Biomedical subjects

X Deng

Publications and source records attributed to X Deng.

At least 127 records · Page 7Linked to original sources

PubMed1998

New Carbon-Silica Composite Adsorbents from Elutrilithe.

Carbon-silica composite adsorbents with high surface area and pore volume were prepared from natural elutrilithe. The elutrilithe was chemically activated with K2CO3 at 1123 K and then dissolved in water. The textural and adsorptive properties of the composite adsorbents can be adjusted by varying the pH and concentration of the sol mixture and the gel aging temperature. Composite adsorbents prepared at low concentration have high adsorption capacities for both water (43.4%) and cyclohexane (32.0%), exceeding those of ordinary commercial silica gel and active carbon. The adsorbents prepared at high concentration are more hydrophobic in nature, with adsorption capacities for water and cyclohexane of 18.5 and 41.5%, respectively. The composite adsorbents are resistant to repetitive adsorption and regeneration cycles. Copyright 1998 Academic Press.

Journal Article↗

PubMed1998

A functional role for mitochondrial protein kinase Calpha in Bcl2 phosphorylation and suppression of apoptosis.

Phosphorylation of Bcl2 at serine 70 may result from activation of a classic protein kinase C (PKC) isoform and is required for functional suppression of apoptosis by Bcl2 in murine growth factor-dependent cell lines (Ito, T., Deng, X., Carr, B., and May, W. S. (1997) J. Biol. Chem. 272, 11671-11673). Human pre-B REH cells express high levels of Bcl2 yet remain sensitive to the chemotherapeutic agents etoposide, cytosine arabinoside, and Adriamycin. In contrast, myeloid leukemia-derived HL60 cells express less than half the level of Bcl-2 but are >10-fold more resistant to apoptosis induced by these drugs. The mechanism responsible for this apparent dichotomy appears to involve a deficiency of mitochondrial PKCalpha since 1) HL60 but not REH cells contain highly phosphorylated Bcl2; 2) PKCalpha is the only classical isoform co-localized with Bcl2 in HL60 but not REH mitochondrial membranes; 3) the natural product and potent PKC activator bryostatin-1 induces mitochondrial localization of PKCalpha in association with Bcl2 phosphorylation and increased REH cell resistance to drug-induced apoptosis; 4) PKCalpha can directly phosphorylate wild-type but not phosphorylation-negative and loss of function S70A Bcl2 in vitro; 5) stable, forced expression of exogenous PKCalpha induces mitochondrial localization of PKCalpha, increased Bcl2 phosphorylation and a >10-fold increase in resistance to drug-induced cell death; and () PKCalpha-transduced cells remain highly sensitive to staurosporine, a potent PKC inhibitor. Furthermore, treatment of the PKCalpha transformants with bryostatin-1 leads to even higher levels of mitochondrial PKCalpha, Bcl2 phosphorylation, and REH cell survival following chemotherapy. While these findings strongly support a role for PKCalpha as a functional Bcl2 kinase that can enhance cell resistance to antileukemic chemotherapy, they do not exclude the possibility that another Bcl2 kinase(s) may also exist. Collectively, these findings identify a functional role for PKCalpha in Bcl2 phosphorylation and in resistance to chemotherapy and suggest a novel target for antileukemic strategies.

Antineoplastic Agents↗

PubMed1998

Characterization of human TCR Vbeta gene promoter. Role of the dodecamer motif in promoter activity.

During T-lymphocyte development, the T-cell antigen receptor (TCR) gene expression is controlled by its promoter and enhancer elements and regulated in tissue- and development stage-specific manner. To uncover the promoter function and to define positive and negative regulatory elements in TCR gene promoters, the promoter activities from 13 human TCR Vbeta genes were determined by the transient transfection system and luciferase reporter assay. Although most of the TCR Vbeta gene promoters that we tested are inactive by themselves, some promoters were found to be constitutively strong. Among them, Vbeta6.7 is the strongest. 5'-Deletion and fragmentation experiments have narrowed the full promoter activity of Vbeta6.7 to a fragment of 147 base pairs immediately 5' to the transcription initiation site. A decanucleotide motif with the consensus sequence AGTGAYRTCA has been found to be conserved in most TCR Vbeta gene promoters. There are three such decamer motifs in the promoter region of Vbeta6.7, and the contribution of each such motif to the promoter activity has been examined. Further site-directed mutagenesis analyses showed that: 1) when two Ts in the decamer were mutated, the promoter activity was totally abolished; 2) when two additional nucleotides 3' to the end of decamer were mutated, the promoter activity was decreased to two-thirds of the full level; and 3) when the element with the sequence AGTGATGTCACT was inserted into other promoters, the original weak promoters become very strong. Taken together, our data suggest that the positive regulatory element in Vbeta6.7 should be considered a dodecamer rather than a decamer and that it confers strong basal transcriptional activity on TCR Vbeta genes.

Alleles↗

PubMed1998

Fluid filtration across the arterial wall under flow conditions: is wall shear rate another factor affecting filtration rate?

The effect of flow on fluid filtration across an arterial wall was investigated in the canine common carotid artery. The arteries were cannulated in situ to maintain their in vivo length and endothelium intact. The excised vessels were pressurized at 120 mmHg through an overflow head-tank system that provided a constant flow rate to the perfused vessels. Filtration rates across the walls of the carotid arteries tested were measured under 4 different experimental conditions: 1) albumin-free Krebs solution under absent flow condition; 2) albumin-free Krebs solution with flow (148 +/- 8 ml/min); 3) Krebs solution containing 1.0 g/dl bovine serum albumin under absent flow condition; 4) Krebs solution containing 1.0 g/dl bovine serum albumin with flow (148 +/- 8 ml/min). Under absent flow conditions, the addition of albumin to the Krebs solution (1.0 g/dl) led to an approximate 25% drop in filtration rate (p < 0.001). It was found that fluid flow affected the filtration rate of the albumin solution, yet failed to affect the filtration rate of albumin-free solution across the arterial wall. The present study suggests that the change in filtration rate of the albumin solution under flow condition may indicate the change in the luminal surface concentration of albumin due to flow.

Animals↗

PubMed1998

Concentration polarization of low density lipoproteins (LDL) in the arterial system.

The atherogenic lipid concentration at the luminal surface of a blood vessel may vary according to its location in the arterial tree because of regional differences in wall shear rate, blood pressure, and vascular permeability. We therefore hypothesized that these local variations in the luminal surface lipid concentration may contribute to the localization of atherosclerosis. To verify this hypothesis, the transport of low-density lipoproteins from flowing blood to the arterial wall was studied numerically under both steady-state and pulsatile flow conditions. Numerical analysis predicted that "concentration polarization" of LDL may occur in the arterial system under these conditions. In contrast to steady-state flow conditions, the luminal surface LDL concentration varied with time in a cardiac cycle. However, its time-average value was slightly higher than the corresponding value under steady-state flow conditions. The time-average value of the luminal surface LDL concentration was 5 to 14% greater than the bulk concentration in a straight segment of an artery. The luminal surface LDL concentration at the arterial wall was flow-dependent, varying linearly with the filtration rate through the vessel wall and inversely with wall shear rate. This may therefore have some significant implications for the pathogenesis and localization of vascular disorders.

Animals↗

PubMed1998

Chromosomal localization and characterization of the stannin (Snn) gene.

Stannin is a protein that has been localized to trimethyltin-sensitive cell populations, and evidence suggests it plays a role in the toxic effects of organotins. In this study, we have isolated a mouse stannin genomic clone and have characterized the gene's intron-exon organization, promoter region, and chromosomal location. We have also isolated a partial human stannin cDNA clone and analyzed the open reading frame. The mouse genomic clone spans approximately 19 kb and consists of one intron and two exons. The splice site consensus sequence was maintained at all intron-exon junctions. Promoter analysis suggests that two putative promoter sites exist, each containing multiple regulatory elements and transcription factor-binding sites. Fluorescence in situ hybridization analysis localized stannin to mouse Chromosome (Chr) 16 at band A2. This region is homologous to the proximal region of human Chr 16 (16p13) to which stannin has been previously mapped. Sequence analysis revealed that the 264-bp open reading frame was identical between rat and mouse. The human sequence was 98% identical, with two amino acid substitutions near the c-terminal end of the peptide. These data suggest that stannin is highly conserved between species, and its unusual pattern of cellular expression may, in part, be explained via cell-specific promoters.

Amino Acid Sequence↗

PubMed1998

The influence of apoptosis on intestinal barrier integrity in rats.

BACKGROUND: Apoptosis is a critical step responsible for maintaining the cellular balance between proliferation and death and for controlling tumorigenesis. Although an increase in intestinal apoptotic cells has been considered to be associated with the pathogenesis of gastrointestinal injury, little is understood concerning the role of apoptosis in the development of intestinal barrier dysfunction. METHODS: Apoptosis induced by intraperitoneal injection of doxorubicin in rats was evaluated by transmission electron microscopy and the TUNEL histochemistry method. Treatment with deoxy-D-glucose (a glycolytic pathway inhibitor) or cycloheximide (a protein synthesis inhibitor) was performed after doxorubicin challenge. Passage of human serum albumin from blood to the intestinal interstitium and the intestinal lumen or from the intestine to the intestinal interstitium and blood was evaluated by means of albumin clearance. RESULTS: A significant increase in gut water content, albumin flux, and bidirectional clearance of albumin accompanied by apoptotic epithelial cell increase was noted in doxorubicin-challenged rats treated with saline. The increase in endothelial and epithelial permeability and the increase of apoptosis could partly be prevented by treatment with deoxy-D-glucose or cycloheximide. CONCLUSION: Doxorubicin-increased epithelial apoptosis within the intestine occurs simultaneously with increased bidirectional permeability of the intestinal barrier, probably associated with both glycolytic and protein synthesis pathways. Apoptosis may thus play a role in the pathogenesis of intestinal barrier dysfunction.

Animals↗

PubMed1998

Alterations in the functions of the reticuloendothelial and protease-antiprotease systems after intraperitoneal injection of zymosan in rats.

OBJECTIVE: To evaluate alterations in the function of the reticuloendothelial system (RES) and potential protective effects of pretreatment with the antioxidants: N-acetyl-L-cysteine (NAC) or dimethyl sulphoxide (DMSO), after intraperitoneal injection of zymosan (0.50 mg/g body weight) in rats. DESIGN: Experimental study. SETTING: University hospital, Sweden. ANIMALS: 81 male Sprague-Dawley rats. INTERVENTION: Intraperitoneal injection of either 4 ml saline or zymosan suspension (0.50 mg/g body weight). One hour before the intraperitoneal injection, 1 ml of saline, or a solution of NAC (150 mg/kg) or DMSO (80 mg/kg) were given intravenously. MAIN OUTCOME MEASURES: Systemic arterial pressure, packed cell volume, concentrations of plasma proteins and plasma protease inhibitors, uptake of 125I-labelled Escherichia coli in organs, blood clearance and body uptake rate of radiolabelled E. coli, and blood flow in organs at 3, 6, and 12 hours after injection. RESULTS: The uptake of radiolabelled E. coli in the liver, spleen and lungs decreased significantly from 3 hours onwards after zymosan challenge (p <(0.05). Blood clearance and body uptake rate also decreased significantly from 3 hours onwards (p < 0.05), but this did not correlate with the reduction in organ blood flow. Significant falls in plasma concentrations of prekallikrein (p < 0.01) and protease inhibitors (p <0.05) suggested possible contact-phase activation and activation of the kallikrein-kinin and fibrinolytic system. Pretreatment with NAC, and to a less extent DMSO, significantly prevented these alterations in RES function. CONCLUSION: Zymosan induced an impairment in RES function that was not initially associated with a reduction in blood flow. Plasma proteolytic activity seems to be involved in the impaired RES function. Pretreatment with NAC or DMSO effectively improved RES function.

Acetylcysteine↗

PubMed1998

Effect of a platelet-activating factor antagonist on pancreatitis-associated gut barrier dysfunction in rats.

Platelet-activating factor (PAF) may play a critical and primary role in the pathogenesis of acute pancreatitis and pancreatitis-associated distant organ injury. The present study evaluated the effect of a PAF antagonist, lexipafant (an (S)-4-methyl-2[methyl-imidazo[4,5-c]pyridin-1-ylmethyl)-benzene sulphonyl]-amino]pentanoic acid ethyl ester, BB-882; British Biotech Ltd.), on the potential prevention of gut barrier dysfunction, by measuring gut origin sepsis, bidirectional permeability of the intestinal barrier, and pancreatic capillary endothelial barrier integrity, in acute pancreatitis induced by intraductal infusion of 5% sodium taurodeoxycholate. Pancreatic endothelial permeability significantly increased in animals with acute pancreatitis, whereas pretreatment with lexipafant had a preventive effect (p < 0.05 vs. pancreatitis with saline). Similarly, alterations noted in hematocrit and plasma levels of lipase and calcium were counteracted by the PAF antagonist. It also prevented the increase in albumin leakage from blood to the mucosal interstitium and from blood to the intestinal lumen in acute pancreatitis. Albumin passage from the gut lumen to blood in animals with pancreatitis pretreated with saline increased from 3 h and on, and lexipafant prevented alterations in mucosal epithelial permeability. Bacterial translocation was commonly seen in pancreatitis, whereas only a few positive cultures were observed in pancreatitis animals given lexipafant. Microthrombosis in intestinal villi seemed less frequent after lexipafant pretreatment. We conclude that (a) PAF may play a role in the pathogenesis of pancreatitis-associated intestinal dysfunction, (b) PAF may be involved in the development of distant organ dysfunction by triggering endothelial barrier dysfunction, and (c) PAF antagonists may provide potential agents for preventing pancreatitis-associated gut barrier dysfunction.

Acute Disease↗

PubMed1998

The influence of intestinal ischemia and reperfusion on bidirectional intestinal barrier permeability, cellular membrane integrity, proteinase inhibitors, and cell death in rats.

Intestinal ischemia and reperfusion injury (I/R) is probably involved in the pathogenesis of intestinal barrier dysfunction, associated with the concomitant translocation of enteric bacteria and toxins and the potential development of multiple organ failure. The intestinal endothelial and epithelial layers play a major role preventing the entry of toxic substances from the gut, but the influence of protease-antiprotease systemic balance on these barrier functions and the relationship between epithelial DNA synthesis, apoptosis, and endothelial and epithelial barrier macromolecule permeability are not fully investigated. Endothelial and epithelial barrier macromolecular permeability, epithelial DNA synthesis, the endothelial and epithelial plasma membrane system, apoptosis and oncosis, plasma levels of proteinase inhibitors, and proenzymes were measured in rats subjected to 20 and 40 min intestinal ischemia and 1, 3, 6, or 12 h reperfusion. Endothelial permeability increased after both 20 and 40 min intestinal ischemia. Epithelial permeability significantly increased during 1-6 h reperfusion after 20 min ischemia and during 1-12 h reperfusion after 40 min ischemia. Epithelial DNA synthesis increased in animals with 20 min ischemia followed by 12 h reperfusion. Plasma levels of prekallikrein, C1-esterase inhibitor, and alpha1-macroglobulin were significantly lower following both 20 and 40 min ischemia from 3 h reperfusion and on. Apoptotic epithelial cells significantly increased in animals subjected to 20 min ischemia followed by 12 h reperfusion. The severity of reperfusion injury in the intestinal endothelial and epithelial barrier seems to correlate with the period of ischemia and the pathway of cell damage and death, together with proteinase-antiproteinase imbalance.

Albumins↗

PubMed1998

NO generation and action during changes in salt intake: roles of nNOS and macula densa.

Micropuncture studies of single nephrons have shown that macula densa solute reabsorption via a furosemide-sensitive pathway activates nitric oxide (NO) generation via neuronal NO synthase (nNOS). This pathway is enhanced during salt loading. We investigated the hypothesis that changes in NO generation via nNOS in the macula densa contribute to changes in whole kidney NO generation and action during alterations in salt intake. Groups of rats (n = 6-10) were equilibrated to high-salt (HS) or low-salt (LS) diets and were administered a vehicle (Veh), 7-nitroindazole (7-NI; a relatively selective inhibitor of nNOS), or furosemide (F; an inhibitor of macula densa solute reabsorption) with volume replacement. Compared with LS, excretion of the NO metabolites, NO2 plus NO3 (NOX) was increased during HS (LS: 9.0 +/- 0.5 vs. HS: 15.7 +/- 0.8 micromol/24 h; P < 0.001), but this difference was prevented by 7-NI (LS: 7.4 +/- 1.3 vs. HS: 9.4 +/- 1.6 micromol/24 h; NS). During nonselective blockade of NOS with NG-nitro-L-arginine methyl ester (L-NAME), renal vascular resistance (RVR) increased more in HS than LS (HS: +160 +/- 17 vs. LS: +83 +/- 10%; P < 0.001). This difference in response to nonselective NOS inhibition was prevented by pretreatment with 7-NI (HS: +28 +/- 6 vs. LS: +34 +/- 8%; NS) or F with volume replacement (HS: +79 +/- 11 vs. LS: +62 +/- 4%; NS). In conclusion, compared with salt restriction, HS intake increases NO generation and renal action that depend on nNOS and macula densa solute reabsorption.

Absorption↗

PubMed1998

[Relationship between osteoporosis and metabolism of calcium and bone].

Using metabolic balance test, bone mineral density measurement, animal models of osteoporosis, bone cell culture, we investigated the relationship between osteoporosis and the metabolism of calcium and bone. We found that the calcium intake was rather low in 20 healthy adults (480 mg per day); the average intestinal net absorption rate(%) of calcium in 124 healthy adult volunteers was 28.9(%), which increased gradually in recent 20 years (from 17.1% in 1978 to 40.6% in 1977), owing to improvement of dietetic structure. We conclude that the insufficiency of sex hormone and calcium are the main causes of osteoporosis. In bone cell culture, the whole process of bone remodelling was observed for 35 days continuously. Calcitonin damaging osteoclast was also investigated. Thus, we suggest new concept of bone remodelling coupling.

Adult↗

PubMed1998

[Detection of telomerase activity and its clinical significance in colonic cancers by PCR-ELISA].

Using the recently developed telomerase PCR-ELISA detection kit, the authors detected the telomerase activity in 12 paired colonic cancer biopsies. It was found that strong telomerase activity was detected in all of the 12 colonic cancer tissues but not in adjacent non-cancerous tissues. These results suggest that the detection of telomerase activity by the PCR-ELISA assay could be used as a supplementary means for the diagnosis of colonic cancer.

Biopsy↗

PubMed1998

[Pulmonary lymphangitic carcinomatosis].

OBJECTIVE: To explore the clinical manifestations of pulmonary lymphangitic carcinomatosis (PLC), to analyse its associated diagnostic methods, and to improve the understanding of PLC and its diagnosis. METHOD: Retrospective analysis of 4 cases of PLC and review of the literature. RESULT: The clinical manifestations of PLC include: (1) dyspnea and cough; (2) normal or restrictive pattern ventilation; (3) diffuse or local reticulonodular infiltrates in the lung like interstitial fibrosis and pleural effusion on chest radiograph; (4) CT and high-resolution CT (HRCT) scans reveal a beaded chain appearance caused by uneven thickening of the interlobular septa and pleural membrane, polygonal thickening of bronchovascular bundles, and mediastinal lymphadenopathy as well. CONCLUSION: These clinical data suggest that any manifestations similar to pulmonary interstitial fibrosis complicated with pleural effusion and paratracheal lymphadenopathy should be further differentiated from PLC by HRCT and pleural-lung tissue biopsy.

Adult↗

PubMed1998

[A study on the spectra of L-fucose].

The concentration of L-fucose will extraordinarily increase in urine in patients with early stage of cancer. It seems that this is a significant clue for early phase diagnosis of cancer. Unfortunately the sensitive detection of L-fucose is difficult. Thus we carried out researches on IR-spectrum, Raman spectrum, ultraviolet absorption spectrum and ultraviolet fluorescence spectrum. We compared the results from patients and healthy subjects. It is confirmed that the spectroscopic method, especially ultraviolet fluorescence spectrophotometry, may be suitable for early stage screening of some kinds of cancer. This test is rapid, inexpensive and painless.

Absorption↗

PubMed1997

Oncogenic c-Ki-ras but not oncogenic c-Ha-ras up-regulates CEA expression and disrupts basolateral polarity in colon epithelial cells.

Colon carcinomas commonly contain mutations in Ki-ras4B, but very rarely in Ha-ras, suggesting that different Ras isoforms may have distinct functions in colon epithelial cell biology. In an earlier study we had demonstrated that oncogenic Ki-ras4BVal-12, but not oncogenic Ha-rasVal-12, blocks the apicobasal polarization of colon epithelial cells by preventing normal glycosylation of the integrin beta1 chain of the collagen receptor. As a result, only the Ki-ras mutated cells exhibited altered cell to substratum attachment, whereas mutation of either Ras isoform activated mitogen-activated protein kinases. We have now asked whether intercellular adhesion proteins implicated in establishing basolateral polarity in colon epithelial cells are modulated by oncogenic Ki-Ras4BVal-12 proteins but not oncogenic Ha-RasVal-12 proteins. The embryonic adhesion protein carcinoembryonic antigen (CEA) was up-regulated on the mRNA and protein levels in each of three stable Ki-rasVal-12 transfectant lines but in none of three stable Ha-rasVal-12 transfectant lines. The elevated protein levels of CEA in Ki-ras4BVal-12 transfectant cells were decreased by blocking expression of Ki-ras4BVal-12 with antisense oligonucleotides. N-cadherin levels were decreased in only the Ki-ras transfectants, whereas E-cadherin levels were unchanged. Immunohistochemical analysis demonstrated that Ki-ras4BVal-12 transfectant cells did not polarize into cells with discrete apical and basal regions and so could not restrict expression of CEA to the apical region. These unpolarized cells displayed elevated levels of CEA all along their surface membrane where CEA mediated random, multilayered associations of tumor cells. This aggregation was both calcium-independent and blocked by Fab' fragments of anti-CEA monoclonal antibody col-1. Trafficking of the lysosomal cysteine protease cathepsin B may also be altered when cell polarity cannot be established. Ki-ras4BVal-12 transfectant cells expressed 2-fold elevated protein levels of the lysosomal cysteine protease cathepsin B but did not up-regulate cathepsin B mRNA expression. One function of oncogenic c-Ki-Ras proteins in colon cancer progression may be to up-regulate CEA and thus to prevent the lateral adhesion of adjacent colon epithelial cells that normally form a monolayer in vivo.

Carcinoembryonic Antigen↗

PubMed1997

Preparation and Characterization of Active Carbon Adsorbents for Wastewater Treatment from Elutrilithe

Active carbon adsorbents were prepared from natural elutrilithe by chemical activation with K2CO3. The effect of pyrolysis temperature and time and K2CO3/elutrilithe ratio on the surface area, porosity, and ash content of the adsorbents was studied. Various prior and post treatments have been tried to improve the quality of the adsorbents. An ideal active carbon adsorbent with a BET surface area of 1236 m2/g and a total pore volume of 0.679 cm3/g has been obtained. The adsorbent is hydrophobic in nature and exhibits large adsorption capacities for various phenolic compounds from aqueous solutions. Copyright 1997Academic Press

Journal Article↗

PubMed1997

Bcl-2 phosphorylation required for anti-apoptosis function.

The protooncogene Bcl-2 functions as a suppressor of apoptosis in growth factor-dependent cells, but a post-receptor signaling mechanism is not known. We recently reported that interleukin 3 (IL-3) and erythropoietin, or the protein kinase C activator bryostatin-1 (Bryo), not only suppresses apoptosis but also stimulates the phosphorylation of Bcl-2 (May, W. S., Tyler, P. G., Ito, T., Armstrong, D. K., Qatsha, K. A., and Davidson, N. E. (1994) J. Biol. Chem. 269, 26865-26870). To test whether phosphorylation is required for Bcl-2 function, conservative serine --> alanine mutations were produced at the seven putative protein kinase C phosphorylation sites in Bcl-2. Results indicate that the S70A Bcl-2 mutant fails to be phosphorylated after IL-3 or Bryo stimulation and is unable to support prolonged cell survival either upon IL-3 deprivation or etoposide treatment when compared with wild-type Bcl-2. In contrast, a Ser --> Glu mutant, S70E, which may mimic a potential phosphate charge, more potently suppressed the etoposide-induced apoptosis than wild type in the absence of IL-3. Since the loss of function S70A mutant can heterodimerize with its partner protein and death effector Bax, these findings demonstrate that Bcl-2:Bax heterodimerization is not sufficient and Bcl-2 phosphorylation is required for full Bcl-2 death suppressor signaling activity.

Alanine↗