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排序方式: 共有928条查询结果,搜索用时 15 毫秒
151.
152.
André S Khayat Adriana C Guimarães Danielle Q Calcagno Aline D Seabra Eleonidas M Lima Mariana F Leal Mário HG Faria Silvia HB Rabenhorst Paulo P Assumpção Samia Demachki Marília AC Smith Rommel R Burbano 《BMC gastroenterology》2009,9(1):55-7
Background
This study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. The p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics. 相似文献153.
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Prudent R Vassal-Stermann E Nguyen CH Pillet C Martinez A Prunier C Barette C Soleilhac E Filhol O Beghin A Valdameri G Honoré S Aci-Sèche S Grierson D Antonipillai J Li R Di Pietro A Dumontet C Braguer D Florent JC Knapp S Bernard O Lafanechère L 《Cancer research》2012,72(17):4429-4439
The emergence of tumor resistance to conventional microtubule-targeting drugs restricts their clinical use. Using a cell-based assay that recognizes microtubule polymerization status to screen for chemicals that interact with regulators of microtubule dynamics, we identified Pyr1, a cell permeable inhibitor of LIM kinase, which is the enzyme that phosphorylates and inactivates the actin-depolymerizing factor cofilin. Pyr1 reversibly stabilized microtubules, blocked actin microfilament dynamics, inhibited cell motility in vitro and showed anticancer properties in vivo, in the absence of major side effects. Pyr1 inhibition of LIM kinase caused a microtubule-stabilizing effect, which was independent of any direct effects on the actin cytoskeleton. In addition, Pyr1 retained its activity in multidrug-resistant cancer cells that were resistant to conventional microtubule-targeting agents. Our findings suggest that LIM kinase functions as a signaling node that controls both actin and microtubule dynamics. LIM kinase may therefore represent a targetable enzyme for cancer treatment. Cancer Res; 72(17); 4429-39. ?2012 AACR. 相似文献
156.
Khalil SN Maposa D Ghelber O Rabb MF Matuszczak M Ganesan BA Tabrizi HK Chuang AZ 《Middle East journal of anesthesiology》2008,19(4):885-899
BACKGROUND: Children with obstructive sleep apnea (OSA) have a higher rate of adverse post-extubation respiratory events, such as laryngospasm, upper airway obstruction, apnea, desaturation and/or need for re-intubation. They are overly sensitive to sedatives and narcotics. Although the etiology of OSA is primarily obstruction (mechanical or neuromuscular), a central element may contribute to OSA. Caffeine citrate has been shown to be effective in treating apnea of prematurity. This study evaluated whether the administration of caffeine benzoate to children with OSA decreases the number of children who experience adverse post-extubation respiratory events. METHODS: In a randomized, double-blind and placebo-controlled study, children with OSA scheduled for adenotonsillectomy (T&A) received either caffeine benzoate, 20 mg/kg IV, (caffeine group, n = 36) or saline (placebo group, n = 36). The primary outcome evaluated the number of children who developed adverse post-extubation respiratory events, and the secondary outcome was the incidence of those events. RESULTS: The results demonstrated the two groups differed in the number of children who developed adverse post-extubation respiratory events (p = 0.032). The overall incidence of adverse postoperative respiratory events was less in the caffeine group than the placebo group (p = 0.0196). CONCLUSION: In children with OSA scheduled for T&A, administration of caffeine benzoate, 20 mg/kg IV, decreased the number of children who developed adverse post-extubation respiratory events and decreased the overall incidence of adverse post-extubation respiratory events. PACU duration, hospital discharge time and postoperative delirium did not differ between groups. 相似文献
157.
定位头影测量方法是评价颅颌面骨骼结构特征的重要手段,广泛运用于颅面生长发育预测及颅颌面骨骼特征等研究^[1]。传统方法诸如Downs分析法、Steiner分析法、Tweed分析法、Wylie分析法、Wits分析法、Ricketts分析法等对颅颌面骨骼结构的评价主要基于角度、线距、比例等,因受面高、颌骨旋转、参照平面变异等影响以及准确度、适用条件等限制,不能充分满足临床需要, 相似文献
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159.
Efficacy of different modes of fractional CO2 laser in the treatment of primary cutaneous amyloidosis: A randomized clinical trial
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Samia M. Esmat MD Marwa M. Fawzi MD Heba I. Gawdat MD Heba S. Ali Safinaz S. Sayed MD 《Lasers in surgery and medicine》2015,47(5):388-395
Background
Primary cutaneous amyloidosis (PCA) comprises three main forms: macular, lichen, and nodular amyloidosis. The current available treatments are quite disappointing.Objectives
Assess and compare the clinical and histological changes induced by different modes of Fractional CO2 laser in treatment of PCA.Patients and Methods
Twenty five patients with PCA (16 macular and 9 lichen amyloidosis) were treated by fractional CO2 using; superficial ablation (area A ) and deep rejuvenation (area B ). Each patient received 4 sessions with 4 weeks intervals. Skin biopsies were obtained from all patients at baseline and one month after the last session. Patients were assessed clinically and histologically (Congo red staining, polarized light). Patients were followed‐up for 3 months after treatment.Results
Both modes yielded significant reduction of pigmentation, thickness, itching, and amyloid deposits (P‐value < 0.001). However, the percentage of reduction of pigmentation was significantly higher in area A (P‐value = 0.003). Pain was significantly higher in area B. Significant reduction in dermal amyloid deposits denotes their trans‐epidermal elimination induced by fractional photothermolysis.Conclusion
Both superficial and deep modes of fractional CO2 laser showed comparable efficacy in treatment of PCA. Superficial mode being better tolerated by patients, is recommended as a valid therapeutic option. Lasers Surg. Med. 47:388–395, 2015. © 2015 Wiley Periodicals, Inc. 相似文献160.
Despite recent advances in the diagnosis and treatment of multiple sclerosis, we still lack a consensus regarding the causes, pathogenesis, and mechanisms of disease progression. Current evidence indicates that multiple sclerosis is an inflammatory neurodegenerative disorder in which both adaptive and innate immunity play important roles in initiation and maintenance of the disease. Recent evidence supports the notion of molecular pathologic abnormalities beyond the plaques and dysfunction of neurons in normal appearing areas, in addition to the multifocal demyelination and axonal loss, as important features that may underlie early reversible changes in the disease. Chronic failure of remyelination, axonal regeneration, and neuronal dysfunction may contribute to disease progression. This article discusses the emerging molecular evidence for the progression of multiple sclerosis with particular focus on alterations in the local central nervous system microenvironment of neural and glial cells. The molecular pathways leading to structural and functional neurodegeneration and those that prevent regeneration need to be identified in order to design new therapeutic strategies that can halt or even reverse disease progression. 相似文献