Biomedical subjects

Jing Li

Publications and source records attributed to Jing Li.

At least 307 records · Page 17Linked to original sources

PubMed2004

N-terminally extended surfactant protein (SP) C isolated from SP-B-deficient children has reduced surface activity and inhibited lipopolysaccharide binding.

In both humans and mice, a deficiency of surfactant protein B (SP-B) is associated with a decreased concentration of mature SP-C and accumulation of a larger SP-C peptide, denoted SP-C(i), which is not observed under normal conditions. Isolation of hydrophobic polypeptides from the lungs of children who died with two different SP-B mutations yielded pure SP-C(i) and showed only trace amounts of mature SP-C. Determination of the SP-C(i) covalent structure revealed a 12-residue N-terminal peptide segment, followed by a 35-residue segment that is identical to mature SP-C. The SP-C(i) structure determined herein is similar to that of a proposed late intermediate in the processing of proSP-C, suggesting that SP-C(i) is the immediate precursor of SP-C. In bronchoalveolar lavage fluid from transgenic mice with a focal deficiency of SP-B, SP-C(i) was detected in the biophysically active, large aggregate fraction and was associated with membrane structures that are typical for a large aggregate surfactant. However, unlike SP-C, SP-C(i) exhibited a very poor ability to promote phospholipid adsorption, gave high surface tension during cyclic film compression, and did not bind lipopolysaccharide in vitro. SP-C(i) is thus capable of associating with surfactant lipids, but its N-terminal dodecapeptide segment must be proteolytically removed to generate a biologically functional peptide. The results of this study indicate that the early postnatal fatal respiratory distress seen in SP-B-deficient children is combined with the near absence of active variants of SP-C.

Amino Acid Sequence↗

PubMed2004

NOD2 3020insC frameshift mutation is not associated with inflammatory bowel disease in Chinese patients of Han nationality.

AIM: An insertion mutation at nucleotide 3020 (3020insC) in the Caspase recruitment domain gene (CARD15), originally reported as NOD2, is strongly associated with Crohn's disease. The C-insertion mutation at nucleotide 3020 (3020inC) in the leucine-rich repeat (LRR) region results in a frameshift in the 10(th) LRR followed by a premature stop codon. This truncation mutation is responsible for the inability to activate nuclear factor (NF)-kappaB in response to bacterial lipopolysaccharide (LPS). The present study aimed to genotype NOD2/CARD15 gene 3020insC frameshift mutation in Chinese patients with inflammatory bowel disease. METHODS: We genotyped an insertion polymorphism affecting the leucine-rich region of the protein product by the allele specific PCR in 74 unrelated patients with ulcerative colitis of Han nationality in Hubei Province of China, 15 patients with Crohn's disease and 172 healthy individuals. RESULTS: No significant differences were found in the genotype and allele frequencies of the C-insertion mutation of NOD2 gene among patients with Crohn's disease and ulcerative colitis and healthy controls. CONCLUSION: NOD2 gene 3020insC frameshift mutation is not a major contributor to the susceptibility to both Crohn's disease and ulcerative colitis in Chinese Han patients.

Asian People↗

PubMed2004

Porphyrins with four monodisperse oligofluorene arms as efficient red light-emitting materials.

A family of red light-emitting star-shaped porphyrins with four monodisperse conjugated oligofluorene arms was prepared by using two key reactions: Lindsey condensation and Suzuki-Miyaura cross coupling reactions. All porphyrins exhibit high quantum yields (about 0.22) and good solubility in common organic solvents, and form high-quality solid films. Optical studies showed that the star-shaped oligomers could absorb blue light and emit saturated red light via efficient energy transfer from the fluorene segments to the porphyrin core.

Journal Article↗

PubMed2004

Molecular analysis of PinX1 in medulloblastomas.

Our group has previously demonstrated a high frequency of allelic loss on the short arm of chromosome 8 and identified a region of homozygous deletion of 1.41 Mb, flanked by D8S520 and D8S1130, on 8p23.1 in medulloblastomas, suggesting the presence of a tumor suppressor gene in this critical deletion region. The aim of our study was to investigate whether PinX1, a newly identified gene whose product is a potent inhibitor of telomerase, is the target gene in the homozygous deletion region identified in medulloblastomas. We assessed for alterations in gene sequence and transcript expression of PinX1, as well as the correlation between PinX1 expression and telomerase activity in a series of 52 medulloblastomas, 3 medulloblastoma cell lines (D283, D341 and Daoy) and 4 primitive neuroectodermal tumors (PNETs). Direct sequence analysis of all 7 exons and splice junctions of the PinX1 gene revealed no somatic mutations but 11 genetic polymorphisms. Transcript expression of PinX1, as evaluated by reverse transcription-polymerase chain reaction, in microdissected tumors and normal cerebellum showed 2 transcript variants, corresponding to the full-length form and an alternative spliced variant lacking exon 6, in all samples. This result indicated that PinX1 expression was not suppressed in medulloblastomas. Using the telomeric repeat amplification protocol (TRAP) assay, 13 of 19 (68%) medulloblastomas, 1 of 2 PNETs and all 3 cell lines showed telomerase activity. There is no significant correlation between PinX1 transcript expression and telomerase activity, but our results showed that telomerase activation is involved in medulloblastomas. Taken together, our results suggest that PinX1 does not play a major role in the oncogenesis of medulloblastomas.

Adolescent↗

PubMed2004

Synthesis of aryl/alkyl building blocks for dendrimer and hyperbranched polymer synthesis.

Several useful aryl/alkyl building blocks for dendrimer and hyperbranched polymer synthesis were prepared by Suzuki-Miyaura cross-coupling reactions and iododesilylation reactions. The iododesilylations were carried out with iodine monochloride (ICl) in methylene chloride and diethyl ether (10:1). This solvent combination lowered the reagents electrophilicity to the point that the iododesilylation still proceeded absolutely cleanly, but no direct iodination of alkyl-substituted aromatics occurred, which otherwise could not be avoided. [reaction: see text]

Journal Article↗

PubMed2004

Visible-light-assisted degradation of dye pollutants over Fe(III)-loaded resin in the presence of H2O2 at neutral pH values.

A novel catalyst was synthesized by direct exchange of ferric ions onto a cationic resin (Amberlite IRA200). Upon visible light irradiation (lambda > 420 nm) in the presence of H2O2, this catalyst was found to be highly effective for the degradation of nonbiodegradable cationic dyes, Malachite green, Rhodamine B, and Methylene blue, even at neutral pH values. It was also easy to separate from the degraded solution. By total organic carbon, FT-IR, and GC-MS analysis, the degradation process of Malachite green was shown to proceed with demethylation and phenyl ring openings into CO2 and small molecular compounds. EPR studies revealed that *OH radicals, other than *OOH/O2*-, were involved as the active species. A possible reaction mechanism is proposed on the basis of all the information obtained under various experimental conditions.

Catalysis↗

PubMed2004

Organochlorine pesticides in the air around the Taihu Lake, China.

Organochlorine (OC) pesticides have been used broadly in China's past, yet very little is known about their atmospheric concentrations and transport. In this work, air samples were collected in the Taihu Lake Region, China, from July 23 to August 11, 2002, to measure concentrations of OC pesticides in air. The average concentrations of alpha and gamma- hexachlorocyclohexane (HCH), hexachlorobenzene (HCB), heptachlor (HEPT), alpha-endosulfan, p,p'-DDT, p,p'-DDE, p,p'-DDD, and o,p'-DDT in the air were 74 and 46, 47, 53, 307, 124, 212, 36, and 767 pg m(-3), respectively. It was interesting to note that the concentrations of p,p'-DDT, p,p'-DDE, and o,p'-DDT were all very high, even though the use of technical DDT has been banned in China since 1983. Moreover, the average concentration ratios of o,p'-DDT/p,p'-DDT and p,p'-DDE/p,p'-DDT were as high as 6.3 and 1.8. This suggested that there could be an unknown source of DDT-related compounds (DDTs), especially o,p'-DDT and p,p'-DDE. It is very likely that this unknown source was the application of dicofol, an acaricide manufactured from technical DDT and used mainly on cotton fields to treat mites in China. Backward trajectory analysis also provided consistent evidence that the high air concentrations of DDTs were related to trajectories from the area north of the Yangtze River, where cotton fields account for a significant fraction of land use.

Agriculture↗

PubMed2004

Microporous metal organic materials: promising candidates as sorbents for hydrogen storage.

Advancement in hydrogen storage techniques represents one of the most important areas of today's materials research. While extensive efforts have been made to the existing techniques, there is no viable storage technology capable of meeting the DOE cost and performance targets at the present time. New materials with significantly improved hydrogen adsorption capability are needed. Microporous metal coordination materials (MMOM) are promising candidates for use as sorbents in hydrogen adsorption. These materials possess physical characteristics similar to those of single-walled carbon nanotubes (SWNTs) but also exhibit a number of improved features. Here, we report a novel MMOM structure and its room-temperature hydrogen adsorption properties.

Journal Article↗

PubMed2004

Reversed-phase liquid chromatography method to determine COL-3, a matrix metalloproteinase inhibitor, in biological samples.

A reversed-phase high-performance liquid chromatographic (HPLC) method with ultraviolet (UV) detection was developed and validated for the quantification of 6-deoxy-6-demethyl-4-dedimethylamino-tetracycline (COL-3), a matrix metalloproteinase (MMPs) inhibitor, in rat serum. This simple, sensitive, rapid and reproducible assay involved a preliminary serum deproteinization by adding a mixture of acetonitrile-methanol-0.5 M oxalic acid (70:20:10 (v/v)), as the combined precipitant and metal blocking agent, into serum samples (2:1 (v/v)). An aliquot (20 microl) of the supernatant was injected into the HPLC system linked to a Waters XTerra RP(18) column (150 mm x 4.6 mm i.d., particle size 5 microm). The compound was eluted by a mixture of acetonitrile-methanol-0.01 M oxalic acid (40:10:50 (v/v), pH 2.00), as the mobile phase, and detected at the wavelength of 350 nm. The total running time was 10 min. The low and high concentration calibration curves were linear in the range of 50-1200 ng/ml and 1200-12,000 ng/ml, respectively. The intra- and inter-day coefficients of variation at three quality control concentrations of 100, 1200, and 12,000 ng/ml were all less than 6%, while the percent error ranged from -2.5 to 6.6%. The limit of quantitation (LOQ) for COL-3 in serum was 50 ng/ml. This assay was successfully employed to study the serum concentration-time profiles of COL-3 after its intravenous and oral administration in rats. The method with some minor modifications in sample pretreatment was also applicable to the determination of the concentrations of COL-3 in rat bile, urine and feces.

Animals↗

PubMed2004

The WRKY70 transcription factor: a node of convergence for jasmonate-mediated and salicylate-mediated signals in plant defense.

Cross talk between salicylic acid (SA)- and jasmonic acid (JA)-dependent defense signaling has been well documented in plants, but how this cross talk is executed and the components involved remain to be elucidated. We demonstrate that the plant-specific transcription factor WRKY70 is a common component in SA- and JA-mediated signal pathways. Expression of WRKY70 is activated by SA and repressed by JA. The early induction of WRKY70 by SA is NPR1-independent, but functional NPR1 is required for full-scale induction. Epistasis analysis suggested that WRKY70 is downstream of NPR1 in an SA-dependent signal pathway. Modulation of WRKY70 transcript levels by constitutive overexpression increases resistance to virulent pathogens and results in constitutive expression of SA-induced pathogenesis-related genes. Conversely, antisense suppression of WRKY70 activates JA-responsive/COI1-dependent genes. The effect of WRKY70 is not caused by subsequent changes in SA or JA levels. We suggest that WRKY70 acts as an activator of SA-induced genes and a repressor of JA-responsive genes, integrating signals from these mutually antagonistic pathways.

Arabidopsis↗

PubMed2004

Inhibitory effects of anti-sense PTTG on malignant phenotype of human ovarian carcinoma cell line SK-OV-3.

To construct eukaryotic expression vector expressing full length anti-sense pituitary tumor transforming gene (PTTG) mRNA and observe its blocking effect on the potential invasion of human ovarian carcinoma cell line SK-OV-3. PCR primers containing designed enzyme cut sites were used for cloning full-length PTTG gene fragment, and the resulting PCR product was inserted into the eukaryotic vector pcDNA3.1 in the antisense direction. The recombinant vector was then transfected into SK-OV-3 by Lipofectamine. The positive cell clone was screened by G418, PTTG and bFGF at protein level expression were detected by Western blot. The biological behavior change of transfection positive cells was observed by colony formation in soft agar assay. Our results showed that SK-OV-3 clones stably expressing full-length recombinant pcDNA3.1-PTTGas were obtained. The expressions of PTTG and bFGF protein in transfected cells were decreased by 61.5% and 52.3%, respectively as compared with non-transfected ones. The number of colony formation was reduced significantly in transfected cells as compared with empty vector transfected and non-transfected cells. It is concluded that the recombinant vector pcDNA3.1-PTTGas is a novel tool and provides an alternative anti-sense gene therapy targeted at PTTG in human carcinoma.

Cell Line, Tumor↗

PubMed2004

Tra2betal regulates P19 neuronal differentiation and the splicing of FGF-2R and GluR-B minigenes.

The present study demonstrates that the expression of Tra2beta1 (Transformer 2-beta1) proteins, an SR (serine/arginine rich) protein, is developmentally up-regulated in a neural-specific pattern. The up-regulation is also observed in RA (retinoic acid) induced neural differentiation of P19 cells. Tra2betal proteins are located in the nuclei of P19 cells, which are consistent with its functional site as an SR protein. The over-expression of Tra2betal proteins promotes RA induced neuronal differentiation of P19 cells. In P19 cells, the splicing of FGF-2R (fibroblast growth factor receptor 2) minigene produces the BEK form, while the alternative splicing of GluR-B (glutamate receptor subunit B) minigene generates two products, the Flop and the Truncated isoforms. Tra2betal inhibits the BEK splicing, but it promotes the Flop splicing. The results therefore suggest that Tra2betal is involved in the regulation of alternative splicing processes during neural development, peculiarly the splicing of FGF-2R and GluR-B genes. Both FGF-2R and GluR-B genes are known to play important roles in neural differentiation.

Alternative Splicing↗

PubMed2004

Temporal associations between interleukin 22 and the extracellular domains of IL-22R and IL-10R2.

Interleukin 22 (IL-22) is a cytokine induced during both innate and adaptive immune responses. It can effect an acute phase response, implicating a role for IL-22 in mechanisms of inflammation. IL-22 requires the presence of the IL-22 receptor (IL-22R) and IL-10 receptor 2 (IL-10R2) chains, two members of the class II cytokine receptor family (CRF2), to effect signal transduction within a cell. We studied the interaction between human IL-22 and the extracellular domains (ECD) of its receptor chains in an enzyme-linked immunoabsorbant assay (ELISA)-based format, using biotinylated IL-22 (bio-IL-22) and receptor-fusions containing the ECD of a receptor fused to the Fc of hIgG1 (IL-22R-Fc and IL-10R2-Fc). IL-22 has measurable affinity for IL-22R-Fc homodimer and undetectable affinity for IL-10R2. IL-22 has substantially greater affinity for IL-22R/IL-10R2-Fc heterodimers. Further analyses involving sequential additions of receptor homodimers and cytokine indicates that the IL-10R2(ECD) binds to a surface created by the interaction between IL-22 and the IL-22R(ECD), and thereby further stabilizes the association of IL-22 within this cytokine-receptor-Fc complex. Both a neutralizing rat monoclonal antibody, specific for human IL-22, and human IL-22BP-Fc, an Fc-fusion of the secreted IL-22 binding-protein and proposed natural antagonist for IL-22, bind to similar cytokine epitopes that may overlap the binding site for IL-22R(ECD). Another rat monoclonal antibody, specific for IL-22, binds to an epitope that may overlap a separate binding site for IL-10R2(ECD). We propose, based on this data, a temporal model for the development of a functional IL-22 cytokine-receptor complex.

Animals↗

PubMed2004

Inducible nuclear factor-kappaB activation contributes to chemotherapy resistance in gastric cancer.

BACKGROUND: Activation of nuclear factor-kappaB (NF-kappaB) inhibits chemotherapy-induced apoptosis in some cancer cell lines. Inhibition of NF-kappaB by adenoviral delivery of an IkappaBalpha superrepressor (Ad.IkappaBalpha-SR) should potentiate 5-fluorouracil (5-FU) and irinotecan chemotherapy in gastric cancer cells. STUDY DESIGN: NCI-N87 and AGS human gastric cancer cells were studied. Chemotherapy-induced NF-kappaB activation was assessed using a luciferase reporter assay. Inhibition of NF-kappaB was assessed by luciferase reporter assay and by electrophoretic mobility shift assay. Cells were pretreated for 1 hour with Ad.IkappaBalpha (25 MOI) and incubated with 5-FU or the active metabolite of irinotecan (SN-38). Cell growth was assessed by cell proliferation assay and induction of apoptosis was determined by flow cytometry and caspase 3/7 assay. RESULTS: 5-FU and SN-38 significantly induced NF-kappaB activation as measured by luciferase reporter assay (p < 0.001). Ad.IkappaBalpha-SR treatment inhibited NF-kappaB binding as demonstrated by electrophoretic mobility shift assay and by luciferase reporter assay. In AGS cells, pretreatment with Ad.IkappaBalpha-SR followed by 5-FU (0.005 mmol/L) or SN-38 (10 ng/mL) led to increased growth inhibition of 13% and 59%, respectively (p < 0.001). Similarly, growth inhibition in NCI cells was significantly increased by pretreatment with Ad.IkappaBalpha followed by 5-FU (0.001 mmol/L) or SN-38 (0.5 ng/mL) (p < 0.001). In both cell lines, Ad.IkappaBalpha-SR enhanced apoptosis by both flow cytometry and caspase 3/7 assay as compared with chemotherapy alone. CONCLUSIONS: NF-kappaB is activated in human gastric cancer in response to chemotherapy and may result in inducible chemoresistance. Inhibition of NF-kappaB by Ad.IkappaBalpha-SR enhances the antitumor effects of chemotherapy and has potential as a novel antineoplastic strategy.

Antimetabolites, Antineoplastic↗

PubMed2004

Inhibition of NF-kappa B augments sensitivity to 5-fluorouracil/folinic acid in colon cancer.

BACKGROUND: 5-fluorouracil (5-FU), the most common antimetabolite used for the treatment of colorectal cancer, exerts its cytotoxic effects through the induction of apoptosis. Folinic acid potentiates the effect of 5-FU. Drug activity is currently limited as a result of inducible chemoresistance. Limited research suggests that the transcription factor nuclear factor kappa-B (NF-kappaB), which has antiapoptotic properties, may play a major role in inducible chemoresistance. MATERIALS AND METHODS: SW48 colon cancer cells were used for all experiments. Cell growth was determined by cell proliferation assay. Apoptosis was assessed by measuring caspase 3 activity. Activation of NF-kappaB was ascertained by electrophoretic mobility shift assay, luciferase reporter assay, and Western blot analysis. RESULTS: Treatment with 5-FU (0.001-10 mm), not only inhibited growth and induced apoptosis but significantly activated NF-kappaB in SW48 cells. Folinic acid alone (0.01-100 mg/L) did not inhibit growth but improved the cytotoxic effect of 5-FU in a dose-dependent manner. Likewise, folinic acid alone did not activate NF-kappaB or induce apoptosis but enhanced 5-FU-mediated NF-kappaB activation and cell apoptosis. Transfection with adenovirus IkappaBalpha super-repressor strongly inhibited constitutive activation of NF-kappaB and significantly enhanced 5-FU and 5-FU/Folinic acid-mediated growth inhibition (P < 0.05). CONCLUSIONS: Treatment with 5-FU activates NF-kappaB. Folinic acid enhances 5-FU-mediated activation of NF-kappaB. Inhibition of NF-kappaB enhances the cytotoxic effect of 5-FU with or without Folinic acid in colon cancer cells.

Adenoviridae↗

PubMed2004

Regulator of G protein signaling 5 marks peripheral arterial smooth muscle cells and is downregulated in atherosclerotic plaque.

OBJECTIVE: Regulator of G protein signaling 5 (RGS5), an inhibitor of Galpha(q) and Galpha(i) activation, was recently identified among genes highly expressed in smooth muscle cells (SMCs) of aorta but not vena cava. This finding prompted the hypothesis that RGS5 provides long-term G protein inhibition specific to normal arterial SMC populations and that loss of expression may in turn contribute to arterial disease. METHODS: To test this hypothesis we characterized RGS5 gene expression throughout the vasculature of nonhuman primates to determine whether RGS5 was restricted to arteries in other vascular beds and whether expression was altered in arterial disease. RESULTS: In situ hybridization localized RGS5 message to medial SMCs of peripheral arteries, including carotid, iliac, mammary, and renal arteries, but not accompanying veins. SMCs of many small arteries and arterioles also expressed RGS5, including glomerular afferent arterioles critical to blood pressure regulation. Differential expression persisted in culture, inasmuch as RGS5 message was significantly higher in SMCs derived from arteries than from veins at real-time polymerase chain reaction. It was remarkable that the only major arterial bed lacking RGS5 was the coronary circulation. In atherosclerotic peripheral arteries RGS5 was expressed in medial SMCs, but was sharply downregulated in plaque SMCs. CONCLUSION: These data identify RGS5 as a new member of a short list of genes uniquely expressed in peripheral arteries but not coronary arteries. Persistence of an arterial pattern of RGS5 expression in culture and lack of expression in coronary arteries support a unique SMC phenotype fixed by distinct lineage or differentiation pathways. The association between loss of expression and arterial wall disease has prompted the new hypothesis that prolonged inhibition by RGS5 of vasoactive or trophic G protein signaling is critical to normal peripheral artery function.

Animals↗

PubMed2004

Wip1-deficient mice are resistant to common cancer genes.

PPM1D encodes WIP1, a serine-threonine phosphatase that had previously been shown to be the driver oncogene of a 17q23 amplicon that is present in approximately 15% of human breast tumors. However, it is unknown whether it has any role in the remaining 85% of breast tumors. A recent study using Wip1-deficient mice revealed that blocking its function significantly impaired RAS and ERBB2-induced breast tumor formation, suggesting that the inhibition of Wip1 could be a broad-spectrum treatment for breast cancer. However, because of the structure of Wip1, the development of small molecule inhibitors is a significant challenge.

Animals↗

PubMed2004

Differential effects of Rho-kinase inhibition on artery wall mass and remodeling.

PURPOSE: Constrictive remodeling and new artery wall mass contribute to lumen narrowing in atherosclerosis and following injury. Rho-kinase, an important regulator of myosin phosphorylation and cytoskeletal reorganization, is critical to smooth muscle cell (SMC) growth and vasoconstriction, but its role in artery wall remodeling is poorly defined. We hypothesized that constrictive artery wall remodeling is dependent on Rho signaling so that blocking Rho-kinase would promote outward artery wall remodeling in response to intimal hyperplasia and thus limit lumen narrowing. METHODS: To test this hypothesis, we first studied the effects of the Rho-kinase inhibitor fasudil on SMC remodeling of collagen matrix in vitro. Mouse aortic SMCs were seeded into three-dimensional collagen gels with and without fasudil, and extent of contraction was measured at 24 hours. We then used the mouse carotid ligation model to study the effects of Rho-kinase inhibition on remodeling and intimal hyperplasia in vivo. C57B6/J mice were randomly assigned to fasudil (100 mg/kg per day) or vehicle and underwent unilateral carotid artery ligation or sham ligation. Remodeling and wall mass were measured after 28 days. RESULTS: Fasudil blocked SMC contraction of collagen gels in a dose-dependent manner. Complete inhibition of collagen gel remodeling was achieved between 10 and 30 micromol/L fasudil. In control mice, carotid ligation caused significant thickening of the adventitia, media, and intima (P <.01) and outward remodeling of the carotid wall. The external elastic lamina (EEL) area increased by 14% versus sham (P <.05), but this increase was insufficient to prevent lumen narrowing (-42% vs sham, P <.05). Fasudil treatment had favorable effects on wall mass, inhibiting neointimal (P =.04), medial (P =.03), and adventitial thickening (P =.07) versus controls. Opposite our hypothesis, however, fasudil did not enhance outward artery wall remodeling or improve lumen caliber. Rather, inhibiting Rho-kinase blocked outward remodeling in response to ligation. EEL area was significantly smaller in treated versus control animals (P =.04) and slightly smaller versus shams (P = NS). These data suggest that Rho activation contributes significantly to both hyperplasia and outward remodeling of the injured artery wall. Rho-kinase may prove an important target to limit intimal hyperplasia and prevent restenosis when remodeling is improved by other means (eg, stents).

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗