Biomedical subjects

C Ji

Publications and source records attributed to C Ji.

At least 37 records · Page 2Linked to original sources

PubMed2000

Embolization with radiopaque microbeads of polyacrylonitrile hydrogel: evaluation in swine.

PURPOSE: To perform in vitro and in vivo studies of radiopaque microbeads of polyacrylonitrile (PAN) hydrogel to evaluate their characteristics as embolic material. MATERIALS AND METHODS: PAN microbeads were analyzed in vitro for swelling in different concentrations of contrast material and saline solution and injected through various microcatheters. In three nonsurvival swine, various organs were embolized with PAN microbeads. In eight survival swine, the rete mirabile was embolized with PAN microbeads or polyvinyl alcohol particles. Follow-up angiograms were obtained regularly, and histopathologic analysis was performed at 1 and 6 months. RESULTS: The microbeads were black with a regular shape and smooth surface. They were easily visible in the syringe and easy to inject through the microcatheters. When wet, their diameters increased by 40%. The microbeads were sufficiently radiopaque to be visible in all vascular territories. Vascular occlusion was not permanent, and even when embolization was adequate, some revascularization was detected at 3 months. The microbeads were intact and still radiopaque at 6 months. Histopathologic examination demonstrated variable inflammatory reactions and foreign-body giant cell reaction and no angionecrosis or hemorrhage. CONCLUSION: Because PAN microbeads are biocompatible, radiopaque, and easy to handle during embolization procedures, they have potential as a therapeutic embolic agent.

Acrylic Resins↗

PubMed2000

Links among growth factors, hormones, and nuclear factors with essential roles in bone formation.

Research performed during the last several years implicates important roles for a variety of growth factors that affect osteoblasts or their precursors during bone development, remodeling, or repair. Of these, three families of growth factors in particular-the transforming growth factor betas (TGF-betas), insulin-like growth factors (IGFs), and bone morphogenetic proteins (BMPs)-are considered to be principal local regulators of osteogenesis, although none is specific for cells of the osteoblast lineage. Therefore, mechanisms to induce skeletal tissue specificity might occur through interactions among these growth factors, with circulating hormones, or through specific intracellular mediators. In the latter case, even more recent studies point to two nuclear transcription factors, termed Core Binding Factor a1 (CBFa1) and CCAAT/Enhancer Binding Protein delta (C/EBPdelta), as significant regulators of the expression or activity of specific bone growth factors or their receptors. Perhaps more importantly, events that link these growth factors to nuclear proteins occur in response to glucocorticoids, sex steroids, parathyroid hormone (PTH), or prostaglandin E2 (PGE2), which themselves have well-known effects on bone biology. In this review, we discuss the situations and processes that initially suggested growth-factor- and hormone-specific interactions on cells within the osteoblast lineage, and present evidence for roles that CBFa1 and C/EBPdelta have on osteoblast function. Finally, we offer examples for how these factors integrate events that are associated with various aspects of bone formation.

Animals↗

PubMed2000

Time- and dose-related interactions between glucocorticoid and cyclic adenosine 3',5'-monophosphate on CCAAT/enhancer-binding protein-dependent insulin-like growth factor I expression by osteoblasts.

Glucocorticoid has complex effects on osteoblasts. Several of these changes appear to be related to steroid concentration, duration of exposure, or specific effects on growth factor expression or activity within bone. One important bone growth factor, insulin-like growth factor I (IGF-I), is induced in osteoblasts by hormones such as PGE2 that increase intracellular cAMP levels. In this way, PGE2 activates transcription factor CCAAT/enhancer-binding protein-delta (C/EBPdelta) and enhances its binding to a specific control element found in exon 1 in the IGF-I gene. Our current studies show that preexposure to glucocorticoid enhanced C/EBPdelta and C/EBPbeta expression by osteoblasts and thereby potentiated IGF-I gene promoter activation in response to PGE2. Importantly, this directly contrasts with inhibitory effects on IGF-I expression that result from sustained or pharmacologically high levels of glucocorticoid exposure. Consistent with the stimulatory effect of IGF-I on bone protein synthesis, pretreatment with glucocorticoid sensitized osteoblasts to PGE2, and in this context significantly enhanced new collagen and noncollagen protein synthesis. Therefore, pharmacological levels of glucocorticoid may reduce IGF-I expression by osteoblasts and cause osteopenic disease, whereas physiological transient increases in glucocorticoid may permit or amplify the effectiveness of hormones that regulate skeletal tissue integrity. These events appear to converge on the important role of C/EBPdelta and C/EBPbeta on IGF-I expression by osteoblasts.

Animals↗

PubMed2000

[Analysis of proteins during recovery from lens opacity--analysis of selenite cataract model using Sprague-Dawley and Wistar rat].

BACKGROUND AND PURPOSE: The cataract in Sprague-Dawley rats injected with selenite is a dense nuclear opacity that appears by 4 or 5 days after selenite injection and becomes irreversible by 7 days. Injection of Wistar rats with selenite resulted in a similar nuclear opacity by 4 or 5 days that began to recover transparency by 7 days. In this report, the cytoplasmic proteins were analyzed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) in lenses from Sprague-Dawley and Wistar rats at 4 and 7 days after injection. RESULTS: In the opaque lens cells, degradation of the 31 kDa protein and cytoskeletal proteins (vimentin, spectrin, and actin) was observed during cataract development using SDS-PAGE and western blot analysis. During recovery from opacity, the decreased 31 kDa protein and the vimentin increased. CONCLUSION: The results suggest that the 31 kDa protein and the vimentin may be important for recovery of transparency in a reversible model of cataract formation.

Animals↗

PubMed1999

Cloning the promoter for transforming growth factor-beta type III receptor. Basal and conditional expression in fetal rat osteoblasts.

Transforming growth factor-beta binds to three high affinity cell surface molecules that directly or indirectly regulate its biological effects. The type III receptor (TRIII) is a proteoglycan that lacks significant intracellular signaling or enzymatic motifs but may facilitate transforming growth factor-beta binding to other receptors, stabilize multimeric receptor complexes, or segregate growth factor from activating receptors. Because various agents or events that regulate osteoblast function rapidly modulate TRIII expression, we cloned the 5' region of the rat TRIII gene to assess possible control elements. DNA fragments from this region directed high reporter gene expression in osteoblasts. Sequencing showed no consensus TATA or CCAAT boxes, whereas several nuclear factors binding sequences within the 3' region of the promoter co-mapped with multiple transcription initiation sites, DNase I footprints, gel mobility shift analysis, or loss of activity by deletion or mutation. An upstream enhancer was evident 5' proximal to nucleotide -979, and a silencer region occurred between nucleotides -2014 and -2194. Glucocorticoid sensitivity mapped between nucleotides -687 and -253, whereas bone morphogenetic protein 2 sensitivity co-mapped within the silencer region. Thus, the TRIII promoter contains cooperative basal elements and dispersed growth factor- and hormone-sensitive regulatory regions that can control TRIII expression by osteoblasts.

Animals↗

PubMed1999

CCAAT/enhancer-binding protein delta is a critical regulator of insulin-like growth factor-I gene transcription in osteoblasts.

Insulin-like growth factor-I (IGF-I) plays a major role in promoting skeletal growth by stimulating bone cell replication and differentiation. Prostaglandin E2 and other agents that induce cAMP production enhance IGF-I gene transcription in cultured rat osteoblasts through a DNA element termed HS3D, located in the proximal part of the major rat IGF-I promoter. We previously determined that CCAAT/enhancer-binding protein delta (C/EBPdelta) is the key cAMP-stimulated regulator of IGF-I transcription in these cells and showed that it transactivates the rat IGF-I promoter through the HS3D site. We now have defined the physical-chemical properties and functional consequences of the interactions between C/EBPdelta and HS3D. C/EBPdelta, expressed in COS-7 cells or purified as a recombinant protein from Escherichia coli, bound to HS3D with an affinity at least equivalent to that of the albumin D-site, a known high affinity C/EBP binding sequence, and both DNA elements competed equally for C/EBPdelta. C/EBPdelta bound to HS3D as a dimer, with protein-DNA contact points located on guanine residues on both DNA strands within and just adjacent to the core C/EBP half-site, GCAAT, as determined by methylation interference footprinting. C/EBPdelta also formed protein-protein dimers in the absence of interactions with its DNA binding site, as indicated by results of glutaraldehyde cross-linking studies. As established by competition gel-mobility shift experiments, the conserved HS3D sequence from rat, human, and chicken also bound C/EBPdelta with similar affinity. We also found that prostaglandin E2-induced expression of reporter genes containing human IGF-I promoter 1 or four tandem copies of the human HS3D element fused to a minimal promoter and show that these effects were enhanced by a co-transfected C/EBPdelta expression plasmid. Taken together, our results provide evidence that C/EBPdelta is a critical activator of IGF-I gene transcription in osteoblasts and potentially in other cell types and species.

Animals↗

PubMed1999

Activation of the insulin-like growth factor-binding protein-5 promoter in osteoblasts by cooperative E box, CCAAT enhancer-binding protein, and nuclear factor-1 deoxyribonucleic acid-binding sequences.

Insulin-like growth factor (IGF)-binding protein-5 (IGFBP-5) has IGF-dependent and -independent actions. PGE2 rapidly increases IGFBP-5 expression by osteoblasts through cAMP-dependent processes. A minimal DNA sequence required for basal and PGE2-stimulated IGFBP-5 promoter activity spans -69 to -35 bp. This region adjoins a functional TATA box and contains E box, CCAAT enhancer-binding protein (C/EBP), nuclear factor-1 (NF-1), and activator protein-2 (AP-2) transcription factor related binding motifs. In this study we compared minimal promoter sequences of -74 to +120 bp, without or with mutations in each potential regulatory element, by reporter gene expression and electrophoretic mobility shift assays. Mutation of the E box-related element reduced basal promoter activity by 50% and eliminated the 2-fold stimulatory effect of PGE2. In contrast, mutations in the C/EBP- or NF-1-related elements also reduced basal promoter activity without fully eliminating the PGE2 effect. Overexpression of C/EBPdelta stimulated basal IGFBP-5 promoter activity, and this effect was eliminated by mutating the C/EBP-binding site. However, mutation of the AP-2-binding site or overexpression of AP-2 did not correlate with basal or PGE2-induced promoter activation. By electrophoretic mobility shift assay, prominent gel shift complexes occurred with osteoblast nuclear extracts and 32P-labeled probes spanning the E box-, C/EBP-, and NF-1-related motifs. These gel shift complexes were depleted by specific binding site mutations and were enhanced by PGE2. Increased binding by extracts from PGE2-treated cultures was blocked by cycloheximide treatment. These results identify several elements as integral binding sequences for both basal and PGE2-stimulated IGFBP-5 promoter activity. They further reveal that multiple sequences within this cluster form a basic transcription unit where nuclear factors can accumulate in a protein synthesis-dependent way and enhance IGFBP-5 expression by osteoblasts in response to PGE2.

Animals↗

PubMed1999

[Prevalence study of congenital heart disease in children aged 0-2 in Zhejiang Province].

OBJECTIVE: To find out the prevalence rate of Congenital Heart Disease (CHD) among infants and toddlers. METHODS: Heart auscultation and echocardiography examination on children aged 0-2 were examined in 13 cities (or counties) in Zhejing province. RESULTS: Findings showed that the prevalence rate in children aged 0-2 was 3.72/1000. The prevalence rates of CHD were quite different among age groups with the highest (5.54/1000) in age group 0, followed by 3.36/1000 in age group 1 and lowest (2.66/1000) in age group 2. No significant difference of prevalence rates was found between different sex. Ventricular septal defects (59.4%) was noticed as the most common lesion. CONCLUSION: The evidence indicated that CHD is one of the most important problems of public health in China. Preventing its occurrence by conducting CHD surveillance and its etiologic research will have great significance for enhancing the qualities of life of children.

Child, Preschool↗

PubMed1999

[A case-control study on cerebral palsy in children].

OBJECTIVE: To identify the risk factors for cerebral palsy (CP) in children. METHODS: A population-based 1:2 matched case-control study was conducted during May to June 1997 in southern Jiangsu Province of China. RESULTS: Risk factors for CP in children could be summarized into four categories, i.e.; (1) fetal growth retardation, preterm delivery and low birth weight; (2) asphyxia at birth, intracranial hemorrhage, ischemic and hypoxic encephalopathy and hyperbilirubinemic encephalopathy; (3) delivery with vaccum suction and traumatic brain injury; and (4) other prenatal factors. CONCLUSION: The first and second categories of risk factors correlated strongly and reproducibly with CP in children. It is emphasized that antenatal care be enforced to prevent occurrence of risk factors, such as low birth weight, etc., and the newborns with asphyxia be vigorously rescued and put under close supervision. For risk factors in the third category, the key measures should be obstetric practice and health education for the parents. But, little about the knowledge of the risk factors in the fourth category has been understood, which could be associated with those in the first two categories.

Asphyxia Neonatorum↗

PubMed1999

[The diagnostic and therapeutic value of flexible bronchoscopy in foreign-body aspiration misdiagnosed as other respiratory diseases].

To explore the causes of missed diagnosis of foreign-body aspiration and summarize the experiences on the diagnostic and therapeutic use of flexible bronchoscopy (FB) in these patients. Twelve cases of foreign-body aspiration misdiagnosed as other respiratory diseases, confirmed by FB examination were analyzed. All of these patients had no histories of foreign-body aspiration, and no foreign-body shadows were found on their chest films. But there were atelectasis, hilar enlargement and obstructive pneumonia found on the films. Among the patients in this group, 7 cases were misdiagnosed as lung cancer, 2 cases of pneumonia and asthma each, and 1 case as tuberculosis. The diagnoses of all the 12 cases were confirmed by FB examinations. The foreign-bodies of the 11 cases were successfully grasped and taken out through the FB. This suggests that FB should be of great diagnostic and therapeutic value in patients with foreign-body aspiration misdiagnosed as other respiratory diseases.

Adolescent↗

PubMed1998

Insulin-like growth factor binding proteins localize to discrete cell culture compartments in periosteal and osteoblast cultures from fetal rat bone.

Insulin-like growth factor (IGF)-I and IGF-II are expressed at biologically effective levels by bone cells. Their stability and activity are modulated by coexpression of IGF binding proteins (IGFBPs). Secreted IGFBPs may partition to soluble, cell-associated, and matrix-bound compartments. Extracellular localization may sequester, store, or present IGFs to appropriate receptors. Of the six IGFBPs known, rat osteoblasts synthesize all but IGFBP-1. Of these, IGFBP-3, -4, and -5 mRNAs are induced by an increase in cAMP. Little is known about extracellular IGFBP localization in bone and nothing about IGFBP expression by nonosteoblastic periosteal bone cells. We compared basal IGFBP expression in periosteal and osteoblast bone cell cultures and assessed the effects of changes in cAMP-dependent protein kinase A or protein kinase C. Basal IGFBP gene expression differed principally in that more IGFBP-2 and -5 occurred in osteoblast cultures, and more IGFBP-3 and -6 occurred in periosteal cultures. An increase in cAMP enhanced IGFBP-3, -4, and -5 mRNAand accordingly increased soluble IGFBP-3, -4, and -5 and matrix-bound IGFBP-3 and -5 in both bone cell populations. In contrast, protein kinase C activators suppressed IGFBP-5 mRNA, and its basal protein levels remained very low. We also detected low Mr bands reactive with antisera to IGFBP-2, -3, and -5, suggesting proteolytic processing or degradation. Our studies reveal that various bone cell populations secrete and bind IGFBPs in selective ways. Importantly, inhibitory IGFBP-4 does not significantly accumulate in cell-associated compartments, even though its secretion is enhanced by cAMP. Because IGFBPs bind IGFs less tightly in cell-bound compartments, they may prolong anabolic effects by agents that increase bone cell cAMP.

Animals↗

PubMed1998

CBFa(AML/PEBP2)-related elements in the TGF-beta type I receptor promoter and expression with osteoblast differentiation.

Organization of the transforming growth factor-beta (TGF-beta) type I receptor (TRI) promoter predicts constitutive transcription, although its activity increases with differentiation status in cultured osteoblasts. Several sequences in the rat TRI promoter comprise cis-acting elements for CBFa (AML/PEBP2alpha) transcription factors. By gel mobility shift and immunological analyses, a principal osteoblast-derived nuclear factor that binds to these sites is CBFa1 (AML-3/PEBP2alphaA). Rat CBFa1 levels parallel expression of the osteoblast phenotype and increase under conditions that promote mineralized bone nodule formation in vitro. Fusion of CBFa binding sequence from the TRI promoter to enhancer-free transfection vector increases reporter gene expression in cells that possess abundant CBFa1, and overexpression of CBFa increase the activity of transfected native TRI promoter/reporter plasmid. Consequently, phenotype-restricted use of cis-acting elements for CBFa transcription factors can contribute to the high levels of TRI that parallel osteoblast differentiation and to the potent effects of TGF-beta on osteoblast function.

Activin Receptors, Type I↗

PubMed1998

Genetics of plant-pathogen interactions

Progress has occurred in understanding the function of disease-resistance genes that govern the resistance of plants to pathogens, and pathogen-produced molecules, called elicitors, that resistance genes key on. Data support the elicitor-receptor model wherein resistant plants contain receptors for pathogen elicitors. This recognition may be complex, however, involving delivery of elicitors to plant cells by specialized pathogen secretion systems and their processing prior to perception. Furthermore, elicitor receptors may not be the resistance gene proteins that govern specificity of the system. It is now also recognized that many elicitors function as virulence factors for the pathogen but have been co-opted by plants as triggers for active resistance. Major recent advances in the cloning and sequencing of clustered plant disease-resistance genes are providing information on the basis of their recognitional specificities and offer the opportunity to engineer new genes that recognize refractory pathogens or exhibit increased efficacy and durability. In combination with the transformation of cloned disease-resistance genes into new plant species, these approaches should facilitate disease control strategies in practical agriculture.

Journal Article↗

PubMed1998

Characterization of a 34-kDa soybean binding protein for the syringolide elicitors.

Syringolides are water-soluble, low-molecular-weight elicitors that trigger defense responses in soybean cultivars carrying the Rpg4 disease-resistance gene but not in rpg4 cultivars. 125I-syringolide 1 previously was shown to bind to a soluble protein(s) in extracts from soybean leaves. A 34-kDa protein that accounted for 125I-syringolide 1 binding activity was isolated with a syringolide affinity-gel column. Partial sequences of internal peptides of the 34-kDa protein were identical to P34, a previously described soybean seed allergen. In soybean seeds, P34 is processed from a 46-kDa precursor protein and was shown to have homology with thiol proteases. P34 is a moderately abundant protein in soybean seeds and cotyledons but its level in leaves is low. cDNAs encoding 46-, 34-, and 32-kDa forms of the soybean protein were cloned into the baculovirus vector, pVL1392, and expressed in insect cells. The resulting 32- and 34-kDa proteins, but not the 46-kDa protein, exhibited ligand-specific 125I-syringolide binding activity. These results suggest that P34 may be the receptor that mediates syringolide signaling.

Allergens↗

PubMed1998

Alternate signaling pathways selectively regulate binding of insulin-like growth factor I and II on fetal rat bone cells.

Bone cells synthesize and respond to IGF-I and IGF-II which contribute to bone remodeling and linear growth. In osteoblasts, prostaglandin (PG)E2 stimulates IGF-I but not IGF-II synthesis through a cAMP-dependent protein kinase A (PKA)-related event. However, protein kinase C (PKC) activation by PGE2 enhances replication and protein synthesis by less differentiated periosteal cells more so than in osteoblast-enriched cultures from fetal rat bone. Using various PGs and other PKA and PKC pathway activators, the importance of these aspects of PGE2 activity has now been examined on IGF receptors in these bone cell culture models. PGE2 and other agents that activate PKA enhanced 125I-IGF-II binding to type 2 IGF receptors on both cell populations. In contrast, agents that activate PKC enhanced 125I-IGF-I binding to type 1 receptors on less differentiated bone cells, and of these, only phorbol myristate acetate (PMA), which activates PKC in a receptor-independent way, was effective in osteoblast-enriched cultures. No stimulator increased total type 1 receptor protein in either cell population. Consequently, ligand binding to type 1 and type 2 IGF receptors is differentially modulated by specific intracellular pathways in bone cells. Importantly, changes in apparent type 1 receptor number occur rapidly and may do so at least in part through post-translational effects. These results may help to predict new ways to manipulate autocrine or paracrine actions by IGFs in skeletal tissue.

Animals↗

PubMed1998

Reduction in transforming growth factor beta receptor I expression and transcription factor CBFa1 on bone cells by glucocorticoid.

Glucocorticoid in excess suppresses bone formation in vivo and disrupts bone matrix protein synthesis by osteoblasts in vitro. In contrast, transforming growth factor beta (TGF-beta) potently enhances bone matrix apposition. The rat TGF-beta type I receptor gene promoter contains cis-acting elements for transcription factor CBFa1, which increases in parallel with osteoblast differentiation. Here we present molecular data linking these events. We show that previously unexplained effects of glucocorticoid on bone loss may be mediated in part by suppression of CBFa1, with a resultant decrease in the expression and activity of the TGF-beta type I receptor on matrix-producing bone cells.

Activin Receptors, Type I↗

PubMed1998

Control of TGF-beta receptor expression in bone.

Bone growth and remodeling are controlled by local and systemic growth factors. The first local bone growth factor purified to homogeneity was transforming growth factor type beta (TGF-beta). On skeletal cells, TGF-beta has multiple effects mediated through at least three distinct cell surface receptors. More recent evidence demonstrated hormone and growth factor dependent alterations in TGF-beta receptor expression on osteoblasts in vitro. Indeed, certain biological responses appear to depend on the proportional expression of the type I TGF-beta receptor. Studies defining the type I TGF-beta receptor gene promoter then revealed that it contained several binding sequences for a nuclear factor that varies in parallel with expression of the osteoblast phenotype. New observations linking these events appear to enhance our understanding of this pivotal growth factor during osteogenesis and systemic bone disease.

Animals↗

PubMed1998

Induction of cell cycle arrest by the endogenous product of lipid peroxidation, malondialdehyde.

We have investigated the effect of the endogenous genotoxin malondialdehyde (MDA) on cell cycle kinetics and the expression and biochemical activity of several cell cycle regulatory proteins. MDA treatment of two human cell lines (RKO and H1299) resulted in a 3- to 6-fold elevation in the levels of the major detectable MDA-DNA adduct, M1G-dR. The increase in M1G-dR was accompanied by irreversible cell cycle arrest, elevation in p53 and p21 protein levels, and inhibition of cyclin E- and cyclin B-associated kinase activities. The decrease in cyclin E- and cyclin B-dependent kinase activities was caused by increased p21 and decreased cdc2 levels, respectively. Comparable levels of p21 induction were observed in RKO (wild-type p53) and H1299 (p53-null) cells. Thus, MDA was able to engage cell cycle checkpoint function in human cell lines when used at concentrations that produce M1G-dR levels of the same magnitude found in human tissues.

Antibiotics, Antineoplastic↗