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Biomedical subjects

J Zhu

Publications and source records attributed to J Zhu.

At least 397 records · Page 22Linked to original sources
PubMed1999

[Clinical study on keratoplasty with corneal cryopreservation].

PURPOSE: To evaluate the clinical application value of the corneal cryopreservation in keratonosus. METHODS: 32 patients with keratonosus treated by corneal transplantation were clinically observed. RESULTS: In 32 keratonosus cases, 59.37% (19 cases) of the grafts remained transparant; in 24 corneal ulcer preforation cases, 45.83% (11 cases) of the grafts were transparent, all eyeballs(100%) were remained. CONCLUSION: Corneal cryopreservation can be a practical, effective method in the treatment of keratonosus in district hospitals.

Adolescent↗
PubMed1999

[Quantitative analysis of Pt-Pd alloys using partition polynomial regression].

A new regression method was developed for X-ray microflurescence analysis of Pt-Pd alloys using X-ray tube excitation. Working curve is divided into four parts based on concentration of Pt in alloys. For each part, polynomial regression method is used to fit the curve. Results show that this procedure is superior to conventional method of polynomial regression which fitting the whole curve with one equation. Homogeneous level of element distribution in standard alloys is also investigated

English Abstract↗
PubMed1998

Partitioning of low molecular combination peptides in aqueous two-phase systems of poly(ethylene glycol) and dextran in the presence of small amounts of K2HPO4/KH2PO4 buffer at 293 K: experimental results and predictions.

Buffered aqueous two-phase systems are effective extraction systems for separating amphoteric hydrocarbons like, for example, polypeptides from aqueous phases. The design and basic engineering of such processes requires the knowledge of the liquid-liquid equilibrium. The study presented here aims to contribute to the development of methods to predict the partitioning of peptides in aqueous two-phase systems. Experimental results are reported for the partitioning of small amounts ( approximately 0.001 g solute per gram of solution) of low molecular combination peptides of glycine, L-glutamic acid, L-phenylalanine, and L-lysine (9 dipeptides, gly-glu, gly-phe, gly-lys, glu-gly, phe-gly, phe-glu, lys-gly, lys-glu, lys-phe; 7 tripeptides, gly-gly-phe, gly-phe-gly, glu-gly-phe, phe-gly-gly, lys-gly-lys, lys-glu-gly, lys-phe-lys) in aqueous two-phase systems of high molecular weight dextran (molecular weight about 500,000) and poly(ethylene glycol) (molecular weight about 6,000 and 35,000, respectively) in the presence of small amounts (about 0.05 mol/kg) of K2HPO4/KH2PO4 buffer at about 293 K. The new data are compared to predictions. Partition coefficients are predicted applying a group contribution excess Gibbs energy model. The model is an osmotic virial equation. It uses surface fractions to encounter for the probability of interactions between solutes. All model parameters were taken from the literature. They were determined exclusively from experimental data for the phase forming systems and for the partitioning of amino acids and their di- and tripeptides (containing only a single amino acid), but no experimental data for the partitioning of combinations peptides were used. In most cases predicted partition coefficients agree favourably with the experimental data.

Amino Acids↗
PubMed1998

Reprogramming of early embryonic blastomeres into endodermal progenitors by a Caenorhabditis elegans GATA factor.

The END-1 GATA factor has been implicated in specifying endoderm in Caenorhabditis elegans and is the earliest known zygotic protein expressed in the lineage of E, the clonal endoderm progenitor. We report that ubiquitous end-1 expression during a critical period in embryogenesis causes all non-endodermal lineages to produce endoderm instead of ectoderm and/or mesoderm. END-1 expression bypasses the requirement for maternal SKN-1 and the maternal Wnt signaling pathway in endoderm formation. This suggests that a primary function of these maternal factors is to regulate zygotic end-1 expression, which is then sufficient to initiate the entire program for endoderm development.

Animals↗
PubMed1998

Role of cAMP-dependent protein kinase A in activation of a voltage-sensitive release mechanism for cardiac contraction in guinea-pig myocytes.

1. Ionic currents and unloaded cell shortening were recorded from guinea-pig ventricular myocytes with single electrode voltage clamp techniques and video edge detection at 37 C. Patch pipettes (1-3 MOmega) were used to provide intracellular dialysis with pipette solutions. 2. Na+ currents were blocked with 200 microM lidocaine. Contractions initiated by the voltage-sensitive release mechanism (VSRM) and Ca2+-induced Ca2+ release (CICR) in response to L-type Ca2+ current (ICa,L) were separated with voltage clamp protocols. 3. Without 8-bromo cyclic adenosine 3',5'-monophosphate (8-Br-cAMP) in the pipette, small VSRM-induced contractions occurred transiently in only 13% of myocytes. In contrast, large ICa,L-induced contractions were demonstrable in 100% of cells. 4. Addition of 10 or 50 microM 8-Br-cAMP to the pipette increased the percentage of cells exhibiting VSRM contractions to 68 and 93%, respectively. With 50 microM 8-Br-cAMP, contractions initiated by the VSRM and ICa,L were not significantly different in amplitude. 5. 8-Br-cAMP-supported VSRM contractions had characteristics of the VSRM shown previously in undialysed myocytes. Cd2+ (100 microM) blocked ICa,L and ICa,L contractions but not VSRM contractions. 8-Br-cAMP-supported contractions exhibited steady-state inactivation with parameters characteristic of the VSRM, as well as sigmoidal contraction-voltage relations. 6. Without 8-Br-cAMP in the pipette, contraction-voltage relations determined with steps from a post-conditioning potential (Vpc) of either -40 or -65 mV were bell shaped, with a threshold near -35 mV. With 50 microM 8-Br-cAMP in the pipette, contraction-voltage relations from a Vpc of -65 mV were sigmoidal and the threshold shifted to near -55 mV. Contraction-voltage relations remained bell shaped in the presence of 8-Br-cAMP when the Vpc was -40 mV. 7. H-89, which inhibits cAMP-dependent protein kinase A (PKA), significantly reduced the amplitudes of VSRM contractions by approximately 84% with 50 microM 8-Br-cAMP in the pipette. H-89 also significantly reduced the amplitudes of peak ICa, L and ICa,L contractions, although to a lesser extent. 8. We conclude that intracellular dialysis with patch pipettes disrupts the adenylyl cyclase-PKA phosphorylation cascade, and that the VSRM requires intracellular phosphorylation to be available for activation. Intracellular dialysis with solutions that do not maintain phosphorylation levels inhibits a major mechanism in cardiac excitation- contraction coupling.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

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↗
PubMed1998

Inductive electron-withdrawal from ammonium ion headgroups of cationic lipids and the influence on DNA transfection.

We have prepared a panel of lipidic ammonium tetrafluoroborate salts that contain trifluoromethyl, trichloromethyl, and methyl groups attached to the headgroup. 19F-NMR analyses of the cationic lipid panel revealed that the differences in electron-withdrawal from the ammonium ion headgroup accounted for differences in ion-pairing. Exchange of the tetrafluoroborate counterion by complexation to DNA-phosphate of a reporter gene enabled us to probe the influence of inductive electron-withdrawal in cationic lipid-mediated DNA transfection. We tested the lipid panel for transfection activity in two cell lines. The results indicate that the inductive effects of electron-withdrawing functionality diminish transfection activity in modest (2-4-fold) increments. The present study suggests that the mechanism whereby poly(alcohol)- or poly(ether)-substituted headgroups improve DNA transfection is not based on electronic activation of the ammonium ion.

Adenocarcinoma↗
PubMed1998

Characterization of kappa-opioid receptor transcripts expressed by T cells and macrophages.

We have found that the immature T cell lines R1.1 and DPK and the macrophage lines P388D1 and WEHI-3 also express kappa-opioid receptor (KOR) mRNA. Characterization of the KOR transcripts in both brain tissue and these T cells has revealed both the normal full-length as well as a truncated form of the mRNA. Our results show that the truncated transcript lacks the second exon. Primary macrophages express this truncated form of the transcript in the absence of detectable levels of the full-length form. These results suggest a degree of heterogeneity in the expression of the opioid receptors which has not previously been reported.

Animals↗
PubMed1998

Resistance and susceptibility to experimental autoimmune neuritis in Sprague-Dawley and Lewis rats correlate with different levels of autoreactive T and B cell responses to myelin antigens.

Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated, inflammatory demyelinating disease of the peripheral nervous system (PNS) that serves as a model for Guillain-Barré syndrome (GBS) in humans. Various mouse and rat strains show different susceptibilities to EAN that can be induced by immunization with bovine PNS myelin (BPM) + Freund's complete adjuvant (FCA). We examined PNS-induced T and B cell responses and cytokine protein production as well as mRNA expression to study the mechanisms behind susceptibility to EAN in Lewis rats and resistance in Sprague-Dawley (SD) rats. Lewis rats with EAN have elevated PNS myelin-reactive interferon-gamma (IFN-gamma) production, TNF-alpha mRNA expression, and increased B cell responses to PNS myelin antigens, but low PNS myelin-reactive transforming growth factor-beta (TGF-beta) and interleukin (IL)-10 mRNA expression in lymph node mononuclear cells (MNC). In contrast, resistance to EAN in SD rats is associated with reduced BPM and P2 peptide-reactive IFN-gamma production, TNF-alpha mRNA expression, and suppressed B cell responses to PNS myelin antigens as well as up-regulation of TGF-beta and IL-10 mRNA expression. Resistance to EAN is also associated with low-grade inflammation or absence of histological evidence of EAN. These results suggest that differential autoreactive T and B cells responses to PNS myelin antigens are strain specific, and the susceptibility to EAN is related to quantitative rather than qualitative differences in distribution between proinflammatory and anti-inflammatory cytokines.

Animals↗
PubMed1998

Linomide suppresses chronic-relapsing experimental autoimmune encephalomyelitis in DA rats.

Linomide (quinoline-3-carboxamide) is a synthetic immunomodulator that suppresses several experimental autoimmune diseases. Here we report the effects of Linomide on chronic progressive and/or relapsing experimental autoimmune encephalomyelitis (PR-EAE), a CD4+ T cell mediated animal model of multiple sclerosis (MS). PR-EAE induced in DA rats by inoculation with homogenized guinea pig spinal cord and Freund's complete adjuvant, was strongly suppressed by Linomide administered daily subcutaneously from the day of inoculation. Linomide dose-dependently delayed the interval between immunization and onset of clinical PR-EAE, reduced severity and relapse of clinical PR-EAE, and shortened clinical PR-EAE. These clinical effects were associated with the down-modulation of CNS antigen-induced T cell responses and production of proinflammatory cytokines (IFN-gamma and TNF-alpha) as well as with upregulation of IL-4 (except in spleen MNC), IL-10 and TGF-beta in both spleen MNC and the spinal cord. These effects indicate that Linomide can suppress PR-EAE and may mediate its suppressive effects by regulation of cytokines.

Adjuvants, Immunologic↗
PubMed1998

Senescence of human fibroblasts induced by oncogenic Raf.

The oncogenes RAS and RAF came to view as agents of neoplastic transformation. However, in normal cells, these genes can have effects that run counter to oncogenic transformation, such as arrest of the cell division cycle, induction of cell differentiation, and apoptosis. Recent work has demonstrated that RAS elicits proliferative arrest and senescence in normal mouse and human fibroblasts. Because the Raf/MEK/MAP kinase signaling cascade is a key effector of signaling from Ras proteins, we examined the ability of conditionally active forms of Raf-1 to elicit cell cycle arrest and senescence in human cells. Activation of Raf-1 in nonimmortalized human lung fibroblasts (IMR-90) led to the prompt and irreversible arrest of cellular proliferation and the premature onset of senescence. Concomitant with the onset of cell cycle arrest, we observed the induction of the cyclin-dependent kinase (CDK) inhibitors p21(Cip1) and p16(Ink4a). Ablation of p53 and p21(Cip1) expression by use of the E6 oncoprotein of HPV16 demonstrated that expression of these proteins was not required for Raf-induced cell cycle arrest or senescence. Furthermore, cell cycle arrest and senescence were elicited in IMR-90 cells by the ectopic expression of p16(Ink4a) alone. Pharmacological inhibition of the Raf/MEK/MAP kinase cascade prevented Raf from inducing p16(Ink4a) and also prevented Raf-induced senescence. We conclude that the kinase cascade initiated by Raf can regulate the expression of p16(Ink4a) and the proliferative arrest and senescence that follows. Induction of senescence may provide a defense against neoplastic transformation when the MAP kinase signaling cascade is inappropriately active.

Animals↗
PubMed1998

Effects of mutations in the human uncoupling protein 3 gene on the respiratory quotient and fat oxidation in severe obesity and type 2 diabetes.

Human uncoupling protein 3 (UCP3) is a mitochondrial transmembrane carrier that uncouples oxidative ATP phosphorylation. With the capacity to participate in thermogenesis and energy balance, UCP3 is an important obesity candidate gene. A missense polymorphism in exon 3 (V102I) was identified in an obese and diabetic proband. A mutation introducing a stop codon in exon 4 (R143X) and a terminal polymorphism in the splice donor junction of exon 6 were also identified in a compound heterozygote that was morbidly obese and diabetic. Allele frequencies of the exon 3 and exon 6 splice junction polymorphisms were determined and found to be similar in Gullah-speaking African Americans and the Mende tribe of Sierra Leone, but absent in Caucasians. Moreover, in exon 6-splice donor heterozygotes, basal fat oxidation rates were reduced by 50%, and the respiratory quotient was markedly increased compared with wild-type individuals, implicating a role for UCP3 in metabolic fuel partitioning.

Alternative Splicing↗
PubMed1998

The potentiation of the effect of radiation treatment by intratumoral delivery of cisplatin.

PURPOSE: To compare potentiation of the effects of acute or fractionated radiation by cisplatin when the drug was delivered intratumorally by implanted biodegradable polymer, by intraperitoneal injection, or by intraperitoneal osmotic pump. METHODS AND MATERIALS: Radiation was delivered to a mouse tumor (RIF-1) either in a single dose or in a fractionated regime in conjunction with cisplatin delivered either as a bolus injection, with an osmotic pump, or with a biodegradable polymer rod containing cisplatin. The osmotic pump was implanted in the intraperitoneal cavity of the mouse while the polymer implants were placed directly in the tumor. As the polymer degrades, the drug is released at the treatment site leading to high local concentrations. The osmotic pump, in contrast, leads to prolonged systemic exposure to the drug at low concentrations. Tumor growth delay (TGD) was used as an endpoint in these experiments. RESULTS: The most effective treatment protocol, in terms of potentiating the effects of radiation was cisplatin delivered by polymer implanted 2 days before an acute dose of radiation (growth modification factor [DMF] = 2.2). Comparison of single and multifraction regimes where polymer implant was on the same day as the commencement of treatment showed greater potentiation of the effect of fractionated than of acute radiation treatment with the DMF for fractionated treatment remaining relatively constant (1.5-1.9) for 5, 8, and 12 fraction treatments. Cisplatin delivered via the osmotic pump did not deliver a high enough dose of cisplatin to produce therapeutic effect in this mouse tumor model and had little impact on response to treatment. CONCLUSIONS: Our results indicated that cisplatin delivered intratumorally by biodegradable polymer implant was effective in potentiating the effect of both acute and fractionated radiation. For the fractionated treatments the effect was maintained with increasing fraction numbers and treatment time.

Animals↗
PubMed1998

Differences between DNA base pair stacking energies are conserved over a wide range of ionic conditions.

Base pair stacking free energy parameters in a low ionic strength solvent were determined from an analysis of DNA fragments using temperature gradient gel electrophoresis (TGGE). Transition midpoint temperatures (Tu) were determined for the first melting domain (52 +/- 4 bp) of 16, 339 bp DNAs that differed from each other by single base pair substitutions. The data were combined with previously obtained Tu data from 17 similar DNAs that had single base pair changes at different sites [Ke, S. H., and Wartell, R. M. (1995) Biochemistry 34, 4593-4599]. The Tu values were used to evaluate free energy differences (deltaDeltaG) between 31 pairs of DNAs. Linear equations relating the deltaDeltaG values to changes in base pair stacking were analyzed by singular value decomposition (SVD) to determine the 10 nearest neighbor free energy parameters. The order of stability of the parameters, TA < AT < AA < AG < GT approximately TC approximately TG < CC < GC approximately CG, was essentially the same as the hierarchy determined in 1 M Na+ [Allawi, H. T., and SantaLucia, J., Jr. (1997) Biochemistry 36, 10581-10594]. The experimental free energy differences were in good agreement with predictions made using nearest-neighbor parameters determined from several previous studies conducted in medium or high salt concentrations. Conversely the parameters determined in the current study produced good predictions of free energy differences previously determined from 59 DNA oligomers in 1 M Na+. The results indicate that differences between base pair stacking energies are conserved across a wide range of ionic conditions, and in both oligomer and polymer DNA contexts.

Bacillus subtilis↗
PubMed1998

Astrocytes induce hyporesponses of myelin basic protein-reactive T and B cell function.

We have isolated infiltrating mononuclear cells (inMNC) and lymph node MNC (lnMNC) from Lewis rats with actively induced experimental allergic encephalomyelitis (EAE), and compared their responses to myelin basic protein (MBP). MBP-induced proliferation and MBP-specific IgG secreting cells were lower in inMNC compared to lnMNC, while MBP-reactive IFN-gamma secreting cells in inMNC were higher. Using an in vitro culture system, we observed that astrocytes derived from newborn Lewis rats not only suppressed T cell proliferation and IFN-gamma production but also reduced MBP-specific IgG production by B cells. Astrocyte-derived soluble factor (s), rather than direct cell-to-cell interactions, seems to be responsible for the inhibitory effect. Supernatants from IFN-gamma-stimulated astrocytes exhibited stronger suppressive effects than supernatants from unstimulated astrocytes, whereas supernatants from microglia did not cause downregulation of T and B cell functions. These results indicate that astrocytes are major effector cells in inhibiting functions of MBP-reactive T and B cells. Astrocytes down-regulated expression of ICAM-1 and MHC class II in lnMNC, but did not induce apoptosis of lnMNC. The results in the present study do not exclude the possibility that astrocytes induce T cell apoptosis in a cognate fashion. Taken together, the inhibitory properties of astrocytes may contribute to the confinement of inflammatory lesions in multiple sclerosis and EAE. Our report compares immunoreactivities of inMNC and lnMNC in EAE and elucidates the role of astrocytes in the inactivation of MBP-reactive T and B cells.

Animals↗
PubMed1998

Effects of phosphorylation on function of the Rad GTPase.

Rad, Gem and Kir possess unique structural features in comparison with other Ras-like GTPases, including a C-terminal 31-residue extension that lacks typical prenylation motifs. We have recently shown that Rad and Gem bind calmodulin in a Ca2+-dependent manner via this C-terminal extension, involving residues 278-297 in human Rad. This domain also contains several consensus sites for serine phosphorylation, and Rad is complexed with calmodulin-dependent protein kinase II (CaMKII) in C2C12 cells. Here we show that Rad serves as a substrate for phosphorylation by CaMKII, cAMP-dependent protein kinase (PKA), protein kinase C (PKC) and casein kinase II (CKII) with stoichiometries in vitro of 0.2-1.3 mol of phosphate/mol of Rad. By deletion and point mutation analysis we show that phosphorylation by CaMKII and PKA occurs on a single serine residue at position 273, whereas PKC and CKII phosphorylate multiple C-terminal serine residues, including Ser214, Ser257, Ser273, Ser290 and Ser299. Incubation of Rad with PKA decreases GTP binding by 60-70%, but this effect seems to be independent of phosphorylation, as it is observed with the Ser273-->Ala mutant of Rad containing a mutation at the site of PKA phosphorylation. The remainder of the serine kinases have no effect on Rad GTP binding, intrinsic GTP hydrolysis or GTP hydrolysis stimulated by the putative tumour metastasis suppressor nm23. However, phosphorylation of Rad by PKC and CKII abolishes the interaction of Rad with calmodulin. These findings suggest that the binding of Rad to calmodulin, as well as its ability to bind GTP, might be regulated by the activation of several serine kinases.

Binding Sites↗
PubMed1998

Salicortin: a repeat-attack new-mechanism-based Agrobacterium faecalis beta-glucosidase inhibitor.

Salicortin, a natural product abundant in most members of the Salicaceae family, is a mechanism-based inactivator of Agrobacterium faecalis beta-glucosidase. Inactivation is delayed in the presence of competitive inhibitors, thereby demonstrating the requirement for an enzyme-bound salicortin before inactivation. Product studies suggest that inactivation proceeds via a quinone methide intermediate formed by the fragmentation of the aglycone of salicortin while it is bound to the enzyme. Tryptic digest and HPLC/MS studies confirm the role of quinone methide attack and also show that the enzyme undergoes multiple modifications. In addition, when the inactivation was run in the presence of a mutant inactive form of the enzyme, HPLC/MS analyses clearly showed no modification of the mutant enzyme, demonstrating that the quinone methide does not exist in free solution and suggesting that inactivation is active-site directed.

1-Deoxynojirimycin↗