The mechanism by which Peganum harmala L. inhibits high glucose-induced tube formation in endothelial cells / 药学学报

The study investigates the mechanism by which Peganum harmala L. (Luotuopeng, LTP) inhibits tube formation in retinal vascular endothelial cells. Tube formation was induced by treatment of retinal vascular endothelial cells with glucose. The cells were divided into a normal group, model group, and an LTP group. The total length of tube formation was measured. The active components, targets, and pathway by which LTP acts in the treatment of diabetic retinopathy was explored by network pharmacology. The mRNA expression levels of targets [extracellular signal-regulated kinase 2 (ERK2), phosphoinositide 3 kinase catalytic alpha polypeptide (PIK3CA), serine/threonine-protein kinase 1 (AKT1)] related to the mitogen-activated protein kinase (MAPK) signaling pathway and vascular endothelial growth factor (VEGF) signaling pathway was measured by real-time PCR. The results of tube formation indicated that compared with the normal group, the total tube length increased in the model group (P < 0.01); after the treatment with LTP, the total tube length decreased compared with the model group (P < 0.01). Network pharmacology revealed that the targets of LTP included PIK3CA, AKT1, and ERK2, and the pathways involved the MAPK signaling pathway and the VEGF signaling pathway. Real-time PCR indicated that compared with the normal group, the mRNA expression levels of ERK2, PIK3CA and AKT1 were elevated in the model group (P < 0.05); after treatment with LTP, the mRNA expression levels of ERK2, PIK3CA and AKT1 decreased compared with the model group (P < 0.05). LTP may inhibit retinal vascular endothelial cell tube formation by regulating the MAPK signaling pathway and the VEGF signaling pathway. This study confirms the multi-targets and multi-pathways of LTP and provides a basis for its use in the treatment of diabetic retinopathy．

Effect of chromodomain helicase/ATPase DNA binding protein 1-like gene on the invasion and metastasis of tongue squamous cell carcinoma CAL27 cells / 华西口腔医学杂志

OBJECTIVES@#A study was conducted to investigate the molecular mechanism of chromodomain helicase/ATPase DNA binding protein 1-like gene (CHD1L) influencing the invasion and metastasis of tongue squamous cell carcinoma and to provide a new target for clinical inhibition of invasion and metastasis of tongue squamous cell carcinoma.@*METHODS@#Ualcan website was used to analyze the expression of CHD1L in normal epithelial tissue and primary head and neck squamous cell carcinoma and to analyze the effect of lymph node metastasis on the expression of CHD1L in tissues with head and neck squamous cell carcinoma. The relationship between CHD1L expression and the survival rate of patients with head and neck squamous cell carcinoma was tested by the GEPIA website. Western blot was used to quantify the levels of CHD1L protein in human tongue squamous cell carcinoma CAL27 and immortalized human skin keratinocyte cell HaCaT. After knocking down CAL27 in human tongue squamous cell carcinoma cells with an RNA interference plasmid, the cells were designated as SiCHD1L/CAL27 and Scr/CAL27. Western blot was utilized to detect the expression of CHD1L in each group of cells. The change in CAL27 cell proliferation ability was tested by EdU proliferation test after CHD1L knockdown. The change of cell migration ability of each group cells was tested through the wound healing assay. Western blot was used to detect epithelial-mesenchymal transition (EMT) marker E-cadherin and Vimentin protein expression levels.@*RESULTS@#Ualcan database showed that the expression of CHD1L in primary head and neck squamous cell carcinoma tissues was higher than in normal epithelial tissues and in head and neck squamous cell carcinoma tissues with lymph node metastasis. GEPIA website analysis showed that the overall survival rate of patients with head and neck squamous cell carcinoma with high expression of CHD1L was significantly lower than that of patients with low expression. Western blot results showed that CHD1L expression in human tongue squamous carcinoma cells CAL27 was higher than that of human normal skin cells HaCaT. CHD1L expression in SiCHD1L/CAL27 cells was much lower than that in Scr/CAL27 cells. Results of EdU proliferation experiments showed the significant reduction in the cell proliferation ability of the SiCHD1L/CAL27 cells. Results of the wound healing experiments showed the reduction in the migration capacity of the SiCHD1L/CAL27 cells. The expression of E-cadherin increased, whereas that of Vimentin decreased, in SiCHD1L/CAL27 cells.@*CONCLUSIONS@#CHD1L promoted the EMT, proliferation, migration, and invasion ability of tongue squamous cell carcinoma cells.

miR-125a-5p suppresses epithelial-mesenchymal transition via GSK-3β/Snail signaling pathway in breast cancer cells / 中国病理生理杂志

AIM:To investigate the function of microRNA-125a-5p (miR-125a-5p) on epithelial-mesenchy-mal transition ( EMT) of breast cancer cells via GSK-3β/Snail signaling pathway. METHODS:The expression of miR-125a-5p in normal breast epithelial cells and breast cancer cells, as well as the transfection efficiency of miR-125a-5p plas-mid in MDA-MB-231 cells was detected by RT-qPCR. The chemotaxis ability and invasion ability were detected by chemo-taxis assay and Transwell invasion assay. The changes of EMT-related markers, the protein level of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) and the nuclear translocation of Snail were determined by Western blot. RESULTS:The expression of miR-125a-5p in the breast cancer cells was significantly lower than that in the normal breast epithelial cells. The expression of miR-125a-5p was significantly higher in MDA-MB-231/miR-125a-5p cells than that in MDA-MB-231/NC cells. The ability of epithelial growth factor (EGF) at 10 μg/L to induce chemotaxis of MDA-MB-231 cells was the stron-gest. Compared with MDA-MB-231/NC group, stimulation of EGF decreased the invasion ability of MDA-MB-231/miR-125a-5p cells, and resulted in the increase in E-cadherin expression, while significantly decreased the protein levels of vi-mentin and p-GSK-3β. Meanwhile, the nuclear localization of Snail was significantly inhibited. The invasion capacity of MDA-MB-231/miR-125a-5p+GAB2 cells was significantly enhanced compared with MDA-MB-231/miR-125a-5p +Con cells, the expression of E-cadherin was decreased, and the protein levels of vimentin and p-GSK-3β were significantly in-creased, while the nuclear localization of Snail was promoted. CONCLUSION:miR-125a-5p suppresses EMT via GSK-3β/Snail signaling pathway, thus inhibiting the invasion ability of breast cancer cells.

Relationship between large artery elasticity function and coronary heart disease, lower extremity arterial disease in patients with carotid plaque / 北京大学学报(医学版)

Objective:To evaluate the relationship between large artery elastic function and coronary heart disease (CHD) or lower extremity arterial disease (LEAD) in patients with carotid plaque.Methods:A total of 491 patients with carotid plaque were enrolled into the study with complete data of arterial stiffness detection and blood test [male:208 and female:283,and mean age:(61.66 11.60) years].All the subjects were divided into 2 groups according to CHD or LEAD,namely non-CHD&LEAD group (neither CHD nor LEAD) and CHD/LEAD group (either CHD or LEAD).According to the mean age level (age ＜61.66 years or age ＞61.66 years),the independent association was analyzed between higher large arterial stiffness (carotid-femoral pulse wave velocity,CF-PWV,CF-PWV ＞ 9 m/s) and CHD/LEAD.Results:In the present research population,the mean level of arterial stiffness was high (the mean CF-PWV was 10.71 m/s),and 76.6％ of them had arteriosclerosis,and 36.9％ CHD/LEAD.The age,male and smoking proportion,systolic blood pressure (SBP),glycosylated hemoglobin (HbA1c),homocysteine (Hcy),creatinine (Cr),CF-PWV,prevalence rate of hypertension and diabetes mellitus,medication on hypertension,diabetes and hyperlipidemia were higher in CHD/LEAD group,and total cholesterol (TC),high density lipoprotein cholesterol (HDL-C),and low density lipoprotein cholesterol (LDL-C) were lower in CHD/LEAD group than in non-CHD&LEAD group (all P ＜ 0.05).In multivariate Logistic regression analysis,the results showed that in the patients with age below 61.66 years,large artery stiffness (CF-PWV ＞ 9 m/s) was an independent risk factor of CHD/LEAD (OR =3.229,95％ CI 1.156-9.022,P ＜ 0.05);In the patients with age above 61.66 years,there was no independent association between large artery stiffness and CHD/LEAD (P ＞ 0.05).Conclusion:The large artery elasticity function in the patients with carotid plaque was poor.In the patients with carotid plaque and higher large artery stiffness below 61.66 years,the risk of the prevalence of CHD/LEAD was increased significantly than with normal arterial stiffness.In the patients with carotid plaque below or above 61.66 years,the independent influencing factors on the prevalence of CHD/LEAD were different.

Effect of metformin on learning and memory ability in mice during aging and the possible underlying mechanisms / 中国比较医学杂志

Objective To explore the effect of metformin on learning and memory ability and hippocampal tissue structure in mice during aging induced by D-galactose, and the possible underling mechanisms. Methods Twenty-four SPF 7-month-old female ICR mice were randomly divided into three groups. Mice of the aging group and aging+metformin group were given subcutaneous injection with D-galactose on the back to induce senescence, and given intragastric gavage with 0. 9% saline or metformin. Mice of the control group were treated with 0. 9% saline. All treatments lasted for 16 weeks. The body weight and food intake were monitored, learning and memory ability and motor function were tested by Mirros water maze and shuttle box tests, HE staining was used to observe the pathology of hippocampus in the mice, and the levels of glutathione (glutathione, GSH) in hippocampus of mice were detected by colorimetry. Results Compared with the aging group, the aging+meformin group showed diverse differences:the body weight was decreased (P < 0. 05), the escape latency and swimming distance were decreased ( P < 0. 01 or P < 0. 05 ) , the swimming time in the target quadrant was prolonged (P < 0. 05) and swimming speed was accelerated (P < 0. 05) in the Morris water maze test. The numbers of active avoidance response were markedly increased in shuttle box test ( P < 0. 05 ) . The neurons with nuclear condensation and deep staining were obviously decreased in the dentate gyrus of hippocampus, however the GSH level was significantly increased ( P < 0. 05 ) . Conclusions Metformin can delay the decline of learning and memory ability, maintain the normal structure of hippocampus during the aging process in mice, which may be related to the reduction of body weight and enhancement of antioxidant levels in the hippocampus.

Notoginsenoside Ft1 down-regulates HIF-1α, inhibits cell proliferation, decreases migration and promotes apoptosis in breast cancer cells / 药学学报

To investigate the effect of notoginsenoside Ft1(Ft1) on proliferation, migration and apoptosis of breast cancer cells, we conducted several assays including CCK-8 assay, EdU staining, single cell migration assay and Hoechst 33258 staining. The effect of Ft1 on expression of apoptosis related proteins, HIF-1α, PI3K/Akt/mTOR/p70S6K and MAPK pathways was examined with Western blot. Ft1 could significantly reduce cell survival and inhibit cell proliferation in breast cancer cells in a dose-dependent manner. Ft1 also increased chromatin condensation of MDA-MB-231 cells. Furthermore, Ft1 decreased protein expression of Bcl-2 and HIF-1α and increased expression of cleaved caspase 3 in MDA-MB-231 cells after 12 h treatment. Ft1 significantly down-regulated the levels of p-Akt, p-mTOR and p-p70S6K as well as p-ERK1/2, but up-regulated that of p-JNK. Ft1 significantly inhibited the level of p-EGFR (Tyr1068) and p-EGFR (Ser1046/1047) in MDA-MB-231 cells. Finally, Ft1 significantly inhibited the migration path length and velocity of HS578T cells when used at the concentration without affecting cell viability. Thus, Ft1 exhibited multiple antitumor effects including inhibition of cell survival and migration, promotion of cell apoptosis in breast cancer cells. Suppression of HIF-1α via Akt/mTOR/p70S6K and MAPK pathways may be involved in the pharmacological effect of Ft1 on cell proliferation and apoptosis of breast cancer cells.

Inhibitory effects of vina-ginsenoside R7 on activation of rat C6 astrocytes induced by LPS and TNF-α combination / 中国中药杂志

To investigate the inhibitory effect and mechanism of vina-ginsenoside R7 (R7) on the activation of rat C6 astrocytes cells induced by LPS/TNF-α, cells in logarithmic growth phase were cultured in DMEM medium without FBS for 24 h. After dissociated using 0.25% EDTA-trypsin, the cells were seeded into respective plates at the density of 1.5×10⁶ cells per mL and cultured overnight. The cells were divided into the following groups： control group (no treatment), model group (treated with LPS 1 μg•mL⁻¹ and TNF-α 10 μg•L⁻¹ treated for 24 h), R7 groups (pre-treated with 6.25, 12.5, 25, 50, and 75 μmol•L⁻¹ R7, 4 μmol•L⁻¹ L-NMMA for 2 h and then stimulated with LPS 1 mg•L⁻¹ and TNF-α 10 μg•L⁻¹ for 24 h). Cell viability was analyzed by CCK-8 kit. Secretion of nitric oxide (NO) in the medium was measured by Greiss method. Concentrations of interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) were assayed by ELISA kits. Gene expressions of inflammatory factors were examined by quantitative-PCR analysis. Activation of NF-κB was detected by dual luciferase reporter gene assay kit. The results showed that R7 could significantly inhibit the secretion of NO from C6 cells in a dose-effect manner, with an IC₅₀ of 34 μmol•L⁻¹. And it could reduce cell proliferation induced by LPS/TNF-α stimulation. Furthermore, R7 at 50 μmol•L⁻¹ significantly down-regulated gene expressions of iNOS (P<0.001), TNF-α (P<0.001), IL-1β(P<0.05), and COX-2 (P<0.001), but could not change gene expression of IL-6. However, R7 reduced the secretion of TNF-α (P<0.001) and IL-6 (P<0.001). Further studies disclosed that, different concentrations of R7 (25, 50, 100 μmol•L⁻¹) could significantly inhibit the transcription activity of NF-κB(P<0.05, P<0.01, and P<0.001). In conclusion, R7 could inhibit inflammatory responses in C6 cells induced by LPS/TNF-α probably by inhibiting the transcription activity of NF-κB, which indicates its possible therapeutic effect in neurological diseases related to neuroinflammation.

Multidrug resistance in breast cancer cells during epithelial-mesenchymal transition is modulated by breast cancer resistant protein / 癌症

<p><b>BACKGROUND AND OBJECTIVE</b>Epithelial-mesenchymal transition (EMT) not only initiates invasion and metastasis of tumors, but also induces multidrug resistance in tumor cells. Our experiment analyzed the dependability between breast cancer resistant protein (BCRP) and EMT in breast cancer to explore the effect of EMT on BCRP-mediated multidrug resistance.</p><p><b>METHODS</b>The expressions of BCRP and transcription inhibitor Snai1 (Snail) in breast cancer were detected by immunohistochemistry. The eukaryotic expression vector pCDNA3.1-Snail was constructed and then transfected into human breast cancer cell line MCF-7. Snail, epithelial marker gene E-cadherin, interstitial marker gene Vimentin, multidrug resistance protein BCRP, and relative drug resistance were measured by immunofluorescence, Western blot, real-time polymerase chain reaction (PCR), and MTT assay.</p><p><b>RESULTS</b>Immunohistochemistry showed that Snail was highly correlated with BCRP in breast cancer. Immunofluorescence, Western blot, real-time PCR revealed that compared with parent cell MCF-7, after transfected with Snail, the expression of E-cadherin in MCF-7 decreased, but Snail, Vimentin, and BCRP increased. MTT displayed that the relative drug resistance increased to 9.93.</p><p><b>CONCLUSION</b>After transfected with eukaryotic expression vector pCDNA3.1-Snail, breast cancer cells MCF-7 showed EMT with BCRP-mediated multidrug resistance.</p>

Effects of integrated disease management program on the outcome of patients with heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the feasibility and efficacy on the outcome of patients with heart failure of integrated disease management program with heart failure clinic, patient education and telephone follow-up.</p><p><b>METHODS</b>A total of 145 hospitalized patients with chronic heart failure and LVEF ≤ 45% or patients with LVEF > 45% and NT-proBNP > 1500 ng/L were divided into conventional group (n = 71) and interventional group (n = 74). Patients were followed for 10 to 12 months.</p><p><b>RESULTS</b>Baseline clinical characteristics, LVEF and dose of evidence-based medicine were similar between the 2 groups. During follow-up, the NYHA functional class was higher in conventional group than interventional group (3.2 ± 0.5 vs 1.4 ± 0.5, P < 0.05), and the LVEF deteriorated in the conventional group and improved from 34% to 40%in the interventional group. The proportions of self-monitoring of weight, blood pressure and pulse rate in the interventional group were significantly higher than those of conventional group (P < 0.05). Among patients with systolic heart failure, 40% patients in the interventional group and 11% patients in the conventional group achieved the target doses of β-blockers (P < 0.05). Cardiovascular event rate of conventional group and interventional group is 91.5% and 27.0% respectively (P < 0.05).</p><p><b>CONCLUSION</b>Integrated disease management program with heart failure clinic, patient education and telephone follow-up can improve patient compliance to heart failure treatment, improve cardiac function and reduce cardiovascular event rate.</p>

Construction of murine CCL21 eukaryotic expression plasmid and chemotactic function of its products / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To construct the murine CCL21 eukaryotic expression plasmid, and to investigate the chemotactic function of its products.</p><p><b>METHODS</b>Murine CCL21 cDNA was amplified by RT-PCR from murine total RNA, and was inserted into eukaryotic expression plasmid pcDNA3.1 after confirmation of sequencing. The recombinant CCL21 plasmid was transferred into mouse forestomach carcinoma (MFC) cells and the chemotactic function of expressed products was detected by chemotaxis assay.</p><p><b>RESULT</b>Gene sequencing, gel electrophoresis of PCR products and restrictive digestion proved the successful construction of CCL21, and its expression was confirmed by Western Blot. The transfected tumor cells had a significant chemotactic function to DC.</p><p><b>CONCLUSION</b>The recombinant murine CCL21 eukaryotic expression plasmid has been successfully constructed, and its expression products in tumor cells have a marked chemotactic function to DC.</p>

The construction of siRNA plasmid targeting mouse HIF-1alpha and in vitro study of its inhibition effect / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To construct effective RNA-interference plasmids targeting mouse HIF-1alpha gene and testify their effects and specificities in interfering HIF-1alpha expression.</p><p><b>METHODS</b>Three RNA-interference plasmids targeting mouse HIF-1alpha gene, pBS/U6/HIF-1alpha-siRNAI~III, were constructed and identified using double digestion method in the present study. RT-PCR, immunostaining and western blotting were employed to detect the expression alterations of HIF-1alpha in 293T cells following transfections of the three plasmids, respectively. The interference effect of pBS/U6/HIF1alphai-II in SH-SY5Y cell line was further investigated.</p><p><b>RESULTS</b>All the three RNA-interference plasmids, especially pBS/U6/HIF1alphai-II, showed significant inhibition in HIF-1alpha expression in 293T cell line. pBS/U6/HIF1alphai-II could also inhibit HIF-1alpha expression in SH-SY5Y cell line, in a dose-dependent way.</p><p><b>CONCLUSION</b>Plasmid pBS/U6/HIF1alphai-II constructed in our study can effectively and specifically inhibit HIF-1alpha expression, and its role in neural tube development and dysfunction will be further investigated. Construct of pBS/U6/HIF1alphai-II plasmid will provide a useful tool to study the role of HIF-1 pathway in embryogenesis, oncogenesis and ischemia development.</p>

Increasing cardiopulmonary bypass flow volume improves outcome of patient with carotid stenosis undergoing coronary artery bypass grafting / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the effect of increasing cardiopulmonary bypass (CPB) flow volume in improving outcome of patients with carotid artery stenosis performed coronary artery bypass grafting (CABG) procedure.</p><p><b>METHODS</b>Fifty-one patients data collected from January 2006 to March 2008 and divided into two groups (A and B) based on the degree of the carotid artery stenosis diagnosed by ultrasound. Group A included 15 cases with one or both carotid artery stenosis more than 50%, 14 male and 1 female, aged (68.5 +/- 7.7) years old, 14 with hypertension, 2 with diabetes, 6 with myocardial infarction, 3 with cerebral infarction. Group B included 36 cases with stenosis less than 50%, 34 male and 2 female, aged (62.4 +/- 10.2) years old, 28 with hypertension, 7 with diabetes, 20 with myocardial infarction. Increasing CPB flow volume in A group to compare cerebral blood flow (CBF) within procedure in both groups.</p><p><b>RESULTS</b>CPB flow volume in group A was much higher than it in group B (P = 0.001). Mean arterial blood pressure in group A was (67.0 +/- 9.1) mm Hg (1 mm Hg = 0.133 kPa), higher than group B (59.0 +/- 7.1) mm Hg (P = 0.009). There was no significant difference of CBF within procedure and neuropsychologic performance in both group as result.</p><p><b>CONCLUSION</b>For the patients presenting with carotid artery stenosis undergoing the procedure of CABG with CPB, increasing CPB flow volume could improve significantly diseased side cerebral blood flow and might reduce neurological complications.</p>

Overexpression of cyclin L2 induces apoptosis and cell-cycle arrest in human lung cancer cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Uncontrolled cell division is one of the hallmarks of tumor growth. Researches have been focused on numerous molecules involved in this process. Cyclins are critical regulatory proteins of cell cycle progression and/or transcription. The present study aimed to investigate the anti-proliferative effect of cyclin L2, and to define its growth regulatory mechanisms using human lung adenocarcinoma cell line A549.</p><p><b>METHODS</b>Human cyclin L2 was transfected into human lung adenocarcinoma cells (A549 cell), and was expressed in a mammalian expression vector pcDNA3.1. The effects and mechanisms of the cyclin L2 in cell growth, cell cycle analysis and apoptosis were studied by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), flow cytometry or Western blot, respectively.</p><p><b>RESULTS</b>Overexpression of cyclin L2 inhibited the growth of A549 cells. Cell cycle analysis in cells transfected with pCCNL2 revealed an increment in proportion in G0/G1 phase ((68.07 +/- 4.2)%) in contrast to (60.39 +/- 2.82)% of the cells transfected with mock vector. Apoptosis occurred in (7.25 +/- 0.98)% cells transfected with pCCNL2, as compared with (1.25 +/- 0.21)% of the mock vector control group. Cyclin L2-induced-G0/G1 arrest and apoptosis involved upregulation of caspase-3 and downregulation of Bcl-2 and survivin.</p><p><b>CONCLUSION</b>The results indicate that overexpression of cyclin L2 protein may promote efficient growth inhibition of human lung adenocarcinoma cells by inducing G0/G1 cell cycle arrest and apoptosis.</p>

Application of functional MRI in epilepsy / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To review the recent development of functional MRI application in epilepsy.</p><p><b>DATA SOURCES</b>Both Chinese and English language literatures were researched using MEDLINE/CD ROM (1996 - 2005) and the Chinese Biomedical Literature Disk (1996 - 2005).</p><p><b>STUDY SELECTION</b>Published articles about functional MRI application and epilepsy were selected.</p><p><b>DATA EXTRACTION</b>Data were mainly extracted from 38 articles which are listed in the reference section of this review.</p><p><b>RESULTS</b>fMRI can be used to localize seizure foci through detecting these cerebral hemodynamic changes produced by epileptiform discharges. EEG-triggered fMRI, which has higher spatial and temporal resolution, helps to detect the spatiotemporal pattern of spike origin and propagation, and define localization of the epileptogenic focus. fMRI is also useful in language and memory cognitive function assessment and presurgical assessment of refractory epilepsy. Atypically distributed cognitive function areas can be detected by fMRI, because of cortical language and memory areas reorganization during long-term epileptic activity in patients with epilepsy.</p><p><b>CONCLUSIONS</b>fMRI technique plays a very important role in cognitive function and presurgical assessment of patients with epilepsy. It is meaningful for understanding pathogenesis of epilepsy.</p>

Change and significance of nuclear factor-kappaB in adriamycin induced cardiomyopathy in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>This study aimed at investigating the change and significance of nuclear factor-kappaB (NF-kappaB) in cardiomyopathy induced by adriamycin (ADR) in rats.</p><p><b>METHODS</b>Sixty male Wistar rats were randomly divided into three groups: control, ADR and ADR + pyrrolidine dithiocarbamate (PDTC) groups. After 30-day experiment, myocardial histopathological observation was performed. Location and distribution of NF-kappaB p50 was examined by immunohistochemical assay. Expression of NF-kappaB p50 protein was examined by immunobolt assay. Electrophoretic Mobility Shift Assay examined activity of NF-kappaB; Myocardium p53 gene expression was examined by RT-PCR analysis.</p><p><b>RESULTS</b>The myocardial lesions of rats were less pronounced in ADR + PDTC group than in ADR group. Compared with control group, there were many myocardium nucleuses, which expressed NF-kappaB p50 and distribute under epicardium. Expression of NF-kappaB p50 protein in nucleus increased significantly in ADR group. The NF-kappaB binding activity increased significantly in ADR group. Myocardium expressions of p53 mRNA increased in ADR group.</p><p><b>CONCLUSIONS</b>The NF-kappaB binding activity increased significantly in cardiomyopathy induced by ADR in rats. Moreover, NF-kappaB plays an important role in causing degeneration of myocardial tissue and regulating expression of related-apoptosis genes.</p>

Diagnostic Value of X-Ray Computed Tomography on Neck Masses in Children / 实用儿科临床杂志

Objective To evaluate diagnostic value of X-ray computed tomography(CT) neck masses in children.Methods Clinic,pathologic diagnosis and CT scans of 26 patients from Jan.2004 to Jun.2006 with neck masses which location,density,edge and near construction were reviewed retrospectively.Results Seven cases in neck anterior area,13 cases in neck lateral area,6 cases in other areas or unconfirmed.Eight cases with lower density than cervical muscles,2 cases with same density,2 cases with higher density,14 cases with mixed density.Inflammatory masses were observed in 13 cases,congenital malformation in 11 cases,thyroiditis in 1 case,pharyngeal tumor-like proliferation in 1 case.Conclusion CT scan is the best choice of diagnosis of neck masses in children,and is valuable to diagnosis associated with history and physical examination.