Tanshinone ⅡA improves Alzheimer’s disease via RNA nuclearenriched abundant transcript 1/microRNA-291a-3p/member RAS oncogene family Rab22a axis

BACKGROUND Alzheimer’s disease(AD)is a neurodegenerative condition characterized by oxidative stress and neuroinflammation.Tanshinone ⅡA(Tan-ⅡA),a bioactive compound isolated from Salvia miltiorrhiza plants,has shown potential neuroprotective effects;however,the mechanisms underlying such a function remain unclear.AIM To investigate potential Tan-ⅡA neuroprotective effects in AD and to elucidate their underlying mechanisms.METHODS Hematoxylin and eosin staining was utilized to analyze structural brain tissue morphology.To assess changes in oxidative stress and neuroinflammation,we performed enzyme-linked immunosorbent assay and western blotting.Additionally,the effect of Tan-ⅡA on AD cell models was evaluated in vitro using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Genetic changes related to the long non-coding RNA(lncRNA)nuclear-enriched abundant transcript 1(NEAT1)/microRNA(miRNA,miR)-291a-3p/member RAS oncogene family Rab22a axis were assessed through reverse transcription quantitative polymerase chain reaction.RESULTS In vivo,Tan-ⅡA treatment improved neuronal morphology and attenuated oxidative stress and neuroinflammation in the brain tissue of AD mice.In vitro experiments showed that Tan-ⅡA dose-dependently ameliorated the amyloid-beta 1-42-induced reduction of neural stem cell viability,apoptosis,oxidative stress,and neuroinflammation.In this process,the lncRNA NEAT1-a potential therapeutic target-is highly expressed in AD mice and downregulated via Tan-ⅡA treatment.Mechanistically,NEAT1 promotes the transcription and translation of Rab22a via miR-291a-3p,which activates nuclear factor kappa-B(NF-κB)signaling,leading to activation of the pro-apoptotic B-cell lymphoma 2-associated X protein and inhibition of the anti-apoptotic B-cell lymphoma 2 protein,which exacerbates AD.Tan-ⅡA intervention effectively blocked this process by inhibiting the NEAT1/miR-291a-3p/Rab22a axis and NF-κB signaling.CONCLUSION This study demonstrates that Tan-ⅡA exerts neuroprotective effects in AD by modulating the NEAT1/miR-291a-3p/Rab22a/NF-κB signaling pathway,serving as a foundation for the development of innovative approaches for AD therapy.

Protective Effect and Mechanism of Sodium Tanshinone ⅡA Sulfonate on Microcirculatory Disturbance of Small Intestine in Rats with Sepsis

To explore the protective effect of sodium tanshinone ⅡA sulfonate（STS） on microcirculatory disturbance of small intestine in rats with sepsis,and the possible mechanism,a rat model of sepsis was induced by cecal ligation and puncture（CLP）.Rats were randomly divided into 3 groups：sham operated group（S）,sepsis group（CLP） and STS treatment group（STS）.STS（1 mg/kg） was slowly injected through the right external jugular vein after CLP.The histopathologic changes in the intestinal tissue and changes of mesenteric microcirculation were observed.The levels of tumor necrosis factor-α（TNF-α） in the intestinal tissue were determined by using enzyme-linked immunoabsorbent assay（ELISA）.The expression of intercellular adhesion molecule-1（ICAM-1） in the intestinal tissue was detected by using immunohistochemisty and Western blot,that of nuclear factor κB（NF-κB） and tissue factor（TF） by using Western blot,and the levels of NF-κB mRNA expression by using RT-PCR respectively.The microcirculatory disturbance of the intestine was aggravated after CLP.The injury of the intestinal tissues was obviously aggravated in CLP group as compared with S group.The expression levels of NF-κB p65,ICAM-1,TF and TNF-α were upregulaed after CLP（P0.01）.STS post-treatment could ameliorate the microcirculatory disturbance,attenuate the injury of the intestinal tissues induced by CLP,and decrease the levels of NF-κB,ICAM-1,TF and TNF-α（P0.01）.It is suggested that STS can ameliorate the microcirculatory disturbance of the small intestine in rats with sepsis,and the mechanism may be associated with the inhibition of inflammatory responses and amelioration of coagulation abnormality.

Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone ⅡA Sulfonate

The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ （AngⅡ）-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate （STS） in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction （RT-PCR）. It was found after cardiomyocytes were treated with AngⅡ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly （P〈0.01）. After treatment with AngⅡ for 24 h, the rate of protein synthesis in AngⅡ group was significantly increased as compared with control group （P〈0.01）. After treatment with AngⅡ for 7 days, the size of cardiomyocytes in AngⅡ group was increased obviously as compared with control group （P〈0.05）. After pretreatment with STS or Valsartan before AngⅡ treatment, both of them could inhibit the above effects of AngⅡ （P〈0.05 or P〈0.01）. It was suggested that STS could ameliorate AngⅡ-induced cardiomyocyte hy- pertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.

Growth-inhibiting and Apoptosis-inducing Effects of Tanshinone ⅡA on Human Gastric Carcinoma Cells

To explore the effects of Tanshinone Ⅱ A on the proliferation, apoptosis and gene expression of p53 and bcl-2 in human gastric carcinoma MKN-45 cells. Cell count and MTT assay were used to study the proliferation-inhibiting effect of Tanshinone Ⅱ A on MKN-45 cells. The effect of Tanshinone Ⅱ A on the cell cycle and apoptosis of MKN-45 cells were examined by propidium iodide （PI） staining and flow cytometry. Semi-quantitative RT-PCR was used to further verify the ex- pression of p53 and bcl-2 gene after exposure to Tanshinone Ⅱ A in MKN-45 cells. The results showed that Tanshinone Ⅱ A significantly inhibited the growth and proliferation of MKN-45 cells in a dose- and time-dependent manner （P〈0.05）. Tanshinone Ⅱ A arrested MKN-45 cells in G2/M phase which led to an obvious accumulation of G2/M phase cells while decreased number of Go/G1 phase cells. This resulted in apoptosis of MKN-45 cells and the apoptosis rate was as high as 43.91% after treatment with 2.0 lag/mL Tanshinone Ⅱ A for 96 h. It was also found that Tanshinone Ⅱ A up-regulated expression of p53 gene and down-regulated expression of bcl-2 gene. The cytostatic and antiproliferative effect of Tanshinone Ⅱ A makes it a promising anticancer agent for the treatment of gastric carcinoma.

Effects of Tanshinone ⅡA on Transforming Growth Factor β1-Smads Signal Pathway in Renal Interstitial Fibroblasts of Rats

The effects of tanshinone ⅡA （TSN） on transforming growth factor β1 （TGFβ1） signal transduction in renal interstitial fibroblasts of rats were studied in order to investigate its mechanism in prevention of renal interstitial fibrosis. Rat renal fibroblasts of the line NRK/49F were cultured in vitro, stimulated with 5 ng/mL TGFβ1 and pretreated with 10-6, 10-5, 10-4 mol/L TSN respectively. The mRNA levels of fibronectin （FN） were examined by RT-PCR. The protein expression of FN and Smads was detected by Western blot. TGFβ1 induced the expression of FN mRNA and Smads in a time-dependent manner in a certain range. Compared with pre-stimulation, the FN mRNA and protein levels were increased by 1.1 times and 1.5 times respectively （P〈0.01, P〈0.01）, and the protein expression of phosphorylated Smad2/3 （p-Smad2/3） increased by 7 times at the end of TGFβ1 stimulation （P〈0.01）. TSN pretreatment may down-regulate the FN and p-Smad2/3 expression in a dose-dependent manner. 10-6 mol/L TSN pretreatment had no effect on the FN and p-Smad2/3 expression （both P〉0.05）. After pretreatment with 10-5 and 10-4 mol/L TSN, the FN mRNA levels were decreased by 28.1% and 43.8% respectively （P〈0.05, P〈0.01）, the FN protein levels were decreased by 40% and 44% respectively （P〈0.05, P〈0.05）, and the p-Smad2/3 protein expression were decreased by 40% and 65% respectively （P〈0.05, P〈0.01）. The inhibitory effect of TSN on renal interstitial fibrosis may be related to its blocking effect on TGFβ1-Smads signal pathway in renal intersti- tial fibroblasts.

Preparation and characterisation of solid dispersions of tanshinone ⅡA, cryptotanshinone and total tanshinones

Total tanshinones are lipophilic active constituents extracted from Salvia miltiorrhiza Bge.Tanshinone ⅡA and cryptotanshinone are the major components in total tanshinones.However, the bioavailability of both compounds is low due to poor water solubility. To enhance the solubility and dissolution rate of tanshinone ⅡA, cryptotanshinone and total tanshinones,three common used hydrophilic carriers including PEG 6000, poloxamer 188 and PVP K30 were used to prepare the solid dispersions at different ratios, respectively. The solid dispersions were characterised by scanning electron microscopy(SEM), differential scanning calorimetry(DSC) and Fourier transform infrared spectroscopy(FTIR). The results of powder X-ray diffraction confirmed the microcrystal state of total tanshinones in solid dispersions and no chemical interaction between total tanshinones and carriers was observed in FTIR spectra. The solubility and dissolution rate of tanshinone ⅡA and cryptotanshinone were significantly increased in all solid dispersions. Regarding tanshinone ⅡA, the solubility and dissolution rate of in solid dispersions prepared with poloxamer 188 were significantly higher than that with PEG 6000 and PVP K30. The higher solubility and dissolution rate of cryptotanshinone were obtained in solid dispersion of PVP K30 than that of PEG 6000 solid dispersions but no significant difference from poloxamer 188 solid dispersions. The results indicate that the superior carrier for preparation of tanshinone ⅡA and total tanshinones solid dispersions is poloxamer 188, and that for cryptotanshinone is PVP K30.

Tanshinone ⅡA improves functional recovery in spinal cord injury-induced lower urinary tract dysfunction

Tanshinone ⅡA, extracted from Salvia miltiorrhiza Bunge, exerts neuroprotective effects through its anti-inflammatory, anti-oxidative and anti-apoptotic properties. This study intravenously injected tanshinone ⅡA 20 mg/kg into rat models of spinal cord injury for 7 consecutive days. Results showed that tanshinone ⅡA could reduce the inflammation, edema as well as compensatory thickening of the bladder tissue, improve urodynamic parameters, attenuate secondary injury, and promote spinal cord regeneration. The number of hypertrophic and apoptotic dorsal root ganglion（L6–S1） cells was less after treatment with tanshinone ⅡA. The effects of tanshinone ⅡA were similar to intravenous injection of 30 mg/kg methylprednisolone. These findings suggested that tanshinone ⅡA improved functional recovery after spinal cord injury-induced lower urinary tract dysfunction by remodeling the spinal pathway involved in lower urinary tract control.

Two-step continuous flow process of sodium tanshinone ⅡA sulfonate using a 3D circular cyclone-type microreactor

A sustainable and practical process is presented for the direct synthesis of sodium tanshinone IIA sulfonate(STS).Our approach was inspired by the well-established and industrially applied batch synthetic route for STS production.We constructed a telescoped two-step continuous flow platform.This involved a continuous tanshinone IIA sulfonation and in-line salt formation.For the setup,we constructed a 3D circular cyclone-type microreactor using femtosecond laser micromachining.Compared to the 68%yield for 2 h in batch,the two-step continuous flow had an STS yield of 90%,achieved for a total residence time of<3.0 min under optimal conditions.The proposed continuous flow method vastly simplified the operation and improved procedural safety,while significantly reducing the required acid content and wastewater production.

Growth Inhibition and Apoptosis Induction in Human Hepatoma Cells by Tanshinone Ⅱ_A

In order to .study the effect of tanshinone ⅡA on growth and apoptosis in human hepatoma cell line BEL-7402 in vitro, the human hepatoma cell line BEL-7402 was treated with tanshinone ⅡA at various concentrations for 72 h. Growth suppression was evaluated by MTT assay; apoptosis-relat-ed alterations in morphology and biochemistry were ascertained under cytochemical staining (Hoechst 33258), transmission electron microscopy (TEM), and DNA agarose gel electrophoresis. Apoptotic rate was quantified by flow cytometry (FCM). The results showed that Tanshinone ⅡA could inhibit the growth of hepatoma cells in a dose-dependent manner, with IC50 value being 6. 28μg/ml. After treatment with 1-10μg/ml tanshinone ⅡA for 72 h, BEL-7402 cells apoptosis with nuclear chro-matin condensation and fragmentation as well as cell shrinkage and the formation of apoptotic bodies were observed. DNA ladder could be demonstrated on DNA electrophoresis. FCM analysis showed hypodiploid peaks on histogram, and the apoptotic rates at μg/ml concentration for 12 h> 24 h, 36 h, 48 h and 72 h were (2. 32±0. 16)%, (3. 01±0. 35) %, (3. 87±0. 43)%, (6. 73±0. 58)% and (20. 85 ± 1. 74) % respectively, which were all significantly higher than those in the control group (1. 07±0. 13) %. It is concluded that Tanshinone ⅡA could induce human hepatoma cell line BEL-7402 apoptosis, which may be related to the mechanism of growth inhibition.

The Effect of TanshinoneⅡ A upon the TGF-beta1/Smads Signaling Pathway in Hypertrophic Myocardium of Hypertensive Rats

To investigate the molecular mechanism by which Tanshinone Ⅱ A （TSN Ⅱ A） prevents left ventricular hypertrophy （LVH）, we examined the expression of AT1R, TGF-β1 and Smads gene in the hypertrophic myocardium of hypertensive rats with abdominal aorta constriction. LVH model was established by creating abdominal aorta constriction. Four weeks later, animals were randomly divided into 4 groups with 8 animals in each. One group was used as model control, the other three groups were treated with TSN ⅡA （20 mg/kg）, TSN ⅡA （10 mg/kg） and valsartan （10 mg/kg）, respectively. Another 8 SD rats were subjected to sham surgery and served as blank control. After 8- week treatment, the caudal artery pressure of the animals was measured. The tissues of left ventricle were taken for the measurement of the left ventricular mass index （LVMI） and pathological sectioning and HE-staining were used for determining the myocardial fiber dimension （MFD）. The mRNA expression of AT1R, protein expression of TGF-betal and activity of Smad-2, 4, 7 were detected by RT-PCR and Western blotting, respectively. Our results showed that （1） the blood pressure of rats treated with TSN Ⅱ A, either at high or low dose, was significantly higher than those in the control and valsartan-treated group （P〈0.01, P〈0.05）; （2） LVMI and MFD in TSN Ⅱ A and valsartan-treated rats were higher than those in the control group （P〈0.05） but significantly lower than those in the model control （P〈0.01）; （3） the high doses of TSN Ⅱ A and valsartan significantly down-regulated the mRNA expression of AT 1R and protein expression of TGF-beta l and Smad-3 in the hypertrophic myocardium （P〈0.01）, and TGF-betal in valsartan-treated animals was more significantly lower than that in rats treated with TSN Ⅱ A; （4） the two doses of TSN Ⅱ A and valsartan significantly up-regulated the protein expression of Smad-7 in the hypertrophic myocardium （P〈0.01）, and Smad-7 in the animals treated with high-dose TSN Ⅱ A was significantly higher than that in rats treated with valsartan. It is concluded that inhibition of myocardial hypertrophy induced by TSN ⅡA independent of blood pressure. The underlying mechanism might be the down-regulated expression of AT1R mRNA and Smad-3, increased production of Smad-7, and blocking effect of TSN Ⅱ A on TGF betal/Smads signal pathway in local myocardium.

Tanshinone ⅡA Protects against Lipopolysaccharides-lnduced Endothelial Cell Injury via Rho/Rho Kinase Pathway

Objective： To test whether tanshinone ⅡA （Tan ⅡA）, a highly valued herb derivative to treat vascular diseases in Chinese medicine, could protect endothelial cells from bacterial endotoxin （lipopolysaccharides, LPS）-induced endothelial injury. Methods： Endothelial cell injury was induced by treating human umbilical vein endothelial cells （HUVECs） with 0.2 μg/mL LPS for 24 h. Y27632 and valsartan were used as positive controls. The effects of tanshinone Ⅱ A on the LPS-induced cell viability and apoptosis rate of HUVECs were tested by flow cytometry, cell migration by transwell, adhesion by a 96-well plate pre-coated with vitronectin and cytoskeleton reorganization by immunofluorescence assay. Rho/Rho kinase （ROCK） pathway- associated gene and protein expression were examined by microarray assay; quantitative real-time polymerase chain reaction and Western blotting were used to confirm the changes observed by microarray. Results： Tan ][ A improved cell viability, suppressed apoptosis and protected cells from LPS-induced reductions in cell migration and adhesion at a comparable magnitude to that of Y27632 and valsartan. Tan II A, Y27632 and valsartan also normalized LPS-induced actomyosin contraction and vinculin protein aggregation. A microarray assay revealed increased levels of fibronectin, integrin A5 （ITG A5）, Ras homolog gene family member A （RheA）, myosin light chain phosphatase, phosphatidylinositol-4,5-bisphosphate 3-kinase （PI3K, or PIP2 in Western blotting）, focal adhesion kinase, vascular endothelial growth factor and vascular endothelial growth factor receptor 2 in the damaged HUVECs, which were attenuated to different degrees by Tan ⅡA, Y27632 and valsartan. Conclusion： Tan ⅡA exerted a strong protective effect on HUVECs, and the mechanism was caused, at least in part, by a blockade in the Rho/ROCK pathway, presumably through the down-regulation of ITG A5.

Tanshinone ⅡA Inhibits Dendritic Cell-mediated Adaptive Immunity:Potential Role in Anti-atherosclerotic Activity

Objective：Antigen-presenting cells such as monocytes and dendritic cells（DCs） stimulate T-ceil proliferation and activation during adaptive immunity.This cellular interaction plays a role in the growth of atherosclerotic plaques.Tanshinone ⅡA（TSN） had been shown to decrease the growth of atherosclerotic lesions.We therefore investigated the ability of TSN to inhibit human monocyte-derived DCs and their T-cellstimulatory capacity.Methods：DCs derived from human monocytes cultured with recombinant human interieukin（IL）-4 and recombinant human granulocyte-macrophage colony-stimulating factor were co-cultured with TSN and lipopolysaccharide for 48 h.Phosphate-buffered saline was used as a negative control.Activation markers and the capacity of DCs for endocytosis were measured by flow cytometry,and proinflammatory cytokines were measured by enzyme-linked immunosorbent assays.DCs were co-cultured with lymphocytes to measure T-cell proliferation and IL-2 secretion by mixed lymphocyte reactions.Results：TSN dose-dependently attenuated DC expression of costimulatory molecules（CD86）,and decreased expression of major histocompatibility complex class I（human loukocyte antigen-DR） and adhesion molecules（CD54）.Moreover,TSN reduced secretion of the proinflammatory cytokines IL-12 and IL-1 by human DCs,and restored the capacity for endocytosis.Finally,TSN-preincubated DCs showed a reduced capacity to stimulate T-cell proliferation and cytokine secretion.Conclusions：TSN inhibits DC maturation and decreases the expression of proinflammatory cytokines,while impairing their capacity to stimulate T-cell proliferation and cytokine secretion.These effects may contribute to the influence of TSN on the progression of atherosclerotic lesions.

Synthesis of tanshinoneⅡA analogues and their inhibitory activities against Cdc25 phosphatases

Two series of tanshinone ⅡA derivatives were synthesized and evaluated for their antitumor activities as Cdc25 phosphatase inhibitors. Most of them demonstrated potent Cdc25 inhibitory activity and powerful cytotoxicity against A549 tumor cell line, producing IC50 values in very low micromolar range. At last, the preliminary SAR was discussed.

红外高光谱大气探测仪(FY-3E/HIRAS-Ⅱ)在轨数据非线性校正方法

风云三号E星(FY-3E)搭载的高光谱大气探测仪(HIRAS-Ⅱ)能够实现大气的垂直探测,具有高光谱、高灵敏度、高精度的特点。仪器在轨之后由于仪器衰减和环境变化的原因产生非线性响应,影响在轨定标精度。针对非线性响应的问题,提出了一种基于带内光谱的非线性校正方法。首先基于带外低频光谱的非线性特征求解非线性校正系数,将此系数作为初值输入到辐射定标模型中,以星上测量的黑体带内光谱与理想光谱的偏差为目标函数,通过迭代优化非线性校正系数。通过辐射定标实验得出,校正后的黑体亮温偏差明显低于未校正和基于带外光谱的校正方法。将HIRAS-Ⅱ的观测数据与IASI进行交叉比对并计算平均亮温偏差和偏差绝对值,经过带内校正法非线性校正后的亮温平均偏差为-0.13 K,优于带外校正方法。

Amplatzer动脉导管封堵器-Ⅱ治疗伴发主动脉窦脱垂室间隔缺损患儿效果分析

目的探讨Amplatzer动脉导管封堵器(ADO)-Ⅱ治疗伴发主动脉窦脱垂室间隔缺损(VSD)患儿的效果。方法回顾性收集2018年1月至2022年9月于湖南省儿童医院住院治疗的94例伴发主动脉窦脱垂VSD患儿临床资料。其中男60例,女34例,年龄为(4.7±3.1)岁;主动脉窦轻中度脱垂83例,VSD为(4.12±0.97)mm,重度脱垂11例,VSD为(4.95±0.51)mm;VSD类型为膜周部54例,嵴内以上40例。分析VSD大小、主动脉窦脱垂程度与ADO-Ⅱ选择的关系,以及术后中期主动脉瓣反流、残余漏变化,明确ADO-Ⅱ对此类患儿的适用性。结果术后中期最终存留主动脉瓣轻度反流6例,多发于使用4-4 mm、5-4 mm型ADO-Ⅱ封堵器;残余漏10例,主要发生于使用5-4 mm、6-4 mm型封堵器。结论ADO-Ⅱ封堵器在置入形态良好状况下,适用于VSD<6 mm伴主动脉窦脱垂患儿。术后有一定的残余漏和主动脉脉瓣反流发生,但能满足介入治疗要求。

血清α1-抗胰蛋白酶、血管紧张素-Ⅱ与获得性免疫缺陷综合征患者预后的关系

目的探讨血清α1-抗胰蛋白酶(α1-AT)、血管紧张素-Ⅱ(Ang-Ⅱ)与获得性免疫缺陷综合征(AIDS)患者预后的关系。方法将该院2019年5月至2022年5月收治的97例首诊AIDS患者纳入研究作为研究组,另选取同期于该院进行体检的健康者97例作为对照组。根据病历收集患者临床资料。对纳入研究者进行α1-AT、Ang-Ⅱ水平检测,并进行分组比较。对纳入研究的AIDS患者进行为期1年的随访,观察患者预后情况,并比较不同预后患者的α1-AT、Ang-Ⅱ水平。采用单因素及多因素Logistic回归分析影响AIDS患者预后的因素。用受试者工作特征(ROC)曲线分析α1-AT、Ang-Ⅱ水平对患者预后的预测效能。结果研究组血清α1-AT和Ang-Ⅱ水平高于对照组(P<0.05)。AIDS患者1年内的预后不良发生率为23.71%(23/97)。预后不良患者血清α1-AT和Ang-Ⅱ水平高于预后良好患者(P<0.05)。单因素分析显示,预后不良患者C反应蛋白(CRP)水平、淋巴细胞计数水平、合并淋巴瘤者所占比例均高于预后良好患者,清蛋白(ALB)水平低于预后良好患者(P<0.05)。多因素Logistic回归分析显示,合并淋巴瘤(OR=2.087)、高α1-AT水平(OR=2.611)、高Ang-Ⅱ水平(OR=2.138)是影响患者预后的独立危险因素(P<0.05)。ROC曲线分析显示,α1-AT预测AIDS患者预后的曲线下面积(AUC)为0.778,Ang-Ⅱ预测的AUC为0.798,α1-AT联合Ang-Ⅱ预测的AUC为0.918。结论α1-AT和Ang-Ⅱ在AIDS患者血清中水平异常升高,而且与患者预后有关,是影响患者预后的独立危险因素。α1-AT和Ang-Ⅱ联合检测可有效预测患者预后。

基于改进NSGA-Ⅱ算法的间歇采油制度优化

对于低渗透率油井,采用间歇采油制度能有效避免空抽磨损,并减少电能消耗量。为此通过分析沉没度和地层流压随抽油机井生产时间变化的规律,从系统节能的角度出发,建立以采油总产量最大、能耗最低为目标的间歇采油制度多目标优化模型。引入NSGA-Ⅱ并改进该算法对间歇采油制度多目标优化模型求解,运用改进算法得到的Pareto最优解的多样性和收敛性,合理优化抽油机的最优停机时间,最大效率地提升采油效率的同时,最小化电能消耗量。试验结果表明,基于Pareto多目标遗传算法的间歇采油机制优化具有明显的优势,在优化系统效率的同时能够有效减少电能消耗。研究结果可为油井间歇采油机制的改进和优化提供有力的技术支持。

掺杂CoFe_(2)O_(4)膨胀石墨对Pb(Ⅱ)的吸附性能

为解决膨胀石墨吸附后回收难的问题,采用柠檬酸基的溶胶-凝胶法将CoFe_(2)O_(4)粒子负载到膨胀石墨中,制备磁性膨胀石墨。利用扫描电子显微镜(SEM)和磁滞回线对样品的微观形貌和磁性能进行表征,研究了膨胀石墨和磁性膨胀石墨对Pb(Ⅱ)吸附性能的影响因素,包括吸附时间、Pb(Ⅱ)初始质量浓度、吸附剂用量和pH值等,并采用吸附动力学和吸附等温线模型对吸附行为及机理进行了分析。结果表明,膨胀石墨和磁性膨胀石墨对Pb(Ⅱ)的最大吸附量分别为95.6、69.8 mg/g,吸附动力学符合二级动力学模型,吸附等温线符合Langmuir模型。掺杂CoFe_(2)O_(4)粒子缩短了膨胀石墨对Pb(Ⅱ)吸附平衡所需的时间,并使最佳吸附pH值向更加中性条件迁移。

基于改进NSGA-Ⅱ的纤维缠绕落纱点轨迹采样特征权重优化

针对基于空间特征曲线特征函数的纤维缠绕落纱点轨迹采样算法无法自动选择特征权重的问题,建立以特征权重为变量,以得到采样点线性插值生成曲线与原曲线的MAE,RMSE为目标函数的双目标优化模型。提出基于改进NSGA-Ⅱ算法的双目标优化求解方法以优化特征权重。实例验证表明,与传统NSGA-Ⅱ算法相比,改进NSGA-Ⅱ算法求得Pareto解集的MAE,RMSE平均下降了0.002和0.105,算法选取特征权重的MAE,RMSE比特征权重为(0.1,0.3)的MAE,RMSE分别降低了约12.9%和8.5%,比特征权重为(0.9,0.1)的MAE,RMSE分别降低了约20.6%和11.4%,有效地提高了落纱点轨迹采样的精度。

基于PROMETHEE-Ⅱ的电网科技项目后评估评价方法研究

为满足双碳背景下电网精准投资的迫切需求,面对目前电网科技项目数量的急剧增加,迫切需要构建一个后评价指标体系,以低碳绿色发展、运营效率和经济效益为特点,以便评估电网发展规模和速度、结构和安全性以及效率和效益,进而带动科技项目成果转化率的提高,加快科研项目向市场的推广进程。从组织管理、技术水平、成果应用以及影响力4个方面构建电网科技项目后评估的评价指标体系,应用三角模糊数和变异系数法结合的组合赋权法确定各评价指标的权重,基于PROMETHEE-Ⅱ方法对电网科技项目进行后评估,确定最终的评价结果。以实际案例分析,验证该模型具有可行性。