ObjectiveTo observe the effect of digital auditory activation and touching intervention on infants with cerebral dysfunction.Methods388 infants with perinatal high-risk factors and abnormal result of Denver Development Screening Test (DDST) were randomly divided into group A (n=135), group B (n=128) and group C (n=125), and treated with digital auditory activation combined with touching (group A), simple touching (group B) and simple drug (group C) with 10 days as a course. All infants were tested with DDST after one therapeutic course, and tested again with DDST after the infants of group B and group C treated continuously for six therapeutic courses; and all infants were assessed with the Gesell development quotient (DQ) after six months.ResultsAfter one therapeutic course, normal rate of DDST was 71.11% in group A, 26.69% in group B and 20.00% in group C. After six therapeutic courses, that was 90.37 % in group A, 62.50 in group B and 40.00% in group C. After six months, the children with the Gesell DQ over 86 scores was 125 (92.60%) in group A, 90 (70.31%) in group B and 62 (49.60%) in group C. There were significant differences among three groups ( P<0.01).ConclusionThe digital auditory activation combined with touching has short therapeutic course and high efficacy, so it is a good therapeutic method for infants with cerebral dysfunction.

Drugs, Chinese Herbal ; therapeutic use ; Humans ; Vascular Diseases ; prevention & control

Objective One typical case with stress cardiomyopathy was reported and the current knowledge of the syndrome was reviewed to improve relevant knowledge.Methods A 71-year-old female patient presented dyspnea and chest pain due to emotional stress.ECG,echocardiography,selective coronary artery angiography,left ventriculography,~(99)Tc~m-MIBI single photon emission computed tomography (SPECT),~(18)F-FDG SPECT and MRI were performed.Results Electrocardiogram at admission showed ST segment elevation and T wave inversion in leads V1—V4.Pathological Q wave occurred 1 week later,it disappeared 1 month later however and severe T wave inversion occurred.Normal or slightly elevated cardiac enzymes in the blood were found during the course.Left ventriculogram at admission showed left ventricular apical ballooning with LVEF of 30%.The ballooning volume was about 3/4 of left ventricular volume, without any corresponding coronary artery diseases found in coronary angiogram.The abnormal apical ballooning decreased significantly in the follow-up left ventriculogram performed one month later.The LVEF rose up to 63.6%.~(99)Tc~m-MIBI and ~(18)F-FDG SPECT showed mismatch of perfusion and metabolism in the corresponding region,indicating presence of viable myocardium.MRI showed left ventricular apical ballooning without perfusion defect and late enhancement,indicating viability of corresponding myocardium. Conclusions Emotional stress can cause transient left ventricular apical ballooning called"stress cardiomyopathy".Either ~(99)Tc~m-MIBI SPECT associated with ~(18)F-FDG SPECT or delayed enhancement MRI plays an important role in identification of myocardial viability,which can efficiently guide clinical treatment.

Objective To study the effect of TLR4 activation with LPS on BMP9-induced osteogenic differentiation of immortalized mouse embryonic fibroblasts ( iMEFs).Methods The activation of TLR4/NF-κB signaling path-way was detected by ICC.iMEFs were treated with LPS,BAY11-7082,Adnovirus GFP and BMP9.The early osteo-genic differentiation capability of iMEFs was detected by ALP staining and quantitative assay .The later osteogenic differentiation capability was detected by alizarin red S staining .The expression of later osteogenic differentiation marker gene OCN and OPN were detected by PCR and Western blot .The change of p-Smad1/5/8 was detected by Western blot.The expression of Runx2 and Dlx5 were detected by PCR and Western blot .Results LPS can effec-tively stimulate TLR4/NF-κB signaling pathway .TLR4 activation inhibited BMP 9-induced osteogenic differentiation . BMP9-induced osteogenic differentiation related gene and Smad 1/5/8 signaling activation were inhibited by TLR4 activation .The inhibition effect was partly reversed by BAY 11-7082 ( P<0.05 ) .Conclusions TLR4 activation with LPS can inhibit BMP9-induced osteogenic differentiation of iMEFs cells via NF-κB signaling pathway .

The apparatus introduced in this paper can be used to measure and record the realtime environmental parameters and such physical information of individual protection equipment as the temperature,thermal current and thermal insulating value.The apparatus has several advantages including high accuracy,practicability,reliability and easy to operate.

Objective To investigate the effect of miR-30a on human osteosarcoma cell 143B in migration,invasion andcellviability.Methods 143BcellswereinfectedortransfectedwithrecombinantadenovirusmiR-30a(Ad-miR30a) and miR-30a inhibitor respectively .Wound healing assay was performed to detect the cell healing ability ( P<0.05 ) .Cell migration and invasion ability were determined by Transwell assay ( P<0.05 ) .The cell viability was analyzed by MTT assay ( P<0.01 ) .Real-time quantitative PCR was performed to analyze the expression of RUNX2 mRNA level and confirmed the adenovirus miR-30a expressed in 143B cells.The expression of RUNX2 was analyzed by Western blot .miR-30a target to RUNX2 was verified by luciferase reported gene assay .Results The ability of migration and invasion was suppressed in osteosarcoma cell 143B by overexpression miR-30a,and the cell viability also decreased .After the endogenous miR-30 a being inhibited , the cell motility and invasion enhanced and the cell viability was promoted .The RUNX2 protein decreased after overexpression miR-30 a as compared with controlgroup.TheluciferaseactivityofRUNX2decreasedbyaddingmiR-30a.Conclusions 143Bcellmigration, invasion and viability were suppressed by miR-30a,and this process is potentially achieved via suppressing RUNX 2 protein expression .

Objective To investigate the effects of the fibrin-derived peptide Bβ15-42 (FgBβ 15-42) on renal inflammation in acute kidney injury (AKI) induced by renal ischemia reperfusion (IR).Methods SD rats were randomly divided into sham group (the abdominal cavity were closed after separating the renal artery),IRI group (renal arteries of rats were occluded with microvascular clamps for 60 min),negative treated group (rats were injected with 3.6 mg/kg random peptide by tail vein) and FgBβ15-42 treated group (rats were injected with 3.6 mg/kg FgBβ15-42 by tail vein).Rats were sacrificed at 24 h or 48 h after reperfusion.Blood and kidney samples were collected and histological changes and renal function were examed.The mRNA and protein expressions of intercellular cell adhesion molecule-1 (ICAM-1) and interleukin-1β (IL-1β) were examined by immunohistochemistry,real-time PCR and Western blotting.Results Compared with sham group,Scr and BUN were obviously increased in IRI group (all P ＜ 0.05),pathologic changes of kidney were more serious (P ＜ 0.05).Compared with IRI group,in FgBβ15-42 treated group Scr and BUN were obviously decreased (all P ＜ 0.05),the injury of kidney tubulointerstitial was less serious (P ＜ 0.05).Compared with sham group,there was increased ICAM-1 and IL-1β in IRI group (all P ＜ 0.05),and they all peaked at 24 h.After treated with FgBβ15-42,the expression of ICAM-1,IL-1β were significantly decreased in kidneys compared to IRI group (all P ＜ 0.05).The above indexes had no significant differences between negative treated group and IRI group (all P ＞ 0.05).Conclusions FgBβ15-42 can protect kidneys against ischemia reperfusion injury in rats.The mechanism may be associated with down-regulated expressions of ICAM-1 and IL-1 β in the kidney.

AIM:To investigate the effect of bone morphogenetic proteins 9 (BMP9) on the migration and in-vasion abilities of human lung squamous-cell carcinoma NCI-H520 cells and its mechanism.METHODS:The expression of BMP9 at mRNA and protein levels in the NCI-H520 cells and human bronchial epithelial ( HBE) cells was detected by RT-PCR and Western blot.The NCI-H520 cells were transfected with the recombinant adenovirus AdBMP9 and the expres-sion of BMP9 at mRNA and protein levels was validated by RT-PCR and Western blot.The migration and invasion abilities of the NCI-H520 cells were determined by wound-healing and Transwell assays.The mRNA and protein levels of the migra-tion-related factor matrix metalloproteinase 2 (MMP2) were detected by RT-PCR and Western blot.The level of phospho-rylated Smad1/5 (p-Smad1/5) was detected by Western blot.Meanwhile, NCI-H520 cells were treated with BMP specific antagonist AdNoggin and AdBMP9.The level of p-Smad1/5 and the cell migration ability were measured by Western blot, wound-healing and Transwell assays.RESULTS:The expression of BMP9 at mRNA and protein levels was lower in NCI-H520 cells than that in HBE cells.After AdBMP9 was stably transfected into the NCI-H520 cells, the expression of BMP9 at mRNA and protein levels was significantly up-regulated, cell migration and invasion abilities were significantly de-creased, and the mRNA and protein levels of MMP2 were decreased.Meanwhile, the level of p-Smad1/5 was increased. Noggin reversed BMP9-caused the increase in p-Smad1/5 and the decrease in cell migration ability.CONCLUSION:O-ver-expression of BMP9 inhibits the migration and invasion abilities of lung squamous-cell carcinoma NCI-H520 cells.The activation of BMP-Smad signaling pathway may be involved in this inhibitory process.

Objective To investigate the mechanism of recombinant human bone morphogenetic protein-2(rhBMP-2)in repairing hematopoietic injury in mice irradiated with γ-ray.To prepare SRY gene probe and study the effect of rhBMP-2 in repairing hematopoietic injury in mice by in situ hybridization.Methods Twenty-two BALB/c female mice were randomly divided into the irradiated group and BMP treated group,respectively.Bone marrow cells of normal male mice were transplanted into 22 female mice post-irradiation to 8.5 Gy of 60 Co γ rays.The left femurs of the survived female mice were re-irradiated with 9 Gy 14 days later.Mice in BMP treated group were given rhBMP-2 20 mg/kg while those in control group were treated with 0.9% saline by intraperitoneal injection every day for 6 days.These mice were killed 14 days later and paraffin sections of femurs were made.The SRY gene was detected with in situ hybridization.Results There were more positive blots in the left femurs of the mice in irradiated group than those in BMP treated group(T=155.0,P＜0.05).The number of positive blots between the left femurs of the mice in irradiated group and the right femurs of the mice in two groups was not significantly different(T=92.0,78.5,P＞0.05).The number of positive blots in the left femurs of the mice in BMPtreated group was significantly less than those in the right femurs of the mice in two groups(T=155.0,55.0,P＜0.05).Conclusions No donor cell of male mice was detected in the left femurs of BMP treated group,suggesting that rhBMP-2 promoted the restoration of residuary bone marrow cells.Thus,rhBMP-2 promotes the proliferation or differentiation of residuary mesenchymal stem cells,improves hematopoietic microenvironment and accelerates the hematopoietic restoration.

Objective To construct the RNA interference eukaryotic expression vector targeting human centromere protein-I (CENP-I) and to observe its effect on the growth of human embryo kidney 293 cells (HEK 293). Methods The expression vectors of pGenesil-1/CENP-I-siRNA-1. pGenesil-1/CENP-I-siRNA-2 and pGenesil-1/CENP-I-siRNA-3 were constructed by gene recombination and then were transfected into the HEK293 cells by liposome. The expressions of CENP-I at the protein and mRNA levels were detected by Western blotting and fluorescence quality PCR (FQ-PCR). The effective vector and the best transfection time were selected. The growth and the cell cycle of the transfected cells were assessed by MTT assay and flow cytometry. Giemsa was used to stain the transfected cells to calculate the mitotic index. Results Sequence-specific siRNAs targeting CENP-I significantly down-regulated the expression of CENP-I in HEK293 cells. The recombinant plasmid of pGenesil-1/CENP-I-siRNA-3 was the effective vector. After transfecting for 72 h the best inhibited efficiency was achieved. In CENP-I-siRNA transfected cells,the rate of cell growth was decreased markedly. Cells at G 2/M phase and the mitotic index were increased conspicuous compared with the cells transfected with the blank vector or untransfected. Conclusion Down-regulation of CENP-I in HEK293 cells by sequence specific siRNA delays the cell growth and postpones the cell division.