地面传热实验的微重力修正模拟

目的 使空间飞行器地面传热实验的结果能够有效地应用到空间微重力条件下。方法 用数值模拟的方法研究了矩形空间内45度对称间隔斜进风以及垂直进风和换热情况,壁面条件为等壁温或等热流。对重力和微重力两种情况进行了对比。结果 对等壁温情况,提出了表征空间飞行器舱内换热的关系式,并且将数值计算所得数据按这些关系式进行了最小二乘拟合,得到了空间微重力工况和地面工况下的换热关系式。对等热流情况,本文列出了重力和微重力条件下的最高壁面温度值,给出了两种情况时最高壁面温度的拟合公式。结论 根据本文的内容,可以对地面模型装置的实验结果进行修正,得到空间飞行器原型内的换热情况。     

不同补钾方式治疗严重低钾血症的临床疗效

目的:探讨不同静脉途径注射高浓度氯化钾治疗重度低钾血症的安全性与疗效。方法:收集本院急诊科2010年1月至2013年6月97例重度低钾血症或者,用微量泵通过中心静脉补钾,将97例重度低钾血症患者随机分为治疗组48例与对照组49例,治疗组经中心静脉置管,6%氯化钾注射液经微量泵20~30 ml/h注射;对照组0.3%氯化钾注射液经输液泵150~250 ml/h注射补钾。结果:与对照相比较,治疗组6 h和12 h血钾明显上升较快,补钾终点时长明显缩短,补钾液体量明显减少,其差异均有显著统计学意义(P<0.01)。结论:在严密监测下经中心静脉微量泵高浓度补钾治疗重度低钾血症,是安全、有效、快速的治疗方法,值得在基层医院推广应用。     

慢性HBV携带小鼠模型评估

【摘要】 目的 研究琥珀酸美托洛尔普通颗粒与自制缓释微丸的药代动力学行为,并验证缓释微丸的缓释特性,为后期开展缓释制剂研究打下基础。方法 将大鼠随机分为普通组、缓释组各6只,每组雌雄各3只,普通组大鼠单次口服琥珀酸美托洛尔普通颗粒,缓释组大鼠单次口服等剂量的琥珀酸美托洛尔缓释微丸。采用LC MS/MS法测定血药浓度,采用DAS 2.1.1版药代动力学软件计算药代动力学参数,采用SPSS130统计学软件进行统计学分析。结果 结果表明,两种剂型的AUC(0 t) 、AUC(0 ∞) 、Cmax以及MRT(0 t)、MRT(0 ∞)、t1/2z、Tmax差异显著,具有统计学意义。结论 琥珀酸美托洛尔自制缓释微丸具有显著的缓释特性。可为新剂型的研制、开发提供资料参考。     

hTERT基因短发夹状RNA表达载体对肾癌细胞生长的抑制作用

目的观察针对hTERT基因的短发夹状RNA（shRNA）表达载体pSilencer-hTERT对人肾癌细胞及移植瘤生长的抑制作用。方法（1）pSilencer-hTERT转染人肾癌Kerr-3细胞，1、3、5、7d后逆转录-聚合酶链反应（RT-PCR）、蛋白印迹技术检测hTERTmRNA、蛋白表达，MTT法检测细胞增殖，原位末端标记法检测凋亡。（2）BALB／C-nu裸鼠接种Ketr-3细胞成瘤，瘤内分别注射pSilencer-hTERT（50μg）、空质粒pSilencer1．0-U6（50μg）及等体积（100μg）生理盐水，隔日1次，共7次。治疗结束后第3天处死小鼠，取瘤组织检测肿瘤体积，免疫组织化学染色检测hTERT表达。结果（1）pSilencer-hTERT转染3d后Ketr-3细胞hTERTmRNA表达（43．2±4．4）％、蛋白表达（42．6±5．6）％最低，细胞增殖抑制率（37．3±6．6）％、凋亡细胞阳性率（30．5±4．7）％最高，分别与空质粒对照组[（98．8±4．7）％、（98．0±3．7）％、（3．3±0．9）％、（10．4±2．4）％]比较，差异均有统计学意义（P〈0．01）。（2）pSilencer-hTERT处理组小鼠肿瘤体积（62．4±36．5）mm^3减小，hTERT表达率（65．7±4．7）％降低，分别与空质粒对照组（83．2±38．7）、（90．7±4．2）％比较，差异均有统计学意义（P〈0．05）。结论pSilencer-hTERT能有效、持续抑制人肾癌Ketr-3细胞及裸鼠肾癌移植瘤生长。     

MicroRNA‐494 Promotes Cyclosporine‐Induced Nephrotoxicity and Epithelial to Mesenchymal Transition by Inhibiting PTEN

A major complication associated with cyclosporine (CsA) treatment is nephrotoxicity. In this study, we examined whether microRNAs play a role in cyclosporine‐induced nephrotoxicity. Treatment of mice with CsA resulted in nephrotoxicity that was associated with an early increase in expression of microRNA mmu‐miR‐494 (miR‐494). Similarly, tubular epithelial cell epithelial‐mesenchymal transition (EMT) induced by CsA toxicity resulted in the upregulation of microRNA‐494 and a decrease in PTEN levels in vitro. miR‐494 directly targeted Pten and negatively regulated its expression. Preventing Pten targeting by miR‐494 was sufficient to prevent CsA induced EMT. Knockdown of miR‐494 prevented the downregulation of PTEN in tubular epithelial cells following CsA treatment and also prevented CsA induced EMT. Thus, miR‐494 plays a major role in promoting CsA induced nephrotoxicity through its ability to target Pten thereby contributing to EMT. We suggest that manipulating miR‐494 expression may represent a novel approach to preventing EMT associated with CsA induced nephrotoxicity.     

Risedronate reduces intracortical porosity in women with osteoporosis

Nonvertebral fractures account for 80% of all fractures and their accompanying morbidity and mortality. Despite this, the effect of drug therapy on cortical morphology has received limited attention, partly because cortical bone is believed to remodel less and decrease less with age than trabecular bone. However, the haversian canals traversing the cortex provide a surface for remodeling that produces bone loss, porosity, and cortical fragility. We developed a new method of 3D micro‐computed tomography (µCT) to quantify intracortical porosity and the effects of treatment. Women with osteoporosis randomized to risedronate (5 mg/day, n = 28) or placebo (n = 21) had paired transiliac biopsies at baseline and 5 years imaged using 3D µCT. Pores determined from 8 to 12 slices were stratified by their minor axis length into those 25 to 100 µm (closing cone of haversian canals), 100 to 300 µm (cutting cone of haversian canals), and >300 µm (coalescent cavities). Porosity was analyzed as pore area (percent bone area) and pore density (pore number/mm²). Medians are reported. Risedronate reduced pore area in the 25 to 100, 100 to 300, and 300 to 500 µm ranges over 5 years (p = .0008, .04, NS, respectively) corresponding to an 18% to 25% reduction. In the placebo group, pore area was unchanged. At 5 years, pore area and pore number/mm² in the 25 to 100 µm range were each 17% lower in the risedronate group than in the placebo group (p = .02 and .04, respectively). Risedronate is likely to maintain bone strength and reduce nonvertebral fracture risk in part by reducing remodeling and therefore the number and size of intracortical cavities. © 2010 American Society for Bone and Mineral Research     

Micro‐computed tomography evaluation of vertebral end‐plate trabecular bone changes in a porcine asymmetric vertebral tether

We conducted a micro‐CT analysis of subchondral bone of the vertebral end‐plates after application of compressive stress. Thoracic and lumbar vertebral units were instrumented by carrying out left asymmetric tether in eleven 4‐week‐old pigs. After 3 months of growth, instrumented units and control units were harvested. Micro‐CT study of subchondral bone was performed on one central and two lateral specimens (fixated side and non‐fixated side). In control units, bone volume fraction (BV/TV), number of trabeculae (Tb.N), trabecular thickness (Tb.Th), and degree of anisotropy (DA) were significantly higher, whereas intertrabecular space (Tb.Sp) was significantly lower in center than in periphery. No significant difference between the fixated and non‐fixated sides was found. In instrumented units, BV/TV, Tb.N, Tb.Th, and DA were significantly higher in center than in periphery. BV/TV, Tb.N, and Conn.D were significantly higher in fixated than in non‐fixated side, while Tb.Sp was significantly lower. We noted BV/TV, Tb.N, and Tb.Th significantly lower, and Tb.Sp significantly higher, in the instrumented levels. This study showed, in instrumented units, two opposing processes generating a reorganization of the trabecular network. First, an osteolytic process (decrease in BV/TV, Tb.N, Tb.Th) by stress‐shielding, greater in center and on non‐fixated side. Second, an osteogenic process (higher BV/TV, Tb.N, Conn.D, and lower Tb.Sp) due to the compressive loading induced by growth on the fixated side. This study demonstrates the densification of the trabecular bone tissue of the vertebral end‐plates after compressive loading, and illustrates the potential risks of excessively rigid spinal instrumentation which may induce premature osteopenia. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:232–240, 2010     

Decrease in particle‐induced osteolysis in ovariectomized mice

Postmenopausal osteoporosis is a common disorder that results from increased osteoclastic activity caused by estrogen deficiency. Whether postmenopausal bone remodeling can alter the response to particulate debris is unknown. The purpose of this study was to evaluate the bone response to polyethylene particles in an ovariectomized murine model. Polyethylene particles were implanted onto the calvaria of seven control mice and seven ovariectomized (OVX) mice, as compared with calvaria from sham‐operated and OVX mice. Calvaria were harvested after 14 days. Skulls were analyzed with a high‐resolution micro‐CT and by histomorphometry after staining with Stevenel blue and picrofuschine, and for tartrate‐specific alkaline phosphatase. As assessed by micro‐CT, particle implantation induced a significant decrease in bone thickness in control mice, while bone thickness remained stable in OVX mice. In particle‐implanted animals, the osteoclast number was 2.84 ± 0.3 in control mice and 1.74 ± 0.22 in OVX mice. Mean bone loss was ?12% ± 1.9% in control mice and ?4.7% ± 1.7% in OVX animals. The reduction of osteolytic response suggests that ovariectomy may have a protective role against particle‐induced bone resorption. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:178–183, 2010     

Long noncoding RNA PR11-387H17.6 as a potential novel diagnostic biomarker of atherosclerotic renal artery stenosis

BackgroundAtherosclerotic renal artery stenosis (ARAS) is frequently related to ischemic nephropathy, secondary hypertension, and end-stage renal failure. Thus, this study aimed to explore whether certain circulating long noncoding RNAs (lncRNAs) may be used as potential specific ARAS biomarkers.MethodsIn the present study, a microarray analysis was performed to screen for lncRNAs in renal artery tissue from four ARAS patients and four non-ARAS individuals. To identify specific lncRNAs as candidate potential biomarkers of ARAS, we used the following criteria: the fold change was set to >3.0 (compared with non-ARAS tissues), and p value cutoff was set at .05. According to these criteria, six lncRNAs were identified from 1150 lncRNAs. After validation by quantitative PCR (qPCR), these lncRNAs were independently validated in blood from groups of 18 ARAS patients, 18 non-ARAS individuals, and 18 healthy volunteers, furthermore, the predictive value of lncRNA PR11-387H17.6 was further assessed using blood from groups of 99 ARAS patients, 49 non-ARAS individuals, and 50 healthy volunteers. A receiver operating characteristic (ROC) curve analysis was performed to assess the performance of these lncRNAs as biomarkers.ResultsIn the ROC analysis, the area under the curve (AUC) of PR11-387H17.6 was 0.733, with 52.5% sensitivity and 84.8% specificity in predicting the occurrence of ARAS. After considering the risk factors, the AUC of PR11-387H17.6 was 0.844, and the optimal sensitivity increased from 52.5% to 74.5%, although the specificity decreased from 84.8% to 81.9%. In the multivariable logistic analysis, PR11-387H17.6 was an independent predictor of major adverse events (OR: 3.039; 95% CI: 1.388–6.654; p= .006).ConclusionsPR11-387H17.6 is a potential diagnostic biomarker of ARAS. The lncRNA levels in blood cells are regulated in ARAS. Thus, further investigations of the role of lncRNAs in ARAS are warranted.     

血管内皮生长因子、血小板反应素1在肾上腺皮质肿瘤中的表达及其意义

目的讨论血管内皮生长因子（VEGF）与血小板反应素1（TSP-1）在肾上腺皮质肿瘤中的表达及其临床意义。方法选取经手术治疗且取得完整临床资料的肾上腺皮质肿瘤石蜡包埋标本37例,其中良性组20例,恶性组（ACC组）17例。采用免疫组化技术,检测并分析良、恶性肾上腺皮质肿瘤中VEGF和TSP-1的表达情况。结果TSP-1在ACC组中呈低表达（5／17,29．41％）,在良性组中表达高（13／20,65．00％）,ACC组与良性组之间TSP-1的表达有显著性差异（P〈0．05）。VEGF在ACC组中呈高表达（70．59％）,在良性组中表达较低（25．00％）,VEGF在ACC组中的表达与在良性组中的表达有显著性差异（P〈0．05）。微血管密度（MVD）在ACC组中的表达为（76．40±15．64）／视野,良性组中为（21．05±8．07）／视野,两者之间有显著性差异（P〈0．05）。VEGF的表达和MVD呈正相关（P〈0．01）,TSP-1的表达和MVD呈负相关（P〈0．01）。VEGF的表达和TSP-1的表达呈负相关（rs＇=-0．386）。结论VEGF与TSP-1表达不平衡可能是肾上腺皮质肿瘤肿瘤性血管生成的重要原因,有望为抗肿瘤靶向治疗在ACC中的应用提供相应的理论依据。