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82.
Marta Pacio Miguez Fernando Santos‐Simarro Sixto García‐Miñaúr Ramón Velázquez Fragua Ángela del Pozo Mario Solís Carmen Jiménez Rodríguez Virginia Rufo‐Rabadán Victoria Eugenia Fernandez Inmaculada Rueda Maria Victoria Gomez del Pozo Natividad Gallego Pablo Lapunzina María Palomares‐Bralo 《American journal of medical genetics. Part A》2020,182(10):2222-2225
83.
Seilicovich A Pisera D Sciascia SA Candolfi M Puntel M Xiong W Jaita G Castro MG 《Current gene therapy》2005,5(6):559-572
Pituitary tumors are the most common primary intracranial neoplasms. Although most pituitary tumors are considered typically benign, others can cause severe and progressive disease. The principal aims of pituitary tumor treatment are the elimination or reduction of the tumor mass, normalization of hormone secretion and preservation of remaining pituitary function. In spite of major advances in the therapy of pituitary tumors, for some of the most difficult tumors, current therapies that include medical, surgical and radiotherapeutic methods are often unsatisfactory and there is a need to develop new treatment strategies. Gene therapy, which uses nucleic acids as drugs, has emerged as an attractive therapeutic option for the treatment of pituitary tumors that do not respond to classical treatment strategies if the patients become intolerant to the therapy. The development of animal models for pituitary tumors and hormone hypersecretion has proven to be critical for the implementation of novel treatment strategies and gene therapy approaches. Preclinical trials using several gene therapy approaches for the treatment of anterior pituitary diseases have been successfully implemented. Several issues need to be addressed before clinical implementation becomes a reality, including the development of more effective and safer viral vectors, uncovering novel therapeutic targets and development of targeted expression of therapeutic transgenes. With the development of efficient gene delivery vectors allowing long-term transgene expression with minimal toxicity, gene therapy will become one of the most promising approaches for treating pituitary adenomas. 相似文献
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86.
API0134对大鼠血浆和血小板血栓素B2生成与血小板聚集的影响 总被引:2,自引:0,他引:2
用放射免疫分析法和比浊法测定PAI0134对大鼠血浆血栓素B2浓度,血小板TXB2生成血小板聚集的影响。静脉注射API013470mg或100mg.kg显著降低血浆TXB2浓度,其降低2率分别为38.8%和51.6%,API0134明显抑制ADP诱导的大鼠血小板聚集和TXB2生成,抑制率分别为27.8%,39.5%,和41.4%,53.6%,两抑制率间呈显著正相关。 相似文献
87.
可切削渗透陶瓷玻璃料对不同堆积密度氧化铝基体的渗透 总被引:1,自引:0,他引:1
探讨了可切削渗透陶瓷 (Infiltration of Machinable- infiltrated- ceramic,MIC)渗透玻璃在不同堆积密度氧化铝基体中的渗透情况及渗透后复合体的颜色表达。在 110 0℃保温 2 h,将玻璃渗透到不同堆积密度的氧化铝基体中 ,分别测得其渗透深度和颜色参数。扫描电镜观察玻璃—氧化铝复合体断面。玻璃渗透深度的平方与氧化铝堆积密度有直线负相关关系 ,最小渗透深度为 3.0 92 m m。复合体的颜色系数与氧化铝堆积密度无相关性。渗透复合体在断裂过程中可见 :裂纹偏转、晶体拔出和穿晶断裂。本实验证实 MIC渗透玻璃的渗透性能达到临床要求。渗透后的复合体颜色稳定 ,强度可靠 相似文献
88.
APOE is a potential modifier gene in an autosomal dominant form of frontotemporal dementia (IBMPFD).
Sarju G Mehta Giles D J Watts Jennifer L Adamson Mike Hutton Geanie Umberger Shuling Xiong Sheena Ramdeen Mark A Lovell Virginia E Kimonis Charles D Smith 《Genetics in medicine》2007,9(1):9-13
PURPOSE: Inclusion-body myopathy, Paget's disease of bone and frontotemporal dementia is an adult-onset autosomal dominant illness (IBMPFD) caused by mutations in the valosin-containing protein (VCP) on chromosome 9p21.1-p12. The penetrance of the gene is 82% for myopathy, 49% for Paget's disease, but may be as low as 30% for frontotemporal dementia. Modifier genes could account for decreased frontotemporal dementia penetrance. In this study apolipoprotein-E (APOE) was evaluated for this role in IBMPFD families based on its known modifier effect in Alzheimer's disease. METHODS: From a database of 231 members of 15 families, 174 had APOE genotype available for analysis. Logistic regressions on APOE genotype and frontotemporal dementia were performed, using appropriate covariates. RESULTS AND CONCLUSION: FTD was associated with APOE 4 genotype (P=0.0002), myopathy (P=0.0006), and age (P=0.01), but not microtubule associated protein tau (MAPT) H2 haplotype (P=0.5) or gender (0.09) after adjustment for membership in pedigrees with at least one APOE 4 genotype. These data suggest a potential link between APOE 4 genotype and the specific form of frontotemporal dementia found in IBMPFD. The molecular basis of this link bears further investigation. We did not observe an association of frontotemporal dementia and H2 MAPT haplotype. 相似文献
89.
Kim NJ Park SJ Choi SH Lee MS Choo EJ Kwak YG Woo JH Ryu J Jeong JY Kim YS 《Microbial drug resistance (Larchmont, N.Y.)》2005,11(3):260-265
To characterize the phenotypes and genotypes of erythromycin-resistant clinical isolates of Streptococcus pneumoniae in Korea and to evaluate the in vitro activity of telithromycin against these erythromycin-resistant isolates, we tested a total of 676 isolates of S. pneumoniae collected from 1997 to 2002 in a tertiary hospital in Seoul, Republic of Korea. MICs for erythromycin and telithromycin were determined by the agar dilution method. The macrolide resistance phenotypes of erythromycin-resistant isolates were determined by the erythromycin- clindamycin-rokitamycin triple disk (ECRTD) and MIC induction tests, whereas their macrolide resistance genotypes were determined by PCR for the erm(B), erm(A), subclass erm(TR), and mef genes. To discriminate between mef(A) and mef(E), PCR-restriction fragment length polymorphism (RFLP) analyses were performed. Of the 676 S. pneumoniae isolates, 459 (67.9%) were resistant to erythromycin. Of the 459 erythromycin-resistant isolates, 343 (74.7%) were assigned to the cMLS phenotype, 48 (10.4%) to the iMcLS phenotype, 4 (0.9%) to the iMLS phenotype, and 64 (14.0%) to the M phenotype. The erm(B) gene was detected in 251 (54.6%) isolates, the mef gene was detected in 64 (14.0%), and both the erm(B) and mef genes were detected in 144 (31.4%) isolates. All of the mef genes detected were identified as mef(E). Of the 459 erythromycin- resistant isolates, all but one were susceptible to telithromycin. The MIC(50)/MIC(90) to telithromycin of isolates carrying erm(B), mef(E), and both genes was 0.06/0.5 microg/ml, 0.03/0.125 microg/ml, and 0.5/1.0 microg/ml, respectively. Although the MICs of telithromycin for the erythromycin-resistant isolates varied according to genotype, telithromycin was very active against these erythromycin-resistant S. pneumoniae. 相似文献
90.
Amyloid-beta peptide (Abeta), the major component of amyloid plaques, can activate brain mononuclear phagocytes (MP; macrophages and microglia), leading to their secretion of neurotoxins. Recent studies strongly suggest that MP-mediated neurotoxicity plays an important role in the pathogenesis of Alzheimer's disease (AD). To further explore this notion, human monocyte-derived macrophages (MDM) were stimulated with naturally secreted alpha-processing soluble amyloid precursor protein/p3 (alphaAPPs/p3) or beta-processing APP/Abeta (betaAPPs/Abeta). MDM conditioned media (MCM) was recovered and tested for its ability to activate recombinant N-methyl-d-aspartate (NMDA) receptor subtype NR1a/NR2B expressed in Xenopus oocytes. Pressure ejection of alphaAPPs/p3- and betaAPPs/Abeta-stimulated MCM produced inward currents of 59.5 +/- 8.9 nA (mean +/- S.E.M., n = 31) and 111.1 +/- 21.0 nA (n = 42) in NR1a/NR2B-expressing oocytes, respectively. The MCM-induced currents were concentration dependent and blocked by 50 microM of the NMDA receptor antagonist 2-amino-5-phosphnovalerate, but not by a non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM). The alphaAPPs/p3- and betaAPPs/Abeta-stimulated MCM placed in non-injected oocytes failed to generate inward current. These results demonstrate that APPs/Abeta-stimulated MCM directly activate NMDA receptor subtypes relevant in the pathogenesis of AD. 相似文献