Adult ; Brachial Plexus ; Female ; Humans ; Male ; Middle Aged ; Neurilemmoma ; surgery ; Treatment Outcome

Objective To investigate whether HIV-1 Nef could promote the angiogenesis and tu-morigenesis induced by KSHV vIL-6 through regulating PTEN/PI3K signaling pathway .Methods Lipo-some transfection was used to transfect cDNA of pPTEN , dominant-negative ( DN) construct of PI3K and control vector into endothelial cells , which stably express KSHV vIL-6 and HIV-1 Nef.Microtubule forma-tion assay and chicken chorioallantoic membrane ( CAM) assay were used to evaluate microtubule formation and angiogenesis , respectively .Expressions of PTEN and PI 3 K were measured by Western blot .Results Both overexpression of PTEN and inhibited expression of PI 3K suppressed the vIL-6-induced microtubule for-mation and angiogenesis in CAM mediated by Nef .Conclusion HIV-1 Nef enhances vIL-6-induced angio-genesis and tumorigenesis through regulating PTEN/PI3K signaling pathway .

Adult ; Aluminum Silicates ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; adverse effects ; statistics & numerical data ; Quartz ; adverse effects ; analysis ; Silicosis ; epidemiology ; mortality

Angiomyoma ; complications ; pathology ; Humans ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; etiology ; Male ; Middle Aged

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective To explore the role of glycogen synthase kinase (GSK)-3β/β-catenin signaling pathway on human immunodeficiency virus 1 (HIV-1) negative factor (Nef) protein promoting of human herpesvirus-8 (HHV-8) viral interleukin-6 (vIL-6)-induced angiogenesis.Methods GSK-3β mutant plasmid GSK-3β-S9A,dominant negative (DN) form GSK-3β-DN and the control vector pcDNA3.1+ were transfected into endothelial cells which stably expressed HHV-8 vIL-6 or HIV-1 Nef,or co-expressed vIL-6 and Nef protein.Microtubule formation assay was performed to explore microtubule formation ability.A chick embryo chorioallantoic membrane (CAM) model was used to detect angiogenesis.The expression of GSK-3β/β-catenin signaling pathway-related kinases in transfected cells and CAM tissue were further detected by Western blot.The measurement data were compared by t test.Results The activity of GSK-3β was decreased and the ability of HIV-1 Nef protein was enhanced by transfection with GSK-3β-DN in promoting vIL-6 induced microtubule formation (3.42 vs 2.51,t =3.67,P＜0.01) and angiogenesis (6.25 vs 3.97,t=4.06,P＜0.01).In contrast,the activity of GSK-3β was significantly increased and these functions of HIV-1 Nef protein mentioned above were inhibited by transfection with GSK-3β-S9A (0.62 vs2.51,t=8.48,P＜0.01; 0.39 vs 3.97,t=8.59,P＜0.01).The results of Western blot showed that with the elevated level of,β-catenin (in cells:3.53 vs 2.07,t=6.60,P＜0.05; in tissues:2.76 vs 1.74,t=17.40,P＜0.01) and vascular endothelial growth factor (VEGF,in cells:2.68 vs 1.87,t=4.28,P＜0.01; in tissues:2.20 vs 1.39,t=7.08,P＜0.01) were increased in the GSK-3β-DN transfected cells or tissues,while the opposite results were achieved in the GSK-3β-S9A-transfected cells (GSK-3β phosphorylation:0.50 vs 1.47,t=7.33,P＜0.01; β-catenin:1.05 vs 2.62,t=29.50,P＜0.01; VEGF:0.74 vs 2.16,t=20.95,P＜0.01) or tissues (GSK-3β phosphorylation:0.35 vs 1.97,t=10.72,P＜0.01; β-catenin:0.79 vs 1.77,t=5.72,P＜0.01; VEGF:0.43 vs 1.65,t=11.89,P＜ 0.01).Conclusion GSK-3β/β-catenin signaling pathway is involved in vIL-6-induced angiogenesis promoted by HIV-1 Nef protein,which would be valuable for the therapy of Kaposi's sarcoma,an acquired immunodeficiency syndrome,as a potential molecular target.

Immunohistochemical and electron microscopic techniques and image analysis were employed to investigate the regulation of cardiac AT1A and AT2 subtype receptors in rats during cardiac remodeling following myocardial infarction (MI). Positive immunostaining for AT1A and AT2 receptors was observed in myocytes and vessels with AT1A being more than AT2. Three days after MI, disappearance of myocardial cross striation and fibroblast hyperplasia were found with electron microscopy. AT1A receptor protein expression in myocardial noninfarcted portion notably increased compared with that in sham-operated control rats (P<0.001). No apparent changes were observed in AT2 receptor (P>0.05). Two weeks after MI, myocyte cross striation and collagen deposition were found. Meanwhile, AT1A receptor staining decreased compared with that of three days after MI (P<0.01), but there was still more than that of the control (P<0.05). AT2 receptor was significantly increased compared with that of the sham-operated control rats (P<0.001). These results suggust that both AT1A and AT2 receptor protein expression was upregulated in noninfarcted myocardium after MI, and the regulation of AT1A and AT2 receptors after MI may be involved in post-infarction cardiac remodeling.

BackgroundDiabetic retinopathy (DR) is the result of the cytokine network disorders,the imbalance of angiogenic factor and vascular inhibitory factor is the start factor.ObjectiveTo analyze the levels of CXC chemotatic factors of type 2 diabetes mellitus patients,evaluate the clinical application value of them in different clinical types of DR using receiver operating characteristic (ROC)analysis and to approach the new way of individualized treatment.Methods This was a prospective research.The gold standard was ophthalmolscope and fundus fluorescein angiography.The levels of CXC chemotatic factors and multiplicaiton factors were measured in 96 cases with type 2 diabetes mellitus (66 cases with retinopathy and 30 cases without retinopathy as control).The assessment tasks were performed for these index and courses of DR with ROC curve.Results The expression of age,course of disease has significant difference in different courses of DR ( F =8.507,P =0.001 ; F =28.143,P =0.000).Compared with the control group,the expression of growth-related oncogene-α ( GROα ) ( t =- 2.172,P =0.035,AUC =0.625 ),whole blood viscosity 200 ( t =- 3.724,P =0.001,AUC =0.904 ) and neutrophilic leukocyte (t=-2.562,P =0.013,AUC =0.577 ) has significant difference in the group of mild NPDR.Compared with the control group,the expression of interferon-γ-inducible protein 10 ( IP-10 ) ( t =-3.591,P =0.001,AUC =0.592 ),platelet derivation growth factor-BB ( PDGF-BB ) ( t =- 3.233,P =0.003,AUC =0.735 ),vascular endothelial growth factor(VEGF) ( t =- 3.617,P =0.001,AUC =0.776 ),C peptide ( t =- 3.366,P =0.002,AUC =0.962 ),leukocyte ( t=-3.201,P =0.003,AUC =0.852) and neutrophilic leukocyte(t =-4.201,P=0.000,AUC =0.852) has significant difference in the group of moderate and severe NPDR.ConclusionsCXC chemotatic factors may act as reactivator in the pathogenesis of DR,GROα and IP-10 may be useful for clinical monitoring of the severity of DR,and evaluating the imbalance state of chemotatic factors maybe a new approach to clinical monitoring and prognosis of DR.

In order to construct an integrated DNA barcoding database for identifying Chinese animal medicine, the authors and their cooperators have completed a lot of researches for identifying Chinese animal medicines using DNA barcoding technology. Sequences from GenBank have been analyzed simultaneously. Three different methods, BLAST, barcoding gap and Tree building, have been used to confirm the reliabilities of barcode records in the database. The integrated DNA barcoding database for identifying Chinese animal medicine has been constructed using three different parts: specimen, sequence and literature information. This database contained about 800 animal medicines and the adulterants and closely related species. Unknown specimens can be identified by pasting their sequence record into the window on the ID page of species identification system for traditional Chinese medicine (www. tcmbarcode. cn). The integrated DNA barcoding database for identifying Chinese animal medicine is significantly important for animal species identification, rare and endangered species conservation and sustainable utilization of animal resources.
Animals ; DNA Barcoding, Taxonomic ; methods ; Databases, Nucleic Acid ; Eukaryota ; classification ; genetics ; Medicine, Chinese Traditional

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.