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Presently, commercially available porous bone substitutes are manufactured by the sacrificial template method, direct foaming method, and polymer replication method (PRM). However, current manufacturing methods provide only the simplest form of the bone scaffold and cannot easily control pore size. Recent developments in medical imaging technology, computer‐aided design, and solid freeform fabrication (SFF), have made it possible to accurately produce porous synthetic bone scaffolds to fit the defected bone shape. Porous scaffolds were fabricated by SFF and PRM for a comparison of physical and mechanical properties of scaffold. The suggested three‐dimensional model has interconnected cubic pores of 500 μm and its calculated porosity is 25%. Whereas hydroxyapatite scaffolds fabricated by SFF had connective macropores, those by PRM formed a closed pore external surface with internally interconnected pores. SFF was supposed to be a proper method for fabricating an interconnected macroporous network. Biocompatibility was confirmed by testing the cytotoxicity, hemolysis, irritation, sensitization, and implantation. In summary, the aim was to verify the safety and efficacy of the scaffolds by biomechanical and biological tests with the hope that this research could promote the feasibility of using the scaffolds as a bone substitute.  相似文献   
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A 70-yr-old man presented with painless gross hematuria. He underwent right nephrectomy for benign disease 9 yr ago. Computed tomography and cystoscopy showed a mass in the distal region of the right ureteral stump. He underwent right ureterectomy and bladder cuff resection. Pathological examination showed T1 and WHO grade 2 transitional cell carcinoma. At 6 months postoperatively, the patient is alive without any evidence of recurrence.  相似文献   
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Quantification of quality of life (QOL) related to disease severity is important in patients with atopic dermatitis (AD), because the assessment provides additional information to the traditional objective clinical scoring systems. To document the impact of AD on QOL for both children and adults as well as to quantify the relationship with disease severity, QOL assessments were performed over a 6-month period on 415 patients with AD. A questionnaire derived from the Infants'' Dermatitis Quality of Life Index (IDQOL), the Children''s Dermatology Life Quality Index (CDLQI) and the Dermatology Life Quality Index (DLQI) was used to determine the QOL for 71 infants, 197 children and 147 adults, respectively. To measure AD severity, both the Rajka & Langeland scoring system and the Scoring of Atopic Dermatitis (SCORAD) index were used. The mean scores were as follows: 7.7 ± 5.5 for IDQOL, 6.6 ± 6.3 for CDLQI, and 10.7 ± 7.9 for DLQI. In conclusion, these QOL scores are correlated with AD severity scores as estimated by the Rajka & Langeland severity score and the SCORAD. The outcome of the QOL instruments in this study demonstrates that atopic dermatitis of both children and adults affects their QOL.  相似文献   
105.

Background and aims  

Pathologic complete remission (CR) of rectal cancer after neoadjuvant chemoradiation therapy (CRT) is generally confirmed by routine hematoxylin and eosin (H&E) staining. The aim of this study was to identify residual rectal cancer cells in primary lesions of patients with pathologic CR by immunohistochemical staining for cytokeratin.  相似文献   
106.
The aim of this study was to review the normal variations and anatomic pitfalls that may mimic diseases on coronary computed tomography angiography (CCTA), based on an echocardiographic correlation. Diverse normal variations and anatomic pitfalls of the heart can be misinterpreted as pathologic processes on radiologic examination. Awareness of normal variations and anatomic pitfalls during CCTA will help avoid misinterpretation of CCTA findings.  相似文献   
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J Oral Pathol Med (2010) 39 : 349–355 Objective: Defects in the mitotic checkpoint lead to aneuploidy and might facilitate tumorigenesis. However, the ploidy status in salivary duct carcinoma (SDC) has been reported to play limited role in prediction of prognosis. Thus, we need more reliable markers to reflect the rapid tumor progression in SDCs. We aimed here to investigate the expression of mitotic checkpoint proteins benzimidazole 1 homolog beta (BUB1B) and mitosis arrest‐deficient 2 like 1 (MAD2L1) in SDCs and to determine their possible role as surrogate prognostic markers. Methods: We analyzed the clinical courses, pathologic findings and immunohistochemical profiles of mitotic checkpoint proteins (BUB1B and MAD2L1) in 27 pathologically confirmed SDCs. The expression status of BUB1B and MAD2L1 was compared with clinicopathologic factors and other molecular markers, such as TGF‐beta, c‐erb‐B2, androgen receptor, vascular endothelial growth factor, and epidermal growth factor receptor, for prognostic significance. Results: High BUB1B expression was detected in 25.9% of subjects, and high MAD2L1 expression was in 55.6% of subjects. However, survival analysis revealed that mitotic checkpoint expression did not have prognostic significance in SDCs, nor did the other studied markers. Rather, the clinical variable of N classification at diagnosis (in N+ status, hazard ratio 5.19, 95% CI 1.26–21.32 for disease‐free survival and hazard ratio 7.18, 95% CI 1.09–46.99 for overall survival) was strongly associated with survival and prognosis based on the Cox proportional hazard model. Conclusions: Mitotic checkpoint proteins appeared to play a limited role in predicting prognosis in SDCs. Further study is required to elucidate the exact role of mitotic checkpoint proteins in SDCs.  相似文献   
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Sphingosine 1-phosphate (S1P) is a bioactive lipid, stored and released from activated platelets, macrophages, and other mammalian cells. We previously reported that S1P induces esophageal smooth muscle contraction in freshly isolated intact cells. Here, we measured S1P-induced ERK1/2 activation and upstream signaling in cultured feline esophageal smooth muscle cells. Activation of ERK1/2 by S1P peaked at 5 min, was sustained up to 30 min, and was blocked by PTX. In contrast, S1P did not activate p38 MAPK or JNK. PTX inhibited S1P-induced ERK1/2 activation. We then used phospholipase inhibitors, DEDA for PLA2, U73122 for PLC, and ρCMB for PLD, to determine that ERK1/2 activation was downstream of PLC activation. The PKC inhibitors, GF109203X and chelerythrine, also suppressed ERK1/2 activation. Whereas the PTK inhibitor, genistein, partially inhibited ERK1/2 activation, the EGFR tyrosine kinase inhibitor, tyrphostin 51, had no effect. Taken together, S1P-induced ERK1/2 activation in cultured ESMCs requires a PTX-sensitive G protein, stimulation of the PLC pathway, and subsequent activation of the PKC and PTK pathways.  相似文献   
110.
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