Neonatal respiratory distress syndrome, neonatal pneumonia, meconium aspiration syndrome, neonatal pulmonary hemorrhage and other common neonatal lung diseases have a risk of radiation damage using traditional chest X-ray examination. Lung ultrasound examination shows no radiation damage. This article summarizes the characteristics of lung ultrasound imaging of common neonatal lung diseases, and briefly reviews the diagnostic value and clinical application of lung ultrasound.

目的 探究小儿哮喘治疗前病程与治疗后肺功能恢复情况的分析.方法 随机选择2017年1月—2020年5月在该院接受治疗的哮喘患儿50例.根据患儿治疗前病程是否在1年以上分成两组,病程超出1年患儿纳入对照组,病程低于1年患儿纳入观察组,记录两组患儿治疗后的肺功能指标,比较分析治疗效果.结果 观察组治疗总有效率是93.33％(28/30),与对照组数据60.00％(12/20)相比,明显更高,差异有统计学意义(χ2=6.380,P<0.05);对照组患儿用力肺活量(79.34±8.56)％、最大通气量(87.45±10.21)L/min、1 s用力呼气量(75.04±10.37)％、呼气流速峰值(63.02±9.56)L/min水平均显著较观察组(87.44±12.45)％、(98.45±12.24)L/min、(88.30±12.43)％、(101.23±11.67)L/min更低,差异有统计学意义(t=2.730、3.446、4.090、12.671,P<0.05).结论 小儿哮喘治疗前病程直接相关于治疗后肺功能恢复状况,病程越短越有利于患儿肺功能恢复,为临床诊治提供参考依据.

OBJECTIVES:To explore the protective effects of Tongmai Yizhi Decoction (, TYD), a Chinese herb complex prescription against the impairment of cognitive functions and memory loss in amyloid beta 1-40 (Aβ1-40) peptide and ibotenic (IBO)-induced Alzheimer's disease (AD) model rats. METHODS:The in vivo model was established by injecting Aβ1-40 and IBO into left hippocampal CA1 area of Sprague-Dawley (SD) rat to mimic AD. Totally 32 SD rats were divided into 4 groups, including sham operation group, AD model group, TYD group [AD rats treated with TYD at the dosage of 19.44 g/(kg•d) for 4 weeks] and huperzine A group [AD rats treated with huperzine A at the dosage of 40.5 μg/(kg•d) for 4 weeks]. Spatial learning and memory level was detected by Morris Water Maze test. Histological morphology in the hippocampus was tested by hematoxylin-eosin (HE) staining. Cyclin-dependent kinase-5 (Cdk5) protein and gene expression level were investigated by Western blot analysis and real-time quantitative polymerase chain reaction (RT-qPCR), respectively. RESULTS:Aβ1-40 and IBO treatment induced longer escape latency of rats, compared with sham operation group from day 25 (P<0.01). However, TYD and huperzine A obviously shortened the escape latency from day 26 (P<0.01). Moreover, the effect of TYD was similar to huperzine A (P>0.05). Furthermore, HE staining also showed that TYD and huperzine A reversed the neuropathological changes in the hippocampus triggered by Aβ1-40 and IBO. TYD and huperzine A effectively reduced the expression levels of Cdk5 protein and gene located in rat hippocampus, compared with the AD model group (P<0.01). CONCLUSION:TYD could be a promising neuroprotective agent for protecting neuron from AD injury through inhibiting Cdk5 expression.

OBJECTIVE To determine the combined cytotoxic effect and the molecular basis of triptolide and sodium cantharidinate on hepatoma cell line 7721.
 METHODS After treating the hepatoma cell line 7721 with triptolide(9, 18, or 36 μg/mL) and/or sodium cantharidinate (2, 5, or 10 μg/mL), cell viability assay and apoptosis were examined by MTT and flocytometry, respectively. The protein levels of caspase 3 and nuclear factor κB were analyzed by Western blot.
 RESULTS Viability of hepatoma cell line 7721 was inhibited by either the therapy of triptolide and/or sodium cantharidinate (P<0.05) in a time- and dose-dependent manner. The combined effects of both drugs were better than those of the single drug (P<0.05). The combined therapy down-regulated the expression of NF-κB p65 (P<0.05) while up-regulated the expression of caspase-3 (P<0.05).
 CONCLUSION Triptolide and sodium cantharidinate exert a synergistic toxic effect on hepatoma cell line 7721, which is related to increasing capase-3 activity and suppression of NF- κB.

目的 从线粒体途径探讨山茱萸活性成分5-羟甲基糠醛对肿瘤坏死因子α(TNF-α)和D-氨基半乳糖(D-GalN)所致肝细胞凋亡的保护作用 方法 体外培养人正常肝L02细胞,用TNF-α(100μg/L)和D-GalN(44 mg/L)诱导肝细胞损伤模型,采用CCK-8细胞增殖检测试剂盒检测细胞活力;流式细胞仪检测5-羟甲基糠醛对细胞凋亡的影响;Western-blot检测线粒体途径凋亡标志蛋白Apaf-l、AIF、cytochrome C、Bcl-2、Bcl-XL、Bax表达水平的变化;分光光度法检测Caspase-3、Caspase-9的活性.结果 与TNF-α和D-GalN模型组相比,不同浓度的5-羟甲基糠醛作用后,可显著减轻L02肝细胞的增殖抑制、降低细胞的凋亡率,并使促凋亡蛋白Apaf-l、AIF、cytochrome C、Bax的表达量明显下降,而使抗凋亡蛋白Bcl-2、Bcl-XL的表达量显著上升,同时使细胞凋亡的关键蛋白酶Caspase-3、Caspase-9的活性显著降低.结论 山茱萸羟甲基糠醛对TNF-α和D-GalN所诱导的肝细胞凋亡具有抑制作用,其机制可能与线粒体介导的凋亡通路以及BCL-2家族成员的表达调控有关.

衰老是本世纪生物学研究的方向之一。衰老涉及面广，机制复杂，对衰老调控的研究始终是生命科学领域中最关键的问题。近年来，随着现代遗传学、分子生物学、细胞生物学、现代遗传学等学科的快速发展，对衰老调控的研究也越来越趋向于分子水平，发现 MicroRNA(miRNA)参与衰老调控的多个方面[1]。衰老对体内细胞的新陈代谢以及维持正常生命活动具有重要意义。同时，细胞衰老过程也参与调控多种相关性疾病，如心血管疾病、肿瘤、纤维化疾病等，发挥着“双刃剑”的作用。随着衰老调控研究的深入，不仅有利于我们认识生长发育的过程，更为我们延缓衰老，提高生活质量提供了可能性。本文将近年来 miRNA在衰老调控中的研究进展综述如下。

5-Hydroxymethylfurfural(5-HMF), a water-soluble compound extracted from wine-processed Fructus corni, is a novel hepatic protectant for treating acute liver injury. The present study was designed to investigate the protective effect of 5-HMF in human L02 hepatocytes injured by D-galactosamine(Gal N) and tumor necrosis factor-α(TNF-α) in vitro and to explore the underlying mechanisms of action. Our results showed that 5-HMF caused significant increase in the viability of L02 cells injured by Gal N/TNF-α, in accordance with a dose-dependent decrease in apoptotic cell death confirmed by morphological and flow cytometric analyses. Based on immunofluorescence and Western blot assays, we found that Gal N/TNF-α induced ER stress in the cells, as indicated by the disturbance of intracellular Ca2+ concentration, the activation of protein kinase RNA(PKR)-like ER kinase(PERK), phosphorylation of eukaryotic initiation factor 2 alpha(e IF2α), and expression of ATF4 and CHOP proteins, which was reversed by 5-HMF pre-treatment in a dose-dependent manner. The anti-apoptotic effect of 5-HMF was further evidenced by balancing the expression of Bcl-2 family members. In addition, the knockdown of PERK suppressed the expression of phospho-PERK, phospho-e IF2α, ATF4, and CHOP, resulting in a significant decrease in cell apoptosis after the treatment with Gal N/TNF-α. 5-HMF could enhance the effects of PERK knockdown, protecting the cells against the Gal N/TNF-α insult. In conclusion, these findings demonstrate that 5-HMF can effectively protect Gal N/TNF-α-injured L02 hepatocytes against ER stress-induced apoptosis through the regulation of the PERKe IF2α signaling pathway, suggesting that it is a possible candidate for liver disease therapy.

目的:研究清络通痹颗粒(QLT)对体外培养的类风湿关节炎患者的成纤维样滑膜细胞(FLS)作用的分子机制.方法:利用基因芯片技术检测QLT作用于FLS 72h后基因表达的变化.结果:QLT对FLS细胞凋亡相关通路Activation of BH3-only proteins、FAS Signaling和Apoptosis有影响,并上调了CASP8、BCL2L1 1、BID等促凋亡基因的表达.此外,差异表达基因涉及到血管生成、免疫调节、炎症等方面.结论:QLT改变细胞凋亡、血管生成及免疫调节等相关基因表达可能是其参与抑制FLS细胞异常增殖的作用过程.

To investigate whether pinching spine (PS, i.e. aeie"S, a traditional Chinese manipulative therapy) is beneficial to ameliorating the depressive state (including behavioral deficit, retardative weight gain and decreased sucrose consumption) in a rat model of depression induced by chronic unpredictable stress (CUS) and to explore the candidate mechanism of action.PS was performed on rats' spine once daily for 1 week after exposure to CUS. The open-field test, body weight measuring, and sucrose intake test were applied on different dates: before stress (d0), at the end of stress (d21) and after PS treatment (d28), respectively. Then the rats' hippocampuses were performed genome-wide microarray analysis, and the expression levels of several genes were evaluated by real-time polymerase chain reaction (PCR).Exposure to CUS resulted in decreases of behavioral activity and sucrose consumption, which were reversed significantly after PS treatment. The expression of several genes relevant to energy metabolism, anti-oxidation, and olfactory receptor, etc., were down-regulated, while the expression of those relevant to hemostasis, immunity-inflammation, and restriction of activities and ingestion, etc., were up-regulated in hippocampuses of rats exposed to CUS. PS treatment significantly inverted these changes. Furthermore, increase or decrease in gene expression evaluated by realtime PCR was concordant with up-regulated or down-regulated expression evaluated by microarray analysis.PS showed a potential antidepressant-like effect, of which the action mechanism might be due to gene expression regulation in hippocampus.

Promoting scientific and technological innovation and modernization of Chinese Medicine is an important task of higher education of traditional Chinese medicine (TCM). The key issue is to train the talents who are well versed in both Chinese and western medicine. The educational reform in western curriculum guiding by the knowledge view of constructivism could take the student as the main body, and the teachers were the partners in the knowledge construction of the students. The reform could fully mobilize the enthusiasm and creativity of the students, enhance the interest and confidence in learning Chinese medicine and western medicine, and promote the connotation construction in Higher Education of Chinese medicine. It is of great significance to the implementation of quality education, cultivating innovative talents of Chinese medicine.

Aim To study effects of loganin and morro-niside on aging astrocytes induced by D-galactose. Methods Cortex astrocytes of newly born rats were cultured in vivo and indentified by immunofluorescence method.Firstly,appropriate D-galactose concentration was selected and effects of loganin and morroniside on proliferation activity of aging astrocytes induced by D-galactose were determined by MTT test.Then SOD, MDA were taken as indicators to study the effects of loganin and morroniside on aging astrocytes induced by D-galactose.Thirdly,growth factors like gliar cell line-derived neurotrophic factor (GDNF),basic fibro-blast growth factor (bFGF)tested by ELISA method and expression of Bax,caspase-3,phospho-extracellu-lar signal-regulated kinese (p-ERK1 /2),phospho-mi-togen-actived protein kinase /extracellular signal-regu-lated kinase kinase (p-MEK1 /2)were taken as indi-cators to discuss the potential protection mechanism. Results Loganin and morroniside exerted certain effects on proliferation of aging astrocytes induced by D-galactose,improving SOD,GDNF,bFGF release and lowering MDA release significantly (P <0.05 ). The expressions of Bax and caspase-3 proteins had no difference between model group and loganin group, morroniside group.While the expressions of p-ERK1 /2,p-MEK1 /2 of loganin group,morroniside group were improved significantly compared with model group.Conclusion Loganin and morroniside have protective effects on aging astrocytes induced by D-ga-lactose,and increase the proliferation ability.Protec-ting their antioxidant systems and improving the expres-sion of p-ERK1 /2,p-MEK1 /2 proteins are possible mechanisms.

The aim was to determine the action mode of cornel iridoid glycoside (CIG) from Fructus corni on hepatoprotective activities, the effects of CIG on human hepatocyte cell line (L02) injured by D-galactosamine (GalN) and tumor necrosis factor-α (TNF-α) were examined.The percentage of cell viability was evaluated by cell counting kit-8 assay. Apoptosis was detected by flow cytometric analysis in human L02 hepatocytes. The expression levels of activating transcription factor-4 (ATF4), and C/EBP homologous protein (CHOP) were detected by western-blot analysis. In addition, the activity of caspase-3 was tested by enzyme-linked immunosorbent assay.The results showed that CIG caused a significant increase in the viability of L02 cells injured by GalN/TNF-α, in accordance with a dose-dependent decrease of apoptotic cell death confirmed by flow cytometric analysis. Based on western blot and colorimetric assay, we found that GalN/TNF-α induced increased expression of ATF4, CHOP, and activation of caspase-3 while CIG pre-treatment had a dose-dependent suppression on them in this cell model.Overall, these findings demonstrate that CIG can effectively protect L02 hepatocytes against apoptosis induced by GalN/TNF-α, suggesting that it is a possible candidate target for liver disease therapy.

Morroniside is a water-soluble compound extracted from the fruit of Cornus officinalis and is used to protect lung activity against aging. In the present study, the manner in which morroniside regulates normal lung and cancer cells was examined. The human embryonic lung fibroblast (HELF) cell line and lung cancer A549 cell line, and their responses to morroniside treatment, were examined. Results showed that morroniside reverses the apoptotic effect of H2O2 on HELF cell growth, protecting cell proliferation and normal cell morphology and inhibiting apoptosis. However, these effects were not present in A549 cells. Western blotting showed that morroniside also markedly downregulated retinoblastoma protein in HELF cells. These results suggest that morroniside treatment exhibits different effects on apoptosis in HELF and A549 cells, making it a viable compound for decreasing the side effects of anticancer medicines in normal cells.

目的 研究没食子酸(gallic acid,GA)体外诱导人肝癌SMMC-7721细胞凋亡及其作用机制.方法 体外培养人肝癌SMMC-7721细胞,噻唑蓝(MTF)法观察细胞增殖;Hoechst-33258、AnnexinⅤ-FITC/PI检测细胞凋亡情况;逆转录聚合酶链式反应(RT-PCR)法研究凋亡抑制基因Survivin mRNA的变化.结果 6.25 ～ 50 μmol· L-1 GA可抑制SMMC-7721细胞的生长,并呈剂量依赖性;不同剂量的GA作用48 h后,SMMC-7721细胞出现明显的凋亡形态,细胞凋亡率有显著的剂量依赖性.RT-PCR法检测结果显示,GA能明显抑制肝癌细胞中Survivin mRNA的表达.结论 GA可抑制人肝癌SMMC-7721细胞的增殖,这可能与下调凋亡抑制基因Survivin有关.

Neural stem cells (NSCs) are self-regenerating cells, but their regenerative capacity is limited. The present study was conducted to investigate the effect of daucosterol (a sterolin) on the promotion of NSC proliferation and determine the corresponding molecular mechanism. Results of cell counting kit-8 (CCK-8) assay showed that daucosterol significantly increased the quantity of viable cells and the effectiveness of daucosterol was similar to that of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). Flow cytometry detection of CFSE-labeled (CFSE, carboxyfluorescein diacetate succinimidyl ester) NSCs showed that Div Index (or the average number of cell divisions) and % Divided (or the percentage of cells that divided at least once) of the cells were increased, indicating that daucosterol increased the percentage of NSCs re-entering the cell cycle. mRNA microarray analysis showed that 333 genes that are mostly involved in the mitotic cell cycle were up-regulated. By contrast, 627 genes that are mostly involved in differentiation were down-regulated. In particular, insulin-like growth factor I (IGF1) was considered as an important regulatory gene that functionally promoted NSC proliferation, and the increased expression of IGF1 protein was validated by ELISA. In addition, the phosphorylation of AKT was increased, indicating that the proliferation-enhancing activity of daucosterol may be involved in IGF1-AKT pathway. Our study provided information about daucosterol as an efficient and inexpensive growth factor alternative that could be used in clinical medicine and research applications.

大脑衰老是人体随年龄增长而出现大脑结构和功能等方面的退行性变化.延缓大脑衰老,就要延缓大脑生理性退化的过程或者减轻因大脑功能退化而出现的病理性改变.肾为先天之本,主骨生髓通脑,决定生长壮老已的生命过程,随年龄增长,出现肾虚证的可能性大大增加.肾虚推动无力,气化失常,精不化血,则脉道枯涩,血行不畅而致瘀.因此,大脑衰老是以肾虚和血瘀并存为基础,补肾活血法延缓大脑衰老具有坚实的理论依据.

目的:观察凉血通瘀方及其君药——大黄单体(大黄酸、大黄素)对出血性中风患者外周血中炎症相关细胞因子的影响,探讨凉血通瘀方治疗出血性中风患者的作用及机制.方法:采集出血性中风患者的全血,培养加药,放射性免疫法检测细胞上清中白介素-1β(IL-1β)、白介素-10(IL-10)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的含量,Western-blot法检测TNF-α、核因子-κB (NF-κB)、一氧化氮合成酶(iNOS)蛋白的表达水平.结果:凉血通瘀方(1g/ml)及大黄酸(25μmol/L)、大黄素(50μmol/L)可降低大鼠IL-1β、IL-6、TNF-α、NF-κB的表达,升高IL-10、iNOS的表达.结论:凉血通瘀方及大黄酸、大黄素降低炎症反应可能是其治疗出血性中风的作用机理之一.

Aim To investigate the proliferative effect and the apoptosis of human hepatoma SMMC-7721 cells induced by gallic acid ( GA ) , and its underlying mechanism. Methods SMMC-7721 cells were cul-tured in vitro. MTT assay was used to observe the pro-liferation of SMMC-7721 cells induced on GA 24 , 48 , 72 h. The morphological and ultra structural changes of the SMMC-7721 cells were observed by inverted micro-scope and transmission electron microscope respective-ly. Annexin V-FITC/PI staining was used to quantify the percentages of apoptosis in the total cell popula-tion. The expression of p53 mRNA was investigated by RT-PCR. Western blot was used to determine the pro-tein expression of p53. Results GA(6. 25~50 μmol ·L-1 ) markedly inhibited the activity of proliferation and induced apoptosis of SMMC-7721 cells after 48 h in a dose-dependent manner. GA significantly induced cell nuclear condensation and fragmentation. RT-PCR and Western blot results showed that GA could improve the expression of p53 mRNA and protein. Conclusion GA can inhibit the proliferation of human hepatoma SMMC-7721 cells and induce cells apoptosis. The mechanism may be associated with improving tumor suppressor gene p53 expression.

从教学现状、理论教学改革、实验教学改革和教改效果4个方面进行探讨,为分子生物学教学改革提供新思路.