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21.
Mackinnon S; Papadopoulos EB; Carabasi MH; Reich L; Collins NH; Boulad F; Castro-Malaspina H; Childs BH; Gillio AP; Kernan NA 《Blood》1995,86(4):1261-1268
Infusions of large numbers (> 10(8)/kg) of donor leukocytes can induce remissions in patients with chronic myeloid leukemia (CML) who relapse after marrow transplantation. We wanted to determine if substantially lower numbers of donor leukocytes could induce remissions and, if so, whether this would reduce the 90% incidence of graft-versus-host disease (GVHD) associated with this therapy. Twenty-two patients with relapsed CML were studied: 2 in molecular relapse, 6 in cytogenetic relapse, 10 in chronic phase, and 4 in accelerated phase. Each patient received escalating doses of donor leukocytes at 4- to 33-week intervals. Leukocyte doses were calculated as T cells per kilogram of recipient weight. There were 8 dose levels between 1 x 10(5) and 5 x 10(8). Lineage-specific chimerism and residual leukemia detection were assessed using sensitive polymerase chain reaction (PCR) methodologies. Nineteen of the 22 patients achieved remission. Remissions were achieved at the following T-cell doses: 1 x 10(7) (n = 8), 5 x 10(7) (n = 4), 1 x 10(8) (n = 3), and 5 x 10(8) (n = 4). To date, 15 of the 17 evaluable patients have become BCR-ABL negative by PCR. The incidence of GVHD was correlated with the dose of T cells administered. Only 1 of the 8 patients who achieved remission at a T-cell dose of 1 x 10(7)/kg developed GVHD, whereas this complication developed in 8 of the 11 responders who received a T-cell dose of > or = 5 x 10(7)/kg. Three patients died in remission, 1 secondary to marrow aplasia, 1 of respiratory failure and 1 of complications of chronic GVHD. Sixteen patients who were mixed T-cell chimeras before treatment became full donor T-cell chimeras at the time of remission. Donor leukocytes with a T-cell content as low as 1 x 10(7)/kg can result in complete donor chimerism together with a potent graft-versus-leukemia (GVL) effect. The dose of donor leukocytes or T cells used may be important in determining both the GVL response and the incidence of GVHD. In many patients, this potent GVL effect can occur in the absence of clinical GVHD. 相似文献
22.
P-selectin is a 140-kD protein found in the alpha-granules of platelets and the Weibel-Palade bodies of endothelial cells that on cell activation is expressed on the cell surface and also secreted into the plasma. The secreted form of P-selectin, like plasma P-selectin, differed from platelet membrane P-selectin in that its molecular mass was approximately 3 kD lower under reducing conditions. Both the secreted and plasma forms of P-selectin contained cytoplasmic sequence as determined by Western blot analysis with an affinity-purified rabbit anti-P-selectin cytoplasmic peptide antibody. We have measured plasma P- selectin and beta-thromboglobulin (beta TG) concurrently in (1) patients with consumptive thrombotic disorders, including disseminated intravascular coagulation (DIC), heparin-induced thrombocytopenia (HIT), and thrombotic thrombocytopenic purpura (TTP)/haemolytic uremic syndrome (HUS); (2) patients with idiopathic thrombocytopenic purpura (ITP); and (3) healthy controls. Patients with DIC, HIT, and TTP/HUS, but not ITP, had significantly elevated plasma P-selectin and beta TG levels when compared with their age-matched healthy controls. The increased plasma P-selectin and beta TG in patients with thrombotic disorders were likely to be the result of in vivo platelet and endothelial cell damage or activation. We also found that avoidance of veno-occlusion and other tedious measures customarily taken during blood collection and sample preparation to prevent in vitro platelet activation did not affect plasma P-selectin assay results. In addition, plasma P-selectin levels were not influenced by the presence of renal failure or heparin administration. These results indicate that plasma P- selectin may be a useful new marker for thrombotic diseases. 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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Hoos A. D'Incan C. Gissmann L. Altmann A. Momburg F. Nindl I. Osen W. Schönning BH. Jochmus I. 《Archives of virology》1996,141(3-4):449-458
Archives of Virology - The low expression of major histocompatibility complex (MHC) class I antigens on human papillomavirus (HPV)-infected cervical carcinoma cells may be responsible for an... 相似文献
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Quantitative liver function in patients with rheumatoid arthritis treated with low-dose methotrexate: a longitudinal study 总被引:4,自引:0,他引:4
Beyeler C; Reichen J; Thomann SR; Lauterburg BH; Gerber NJ 《Rheumatology (Oxford, England)》1997,36(3):338-344
The objectives were to determine quantitative liver function prospectively
in patients with rheumatoid arthritis (RA) treated with low-dose
methotrexate (MTX), to search for risk factors for a loss of quantitative
liver function and to assess the relationship between quantitative liver
function and histological staging. A total of 117 patients with RA (ACR
criteria, 85 women, mean age 59 yr) had measurements of galactose
elimination capacity (GEC), aminopyrine breath test (ABT) and liver enzymes
[aspartate amino transferase (AST), alanine amino transferase (ALT),
alkaline phosphatase (AP), 7-glutamyl transferase (GGT), bile acids,
bilirubin, albumin] before treatment with weekly i.m. MTX injections and
every year thereafter. In 16 patients, liver biopsies were performed.
Before the introduction of MTX, mean GEC was 6.6 mg/min/kg [5th to 95th
percentile (5-95 PC) 5.1- 8.5; reference range 6.0-9.1] and mean ABT was
0.80% kg/mmol (5-95 PC 0.42-1.30: reference range 0.6-1.0). During
treatment with MTX [mean weekly dose 11.8 mg (5-95 PC 5.4-20.2), mean
observation period 3.8 yr (5-95 PC 0.4-6.9)], significant declines of GEC
(-0.12 mg/min/kg per year. t = 3.30, P < 0.002) and ABT (-0.06% kg/mmol
per year, t = 4.81, P < 0.001) were observed. Negative correlations were
found between the annual change in GEC and GEC at baseline (Rs = -0.40, P
< 0.0001), and the annual change in ABT and ABT at baseline (Rs = -0.43,
P < 0.0001). No correlations were found between the annual change in GEC
or ABT and weekly MTX dose, age or percentage of increased liver enzymes,
and no effect of a history of alcohol consumption > 30 g/week became
evident. Two patients with Roenigk grade III had impaired quantitative
liver function, while 14 patients with Roenigk grades I and II exhibited a
high variability of GEC and ABT from normal to abnormal values. The
continuous declines in GEC and ABT observed deserve attention in patients
with prolonged treatment. Patients with a low GEC or ABT at baseline seem
not to be at increased risk for a further loss of quantitative liver
function. An impaired GEC or ABT does not necessarily concur with hepatic
fibrosis on histological examination.
相似文献
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Work in progress: [18F] fluorodeoxyglucose and positron emission tomography in the evaluation of radiation necrosis of the brain 总被引:3,自引:0,他引:3