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Biomedical subjects

Bing Ma

Publications and source records attributed to Bing Ma.

At least 37 records · Page 2Linked to original sources
PubMed2005

[Model for predicting survival of patients with severe virus hepatitis and its clinical application].

OBJECTIVE: To study prospectively the short-time survival of patients with severe virus hepatitis using model of severe liver diseases (MSLD) established by our previous study. METHODS: One hundred and three patients with severe hepatitis were included by cohort study. Of them, there were 85 patients with severe chronic hepatitis patients, 10 acute and 8 subacute severe hepatitis patients, respectively. The follow-up endpoint was 6 months. The cutoff score of the MSLD was determined by receiver operating characteristic cure (ROC) statistic analysis, and the survival of severe hepatitis patients in 2 weeks, 4 weeks, 3 months and 6 months were estimated by Kaplan-Meier statistic analysis. RESULTS: The cutoff MSLD score for predicting survival was 5. The survival curves of group A (total MSLD score< or =4) was significantly better than group B (total MSLD score> or =5, P<0.000). After treatment for 2 weeks, the survival rate in 2 weeks and 4 weeks was 37.9% and 3.5%, respectively, if MSLD score had no change or increased. The survival rate in 2 weeks, 4 weeks and 3 months was respectively 61.5%, 15.4%, 5.8% if the MSLD score decreased 1. Then, the survival in 2 weeks, 4 weeks, 3 months and 6 months was respectively 95.0%, 90.0%, 63.9% and 52.4% if MSLD score decreased 2 or more. CONCLUSION: It is suggested that MSLD may be valuable in predicting 6-month survival of severe virus hepatitis patients. It may be used to determine the efficacy of medical treatment and to guide clinical decision.

Adolescent↗
PubMed2005

[Study on the changes in the distribution and chemical states of the hepatic intra-and extra-cellular sodium ion in the rats with severe burns at early stage].

OBJECTIVE: To investigate the changes in the distribution and chemical states of the hepatic intra- and extra-cellular sodium ion in the rats with severe burns, so as to provide guidance for fluid resuscitation at early postburn stage. METHODS: Nineteen adult male Sprague-Dawley (SD) rats were employed in the study and were randomly divided into control (n = 12) and burn (n = 7) groups. The changes in the longitudinal (T1) and transverse (T2) relaxation times of hepatic intra-cellular and extra-cellular sodium in the two groups were studied with 23Na NMR spectroscopy and a shift reagent. RESULTS: After infusion of the shift reagent,the extra-cellular sodium content in rat liver decreased by 17%, with obvious increase in fast T2 component (P < 0.01), indicating an increase in the fraction of Na+ binding sites in the extra-cellular space. The characteristics of relaxation of intra-cellular sodium remained unchanged despite a 57% increment in intra-cellular sodium content. CONCLUSION: The deficiency of sodium as a permeable molecule might be related to the postburn movement of hypertonic sodium from extra-cellular to intra-cellular space. The results indicated that it is reasonable to administer high concentration of sodium in fluid resuscitation during the first 24 postburn hours.

Animals↗
PubMed2004

The protein profile of acetazolamide-treated sera in mice bearing Lewis neoplasm.

The aim of the present research is to analyze the proteome of neoplasm serum before and after treated with acetazolamide (20, 40, 80 mg kg(-1) d(-1) for 3 days p.o.). The Lewis lung carcinoma mice were used and carried out a comprehensive proteomic analysis by using the technologies of high-resolution two-dimensional polyacrylamide gel electrophoresis (2D PAGE) and mass spectrometry (MS). The results showed that the acetazolamide could dramatically reduce the lung metastasis and primary tumor growth. Its most potent inhibition rate on lung metastases was reach to 77.7% at the dose of 80 mg kg(-1) d(-1). The two dimension electrophoresis and software analysis reveal 393 protein spots in control gel, 385 protein spots were detected in treated gel and matched 209 protein spots with control gel, indicating that intensive changes had occurred during the process of treatment. Two obviously different spots were cut off from gel and for the peptide mass fingerprinting. Data base searching showed the two proteins' peptide much more mach with Histone H2B fragment and Ubc-like protein CROC1 fragment. The results suggest that acetazolamide has a strong anti-tumor and anti-metastasis effect on Lewis-lung-carcinoma. The mechanism may be related to its regulation on plenty of proteins, in particular, on upregulation of H2B and CROC-1 expression of postreplicational DNA repair related protein in serum.

Acetazolamide↗
PubMed2004

The C10/CCL6 chemokine and CCR1 play critical roles in the pathogenesis of IL-13-induced inflammation and remodeling.

IL-13 is a potent stimulator of inflammation and tissue remodeling that plays a key role in the pathogenesis of a wide variety of human disorders. To further understand these responses, studies were undertaken to define the role(s) of the chemokine C10/CCL6 in the pathogenesis of IL-13-induced alterations in the murine lung. IL-13 was a very potent stimulator of C10/CCL6 mRNA and protein, and IL-13-induced inflammation, alveolar remodeling, and compliance alterations were markedly ameliorated after C10/CCL6 neutralization. Treatment with anti-C10/CCL6 decreased the levels of mRNA encoding matrix metalloproteinase-2 (MMP-2), MMP-9, and tissue inhibitor of metalloproteinase-4 (TIMP-4) in lungs from wild-type mice. C10/CCL6 neutralization also decreased the ability of IL-13 to stimulate the production of monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, MMP-2, MMP-9, and cathepsins-K, -L, and -S and the ability of IL-13 to inhibit alpha1-antitrypsin. In accord with these findings, a targeted null mutation of CCR1, a putative C10/CCL6 receptor, also decreased IL-13-induced inflammation and alveolar remodeling and caused alterations in chemokines, proteases, and antiproteases comparable to those seen after C10/CCL6 neutralization. These C10/CCL6 and CCR1 manipulations did not alter the production of transgenic IL-13. These studies demonstrate that IL-13 is a potent stimulator of C10/CCL6 and highlight the importance of C10/CCL6 and signaling via CCR1 in the pathogenesis of the IL-13-induced pulmonary phenotype. They also describe a C10/CCL6 target gene cascade in which C10/CCL6 induction is required for optimal IL-13 stimulation of selected chemokines (monocyte chemoattractant protein-1 and MIP-1alpha) and proteases (MMP-2, MMP-9, and cathepsins-K, -L, and -S) and the inhibition of alpha1-antitrypsin.

Animals↗
PubMed2004

Sensitivity of [11C]N-methylpyrrolidinyl benzilate ([11C]NMPYB) to endogenous acetylcholine: PET imaging vs tissue sampling methods.

Administration of phenserine, an acetylcholinesterase inhibitor, raises endogenous brain acetylcholine levels and has been previously shown to reduce in vivo binding of the muscarinic cholinergic receptor antagonist [(11)C]N-methylpyrrolidinyl benzilate ([(11)C]NMPYB) in the awake rat brain. In this study, phenserine pretreatment was studied in both awake and isoflurane-anesthetized rats using the techniques of ex vivo dissection or in vivo microPET imaging. In ex vivo dissection experiments, a statistically significant 10% inhibition of [(11)C]NMPYB binding could be demonstrated in both awake and anesthetized animals after phenserine pretreatment, showing no deleterious effect of using isoflurane anesthesia. However, microPET imaging in anesthetized animals failed to successfully demonstrate inhibition of [(11)C]NMPYB binding following the identical phenserine treatment protocol. These results demonstrate that in small numbers of subjects ex vivo dissection may be a more sensitive experimental method for determining small changes of in vivo radiotracer binding in this model of neurotransmitter competition for brain receptor sites.

Acetylcholine↗
PubMed2004

Gene expression of early hypertrophic scar tissue screened by means of cDNA microarrays.

BACKGROUND: Hypertrophic scar is an excessive healing response that often follows thermal injury. The most outstanding morphologic change is the overdeposition of collagen, which is caused by imbalance between synthesis and metabolism of collagen. Previous studies also found that transforming growth factor-beta was the key factor controlling scar formation. However, neither anti-transforming growth factor-beta nor other methods could completely control scar formation and contraction. This fact suggests a multifactorial cause. Fortunately, cDNA microarray throws light on the general alteration at the gene level, and thus could allow us to find some new clues for understanding scar formation and contraction. METHODS: In this article, we report the results obtained from the scanning of gene expression of hypertrophic scar by means of cDNA microarray. Five cases of early human postburn hypertrophic scars were selected. Total tissue RNA was extracted from each hypertrophic scar sample and the corresponding uninjured region skin tissue; mRNA was further purified by Oligotex and then was reversely transcribed to cDNAs with the incorporation of fluorescent dUTP to prepare the hybridization probes. The mixed probes were hybridized to the cDNA microarray containing 4,096 genes on a type of chemical material-coated glass slide. After high-stringent washing, the hybridized slides were scanned for fluorescent signal detection. Then, the expression and distribution of cytoskeletal genes such as alpha-smooth muscle actin (alpha-SMA) gene; fibroblast tropomyosin TM30(pl) gene; vimentin gene; profilin gene; and BM40 gene of hypertrophic scar at 3, 6, 9, and 12 months age were further quantitatively studied by in situ hybridization or immunohistochemistry. RESULTS: Our data indicated that there were 94 genes overexpressed and 3 genes down-regulated in early postburn hypertrophic scar. These altered genes were related to proto-oncogenes, apoptosis, immune regulatory genes, cytoskeletal elements, metabolism, and so forth. We also found that the detected cytoskeletal gene expression was much more intense at all time points than the control group. Consistent with clinical observation, cytoskeletal genes reached a peak at an early stage and gradually decreased. CONCLUSION: Our study implied that multiple genes are involved in scar formation and contraction. Interferon is an autosecreted cytokine that might be responsible for self-control of overgrowth of cells in wounds. The early period of hypertrophic scar formation might be a good time for preventing overgrowth and contraction of hypertrophic scar by gene therapy.

Actins↗
PubMed2004

Inhibitory effect of topiramate on Lewis lung carcinoma metastasis and its relation with AQP1 water channel.

AIM: To study the effect of topiramate on tumor metastasis and its relation with aquaporin 1 (AQP1) water channel. METHODS: Lewis lung carcinoma metastatic model was used to determine the effect of topiramate on tumor growth and metastasis. Colorimetric estimation was used to investigate the action of topiramate on carbonic anhydrase (CA) activity. Western blotting and immunohistochemical analysis were used to study the influence of topiramate on AQP1 water channel expression in lungs or tumor tissues of mice bearing Lewis lung carcinoma. RESULTS: Treatment with topiramate (120 mg/kg/d, ig for 20 d) reduced the growth of primary tumor significantly (P<0.05). Its inhibitory rate of metastasis was 81.25 %. Topiramate inhibited CA activity in lungs of mice in a dose-dependent manner. Topiramate apparently decreased AQP1 protein expression and immunostaining in lungs or in tumor microvessel endothelial cells of mice. CONCLUSION: Suppression of AQP1 water channel expression may be an important pathway for the inhibitory effect of topiramate on tumor metastasis.

Animals↗
PubMed2004

Effects of acetazolamide and anordiol on osmotic water permeability in AQP1-cRNA injected Xenopus oocyte.

AIM: To study the effects of acetazolamide and anordiol on osmotic water permeability in aquaporin 1 (AQP1)-cRNA injected Xenopus oocyte and their mechanisms. METHODS: AQP1 gene constructed in pBluescript was transcripted into cRNA in vitro and then the cRNA was injected in Xenopus oocytes. The effects of acetazolamide and anordiol on the water transport function of AQP1 were observed by assaying the osmotic swelling of oocytes. In addition, their effects on protein expression of AQP1 were quantitatively investigated by Western blotting method. RESULTS: After incubation for 15 min or 72 h, acetazolamide, a carbonic anhydrase inhibitor, equally reduced the water permeability of AQP1-cRNA injected oocyte in a dose-dependent manner. After incubation for 72 h, anordiol, an antiestrogen with partial estrogenic activity, reduced the osmotic water permeability dose dependently as well; however, no discernable action was observed after incubation with anordiol for 15 min. The Western blotting analysis showed that acetazolamide did not influence the protein expression of AQP1. However, after incubation for 72 h with anordiol (10 micromol/L), the quantity of AQP1 in the oocyte membrane was decreased dramatically (P<0.05). CONCLUSION: Both acetazolamide and anordiol inhibited the osmotic water permeability of AQP1-cRNA injected oocyte, but their mechanisms were different. Acetazolamide functionally inhibited the osmotic water permeability of AQP1, whereas anordiol primarily decreased the amount of AQP1 protein in the oocyte membrane.

Acetazolamide↗
PubMed2004

Acetazolamide inhibits aquaporin-1 protein expression and angiogenesis.

AIM: To study effects of acetazolamide on aquaporin-1 (AQP(1)) protein expression and angiogenesis. METHODS: Establishing Lewis-lung-carcinoma model, the localization of AQP(1) in tumor tissues was investigated by immunohistochemical methods; The biological activity of acetazolamide was detected by endothelial cells proliferation test (MTT) assay and chorioallantoic membrane (CAM) vascular inhibition test. RESULTS: Immunohistochemical localization of AQP(1) in mice tumor was labeled in capillaries, post capillary venules endothelial cells. After being treated with acetazolamide, the number of capillaries and post capillary venules was significantly decreased in tumor tissue. Acetazolamide showed significant inhibitory effect on angiogenesis in CAM and endothelial cell proliferation. CONCLUSION: Acetazolamide might be identified and developed as one of potential lead compounds for a new therapeutic intervention in inhibiting cancer angiogenesis.

Acetazolamide↗
PubMed2004

[Experimental study on the antibacterial effects of zirconium phosphate gauze loaded with silver on the common bacteria on rat burn wound].

OBJECTIVE: To investigate the antibacterial effects of zirconium phosphate gauze loaded with silver on rat burn wounds seeded with commonly seen bacteria. METHODS: Wistar rats were employed in the study and were scalded and infected. The minimum inhibition concentration (MIC) and minimum bactericidal concentration (MBC) of zirconium phosphate loaded with silver were determined by double dilution in tubes. The effect on wound healing and the subeschar bacterial count of the rat burn wounds were observed after the wounds had been covered by gauze loaded with zirconium phosphate and silver, and also with the gauze which has been rinsed for 20 times. RESULTS: The MIC of silver loaded zirconium phosphate on Staphylococcus aureus, Pseudomonas aeruginosa and E. coli were 8, 8 and 16 mg/L, respectively, while the MBC were 16, 8 and 32 mg/L, respectively. The subeschar bacterial count in the burn wounds with the gauze with silver loaded zirconium phosphate was ten times lower than that in those which were treated with gauze with SD-Ag and 100 times lower than that with ordinary gauze. But there was no difference in the bacterial count between the wounds which were treated with fresh gauze with silver loaded zirconium phosphate and that with the gauze which has been rinsed for 20 times (P > 0.05). Furthermore, wound healing seemed to be better with the gauze with silver loaded zirconium phosphate when compared with those by the other two kinds of gauze. CONCLUSION: The silver loaded zirconium phosphate was found to be bacteriocidal against bacteria commonly seen in the burn wounds.

Animals↗
PubMed2003

C-terminal amino acids of Helicobacter pylori alpha1,3/4 fucosyltransferases determine type I and type II transfer.

The alpha1,3/4 fucosyltransferase (FucT) enzyme from Helicobacter pylori catalyzes fucose transfer from donor GDP-beta-l-fucose to the GlcNAc group of two series of acceptor substrates in H. pylori lipopolysaccharide: betaGal1,3betaGlcNAc (Type I) or betaGal1,4betaGlcNAc (Type II). Fucose is added either in alpha1,3 linkage of Type II acceptor to produce Lewis X or in alpha1,4 linkage of Type I acceptor to produce Lewis A, respectively. H. pylori FucTs from different strains have distinct Type I or Type II substrate specificities. FucT in H. pylori strain NCTC11639 has an exclusive alpha1,3 activity because it recognizes only Type II substrates, whereas FucT in H. pylori strain UA948 can utilize both Type II and Type I acceptors; thus it has both alpha1,3 and alpha1,4 activity, respectively. To identify elements conferring substrate specificity, 12 chimeric FucTs were constructed by domain swapping between 11639FucT and UA948FucT and characterized for their ability to transfer fucose to Type I and Type II acceptors. Our results indicate that the C-terminal region of H. pylori FucTs controls Type I and Type II acceptor specificity. In particular, the highly divergent C-terminal portion, seven amino acids DNPFIFC at positions 347-353 in 11639FucT, and the corresponding 10 amino acids CNDAHYSALH at positions 345-354 in UA948FucT, controls the Type I and Type II acceptor recognition. This is the opposite of mammalian FucTs where acceptor preference is determined primarily by the N-terminal residues in the hypervariable stem domain.

Amino Acid Sequence↗
PubMed2003

Performance of a 41 x 41 cm2 amorphous silicon flat panel x-ray detector designed for angiographic and R&F imaging applications.

We measured the physical imaging performance of a 41 x 41 cm2 amorphous silicon flat panel detector designed for angiographic and R&F imaging applications using methods from the emerging IEC standard for the measurement of detective quantum efficiency (DQE) in digital radiographic detectors. Measurements on 12 production detectors demonstrate consistent performance. The mean DQE at the detector center is about 0.77 at zero frequency and 0.27 at the Nyquist frequency (2.5 cycles/mm) when measured with a 7 mm of Al HVL spectrum at about 3.6 microGy. The mean MTF at the center of the detector for this spectrum is 0.24 at the Nyquist frequency. For radiographic operation all 2048 x 2048 detector elements are read out individually. For fluoroscopy, the detector operates in two 30 frame per second modes: either the center 1024 x 1024 detector elements are read out or the entire detector is read out with 2 x 2 pixel binning. A model was developed to predict differences in performance between the modes, and measurements demonstrate agreement with the model. Lag was measured using a quasi-equilibrium exposure method and was found to be 0.044 in the first frame and less than 0.007 after 1 s. We demonstrated that it is possible to use the lag data to correct for temporal correlation in images when measuring DQE with a fluoroscopic imaging technique. Measurements as a function of position on the detector demonstrate a high degree of uniformity. We also characterized dependences on spectrum, exposure level, and direction. Finally, we measured the DQE of a current state of the art image intensifier/CCD system using the same method as for the flat panel. We found the image intensifier system to have lower DQE than the flat panel at high exposure levels and approximately equivalent DQE at fluoroscopic levels.

Angiography↗
PubMed2003

Transgenic modeling of interleukin-13 in the lung.

Interleukin (IL)-13 is a key cytokine in asthma pathogenesis. We used constitutive and inducible overexpression transgenic mice to characterize the mechanisms by which IL-13 causes phenotypic alterations in the lung. These studies demonstrated that chemokine receptor-2, transforming growth factor-beta(1), and IL-11 play an important role in the regulation of inflammation and remodeling in the IL-13-treated lung. The study results also demonstrated that IL-13 induces vascular endothelial growth factor, which causes bronchial circulation neovascularization in the murine airway. Last, it was demonstrated that IL-13 induces adenosine accumulation and that adenosine in turn stimulates IL-13 elaboration. These approaches validated in vivo genetic targets against which therapies can be directed to selectively regulate aspects of the IL-13 phenotype.

Animals↗
PubMed2003

[An experimental study on the role of indirect antigen presentation pathway on the immunogenetic of epidermal cells].

OBJECTIVE: To explore the role of indirect antigen presentation pathway on the immunogenecity of epidermal cells. METHODS: Human epidermal cells (HEC), allogeneic human peripheral blood lymphocytes (PBL) and mononuclear cells (PBM, including monocytes) were isolated and cultured in vitro. HECs were transfected by human-originated CTLA4Ig-adenovirus vector. The CTLA4Ig expression was observed. Allogeneic PBLs or PBMs were added to the transfected and non-transfected HECs with simple cultured PBLs and PBMs as the control. The proliferation of PBL and PBM was determined by (3)H-TdR incooperation. RESULTS: HECs could be successfully transfected by CTLA4Ig-adenovirus vector and expressed corresponding proteins. The non-transfected HECs could stimulate slight proliferation of allogeneic PBLs (P < 0.05) and stimulate remarkable proliferation of PBMs (including monocytes) (P < 0.05). The proliferation reaction of PBLs and PBMs decreased significantly (P < 0.05) after being stimulated by HEC which was modulated by CTLA4Ig genes. CONCLUSION: Indirect antigen presentation pathway might play important roles in the HEC immunogenicity which could be evidently inhibited by CTLA4Ig.

Adenoviridae↗
PubMed2003

[Differential protein analysis in rat renal proximal tubule epithelial cells in response to acetazolamide and its relation with the inhibition of AQP1].

AIM: To study the endogenous mechanism for the inhibition of aquaporin-1 expression in rat renal proximal tubule epithelial cells in response to acetazolamide. METHODS: Primary cultured rat renal proximal tubule epithelia cells were divided into two groups: one was subjected to 1 x 10(-5) mol.L-1 acetazolamide, the other served as normal control. When grown to sub-confluency, the cells were disintegrated to perform isoelectrofocusing electrophoresis in order to find the differential proteins induced by the acetazolamide treatment. The differential proteins were defined by peptide mass fingerprinting technology. RESULTS: Two differential proteins were found in the cell disintegrant. The pI 3.8 protein was reduced after treatment, which showed 21.4% similarity with the brush border membrane myosin from rat brain and testis, and 27% with glycogen phosphorylase; The pI 5.5 protein was increased on the contrary, with 20% similarity to phosphatidylinositol transfer protein alpha isoform. CONCLUSION: Acetazolamide inhibited AQP1 expression probably by affecting the expression of pI 3.8 and pI 5.5 proteins.

Acetazolamide↗
PubMed2002

IL-13-induced chemokine responses in the lung: role of CCR2 in the pathogenesis of IL-13-induced inflammation and remodeling.

IL-13 stimulates inflammatory and remodeling responses and contributes to the pathogenesis of human airways disorders. To further understand the cellular and molecular events that mediate these responses, we characterized the effects of IL-13 on monocyte chemotactic proteins (MCPs) and compared the tissue effects of transgenic IL-13 in mice with wild-type (+/+) and null (-/-) CCR2 loci. Transgenic IL-13 was a potent stimulator of MCP-1, -2, -3, and -5. This stimulation was not specific for MCPs because macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, MIP-2, MIP-3alpha, thymus- and activation-regulated chemokine, thymus-expressed chemokine, eotaxin, eotaxin 2, macrophage-derived chemokines, and C10 were also induced. The ability of IL-13 to increase lung size, alveolar size, and lung compliance, to stimulate pulmonary inflammation, hyaluronic acid accumulation, and tissue fibrosis, and to cause respiratory failure and death were markedly decreased, whereas mucus metaplasia was not altered in CCR2(-/-) mice. CCR2 deficiency did not decrease the basal or IL-13-stimulated expression of target matrix metalloproteinases or cathepsins but did increase the levels of mRNA encoding alpha1-antitrypsin, tissue inhibitor of metalloproteinase-1, -2, and -4, and secretory leukocyte proteinase inhibitor. In addition, the levels of bioactive and total TGF-beta(1) were decreased in lavage fluids from IL-13 transgenic mice with -/- CCR2 loci. These studies demonstrate that IL-13 is a potent stimulator of MCPs and other CC chemokines and document the importance of MCP-CCR2 signaling in the pathogenesis of the IL-13-induced pulmonary phenotype.

Animals↗
PubMed2002

Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure.

Interleukin (IL)-13, a key mediator of Th2-mediated immunity, contributes to the pathogenesis of asthma and other pulmonary diseases via its ability to generate fibrosis, mucus metaplasia, eosinophilic inflammation, and airway hyperresponsiveness. In these studies, we compared surfactant accumulation in wild-type mice and mice in which IL-13 was overexpressed in the lung. When compared with littermate controls, transgenic animals showed alveolar type II cell hypertrophy under light and electron microscopy. Over time, their alveoli also filled with surfactant in a pulmonary alveolar proteinosis pattern. At the same time, prominent interstitial fibrosis occurs. Bronchoalveolar lavage fluid from these mice had a three- to sixfold increase in surfactant phospholipids. Surfactant proteins (SP)-A, -B, and -C showed two- to threefold increases, whereas SP-D increased 70-fold. These results indicate that IL-13 is a potent stimulator of surfactant phospholipid and surfactant accumulation in the lung. IL-13 may therefore play a central role in the broad range of chronic pulmonary conditions in which fibrosis, type II cell hypertrophy, and surfactant accumulation occur.

Animals↗