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Jie Ding

Publications and source records attributed to Jie Ding.

At least 19 recordsLinked to original sources
PubMed2025

Mendelian randomization reveals causal relationships between cytokines and male reproductive diseases.

This study aims to explore the causal links between cytokines and four male reproductive disorders, namely abnormal spermatozoa (AS), male infertility, erectile dysfunction (ED), and hyperplasia of prostate (HP), employing a two-sample Mendelian randomization (MR) approach. Genetic associations with male reproductive diseases were derived from the IEU OpenGWAS project, with cytokine data from two GWASs focused on the human proteome and cytokines. Estimations were derived using inverse variance weighting, MR-Egger regression, weighted median, weighted model, and simple mode. Furthermore, the robustness of the findings was evaluated through Cochran's Q-test, MR-Egger regression, and leave-one-out sensitivity analysis. Fifteen unique cytokines were identified as having causal relationships with the risk of four male reproductive disorders. Specifically, for AS, interleukin-22 (IL-22), IL-12, and macrophage migration inhibitory factor were negatively correlated with AS, while tumor necrosis factor β levels were positively correlated with AS. In the context of male infertility, IL-2 receptor antagonist levels, IL-34, and granulocyte-colony stimulating factor levels were positively linked to male infertility, whereas IL-21 showed a negative relationship. Regarding ED, IL-19, IL-1β, and eotaxin levels were negatively associated with ED risk, while macrophage inflammatory protein 1β (MIP-1β) levels and interferon gamma-induced protein 10 levels were positively associated. As for HP, stromal-cell-derived factor 1α levels and MIP-1α levels revealed negative associations with HP. In conclusion, this MR analysis revealed that several cytokines were causally associated with male reproductive diseases and could be valuable in offering new insights for further mechanistic and clinical investigations of cytokines-associated male reproductive diseases.

Male↗
PubMed2006

Optimising the incorporation and release of a neurotrophic factor using conducting polypyrrole.

In this study, a neurotrophin delivery system based on an inherently conducting polymer (ICP) has been developed. Direct incorporation of neurotrophin-3 (NT-3) was investigated and controlled release was tested under various electrochemical conditions. The loading capacity and amount of NT-3 released from the polymer was determined using (125)I-labelled NT-3. Electrochemical stimulation of polypyrrole by pulsed voltage, pulsed current or cyclic voltammetry promoted the release of NT-3 at a greater rate than natural diffusion of NT-3. NT-3 was released from polypyrrole as an initial burst in the first 24 h followed by prolonged release over a subsequent 6 days of sampling. The amount of NT-3 incorporated into the polymer could be controlled by varying the polymerisation time, with longer growth periods incorporating more NT-3. The NT-3 release results indicated that the polymers grown for longer released a lower percentage of the incorporated NT-3 compared to the polymers grown for shorter times. Polymer-based neurotrophin delivery systems have the potential to be incorporated into future treatments for nerve injuries to prevent nerve degradation and promote nerve protection.

Delayed-Action Preparations↗
PubMed2006

Monte Carlo pedigree disequilibrium test for markers on the X chromosome.

Because of the need for fine mapping of disease loci and the availability of dense single-nucleotide-polymorphism markers, many forms of association tests have been developed. Most of them are applicable only to triads, whereas some are amenable to nuclear families (sibships). Although there are a number of methods that can deal with extended families (e.g., the pedigree disequilibrium test [PDT]), most of them cannot accommodate incomplete data. Furthermore, despite a large body of literature on association mapping, only a very limited number of publications are applicable to X-chromosomal markers. In this report, we first extend the PDT to markers on the X chromosome for testing linkage disequilibrium in the presence of linkage. This method is applicable to any pedigree structure and is termed "X-chromosomal pedigree disequilibrium test" (XPDT). We then further extend the XPDT to accommodate pedigrees with missing genotypes in some of the individuals, especially founders. Monte Carlo (MC) samples of the missing genotypes are generated and used to calculate the XMCPDT (X-chromosomal MC PDT) statistic, which is defined as the conditional expectation of the XPDT statistic given the incomplete (observed) data. This MC version of the XPDT remains a valid test for association under linkage with the assumption that the pedigrees and their associated affection patterns are drawn randomly from a population of pedigrees with at least one affected offspring. This set of methods was compared with existing approaches through simulation, and substantial power gains were observed in all settings considered, with type I error rates closely tracking their nominal values.

Chromosomes, Human, X↗
PubMed2006

Genetic variations of the NR3C1 gene in children with sporadic nephrotic syndrome.

Previous studies have demonstrated that the genetic variations of glucocorticoid receptor gene (NR3C1) are associated with both familial steroid resistance and acquired steroid resistance in some diseases, such as Cushing's disease, leukemia, lupus nephritis, and female pseudohermaphroditism. In this study, we examined the genetic variations of NR3C1 in 35 children with sporadic steroid-resistant nephrotic syndrome (SRNS), and in 83 cases with sporadic steroid-sensitive NS (SSNS) using polymerase chain reaction, denaturing high-performance liquid chromatography and DNA sequencing, and analyzed possible associations between NR3C1 variants and steroid resistance in sporadic NS. No causative mutations were found; however, six previously identified and six novel polymorphisms, 1206C > T, 1374A > G, 2382C > T, 2193T > G, IVS7-68_-63delAAAAAA, and IVS8-9C > G, were detected. Two novel haplotypes, [1374A > G; IVS7-68_-63delAAAAAA; IVS8-9C > G; 2382C > T] and [1896C > T; 2166C > T; 2430T > C], of NR3C1 were also identified in sporadic NS and controls. The odds ratios (95% Confidence Interval) for the two novel NR3C1 haplotypes in the sporadic nephrotic children at risk of steroid resistance were 4.970 (0.889-27.788) and 2.194 (0.764-6.306), respectively, but the association between NR3C1 haplotypes and steroid resistance was not significant. Further studies on the possible association between the two novel NR3C1 haplotypes and steroid resistance in sporadic NS in larger cohorts are required.

Adolescent↗
PubMed2006

Structural and functional characterization of transmembrane segment VII of the Na+/H+ exchanger isoform 1.

The Na(+)/H(+) exchanger isoform 1 is an integral membrane protein that regulates intracellular pH by exchanging one intracellular H(+) for one extracellular Na(+). It is composed of an N-terminal membrane domain of 12 transmembrane segments and an intracellular C-terminal regulatory domain. We characterized the structural and functional aspects of the critical transmembrane segment VII (TM VII, residues 251-273) by using alanine scanning mutagenesis and high resolution NMR. Each residue of TM VII was mutated to alanine, the full-length protein expressed, and its activity characterized. TM VII was sensitive to mutation. Mutations at 13 of 22 residues resulted in severely reduced activity, whereas other mutants exhibited varying degrees of decreases in activity. The impaired activities sometimes resulted from low expression and/or low surface targeting. Three of the alanine scanning mutant proteins displayed increased, and two displayed decreased resistance to the Na(+)/H(+) exchanger isoform 1 inhibitor EMD87580. The structure of a peptide of TM VII was determined by using high resolution NMR in dodecylphosphocholine micelles. TM VII is predominantly alpha-helical, with a break in the helix at the functionally critical residues Gly(261)-Glu(262). The relative positions and orientations of the N- and C-terminal helical segments are seen to vary about this extended segment in the ensemble of NMR structures. Our results show that TM VII is a critical transmembrane segment structured as an interrupted helix, with several residues that are essential to both protein function and sensitivity to inhibition.

Alanine↗
PubMed2006

Screening and identification of vascular-endothelial-cell-specific binding peptide in gastric cancer.

Antiangiogenesis therapy has become a hot field in cancer research. Blood vessels of tumor carry specific markers that are usually related to angiogenesis. Study of these heterogeneous molecules in different tumor vessels may be beneficial for promoting antiangiogenic therapy. In this study, we established an in vitro co-culture model of human umbilical vein endothelial cells (HUVECs) and gastric adenocarcinoma cell line SGC7901, screened the peptides binding specifically to the HUVECs co-cultured with gastric cancer cells (Co-HUVECs) using phage display peptides library, and studied the affinity of these peptides to gastric cancer vascular endothelial cells. After four rounds of panning, there was an obvious enrichment for the phages specifically binding to the Co-HUVECs, and the output/input ratio of Co-HUVECs increased about 590-fold (from 0.95x10(-7) to 561.25x10(-7)). Five phage clones (M6, M3, M9, IN12, IN11), which could strongly bind to Co-HUVECs instead of wild-type HUVECs, were characterized by ELISA. In vitro cellular binding assay showed that phage IN11 preferably bound to Co-HUVECs rather than control HUVECs, and the number of the phage IN11 recovered from Co-HUVECs was 5.7- and 16.9-folds, respectively, as much as those from control HUVECs and GES cells. Immunocytochemical and immunohistochemical staining confirmed that phage IN11 could specifically bind to Co-HUVECs as well as vascular endothelial cells in gastric cancer tissue sections. Competitive and inhibitory assay revealed the synthetic peptide GEBP11 (CTKNSYLMC) displayed on phage IN11 could competitively inhibit binding of the phage IN11 to Co-HUVECs. Immunofluorescence microscopy showed that the fluorescence-labeled peptide GEBP11 was located at the membrane and perinuclear cytoplasm of Co-HUVECs. Meanwhile, GEBP11 was found to be able to target the gastric cancer vascular endothelial cells. Therefore, GEBP11 may be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of gastric cancer.

Amino Acid Sequence↗
PubMed2006

Cyclooxygenase isozymes are expressed in human myeloma cells but not involved in anti-proliferative effect of cyclooxygenase inhibitors.

Considering possible tumorigenic activity of cyclooxygenase (COX) isozymes in myeloma, we examined expression levels of COX-1 and -2 in seven human myeloma cell lines (ARH-77, IM-9, RPMI-8226, HPC, HS-Sultan, TSPC-1, and U-266). As analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR), all the cell lines constitutively expressed COX-1, while COX-2 levels markedly varied among different cell lines. Induction of COX-2 by phorbol ester was observed in RPMI-8226 and HPC cells. In contrast, COX-2 was constitutively expressed in ARH-77 and IM-9 cells. Moreover, the high expression level of COX-2 protein in ARH-77 cells was verified by Western blotting. Intact cells of ARH-77 converted 14C-labeled arachidonic acid to prostaglandin E2, F2alpha, and D2, and this activity was dose-dependently inhibited by selective COX-2 inhibitors (SC-58125 and NS-398), a non-selective COX inhibitor (indomethacin), and relatively high concentrations of a selective COX-1 inhibitor (SC-560). These COX inhibitors also suppressed the proliferation of ARH-77 cells, but significant suppression was seen only at 100 microM, a much higher concentration than those sufficient for the COX inhibition. Moreover, proliferation of the myeloma cells lacking COX-2 was also suppressed by 100 microM of SC-58125. These results suggested that the anti-proliferative effect of the COX inhibitors is independent of the inhibition of COX-2.

Arachidonic Acid↗
PubMed2006

Prospective randomized clinical trial of two drug delivery pathway in the treatment of inoperable advanced pancreatic carcinoma.

OBJECTIVES: Evaluate the effect of an implanted percutaneous left subclavian artery port-catheter drug delivery system for regional chemotherapy of inoperable pancreatic carcinoma. METHODS: One hundred and forty patients with inoperable pancreatic carcinoma were enrolled and randomized into two groups to receive the FAM regimen on a 6-day cycle at 1-month intervals: 70 patients in the regional interventional chemotherapy group in which treatment was infused directly into the common hepatic artery, and 70 patients who received the same chemotherapy regimen via the peripheral vein. RESULT: In the interventional chemotherapy group, there were 5 cases of complete remission (CR) and 49 cases of partial remission (PR), giving a response rate (CR+PR) of 77.1%; pain control was effective in 95.7% cases; survival time was 3-34 months (median 13.5). There was no case of CR in the systemic chemotherapy group, and 25 cases of PR, giving a response rate of 35.7%; pain control was effective in 35.7%, and survival time was 1-13 months (median 6.2). The differences between the two groups in response rate and survival were statistically significant (P < 0.005). Nausea and vomiting occurred in 48.6% of the interventional chemotherapy group and 41.3% of the systemic chemotherapy group (NS). There were three cases of serious myelosuppression in the systemic chemotherapy group and one case died. There was a significant difference between the two groups in white blood cell count after the chemotherapy, indicating that the myelosuppressive effect was serious in the systemic chemotherapy group. CONCLUSION: Interventional arterial infusion chemotherapy could significantly improve quality of life and prolong the survival of patients with inoperable pancreatic carcinoma.

Adult↗
PubMed2006

Diversities of podocyte molecular changes induced by different antiproteinuria drugs.

Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. Studies have shown that angiotensin-converting enzyme inhibitors, glucocorticoids, and all-trans retinoic acid (ATRA) have antiproteinuric effects. However, it is still unclear whether these drugs, with different pharmacological mechanisms, lead to a reduction in proteinuria by changing the expression and distribution of these important podocyte proteins. In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. Nephropathy was induced by an intravenous injection of Adriamycin. After Adriamycin injection, rats received lisinopril, prednisone, and ATRA treatment, respectively. Renal tissues were collected at Days 3, 7, 14, and 28. The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. There was no change in the expression of alpha-actinin-4 molecule. In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. The pattern in the change of podocyte molecules after lisinopril and prednisone intervention was similar, but the pattern in the change of podocyte molecules after ATRA intervention was different from that of lisinopril or prednisone intervention.

Actinin↗
PubMed2006

[Fifteen short tandem repeat polymorphisms in Han race of North China].

OBJECTIVE: To research on the genetic polymorphism distributions of 15 short tandem repeat (STR) loci in Han race of North China and the genetic data of population genetics. METHODS: The capillary electrophoresis and five-color fluorescent multi-amplifying were applied to detect the genotypes of 15 STR loci in 597 unrelated Chinese Han individuals. RESULTS: No significant deviation from the Hardy-Weinberg Equilibrium was observed. High polymorphism was detected in the loci. Statistical analysis was carried out to obtain some parameters of forensic medicine. The heterozygosity of 15 loci was above 0.62. The values of discrimination power (DP) at 15 STRs ranged from 0.802 to 0.967. The values of excluding probability of paternity (EP) ranged from 0.320 to 0.697. The values of probability matching (Pm) ranged from 0.033 to 0.198. The fifteen loci showed an accumulated total discrimination power (TDP) more than 0.999999, a cumulative excluding probability of paternity (CEP) as 0.99999571, and total probability matching to be 8.93 x 10(-18). CONCLUSION: The data indicated that detecting combined 15 STRs is sensitive and reliable, and can be used to forensic and individual identification cases in Chinese group.

Asian People↗
PubMed2006

[Preparation and characterization of anti-Drosophila Dnop5 antibody].

AIM: To prepare the rabbit antibody against Dnop5 and identify its specificity. METHODS: Dnop5 cDNA was amplified by RT-PCR, and then was subcloned into the fusion expression vectors pET28a(+). After being expressed in E.coli BL21, the truncated Dnop5 protein was purified and used to immunize rabbit. Purified antibody was obtained through affinity chromatography column with the expressed Dnop5. The specificity of the purified antibody was characterized by Western blot and immunohistochemical staining. RESULTS: The Dnop5 gene was successfully inserted into pET28a(+). After induction, the fusion protein was expressed in the form of inclusion body. The purified fusion protein was obtained by affinity chromatography. After immunization of rabbits, the antibody against Dnop5 was obtained. Western blot analysis and immunohistochemical staining showed that the antibody had a good specificity. CONCLUSION: The rabbit antibody against Dnop5 has been successfully prepared, which lays the foundation for further study on the Dnop5 function.

Animals↗
PubMed2006

[Study on the predictive model for Yersinia enterocolitica growth at different temperatures].

OBJECTIVE: A predictive model for Yersinia enterocolitica growth in MTSB at different temperatures was studied. According to this model, if food has been contaminated by a few Yersinia enterocolitica, the growth rate, generation time, lag time and total bacterial number at any time and any effective temperature can be predicted. Under the same condition, the parameters for Yersinia enterocolitica serotype O:3 and Yersinia enterocolitica O:9 were compared, respectively. RESULTS: 1. The minimum growth temperature for Yersinia enterocolitica serotype O:3 and O:9 were--17.8 degrees C and--10.3 degrees C, respectively. 2. In the range of 4 degrees C and 30 degrees C, the growth rate of Yersinia enterocolitica serotype O:3 or O:9 increase with temperature going up. 3. In the range of 4 degrees C and 15.7 degrees C, the growth rate of Yersinia enterocolitica serotype O:3 is higher than that of Yersinia enterocolitica serotype O:9. In the range of 15.7 degrees C and 30 degrees C, the growth rate of Yersinia enterocolitica serotype O:9 is higher than that of Yersinia enterocolitica serotype O:3. 4. We get a predictive model for Yersinia enterocolitica in MTSB: Yersinia enterocolitica serotype O:3, square root of M = 0.0134 (T-255.1866). Yersinia Enterocolitica serotype O:9, square root of M = 0.0173 (T-262.7457).

Food Microbiology↗
PubMed2005

Comparisons of methods for linkage analysis and haplotype reconstruction using extended pedigree data.

We compare and contrast the performance of SIMPLE, a Monte Carlo based software, with that of several other methods for linkage and haplotype analyses, focusing on the simulated data from the New York City population. First, a whole-genome scan study based on the microsatellite markers was performed using GENEHUNTER. Because GENEHUNTER had to drop individuals for many of the pedigrees, we performed a follow-up study focusing on several regions of interest using SIMPLE, which can handle all pedigrees in their entirety. Second, 3 haplotyping programs, including that in SIMPLE, were used to reconstruct haplotypic configurations in pedigrees. SIMPLE emerges clearly as a preferred tool, as it can handle large pedigrees and produces haplotypic configurations without double recombinant haplotypes. For this study, we had knowledge of the simulating models at the time we performed the analysis.

Chromosome Mapping↗
PubMed2005

Mad2beta, an alternative variant of Mad2 reducing mitotic arrest and apoptosis induced by adriamycin in gastric cancer cells.

Mad2beta is an alternative splicing variant of spindle checkpoint gene mad2, which was previously found by us and was related to the drug resistance in gastric cancer cells. In this paper, we explored the molecular mechanisms that Mad2beta variant promoted the formation of multidrug resistance in gastric cancer cells. We found that Mad2beta variant was detected only in the two human drug resistant gastric cancer cell sublines SGC7901/VCR and SGC7901/ADR, and it did not appear in its parental cell line SGC7901 and other detected gastric cancer cell lines. Expressions of Mad2 mRNA and protein in SGC7901 cells transfected with Mad2beta, SGC7901/VCR and SGC7901/ADR were significantly lower than that in SGC7901 cells. Moreover, SGC7901 cells overexpressing Mad2beta variant became more resistant to adriamycin, vincristine and mitomycin by abrogating mitotic arrest and apoptosis. This suggests that expression of Mad2beta variant decreases the relative expression of efficient MAD2, which may help gastric cancer cells to develop the phenotype of multidrug resistance.

Alternative Splicing↗
PubMed2005

Tumor suppressor gene Runx3 sensitizes gastric cancer cells to chemotherapeutic drugs by downregulating Bcl-2, MDR-1 and MRP-1.

The Runx3 gene is a member of the runt domain family transcription factors, key regulators of development and differentiation in metazoan. Recently, Runx3 was identified as a tumor suppressor gene. Loss of Runx3 was found to be associated with genesis and progression of gastric cancer. In this study, we transfected the gastric cancer cell line SGC7901 with eukaryotic expression vector of Runx3. In vitro drug sensitivity assay suggested that SGC7901/Runx3 cells were more sensitive to various chemotherapeutic drugs. Blocking Runx3 expression in immortalized stomach mucosal cells (GES-1) or gastric cancer cells (SGC7901) by Runx3-specific small interfering RNA conferred the cells resistance to chemotherapeutic drugs. Flow cytometry examination suggested that expression of Runx3 in gastric cancer cells increased the intracellular accumulation and retention of adriamycin. Semiquantitative RT-PCR and Western blot suggested that Runx3 downregulated expression of Bcl-2, MDR-1 (P-gp) and MRP-1. Binding of Runx3 to promoter sequences of Bcl-2, MDR-1 and MRP-1 gene was detected by eletrophoretic mobility shift assay (EMSA) and supershift EMSA. We cloned the MDR-1 and MRP-1 gene promoters containing Runx binding sites and constructed the luciferase reporter vectors of these 2 promoters. Luciferase reporter assay suggested that Runx3 inhibited the promoter activity of the MDR-1 and MRP-1 promoter in SGC7901 cells. Taken together, our findings suggested that overexpression of Runx3 could sensitize gastric cancer cells to chemotherapeutic drugs by downregulating the Bcl-2, MDR-1 and MRP-1.

Adenocarcinoma↗
PubMed2005

Regulation of vascular endothelial growth factor (VEGF) production and angiogenesis by tissue Factor (TF) in SGC-7901 gastric cancer cells.

Tissue factor (TF), an initiator of the extrinsic coagulation cascade, is expressed in a wide range of cancer cells and plays important roles in cancer progression and metastasis. We demonstrated between TF and vascular endothelial growth factor (VEGF) production differences in four human gastric cell lines. One of these cell lines, SGC-7901, a high TF and VEGF producer, was grown subcutaneously in severe combined immuno-deficient (SCID) mice. The SCID mice generated solid tumors characterized by intense vascularity. In contrast, SGC-7901 cells transfected with antisense TF cDNA generated relatively avascular tumors in SCID mice, as determined by immunohistochemical staining of tumor vascular endothelial cells with anti-VIII factor antibody. To investigate the structure-function relationship between TF and VEGF, the SGC-7901 cell line was transfected with antisense a full-length TF cDNA, a cytoplasmic deletion mutant lacking the distal three serine residues (potential substrates for protein kinase C), or an extracellular domain mutant, which has markedly diminished function for activation of factor X. Cells transfected with the full-length antisense TF sequence produced decreased levels of both TF and VEGF. Transfectants with the extracellular domain mutant produced high levels of VEGF mRNA. However, cells transfected with the cytoplasmic deletion mutant construct produced increased levels of TF, but little or no VEGF. Thus, the cytoplasmic tail of TF may signal VEGF expression in some tumor cells.

Animals↗