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Biomedical subjects

Wei Jiang

Publications and source records attributed to Wei Jiang.

At least 73 records · Page 4Linked to original sources
PubMed2005

Ghrelin blunted vascular calcification in vivo and in vitro in rats.

Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification. Calcification increased total Ca2+ content and 45Ca2+ deposition in aortas and VSMCs and alkaline phosphatase (ALP) activation in plasma, aortas and VSMCs. However, calcified aortas and VSMCs showed a significant decrease in osteopontin (OPN) mRNA expression and a marked reduction of ghrelin levels in plasma and its mRNA expression in aortas. The aortic calcification was significantly attenuated by subcutaneous administration of ghrelin 30 and 300 nmol kg(-1) day(-1) for 4 weeks, and the latter dosage was more potent than the former. Ghrelin treatment at the two dosages reduced the total aorta Ca2+ content by 24.4% and 28.1%, aortic 45Ca2+ deposition by 18.4% and 24.9%, plasma ALP activity by 36.6% and 76.7%, and aortic ALP activity by 10.3% and 47.6% (all P < 0.01 or 0.05), respectively. Ghrelin at 10(-8)-10(-6) mol/L attenuated the calcification in cultured VSMCs, with decreased total Ca2+ content, 45Ca2+ deposition and ALP activity and increased OPN mRNA expression, in a concentration-dependent manner. In addition, endothelin levels in plasma and aortas and its mRNA expression in aortas significantly increased with calcification, but ghrelin treatment significantly decreased endothelin levels and mRNA expression, with the high dosage being more potent than the lower dosage. These results indicate that local ghrelin in vascular was down-regulated during vascular calcification, whereas administration of ghrelin effectively attenuated vascular and VSMCs calcification.

Animals↗
PubMed2005

Adrenomedullin(27-52) inhibits vascular calcification in rats.

Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52). The rat vascular calcific model was replicated with vitamin D3 and nicotine. ADM or/and ADM(27-52) were systemically administrated with mini-osmotic pump beginning at seventh day after the model replication for 25 days. Vascular calcific nodules histomorphometry, vascular calcium content, vascular calcium uptake, alkaline phosphatase activity, and osteopontin-mRNA quantification in aorta were assessed. ADM limited 40.2% vascular calcific nodules (P<0.01), did not effect on calcium content (P>0.05), reduced 44.4% calcium uptake (P<0.01), lowered 21.1% alkaline phosphatase activity (P<0.01), and regulated 40.9% downwards osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. ADM(27-52) receded 32.0% vascular calcific nodules (P<0.01), taken from 55.5% calcium content (P<0.01), did not affect calcium uptake (P>0.05), inhibited 22.5% alkaline phosphatase activity (P<0.01), and restrained 21.9% osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. Both of ADM and ADM(27-52) did interact on vascular calcification each other. ADM could partially antagonize the effects of ADM(27-52) in taking from calcium content (17.5%, P<0.01) and in receding vascular calcific nodules (18.6%, P<0.01). ADM could obviously enhance the action of ADM(27-52) in inhibiting alkaline phosphatase activity (14.4%, P<0.01) and in reducing calcium uptake (11.4%, P<0.01). ADM(27-52) could partially antagonize the effects of ADM on regulating downwards osteopontin-mRNA expression (17.0%, P<0.01). It is concluded that ADM(27-52) derived from ADM acts as an inhibitory agent on vascular calcification, with special mechanisms different from ADM derived from ADM progenitor molecule.

Adrenomedullin↗
PubMed2005

Recruitment of MKLP1 to the spindle midzone/midbody by INCENP is essential for midbody formation and completion of cytokinesis in human cells.

The INCENP (inner centromere protein) is a chromosomal passenger protein that plays multiple roles in regulating mitosis and cytokinesis. The MKLP1 (mitotic kinesin-like protein) is a component of centralspindlin complex that has been implicated in assembly of midzone/midbody during mitosis and is essential for cytokinesis. In the present study, we investigated functions of INCNEP and MKLP1 and their interplay in regulating spindle midzone/midbody formation and cytokinesis in human cells. Immunofluorescence and live-cell imaging analyses have shown that, in addition to multiple chromosome segregation defects, cells that lacked INCENP by RNAi (RNA interference) exhibit abnormal spindle midzone/midbody formation, resulting in formation of binucleated/multinucleated cells. Suppression of MKLP1 expression by siRNA (small interfering RNA) did not cause any abnormality of chromosome segregation and midzone formation, but abrogated midbody formation and completion of cytokinesis. Furthermore, we show that INCENP is required for recruiting MKLP1 to the spindle midzone/midbody. Three-dimensional reconstruction imaging analysis suggests that recruitment of MKLP1 to the midzone/midbody by INCENP is a crucial step for the midbody formation and completion of cytokinesis in mammalian cells.

Chromosomal Proteins, Non-Histone↗
PubMed2005

Peripheral S-phase T cells in HIV disease have a central memory phenotype and rarely have evidence of recent T cell receptor engagement.

Heightened proliferation and death of T lymphocytes may play a key role in human immunodeficiency virus (HIV) pathogenesis; however, the mechanism that mediates this effect and the phenotype of the proliferating T cells have not been clearly determined. We assessed S-phase cell frequencies and phenotype by ex vivo bromodeoxyuridine incorporation and flow-cytometric analysis in a group of 35 HIV-infected individuals. Frequencies of S-phase T cells were increased in HIV disease and were related to plasma HIV RNA levels but not to CD4 cell, total T cell, or total lymphocyte counts. S-phase cells were phenotypically defined as "central memory" cells (CD45RO+CD62L+CCR7+). Although activated (CD38+), S-phase cells lacked CD69 expression, rarely expressed CD25, and were not overrepresented among HIV-specific cells, as might have been expected if these cells had recently been activated by HIV antigens. Thus, in HIV infection, central memory T cells may be highly susceptible to bystander mechanisms of immune activation, leading to S-phase entry.

Adult↗
PubMed2005

Self-assembly of ABA amphiphilic triblock copolymers into vesicles in dilute solution.

Self-assembly of an ABA amphiphilic triblock copolymer into vesicles in dilute solution was studied by successfully combining experimental methods and a real-space self-consistent field theory in three-dimensional space. It was found experimentally that vesicle size was sensitive to the initial copolymer concentration in the organic solvent. Also, the aggregate morphologies and vesicles sizes were found to be dependent on the annealing time. A number of complex vesicles, such as global, long-style, trigonal, and necklacelike vesicles, were obtained in our experiments. Moreover, the corresponding microstructures were produced in our simulations. The results show that various vesicles in dilute solution are formed solely on account of the inhomogeneous density distribution in the local region in nature. Our simulations confirm that the structural complexity coexisting behavior in the single-amphiphile systems is largely attributed to the metastability rather than the polydispersity of the triblock copolymer. These metastable states should strongly depend on the pathway of the system on the free energy landscapes, which is governed by the initial condition.

Journal Article↗
PubMed2005

Functional analysis of human microtubule-based motor proteins, the kinesins and dyneins, in mitosis/cytokinesis using RNA interference.

Microtubule (MT)-based motor proteins, kinesins and dyneins, play important roles in multiple cellular processes including cell division. In this study, we describe the generation and use of an Escherichia coli RNase III-prepared human kinesin/dynein esiRNA library to systematically analyze the functions of all human kinesin/dynein MT motor proteins. Our results indicate that at least 12 kinesins are involved in mitosis and cytokinesis. Eg5 (a member of the kinesin-5 family), Kif2A (a member of the kinesin-13 family), and KifC1 (a member of the kinesin-14 family) are crucial for spindle formation; KifC1, MCAK (a member of the kinesin-13 family), CENP-E (a member of the kinesin-7 family), Kif14 (a member of the kinesin-3 family), Kif18 (a member of the kinesin-8 family), and Kid (a member of the kinesin-10 family) are required for chromosome congression and alignment; Kif4A and Kif4B (members of the kinesin-4 family) have roles in anaphase spindle dynamics; and Kif4A, Kif4B, MKLP1, and MKLP2 (members of the kinesin-6 family) are essential for cytokinesis. Using immunofluorescence analysis, time-lapse microscopy, and rescue experiments, we investigate the roles of these 12 kinesins in detail.

3' Untranslated Regions↗
PubMed2005

The tumor suppressor DAL-1/4.1B modulates protein arginine N-methyltransferase 5 activity in a substrate-specific manner.

We previously identified DAL-1/4.1B as a growth suppression protein involved in the pathogenesis of lung, breast, and meningioma tumors. Using yeast two-hybrid interaction cloning, protein arginine N-methyltransferase 3 (PRMT3) was originally identified as a DAL-1/4.1B-interacting protein. PRMTs catalyze the sequential transfer of methyl groups from S-adeonsyl-l-methionine to the guanidino nitrogens of arginine residues in proteins, the effect of which can include regulation of signal transduction, transcription regulation, and RNA transport, suggesting that modulating this event may have far-reaching impact. In this study, we assessed the impact of DAL-1/4.1B binding on the activity of another family member, PRMT5, both in vitro and in cells. In contrast to PRMT3, DAL-1/4.1B was found to mediate PRMT5 by either inhibiting (Sm proteins) or enhancing (myelin basic protein) protein methylation. We propose that this interaction between a tumor suppressor and a post-translational methylation enzyme is of biological importance in controlling tumorigenesis.

Binding Sites↗
PubMed2005

Defective N-acetylaspartate catabolism reduces brain acetate levels and myelin lipid synthesis in Canavan's disease.

Canavan's disease (CD) is a fatal, hereditary disorder of CNS development that has been linked to mutations in the gene for the enzyme aspartoacylase (ASPA) (EC 3.5.1.15). ASPA acts to hydrolyze N-acetylaspartate (NAA) into l-aspartate and acetate, but the connection between ASPA deficiency and the failure of proper CNS development is unclear. We hypothesize that one function of ASPA is to provide acetate for the increased lipid synthesis that occurs during postnatal CNS myelination. The gene encoding ASPA has been inactivated in the mouse model of CD, and here we show significant decreases in the synthesis of six classes of myelin-associated lipids, as well as reduced acetate levels, in the brains of these mice at the time of peak postnatal CNS myelination. Analysis of the lipid content of white matter from a human CD patient showed decreased cerebroside and sulfatide relative to normal white matter. These results demonstrate that myelin lipid synthesis is significantly compromised in CD and provide direct evidence that defective myelin synthesis, resulting from a deficiency of NAA-derived acetate, is involved in the pathogenesis of CD.

Acetic Acid↗
PubMed2005

[The treatment of middle and lower thirds fractures of humerus by anterior plate fixation].

OBJECTIVE: To study the effect of anterior plate fixation on the treatment of middle and lower thirds fractures of humerus and the possibility of operating without injuring the radial nerve. METHODS: Forty-nine patients with the middle and lower thirds fractures of the humerus were treated with anterior plate fixation from March 1998 to December 2002. Of the 49 patients, 27 were with new fractures, 12 with old fractures, and 10 with nonunion fractures. According to AO classification, of the 49 patients, there were 19 type A, 14 type B1, 9 type B2, 5 type B3, 2 type C1. Thirty-seven patients had closed fractures and 12 had open fractures. Of the 12 patients, 8 were type Gustilo I , 4 were type Gustilo I . Four out of the 49 patients were associated with radial nerve palsy. All patients were treated with anterior plate fixation through the anterior approach to the humerus. The radial nerves injured were explored. RESULTS: Of the 49 patients, 48 were followed up 6 to 48 months (28.7 months on average). All fractures were healed within 3 to 9 months(4.7 months on average). Fixed plates of 37 patients out of the 49 were removed. No iatrogenic radial nerve injury occurred in the 82 times of the operations among the 49 patients. CONCLUSION: The treatment of middle and lower thirds fractures of humerus by anterior plate fixation through the anterior approach to the humerus does not interfere with the fracture healing and can prevent the iatrogenic radial nerve injury.

Adolescent↗
PubMed2005

Effects of a plasmid expressing antisense tissue inhibitor of metalloproteinase-1 on liver fibrosis in rats.

BACKGROUND: No efficient therapy for liver fibrosis has been available. This study was aimed to provide evidence that the introduction of a plasmid expressing antisense tissue inhibitor of metalloproteinase-1 (TIMP-1) into a rat model of immunologically induced liver fibrosis can result in the increased activity of interstitial collagenase, thus enhancing the degradation of collagen. METHODS: Real-time nested polymerase chain reaction (RT-Nested-PCR) and gene recombination techniques were used to construct a rat antisense TIMP-1 recombinant plasmid that can be expressed in eukaryotic cells. Both the recombinant plasmid and an empty vector (pcDNA3) were encapsulated with glycosyl-poly-L-lysine and injected into rats suffering from pig serum-induced liver fibrosis. The expression of exogenous transfected plasmid was assessed by Northern blot, RT-PCR, and Western blot. Hepatic interstitial collagenase activity was detected using fluorescinisothiocyanate (FITC)-labeled type I collagen. In addition to hepatic hydroxyproline content, hepatic collagen types I and III were detected by immunohistochemical staining, and the stages of liver fibrosis by Van Gieson staining. RESULTS: Exogenous antisense TIMP-1 was successfully expressed in vivo and could block the gene and protein expression of TIMP-1. Active and latent hepatic interstitial collagenase activities were elevated (P < 0.01), hepatic hydroxyproline content and the accumulation of collagen types I and III were lowered, and liver fibrosis was alleviated in the antisense TIMP-1 group (P < 0.01) as compared with the model group. CONCLUSION: The results demonstrate that antisense TIMP-1 recombinant plasmids have some inhibitory effect on liver fibrosis.

Animals↗
PubMed2005

An FF domain-dependent protein interaction mediates a signaling pathway for growth factor-induced gene expression.

FF domains are poorly understood protein motifs found in all eukaryotes but in a very small number of proteins. They typically occur in tandem arrays and appear predominantly in splicing and transcription factors. Curiously, they are also present in the p190 family of cytoplasmic Rho GTPase activating proteins (GAPs). We identified the serum-responsive transcriptional regulator TFII-I as a specific interactor with the p190 RhoGAP FF domains. p190 sequesters TFII-I in the cytoplasm via the FF domains, but upon PDGF receptor-mediated phosphorylation of an FF domain, TFII-I is released from p190 and translocates to the nucleus where it can activate transcription of serum-inducible genes including c-fos. These findings reveal a pathway by which mitogens promote gene transcription and indicate a role for FF domains in phosphorylation-mediated signal transduction.

Active Transport, Cell Nucleus↗
PubMed2005

An orthotopic model of human osteosarcoma growth and spontaneous pulmonary metastasis.

Osteosarcoma is the most common primary malignancy of bone and patients often develop pulmonary metastases. In order to investigate the pathogenesis of human osteosarcoma, there is a great need to develop a clinically relevant animal model. Here we report the development of an osteosarcoma animal model using three related human osteosarcoma lines, the parental TE-85 and two derivative lines MNNG/HOS and 143B. In vitro characterization demonstrated that the 143B line had the greatest cell migration and the least cell adhesion activities among the three lines. The 143B line also exhibited the greatest ability for anchorage independent growth. When GFP-tagged osteosarcoma cells were injected into the proximal tibia of athymic mice, we found that 143B cells were highly tumorigenic and metastatic, and MNNG/HOS cells were tumorigenic but significantly less metastatic. TE85 cells were neither tumorigenic nor metastatic. The number of pulmonary metastases was found 50-fold higher in 143B injected animals than that in MNNG/HOS injected mice. No pulmonary metastases were detected in TE85 injected animals for up to 8 weeks. Primary tumors formed by MNNG/HOS and 143B cells could be visualized by whole body fluorescence imaging, while the pulmonary metastases were visualized on the necropsied samples. The GFP tagged 143B cells (and to a lesser extent, MNNG/HOS cells) were readily recovered from lung metastases. This clinically relevant model of human osteosarcoma provides varying degrees of tumor growth at the primary site and metastatic potential. Thus, this orthotopic model should be a valuable tool to investigate factors that promote or inhibit osteosarcoma growth and/or metastasis.

Animals↗
PubMed2005

Antidepressant therapy in patients with ischemic heart disease.

Depressive disorders are common in patients with ischemic heart disease and have serious consequences in terms of the risk of further cardiac events and cardiac mortality. Among survivors of acute myocardial infarction, up to one fifth meet diagnostic criteria for major depression, and the presence of major depression carries a >5-fold increased risk for cardiac mortality within 6 months. This article reviews clinical trial data on the cardiac safety profiles of antidepressant agents with the aim of discussing clinical considerations in selecting the most appropriate treatment of comorbid depression in patients with ischemic heart disease. Tricyclic antidepressants are effective against depression but are associated with cardiovascular side effects including orthostatic hypotension, slowed cardiac conduction, antiarrhythmic activity, and increased heart rate. Selective serotonin reuptake inhibitors, by contrast, have benign cardiovascular profiles and are well tolerated in patients with cardiac disease. The safety of dual-acting serotonin and noradrenaline reuptake inhibitors has not been well studied. Intervention with a selective serotonin reuptake inhibitors has the potential to provide the depressed patient with ischemic heart disease relief from their depressive symptoms and may offer a potential improvement in their cardiovascular risk profile.

Antidepressive Agents↗
PubMed2005

Adsorption of arsenate on soils. Part 1: laboratory batch experiments using 16 Chinese soils with different physiochemical properties.

Laboratory batch experiments were carried out to study the adsorption of arsenate on 16 Chinese soils with different physicochemical properties. Wide differences in arsenate adsorption were observed, and the Jiangxi and Hubei soils were more effective sorbents for arsenate than other soils. The Langmuir one-surface and two-surface equations were used to model the arsenate adsorption data. Except for the Jiangxi and Hubei soils, the Langmuir one-surface equation gave reasonably good fits to the arsenate adsorption data. However, the Langmuir two-surface equation generally provided a better fit than the Langmuir one-surface equation. For soils with relative high organic matter (OM), dissolved organic carbon (DOC) or extractable phosphate, the Langmuir one-surface and two-surface equations described the adsorption isotherms similarly. In contrast, for soils with relatively low contents of OM, DOC or extractable phosphate, the Langmuir two-surface equation gave the better fit to the arsenate adsorption data.

Adsorption↗
PubMed2005

Adsorption of arsenate on soils. Part 2: modeling the relationship between adsorption capacity and soil physiochemical properties using 16 Chinese soils.

An attempt has been made to elucidate the effects of soil properties on arsenate adsorption by modeling the relationships between adsorption capacity and the properties of 16 Chinese soils. The model produced was validated against three Australian and three American soils. The results showed that nearly 93.8% of the variability in arsenate adsorption on the low-energy surface could be described by citrate-dithionite extractable Fe (Fe(CD)), clay content, organic matter content (OM) and dissolved organic carbon (DOC); nearly 87.6% of the variability in arsenate adsorption on the high-energy surface could be described by Fe(CD), DOC and total arsenic in soils. Fe(CD) exhibited the most important positive influence on arsenate adsorption. Oxalate extractable Al (Al(OX)), citrate-dithionite extractable Al (Al(CD)), extractable P and soil pH appeared relatively unimportant for adsorption of arsenate by soils.

Adsorption↗
PubMed2005

A robust hybrid between genetic algorithm and support vector machine for extracting an optimal feature gene subset.

Development of a robust and efficient approach for extracting useful information from microarray data continues to be a significant and challenging task. Microarray data are characterized by a high dimension, high signal-to-noise ratio, and high correlations between genes, but with a relatively small sample size. Current methods for dimensional reduction can further be improved for the scenario of the presence of a single (or a few) high influential gene(s) in which its effect in the feature subset would prohibit inclusion of other important genes. We have formalized a robust gene selection approach based on a hybrid between genetic algorithm and support vector machine. The major goal of this hybridization was to exploit fully their respective merits (e.g., robustness to the size of solution space and capability of handling a very large dimension of feature genes) for identification of key feature genes (or molecular signatures) for a complex biological phenotype. We have applied the approach to the microarray data of diffuse large B cell lymphoma to demonstrate its behaviors and properties for mining the high-dimension data of genome-wide gene expression profiles. The resulting classifier(s) (the optimal gene subset(s)) has achieved the highest accuracy (99%) for prediction of independent microarray samples in comparisons with marginal filters and a hybrid between genetic algorithm and K nearest neighbors.

Algorithms↗
PubMed2005

Enhanced efficiency and specificity of ovarian cancer gene therapy in rats with a novel nonviral gene delivery system (GE7) via intraovarian artery perfusion approach.

Transfer of the herpes simplex virus type I-thymidine kinase gene, followed by the administration of ganciclovir (HSV1-tk/GCV) into ovarian cancer-derived cell line either in vitro or transplanted into nude mice has been shown to provide a potential strategy for the gene therapy of ovarian cancer. We investigated the antitumor effects of HSV1-tk/GCV strategy with a chemically induced rat ovarian cancer model and a tumor-selective gene delivery by a novel nonviral gene delivery system (GE7) through the ovarian artery and tail vein. We demonstrated the expression of a reporter gene, beta-gal gene, as well as HSV1-tk gene in tumors and other organs, evaluated the overall antitumor effects after the GCV treatment and analyzed the tumor cell cycle phase distribution. Via the ovarian artery route, the expressions of beta-gal and HSV1-tk in tumors were significantly stronger than those expressed in such organs as the hearts, livers, spleens, lungs and kidneys. However, no beta-gal and HSV1-tk were detected in the tumor tissues when administrated via the tail vein, and little was found in other organs. The cell cycle analysis showed that the total S-phase of tumor cells in the test intra-arterial treatment group was considerably higher than that of the controls. The weight of the tumor tissues in the group treated by the intra-arterial route (4.06+/-2.12 g) was much less than the group treated intravenously (18.25+/-8.34 g) (P<.01). These findings indicated that the administration of GE7/HSV1-tk complex via the ovarian artery route could be a promising avenue of future human ovarian cancer treatment.

9,10-Dimethyl-1,2-benzanthracene↗