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1.
目的 探讨煅烧温度对羟基磷灰石结晶性能、晶粒尺寸、形貌的影响.方法 以四水硝酸钙和五氧化二磷为原料,无水乙醇为溶剂,采用溶胶-凝胶法制备出羟基磷灰石(HAP)纳米粉体.利用X射线衍射分析(XRD)和红外光谱(FTIR)研究煅烧温度对羟基磷灰石结晶性能、晶粒尺寸、形貌的影响.采用扫描电镜(SEM)观察制备粉体的表面形貌和尺寸.结果 500℃可初步形成结晶度不太高的HAP;650℃则晶化程度提高;到800℃时晶化程度更高.凝胶HAP经500℃煅烧后,颗粒以团聚为主,边界不清;650℃时结晶粒度大小为48 nm,800 ℃时为78 nm.结论 采用溶胶凝胶法,650℃处理可得到结晶性能良好、分散均匀、50 nm左右大小的羟基磷灰石粉体.煅烧温度对羟基磷灰石粉体的制备有重要影响,温度过低,晶化程度差,晶粒尺度小,提高煅烧温度有利于HAP晶化程度的提高.  相似文献   

2.
目的研究羟基磷灰石纳米粒子细胞毒性和血液相容性。方法将羟基磷灰石纳米粒子以不同分散剂、不同终浓度作用于L929细胞,用MTT比色法观察其细胞毒性;用溶血试验检测其血液相容性。结果 MTT实验表明,不同浓度羟基磷灰石纳米粒子作用细胞后,细胞生长受到不同程度的抑制,这一抑制作用随羟基磷灰石纳米粒子浓度的升高而增强,同一样品各个浓度之间存在显著性差异。对于同一浓度,三种纳米粒子细胞毒性大小依次为:HAP3〉HAP2〉HAP1,而三种分散剂对细胞增殖的影响没有显著性差异。溶血试验表明,溶剂肝素钠、聚丙烯酸纳和三种不同浓度的HAP1纳米粒子均无溶血现象,而三种不同浓度的HAP2和HAP3均有溶血现象,HAP2对浓度存在依赖性,HAP3纳米粒子的三种浓度之间无显著性差异。结论羟基磷灰石纳米粒子对L929细胞增殖有抑制作用,血液相容性与不同的分散剂和纳米粒子浓度有关。  相似文献   

3.
目的探讨煅烧温度对羟基磷灰石结晶性能、晶粒尺寸、形貌的影响。方法以四水硝酸钙和五氧化二磷为原料,无水乙醇为溶剂,采用溶胶-凝胶法制备出羟基磷灰石(HAP)纳米粉体。利用X射线衍射分析(XRD)和红外光谱(FTIR)研究煅烧温度对羟基磷灰石结晶性能、晶粒尺寸、形貌的影响。采用扫描电镜(SEM)观察制备粉体的表面形貌和尺寸。结果500℃可初步形成结晶度不太高的HAP;650℃则晶化程度提高;到800℃时晶化程度更高。凝胶HAP经500℃煅烧后,颗粒以团聚为主,边界不清;650℃时结晶粒度大小为48nm,800℃时为78nm。结论采用溶胶凝胶法,650℃处理可得到结晶性能良好、分散均匀、50nm左右大小的羟基磷灰石粉体。煅烧温度对羟基磷灰石粉体的制备有重要影响,温度过低,晶化程度差,晶粒尺度小,提高煅烧温度有利于HAP晶化程度的提高。  相似文献   

4.
为了得到稳定分散的纳米羟基磷灰石水悬浮液,以羧甲基纤维素钠(CMCNa)作分散剂,采用吸光率实验考察了羧甲基纤维素钠的用量及超声分散时间对纳米羟基磷灰石水悬浮液稳定性的影响,并对其分散机理进行了初步的探讨。结果表明:CMCNa作分散剂时,能有效地分散纳米羟基磷灰石粒子,得到均匀、稳定的纳米羟基磷灰石水悬浮液体系;当CMCNa用量为0.35wt%、超声时间为150s时分散效果最佳;CMCNa分散后,体系的Zeta电位的绝对值提高了69.82mV;CMCNa对纳米HAP悬浮液的稳定分散作用主要是通过粒子间的静电作用和空间位阻来实现的。由此可见,CMCNa对HAP纳米粒子具有较好的分散效果,是制备高分散稳定HAP的理想分散剂。  相似文献   

5.
纳米羟基磷灰石的制备及其抗肿瘤活性的研究   总被引:18,自引:0,他引:18  
采用溶胶凝胶法合成了含CO32 - 的纳米羟基磷灰石 ,研究了热处理温度对羟基磷灰石结晶性能、粒子大小和形貌的影响。并采用体外细胞培养的方法对含CO32 - 纳米羟基磷灰石的抗肿瘤活性进行了初步的探索。结果表明 :以Ca(NO3) 2 ·4H2 O和PO(CH3O) 3为原料 ,采用溶胶凝胶法 ,6 0 0℃处理可得到结晶性能良好、分散均匀、5 0nm左右大小的含CO32 - 的羟基磷灰石粉体。MTT比色法研究结果表明纳米HAP粒子对正常肝细胞L 0 2的抑制率较小 ,而对BEL 74 0 2肝癌细胞有明显的抑制作用 ,且呈现明显的浓度和时间依赖性。荧光显微照片显示纳米HAP粒子能够诱导BEL 74 0 2肝癌细胞的凋亡。  相似文献   

6.
目的利用溶胶-凝胶法制备纳米羟基磷灰石粉体的方法进行研究.方法综述了溶胶-凝胶法的基本原理和分类,介绍了制备纳米羟基磷灰石粉体采用的溶胶-凝胶方法,提出了相关待解决的问题.结果溶胶-凝胶法的研究已取得一定的进展.结论利用该方法有望制备出形状可控、粒度均匀的纳米羟基磷灰石粉体.  相似文献   

7.
目的通过不同浓度的羟基磷灰石(HAP)纳米粒子作用于肝癌H22小鼠肿瘤细胞,研究其对肿瘤细胞凋亡的影响。方法100只肝癌H22小鼠随即分组并连续服用不同剂量的HAP纳米粒子,11d后处死小鼠,计算抑瘤率和细胞凋亡率,评价不同剂量的HAP纳米粒子与H22小鼠肿瘤细胞生长的关系。结果肝癌H22小鼠肿瘤细胞对纳米羟基磷灰石(HAP)较敏感,能明显延长小鼠生存期,高剂量组与丝裂霉素结果相近(P>0.05)。实验后小鼠体重没有明显下降,抑瘤率和细胞的凋亡率随浓度升高而增大,呈明显的剂量依赖性(P<0.01)。结论不同浓度的羟基磷灰石(HAP)纳米粒子能够抑制H22肿瘤细胞的增殖,诱导肿瘤细胞的凋亡,并呈剂量依赖性。  相似文献   

8.
评价用聚乙二醇系列的表面改性剂PEG、F127及PELA改性的纳米羟基磷灰石/聚乳酸复合材料的亲水性和溶胀性,先对纳米羟基磷灰石进行表面改性处理后,再综合用传统的溶液共混、流延法及热压法将改性的和未改性的纳米羟基磷灰石分别与聚乳酸制备成复合薄膜。检测结果表明:改性剂分别被涂敷于纳米羟基磷灰石上,改性处理能够改善纳米颗粒在基材内的分布;改性的纳米羟基磷灰石/聚乳酸复合材料比未改性的对比材料的表面接触角小、表面能大、亲水性好、溶胀度大,达到饱和溶胀度的时间长。改性的纳米羟基磷灰石比未改性的羟基磷灰石改善基体聚乳酸的亲水性和溶胀性效果更显著。  相似文献   

9.
本文综合论述了羟基磷灰石粉体的主要制备方法.在对纳米羟基磷灰石颗粒团聚机理探讨的基础上,分析了该粉体几种主要分散技术研究现状,提出通过改进湿法制备工艺获得高分散性医用羟基磷灰石粉体的技术思路.  相似文献   

10.
目的 利用溶胶凝胶法制备纳米羟基磷灰石粉体的方法进行研究。方法综述了溶胶凝胶法的基本原理和分类,介绍了制备纳米羟基磷灰石粉体采用的溶胶-凝胶方法,提出了相关待解决的问题。结果溶胶-凝胶法的研究已取得一定的进展。结论利用该方法有望制备出形状可控、粒度均匀的纳米羟基磷灰石粉体。  相似文献   

11.
12.
K Tobita  K Ohori 《Acta virologica》1979,23(3):263-266
Virus particles produced by MDCK cells mixedly infected with 3 PFU/cell each of A/Aichi/2/68 (H3N2) (Aichi) and B/Massachusetts/1/71 (Mass) influenza viruses exclusively possessed haemagglutinin (HA) of Mass, although approximately one-fifth of the mixed yield had coding potential for Aichi serotype. Synthesis of major viral proteins of Aichi was markedly suppressed by co-infecting Mass. By increasing the multiplicity of co-infecting Aichi to 30 PFU/cell, interference became reciprocal. Aichi interfered with replication of Mass more severely than Mass did with replication of Aichi. All the major viral proteins of both Aichi and Mass were expressed within the infected cells.  相似文献   

13.
14.
Infection of 1-day-old chicks with PMV-3/parakeet/Netherlands/449/75 (449) by intramuscular, intranasal or contact routes resulted in severe impairment of growth in all groups compared to uninfected control birds. In the group infected intramuscularly with 449 virus 16/22 birds died within 14 days of infection. No clinical signs were seen in 6-week-old chickens infected with 449 by intramuscular, intranasal or contact routes. One-day-old chicks infected with a large dose of NDV-B(1) and one-day-old chicks placed in contact with these birds also showed significant impairment of growth compared to uninfected controls.  相似文献   

15.
Ultraviolet radiation (UVR) may protect against prostate cancer via a mechanism involving vitamin D. Thus, the vitamin D receptor (VDR) gene is a susceptibility candidate, though published data are discrepant. We studied the association of prostate cancer risk with five VDR single nucleotide polymorphisms (SNPs): G/A1229 (SNP 1), A/G3944 (SNP 2), T/C30875 (SNP 3), C/T48200 (SNP 4) and C/T65013 (SNP 5), in 430 cancer and 310 benign prostatic hypertrophy (BPH) patients. The SNP 2 GG genotype frequency was lower in cancer than BPH patients (odds ratio = 0.63, 95% CI = 0.41–0.98, p = 0.039). SNPs 1 and 2, and SNPs 4 and 5, were in linkage disequilibrium. Two copies of haplotypes comprising SNPs 1‐2, G‐G (odds ratio = 0.63, p = 0.039), SNPs 2‐3 G‐C (odds ratio = 0.45, p = 0.008) and SNPs 1‐2‐3 G‐G‐C (odds ratio = 0.44, p = 0.006), but not SNPs 1‐3, G‐C (odds ratio = 0.81, p = 0.34), were associated with reduced risk (reference, no copies of the haplotypes) . These associations were observed after stratification of subjects by extent of UVR exposure. These data show that SNP 2 GG genotype mediates prostate cancer risk, complementing studies reporting this allele is protective in malignant melanoma pathogenesis. They further suggest that published associations of risk with SNP 1 may result from linkage disequilibrium with SNP 2.  相似文献   

16.
In this study, through the analysis of Vibrio cholerae 2740-80 mutant strains produced by the cholera toxin subunit B gene containing Mariner-based transposon, we found that disruption of the varS gene, a member of the recently reported sensory system VarS/VarA–CsrA/B/C/D, resulted in altered expression of hemagglutinin/protease A. To further investigate the connection between VarS and HapA, we generated an additional varS mutant, V. cholerae 2740-80-VS, and examined the effect of this mutation on expression of HapA and of genes in the VarS/VarA–CsrA/B/C/D system. 2740-80-VS showed decreased expression of varS, csrB/C, hapR, and hapA along with increased biofilm production. Interestingly, expression of the alternative sigma factor σs, which is important for adaptation to environmental stress, was also decreased in this mutant. These results indicate that the VarS/VarA–CsrA/B/C/D system is involved in the control of HapA expression and biofilm production in V. cholerae 2740-80 through HapR regulation, and also that VarS/VarA controls expression of σs for HapA regulation.  相似文献   

17.
Summary Three recent wild-type H1N1 influenza virus isolates (A/USSR/90/77, A/Fiji/15899/83 and A/Firenze/13/83) replicated poorly in organ cultures of ferret bronchial tissue compared with the replication of an H3N2 wild-type virus (A/England/939/69). All four viruses replicated well in nasal turbinate tissue. Examination of one H1N1 virus (A/USSR/90/77)in vivo showed heavy infection in the upper respiratory tract of ferrets but little in the lower respiratory tract. These results raise the possibility that the mildness of human influenza arising from the H1N1 strains may be due to lack of capacity to attack the lower respiratory tract as well as the presence of antibody in previously exposed persons.With 1 Figure  相似文献   

18.
The immunogenicity of the Russian cold-adapted (ca) donor stains, A/Leningrad (Len)/134/17/57 and A/Leningrad/134/47/57, and the US strain A/Ann Arbor (AA)/6/60-ca, were compared in BALB/c mice with their respective wild-type parental viruses. Each ca donor strain was less immunogenic than its wild-type parent. The vaccinating dose, when administered twice, which prevented multiplication of a standard challenge of parental wild-type virus in 50% of mice (the 50% protective dose or PD(50)), was shown for A/Len/134/17/57-ca, A/Len/134/47/57-ca, and A/AA/6/60-ca to be 10(3.77), 10(4.32), and 10(4.70), respectively. These findings were extended by measuring the number of antibody secreting cells induced in the lungs and mediastinal lymph nodes of mice infected with the same ca donors using an ELISPOT assay. When each donor strain was administered twice at a dose of 100 PD(50) over a 3-week interval, the overall immunoglobulin isotype antibody secreting cell profiles were shown to be similar. However, A/Len/134/17/57-ca and A/Len/134/47/57-ca induced significantly higher total immunoglobulin responses in the lungs than A/AA/6/60-ca (P < 0.05). A/Len/134/17/57-ca also induced a significantly greater IgA response in the lungs than A/AA/6/60-ca (P < 0.05). These results suggest that A/Len/134/17/57-ca is a superior immunogen to A/Len/134/47/57-ca which in turn is more immunogenic than A/AA/6/60-ca.  相似文献   

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Under the conditions of both an increased red cell affinity for O(2) at a constant rate of O(2) delivery (arterial O(2) content x flow) and a decrease in the rate of O(2) delivery induced by hypoxic hypoxia at constant blood flow, we have obtained a linear relationship between the partial pressure of O(2) in the muscle venous effluent (P(v,)(O(2))) and O(2) uptake (.V(O(2))). The relationship is described by the equation .V(O(2)) = D(a) x P(v,)(O(2)) + .V(O(2)conv)) where D(a) is the apparent O(2) diffusion capacity and .V(O(2)conv)) is O(2) delivery-limited .V(O(2)), and D(a) x P(v,)(O(2)) represents the O(2) diffusion-limited .V(O(2)) .V(O(2)diff)). From these observations, we propose the hypothesis that .V(O(2)) consists of two additive values, .V(O(2)conv)) and .V(O(2)diff)). The mechanism underlying the reduction in .V(O(2)) that is induced by reducing O(2) delivery to markedly below the .V(O(2)conv)) value has only been investigated using a model based on the single compartment of diffusion-limited .V(O(2)), and has not been investigated in terms of this additive .V(O(2)) model. The single compartment analysis appears to overestimate the role of O(2) diffusion in limiting the reduction of .V(O(2)) that occurs in response to a decrease in O(2) diffusion capacity, as reflected by the .V(O(2))/P(v,)(O(2)) ratio. To gain better insight into the mechanism involved, we altered the rate of O(2) delivery by changing arterial P(O(2)) from normoxia (with inhalation of air) to hypoxia (by inhalation of 10-11 % O(2)) and blood flow (with high and low flow rates (n = 7 for both groups), and very low and ischaemic flow rates (n = 4 for both groups)) in pump-perfused dog gastrocnemius preparations during tetanic isometric contractions at 1 Hz. As rates of O(2) delivery were reduced from 23.2 to 10.9 ml min(-1) (100 g)(-1), significant decreases in P(v,)(O(2)) and .V(O(2)) were observed (P < 0.05). From the data of P(v,)(O(2)) and .V(O(2)) values within this range of O(2) delivery rates, we obtained the regression equation .V(O(2)) = 0.22 x P(v,)(O(2)) + 8.14 (r = 0.58). From the equation, the intercept of the .V(O(2))-axis was significantly different from zero (P < 0.05), in accordance with the observation that the .V(O(2)) /P(v,)(O(2)) ratio (ml min(-1) (100 g)(-1) Torr(-1)) increased from 0.54 to 1.35 (P < 0.05). However, at extremely low rates of O(2) delivery (5.6 and 7.3 ml min(-1) (100 g)(-1) the .V(O(2))/P(v,)(O(2)) ratio was 1.51 and 2.80 (P < 0.05), respectively. This indicates a break in the linear .V(O(2))-P(v,)(O(2)) relationship as the rate of O(2) delivery was reduced to below the .V(O(2)conv)) value of the .V(O(2))-axis intercept. These results suggest that the reduction in .V(O(2)) caused by extreme reductions in the rate of O(2) delivery is not attributable to a reduction in O(2) diffusion capacity, as expected from the .V(O(2))/P(v,)(O(2)) ratio, but to a reduction in the O(2) delivery-limited .V(O(2)) component, as evaluated by the .V(O(2))-axis intercept of the linear .V(O(2))-P(v,)(O(2)) relationship.  相似文献   

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