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1.
D Soldateschi S Censini V de Gori G Antoni A Tagliabue D Boraschi 《Immunobiology》1984,166(3):251-262
Mouse peritoneal M phi and human blood monocytes were assayed for their antitumor activity in vitro with a cytolysis, a cytostasis and a cytotoxicity test performed in parallel. Both natural and stimulus-induced M phi antitumor capacities were assessed. Results indicate that natural cytolytic activity of unstimulated M phi is generally unable to restrict final tumor cell growth, since it is not coupled with cytostatic capacity. In contrast, exposure of M phi in vitro to either MAF or IFN-beta, besides augmenting M phi cytolytic capacity, induced a very significant cytostatic activity and thus efficiently restricted the survival of tumor cells. 相似文献
2.
David J. Tester Leonie C.H. Wong Pritha Chanana Amie Jaye Jared M. Evans David R. FitzPatrick Margaret J. Evans Peter Fleming Iona Jeffrey Marta C. Cohen Jacob Tfelt-Hansen Michael A. Simpson Elijah R. Behr Michael J. Ackerman 《Journal of the American College of Cardiology》2018,71(11):1217-1227
Background
Sudden infant death syndrome (SIDS) is a leading cause of postneonatal mortality. Genetic heart diseases (GHDs) underlie some cases of SIDS.Objectives
This study aimed to determine the spectrum and prevalence of GHD-associated mutations as a potential monogenic basis for SIDS.Methods
A cohort of 419 unrelated SIDS cases (257 male; average age 2.7 ± 1.9 months) underwent whole exome sequencing and a targeted analysis of 90 GHD-susceptibility genes. The yield of “potentially informative,” ultra-rare variants (minor allele frequency <0.00005) in GHD-associated genes was assessed.Results
Overall, 53 of 419 (12.6%) SIDS cases had ≥1 “potentially informative,” GHD-associated variant. The yield was 14.9% (21 of 141) for mixed-European ancestry cases and 11.5% (32 of 278) for European ancestry SIDS cases. Infants older than 4 months were more likely to host a “potentially informative” GHD-associated variant. There was significant overrepresentation of ultra-rare nonsynonymous variants in European SIDS cases (18 of 278 [6.5%]) versus European control subjects (30 of 973 [3.1%]; p = 0.013) when combining all 4 major cardiac channelopathy genes (KCNQ1, KCNH2, SCN5A, and RYR2). According to the American College of Medical Genetics guidelines, only 18 of 419 (4.3%) SIDS cases hosted a “pathogenic” or “likely pathogenic” variant.Conclusions
Less than 15% of more than 400 SIDS cases had a “potentially informative” variant in a GHD-susceptibility gene, predominantly in the 4- to 12-month age group. Only 4.3% of cases possessed immediately clinically actionable variants. Consistent with previous studies, ultra-rare, nonsynonymous variants within the major cardiac channelopathy-associated genes were overrepresented in SIDS cases in infants of European ethnicity. These findings have major implications for the investigation of SIDS cases and families. 相似文献3.
Marcello Niceta Domenico Barbuti Neerja Gupta Carlos Ruggiero Eduardo F. Tizzano Luitgard Graul-Neumann Sabina Barresi Gen Nishimura Irene Valenzuela Fermina López-Grondona Paula Fernandez-Alvarez Chiara Leoni Christiane Zweier Andreas Tzschach Emilia Stellacci Andrea Del Fattore Bruno Dallapiccola Giuseppe Zampino Marco Tartaglia 《Clinical genetics》2020,97(2):362-369
4.
Cristian Bonvicini Alessandra Minelli Catia Scassellati Marco Bortolomasi Matilde Segala Riccardo Sartori Mario Giacopuzzi Massimo Gennarelli 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Major Depression Disorder (MDD) is a serious mental illness that is one of the most disabling diseases worldwide. In addition, approximately 15% of depression patients are defined treatment-resistant (TRD). Preclinical and genetic studies show that serotonin modulation dysfunction exists in patients with TRD. Some polymorphisms in the promoter region of the serotonin transporter gene (SLC6A4) are likely to be involved in the pathogenesis/treatment of MDD; however, no data are available concerning TRD. 相似文献
5.
The phenotype of lymphocytes, obtained from mice immunized with allogeneic tumor cells, with the capacity to induce macrophage cytotoxicity was determined. Macrophage cytotoxicity was induced, either by incubating the macrophages with Macrophage Arming Factor (MAF) containing supernatants of cultures of sensitized lymphocytes and tumor cells (arming) or by incubating the macrophages directly with sensitized lymphocytes and tumor cells (activation). The MAF producing or activating capacity of the lymphocytes was not only "triggered" by the sensitizing tumor cells but also by normal cells and other tumor cells bearing the H-2 determinants of the sensitizing tumor cell. The capacity to render macrophages cytotoxic was not reduced after treatment of the lymphocytes with mitomycin-C or treatment with anti-murine Ig and complement. This capacity of the lymphocytes was abrogated after treatment with anti-T-cell serum or anti-Thy 1.2 serum and complement. After treatment with anti-Lyt 1 or anti-Lyt 2 serum and complement, the activating capacity was significantly reduced and the MAF producing capacity of the lymphocytes abrogated. Mixing the Lyt 1 depleted and Lyt 2 depleted lymphocytes or addition of normal lymphocytes to the Lyt 1 depleted or Lyt 2 depleted populations did not restore the MAF producing and activating capacities. This indicated that the lymphocytes inducing macrophage cytotoxicity in this allogeneic system are Lyt-1+2+ T-lymphocytes, which do not need to divide prior to perform their action. 相似文献
6.
7.
Annukka Holster Johanna Teräsjärvi Eero Lauhkonen Sari Törmänen Merja Helminen Petri Koponen Matti Korppi Ville Peltola Qiushui He Kirsi Nuolivirta 《Allergology international》2018,67(1):109-113
Background
Interleukin-17 (IL-17A) is a mainly pro-inflammatory cytokine, and IL-17 signaling implicates in the development of allergic asthma. The polymorphism rs2275913 in the promoter region of the IL-17A gene has in previous studies been associated with asthma susceptibility. The objective was to evaluate the association between IL-17A rs2275913 (-197G>A) polymorphism and post-bronchiolitis asthma and/or allergic rhinitis in a prospective 11–13 years post-bronchiolitis follow-up.Methods
166 previously healthy full-term infants, hospitalized for bronchiolitis at age less than 6 months, were invited to follow-up visits at the ages of 5–7 years and 11–13 years. Asthma diagnoses and presumptive symptoms, allergic rhinitis and use of inhaled corticosteroids (ICS) were registered. Blood samples for IL-17A rs2275913 (-197G>A) polymorphism were obtained during hospitalization or at the 5–7 years control visit.Results
There were no significant differences between children with the wild GG and variant GA or AA genotype in the severity of bronchiolitis during hospitalization or in the outcomes until the age 5–7 years. At 11–13 years of age, children with the variant GA or AA genotype had significantly less often current asthma, use of ICSs during last 12 months or allergic rhinitis than those with the wild GG genotype. The ICS use during last 12 months retained the statistical significance in adjusted analyses (adjusted OR 0.25), whereas current asthma and allergic rhinitis marginally lost it.Conclusions
The IL-17A rs2275913 (-197G>A) polymorphism decreased the risk of post-bronchiolitis asthma at 11–13 years of age, but not earlier in life, in the present prospective, long-term follow-up study. 相似文献8.
9.
Matt J. Neville Wanseon Lee Peter Humburg Daniel Wong Martin Barnardo Fredrik Karpe Julian C. Knight 《Human immunology》2017,78(3):242-251
This study aimed to establish the occurrence and frequency of HLA alleles and haplotypes for a healthy British Caucasian population bioresource from Oxfordshire. We present the results of imputation from HLA SNP genotyping data using SNP2HLA for 5553 individuals from Oxford Biobank, defining one- and two-field alleles together with amino acid polymorphisms. We show that this achieves a high level of accuracy with validation using sequence-specific primer amplification PCR. We define six- and eight-locus HLA haplotypes for this population by Bayesian methods implemented using PHASE. We determine patterns of linkage disequilibrium and recombination for these individuals involving classical HLA loci and show how analysis within a haplotype block structure may be more tractable for imputed data. Our findings contribute to knowledge of HLA diversity in healthy populations and further validate future large-scale use of HLA imputation as an informative approach in population bioresources. 相似文献
10.
Nicolas Bonhoure Ashlee Byrnes Robyn D. Moir Wassim Hodroj Frédéric Preitner Viviane Praz Genevieve Marcelin Streamson C. Chua Jr. Nuria Martinez-Lopez Rajat Singh Norman Moullan Johan Auwerx Gilles Willemin Hardik Shah Kirsten Hartil Bhavapriya Vaitheesvaran Irwin Kurland Nouria Hernandez Ian M. Willis 《Genes & development》2015,29(9):934-947