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91.

Background

The relationship between anxiety and depression in pain patients has not been clarified comprehensively. Previous research has identified a common factor in anxiety and depression, which may explain why depression and anxiety are strongly correlated. However, the specific clinical features of anxiety and depression seem to pull in opposite directions.

Objective

The purpose of this study is to develop a statistical model of depression and anxiety, based on data from pain patients using Hospital Anxiety and Depression Scale (HADS). This model should account for the positive correlation between depression and anxiety in terms of a general factor and also demonstrate a latent negative correlation between the specific factors underlying depression and anxiety.

Methods

The anxiety and depression symptoms of pain patients were evaluated using the HADS and the severity of their pain was assessed with the visual analogue scale (VAS). We developed a hierarchical model of the data using an IRT method called bifactor analysis. In addition, we tested this hierarchical model with model fit comparisons with unidimensional, bidimensional, and tridimensional models. The correlations among anxiety, depression, and pain severity were compared, based on both the bidimensional model and our hierarchical model.

Results

The bidimensional model analysis found that there was a large positive correlation between anxiety and depression (r = 0.638), and both scores were significantly positively correlated with pain severity. After extracting general factor of distress using bifactor analysis, the specific factors underlying anxiety and depression were weakly but significantly negatively correlated (r = −0.245) and only the general factor was significantly correlated with pain severity. Compared with the three first-order models, the bifactor hierarchical model had the best model fit.

Conclusion

Our results support the hypothesis that apart from distress, anxiety and depression are inversely correlated. This finding has not been convincingly demonstrated in previous research.  相似文献   
92.
铜锌超氧化物歧化酶(Cu, Zn-SOD)表面的赖氨酸经化学修饰后, 酶的稳定性显著提高. 赖氨酸被修饰后, 酶的电荷结构遂发生变化, 从而影响到酶分子电场. 使用FDPB方法(有限差分法求解Poission-Boltzman方程)计算了酶修饰前后的静电场变化, 以及对维持酶的结构稳定起重要作用的Cu, Zn配位结构的影响.结果表明, Cu, Zn配位体的两级离解常数在酶修饰后分别约下降103, 106.  相似文献   
93.
土壤中含EB病毒诱导物的检测   总被引:1,自引:0,他引:1  
从广西壮族自治区梧州市、苍梧县、罗城县和北京市收集的土壤标本中发现有EB病毒诱导物。梧州市和苍梧县沿公路和江河两旁桐油树下的土壤标本,对EB病毒早期抗原诱导的阳性率为40~58%。在其他大戟科植物下的土壤标本中,也发现有EB病毒诱导物。对桐油树下土壤中EB病毒诱导物与鼻咽癌发生的可能关系进行了讨论。  相似文献   
94.
最近的研究表明,蛋白质内含子(intein)介导的B区缺失型凝血因子Ⅷ (BDD-FⅧ)的轻链和重链剪接可顺式促进后者的分泌,而且剪接反应在细胞内、外均可发生.为进一步提高基于蛋白质内含子的双载体转BDD-FⅧ基因的功效,将具有促进重链分泌作用的位于Pro1640~Ser1690的酸性区3(acidic region-3,AR-3)引入重链,检验对蛋白质内含子剪接的BDD-FⅧ蛋白分泌和活性的影响.用融合蛋白内含子的附加ar-3重链(HCAR3IntN)基因和轻链(IntCLC)基因共转染培养的HEK293细胞,分别用ELISA和Coatest法定量分析分泌至培养上清中剪接BDD-FⅧ蛋白量和生物活性,并用免疫印迹观察了细胞内的BDD-FⅧ剪接.结果显示,共转HCAR3IntNIntCLC基因细胞,分泌至上清的剪接BDD-FⅧ蛋白量和活性分别为(173±26) μg/L和(1.31±0.15) U/ml,明显高于未添加ar-3的蛋白质内含子融合重链(HCIntN)与轻链(IntCLC)基因共转染细胞[(102±12) μg/L和(0.79±0.09) U/ml],提示AR-3对蛋白质内含子剪接的BDD-FⅧ蛋白分泌和活性有明显改善作用.而且,分别转HCAR3IntNIntCLC基因细胞混合培养后的上清中,亦检测到剪接的BDD-FⅧ蛋白和活性[(35±7) μg/L和(0.28±0.08) U/ml],表明蛋白质内含子可进行不依赖细胞机制的蛋白质剪接.另外,转基因细胞总蛋白呈现明显的可与FⅧ多克隆抗体进行反应的剪接BDD-FⅧ蛋白条带,直观地反映细胞内BDD-FⅧ的剪接.为动物模体内运用蛋白质反式剪接技术的双腺相关病毒载体(AAV)转BDD-FⅧ基因实验提供了依据.  相似文献   
95.
Assembly of N,N′-bis(4-picolinoyl)hydrazine (H2L) with cadmium nitrate in the presence of dicyanamide anion (dca) affords a new coordination polymer {[Cd(HL)(dca)] · (H2O)0.5}n (1), in which the [Cd(HL)]n layers are extended by dca bridges to result in a three-dimensional (3-D) coordination framework. The network structure of 1 has unusual (3,5)-connectivity and represents a new type of (4·62)(4·66·83) topology. Two such identical and complementary networks are entangled to generate a twofold parallel interpenetrating supramolecular lattice.  相似文献   
96.
Niemann-Pick C1-like 1 (NPC1L1) plays a critical role in the enterohepatic absorption of free cholesterol. Cellular cholesterol depletion induces the transport of NPC1L1 from the endocytic recycling compartment to the plasma membrane (PM), and cholesterol replenishment causes the internalization of NPC1L1 together with cholesterol via clathrin-mediated endocytosis. Although NPC1L1 has been characterized, the other proteins involved in cholesterol absorption and the endocytic recycling of NPC1L1 are largely unknown. Most of the vesicular trafficking events are dependent on the cytoskeleton and motor proteins. Here, we investigated the roles of the microfilament and microfilament-associated triple complex composed of myosin Vb, Rab11a, and Rab11-FIP2 in the transport of NPC1L1 from the endocytic recycling compartment to the PM. Interfering with the dynamics of the microfilament by pharmacological treatment delayed the transport of NPC1L1 to the cell surface. Meanwhile, inactivation of any component of the myosin Vb·Rab11a·Rab11-FIP2 triple complex inhibited the export of NPC1L1. Expression of the dominant-negative mutants of myosin Vb, Rab11a, or Rab11-FIP2 decreased the cellular cholesterol uptake by blocking the transport of NPC1L1 to the PM. These results suggest that the efficient transport of NPC1L1 to the PM is dependent on the microfilament-associated myosin Vb·Rab11a·Rab11-FIP2 triple complex.Cholesterol homeostasis in human bodies is maintained through regulated cholesterol synthesis, absorption, and excretion. Intestinal cholesterol absorption is one of the major pathways to maintain cholesterol balance. NPC1L1 (Niemann-Pick C1-like protein 1), a polytopic transmembrane protein highly expressed in the intestine and liver, is required for dietary cholesterol uptake and biliary cholesterol reabsorption (14). Genetic or pharmaceutical inactivation of NPC1L1 significantly inhibits cholesterol absorption and confers the resistance to diet-induced hypercholesterolemia (1, 2, 4). Ezetimibe, an NPC1L1-specific inhibitor, is currently used to prevent and treat cardiovascular diseases (5).Human NPC1L1 contains 1,332 residues with 13 transmembrane domains (6). The third to seventh transmembrane helices constitute a conserved sterol-sensing domain (4, 7). NPC1L1 recycles between the endocytic recycling compartment (ERC)3 and the plasma membrane (PM) in response to the changes of cholesterol level (8). ERC is a part of early endosomes that is involved in the recycling of many transmembrane proteins. It is also reported that ERC is a pool for free cholesterol storage (9). When cellular cholesterol concentration is low, NPC1L1 moves from the ERC to the PM (8, 10). Under cholesterol-replenishing conditions, NPC1L1 and cholesterol are internalized together and transported to the ERC (8). Disruption of microfilament, depletion of the clathrin·AP2 complex, or ezetimibe treatment can impede the endocytosis of NPC1L1, thereby decreasing cholesterol internalization (8, 10, 11).The microfilament (MF) system, part of the cytoskeleton network, is required for multiple cellular functions such as cell shape maintenance, cell motility, mitosis, protein secretion, and endocytosis (12, 13). The major players in the microfilament system are actin fibers and motor proteins (14). Actin fibers form a network that serves as the tracks for vesicular transport (15, 16). Meanwhile, the dynamic assembly and disassembly of actin fibers and the motor proteins provides the driving force for a multitude of membrane dynamics including endocytosis, exocytosis, and vesicular trafficking between compartments (15, 16).Myosins are a large family of motor proteins that are responsible for actin-based mobility (14). Class V myosins (17, 18), comprising myosin Va, Vb, and Vc, are involved in a wide range of vesicular trafficking events in different mammalian tissues. Myosin Va is expressed mainly in neuronal tissues (19, 20), whereas myosins Vb and Vc are universally expressed with enrichment in epithelial cells (21, 22). Class V myosins are recruited to their targeting vesicles by small GTPase proteins (Rab) (23). Rab11a and Rab11 family-interacting protein 2 (Rab11-FIP2) facilitate the binding of myosin Vb to the cargo proteins of endocytic recycling vesicles (2428).Myosin Vb binds Rab11a and Rab11-FIP2 through the C-terminal tail (CT) domain. The triple complex of myosin Vb, Rab11a, and Rab11-FIP2 is critical for endocytic vesicular transport and the recycling of many proteins including transferrin receptor (29), AMPA receptors (30), CFTR (28), GLUT4 (31, 32), aquaporin-2 (26), and β2-adrenergic receptors (33). The myosin Vb-CT domain (24) competes for binding to Rab11a and Rab11-FIP2 and functions as a dominant-negative form. Expression of the CT domain substantially impairs the transport of vesicles. Deficient endocytic trafficking is also observed in cells expressing the GDP-locked form of Rab11a (S25N) (34) or a truncated Rab11-FIP2, which competes for the rab11a binding (35).Here we investigated the roles of actin fibers and motor proteins in the cholesterol-regulated endocytic recycling of NPC1L1. Using pharmaceutical inactivation, dominant-negative forms, and an siRNA technique, we demonstrated that actin fibers and myosin Vb·Rab11a·Rab11-FIP2 triple complex are involved in the export of NPC1L1 to the PM and that this intact MF-associated triple complex is required for efficient cholesterol uptake. Characterization of the molecules involved in the recycling of NPC1L1 may shed new light upon the mechanism of cholesterol absorption.  相似文献   
97.
The effect of ultraviolet-B (UV-B) radiation on Antarctic phytoplankton has become an attractive ecological issue as a result of annual springtime ozone depletion. The effects of UV-B radiation on the growth and antioxidant enzymes were investigated using Antarctic sea ice microalgae Chlamydomonas sp. ICE-L as the material in this study. The results demonstrated that UV-B radiation could notably inhibit the growth, especially at high UV-B radiation intensity (70 μW cm−2). Malondialdehyde and O2 ·− content in ICE-L increased rapidly in early days (1–3 days) exposed to UV-B radiation enhancement, then decreased rapidly. In the stress of UV-B radiation enhancement, the superoxide dismutase, peroxidase and Catalase activities of 1–4 days in ICE-L were obviously higher than those in the control, and their activities became higher at high UV-B radiation intensity (70 μW cm−2). These enzymes activity of 7 days would kept stable at low UV-B radiation intensity (35 μW cm−2), but kept high level at high UV-B radiation intensity (70 μW cm−2). However, the ascorbate peroxidase activity in ICE-L kept stable under the stress of UV-B radiation enhancement. The above experimental results indicated that the antioxidant enzyme system played an important role in the adaptation of Antarctic ice microalgae under the UV-B radiation change of Antarctic ecosystems.  相似文献   
98.
为构建含东北地区人乳头瘤病毒16型(HPV16)全基因组的HPV16.HaCaT细胞模型,收集中国东北地区HPV16单一感染患者宫颈脱落细胞,提取DNA,将HPV16全基因组分成4个区段,通过4对特异性引物对HPV16全基因组进行分段扩增,测序后进行序列拼接及核酸序列分析,克隆HPV16全基因组序列;通过细胞转染,构建含HPV16全基因组的HPV16.HaCaT重组细胞模型;利用聚合酶链式反应(PCR)和细胞免疫荧光法检测重组细胞内HPV16早期基因的表达.成功克隆出中国东北地区HPV16全基因组序列(GenBank登录号:MW320358);构建了东北地区HPV16全基因组的重组质粒及HPV16.HaCaT重组细胞模型;证明了 HPV16早期基因E1-E4、E5、E6和E7在重组细胞模型内均有表达,从而获得中国东北地区HPV16全基因组序列及含有HPV16全基因组的HPV16.HaCaT重组细胞模型.  相似文献   
99.
100.
Summary A psychrotrophic bacterium Colwellia sp. NJ341 from Antarctic sea ice could grow at −5 and 22 °C, and the extent of cellular protein content and growth were greater at low temperatures (0–10 °C) than at higher temperatures. SDS-PAGE analysis demonstrated the presence of a 7 kDa cold-shock protein. The further result of two-dimensional electrophoresis (2-DE) showed that two proteins a and c were newly synthesized at near-freezing temperatures. With matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOF MS) analysis, proteins a and c were identified as glutathione S-transferase (GST) and cold-shock protein A (CspA), respectively, which were involved in cold-adaptation at near-freezing temperature in an Antarctic psychrophilic bacterium Colwellia sp. NJ341.  相似文献   
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