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排序方式: 共有385条查询结果,搜索用时 15 毫秒
381.
CH Siar K Nakano KH Ng M Tomida H Nagatsuka T Kawakami 《European journal of medical research》2010,15(4):180-184
Background
Squamous odontogenic tumor (SOT) is a rare benign odontogenic epithelial neoplasm. A slow-growing painless expansive swelling is the common presenting symptom. Histopathologically, SOT can be easily misdiagnosed as an acanthomatous ameloblastoma. Although Notch receptors and ligands have been shown to play a role in cell fate decisions in ameloblastomas, the role of these cell signaling molecules in SOT is unknown.Case report
This paper describes a case of SOT affecting the anterior mandible of a 10-year-old Indian female. The patient was treated by local surgical excision and there has been no follow-up clinical record of recurrence 5 years after primary treatment. Histopathological examination revealed a solid, locally-infiltrative neoplasm composed of bland-looking squamatoid islands scattered in a mature fibrous connective tissue stroma and the diagnosis was SOT. Immunohistochemical evaluation showed positive reactivity of varying intensity in the neoplastic epithelial cells for Notch1, Notch3, Notch4, and their ligands Jagged1 and Delta1. Expression patterns showed considerable overlap. No immunoreactivity was detected for Notch2 and Jagged2.Conclusions
Present findings suggest that Notch receptors and their ligands play differential roles in the cytodifferentiation of SOT. 相似文献382.
383.
Marieke Emonts Mieke JMW Hazes Jeanine J Houwing-Duistermaat Christa E van der Gaast-de Jongh Lisette de Vogel Huub KH Han Jacques MGW Wouters Jon D Laman Radboud JEM Dolhain 《BMC medical genetics》2011,12(1):36
Background
Various cytokines and inflammatory mediators are known to be involved in the pathogenesis of rheumatoid arthritis (RA). We hypothesized that polymorphisms in selected inflammatory response and tissue repair genes contribute to the susceptibility to and severity of RA. 相似文献384.
Computed tomography densitometry of the lung: a method to assess perfusion defects in acute pulmonary embolism 总被引:11,自引:0,他引:11
Groell R Peichel KH Uggowitzer MM Schmid F Hartwagner K 《European journal of radiology》1999,32(3):192-196
OBJECTIVE: To evaluate the potential of spiral computed tomography (CT) densitometry of the lung to assess segmental perfusion defects in patients with acute pulmonary embolism. MATERIALS AND METHODS: Ten patients with known segmental or lobar perfusion defects on ventilation/perfusion scintigraphy and with normal findings in the contralateral lung segment underwent spiral CT of the thorax before and after the administration of contrast material. Regions of interest were defined in 14 segments with normal perfusion and in 14 segments with reduced perfusion. Three consecutive densitometry measurements were performed in each segment. RESULTS: Those segments with reduced perfusion showed a significantly lower mean CT value on the enhanced scans (-813.4 +/- 57.1 Hounsfield units (HU) vs -794.0 +/- 44.8 HU, P = 0.01) and a significantly decreased contrast enhancement (12.3 +/- 18.2 HU vs 29.8 +/- 16.6 HU, P <0.01) when compared to segments with normal perfusion. Measurements from the unenhanced CT scans were not statistically different between segments with reduced and normal perfusion. CONCLUSIONS: Spiral CT densitometry allows the assessment of at least segmental perfusion defects in patients with acute pulmonary embolism. 相似文献
385.
Kirsten Bomblies Catherine L. Peichel 《Proceedings of the National Academy of Sciences of the United States of America》2022,119(30)
The rediscovery of Mendel’s work showing that the heredity of phenotypes is controlled by discrete genes was followed by the reconciliation of Mendelian genetics with evolution by natural selection in the middle of the last century with the Modern Synthesis. In the past two decades, dramatic advances in genomic methods have facilitated the identification of the loci, genes, and even individual mutations that underlie phenotypic variants that are the putative targets of natural selection. Moreover, these methods have also changed how we can study adaptation by flipping the problem around, allowing us to first examine what loci show evidence of having been under selection, and then connecting these genetic variants to phenotypic variation. As a result, we now have an expanding list of actual genetic changes that underlie potentially adaptive phenotypic variation. Here, we synthesize how considering the effects of these adaptive loci in the context of cellular environments, genomes, organisms, and populations has provided new insights to the genetic architecture of adaptation. 相似文献