ADO在慢性阻塞性肺疾病患者近期预后评估中的价值

目的探讨呼吸困难指数气流受限程度指数(dyspnea index air flow restriction degree,ADO)在慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者近期预后评估中的价值。方法选取新疆医科大学第二附属医院呼吸内科自2021年3月—2023年3月的COPD患者120例,并依照患者最终转归情况将其分为存活组(n=95)与死亡组(n=25)。观察2组患者的基础病情况及患者性别、年龄、第1秒用力呼气容积(first second forced expiratory volume,FEV1)占预计值的百分比和ADO指数等相关指标。比较ADO指数不同分数患者病死率。比较ADO指数预测180 d死亡的受试者工作特征(receiver operating characteristic,ROC)曲线面积。结果2组患者的高血压、冠心病、心律失常、糖尿病、慢性肝病、慢性肾病、亚临床甲减发生情况对比,差异无统计学意义(P>0.05)。死亡组患者的FEV1占预计值的百分比、FEV1占预计值的百分比评分、呼吸困难分[英国医学研究委员会(the Medical Research Council,MRC)]评分以及ADO指数均高于存活组患者(P<0.05)。ADO指数<5分者的死亡率高于ADO指数≥5分者(P<0.05)。ADO指数预测180 d死亡的ROC曲线面积为0.851(95%CI:0.767~0.928,P<0.001),ADO指数为5.5时,约登指数最大,为0.565。结论ADO可有效反映COPD病情严重程度,对于患者而言可准确反映其病情进展情况,帮助其获得良好的疾病治疗效果,对于患者近期预后而言也具有积极意义,临床应用效果良好。

戏剧翻译中可表演性的重塑与再现——以Much Ado About Nothing译本为例

戏剧翻译缺乏系统性、层次性、逻辑性、操作性与全面性,亟须再次厘定明晰具体可行的翻译标准。基于此,以英国经典戏剧Much Ado About Nothing译本为例,针对戏剧译本进入目的语文化中受众域的多样性,辨析文本读者、舞台演员、表演观众、幕后人员对戏剧译本的语用期待,将可表演性原则细化为文学鉴赏性、表演呈现性、通俗简要性和舞台操作性四个标准。戏剧译介标准探析有助于经典戏剧在全球进行跨文化传播,可以为各国人民还原戏剧艺术的本真价值,也可以为戏剧翻译实践者提供借鉴与思考。

Adenosine A_(2A)receptor blockade attenuates excitotoxicity in rat striatal medium spiny neurons during an ischemic-like insult

During brain ischemia,excitotoxicity and peri-infarct depolarization injuries occur and cause cerebral tissue damage.Indeed,anoxic depolarization,consisting of massive neuronal depolarization due to the loss of membrane ion gradients,occurs in vivo or in vitro during an energy failure.The neuromodulator adenosine is released in huge amounts during cerebral ischemia and exerts its effects by activating specific metabotropic receptors,namely:A_(1),A_(2A),A_(2B),and A_(3).The A_(2A)receptor subtype is highly expressed in striatal medium spiny neurons,which are particularly susceptible to ischemic damage.Evidence indicates that the A2Areceptors are upregulated in the rat striatum after stroke and the selective antagonist SCH58261 protects from exaggerated glutamate release within the first 4 hours from the insult and alleviates neurological impairment and histological injury in the following 24 hours.We recently added new knowledge to the mechanisms by which the adenosine A2Areceptor subtype participates in ischemia-induced neuronal death by performing patch-clamp recordings from medium spiny neurons in rat striatal brain slices exposed to oxygen and glucose deprivation.We demonstrated that the selective block of A2Areceptors by SCH58261 significantly reduced ionic imbalance and delayed the anoxic depolarization in medium spiny neurons during oxygen and glucose deprivation and that the mechanism involves voltage-gated K+channel modulation and a presynaptic inhibition of glutamate release by the A2Areceptor antagonist.The present review summarizes the latest findings in the literature about the possibility of developing selective ligands of A2Areceptors as advantageous therapeutic tools that may contribute to counteracting neurodegeneration after brain ischemia.

ADORA2A基因多态性与精神分裂症患者攻击行为的相关性

目的探讨腺苷A2A受体(ADORA2A)基因单核苷酸多态性(SNP)与精神分裂症患者攻击行为的相关性。方法选取2015年6月—2019年6月深圳市康宁医院精神分裂症患者282例,根据外显攻击行为量表(MOAS)评分将所有患者分为攻击组(109例,MOAS评分≥4分)和非攻击组(173例,MOAS评分<4分)。收集所有患者的一般资料和实验室检测结果,并检测ADORA2A基因rs5996696位点和rs2298383位点的多态性。采用Logistic回归分析评估精神分裂症患者发生攻击行为的危险因素及其与ADORA2A基因SNP的交互作用。构建列线图预测模型并进行验证。结果攻击组男性所占比例、饮酒史、阳性和阴性精神症状评分量表(PANSS)评分阳性症状总分、非自愿住院、既往有攻击行为、无业或失业、近期严重应激事件、总三碘甲状腺原氨酸(TT_(3))升高率、白细胞介素-17(IL-17)、白细胞介素-23(IL-23)、ADORA2A rs2298383位点CC基因型频率均高于非攻击组(P<0.05)。多因素Logistic回归分析结果显示,PANSS评分阳性症状总分≥20分、IL-17≥16.13 pg·mL^(-1)、TT_(3)升高、既往有攻击行为、携带ADORA2A rs2298383位点CC基因型是精神分裂症患者发生攻击行为的独立危险因素(P<0.05)。ADORA2A rs2298383位点CC基因型与PANSS评分阳性症状总分、TT_(3)升高率、IL-17水平和既往有攻击行为均有正交互作用。列线图模型预测攻击行为的总风险值为0.93,受试者工作特征(ROC)曲线的曲线下面积(AUC)为0.874,校准曲线拟合优度检验差异无统计学意义(P>0.05)。结论携带ADORA2A rs2298383位点CC基因型与精神分裂症患者的攻击行为密切相关,且与精神分裂症患者发生攻击行为的相关危险因素均呈正交互作用。

数字营销研究的整合框架和未来展望——基于TCCM框架和ADO框架的研究

在数字经济时代,数字营销的战略价值和应用前景日益明显,已成为理论和实践探索的前沿与焦点。通过整合TCCM框架和ADO框架,文章对数字营销相关研究进行了系统梳理,构建了数字营销研究的整合框架,对既有研究中有关数字营销的前因与效果、影响机制和理论基础以及研究方法与研究场景等进行了总结和剖析,并深度解析了数字营销的内在机理。在此基础上,文章进一步揭示出既有数字营销研究在顾客隐私悖论、智能算法黑箱、区块链营销、数字营销能力、数字定制、敏捷营销、理论构建和使用、情境和方法匹配等方面存在的主要问题。最后结合有关理论与实践难题,提炼并识别出数字营销未来的关键研究问题,以期为数字营销理论探索和实践提供有益参考和借鉴。

The seeming paradox of adenosine receptors as targets for the treatment of Alzheimer's disease: agonists or antagonists?

Alzheimer＇s disease （AD） is the most common neurodegenerative disorder, and its incidence is relatively high among elderly people, affecting about 1-2% of the population between 60-65 years old and rising dramatically （about 30%） in people aged 80 years or older （Selkoe, 2002）. Nowadays, considering the increasing mean lifespan of populations in developed countries, the disease is becoming more and more a health concern, and the search for an effective cure has turned into＂a real need＂.

Metformin promotes angiogenesis and functional recovery in aged mice after spinal cord injury by adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway

Treatment with metformin can lead to the recovery of pleiotropic biological activities after spinal cord injury.However,its effect on spinal cord injury in aged mice remains unclear.Considering the essential role of angiogenesis during the regeneration process,we hypothesized that metformin activates the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway in endothelial cells,thereby promoting microvascular regeneration in aged mice after spinal cord injury.In this study,we established young and aged mouse models of contusive spinal cord injury using a modified Allen method.We found that aging hindered the recovery of neurological function and the formation of blood vessels in the spinal cord.Treatment with metformin promoted spinal cord microvascular endothelial cell migration and blood vessel formation in vitro.Furthermore,intraperitoneal injection of metformin in an in vivo model promoted endothelial cell proliferation and increased the density of new blood vessels in the spinal cord,thereby improving neurological function.The role of metformin was reversed by compound C,an adenosine monophosphate-activated protein kinase inhibitor,both in vivo and in vitro,suggesting that the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway likely regulates metformin-mediated angiogenesis after spinal cord injury.These findings suggest that metformin promotes vascular regeneration in the injured spinal cord by activating the adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway,thereby improving the neurological function of aged mice after spinal cord injury.

Exploring Gender Differences in Adolescent Dissociative Symptoms via A Structural Equation Model

Adolescent dissociative disorders(ADDs)have been recognized as significant psychological issues with an estimated prevalence of 45.2%in psychiatric outpatient clinics^([1]).Previous studies have demonstrated that dissociative symptoms(DSs)manifest as early signs of dissociative disorders(DDs)^([2]).DSs are characterized as aberrations in one's feelings,experiences,and thoughts in the realm of awareness and memory^([3]).

Adenosine triphosphate induced cell death: Mechanisms and implications in cancer biology and therapy

Adenosine triphosphate(ATP)induced cell death(AICD)is a critical cellular process that has garnered substantial scientific interest for its profound relevance to cancer biology and to therapeutic interventions.This comprehensive review unveils the intricate web of AICD mechanisms and their intricate connections with cancer biology.This review offers a comprehensive framework for comprehending the multifaceted role of AICD in the context of cancer.This is achieved by elucidating the dynamic interplay between systemic and cellular ATP homeostasis,deciphering the intricate mechanisms governing AICD,elucidating its intricate involvement in cancer signaling pathways,and scrutinizing validated key genes.Moreover,the exploration of AICD as a potential avenue for cancer treatment underscores its essential role in shaping the future landscape of cancer therapeutics.

ADO品质家宽分析能力创新实践

随着“双千兆”网络建设和互联网业务的发展,提升用户体验管理能力、提高体验劣化类投诉解决效率的需求日益迫切。为了快速构建家宽端到端质量智能分析能力,提前预判潜在不满意问题,改善客户感知,故在本地开展了ADO(Agile Digital Operations,敏捷数字化运营系统)品质家庭宽带分析的试点部署,通过该系统为电信提供业务差异服务能力,支撑智慧家庭工程师对客户的精确营销和精准派单整治处理,确保电信家庭宽带网络优势。

Adenosine 2A receptor contributes to the facilitation of postinfectious irritable bowel syndrome by γδ T cells via the PKA/CREB/NF-κB signaling pathway

BACKGROUND Immunological dysfunction-induced low-grade inflammation is regarded as one of the predominant pathogenetic mechanisms in post-infectious irritable bowel syndrome(PI-IBS).γδT cells play a crucial role in innate and adaptive immunity.Adenosine receptors expressed on the surface ofγδT cells participate in intestinal inflammation and immunity regulation.AIM To investigate the role ofγδT cell regulated by adenosine 2A receptor(A2AR)in PI-IBS.METHODS The PI-IBS mouse model has been established with Trichinella spiralis(T.spiralis)infection.The intestinal A2AR and A2AR inγδT cells were detected by immunohistochemistry,and the inflammatory cytokines were measured by western blot.The role of A2AR on the isolatedγδT cells,including proliferation,apoptosis,and cytokine production,were evaluated in vitro.Their A2AR expression was measured by western blot and reverse transcription polymerase chain reaction(RT-PCR).The animals were administered with A2AR agonist,or A2AR antagonist.Besides,γδT cells were also injected back into the animals,and the parameters described above were examined,as well as the clinical features.Furthermore,the A2AR-associated signaling pathway molecules were assessed by western blot and RT-PCR.RESULTS PI-IBS mice exhibited elevated ATP content and A2AR expression(P<0.05),and suppression of A2AR enhanced PI-IBS clinical characteristics,indicated by the abdominal withdrawal reflex and colon transportation test.PI-IBS was associated with an increase in intestinal T cells,and cytokine levels of interleukin-1(IL-1),IL-6,IL-17A,and interferon-α(IFN-α).Also,γδT cells expressed A2AR in vitro and generated IL-1,IL-6,IL-17A,and IFN-α,which can be controlled by A2AR agonist and antagonist.Mechanistic studies demonstrated that the A2AR antagonist improved the function ofγδT cells through the PKA/CREB/NF-κB signaling pathway.CONCLUSION Our results revealed that A2AR contributes to the facilitation of PI-IBS by regulating the function ofγδT cells via the PKA/CREB/NF-κB signaling pathway.

Adenosine cyclic phosphate with ultrasonic-assisted pectinase extraction alleviated allergic reactions in RBL-2H3 through inhibiting the influx of intracellular Ca^(2+)

Jujube contains abundant cyclic adenosine monophosphate(cAMP)and the ultrasonic-assisted pectinase extraction(UAPE)conditions for obtaining the maximum cAMP yield from jujube were optimized.Orthogonal array design was applied to evaluate the effects of 4 variables by UAPE on cAMP yield.The results showed that the optimal cAMP yield(783.0μg/g)was derived at ratio of liquid to solid 5 mL/g,ratio of pectinase to raw material 1.5%,time 60 min and temperature 40℃.Moreover,the effect of cAMP on the anti-allergic function of action induced by immunoglobulin E(IgE)and its meschanism was investigated through establishing the sensitized cell model in rat basophilic leukemia(RBL-2 H3)cells using dinitrophenylated(DNP)-bovine serum albumin(BSA)-IgE.The results showed that cAMP interfered with sensitized cells,effectively inhibited the occurrence of basophil degranulation in dose dependence,and significantly reduced the activity ofβ-hexosamindase(β-hex),at the optimal concentration of 50μg/mL.The level of anti-inflammatory factor interleukin-10(IL-10)was promoted and the content of pro-inflammatory factor tumor necrosis factor-α(TNF-α)was suppressed by cAMP.In addition,influx of intracellular Ca^(2+) was repressed effectively.Our results demonstrate that jujube cAMP regulated the cytokine balance in the allergy pathway through blocking the influx of extracellular Ca^(2+),with the prevention of allergy symptoms.

Dopamine and cyclic adenosine monophosphate-regulated phosphoprotein with an apparent Mr of 32000 promotes colorectal cancer growth

BACKGROUND Dopamine and cyclic adenosine monophosphate(cAMP)-regulated phosphop-rotein with an apparent Mr of 32000(DARPP-32)is a protein that is involved in regulating dopamine and cAMP signaling pathways in the brain.However,recent studies have shown that DARPP-32 is also expressed in other tissues,including colorectal cancer(CRC),where its function is not well understood.AIM To explore the effect of DARPP-32 on CRC progression.METHODS The expression levels of DARPP-32 were assessed in CRC tissues using both quantitative polymerase chain reaction and immunohistochemistry assays.The proliferative capacity of CRC cell lines was evaluated with Cell Counting Kit-8 and 5-ethynyl-2’-deoxyuridine assays,while apoptosis was measured by flow cytometry.The migratory and invasive potential of CRC cell lines were deter-mined using wound healing and transwell chamber assays.In vivo studies involved monitoring the growth rate of xenograft tumors.Finally,the underlying molecular mechanism of DARPP-32 was investigated through RNA-sequencing and western blot analyses.RESULTS DARPP-32 was frequently upregulated in CRC and associated with abnormal clinicopathological features in CRC.Overexpression of DARPP-32 was shown to promote cancer cell proliferation,migration,and invasion and reduce apoptosis.DARPP-32 knockdown resulted in the opposite functional effects.Mechanistically,DARPP-32 may regulate the phosphoinositide 3-kinase(PI3K)/AKT signaling pathway in order to carry out its biological function.CONCLUSION DARPP-32 promotes CRC progression via the PI3K/AKT signaling pathway.

Suppressing high mobility group box-1 release alleviates morphine tolerance via the adenosine5'-monophosphate-activated protein kinase/heme oxygenase-1 pathway

Opioids,such as morphine,are the most potent drugs used to treat pain.Long-term use results in high tolerance to morphine.High mobility group box-1(HMGB1) has been shown to participate in neuropathic or inflammatory pain,but its role in morphine tolerance is unclear.In this study,we established rat and mouse models of morphine tolerance by intrathecal injection of morphine for 7 consecutive days.We found that morphine induced rat spinal cord neurons to release a large amount of HMGB1.HMGB1 regulated nuclear factor κB p65 phosphorylation and interleukin-1β production by increasing Toll-like receptor 4receptor expression in microglia,thereby inducing morphine tolerance.Glycyrrhizin,an HMGB1 inhibito r,markedly attenuated chronic morphine tole rance in the mouse model.Finally,compound C(adenosine 5’-monophosphate-activated protein kinase inhibitor) and zinc protoporphyrin(heme oxygenase-1 inhibitor)alleviated the morphine-induced release of HMGB1 and reduced nuclear factor κB p65 phosphorylation and interleukin-1β production in a mouse model of morphine tolerance and an SH-SY5Y cell model of morphine tole rance,and alleviated morphine tolerance in the mouse model.These findings suggest that morphine induces HMGB1 release via the adenosine 5’-monophosphate-activated protein kinase/heme oxygenase-1 signaling pathway,and that inhibiting this signaling pathway can effectively reduce morphine tole rance.

基于转录组学分析ADORA3在牙周炎中的表达及调控

目的:探讨腺苷A3受体(adenosine A3 receptor,ADORA3)在牙周炎中的表达模式及调控作用。方法:构建牙周炎动物模型,micro-CT和HE染色观察各组小鼠牙槽骨丧失和牙周组织病理形态,并对结扎侧和对照侧牙龈组织进行转录组测序分析Adora3表达差异,RT-qPCR法检测ADORA3在人和小鼠牙龈组织及巨噬细胞中表达情况,转录组测序分析ADORA3与下游靶基因相关性并通过RT-qPCR法验证。结果:小鼠牙周炎模型构建成功,结扎侧牙龈组织中Adora3表达上调。牙周炎患者牙龈组织中ADORA3表达上调,炎症微环境下Adora3表达降低。转录组测序分析显示Adora3表达与下游靶基因抑制蛋白β-2(arrestin beta-2,ARRB2)呈正相关,且Arrb2基因敲除后Adora3表达下调。结论:基于转录组学分析及体外实验验证,ADORA3在不同来源牙龈组织及巨噬细胞中差异表达,且ADORA3表达水平与ARRB2呈正相关。

淫羊藿苷调控mTOR/Akt/CREB通路对高糖诱导的足细胞自噬及凋亡的影响

目的 探讨淫羊藿苷对高糖诱导的足细胞自噬、凋亡及哺乳动物雷帕霉素靶蛋白(mTOR)/丝氨酸苏氨酸蛋白激酶(Akt)/环磷酸腺苷反应元件结合蛋白(CREB)通路的影响。方法 将小鼠足细胞MPC5分为5组:正常对照组(5.5 mmol·L^(-1)葡萄糖)、高糖组(30 mmol·L^(-1)葡萄糖)、淫羊藿苷组(30 mmol·L^(-1)葡萄糖+5μmol·L^(-1)淫羊藿苷)、GDC-0349组(30 mmol·L^(-1)葡萄糖+50μmol·L^(-1)GDC-0349)、淫羊藿苷+GDC-0349组(30 mmol·L^(-1)葡萄糖+5μmol·L^(-1)淫羊藿苷+50μmol·L^(-1)GDC-0349)。培养48 h后,噻唑蓝法检测MPC5细胞活力;吖啶橙染色观察MPC5细胞自噬情况;流式细胞术检测MPC5细胞凋亡;蛋白印迹法检测MPC5细胞自噬[微管相关蛋白1轻链3(LC3)Ⅱ、LC3Ⅰ、自噬相关蛋白(Beclin-1)]、凋亡[Bcl-2相关X蛋白(Bax)、B淋巴细胞瘤-2(Bcl-2)]和mTOR/Akt/CREB通路相关蛋白的表达。结果 与正常对照组比较,高糖组MPC5细胞活力、Bcl-2、磷酸化mTOR(p-mTOR)/mTOR、磷酸化Akt(p-Akt)/Akt、磷酸化CREB(p-CREB)/CREB蛋白表达水平显著降低(P<0.05),自噬能力增强,自噬体表现出橙色荧光,细胞凋亡率、LC3Ⅱ/LC3Ⅰ、Beclin-1、Bax蛋白表达水平显著升高(P<0.05)。与高糖组比较,淫羊藿苷组MPC5细胞活力、LC3Ⅱ/LC3Ⅰ、Beclin-1、Bcl-2、p-mTOR/mTOR、p-Akt/Akt、p-CREB/CREB蛋白表达水平显著升高,自噬能力进一步增强,自噬体数量增多,自噬体呈现出砖红色荧光(P<0.05),细胞凋亡率、Bax蛋白表达水平显著降低(P<0.05);GDC-0349组MPC5细胞活力、LC3Ⅱ/LC3Ⅰ、Beclin-1、Bcl-2、p-mTOR/mTOR、p-Akt/Akt、p-CREB/CREB蛋白表达水平显著降低,自噬能力减弱,自噬体数量减少,自噬体表现出橙色荧光(P<0.05),细胞凋亡率、Bax蛋白表达水平显著升高(P<0.05);淫羊藿苷+GDC-0349可逆转淫羊藿苷对高糖诱导MPC5细胞的作用效果(P<0.05)。结论 淫羊藿苷通过激活mTOR/Akt/CREB通路促进高糖诱导的足细胞自噬抑制细胞凋亡。

黄芩苷调节cAMP/PKA/CREB信号通路对湿疹大鼠皮肤屏障功能的影响

目的探讨黄芩苷(BA)调节环磷酸腺苷(cAMP)/蛋白激酶A(PKA)/cAMP反应元件结合蛋白(CREB)通路对湿疹大鼠皮肤屏障功能的影响。方法将SD大鼠随机分为对照组(NC组)、Model组、低剂量BA组(BA-L组,25 mg/kg)、中剂量BA组(BA-M组,50 mg/kg)、高剂量BA组(BA-H组,100 mg/kg)、泼尼松组(PNS组,25 mg/kg)、BAH+cAMP抑制剂(SQ22536)组(100 mg/kg+2.13 mg/kg)、BA-H+PKA抑制剂(H-89)组(100 mg/kg+5 mg/kg),每组12只。除NC组外,其余组大鼠均构建湿疹大鼠模型。建模成功2 d后,分组进行给药处理。检测湿疹面积及严重度指数(EASI)评分、经皮肤水分流失量(TEWL)、角质层含水量(WCSC)变化;酶联免疫吸附试验(ELISA)检测大鼠血清中免疫球蛋白E(IgE)、干扰素-γ(IFN-γ)、白细胞介素-4(IL-4)水平及大鼠背部受试区皮损组织中c AMP蛋白表达;HE染色检测大鼠背部受试区皮损组织病理变化;Western blot检测大鼠背部受试区皮损组织中水通道蛋白3(AQP3)、cathelicidin相关抗菌肽(CRAMP)、p-PKA、p-CREB蛋白表达。结果与NC组比较,Model组大鼠背部受试区皮损组织病理损伤严重,EASI评分、TEWL、IgE、IL-4水平升高,WCSC、IFN-γ水平、AQP3、CRAMP、cAMP、p-PKA、p-CREB蛋白水平降低(P<0.05)。与Model组比较,BA-L组、BA-M组、BA-H组、PNS组大鼠背部受试区皮损组织病理损伤减轻,EASI评分、TEWL、IgE、IL-4水平降低,WCSC、IFN-γ水平、AQP3、CRAMP、cAMP、p-PKA、p-CREB蛋白水平升高(P<0.05);且BA-L组、BA-M组、BA-H组上述指标变化呈剂量依赖性。SQ22536或H-89减弱了高剂量BA对湿疹大鼠皮肤屏障功能的改善作用。结论BA可能通过激活cAMP/PKA/CREB信号通路改善湿疹大鼠皮肤屏障功能。

熊果苷对心肌纤维化模型大鼠的改善作用及机制研究

目的研究熊果苷对心肌纤维化(MF)模型大鼠的改善作用及机制。方法采用网络药理学方法预测熊果苷改善MF的潜在靶点并进行分子对接验证。将50只SD大鼠皮下注射异丙肾上腺素(5 mg/kg,每天1次,连续14 d)复制MF模型。将造模成功的大鼠随机分为模型组、卡托普利组(9 mg/kg)和熊果苷低、中、高剂量组(50、100、200 mg/kg),每组10只;另取10只未造模大鼠作为正常组。各组大鼠给予相应药物干预,每天1次,连续28 d。末次给药24 h后,检测大鼠心电图、心脏相关指数[心脏质量指数(HWI)、左心室质量指数(LVWI)],检测大鼠心肌组织中肌酸激酶(CK)、乳酸脱氢酶(LDH)、N末端前脑钠肽前体(NT-proBNP)、Ⅰ型胶原蛋白(ColⅠ)、ColⅢ水平,观察大鼠心肌组织病理形态学变化,检测大鼠心肌组织中腺苷脱氨酶(ADA)、腺苷激酶(ADK)蛋白及其mRNA表达水平。结果网络药理学结果显示,熊果苷改善MF的主要靶点为ADA、ADK。分子对接结果显示,熊果苷与ADA、ADK结合稳定。验证实验结果显示,与模型组比较,各给药组大鼠心电图ST波段和T波的振幅有所恢复,心房出现扑动的症状减轻;HWI(熊果苷中剂量组除外)、LVWI和心肌组织中CK、LDH、NT-proBNP、ColⅠ、ColⅢ水平均显著降低(P<0.05);大鼠心肌纤维化程度减轻;心肌组织中ADA、ADK蛋白及其mRNA表达水平均显著升高(P<0.05)。结论熊果苷可改善MF模型大鼠心脏纤维化和心脏功能,其作用机制可能与上调ADA、ADK蛋白及其mRNA表达,影响核苷酸代谢及胶原生成有关。

应用D-SPECT评估远程缺血预适应联合腺苷注射液在PCI患者中的作用

目的应用D-SPECT评价远程缺血预适应联合腺苷注射液在经皮冠状动脉介入治疗(PCI)患者中的作用。方法选择需行冠状动脉造影术及支架植入术患者300例,按照随机数字表法分为常规治疗组(150例)和试验组(150例),常规治疗组给予冠状动脉粥样硬化性心脏病PCI术常规治疗,试验组在PCI术当日通过血压计袖带分别在左、右上臂充气至200 mmHg,持续加压5 min诱导2次远程缺血预适应,然后在患者PCI术中以50μg/(kg·min)泵入腺苷注射液至术毕,其他治疗同常规治疗组,并对所有患者进行冠状动脉SYNTAXⅡ评分。应用静息D-SPECT+瑞加诺生负荷D-SPECT评估PCI术前及PCI术后7 d的心肌17节段分布下心肌灌注总积分、心肌缺血总节段数和左心室射血分数情况。结果PCI术前2组患者心肌缺血节段数、心肌灌注总积分、左心室射血分数情况差异无统计学意义(P>0.05),PCI术后7 d试验组的心肌缺血节段数、心肌灌注总积分、左心室射血分数情况显著优于常规治疗组(P<0.05),2组患者在药物不良反应方面差异无统计学意义(P>0.05)。结论远程缺血预适应联合腺苷注射液在PCI患者中应用安全有效。

沉积模拟实验信息系统的设计与实现

多年来,国内外地质学家在沉积模拟实验研究中积累了海量的实验数据和资料,但目前缺少对此类信息进行规范化管理和共享应用的软件系统。对此,提出浏览器/服务器(B/S)模式的沉积模拟实验信息系统,实现了沉积模拟实验的实验设计方案、实验观测数据、实验结果等信息的集成管理、高效检索和可视化分析等功能,从而为沉积模拟实验的网上信息化管理与分析应用提供可行方案。最后,以某油田辫状河储层沉积模拟实验为例,介绍了系统中实验项目检索、实验详情浏览、砂体测量数据的统计分析等功能的应用效果,说明了本系统的实用性。本系统的研发与应用可极大地方便沉积模拟实验数据的管理、分享及分析工作。