基于SIMD的AVS3并行率失真优化量化算法

针对第三代音频视频标准(the third generation audio video coding standard,AVS3)中的率失真优化量化(rate-distortion optimization quantization,RDOQ)过程的编码效率问题,提出一种基于单指令多数据(single instruction multiple data,SIMD)的并行RDOQ算法。首先,在最优系数决策(optimal coefficient decision,OCD)阶段,通过优化,仅保留扫描线内的依赖关系。然后,在最后一个非零位置决策(last non-zero position decision,LNPD)阶段,基于分治策略,通过将Zig-Zag扫描线分解成多个独立扫描线,实现每条扫描线上最优系数位置的并行计算。最后,采用SIMD指令进行并行加速,以提高整个率失真优化量化的计算效率。实验结果表明,该算法在AI配置下,可以降低29.46%的编码时间,而BD-Rate仅损失0.25%。

miR-143-3p通过靶向integrinβ1抑制肝癌进展

目的探讨肝癌中miR-143-3p的表达及其对肝癌细胞恶性生物学行为的影响,并分析潜在的机制。方法收集肝癌组织,用RT-qPCR和Western blot法分别检测miR-143-3p和integrinβ1的表达。体外培养肝癌细胞,并用miR-143-3p mimics转染后,用XTT和EDU法检测过表达miR-143-3p对细胞增殖活力的影响,用Transwell法检测过表达miR-143-3p对细胞迁移与侵袭的影响,Western blot法检测过表达miR-143-3p对integrinβ1表达的影响。用荧光素酶活性法检测miR-143-3p与integrinβ1的靶向关系。用XTT、EdU和Transwell法检测过表达integrinβ1对已转染miR-143-3p mimics的肝癌细胞增殖、迁移与侵袭的影响。结果与癌旁正常组织比较,肝癌组织中miR-143-3p表达降低,integrinβ1表达升高,且二者均随疾病分期进展进一步降低或增高。过表达miR-143-3p能抑制肝癌细胞增殖、迁移和侵袭,并能下调integrinβ1表达。过表达integrinβ1能逆转miR-143-3p对肝癌细胞的抑制作用。integrinβ1为miR-143-3p的靶点。结论miR-143-3p在肝癌中表达下调,而上调miR-143-3p能通过靶向integrinβ1抑制肝癌细胞增殖、迁移与侵袭。

粘附分子CD44V6及Integrinαvβ_3在胆囊癌中的表达及意义

目的研究粘附分子CD44V6及Integrinαvβ_3在胆囊癌组织及胆囊炎中表达是否存在统计学意义的差异,其表达量与胆囊癌的分化程度之间的关系。方法应用免疫组织化学的方法检测20例胆囊癌及20例慢性胆囊炎组织中CD44V6及Integrinαvβ_3的表达,结合临床病理结果进行分析。结果在胆囊癌中CD44V6和Integrinαvβ_3表达阳性率分别为80.0%和70.0%。CD44V6及Integrinαvβ_3在胆囊癌中表达存在协同性,与胆囊癌分化程度呈正相关(均P<0.05)。结论 CD44V6及Integrinαvβ_3在胆囊癌中高表达(显著高于对照组),并且随着胆囊癌的分化程度降低其表达阳性分值增高;CD44V6及Integrinαvβ_3的表达与原发性胆囊癌的良恶性及分化程度相关;在相同标本中,CD44V6高表达往往伴有Integrinαvβ_3高表达,在胆囊癌的诊断上具有一致性,可联合作为临床监测胆囊癌发生、转移的参考指标。

CXCR4通过integrinαVβ3调控头颈部鳞癌细胞迁移的机制研究

目的:研究C-X-C型趋化因子受体4(CXCR4)-整合素αVβ3(integrinαVβ3)介导头颈部鳞癌细胞迁移的分子生物学机制。方法:应用头颈部鳞癌细胞株HN-5,采用慢病毒转染方法构建CXCR4过表达的细胞株,用荧光显微镜观察基因表达情况;采用脂质体法将CXCR4-siRNA、integrinαVβ3-siRNA分别转染至HN-5细胞和CXCR4过表达的HN-5细胞中,Transwell小室实验检测HN-5细胞迁移能力,Western blot实验检测CXCR4、integrinαVβ3、基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶-2(MMP-2)和黏附斑激酶(FAK)-非受体型酪氨酸蛋白激酶(SRC)-细胞外信号调节激酶(ERK)信号通路相关蛋白的表达情况。结果:CXCR4过表达可上调HN-5细胞中integrinαVβ3表达水平,而抑制CXCR4表达可下调integrinαVβ3表达;CXCR4过表达可调控MMP-2和MMP-9促进癌细胞迁移,并激活FAK-SRC-ERK信号通路;而抑制integrinαVβ3表达可明显逆转CXCR4过表达对HN-5细胞的上述作用。结论:CXCR4过表达可通过integrinαVβ3促进头颈部鳞癌细胞迁移,其作用机制可能与激活FAK-SRC-ERK通路有关。

Integrin beta 3-overexpressing mesenchymal stromal cells display enhanced homing and can reduce atherosclerotic plaque

BACKGROUND Umbilical cord(UC)mesenchymal stem cell(MSC)transplantation is a potential therapeutic intervention for atherosclerotic vascular disease.Integrin beta 3(ITGB3)promotes cell migration in several cell types.However,whether ITGBmodified MSCs can migrate to plaque sites in vivo and play an anti-atherosclerotic role remains unclear.AIM To investigate whether ITGB3-overexpressing MSCs(MSCs^(ITGB3))would exhibit improved homing efficacy in atherosclerosis.METHODS UC MSCs were isolated and expanded.Lentiviral vectors encoding ITGB3 or green fluorescent protein(GFP)as control were transfected into MSCs.Sixty male apolipoprotein E-/-mice were acquired from Beijing Vital River Lab Animal Technology Co.,Ltd and fed with a high-fat diet(HFD)for 12 wk to induce the formation of atherosclerotic lesions.These HFD-fed mice were randomly separated into three clusters.GFP-labeled MSCs(MSCs^(GFP))or MSCs^(ITGB3)were transplanted into the mice intravenously via the tail vein.Immunofluorescence staining,Oil red O staining,histological analyses,western blotting,enzymelinked immunosorbent assay,and quantitative real-time polymerase chain reaction were used for the analyses.RESULTS ITGB3 modified MSCs successfully differentiated into the“osteocyte”and“adipocyte”phenotypes and were characterized by positive expression(>91.3%)of CD29,CD73,and CD105 and negative expression(<1.35%)of CD34 and Human Leukocyte Antigen-DR.In a transwell assay,MSCs^(ITGB3)showed significantly faster migration than MSCsGFP.ITGB3 overexpression had no effects on MSC viability,differentiation,and secretion.Immunofluorescence staining revealed that ITGB3 overexpression substantially enhanced the homing of MSCs to plaque sites.Oil red O staining and histological analyses further confirmed the therapeutic effects of MSCs^(ITGB3),significantly reducing the plaque area.Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction revealed that MSC^(ITGB3)transplantation considerably decreased the inflammatory response in pathological tissues by improving the dynamic equilibrium of pro-and anti-inflammatory cytokines.CONCLUSION These results showed that ITGB3 overexpression enhanced the MSC homing ability,providing a potential approach for MSC delivery to plaque sites,thereby optimizing their therapeutic effects.

Inhibitory Effects of Alpha-zearalenol on Angiotensin II-Induced Integrin β_3 mRNA via Suppression of Nuclear Factor-κB

To investigate the effect of α-zearalenol on angiotensin If-induced β3 integrin mRNA expression in human umbilical vein endothelial cells （HUVECs）. Methods The mRNA level in integrin β3 was determined by reverse transcription-polymerase chain reaction. Endothelial NF-κB activity was determined by the luciferase activity assay of plasmid NF-κB-LUC. Results The angiotensin Ⅱ- induced β3 integrin mRNA expression was inhibited by α-zearalenol and 17β-estradiol （10nmol/L ^-1 μmol/L）, but not influenced by ICI 182, 780, a pure competitive antagonist for estrogen receptor or a nitric oxide inhibitor N^ω-Nitro-L-arginine methyl ester hydrochloride. Alpha-zearalenol and 17β-estradiol suppressed the angiotensin Ⅱ-induced activation of NF-κB in endothelial cells. Condusion Alpha-zearalenol inhibits angiotensin Ⅱ-induced integrin β3 mRNA expression by suppressing NF-κB activation in endothelial cells.

Impacts of PI3K/protein kinase B pathway activation in reactive astrocytes: from detrimental effects to protective functions

Astrocytes are the most abundant type of glial cell in the central nervous system.Upon injury and inflammation,astrocytes become reactive and undergo morphological and functional changes.Depending on their phenotypic classification as A1 or A2,reactive astrocytes contribute to both neurotoxic and neuroprotective responses,respectively.However,this binary classification does not fully capture the diversity of astrocyte responses observed across different diseases and injuries.Transcriptomic analysis has revealed that reactive astrocytes have a complex landscape of gene expression profiles,which emphasizes the heterogeneous nature of their reactivity.Astrocytes actively participate in regulating central nervous system inflammation by interacting with microglia and other cell types,releasing cytokines,and influencing the immune response.The phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway is a central player in astrocyte reactivity and impacts various aspects of astrocyte behavior,as evidenced by in silico,in vitro,and in vivo results.In astrocytes,inflammatory cues trigger a cascade of molecular events,where nuclear factor-κB serves as a central mediator of the pro-inflammatory responses.Here,we review the heterogeneity of reactive astrocytes and the molecular mechanisms underlying their activation.We highlight the involvement of various signaling pathways that regulate astrocyte reactivity,including the PI3K/AKT/mammalian target of rapamycin(mTOR),αvβ3 integrin/PI3K/AKT/connexin 43,and Notch/PI3K/AKT pathways.While targeting the inactivation of the PI3K/AKT cellular signaling pathway to control reactive astrocytes and prevent central nervous system damage,evidence suggests that activating this pathway could also yield beneficial outcomes.This dual function of the PI3K/AKT pathway underscores its complexity in astrocyte reactivity and brain function modulation.The review emphasizes the importance of employing astrocyte-exclusive models to understand their functions accurately and these models are essential for clarifying astrocyte behavior.The findings should then be validated using in vivo models to ensure real-life relevance.The review also highlights the significance of PI3K/AKT pathway modulation in preventing central nervous system damage,although further studies are required to fully comprehend its role due to varying factors such as different cell types,astrocyte responses to inflammation,and disease contexts.Specific strategies are clearly necessary to address these variables effectively.

Changes of β_3 Integrins and Extracellular Matrix Proteins in the Endometrium of Unexplained Infertility

The purpose of this study was to investigate changes of β 3 integrins and extra cellular matrix proteins including fibronectin (FN), laminin (LN) and collagen type Ⅳ (CL typeⅣ) on the endometrium of secretory phase from 31 fertile women (fertility group)and 34 women with unexplained infertility (infertility group) by a histochemical method.The results were as follows:In glandular epithelium, β 3 integrin appeared in the mid secretory phase and continued to late secretory phase in the fertility group, but was not expressed during the secretory phase in the infertility group. Extracellular matrix proteins from the fertility group were expressed more strongly in mid secretory phase than that in the early secretory phase, and were weakest in the late secretory phase. Compared with the fertility group, the levels of extracellular matrix proteins in the infertility group were elevated in the secretory phase. In conclusion: our current study demonstrate that β 3 integrin and extracellular matrix proteins are expressed at different levels in the endometrium during the menstrual cycle. They are involved in endometrial changes during the menstrual cycle and during the implantation of the blastocyst. Their unusual expression result in the failure of implantation.

Ischemic preconditioning partially suppresses and postpones integrin α_Vβ_3 mRNA expression following transient global cerebral ischemia in C57BL/6 mice

Previous studies of integrin αvβ3 have focused on ischemic brain damage, although the role of integrin αvβ3 in ischemic preconditioning （IP） has rarely been reported. The present study analyzed the effects of IP on integrin αvβ3 mRNA expression following cerebral ischemia through the use of hematoxylin-eosin staining and real-time quantitative polymerase chain reaction techniques. Integrin avid3 mRNA expression in the ischemia group peaked at 24 hours after ischemia-reperfusion. In the IP ＋ ischemia group, integrin αvβ3 mRNA expression increased after 24 hours, but remained significantly less than the ischemia group, and expression continued to increase until 7 days after ischemiaJreperfusion. These results demonstrate that IP effectively attenuated upregulation of integrin αvβ3 mRNA expression at 24 hours after ischemia.

子宫内膜异位症不孕患者子宫内膜整合素av、β3表达的初步探讨

目的：探讨子宫内膜异位症是否影响子宫内膜容受性而造成不孕。方法：前瞻性研究我院2004年1月到2005年6月经手术病理确诊的子宫内膜异位症不孕患者胚胎种植窗期血清孕激素、雌激素浓度，组织学分期和子宫内膜整合素av、β3的表达，并与同期已育妇女的指标作比较。结果：15例子宫内膜异位症不孕患者中工期和Ⅱ期共8例（研究1组），Ⅲ期和Ⅳ期共7例（研究2组），与16例对照组比较，血清孕激素和雌激素浓度差异无统计学意义。病理组织学确诊的黄体功能不足差异无统计学意义。子宫内膜整合素β3的表达差异无统计学意义，子宫内膜整合素av的表达差异有统计学意义（P〈0．05），且仅Ⅲ期和Ⅳ期子宫内膜异位症子宫内膜整合素av的表达差异有统计学意义（P〈0．01）。结论：初步证实Ⅲ～Ⅳ期子宫内膜异位症不孕患者子宫内膜容受性标记物-子宫内膜整合素av的表达下降，与其导致不孕和流产相关，值得进一步进行大样本的研究。

整合素avβ3单克隆抗体对小鼠子宫内膜异位病灶的抑制作用

目的研究整合素avβ3单克隆抗体对SCID小鼠子宫内膜异位病灶生长和微血管形成的影响。方法建立人子宫内膜异位症小鼠皮下移植病灶模型。治疗组尾静脉注射整合素avβ3单克隆抗体Lm609(250μg/只),对照组给予相应体积的PBS,1周2次。4周后处死动物,测量病灶,采用免疫组化法检测病灶微血管密度(MVD)及整合素avβ3的表达。结果治疗组与对照组皮下移植病灶质量分别为(0.82±0.09)g和(0.51±0.93)g(P<0.05),病灶组织中MVD则分别为31.2±4.4和14.4±1.8(P<0.05),治疗组病灶受到显著抑制。结论整合素avβ3单克隆抗体通过抑制微血管形成而抑制子宫内膜异位病灶的生长。

整合素α_vβ_3放射性配体^(99)Tc^m-TP1326的制备及其正常兔显像研究

目的制备99Tcm-TP1326,鉴定其理化性质,研究其在兔体内的示踪动力学及组织器官分布特点。方法化学合成制备GA(D)GG-Aba-RGD-4CK(TP1326),并以氯化亚锡为还原剂进行99Tcm标记,纸层析法测定标记率;采用体外稳定性实验、血清蛋白结合实验及油/水分配实验鉴定标记物的理化性质;测定标记物经健康大耳兔静脉注射后不同时相血液放射性浓度,利用药代动力学分析软件判断其最佳房室模型,并得出药代动力学参数;经健康兔耳缘静脉注射99Tcm-TP1326,SPECT动态显像,观察主要组织器官的放射性分布变化。结果 99 Tcm-TP1326的标记率为(95.86±0.83)%,比活度为(38.62±0.32)TBq/mmol。室温放置4 h后放化纯度为(91.76±2.75)%;柱层析未见蛋白结合放射峰;油/水分配系数为-(1.76±0.06)。99Tcm-TP1326在健康兔体内动力学符合权重为1/c的二室模型,t1/2α、t1/2β分别为(3.115±0.771)、(76.978±22.460)min。SPECT显像示血池影消退迅速,放射性主要经肾脏清除,肠道、胃区、颈部未见明显放射性浓聚,脑呈低放射性本底。结论 99Tcm-TP1326标记方法简便,标记率高,体内外稳定性好,动力学特性优良,血液清除快,主要通过泌尿系统排泄,是一种具有潜在应用价值的肿瘤αvβ3受体分子显像剂。

整合素素α_Ⅴβ_3受体显像剂^(18)F标记RGD肽的研究进展

血管新生是肿瘤生长、转移过程中不可缺少的生物过程。整合素αⅤβ3受体在新生血管内皮细胞和多种肿瘤细胞表面高表达,在肿瘤血管新生中起着关键作用,目前已成为肿瘤诊断与治疗的一个重要靶点。精氨酸-甘氨酸-天冬氨酸(Arg-Gly-Asp,RGD)肽可特异性地与整合素αⅤβ3受体结合,18 F标记的RGD肽类化合物PET显像可无创、动态地定量监测整合素αⅤβ3受体表达,在肿瘤早期诊断、疗效监测及抗血管新生评价上发挥着重要作用。本文就近年来国内外18F标记RGD肽在肿瘤αⅤβ3受体显像中的研究进展作简要综述。

整合素β_3及细胞外基质分子纤粘连蛋白、层粘连蛋白在早孕药物流产蜕膜与绒毛中的表达

为了解整合素β３ 及细胞外基质中纤粘连蛋白（ＦＮ）、层粘连蛋白（ＬＭ）在米非司酮抗早孕蜕膜与绒毛组织中的表达。将２０ 例停经≤４９ 天，要求流产的早孕妇女随机分成２ 组，对照组１０ 例，药物流产（药流）组１０ 例，应用流式细胞定性定量分析技术，对经免疫荧光标记的蜕膜、绒毛组织中整合素β３、ＦＮ、ＬＭ 进行分析测定。结果表明，药流组绒毛与蜕膜组织中整合素β３ 及ＬＭ 与正常早孕组比较，呈同步性降低（Ｐ＜ ０．００１～０．０５）；ＦＮ 则无明显变化（Ｐ＞ ０．０５）。提示整合素β３ 和ＬＭ 在维持早孕中具有重要作用，米非司酮可降低绒毛、蜕膜组织中整合素β３ 和ＬＭ

外源性LIF和IL-1对围着床期小鼠子宫内膜整合素β_3亚基表达的调节

Objective:To study regulation of external leukemia inhibitory factor(LIF) and interlukin 1(IL 1) on the expression of integrin β 3 in the mouse endometrium during peri implantation period and explore the mechanism which LIF participate in embryonic implantation.Methods:The mice were injected peritoneally with LIF,IL 1 or IL 1ra at different administration on day 2～4 of pregnancy.The level of integrin β 3 protein was measured with Westernblot method and mRNA measured with RT PCR.Results:The levels of integrin β 3 protein and mRNA were increased by LIF and IL 1(P<0.05) and which relied on administration.The level of integrin β 3 mRNA was decreased by IL 1ra (P<0.05).Conclusion:LIF and IL 1 of cytokines can improve the expression of integrin β 3 in the peri implantation endometrium of mouse.Both of them may take part in implantation by regulating cell adhesion molecules.

来曲唑与克罗米酚对子宫内膜整合素α_Vβ_3和基质金属蛋白酶组织抑制因子-3表达的影响

目的 比较来曲唑（LE）与克罗米酚（CC）促排卵治疗时对植入窗期子宫内膜整合素αvβ3和基质金属蛋白酶组织抑制因子-3（TIMP-3）表达的影响。方法 收集2004年3～10月在本中心服用LE或CC促排卵治疗20例患者植入窗期子宫内膜（LE组9例，CC组11例），另取12例自然月经周期的相应时期内膜作为对照。通过免疫组织化学法测定整合素αvβ3和TIMP-3的表达强度。结果 三组子宫内膜整合素αvβ3的表达强度无显著性差异；TIMP-3表达强度CC组高于LE和对照组。结论 LE和CC都不影响植入窗期子宫内膜中整合素αvβ3的表达。CC使TIMP-3的表达信号明显加强。

抗人整合素ανβ_3单链抗体的构建和表达

目的 :利用基因工程抗体技术构建抗人整合素ανβ3 单链抗体(scFv)。方法 :从分泌抗人整合素ανβ3 单抗 (mAb)的杂交瘤细胞E10总RNA中 ,用RT PCR扩增VH 和VL 基因 ,对其核苷酸序列分析后 ,通过PCR在VH 和VL 基因间插入柔性连接子(Gly4Ser) 3,组装成scFv基因 ,并克隆至原核表达载体pTIG TRX中。以重组子转化大肠杆菌BL2 1(DE3 )诱导目的基因表达。结果 :转化菌可表达相对分子质量 (Mr)为 3 10 0 0的scFv。Westernblot证实 ,具有His6标签蛋白的表达。经低剂量的IPTG诱导和较低温度培养 ,scFv获得了可溶性形式表达。表达产物经Ni NTA琼脂糖层析纯化后纯度达 91%以上。ELISA鉴定证实 ,scFv具有良好的抗原结合活性。结论 :成功地构建并表达抗人整合素ανβ3 的scFv ,为进一步临床研究奠定了基础。

自噬相关蛋白LC3Av1在口腔鳞状细胞癌中表达及甲基化对其的影响

目的:检测自噬相关基因LC3Av1在口腔鳞状细胞癌中的表达,及甲基化对表达的影响,初步探讨自噬与口腔肿瘤发生的关系。方法:提取18株口腔鳞癌细胞系的总RNA,检测LC3Av1的转录水平表达。并采用COBRA法检测LC3Av1启动子区域CpG岛的甲基化程度。结果:LC3Av1在18株口腔鳞癌中仅有3株表达(表达率为16.7%),而LC3B全部表达。有17株LC3Av1可检测出甲基化。结论:在口腔鳞癌中LC3Av1表达水平降低,提示口腔鳞癌的发生可能与LC3Av1依赖的细胞自噬障碍有关,其表达缺失可能与高甲基化相关。

面向高清和3D电视的视频编解码标准AVS+

介绍了AVS+(GY/T 257—2012《广播电视先进音视频编解码第1部分:视频》)标准的制定背景与过程,重点介绍了AVS+新增加的编码工具以及新特性,介绍了AVS+与AVS、AVC/H.264 HP(High Profile,高级档次)的性能对比,说明了AVS+与AVC HP性能相当。AVS+在多个部委的支持与推进下,将在中国高清与立体电视播出中得到应用。

压力诱导血管平滑肌细胞整合素β_3、桩蛋白和纽蛋白的变化

目的 研究压力对大鼠颈总动脉血管平滑肌细胞整合素 β3、桩蛋白和纽蛋白的分布与表达的影响 ,探讨它们在血管平滑肌细胞的机械应力信号转导中的作用。 方法 不同压力 (16 0mmHg和 80mmHg)灌流大鼠颈总动脉 30min ,免疫组织化学和免疫电镜观察整合素 β3、桩蛋白和纽蛋白在血管平滑肌细胞上的表达和分布变化。 结果 高压和常压灌流对大鼠颈总动脉平滑肌细胞的整合素 β3、桩蛋白和纽蛋白的表达无明显影响 ,但高压使整合素β3、桩蛋白和纽蛋白在平滑肌细胞膜上的分布发生改变 ,向离管腔面的平滑肌细胞膜聚集。 结论 高压诱导了整合素 β3、桩蛋白和纽蛋白向离管腔面的平滑肌细胞膜聚集。提示整合素 β3。