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Biomedical subjects

X Ma

Publications and source records attributed to X Ma.

At least 199 records · Page 11Linked to original sources
PubMed1999

[The extraction of DNA from milligram amounts of wild mountain ginseng tissues].

OBJECTIVE: To keep wild mountain ginseng, a rare medicinal remedy, as intact as possible when extracting DNA from it, a new way to extract DNA has been explored. METHOD: The CTAB method was improved and a simple and direct way was developed. RESULT: From 0.001 g of dried samples of ginseng root DNA was obtained in an amount up to 2.25 micrograms. CONCLUSION: The RAPD fingerprinting generated by this DNA is as good as that by CTAB method. This new method may also be used for extraction of other precious Chinese medicinal materials.

DNA, Plant↗
PubMed1999

[Complete overdenture retained with implants and bar-clip attachments].

OBJECTIVE: To sum up and evaluate the applied experience and applied effects of implants and bar-clip attachments in complete overdenture. METHODS: Bar-clip attachments were used as a super structure of implant to manufacture complete overdenture in three designs: mucosa, implant-mucosa, and implant supporting way. The retentive force of the overdenture was measured with measuring instrument of retentive force of prosthesis. RESULTS: All three designs could obtain good retentive effect, specially implant-mucosa supporting and implant supporting designs, which were of more better stability and supporting effect; 2-3 nelon clips could supply 10-15 N retentive force to the overdenture. CONCLUSION: The complete overdenture retained with implant and bar-clips attachments is a very effective way for restoration of endtulous patients, which should be applied more popularly.

Dental Implants↗
PubMed1999

[Separation of p-aminobenzenearsonic acid and its oxide by ion-pair reversed-phase high performance liquid chromatography].

To study the separation of p-aminobenzenearsonic acid (PABAA) and its oxide, p-aminophenylarsine oxide (PAPAO), both the absorption spectra were scanned at the wavelengths from 200 nm to 380 nm. PABAA had absorption maximum at 254 nm and PAPAO 258 nm. The effects of salt concentration, column temperature, methanol and ion-pair agent concentrations on the capacity factor were investigated. Compounds of high polarity showed almost no retention on reversed-phase column; as the volume fraction of the methanol decreased from 90% to 10%, the retention time of PABAA gradually increased with broad peak, and partially eluted when methanol volume fraction being below 20%. With temperature rising, the retention time of PABAA was decreased. But PABAA capacity factor can be increased by selecting an appropriate salt concentration for the mobile phase. The cetyltrimethyl and tetrabutyl ammonium ions were separately added as ion-pair agents to the mobile phase containing methanol in phosphate buffer of 10 mmol/L, the changes of retention time were observed. The mechanism of retention based on reversed phase ion-pair model is proposed. Besides, the retention behaviour is also influenced by size exclusion in stationary phase as well as polar interactions with residual silanol group on the silica surface.

Arsanilic Acid↗
PubMed1999

[Influence of the synthetic peptide recognized by neutralizing antibody on IFN-induced biological responses].

OBJECTIVE: The influence of synthetic peptide WLDPRH on IFN-induced biologic activity was studied. METHODS: Based on our earlier studies in which two peptides were recognized by neutralizing antibody from the hexapeptide library displayed on the phage, one of the peptides synthesized, with amino acid sequence WLDPRH. RESULTS: Computer-building approach showed that the synthetic peptide WLDPRH exhibited structural homology with LoopAB (29-35), the binding domain of type I IFN receptor. In the competitive ELISA studies, the synthetic peptide WLDPRH in 25 micrograms/ml could inhibit IFN binding neutralizing antibody 4C1. IFN-induced antiviral assay showed that the protective effects of suboptimal dose (20-70 pg/ml) of IFN were increased from 40% to 86% in the presence of the synthetic peptide WLDPRH and 1.4 micrograms/ml of the synthetic peptide WLDPRH was the lowest dose with the best protection. But potentiating effect on IFN-induced growth inhibition was fewer noticeable in 1.4 micrograms/ml of synthetic peptide. CONCLUSION: The results indicated that synthetic peptide WLDPRH can mimic the structure and activity of Loop AB in the IFN molecule and can be applied to immunotherapy as well as the mimic minimolecular design of IFN.

Antibodies, Monoclonal↗
PubMed1999

[Study on laser flash spectroscopy of laser-induced interaction of DNA and polynucleotides with SO4*-].

The interactions of DNA and polynucleotides (poly[G],poly[A] and poly[C]) with SO4*- were investigated by 248 nm laser flash photolysis. The results show that, the reactions of poly[G] or poly[A] with SO4*- yield predominantly the corresponding one-electron-oxidated base radicals. With poly[C], it is suggested that SO4*- radical reacts predominantly by addition to the base moiety to produce C5-yl and C6-yl sulphate radical adducts,and subsequently H-abstraction yields C2'-sugar radical. The predominant species resulting from the reaction of DNA with SO4*- is DNA guanyl radical.

DNA↗
PubMed1999

[Study on laser flash spectroscopy of processes of photoionization of tyrosine: pH effects].

The processes of photoionization of tyrosine on three different pH value solutions were investigated by 248 nm laser flash photolysis. The results showed that the processes of photoionization of tyrosine were affected by pH value of the solution. With pH value increasing, the molecule number of photoionization increases via a monophotonic process, and decreases via a biphotonic process. Furthermore, the pH effect of photoionization of tyrosine resulting from deprotonation of phenolic hydroxyl group in alkaline solution was demonstrated.

Hydrogen-Ion Concentration↗
PubMed1998

Preparation, Characterization, and Catalytic Properties of Polymer-Stabilized Ruthenium Colloids.

Poly(N-vinyl-2-pyrrolidone) (PVP)-stabilized ruthenium colloids were prepared by NaBH4 reduction at room temperature and characterized by transmission electron microscopy and x-ray photoelectron spectra. The average diameters of the colloids were 1.3-1.8 nm with final sigma = 0.4-0.7 nm with respect to the preparation conditions. The PVP-stabilized ruthenium colloids were used as catalysts in the hydrogenations of cyclooctene and n-heptene and the selective hydrogenation of citronellal to citronellol. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

The developmentally regulated avian protein IFAPa-400 is transitin.

Transitin and IFAPa-400 are developmentally regulated high M(r) proteins expressed transiently in early chick embryogenesis. Both are associated with radially oriented fibers in the developing CNS and with various neural and myogenic tissues before their down-regulation at later stages. Previous studies have shown that IFAPa-400 colocalized and copurified with intermediate filament proteins and recent molecular cloning has indicated that transitin is a member of this family of cytoskeletal proteins. Here, we provide evidence that IFAPa-400 and transitin are the same protein. The sequence of a composite cDNA corresponding to more than 700 amino acids of IFAPa-400 carboxy-terminal extremity is identical to that of transitin. Both proteins exhibit identical apparent M(r) and isoelectric point. Immunopurified IFAPa-400 reacts with different antibodies to transitin and vice-versa. The patterns of expression of both proteins show a perfect coincidence at the tissue level. At the subcellular level, most antibodies to IFAPa-400/transitin decorate a typical intermediate filament network. However, monoclonal antibody A2B11, at the origin of transitin identification, exhibits a staining more typical of a cortical component, suggesting that different populations of transitin exist within the cell.

Animals↗
PubMed1998

A novel role for ursodeoxycholic acid in inhibiting apoptosis by modulating mitochondrial membrane perturbation.

The hydrophilic bile salt ursodeoxycholic acid (UDCA) protects against the membrane-damaging effects associated with hydrophobic bile acids. This study was undertaken to (a) determine if UDCA inhibits apoptosis from deoxycholic acid (DCA), as well as from ethanol, TGF-beta1, Fas ligand, and okadaic acid; and to (b) determine whether mitochondrial membrane perturbation is modulated by UDCA. DCA induced significant hepatocyte apoptosis in vivo and in isolated hepatocytes determined by terminal transferase-mediated dUTP-digoxigenin nick end-labeling assay and nuclear staining, respectively (P < 0.001). Apoptosis in isolated rat hepatocytes increased 12-fold after incubation with 0.5% ethanol (P < 0.001). HuH-7 cells exhibited increased apoptosis with 1 nM TGF-beta1 (P < 0. 001) or DCA at >/= 100 microM (P < 0.001), as did Hep G2 cells after incubation with anti-Fas antibody (P < 0.001). Finally, incubation with okadaic acid induced significant apoptosis in HuH-7, Saos-2, Cos-7, and HeLa cells. Coadministration of UDCA with each of the apoptosis-inducing agents was associated with a 50-100% inhibition of apoptotic changes (P < 0.001) in all the cell types. Also, UDCA reduced the mitochondrial membrane permeability transition (MPT) in isolated mitochondria associated with both DCA and phenylarsine oxide by > 40 and 50%, respectively (P < 0.001). FACS(R) analysis revealed that the apoptosis-inducing agents decreased the mitochondrial transmembrane potential and increased reactive oxygen species production (P < 0.05). Coadministration of UDCA was associated with significant prevention of mitochondrial membrane alterations in all cell types. The results suggest that UDCA plays a central role in modulating the apoptotic threshold in both hepatocytes and nonliver cells, and inhibition of MPT is at least one pathway by which UDCA protects against apoptosis.

Animals↗
PubMed1998

Molecular mechanisms of the induction of IL-12 and its inhibition by IL-10.

Exogenously added IL-10 rapidly inhibited Staphylococcus aureus- or LPS-induced cytokine mRNA expression in human PBMCs and monocytes, with a maximal effect observed when IL-10 was added from 20 h before until 1 h after the addition of the inducers. Nuclear run-on assays revealed that the inhibition of IL-12 p40, IL-12 p35, and TNF-alpha was at the gene transcriptional level and that the addition of IL-10 to S. aureus- or LPS-treated PBMCs did not affect mRNA stability. The inhibitory activity of IL-10 was abrogated by cycloheximide (CHX), suggesting the involvement of a newly synthesized protein(s). The addition of CHX at 2 h before S. aureus or LPS also inhibited the accumulation of IL-12 p40 mRNA, but did not inhibit IL-12 p35 and TNF-alpha mRNA. This finding suggests that p40 transcription is regulated through a de novo synthesized protein factor(s), whereas the addition of CHX at 2 h after S. aureus activation caused superinduction of the IL-12 p40, IL-12 p35, and TNF-alpha genes. These results indicate that in human monocytes, the mechanism(s) of IL-10 suppression of both IL-12 p40 and IL-12 p35 genes is primarily seen at the transcriptional level, and that the induction of the IL-12 p40 and p35 genes have different requirements for de novo protein synthesis.

Animals↗
PubMed1998

Synergistic regulation of the human interleukin-12 p40 promoter by NFkappaB and Ets transcription factors in Epstein-Barr virus-transformed B cells and macrophages.

Monocytes/macrophages produce interleukin-12 (IL-12) in response to pathogenic stimulation, whereas most Epstein-Barr virus-transformed (EBV+) B cells constitutively secrete IL-12. The molecular mechanism regulating the constitutive IL-12 gene expression in EBV+ B cells has not been addressed. In this study, using the EBV+ B cell line RPMI-8866, we localized to the human IL-12 p40 promoter two essential cis elements, the NFkappaB site and the Ets site. The NFkappaB site was shown to interact with members of the NFkappaB family: p50 and c-Rel. The Ets site constitutively bound a multi-component Ets-2-containing complex. While the NFkappaB and Ets sites appear equally critical for inducible p40 promoter activity in macrophage cell lines, NFkappaB plays a more dominant role in the constitutive p40 promoter activity in EBV+ B cells. Transient expression of Ets-2 and c-Rel in B, T, and monocytic cell lines synergistically activated the IL-12 p40 promoter, apparently overcoming the requirement for cell type- or stimulant-specific transcription factors. These data provide new evidence that full activation of the human IL-12 p40 promoter may result primarily from the interplay between NFkappaB and Ets family members.

B-Lymphocytes↗
PubMed1998

Potent suppression of IL-12 production from monocytes and dendritic cells during endotoxin tolerance.

Endotoxin tolerance, the down-regulation of a subset of endotoxin-driven responses after an initial exposure to endotoxin, may provide protection from the uncontrolled immunological activation of acute endotoxic shock. Recent data suggest, however, that the inhibition of monocyte/macrophage function associated with endotoxin tolerance can lead to an inability to respond appropriately to secondary infections in survivors of endotoxic shock. IL-12 production by antigen-presenting cells is central to the orchestration of both innate and acquired cell-mediated immune responses to many pathogens. IL-12 has also been shown to play an important role in pathological responses to endotoxin. We therefore examined the regulation of IL-12 during endotoxin tolerance. Priming doses of lipopolysaccharide ablate the IL-12 productive capacity of primary human monocytes. This suppression of IL-12 production is primarily transcriptional. Unlike the down-regulation of TNF-alpha under such conditions, the mechanism of IL-12 suppression during endotoxin tolerance is not dependent upon IL-10 or transforming growth factor-beta, nor is IL-12 production rescued by IFN-gamma or granulocyte-macrophage colony-stimulating factor. Of note, human dendritic cells also undergo endotoxin tolerance, with potent down-regulation of IL-12 production. Endotoxin tolerance-related suppression of IL-12 production provides a likely mechanism for the anergy seen during the immunological paralysis which follows septic shock.

Cells, Cultured↗
PubMed1998

Chronic effects of traumatic brain injury on hippocampal vesicular acetylcholine transporter and M2 muscarinic receptor protein in rats.

Experimental traumatic brain injury (TBI) produces cholinergic neurotransmission deficits that may contribute to chronic spatial memory deficits. Cholinergic neurotransmission deficits may be due to presynaptic alterations in the storage and release of acetylcholine (ACh) or from changes in the receptors for ACh. The vesicular ACh transporter (VAChT) mediates accumulation of ACh into secretory vesicles, and M2 receptors can modulate cholinergic neurotransmission via a presynaptic inhibitory feedback mechanism. We examined the effects of controlled cortical impact (CCI) injury on hippocampal VAChT and M2 muscarinic subtype receptor protein levels at four time points: 1 day, 1 week, 2 weeks, and 4 weeks following injury. Rats were anesthetized and surgically prepared for controlled cortical impact injury (4 m/s, 2.5- to 2.9-mm depth) and sham surgery. Animals were sacrificed and coronal sections (35 micro(m) thick) were cut through the dorsal hippocampus for VAChT and M2 immunohistochemistry. Semiquantitative measurements of VAChT and M2 protein in hippocampal homogenates from injured and sham rats were assessed using Western blot analysis. Immunohistochemistry showed no obvious changes in VAChT and M2 immunoreactivity at 1 day and 1 week postinjury. At 2 and 4 weeks postinjury, an increase in hippocampal VAChT protein and a corresponding loss of hippocampal M2 protein was observed compared to sham controls. Consistent with these results, Western blot analyses at 4 weeks postinjury demonstrated a 40-50% increase in VAChT and a 25-30% decrease in M2. These changes may represent a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission chronically after TBI, by upregulating the storage capacity and subsequent release of ACh and downregulating presynaptic inhibitory receptors.

Acetylcholine↗
PubMed1998

I-2190A is a potent immunosuppressive drug for vascularized heart transplantation in rats.

The effect of a new immunosuppressant-I-2190A was tested in a rodent heart allograft model. Grafts were transplanted to recipients heterotopically. There were 5 groups: group 1 received no immunosuppressive agents; group 2 was given CsA (2.0 mg/kg, i.p.); group 3 was administered I-2190A (0.1 mg/kg, i.p.) in carboxymethyl cellulose (CMC); group 4 received injection of I-2190A (0.5 mg/kg, i.p. in CMC); group 5 received the combination treatment of I-2190A (0.1 mg/kg) and CsA (2.0 mg/kg). Immunosuppressants were discontinued 14 days after operation. No statistically significant difference in grafts median survival time (MST) was found between group 2 (9.5 days) and group 1 (9 days). The MSTs of grafts in group 3 (22 days, P < 0.05), group 4 (> 100 days, P < 0.01) and group 5 (> 100 days, P < 0.01) were significantly prolonged compared with control group 1 (9 days). Our results suggest that I-2190A is a potent immunosuppressant able to significantly prolong heart allograft survival in rats after a short time treatment, Low-dose I-2190A could potentiate the effect of sub-therapeutic dose of CsA as well.

Animals↗
PubMed1998

Tumor cell responses to IFNgamma affect tumorigenicity and response to IL-12 therapy and antiangiogenesis.

Expression of a dominant negative mutant IFNgammaR1 in murine SCK and K1735 tumor cells rendered them relatively unresponsive to IFNgamma in vitro and more tumorigenic and less responsive to IL-12 therapy in vivo. IL-12 induced histologic evidence of ischemic damage only in IFNgamma-responsive tumors, and in vivo Matrigel vascularization assays revealed that while IFNgamma-responsive and -unresponsive tumor cells induced angiogenesis equally well, IL-12 and its downstream mediator IFNgamma only inhibited angiogenesis induced by the responsive cells. IL-12 induced angiogenesis inhibitory activity in the responsive cells, which may be attributable to production of the chemokine IP-10. Thus, IL-12 and IFNgamma inhibit tumor growth by inducing tumor cells to generate antiangiogenic activity.

Animals↗