牙列缺损的计算机三维建模

目的 建立牙列缺损的计算机三维模型。方法 采用表面绘制法,依据CT扫描头颅骨标本获得的二维断层图像数据在3D Studio Max中沿牙体长轴放样、微调并赋以材质,得到牙列缺损的计算机三维模型。结果 能在计算机中方便快速地模拟任意类型的牙列缺损,并可全方位地旋转、放大和缩小。结论 提供了一种牙列缺损三维建模的新方法,有利于三维义齿专家系统的开发和计算机辅助教学。     

组织工程化人形下颌骨髁状突的实验研究

目的　评价采用组织工程技术构建人下颌骨髁状突软骨复合组织的可行性。方法　以可降解生物材料聚羟基乙酸 (polyglycolicacid ,PGA) /聚乳酸 (polylacticacid ,PLA)预制人下颌骨髁状突模型 ,体外培养扩增牛骨膜成骨细胞和牛关节表面软骨。实验分 3组 :第 1组 ,模型内仅注入 1.5 %藻酸钙和 30 %氧化乙丙烯 ;第 2组 ,模型内分别注入成骨细胞和软骨细胞悬液 ,浓度为 5× 10 7/ml;第 3组 ,模型内接种成骨细胞藻酸钙悬液 ,同时在模型关节表面涂敷软骨细胞 PluronicF12 7悬液 ,浓度为 5× 10 7/ml。分别植入裸鼠皮下 ,12周后取材 ,作大体和组织学观察。结果　第 1组无骨和软骨形成 ,模型支架明显缩小 ,形态不规则 ;第 2组仅留残缺不全的组织结构 ,标本体积缩小变形 ;第 3组形态结构与原植入模型支架相同 ,组织学观察有骨和软骨组织结构 ,两者界面连接有序 ,骨组织内有大量新生骨板。结论　以人工合成生物材料预制人下颌骨髁状突支架 ,采用组织工程技术 ,可以在裸鼠体内构建具有骨软骨复合结构的正常形态的人形下颌骨髁状突 ,从而为进一步临床应用提供了理论依据     

Total radical trapping antioxidant potential (TRAP) and exercise

The relationship between physical activity, physical fitness and total radical trapping antioxidant potential (TRAP) was examined in the Northern Ireland Health and Activity Survey. This was a cross-sectional population study (n = 1600) using a two-stage probability sample of the population. TRAP was calculated using the sum of the individual serum antioxidant concentrations (urate, protein thiols, ascorbate, alpha tocopherol and bilirubin) multiplied by their respective stoichiometric values. Physical fitness was determined by estimation of VO2max by extrapolation from submaximal oxygen uptake, and physical activity was recorded by computer-assisted interview. Mean serum TRAP concentrations were significantly higher in males (653 +/- 8.2 mumol/l, mean +/- SEM) compared to females (564 +/- 8.0 mumol/l) (p < 0.0001). Both male and female smokers had significantly lower TRAP values than non-smokers (males p < 0.0001, females p = 0.02). In females, there was a positive relationship of TRAP with age (p < 0.001) and body mass index (p < 0.001) but a negative relationship with physical fitness (p < 0.05). The known beneficial effects of exercise and activity do not appear to be directly mediated through increased antioxidant status.      

Mechanism of action of doxepin in the treatment of chronic urticaria

The present study examined 15 patients previously resistant to conventional antihistamines, in which doxepin at doses in the range of 50-75 mg/day was shown to be effective in treatment of chronic urticaria and without significant adverse side effects. However, some controversy remains about its mechanism of action in this particular disease. The aim of the present study was to examine the muscarinic, H1 and H2 blocking activity of doxepin. The following methods were used: a) gastric acid hypersecretion induced by histamine and carbachol in the pylorus-ligated rat preparation; b) contractile dose-response curves to histamine and carbachol in the guinea pig ileum; c) dimaprit-stimulated guinea pig atrium in vitro. pA2 values were determined for atropine, mepyramine, cimetidine and doxepin. As regards histamine, doxepin (50 mg/kg, po) increased gastric pH and decreased secretion volume, gastric acid concentration and total acid output; with carbachol, doxepin weakly antagonized those values. In the ileum, doxepin competitively antagonized carbachol (pA2 = 7.08) and histamine (pA2 = 9.72); pA2 values for atropine and mepyramine against carbachol and histamine were 9.11 and 8.82, respectively. In the atria, the dose-response curve to dimaprit was also competitively displaced by cimetidine (pA2 = 6.69) and doxepin (pA2 = 6.00). Doxepin displayed a very high affinity for H1 histamine receptor, being 8-fold more potent than mepyramine. Doxepin showed significant H2 blocking activity which was 5 times less potent than that of cimetidine. Doxepin competitively antagonized carbachol in the guinea pig ileum, and was 107 times less potent than atropine. The combined H1, H2 and muscarinic blocking activities of doxepin may contribute towards explaining its clinical efficacy in the treatment of chronic urticaria.     

A study of confidential unit exclusion

The effectiveness of the confidential unit exclusion (CUE) procedure recommended by the Food and Drug Administration has been questioned by the blood banking community. The purpose of this study was to determine whether donors were informing the blood center correctly regarding the disposition (transfuse or do not transfuse) of their donated blood. A letter explaining the confidential study and requesting permission to send the participant a questionnaire noting his or her self-exclusion choice was mailed to 230 donors who had chosen transfuse and 276 donors who had chosen do not transfuse. After consent was obtained, participants were sent a second packet and asked to indicate whether they had chosen correctly and, if not, to identify reasons for that incorrect choice. A seven-word terminology quiz made up of words from the CUE form was also enclosed. All participants who had chosen transfuse indicated that this was the correct choice. Approximately 50 percent of those who had chosen do not transfuse indicated that this was an incorrect choice; the most common reason was that "I was not paying attention." The most frequently misunderstood term was "confidential." Donors who chose do not transfuse had a significantly higher rate of error on the terminology quiz (p less than 0.01) than did those who chose transfuse.     

两种不同固位结构附着体义齿修复游离端缺失基牙及缺牙区牙槽嵴应力分布的比较

目的探讨不同固位结构的附着体义齿应力分布特点,为临床应用附着体义齿种类的选择提供依据。方法应用三维有限元的方法分别测定并比较应用键槽缓冲式附着体和柱状附着体修复下颌单侧游离端缺失基牙及牙槽嵴应力分布情况。结果键槽缓冲式附着体义齿对基牙产生应力值小于柱状附着体义齿,对缺牙区牙槽嵴应力大于柱状附着体义齿。结论键槽缓冲式附着体义齿较适合于基牙条件差的义齿修复,柱状附着体义齿较适合于缺牙区牙槽嵴条件差的义齿修复。     

Adaptive differentiation of murine lymphocytes. IV. (Responder × Nonresponder) F(1) T cells can be taught to preferentially help nonresponder,rather than responder, B cells

Responses to the synthetic terpolymer L-glutamic acid, L-lysine, L-tyrosine (GLT) in the mouse are controlled by H-2-1inked Ir-GLTgenes. (Responder × nonresponder) F(1) hybrid mice, themselves phenotypic responders, can be primed with GLT to develop specific helper cells capable of interacting with 2,4-dinitrophenyl hapten (DNP)-primed F(1) B cells in response to DNP-GLT. Unlike the indiscriminant ability of F(1) helper T cells for conventional antigens (i.e. not Ir gene-controlled), which can help B cells of either parental type (as well as F(1)) equally well, GLT-primed F(1) T cells can only provide help under normal circumstances for B lymphocytes of responder parent origin; they are unable to communicate effectively with nonresponder parental B cells (1, and the present studies). The present studies reveal, however, that the induction of a parental cell-induced allogeneic effect during priming of F(1) mice to GLT actually dictates the direction of cooperating preference that will be displayed by such F(1) helper cells for B cells of one parental type or the other. Thus, F(1) T cells, primed to GLT under the influence of an allogeneic effect induced by parental BALB/c cells, develop into effective helpers for nonresponder A/J B cells, but fail to develop effective helpers for responder BALB/c B cells, and vice-versa. In contrast, F(1) T cells, primed to GLT under the influence of an allogeneic effect induced by either parental type, display significantly enhanced levels of helper activity for B cells derived from F(1) donors. These results are interpreted to reflect the existence of two interdependent events provoked by the allogeneic effect: one event augments the differentiation of GLT-specific helper T cells belonging to the subset corresponding to the opposite parental type; this would explain the development of increased helper activity provided to partner B cells of opposite parental type (as well as of F(1) origin). The second event, we postulate, involves the production of responses against the receptors which normally self-recognize native cell interaction determinants; this form of anti-idiotype response is restricted against self- recognizing receptors of the same parental type used for induction of the allogeneic effect, hence explaining diminished helper activity of such F(1) cells for partner B lymphocytes of corresponding parental type.     

Effect of transfusion of fresh frozen plasma on parameters of endothelial condition and inflammatory status in non-bleeding critically ill patients: a prospective substudy of a randomized trial

IntroductionMuch controversy exists on the effect of a fresh frozen plasma (FFP) transfusion on systemic inflammation and endothelial damage. Adverse effects of FFP have been well described, including acute lung injury. However, it is also suggested that a higher amount of FFP decreases mortality in trauma patients requiring a massive transfusion. Furthermore, FFP has an endothelial stabilizing effect in experimental models. We investigated the effect of fresh frozen plasma transfusion on systemic inflammation and endothelial condition.MethodsA prospective predefined substudy of a randomized trial in coagulopathic non-bleeding critically ill patients receiving a prophylactic transfusion of FFP (12 ml/kg) prior to an invasive procedure. Levels of inflammatory cytokines and markers of endothelial condition were measured in paired samples of 33 patients before and after transfusion. The statistical tests used were paired t test or the Wilcoxon signed-rank test.ResultsAt baseline, systemic cytokine levels were mildly elevated in critically ill patients. FFP transfusion resulted in a decrease of levels of TNF-α (from 11.3 to 2.3 pg/ml, P = 0.01). Other cytokines were not affected. FFP also resulted in a decrease in systemic syndecan-1 levels (from 675 to 565 pg/ml, P = 0.01) and a decrease in factor VIII levels (from 246 to 246%, P <0.01), suggestive of an improved endothelial condition. This was associated with an increase in ADAMTS13 levels (from 24 to 32%, P <0.01) and a concomitant decrease in von Willebrand factor (vWF) levels (from 474 to 423%, P <0.01).ConclusionsA fixed dose of FFP transfusion in critically ill patients decreases syndecan-1 and factor VIII levels, suggesting a stabilized endothelial condition, possibly by increasing ADAMTS13, which is capable of cleaving vWF.

Trial registrations

Trialregister.nl NTR2262, registered 26 March 2010 and Clinicaltrials.gov {"type":"clinical-trial","attrs":{"text":"NCT01143909","term_id":"NCT01143909"}}NCT01143909, registered 14 June 2010.