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21.
Background
The Rh blood system is one of the most polymorphic and immunogenic systems known to humans. The expression of Rh blood group antigen is complex. The Rh D antigen is the most important of the antigens that constitute the Rh antigen system. In most cases, D antigen can easily be detected. However, due to variability of expression, weak forms antigen are encountered. The reactivity of weak D with antisera is variable and presents as a problem in blood banking.Methods
A retrospective analysis for a five-year period was done. Blood samples that were negative for Rh D by immediate spin tube method were tested for weak D antigen by additional lab tests.Result
Of 34932 serial Rh grouping tests done in our Blood Bank, the incidence of weak D Rh antigen was 0.189%. All these were confirmed by the antiglobulin test.Conclusion
These patients present as a problem for the blood banker and a curiosity to the clinician. Although uncommon, all health care workers should be aware of this entity to avoid anti D alloimmunisation.Key Words: Weak D, Rh Blood Group 相似文献22.
Human monocytes express interleukin-2 receptor beta (IL-2R beta) constitutively; however, the function of these receptors has not been fully delineated. We discovered that IL-2R beta directs two biologic activities in human monocytes, the release of granulocyte-macrophage colony-stimulating factor (GM-CSF) and increased susceptibility to lysis by lymphokine-activated killer cells (LAK) cells. Human monocytes were purified from peripheral blood mononuclear cells by plastic adherence and anti-CD2 plus complement lysis. By a 5-hour 51Cr-release assay, monocytes cultured in IL-2 were found to gain increasing susceptibility to LAK cells with time and this effect was dose dependent. Maximal susceptibility was obtained with a 4-day culture in 1,000 U/mL of IL-2. Monocytes were also found to release GM-CSF in response to IL-2 using a CSF-dependent cell line, Mo7e. Because IL-2- induced GM-CSF release coincides with LAK lysis of IL-2-cultured monocytes, we treated monocytes with anti-GM-CSF and anti-IL-2R beta to determine whether GM-CSF release and LAK susceptibility were dependent or independent events. We found that both phenomena were inhibited by either antibody. Therefore, we conclude that IL-2-induced release of GM- CSF is mediated by IL-2R beta, which then acts to modulate the susceptibility of monocytes to lysis by LAK cells. 相似文献
23.
Hasegawa DK; Bennett AJ; Coccia PF; Ramsay NK; Nesbit ME; Krivit W; Edson JR 《Blood》1980,56(4):585-595
Factor V deficiency has been identified in 8 of 8 patients 7--20 yr of age, with Philadelphia-positive (Ph1+) chronic myelogenous leukemia (CML). In these 8 patients, factor V deficiency was not due to hepatic dysfunction, factor V inhibitors, or disseminated intravascular coagulation. In 3 patients, factor V activity rose 10%--12% (0.10--0.12 U/ml) after the infusion of 28--31 ml/kg body weight of fresh frozen plasma (FFP). The rise persisted less than 14 hr. The mean measured postinfusion rise in factor V was 18% of the expected rise calculated from the volume of FFP infused in the patients' plasma volume. In 4 patients, a small transient rise in factor V activity occurred after splenectomy or plateletpheresis. Factor V deficiency was completely corrected after a marked reduction in bone marrow cellularity in 2 patients with Ph1+ CML treated with extensive chemotherapy, total body irradiation, and bone marrow transplantation. Factor V deficiency was retrospectively observed in 6 of 20 patients, ages 20--80 yr, with Ph1+ CML and 3 of 6 patients with other myeloproliferative disorders. The factor V deficiency appears to be associated with the large myeloid- megakaryocytic cell mass characteristic of CML and other myeloproliferative disorders. 相似文献
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Anorexia nervosa (AN) is a serious life-threatening illness that typically has its onset during the adolescent years. Evidence regarding the optimal treatment of AN in children and teenagers is growing; however, much remains unknown. Although current treatment approaches vary in Canada and elsewhere, the evidence to date indicates that family-based treatment (FBT) is the most effective treatment for children and teenagers with AN. A key component of the FBT model is that the parents are given the responsibility to return their child to physical health and ensure full weight restoration. An understanding of the basic principles and philosophy underlying FBT allows the physician to initiate elements of this evidence-based intervention to young patients with AN and their families. 相似文献
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W Oh DK Stevenson JE Tyson BH Morris CE Ahlfors G Jesse Bender RJ Wong R Perritt BR Vohr KP Van Meurs HJ Vreman A Das DL Phelps T Michael O’Shea RD Higgins 《Acta paediatrica (Oslo, Norway : 1992)》2010,99(5):673-678
Objectives: To assess the influence of clinical status on the association between total plasma bilirubin and unbound bilirubin on death or adverse neurodevelopmental outcomes at 18–22 months corrected age in extremely low birth weight infants. Method: Total plasma bilirubin and unbound bilirubin were measured in 1101 extremely low birth weight infants at 5 ± 1 days of age. Clinical criteria were used to classify infants as clinically stable or unstable. Survivors were examined at 18–22 months corrected age by certified examiners. Outcome variables were death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death prior to follow‐up. For all outcomes, the interaction between bilirubin variables and clinical status was assessed in logistic regression analyses adjusted for multiple risk factors. Results: Regardless of clinical status, an increasing level of unbound bilirubin was associated with higher rates of death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss and death before follow‐up. Total plasma bilirubin values were directly associated with death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death before follow‐up in unstable infants, but not in stable infants. An inverse association between total plasma bilirubin and death or cerebral palsy was found in stable infants. Conclusions: In extremely low birth weight infants, clinical status at 5 days of age affects the association between total plasma bilirubin and death or adverse neurodevelopmental outcomes at 18–22 months of corrected age. An increasing level of UB is associated a higher risk of death or adverse neurodevelopmental outcomes regardless of clinical status. Increasing levels of total plasma bilirubin are directly associated with increasing risk of death or adverse neurodevelopmental outcomes in unstable, but not in stable infants. 相似文献
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