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Wierzbowski AK Hoban DJ Hisanaga T Decorby M Zhanel GG 《Current infectious disease reports》2005,7(3):175-184
Antimicrobial resistance is a growing problem among upper respiratory tract pathogens. Resistance to β-lactam drugs among
Streptococcus pneumoniae, Haemophilus influenzae, and Streptococcus pyogenes is increasing. As safe and well-tolerated antibiotics, macrolides play a key role in the treatment of community-acquired
upper respiratory tract infections (RTIs). Their broad spectrum of activity against gram-positive cocci, such as S. pneumoniae and S. pyogenes, atypical pathogens, H. influenzae (azithromycin and clarithromycin), and Moraxella catarrhalis, has led to the widespread use of macrolides for empiric treatment
of upper RTIs and as alternatives for patients allergic to β-lactams. Macrolide resistance is increasing among pneumococci
and recently among S. pyogenes, and is associated with increasing use of the newer macrolides, such as azithromycin. Ribosomal target modification mediated
by erm(A) [erm(TR)] and erm(B) genes and active efflux due to mef(A) and mef(E) are the principal mechanisms of resistance in S. pneumoniae and S. pyogenes. Recently, ribosomal protein and RNA mutations have been found responsible for acquired resistance to macrolides in S. pneumoniae, S. pyogenes, and H. influenzae. Although macrolides are only weakly active against macrolide-resistant streptococci species producing an efflux pump (mef) and are inactive against pathogens with ribosomal target modification (erm), treatment failures are uncommon. Therefore, macrolide therapy, for now, remains a good alternative for treatment of upper
RTIs; however, continuous monitoring of the local resistance patterns is essential. 相似文献
35.
Suzuki HI Hangaishi A Hosoya N Watanabe T Kanda Y Motokura T Chiba S Kurokawa M 《International journal of hematology》2008,87(5):538-541
Neurological complications during the treatment of hematological malignancies have a wide range of causes. Treatment-related leukoencephalopathy has been recognized as a major complication of combined chemotherapy and radiotherapy for central nervous system (CNS) lymphoma, and can complicate the diagnosis of CNS infection. Herein, we present a patient with diffuse large B-cell lymphoma who developed herpes simplex encephalitis (HSE) and subsequent cytomegalovirus encephalitis after chemoradiotherapy for CNS relapse. Although cerebrospinal fluid examination (CSF) showed no significant pleocytosis, brain magnetic resonance imaging and polymerase chain reaction analysis of the CSF were useful in the diagnosis. With a review of the literature on the association between HSE and radiotherapy for CNS malignancies, our case suggests that an awareness of viral encephalitis is important in the differential diagnosis of acute neurologic disturbance during chemoradiotherapy for CNS lymphoma. 相似文献
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Masayuki Itoh Koji Kishi Hiroyuki Nakamura Hidekazu Hatao Kiwamu Kioi Akihiko Sudou Katsuyuki Kobayasi Fumihiro Tuchida Hideki Adachi Hisanaga Yagyuu Shuji Oh-ishi Takeshi Matsuoka 《Nihon Kokyūki Gakkai zasshi》2002,40(7):617-621
In this case, a 30-year-old man had been treated for chronic sinusitis and bronchiectasis since 2000, and presented at our outpatient clinic in May 2001 with chief complaints of massive yellow sputum expectoration and dyspnea. After he was admitted by our hospital, Pseudomonas aeruginosa bacteria were isolated at the rate of 10(8)/ml from his sputum culture. In electron-microscopic observation, the cilia of the bronchial epithelium were found to lack dynein arms. Semen examination revealed decreased sperm motility. Thus, the following diagnosis was made: diffuse bronchiectasis associated with the immotile-dyskinetic cilia syndrome, complicated with a P. aeruginosa infection. After the airway infection was ameliorated, 40 mg/day of clenbuterol hydrochloride was administered in combination with 250 mg of azithromycin, which was given twice a week, and which led to a markedly decreased frequency of exacerbation of airway infection. Moreover, chest CT scanning and respiratory function testing also indicated improvements. It was hypothesized that the decreased cilia motility due to P. aeruginosa-produced pyocyanin would be ameliorated with a b2 stimulant, and the inhibitory effect of a macrolide on the P. aeruginosa biofilm and production of pyocyanin would also be involved in the improvement of this case. 相似文献
37.
Kanekura T Kawahara K Maruyama I Kanzaki T 《Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy》2005,9(4):292-296
Pyoderma gangrenosum is an intractable skin disorder characterized by the development of erythematous pustules or nodules that rapidly progress to destructive, necrotizing, non-infective ulcers. We assessed the efficacy of granulocyte and monocyte adsorption apheresis (GCAP) therapy in two new patients, a 67-year-old man with ulcerations on his lower leg, and a 44-year-old man with turgid erythematous lesions with burrowing abscesses and sinus formation on his hip, groin, and thighs. Both patients received 10 GCAP treatments at 5-day intervals. Their skin lesions responded well. The 9 cmx6 cm ulcer on the lower right leg of the 67-year-old patient was completely covered by regenerated skin at the completion of therapy. The turgid skin lesions containing pustules and ulcers of the other patient showed amelioration and a marked decrease in the volume of exudate. Our results suggest that GCAP is a useful treatment modality for pyoderma gangrenosum. 相似文献
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Hidden Genetic Variation in LCA9‐Associated Congenital Blindness Explained by 5′UTR Mutations and Copy‐Number Variations of NMNAT1
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Frauke Coppieters Anne Laure Todeschini Takuro Fujimaki Annelot Baert Marieke De Bruyne Caroline Van Cauwenbergh Hannah Verdin Miriam Bauwens Maté Ongenaert Mineo Kondo Françoise Meire Akira Murakami Reiner A. Veitia Bart P. Leroy Elfride De Baere 《Human mutation》2015,36(12):1188-1196
Leber congenital amaurosis (LCA) is a severe autosomal‐recessive retinal dystrophy leading to congenital blindness. A recently identified LCA gene is NMNAT1, located in the LCA9 locus. Although most mutations in blindness genes are coding variations, there is accumulating evidence for hidden noncoding defects or structural variations (SVs). The starting point of this study was an LCA9‐associated consanguineous family in which no coding mutations were found in the LCA9 region. Exploring the untranslated regions of NMNAT1 revealed a novel homozygous 5′UTR variant, c.‐70A>T. Moreover, an adjacent 5′UTR variant, c.‐69C>T, was identified in a second consanguineous family displaying a similar phenotype. Both 5′UTR variants resulted in decreased NMNAT1 mRNA abundance in patients’ lymphocytes, and caused decreased luciferase activity in human retinal pigment epithelial RPE‐1 cells. Second, we unraveled pseudohomozygosity of a coding NMNAT1 mutation in two unrelated LCA patients by the identification of two distinct heterozygous partial NMNAT1 deletions. Molecular characterization of the breakpoint junctions revealed a complex Alu‐rich genomic architecture. Our study uncovered hidden genetic variation in NMNAT1‐associated LCA and emphasized a shift from coding to noncoding regulatory mutations and repeat‐mediated SVs in the molecular pathogenesis of heterogeneous recessive disorders such as hereditary blindness. 相似文献
40.
Tatsuya Kondo Sayaka Kitano Nobukazu Miyakawa Takuro Watanabe Rieko Goto Miki Sato Satoko Hanatani Masaji Sakaguchi Motoyuki Igata Junji Kawashima Hiroyuki Motoshima Takeshi Matsumura Eiichi Araki 《Internal medicine (Tokyo, Japan)》2021,60(9):1433
The gastrointestinal tract is considered an important endocrine organ for controlling glucose homeostasis via the production of incretins. A 21-year-old man emergently underwent total colectomy due to severe ulcerative colitis, and overt diabetes became evident. Weekly administration of a glucagon-like peptide (GLP)-1 receptor agonist (RA) dramatically improved his glucose control. Levels of GLP-1 or gastric inhibitory polypeptide (GIP) were low at the baseline in the duodenum and serum of the patient. After 11 months of GLP-1RA treatment, his HbA1c worsened again, and intensive insulin therapy was necessary to control his glucose levels. Our report may explain the significance of residual incretin for maintaining the pancreatic β-cell function. 相似文献