人工全髋关节置换患者术前疾病不确定感与焦虑水平的关系

目的 探讨人工全髋关节置换患者术前疾病不确定感与其焦虑水平的关系.方法 选定本院2018年11月～2019年11月住院治疗的200例人工全髋关节置换术患者,采用疾病不确定感量表(MUIS)评估患者术前疾病不确定感,采用焦虑自评量表(SAS)评估焦虑水平,通过比较不同疾病MUIS组的SAS评分和不同焦虑水平组的MUIS评分以及Spearman相关性分析来探讨MUIS量表各维度与焦虑情绪的相关性.结果 200例患者MUIS评分71.5～139.4分,平均(105.26±4.64)分.其中21例是高水平不确定感,占10.50％,MUIS评分(60.25±4.14)分;118例是中水平不确定感,占59.00％,MUIS评分(92.52±10.44)分;61例是低水平不确定感,占30.50％,MUIS评分(138.26±6.44)分.200例患者中46例轻度焦虑,占23.00％;101例中度焦虑,占50.50％;53例重度焦虑,占26.50％.重度焦虑组MUIS评分高于中度焦虑组,中度焦虑组MUIS评分高于轻度焦虑组(P＜0.05).MUIS量表不可预测性、信息缺乏、不确定性、复杂性与焦虑水平均为正相关(P＜0.05).结论 人工全髋关节置换术患者的术前不确定感和焦虑水平均处于中等水平,不确定感和患者的焦虑水平呈正相关,临床应及早予以处理,尽可能减轻患者不确定感、焦虑水平.     

SH-SY5Y细胞凋亡过程中Cpne5蛋白表达的变化

目的探讨Cpne5蛋白在SH-SY5Y细胞凋亡中表达量的变化。方法显微镜观察细胞形态及流式细胞术检测凋亡率,鉴定A23187诱导SH-SY5Y细胞凋亡及血清剥夺诱导凋亡的模型;免疫印迹法检测两种凋亡过程中Cpne5蛋白表达量的变化。结果 10μmol/L A23187诱导SH-SY5Y细胞24h,细胞出现皱缩、凋亡率增加。A23187诱导0.5h,Cpne5蛋白表达量即出现明显的上升,持续至12h;在24h时Cpne5蛋白表达量回落至诱导前水平。血清剥夺72h的SH-SY5Y细胞24份,凋亡率为23.2±2.1%,与对照组1.1±0.1%比,差异有统计学意义（P〈0.01）。免疫印迹结果表明,SH-SY5Y细胞分别经血清剥夺1h、6h、12h、24h、72h对Cpne5蛋白表达量无明显变化。结论 A23187诱导SH-SY5Y细胞凋亡早期Cpne5蛋白表达量有显著变化;提示Cpne5基因可能参与凋亡调控的钙信号通路。     

小鼠Cpne5基因mRNA水平的表达分布及其在胚胎的表达定位

目的明确小鼠Cpne5基因在mRNA水平的组织表达分布及其在胚胎的表达定位。方法提取新生、成年小鼠主要脏器的总RNA,利用RT-PCR法检测Cpne5 mRNA的表达量;合成针对Cpne5 mRNA的杂交探针,取不同胎龄胎鼠进行整体原位杂交。结果 Cpne5 mRNA在成年小鼠10种脏器组织均有不同程度的表达,以大脑,小脑,睾丸和肺脏表达量较高;而肝脏和肌肉未表达。新生小鼠9种脏器中,Cpne5表达量最高的是脑组织,眼和肾次之,肺和肝脏表达量很少。制备并评估Cpne5原杂探针的产量,SP6转录的反义探针浓度为100ng/μL,T7转录的正义探针浓度为10ng/μL,原位杂交结果显示Cpne5 mRNA主要表达于胎鼠的端脑、间脑、中脑及菱脑原节。结论在新生和成年小鼠的脑组织中Cpne5基因mRNA高水平表达,并在胎鼠发育过程中定位于胎脑。     

载碱性成纤维细胞生长因子温敏水凝胶对大鼠骨髓间充质干细胞体外成骨分化的作用研究

目的:实验合成载碱性成纤维细胞生长因子(bFGF)壳聚糖/β-甘油磷酸钠/明胶温敏水凝胶,研究其对骨髓间充质干细胞(BMMSCs)成骨分化的作用.方法:制备壳聚糖/β-甘油磷酸钠/明胶水凝胶,冻干后电子显微镜下观察其表征;检测水凝胶毒性;CCK-8法筛选出载bFGF温敏水凝胶促BMMSCs增殖最适浓度并用于后续研究;碱性磷酸酶染色、茜素红染色及钙结节半定量分析观察其对BMMSCs成骨向分化能力的作用;实时荧光定量PCR检测其对BMMSCs成骨相关基因表达的影响.结果:(1)成功制备壳聚糖/β-甘油磷酸钠/明胶温敏水凝胶,扫描电镜下冻干后的水凝胶孔径为20～80μm.(2)活/死细胞染色结果显示壳聚糖/β-甘油磷酸钠/明胶温敏水凝胶具有良好的生物相容性.(3)载bFGF温敏水凝胶能显著促进BMMSCs增殖,并呈剂量依赖性,最适浓度为100 ng/mL(P<0.01).(4)载bFGF温敏水凝胶组碱性磷酸酶表达增多,钙结节形成增多(P<0.05).(5)载bFGF温敏水凝胶组成骨相关基因(ALP、BMP-2、Runx2)表达增高.结论:载bFGF温敏水凝胶能促进大鼠BMMSCs成骨分化.     

新型冠状病毒肺炎患者的治疗及不良反应监护

目的探讨新型冠状病毒肺炎患者药物治疗与药物不良反应监护。方法隔离收治明确诊断的15例新型冠状病毒感染的肺炎患者,分轻型、普通型、重型及危重型,使用重组人干扰素α-2a、洛匹那韦/利托那韦片、盐酸阿比多尔片、磷酸氯喹、利巴韦林注射液等抗病毒药物治疗,联合抗病毒用药≤3种,同时进行对症支持治疗,在药物治疗过程中实施药学监护,及时发现药物不良反应并对症处理。结果截至2020年3月5日,治愈出院患者9例,在院患者6例,3例患者临床症状及胸部CT均好转,核酸检测为阳性,1例重型患者转为普通型,2例危重型患者转为重型;治疗过程中11例患者出现不同症状、不同程度的不良反应,不良反应发生率达73.33%,8例患者出现消化系统症状,2例患者出现皮疹伴瘙痒,1例患者治疗过程中肝酶轻微升高,根据国家不良反应监测中心分级,2例为新的不良反应,9例为一般的不良反应。结论目前没有经过临床验证有效的治疗方法治疗新型冠状病毒肺炎,在有限的诊疗方案推荐下需要摸索相关的药物治疗,包括药物选择、用法用量及疗程,药物在临床治疗时需进行不良反应监护,及时发现并对症处理,避免因药物引起的机体损害。     

DTI技术在四肢软组织肿瘤良恶性鉴别中的价值

目的探讨扩散张量成像(diffusion tensor imaging,DTI)技术在四肢软组织肿瘤良恶性鉴别中的价值。方法回顾性分析22例经手术病理证实的四肢软组织肿瘤的DTI资料(恶性肿瘤12例,良性肿瘤10例),定量分析良恶性肿瘤部分各向异性值(fractional anisotropy,FA)、相对各向异性值(relative anisotropy,RA)及表观弥散系数值(apparent diffusion coefficient,ADC),并对可疑肿瘤侵犯部位进行肌纤维示踪,评估肌纤维形态。结果四肢软组织恶性肿瘤的FA值、RA值及ADC值分别为0.30±0.11、0.25±0.10、(0.91±0.16)×10-3 mm2/s,良性肿瘤的FA值、RA值及ADC值分别为0.11±0.09、0.12±0.08、(1.39±0.25)×10-3 mm2/s,良恶性肿瘤的FA值、RA值及ADC值均有统计学差异(P0.05)。良性肿瘤周围肌纤维形态学改变为水肿、移位,恶性肿瘤的周围肌纤维主要为侵犯、破坏。结论 DTI通过显示肿瘤周围肌纤维形态变化并对肿瘤实质进行定量测量,可提高四肢软组织肿瘤正确诊断率。     

Cellular and peptide requirements for in vitro clonal deletion of immature thymocytes.

Thymocytes from DO10 T-cell-receptor transgenic mice undergo apoptosis, or programmed cell death, when chicken ovalbumin-(323-339) peptide is administered in vivo. Using DO10 mice thymocytes, we have now developed a simple in vitro model system that recapitulates the in vivo clonal-deletion process. When transgenic thymocytes were cocultured with fibroblasts, B cells, or thymic nurse cell lines (all bearing I-Ad) in the presence of chicken ovalbumin-(323-339), deletion of the transgenic TCR+CD4+CD8+ thymocytes was seen within 8-20 hr. Thymocytes designed to bear I-Ad on their surface could mediate the deletion themselves. Thus, thymocyte clonal deletion entirely depends on the stage at which the thymocytes are vulnerable to the onset of apoptosis, rather than on the nature of the peptide antigen-presenting cells. Furthermore, thymic nurse cell line TNC-R3.1 could cause deletion, strongly suggesting that some thymic epithelial/stromal components are potentially capable of participating in negative selection. In all cases examined, little deletion could be induced at a peptide concentration less than 10 nM, thus defining the minimum amount of peptide antigen required for negative selection. The peptide-dependent in vitro negative-selection system will allow further dissection of the molecular and cellular processes involved in clonal deletion due to apoptosis in the thymus.     

IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms

Myeloproliferative neoplasms (MPNs) are characterized by the clonal expansion of one or more myeloid cell lineage. In most cases, proliferation of the malignant clone is ascribed to defined genetic alterations. MPNs are also associated with aberrant expression and activity of multiple cytokines; however, the mechanisms by which these cytokines contribute to disease pathogenesis are poorly understood. Here, we reveal a non-redundant role for steady-state IL-33 in supporting dysregulated myelopoiesis in a murine model of MPN. Genetic ablation of the IL-33 signaling pathway was sufficient and necessary to restore normal hematopoiesis and abrogate MPN-like disease in animals lacking the inositol phosphatase SHIP. Stromal cell–derived IL-33 stimulated the secretion of cytokines and growth factors by myeloid and non-hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals. Additionally, in the transgenic JAK2^V617F model, the onset of MPN was delayed in animals lacking IL-33 in radio-resistant cells. In human BM, we detected increased numbers of IL-33–expressing cells, specifically in biopsies from MPN patients. Exogenous IL-33 promoted cytokine production and colony formation by primary CD34⁺ MPN stem/progenitor cells from patients. Moreover, IL-33 improved the survival of JAK2^V617F-positive cell lines. Together, these data indicate a central role for IL-33 signaling in the pathogenesis of MPNs.     

Effect of cytokines on liver necrosis

AIM To investigate the effect of cytokines on the liver necrosis.METHODS rIL (interleukin)-1, rIL-6, rIFN (interferon), rTNF (tumor necrosis factor) α with or without D-galactosamine (D-GAL) were injected into the abdominal cavity of mice separately. ALT, TBIL (total bilirubin) and histological changes were observed.RESULTS There was no effect on hepatocyte of normal mice after injection of rIL-1, rIL-6, rIFN alone or together. The serum total bilirubin (TBIL) and liver necrosis of mice increased after rTNFα, rIL-6 or rIFN were used separately with D-GAL. The TBIL level (μmol/L) was 46.19±10.62, 44.55±12.9 and 41.94±14.9, higher than that caused by D-GAL alone (TBIL, 26.67μmol/L±11.14μmol/L). The serum TBIL of mice and the degree of liver necrosis increased after injection of IL-1, IL-6 with D-GAL and rTNFα.CONCLUSION Cytokines, like IL-1,IL-6, IFN and TNFα joined in the process of hepatocyte necrosis. They can enhance the degree of liver necrosis induced by D-GAL.