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Biomedical subjects

J Jiang

Publications and source records attributed to J Jiang.

At least 253 records · Page 14Linked to original sources

[Immunocytochemical localization of two facilitated glucose transporters of Schistosoma mansoni in the tegument of Schistosoma japonicum].

AIM: To observe the distribution of Schistosoma mansoni glucose transport proteins, SGTP1 and SGTP4, in the tegument of Schistosoma japonicum. METHODS: The rapidly frozen fixation technique and ultracryomicrotomy were adopted for preparing ultrathin cryosections of S. japonicum. Anti-SGTP1 and anti-SGTP4 antibodies were used to localize the corresponding antigens in the tegument of adult S. japonicum by immunocytochemical technique. RESULTS: SGTP1 was localized on the basal membrane of the tegument and its infoldings, SGTP4 was localized on the apical membrane of the tegument and its invaginations of S. japonicum. CONCLUSION: The same localization for SGTP 1 and SGTP4 in the tegument of S. japonicum and S. mansoni exhibited apparent homology between SGTPs of the two schistosomes.

Animals↗

[In vivo anti-fecundity effect of recombinant Sjc26 GST against Schistosoma japonicum in immunized mice].

AIM: To observe the anti-fecundity effect of recombinant Sjc26 GST against Schistosoma japonicum and its mechanism. METHODS: Male ICR mice were immunized with rSjc26 GST. Five days after final injection, mice of the immunization and control groups were challenged with 40 +/- 1 S. japonicum cercariae. All mice were sacrified at 6 weeks after challenge. RESULTS: The worm reduction rate was 30.0%, and the egg reduction rates in the liver and in the spleen were 57.1% and 79.9%, respectively. Inhibition of the vitelline gland and testis was also observed by transmission electron microscopy. The number of vitelline globes, vitelline droplets and lipid droplets in the cytoplasm of vitelline cell and the number of lipid droplets in the supporting cells and the number of spermatids in the testis were apparently reduced. CONCLUSION: The damage of the main reproductive organs of Schistosoma japonicum was one of the factors responsible for rSjc26 GST-bound anti-fecundity action.

Animals↗

[The meaning of the expression of PCNA and c-erbB-2 in the hyperplasia of laryngeal epithelium].

OBJECTIVE: This study was performed to examine the relationship between PCNA and c-erbB-2 expression and histological diagnosis. METHOD: The percentages of PCNA-positive nuclei (PCNA index) were evaluated in biopsies of 10 with epithelial simple hyperplasia, 26 with dysplasia and 30 with squamous carcinoma by immunohistochemical staining. RESULT: The PCNA indices were 6.64%, 29.36% and 62.67% respectively. There were significant statistic correlation between these indices and their histological gradies of lesions (P < 0.01). C-erbB-2 was not positive in all of dysplastic lesion and weak in carcinoma (20%). CONCLUSION: The PCNA activity in dysplastic lesions of laryngeal premalignancis is higher than that in simple hyperplastic lesions but lower than that in carcinoma. The severe dysplasia with high PCNA indices should be treated clinically as the early invasive carcinom. The method should be regarded as a useful adjunct to traditional histological techniques with allowing more objective grading of epithelial hyperplastic lesions of larynx. There was no relationship between c-erbB-2 expression and histolotical diagnosis of hyperplastic lesions.

Adult↗

[Plasma branched-chain ketoacids metabolism in patients with chronic renal failure after oral administration of ketosteril].

OBJECTIVE: To investigate the metabolism of branched-chain ketoacids (BCKA) in patients with chronic renal failure (CRF) and healthy control after an oral dose of ketosteril. METHODS: To determine plasma concentration of BCKA by gas chromatography/mass spectrography(GC/MS). RESULTS: Fasting plasma concentration of ketoisocaproate (KICA) and ketomethylvalerate(KMVA) in patients with CRF were lower than that of healthy control; The Cmax of KICA, KMVA and ketoisovalerate (KIVA) were (67.7 +/- 12.9), (57.8 +/- 10.3), (30.3 +/- 5.3) mumol/L; Tmax were (43.8 +/- 5.7), (58.1 +/- 4.6), (43.8 +/- 4.5) min; T1/2 were (108.5 +/- 12), (105 +/- 16.6), (116.8 +/- 18) min respectively. CONCLUSIONS: Absorption of BCKA in ketosteril had no significant difference between CRF patients and healthy controls; ketosteril could be used to treat CRF patients effectively.

Administration, Oral↗

[Effects of antisense N-myc gene on nerve growth factor-induced differentiation of neuroblastoma cell line].

OBJECTIVE: The purpose of this study is to investigate the effects of antisense N-myc gene transfection on nerve growth factor-induced differentiation of neuroblastoma cell line. METHODS: Recombinant retroviral vector expressing antisense N-myc gene was constructed. Using the Transfectam Reagent, the recombinant vector was transduced into the human neuroblastoma cell line, IMR-32/NGFR, which was previously transfected by nerve growth factor receptor gene. The transformant cell line expressing antisense N-myc was established and studied by single chain RNA probe hybridization, immunocytochemistry, and nerve growth factor treatment to see whether nerve growth factor can induce differentiation in this transformant cell line and inhibition of N-myc expression. The TUNEL technique and electromicroscopy were used to detect apoptosis of the tumor cells. RESULTS: The cell line transduced by antisense N-myc expressed much less amount of N-myc both on mRNA and protein levels. After nerve growth factor treatment, remarkable morphological differentiation appeared in these cells. Apoptosis was also enhanced in these cells. CONCLUSIONS: Antisense N-myc transfection could specifically inhibit the expression of N-myc and promoted the nerve growth factor-induced differentiation of neuroblastoma cell line. Transfection of antisense N-myc could also enhance the process of apoptosis of the tumor cells.

Animals↗

[Study on application of crosslinked chitosan to the speciation analysis of selenium].

The adsorption of Se(IV)/Se(VI) by crosslinked chitosan was studied and the adsorption mechanism was concerned. The results indicated that the adsorption of Se(VI) was 95% at pH=4, while almost no adsorption for Se(IV). The adsorbed Se(VI) was quantitatively desorbed with 1 mol/L HCl after adsorption of Se(VI). A new method for the determination of trace Se(IV)/Se(VI) and organic selenium in environmental samples with hydride generation and atomic absorption spectphotometry has been developed. The detection limit of this method was 20 ng/L, the recovery was 93%-106% and the coefficient of variation was 2.0%-5.0%.

Adsorption↗

Growth hormone-dependent tyrosine phosphorylation of a GH receptor-associated high molecular WEIGHT protein immunologically related to JAK2.

A critical step in growth hormone (GH) signalling is the GH-induced activation of the GH receptor (GHR)-associated tyrosine kinase, JAK2. JAK2 is a 120 kD member of the Janus family of tyrosine kinases, whose other mammalian members include JAK1, JAK3, and TYK2. Using 3T3-F442A murine preadipocytes, we now report detection of a Mr approximately 170 kD protein, referred to as HMW ("high molecular weight") JAK2, that is specifically reactive in immunoprecipitation and immunoblotting experiments with three independently-derived anti-JAK2 antibodies--two directed at carboxyl-terminal regions of the molecule and one directed at the amino-terminus. Like JAK2, HMW JAK2 is tyrosine phosphorylated in response to GH treatment of cells and is coimmunoprecipitated with anti-GHR serum. Thus, HMW JAK2 is a protein not heretofore described that is immunologically related to JAK2 and is physically and functionally associated with the GHR.

3T3 Cells↗

Effect of major histocompatibility complex expression on murine intestinal graft survival.

BACKGROUND: Clinical intestinal transplantation has been plagued by frequent and severe graft rejection. It has been proposed that the major histocompatibility complex (MHC) antigens might play a critical role in this process owing to their extensive expression on enterocytes and mucosa-associated immune cells. METHODS: The present study examined the role of MHC antigens in intestinal graft rejection using MHC class I-deficient and MHC class II-deficient donors. RESULTS: Grafts with normal MHC expression were rejected by 9 days, whereas survival was prolonged to 14 days in the MHC class II-deficient grafts (P=NS) and to 20 days in the MHC I-deficient grafts (P<0.002). In all groups, early rejection was characterized by (1) increased crypt cell apoptosis, as detected by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique of in situ labeling; and (2) the increased expression of perforin and a CD8 phenotype in the graft-infiltrating cells. CONCLUSIONS: These data suggest that MHC antigens, CD8-positive T cells, and perforin-expressing cells contribute to intestinal graft rejection. Apoptosis of the progenitor epithelial crypt cells during early intestinal rejection may impair the gut's ability to regenerate and repair mucosal damage.

Animals↗

The potential tumor suppressor p73 differentially regulates cellular p53 target genes.

p73, a potential tumor suppressor, is a p53 homologue. Transient over expression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53-dependent cell cycle arrest. To further characterize the role of p73 in tumor suppression, we established several groups of cell lines that inducibly express p73 under a tetracycline-regulated promoter. By using these cell lines, we found that p73 can induce both cell cycle arrest and apoptosis. We also found that p73 can activate some but not all of the previously identified p53 cellular target genes. Furthermore, we found that the transcriptional activities of p53, p73 alpha, and p73 beta to induce their common cellular target genes differ among one another. These results suggest that p73 is both similar to and different from p53 in their signaling pathways leading to tumor suppression.

Apoptosis↗

Protein Data Bank (PDB): database of three-dimensional structural information of biological macromolecules.

The Protein Data Bank (PDB) at Brookhaven National Laboratory, is a database containing experimentally determined three-dimensional structures of proteins, nucleic acids and other biological macromolecules, with approximately 8000 entries. Data are easily submitted via PDB's WWW-based tool AutoDep, in either mmCIF or PDB format, and are most conveniently examined via PDB's WWW-based tool 3DB Browser.

Database Management Systems↗

Rice (Oryza sativa) centromeric regions consist of complex DNA.

Rice bacterial artificial chromosome clones containing centromeric DNA were isolated by using a DNA sequence (pSau3A9) that is present in the centromeres of Gramineae species. Seven distinct repetitive DNA elements were isolated from a 75-kilobase rice bacterial artificial chromosome clone. All seven DNA elements are present in every rice centromere as demonstrated by fluorescence in situ hybridization. Six of the elements are middle repetitive, and their copy numbers range from approximately 50 to approximately 300 in the rice genome. Five of these six middle repetitive DNA elements are present in all of the Gramineae species, and the other element is detected only in species within the Bambusoideae subfamily of Gramineae. All six middle repetitive DNA elements are dispersed in the centromeric regions. The seventh element, the RCS2 family, is a tandem repeat of a 168-bp sequence that is represented approximately 6,000 times in the rice genome and is detected only in Oryza species. Fiber-fluorescence in situ hybridization analysis revealed that the RCS2 family is organized into long uninterrupted arrays and resembles previously reported tandem repeats located in the centromeres of human and Arabidopsis thaliana chromosomes. We characterized a large DNA fragment derived from a plant centromere and demonstrated that rice centromeres consist of complex DNA, including both highly and middle repetitive DNA sequences.

Base Sequence↗

Identification of a novel p53 functional domain that is necessary for mediating apoptosis.

The ability of p53 to induce apoptosis requires its sequence-specific DNA binding activity; however, the transactivation-deficient p53(Gln22-Ser23) can still induce apoptosis. Previously, we have shown that the region between residues 23 and 97 in p53 is necessary for such activity. In an effort to more precisely map a domain necessary for apoptosis within the N terminus, we found that deletion of the N-terminal 23 amino acids compromises, but does not abolish, p53 induction of apoptosis. Surprisingly, p53(Delta1-42), which lacks the N-terminal 42 amino acids and the previously defined activation domain, retains the ability to induce apoptosis to an even higher level than wild-type p53. A more extensive deletion, which eliminates the N-terminal 63 amino acids, renders p53 completely inert in mediating apoptosis. In addition, we found that both p53(Delta1-42) and p53(Gln22-Ser23) can activate a subset of cellular p53 targets. Furthermore, we showed that residues 53 and 54 are critical for the apoptotic and transcriptional activities of both p53(Delta1-42) and p53(Gln22-Ser23). Taken together, these data suggest that within residues 43-63 lie an apoptotic domain as well as another transcriptional activation domain. We therefore postulate that the apoptotic activity in p53(Gln22-Ser23) and p53(Delta1-42) is still transcription-dependent.

Apoptosis↗

HFE gene knockout produces mouse model of hereditary hemochromatosis.

Hereditary hemochromatosis (HH) is a common autosomal recessive disease characterized by increased iron absorption and progressive iron storage that results in damage to major organs in the body. Recently, a candidate gene for HH called HFE encoding a major histocompatibility complex class I-like protein was identified by positional cloning. Nearly 90% of Caucasian HH patients have been found to be homozygous for the same mutation (C282Y) in the HFE gene. To test the hypothesis that the HFE gene is involved in regulation of iron homeostasis, we studied the effects of a targeted disruption of the murine homologue of the HFE gene. The HFE-deficient mice showed profound differences in parameters of iron homeostasis. Even on a standard diet, by 10 weeks of age, fasting transferrin saturation was significantly elevated compared with normal littermates (96 +/- 5% vs. 77 +/- 3%, P < 0.007), and hepatic iron concentration was 8-fold higher than that of wild-type littermates (2,071 +/- 450 vs. 255 +/- 23 microg/g dry wt, P < 0.002). Stainable hepatic iron in the HFE mutant mice was predominantly in hepatocytes in a periportal distribution. Iron concentrations in spleen, heart, and kidney were not significantly different. Erythroid parameters were normal, indicating that the anemia did not contribute to the increased iron storage. This study shows that the HFE protein is involved in the regulation of iron homeostasis and that mutations in this gene are responsible for HH. The knockout mouse model of HH will facilitate investigation into the pathogenesis of increased iron accumulation in HH and provide opportunities to evaluate therapeutic strategies for prevention or correction of iron overload.

Animals↗

Regulation of the Hedgehog and Wingless signalling pathways by the F-box/WD40-repeat protein Slimb.

Members of the Hedgehog (Hh) and Wnt/Wingless (Wg) families of secreted proteins control many aspects of growth and patterning during animal development. Hh signal transduction leads to increased stability of a transcription factor, Cubitus interruptus (Ci), whereas Wg signal transduction causes increased stability of Armadillo (Arm/beta-catenin), a possible co-factor for the transcriptional regulator Lef1/TCF. Here we describe a new gene, slimb (for supernumerary limbs), which negatively regulates both of these signal transduction pathways. Loss of function of slimb results in a cell-autonomous accumulation of high levels of both Ci and Arm, and the ectopic expression of both Hh- and Wg- responsive genes. The slimb gene encodes a conserved F-box/WD40-repeat protein related to Cdc4p, a protein in budding yeast that targets cell-cycle regulators for degradation by the ubiquitin/proteasome pathway. We propose that Slimb protein normally targets Ci and Arm for processing or degradation by the ubiquitin/proteasome pathway, and that Hh and Wg regulate gene expression at least in part by inducing changes in Ci and Arm, which protect them from Slimb-mediated proteolysis.

Amino Acid Sequence↗

Involvement of the Src homology 2-containing tyrosine phosphatase SHP-2 in growth hormone signaling.

Growth hormone (GH) signaling requires activation of the GH receptor (GHR)-associated tyrosine kinase, JAK2. JAK2 activation by GH is believed to facilitate initiation of various pathways including the Ras, mitogen-activated protein kinase, STAT, insulin receptor substrate (IRS), and phosphatidylinositol 3-kinase systems. In the present study, we explore the biochemical and functional involvement of the Src homology 2 (SH2)-containing protein-tyrosine phosphatase, SHP-2, in GH signaling. GH stimulation of murine NIH 3T3-F442A fibroblasts, cells that homologously express GHRs, resulted in tyrosine phosphorylation of SHP-2. As assessed specifically by anti-SHP-2 coimmunoprecipitation and by affinity precipitation with a glutathione S-transferase fusion protein incorporating the SH2 domains of SHP-2, GH induced formation of a complex of tyrosine phosphoproteins including SHP-2, GHR, JAK2, and a glycoprotein with properties consistent with being a SIRP-alpha-like molecule. A reciprocal binding assay using IM-9 cells as a source of SHP-1 and SHP-2 revealed specific association of SHP-2 (but not SHP-1) with a glutathione S-transferase fusion incorporating GHR cytoplasmic domain residues 485-620, but only if the fusion was first rendered tyrosine-phosphorylated. GH-dependent tyrosine phosphorylation of SHP-2 was also observed in murine 32D cells (which lack IRS-1 and -2) stably transfected with the GHR. Further, GH-dependent anti-SHP-2 coimmunoprecipitation of the Grb2 adapter protein was detected in both 3T3-F442A and 32D-rGHR cells, indicating that biochemical involvement of SHP-2 in GH signaling may not require IRS-1 or -2. Finally, GH-induced transactivation of a c-Fos enhancer-driven luciferase reporter in GHR- and JAK2-transfected COS-7 cells was significantly reduced when a catalytically inactive SHP-2 mutant (but not wild-type SHP-2) was coexpressed; in contrast, expression of a catalytically inactive SHP-1 mutant allowed modestly enhanced GH-induced transactivation of the reporter in comparison with that found with expression of wild-type SHP-1. Collectively, these biochemical and functional data imply a positive role for SHP-2 in GH signaling.

3T3 Cells↗

Insulin-like growth factor-1 is a radial cell-associated neurotrophin that promotes neuronal recruitment from the adult songbird edpendyma/subependyma.

In the adult songbird forebrain, neurons continue to be produced from precursor cells in the forebrain ependymal/subependymal zone (SZ), from which they migrate upon radial guide fibers. The new neurons and their radial cell partners may coderive from a common SZ progenitor, which may be the radial cell itself. On this basis, we asked whether radial cells might provide trophic support for the migration or survival of newly generated neurons. We focused upon the insulin-like growth factors (IGFs) IGF-1 and IGF-2, which have previously been shown to support the survival and differentiation of neural progenitor cells. We found that IGF-1 immunoreactivity was expressed heavily by adult zebra finch radial cells and their fibers, with little expression otherwise. IGF-2, in contrast, was expressed by parenchymal astrocytes and exhibited little radial cell expression. Despite their distinct distributions, IGF-1 and IGF-2 exerted similar trophic effects on finch SZ cells in vitro; both greatly increased the number of neurons migrating from explants of the adult finch SZ, relative to explants raised in low-insulin, IGF-1-deficient media. However, neither factor extended neuronal survival. These results suggest that in neurogenic regions of the adult avian forebrain, IGF-1 acts as a radial cell-associated neuronal differentiation and/or departure factor, which may serve to regulate neuronal recruitment into the adult brain.

Animals↗

Surgical technique for vascularized ear transplantation in mice.

Traditionally, the mouse nonvascularized skin graft has been widely used in organ transplant research. There are, however, several limitations with this model, the main one being the different immune response of vascularized vs. nonvascularized grafts. We have recently developed a vascularized, orthotopic ear transplant model in mice. This model has several advantages that make it a useful tool to study many aspects of transplantation. The donor operation consists of harvesting the ear with intact arterial and venous pedicles. The arterial pedicle is dissected down to the common carotid artery with ligation of all branches except the auricular artery. The venous pedicle is based on the jugular vein with preservation of the auricular veins draining into the posterior facial vein. In the subsequent recipient operation, the graft is transplanted into an orthotopic position using the common carotid artery for arterial inflow and the jugular vein for venous outflow. We performed 16 such transplants (6 isografts, 5 allografts, and 5 xenografts), with a success rate of 94% (15/16). The donor operation time was 1.5 hours and the recipient operation time was 2.5 hours. The total time for anastamosis was 45 +/- 5 minutes. Serial biopsies were obtained on days 3, 5, and 7, and correlated with gross findings. In summary, this study illustrates that it is technically possible to transplant a mouse ear graft. The main advantage of this model is that it is a vascularized graft that can be visibly observed and easily biopsied, thus allowing for good correlation between gross and histological findings after transplantation. We plan to use this model further to study in detail the rejection patterns in an allograft and xenograft setting.

Animals↗