A review of the literature of similar cases is presented, emphasizing the notion that concurrent thyroid pathology is a risk factor for airway compromise after seemingly benign trauma and that airway compromise can present in a delayed fashion. 相似文献
60.
The I-J subregion codes for determinants on suppressor factor(s) which limit the contact sensitivity response to picryl chloride 下载免费PDF全文
The cell-mediated immune reactivity (CMI) of mice to contact chemicals such as picryl chloride (PCI) is influenced by thymus-derived suppressor T lymphocytes (1,2). The development of these suppressor T lymphocytes is stimulated by the intravenous administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Zembala and Asherson have further demonstrated that a specific suppressor factor(s) can be detected in the supernates of cultured suppressor T cells. This factor suppresses the transfer of contact sensitivity (CS) to PCl (1,2). In experiments reported elsewhere (3), we have shown that the PCl suppressor supernates of Zembala and Asherson can also suppress the development of contact sensitivity to PCl. The immunochemical analysis of suppressor factor (SF) operative in the CS response to PCl has revealed many similar properties (3) to other suppressive moieties functioning to limit the plaque-forming cell (PFC) response to dinitrophenylated-keyhole limpet hemocyanin (DNP-KLH) as well as the strict antigen specificity of each respective suppressive factor, suggested that there might be a common origin of these substances. Indeed, in each case these respective factors were found to bear determinants controlled by the H-2 gene complex (4,5). Recently, in selected systems, the I-J subregion has been found to code for the Ia determinants present on suppressor cells (6) and suppressor factors (4,5). In accord with these findings, we report that antigen-specific SF which limit the CS response to PCl bear I-J determinants, implying that analogous suppressive regulatory mechanisms in CMI as well as antibody responses may be determined by genes of one subregion of the H-2 complex. 相似文献