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排序方式: 共有100条查询结果,搜索用时 15 毫秒
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2.
Ana M. Gómez Guillermo E. Umpierrez Oscar M. Mu?oz Felipe Herrera Claudia Rubio Pablo Aschner Richard Buendia 《Journal of diabetes science and technology》2016,10(2):325-329
Background:
Continuous glucose monitoring (CGM) may improve the management of patients with type 2 diabetes hospitalized in the general ward by facilitating the detection of hyper- and hypoglycemic episodes. However, the lack of data on the accuracy and safety of CGM have limited its application.Methods:
A prospective pilot study was conducted including 38 patients hospitalized in the general ward with a known diagnosis of type 2 diabetes mellitus (DM) and hyperglycemic individuals without a history of DM with a blood sugar of 140-400 mg on admission treated with a basal bolus insulin regimen. Inpatient glycemic control and the incidence of hypoglycemic episodes were compared between detection by CGM of interstitial fluid for up to 6 days and point-of-care (POC) capillary blood glucose monitoring performed pre- and postprandially, before bedtime and at 3 am.Results:
No differences in average daily glucose levels were observed between CGM and POC (176.2 ± 33.9 vs 176.6 ± 33.7 mg/dl, P = .828). However, CGM detected a higher number of hypoglycemic episodes than POC (55 vs 12, P < .01). Glucose measurements were clinically valid, with 91.9% of patients falling within the Clarke error grid A and B zones.Conclusions:
Our preliminary results indicate that the use of CGM in type 2 patients hospitalized in the general ward provides accurate estimation of blood sugar levels and is more effective than POC for the detection of hypoglycemic episodes and asymptomatic hypoglycemia. 相似文献3.
A Buendia F Attie J Ovseyevitz A Zghaib C Zamora D Zavaleta J Vargas-Barron R Richheimer 《Heart (British Cardiac Society)》1983,50(1):31-41
Congenital absence of pulmonary valve leaflets is an uncommon condition usually associated with ventricular septal defect and an obstructive pulmonary valve ring. Twenty-one patients with these malformations are described. Twenty had an associated ventricular septal defect with ventriculoarterial concordance, and one also had transposition of the great arteries, ventricular septal defect, and obstructive pulmonary valve ring. The clinical features, cardiac catheterisation findings, and angiocardiographic results are presented. Twelve patients underwent cardiac surgery. Three patients died, one in the early, and the other two in the late postoperative period. The results, according to the surgical technique employed and postoperative cardiac catheterisation findings, showed that patients in whom the bioprostheses were implanted in the pulmonary position had a better late follow-up. 相似文献
4.
The low-affinity IgE receptor (FcεRII/CD23) plays a role in IgE production. Cytokines participating in IgE synthesis also modulate CD23 expression on lymphocytes, but whether this modulation is different in atopic subjects remains unclear. We studied CD23 expression on B and T lymphocytes in 10 asthmatic patients with Dermatophagoides pteronyssinus hypersensitivity and 10 healthy non-atopic subjects. Studies were performed by flow cytometry, in phytohaemagglutinin (PHA) or IL-4-stimulated mononuclear cell cultures, alone or in the presence of IFN-γ. Soluble CD23 (sCD23) released in the culture supernatants was measured by enzyme-linked immunoassay. Both PHA and IL-4 induced the expression of CD23 on lymphocytes of atopic and non-atopic subjects. Whereas PHA increased both the percentage and mean fluorescence intensity of CD23+ B and T cells, IL-4 alone did not increase the percentage of CD23+ T cells. The effects of IFN-γ were different in both groups, since it was able to reduce the percentage of PHA-stimulated CD23+ T cells only in non-atopic individuals. In non-atopic subjects more than atopic, levels of sCD23 were increased in the supernatants of PHA and IL-4 cultures. These results show that the modulation of CD23 expression is different on B and T cells, and that IFN-γ acts differently in atopic and non-atopic individuals. 相似文献
5.
Enrique Luengo Izaskun Buendia Cristina Fernndez‐Mendívil Paula Trigo‐Alonso Pilar Negredo Patrycja Michalska Borja Hernndez‐García Cristina Snchez‐Ramos Juan A. Bernal Tsuneya Ikezu Rafael Len Manuela G. Lpez 《Journal of pineal research》2019,67(1)
Alterations in autophagy are increasingly being recognized in the pathogenesis of proteinopathies like Alzheimer's disease (AD). This study was conducted to evaluate whether melatonin treatment could provide beneficial effects in an Alzheimer model related to tauopathy by improving the autophagic flux and, thereby, prevent cognitive decline. The injection of AAV‐hTauP301L viral vectors and treatment/injection with okadaic acid were used to achieve mouse and human ex vivo, and in vivo tau‐related models. Melatonin (10 μmol/L) impeded oxidative stress, tau hyperphosphorylation, and cell death by restoring autophagy flux in the ex vivo models. In the in vivo studies, intracerebroventricular injection of AAV‐hTauP301L increased oxidative stress, neuroinflammation, and tau hyperphosphorylation in the hippocampus 7 days after the injection, without inducing cognitive impairment; however, when animals were maintained for 28 days, cognitive decline was apparent. Interestingly, late melatonin treatment (10 mg/kg), starting once the alterations mentioned above were established (from day 7 to day 28), reduced oxidative stress, neuroinflammation, tau hyperphosphorylation, and caspase‐3 activation; these observations correlated with restoration of the autophagy flux and memory improvement. This study highlights the importance of autophagic dysregulation in tauopathy and how administration of pharmacological doses of melatonin, once tauopathy is initiated, can restore the autophagy flux, reduce proteinopathy, and prevent cognitive decline. We therefore propose exogenous melatonin supplementation or the development of melatonin derivatives to improve autophagy flux for the treatment of proteinopathies like AD. 相似文献
6.
Hepatocellular carcinoma in WHV/N-myc2 transgenic mice: oncogenic mutations of beta-catenin and synergistic effect of p53 null alleles 总被引:8,自引:0,他引:8
Renard CA Fourel G Bralet MP Degott C De La Coste A Perret C Tiollais P Buendia MA 《Oncogene》2000,19(22):2678-2686
The intronless N-myc2 gene was originally identified as the major target of hepatitis virus insertion in woodchuck liver tumors. Here we report that transgenic mice carrying the N-myc2 gene controlled by woodchuck hepatitis virus (WHV) regulatory sequences are highly predisposed to liver cancer. In a WHV/N-myc2 transgenic line, hepatocellular carcinomas or adenomas arose in over 70% of mice, despite barely detectable expression of the methylated transgene in liver cells. Furthermore, a transgenic founder carrying unmethylated transgene sequences succumbed to a large liver tumor by the age of two months, demonstrating the high oncogenicity of the woodchuck N-myc2 retroposon. Stabilizing mutations or deletions of beta-catenin were found in 25% of liver tumors and correlated with reduced tumor latency (P<0.05), confirming the important role of beta-catenin activation in Myc-induced tumorigenesis. The ability of the tumor suppressor gene p53 to cooperate with N-myc2 in liver cell transformation was tested by introducing a p53-null allele into WHV/N-myc2 transgenic mice. The loss of one p53 allele in transgenic animals markedly accelerated the onset of liver cancer (P=0.0001), and most tumors of WHV/N-myc2 p53+/Delta mice harbored either a deletion of the wt p53 allele or a beta-catenin mutation. These findings provide direct evidence that activation of N-myc2 and reduction of p53 levels act synergistically during multistage carcinogenesis in vivo and suggest that different genetic pathways may underlie liver carcinogenesis initiated by a myc transgene. Oncogene (2000). 相似文献
7.
Ana Merino José Portolés Rafael Selgas Raquel Ojeda Paula Buendia Javier Oca?a M. Auxiliadora Bajo Gloria del Peso Julia Carracedo Rafael Ramírez Alejandro Martín-Malo Pedro Aljama 《Clinical journal of the American Society of Nephrology》2010,5(2):227-234
Background and objectives: We studied the relationship between microinflammation and endothelial damage in chronic kidney disease (CKD) patients on different dialysis modalities.Design, setting, participants, & measurements: Four groups of CKD stage 5 patients were studied: 1) 14 nondialysis CKD patients (CKD-NonD); 2) 15 hemodialysis patients (HD); 3) 12 peritoneal dialysis patients with residual renal function >1 ml/min (PD-RRF >1); and 4) 13 peritoneal dialysis patients with residual renal function ≤1 ml/min (PD-RRF ≤1). Ten healthy subjects served as controls. CD14+CD16+ cells and apoptotic endothelial microparticles (EMPs) were measured by flow cytometry. Serum vascular endothelial growth factor (VEGF) was measured by ELISA.Results: CKD-NonD and HD patients had a higher percentage of CD14+CD16+ monocytes than PD groups and controls. CD14+CD16+ was similar in the PD groups, regardless of their RRF, and controls. The four uremic groups displayed a marked increase in apoptotic EMPs and VEGF compared with controls. Apoptotic EMPs and VEGF were significantly higher in HD patients than in CKD-NonD and both PD groups. However, there were no significant differences between CKD-NonD and the two PD groups. There was a correlation between CD14+CD16+ and endothelial damage in CKD-NonD and HD patients, but not in PD and controls.Conclusions: There was an increase in CD14+CD16+ only in CKD-NonD and HD patients. In these patients, there was a relationship between increased CD14+CD16+ and endothelial damage. These results strongly suggest that other factors unrelated to the microinflammatory status mediated by CD14+CD16+ are promoting the endothelial damage in PD, regardless of their RRF.Chronic kidney disease (CKD) patients have a higher rate of mortality than the general population, which has been attributed to a higher rate of cardiovascular mortality (1–3). Several studies have also reported a strong association between endothelial damage and chronic inflammation in CKD patients (4–7).The percentage of proinflammatory blood monocytes with the CD14+CD16+ phenotype is higher in hemodialysis (HD) patients (8,9), suggesting that these cells play an important role in the chronic inflammatory disease associated with uremia. CD14+CD16+ cells have been described as a subset of human peripheral monocytes that are phenotypically more differentiated than CD14++ and produce proinflammatory cytokines, such as TNF and IL-6 (10,11). In addition, a higher percentage of CD14+CD16+ monocytes is correlated with endothelial damage in CKD patients (12) and, interestingly, the high levels of CD14+CD16+ also predicted the appearance of cardiovascular disease.Recently, we reported that a decrease in the percentage of proinflammatory CD14+CD16+ cells in uremic patients was associated with a greater clearance of large uremic toxins. In fact, we have demonstrated that on-line hemodiafiltration with a high convective transport reduced the percentage of proinflammatory CD14+CD16+ cells in comparison with high-flux HD (13). Furthermore, we have also observed that higher levels of CD14+CD16+ in CKD patients were correlated with high plasma levels of endothelial microparticles, an early feature of endothelial damage (14).The aim of the present study was to evaluate the effects of different dialysis modalities on microinflammation as assessed by the percentage of CD14+CD16+ monocytes and endothelial damage associated with the CKD. 相似文献
8.
H Fabra-Campos F J Dalmases M Buendia R M Cibriàn 《Endodontics & dental traumatology》1991,7(1):10-14
Tooth fracture by impact is the most common cause of fracture in human incisors. We have designed an experimental system to measure the dynamic fracture force of teeth in vitro, and initial results obtained from a sample of healthy, recently removed human incisors are reported. The method was reproducible and reliable, and the results provide a baseline for studies evaluating the effect of endodontic procedures on the dynamic fracture force of teeth. 相似文献
9.
Integration of woodchuck hepatitis and N-myc rearrangement determine size and histologic grade of hepatic tumors 总被引:9,自引:0,他引:9
Jacob JR Sterczer A Toshkov IA Yeager AE Korba BE Cote PJ Buendia MA Gerin JL Tennant BC 《Hepatology (Baltimore, Md.)》2004,39(4):1008-1016
Integrations of woodchuck hepatitis virus (WHV) DNA and rearrangements of the N-myc 2 gene have been detected frequently in hepatocellular carcinoma (HCC) of Eastern woodchucks (Marmota monax) chronically infected with WHV. Fifty-five hepatocellular neoplasms and matched nontumor hepatic tissue specimens obtained postmortem from 13 chronic WHV carriers were analyzed and the frequency of WHV DNA integrations and of N-myc rearrangements compared in tumors of different size and histologic grade. Four small tumor nodules were classified histologically as adenomas and integrated sequences of WHV DNA were detected in two of the four tumor nodules. In one of the two nodules, there was evidence of N-myc rearrangement. Fifty-one neoplasms were classified as HCC. Seven were grade 1 HCCs. WHV DNA integrations were demonstrated in 43% but none had N-myc rearrangements. Twenty grade 2 HCCs had WHV DNA integrations in 80% and in 38% N-myc rearrangements were present. Twenty-four grade 3 HCCs had integrations of WHV DNA in 79% and N-myc rearrangements in 74%. In two other grade 3 HCCs, rearrangements of N-myc were detected in the absence of WHV DNA integrations. The 12 largest tumors in the series all were grade 2 or 3 HCCs, and in 83%, both WHV DNA integrations and N-myc rearrangements were demonstrated. In conclusion, molecular changes observed in this study suggest a progression of genetic alterations providing either a significant proliferative stimulation and/or a growth advantage in hepatocarcinogenesis of woodchucks with chronic WHV infection. 相似文献
10.
Caux F Dubosclard E Lascols O Buendia B Chazouillères O Cohen A Courvalin JC Laroche L Capeau J Vigouroux C Christin-Maitre S 《The Journal of clinical endocrinology and metabolism》2003,88(3):1006-1013
A-Type lamins, arising from the LMNA gene, are intermediate filaments proteins that belong to the lamina, a ubiquitous nuclear network. Naturally occurring mutations in these proteins have been shown to be responsible for several distinct diseases that display skeletal and/or cardiac muscle or peripheral nerve involvement. These include familial partial lipodystrophy of the Dunnigan type and the mandibuloacral dysplasia syndrome. The pathophysiology of this group of diseases, often referred to as laminopathies, remains elusive. We report a new condition in a 30-yr-old man exhibiting a previously undescribed heterozygous R133L LMNA mutation. His phenotype associated generalized acquired lipoatrophy with insulin-resistant diabetes, hypertriglyceridemia, hepatic steatosis, hypertrophic cardiomyopathy with valvular involvement, and disseminated whitish papules. Immunofluorescence microscopic analysis of the patient's cultured skin fibroblasts revealed nuclear disorganization and abnormal distribution of A-type lamins, similar to that observed in patients harboring other LMNA mutations. This observation broadens the clinical spectrum of laminopathies, pointing out the clinical variability of lipodystrophy and the unreported possibility of hypertrophic cardiomyopathy and skin involvement. It emphasizes the fact that the diagnosis of genetic alterations in A-type lamins requires careful and complete clinical and morphological investigations in patients regardless of the presenting signs. 相似文献