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Biomedical subjects

X Q Yu

Publications and source records attributed to X Q Yu.

At least 37 records · Page 2Linked to original sources
PubMed1999

IL-1 up-regulates osteopontin expression in experimental crescentic glomerulonephritis in the rat.

Osteopontin (OPN) is a macrophage chemotactic and adhesion molecule that acts to promote macrophage infiltration in rat anti-glomerular basement membrane (GBM) glomerulonephritis. The present study investigated the role of interleukin-1 (IL-1) in the up-regulation of renal OPN expression in this disease model. Accelerated anti-GBM glomerulonephritis was induced in groups of six rats. Animals were treated by a constant infusion of the IL-1 receptor antagonist or saline (control) over days -1 to 14 (induction phase) or days 7 to 21 (established disease). In normal rat kidney, OPN was expressed in a few tubules (<5%) and absent from glomeruli. During the development of rat anti-GBM disease (days 7 to 21), there was substantial up-regulation of OPN mRNA and protein expression in glomeruli (>5 cells per glomerular cross-section) and tubular epithelial cells (50-75% OPN-positive). Up-regulation of OPN expression was associated with macrophage accumulation within the kidney, severe proteinuria, loss of renal function, and severe histological damage including glomerular crescentic formation and tubulointerstitial fibrosis. In contrast, IL-1 receptor antagonist treatment of either the induction phase of disease or established disease significantly reduced OPN mRNA and protein expression in glomeruli (/75-85%, P < 0.001) and tubules (/45-60%, P < 0.001). The reduction in OPN expression was associated with significant inhibition of macrophage accumulation and progressive renal injury. In vitro, the addition of IL-1 to the normal rat tubular epithelial cell line NRK52E up-regulated OPN mRNA and protein levels, an effect that was dose-dependent and inhibited by the addition of IL-1 receptor antagonist, thus demonstrating that IL-1 can act directly to up-regulate renal OPN expression. In conclusion, this study provides in vivo and in vitro evidence that IL-1 up-regulates OPN expression in experimental kidney disease and support for the argument that inhibition of OPN expression is one mechanism by which IL-1 receptor antagonist treatment suppresses macrophage-mediated renal injury.

Animals↗
PubMed1999

Immulectin, an inducible C-type lectin from an insect, Manduca sexta, stimulates activation of plasma prophenol oxidase.

Immulectin, a C-type lectin from the tobacco hornworm, Manduca sexta, was cloned from a larval fat body cDNA library. The immulectin cDNA encodes a 309 residue polypeptide. Immulectin synthesis was induced by injection of killed gram-positive or gram-negative bacteria or yeast. After injection of bacteria, immulectin mRNA appeared in fat body and immulectin protein was detected in hemolymph. Immulectin contains two carbohydrate recognition domains. The carboxyl-terminal carbohydrate recognition domain is most similar (36% identity) to a lipopolysaccharide-binding protein from the American cockroach, Periplaneta americana. It also shares 26-35% identity to carbohydrate recognition domains of various mammalian C-type lectins. Two immulectin isoforms were identified in the hemolymph of bacteria-injected larvae. Recombinant immulectin agglutinated gram-positive and gram-negative bacteria and yeast. Addition of recombinant immulectin to M. sexta plasma stimulated activation of phenol oxidase. A combination of immulectin with lipopolysaccharide from E. coli activated phenol oxidase more rapidly and to a higher level than immulectin alone, whereas lipopolysaccharide by itself had little effect on phenol oxidase activation. Immulectin synthesized in response to bacterial or fungal infection may help to trigger protective responses in M. sexta in a manner similar to mannose-binding protein, a C-type lectin that functions in the mammalian innate immune system.

Adipose Tissue↗
PubMed1999

Structure of a paralytic peptide from an insect, Manduca sexta.

Paralytic peptide 1 (PP1) from a moth, Manduca sexta, is a 23-residue peptide (Glu-Asn-Phe-Ala-Gly-Gly-Cys-Ala-Thr-Gly-Tyr-Leu-Arg-Thr-Ala-Asp-Gly-Arg -Cys-Lys-Pro-Thr-Phe) that was first found to have paralytic activity when injected into M. sexta larvae. Recent studies demonstrated that PP1 also stimulated the spreading and aggregation of a blood cell type called plasmatocytes and inhibited bleeding from wounds. We determined the solution structure of PP1 by two-dimensional 1H NMR spectroscopy to begin to understand structural-functional relationships of this peptide. PP1 has an ordered structure, which is composed of a short antiparallel beta-sheet at residues Tyr11-Thr14 and Arg18-Pro21, three beta turns at residues Phe3-Gly6, Ala8-Tyr11 and Thr14-Gly17, and a half turn at the carboxyl-terminus (residues Lys20-Phe23). The well-defined secondary and tertiary structure was stabilized by hydrogen bonding and side-chain hydrophobic interactions. In comparison with two related insect peptides, whose structures have been solved recently, the amino-terminal region of PP1 is substantially more ordered. The short antiparallel beta-sheet of PP1 has a folding pattern similar to the carboxyl-terminal subdomain of epidermal growth factor (EGF). Therefore, PP1 may interact with EGF receptor-like molecules to trigger its different biological activities.

Amino Acid Sequence↗
PubMed1999

Sodium nitroprusside prevents oxygen-free-radical-induced pulmonary vasoconstriction in newborn piglets.

The aim of the present study was to test whether hypoxanthine-xanthine oxidase (XO) induced a pulmonary vasoconstriction in newborn piglets, and whether this vasoconstriction could be attenuated or abolished by pretreatment of nitric oxide (NO) donor sodium nitroprusside (SNP). Twenty-five anesthetized newborn piglets (1-3 days old) were randomly assigned to the following four groups: the control group received saline intravenously only; the XO group received 0.1 mmol/kg of hypoxanthine subsequent with XO (1.5 U/kg); the SNP group received the same dosages of hypoxanthine/ XO together with SNP intravenously, allopurinol (ALP) group received ALP intravenously prior to hypoxanthine and XO injection. After giving XO, the pulmonary arterial pressure (PAP) and vascular resistance (PVR) increased, while the cardiac index decreased significantly in the XO group. By contrast, these variables were not significantly modified by XO injection in the SNP and ALP groups. The data suggest that oxygen free radicals induce a pulmonary vasoconstriction in newborn piglets, and this vasoconstriction can be prevented by infusion of the NO donor SNP.

Animals↗
PubMed1999

Nebulization of sodium nitroprusside in lung-lavaged newborn piglets.

The aim of the present study was to test the hypothesis that nebulization of the nitric oxide donor sodium nitroprusside may selectively reduce pulmonary vascular resistance and improve oxygenation in lung-lavaged newborn piglets. Thirteen anesthetized piglets (1-3 d old) were subjected to repeated lung lavages and then randomly assigned to one of the following two groups: 1) an SNP group, which received SNP nebulization, and 2) a saline group, which received saline nebulization. Pulmonary arterial pressure and pulmonary vascular resistance increased significantly after lung lavage, whereas cardiac output decreased significantly in both groups. After SNP nebulization, pulmonary arterial pressure decreased from 32+/-1 to 17+/-1 mm Hg (p < 0.01) and PVR decreased from 255+/-20 to 172+/-15 mm Hg L(-1) min(-1) kg(-1) (p < 0.01). The arterial tension of oxygen concomitantly increased from 9.4+/-4.0 to 17.0+/-3.0 kPa (p < 0.01), and the arterial/alveolar ratio of oxygen tension increased from 0.11+/-0.01 to 0.22+/-0.03 (p < 0.01). Systemic hemodynamics were not modified significantly during nebulization of SNP. On the other hand, all variables were stable during nebulization of saline. These data suggest that SNP nebulization produces a selective pulmonary vasodilatation and improves oxygenation in lung-lavaged newborn piglets.

Acid-Base Equilibrium↗
PubMed1998

De novo glomerular osteopontin expression in rat crescentic glomerulonephritis.

Osteopontin (OPN) is a secreted acidic glycoprotein that has potent monocyte chemoattractant and adhesive properties. Up-regulation of tubular OPN expression is thought to promote interstitial macrophage infiltration in experimental nephritis; however, the role of OPN in glomerular lesions, particularly crescent formation, is unknown. The present study used Northern blotting, in situ hybridization and immunohistochemistry to examine OPN expression in a rat model of accelerated anti-GBM glomerulonephritis. Osteopontin mRNA and protein is expressed by some parietal epithelial cells, thick ascending limbs of Henle and medullary tubules and collecting ducts in normal rat kidney. De novo OPN mRNA and protein expression was evident in glomerular visceral and parietal epithelial cells in anti-GBM glomerulonephritis. Glomerular OPN expression preceded and correlated with macrophage infiltration in the development of hypercellularity, focal and segmental lesions and, notably, crescent formation. There was marked up-regulation of OPN expression by tubular epithelial cells that also preceded and correlated with interstitial macrophage (r = 0.93, P < 0.001) and T-cell infiltration (r = 0.85, P < 0.001). Both glomerular and tubular OPN expression correlated significantly with proteinuria (P < 0.001) and a reduction in creatinine clearance (P < 0.01). In addition, double immunohistochemistry showed co-expression of osteopontin and one of its ligands, CD44, in intrinsic renal cells. CD44 and OPN expression by parietal epithelial cells was evident in crescent formation, while virtually all OPN-positive tubules expressed CD44. Infiltrating macrophages and T-cells were CD44-positive, but only a small proportion of T-cells and few macrophages showed OPN expression. Interestingly, strong OPN mRNA and protein expression was seen in macrophage multinucleated giant cells. In summary, this study suggests that OPN promotes macrophage and T-cell infiltration in the development of renal lesions in rat anti-GBM glomerulonephritis, including glomerular crescent and multinucleated giant cell formation.

Animals↗
PubMed1998

Acute effects on systemic circulation after intratracheal instillation of Curosurf or Survanta in surfactant-depleted newborn piglets.

Systemic vasodilatation in surfactant-depleted newborn piglets is induced by 200 mg/kg of modified porcine lung surfactant (Curosurf). The aim of this investigation was to study whether this effect is dependent on dose and could further be induced by instillation of a bovine surfactant preparation (Survanta). Twenty-two 3-5-d old piglets were subjected to repeated saline lung lavage and then randomized to one of three groups. Instillation of either Curosurf l00 mg/kg (n=8), Survanta l00 mg/kg (n=7) or Curosurf 200 mg/kg (n=7) was performed through the endotracheal tube. Systemic vascular resistance decreased 7 (+/-4)%, 15 (+/-12)% and 18 (+/-6)% in the three groups, respectively (p < 0.05 in all three groups). A significant difference between the high and low dose Curosurf groups was found (p < 0.05), whereas no significant difference was seen between the Curosurf 100 mg group and the Survanta group. The decrease in vascular resistance was compensated by an increase in cardiac output, resulting in a stable mean arterial blood pressure. In conclusion, both Curosurf and Survanta induce a significant decrease in systemic vascular resistance in surfactant-depleted newborn piglets. A more pronounced effect was observed after 200 mg/kg than after 100mg/kg of Curosurf.

Animals↗
PubMed1998

Pulmonary hemodynamics and plasma endothelin-1 during hypoxemia and reoxygenation with room air or 100% oxygen in a piglet model.

The immediate effect on the pulmonary circulation of reoxygenation with either room air or 100% O2 was studied in newborn piglets. Hypoxemia was induced by ventilation with 8% O2 until base excess was <-20 mmol/L or mean arterial blood pressure was <20 mm Hg. Reoxygenation was performed with either room air (n = 9) or 100% O2 (n = 9). Mean pulmonary artery pressure increased during hypoxemia (p = 0.012). After 5 min of reoxygenation, pulmonary artery pressure increased further from 24 +/- 2 mm Hg at the end of hypoxemia to 35 +/- 3 mm Hg (p = 0.0077 versus baseline) in the room air group and from 27 +/- 3 mm Hg at the end of hypoxemia to 30 +/- 2 mm Hg (p = 0.011 versus baseline) in the O2 group (NS between groups). Pulmonary vascular resistance index increased (p = 0.0005) during hypoxemia. During early reoxygenation pulmonary vascular resistance index decreased rapidly to values comparable to baseline within 5 min of reoxygenation in both groups (NS between groups). Plasma endothelin-1 (ET-1) decreased during hypoxemia from 1.5 +/- 0.1 ng/L at baseline to 1.2 +/- 0.1 ng/L at the end of hypoxemia (p = 0.003). After 30 min of reoxygenation plasma ET-1 increased to 1.8 +/- 0.3 and 1.5 +/- 0.2 ng/L in the room air and O2 groups, respectively (p = 0.0077 in each group versus end hypoxemia; NS between groups). We conclude that hypoxemic pulmonary hypertension and plasma ET-1 normalizes as quickly when reoxygenation is performed with room air as with 100% O2 in this hypoxia model with newborn piglets.

Acid-Base Equilibrium↗
PubMed1997

Effects of hypoxemia and reoxygenation with 21% or 100% oxygen in newborn piglets: extracellular hypoxanthine in cerebral cortex and femoral muscle.

OBJECTIVE: To determine whether reoxygenation with an FIO2 of 0.21 (21% oxygen) is preferable to an FIO2 of 1.0 (100% oxygen) in normalizing brain and muscle hypoxia in the newborn. DESIGN: Prospective, randomized, animal study. SETTING: Hospital surgical research laboratory. SUBJECTS: Twenty-six anesthetized, mechanically ventilated, domestic piglets, 2 to 5 days of age. INTERVENTIONS: The piglets were randomized to control or hypoxemia groups. Hypoxemia was induced by ventilating the piglets with 8% oxygen in nitrogen, which was continued until mean arterial pressure decreased to <20 mm Hg. After hypoxemia, the piglets were further randomized to receive reoxygenation with an FIO2 of 0.21 (21% oxygen group, n = 9) or an FIO2 of 1.0 for 30 mins followed by an FIO2 of 0.21 (100% oxygen group, n = 9), and followed for 5 hrs. The piglets in the control group were mechanically ventilated with 21% oxygen (n = 8). MEASUREMENTS AND MAIN RESULTS: We measured extracellular concentrations of hypoxanthine in the cerebral cortex and femoral muscle (in vivo microdialysis), plasma hypoxanthine concentrations, cerebral arterial-venous differences for hypoxanthine, acid base balances, arterial and venous (sagittal sinus) blood gases, and mean arterial pressures. The lowest pH values of 6.91 +/- 0.11 (21% oxygen group, mean +/- SD) and 6.90 +/- 0.07 (100% oxygen group) were reached at the end of hypoxemia and then normalized during the reoxygenation period. Plasma hypoxanthine increased during hypoxemia from 28.1 +/- 9.3 to 119.1 +/- 31.9 micromol/L in the 21% oxygen group (p < .001) and from 32.6 +/0- 14.5 to 135.0 +/- 31.4 micromol/L in the 100% oxygen group (p <.001). Plasma hypoxanthine concentrations then normalized over the next 2 hrs in both groups. In the cerebral cortex, extracellular concentrations of hypoxanthine increased during hypoxemia from 3.9 +/- 2.8 to 20.2 +/- 7.4 micromol/L in the 21% oxygen group (p < .001) and from 5.9 +/- 5.0 to 25.1 +/- 7.1 micromol/L in the 100% oxygen group (p < .001). In contrast to plasma hypoxanthine, extracellular hypoxanthine in the cerebral cortex increased significantly further during early reoxygenation, and, within the first 30 mins, reached maximum values of 24.9 +/- 6.3 micromol/L in the 21% oxygen group (p < .01) and 34.8 +/- 10.9 micromol/L in the 100% oxygen group (p < .001). This increase was significantly larger in the 100% oxygen group than in the 21% oxygen group (9.7 +/- 4.7 vs. 4.7 +/- 2.6 micromol/L, p < .05). There were no significant differences between the two reoxygenated groups in duration of hypoxemia, hypoxanthine concentrations in femoral muscle, plasma hypoxanthine concentrations, pH, or mean arterial pressure. The cerebral arterial-venous difference for hypoxanthine was positive both at baseline, at the end of hypoxemia, and after 30 mins and 300 mins of reoxygenation, and no differences were found between the two reoxygenated groups. CONCLUSIONS: Significantly higher extracellular concentrations of hypoxanthine were found in the cerebral cortex during the initial period of reoxygenation with 100% oxygen compared with 21% oxygen. Hypoxanthine is a marker of hypoxia, and reflects the intracellular energy status. These results therefore suggest a possibly more severe impairment of energy metabolism in the cerebral cortex or an increased blood-brain barrier damage during reoxygenation with 100% oxygen compared with 21% oxygen in this newborn piglet hypoxia model.

Animals↗
PubMed1997

Acute effects on systemic and pulmonary hemodynamics of intratracheal instillation of porcine surfactant or saline in surfactant-depleted newborn piglets.

Surfactant instillation may affect systemic and pulmonary hemodynamics. The aim of this study was to investigate whether this effect is specific to surfactant or if it can be triggered by instillation of the same volume of saline. Piglets 3-5-d-old were subjected to repeated lung lavage using 20 mL/kg 0.9% saline until the partial pressure of arterial O2 was < 10 kPa and partial pressure of arterial CO2 was between 4.0 and 6.0 kPa with fraction of inspired oxygen (FiO2) 1.0 and peak inspiratory pressure 25 cm H2O. Porcine surfactant 200 mg/kg (80 mg/mL) or the same volume of 0.9% saline was instilled into the lungs through a feeding catheter entered through the endotracheal tube. Mean arterial blood pressure, pulmonary artery pressure, and cardiac output were measured continuously. There was a significant decrease in mean arterial blood pressure from 67 (+/- 13) mm Hg to 52 (+/- 18) mm Hg (p < 0.05) 210 s after instillation of surfactant. Systemic vascular resistance decreased from 0.42 (+/- 0.18) to 0.34 (+/- 0.18) mm Hg x mL-1 x min x kg (p < 0.05) from 0 min to 180 s after instillation of surfactant. In the group receiving saline instillations there were no significant changes in mean arterial blood pressure or systemic vascular resistance. A transient but significant increase in mean pulmonary artery pressure was seen 120 s after instillation in both groups with a return to presurfactant level 240 s after instillation. Pulmonary vascular resistance increased transiently and significantly only in the group receiving surfactant. We conclude that porcine surfactant causes a decrease in systemic vascular resistance, resulting in a decrease in mean arterial blood pressure in newborn lung-lavaged piglets not seen after instillation of the same volume of saline.

Animals↗
PubMed1997

Nitric oxide contributes to surfactant-induced vasodilation in surfactant-depleted newborn piglets.

To investigate whether nitric oxide (NO) is involved in surfactant-induced systemic and pulmonary vasodilatation in newborn piglets with surfactant deficiency, 2-6-d-old piglets were subjected to repeated saline lung lavages. They were then randomly assigned to one of two groups (seven in each group): the N(omega)-nitro-L-arginine methyl ester (L-NAME) group received 3 mg/kg L-NAME i.v. 45 min before endotracheal instillation of 200 mg/kg porcine surfactant; the saline group received saline i.v. at the same time point, and instillation of 200 mg/kg surfactant. Mean arterial blood pressure, systemic vascular resistance, pulmonary arterial pressure, and pulmonary vascular resistance increased significantly after injection of L-NAME (all p < 0.01), whereas the cardiac index decreased significantly (p < 0.05). Saline injection did not change any variable. Significant decreases in mean arterial blood pressure (from a mean +/- SD of 66 +/- 10 to 53 +/- 9 mm Hg, p < 0.01), pulmonary arterial pressure (from 29 +/- 6 to 23 +/- 6 mm Hg, p < 0.01), and systemic vascular resistance (from 0.40 +/- 0.13 to 0.33 +/- 0.12 mm Hg/mL/min/kg, p < 0.05) were observed only in the saline group after surfactant instillation, whereas the decrease in pulmonary vascular resistance was not significant after surfactant instillation (p = 0.06). In contrast to the saline group, these variables were not modified in the L-NAME group after surfactant instillation. We conclude that the vasodilatory effect of porcine surfactant instillation in newborn piglets with surfactant deficiency is associated with activation of NO synthase.

Animals↗
PubMed1997

The design and application of a pediatric centrifugal pump.

This centrifugal pump (CP) includes two parts: the blood pump and the driving apparatus. They are connected by six twin magnetic disc plates and driven by a magnetic DC motor (120W). The blood pump had six leaves deadlocked between two plastic discs. Six leaves were set at 30 degrees angles, separately. In the lower chamber of the CP, there was an inlay magnetic disc, which is connected with the disc leaves by an axis. This axis was sealed by silicon rubber and a ceramic ring. The priming volume of the blood chamber was 34 ml. In vitro testing showed that the free hemoglobin caused by the CP was much less than that caused by a roller pump after 180 min. The effect of this CP on blood cell damage was also studied in an animal model. Six goats were placed on cardiopulmonary bypass for 180 min. Perfusion flow rates were maintained between 1.5 and 2.5 L/min. The plasma free hemoglobin was lower in the CP group (6.04 mg/dL) than in the roller pump group (32.25 mg/dL), p < 0.01. The CP has been used in ten pediatric patients undergoing cardiopulmonary bypass surgery. The patients' ages were from three to five years, and body weights were from 15 to 20 kg. Perfusion flow rates were maintained between 1.8 and 2.5 L/min, and bypass times were from 30 to 50 min. The rotation speeds were from 2000 to 2500 rpm. All the patients recovered smoothly, and no hemoglobinuria occurred.

Animals↗
PubMed1996

Effects of chloral hydrate on the cardiorespiratory response to hypoxia in newborn piglets.

To assess the effects of chloral hydrate (CH) on the cardiorespiratory response to hypoxia in the neonate, 17 newborn piglets were chronically instrumented 48-72 h before study and randomly assigned to a CH group (100 mg/kg, i.p.) or saline group. The animals were intubated and studied under quiet sleep which was determined by behavioral states, and continuous electro-oculographic and electroencephalographic monitoring. Minute ventilation (VE), tidal volume, respiratory rate, arterial blood gases (ABG), oxygen consumption (VO2), arterial blood pressure (ABP) and heart rate (HR) were measured before and after CH or saline administration during room air and after 10 min of hypoxia (fraction of inspired oxygen concentration = 0.10). Cardiorespiratory response to hypoxia was similar before and after saline infusion. Basal VE and the ventilatory response to hypoxia were similar before and after CH administration. In contrast, the basal ABP decreased significantly (p < 0.05) after CH administration, but the ABP response to hypoxia was similar before and after CH. A significant increase in both basal HR and HR with hypoxia was observed after CH administration. In addition, VO2 and ABG were not modified by CH treatment during normoxia and hypoxia. These data demonstrate that a sedative dose of CH does not significantly modify the ventilatory response to hypoxia in newborn piglets. However, CH produced some changes in the cardiovascular system which should be considered when using it in infants with hemodynamic derangements.

Animals↗
PubMed1991

Application of neural computing in pharmaceutical product development.

Neural computing technology is capable of solving problems involving complex pattern recognition. This technology is applied here to pharmaceutical product development. The most commonly used computational algorithm, the delta back-propagation network, was utilized to recognize the complex relationship between the formulation variables and the in vitro drug release parameters for a hydrophilic matrix capsule system. This new computational technique was also compared with the response surface methodology (RSM). Artificial neural network (ANN) analysis was able to predict the response values for a series of validation experiments more precisely than RSM. ANN may offer an alternative to RSM because it allows for the development of a system that can incorporate literature and experimental data to solve common problems in the pharmaceutical industry.

Algorithms↗
PubMed1991

B subunit of cholera toxin produced in Escherichia coli.

An engineered E. coli strain containing high expression level of CT-B subunits has been obtained by the application of recombinant DNA techniques. The B subunit can be secreted into the medium and reaches 20-40 micrograms/ml when this strain is incubated in a 50 l fermentation tank. The CT-B subunit purified with affinity chromatography in E. coli has the same characters as the natural CT-B subunit in molecular weight, N terminal amino acid analysis and antigenicity. The CT-B subunit has good immunogenicity and can be used as a preparation for protecting against diarrhea caused by V. cholera and enterotoxigenic E. coli. It can also be used as a vector for hepatins.

Animals↗
PubMed1990

Construction of a bivalent oral vaccine for prevention of typhoid fever and cholera diarrhea.

A recombinant plasmid pMM-CTB containing the gene for production of the nontoxic B subunit of Vibrio cholera was transferred into a safe, effective and attenuated oral vaccine Ty21a strain of Salmonella typhi. The resulting Ty21a (pMM-CTB) could steadily produce CT-B subunit that was secreted extracellularly and had the same antigenicity as CT-B produced by V. cholera. Furthermore, the characteristics of the antigenicity, the persistance in mice and the galactose sensitivity possessed in the strain of Ty21a were also retained in Ty21a (pMM-CTB). A bivalent vaccine containing Ty21a (pMM-CTB) and the killed whole cell of V. cholera was then constructed which had good immunogenecity for typhoid fever and cholera diarrhea.

Animals↗
PubMed1989

The expression of enterotoxin A-B+ gene of V. cholerae in E. coli.

The cloning in E. coli of a cholerae toxin gene that is A-B+ has been successfully constructed by using DNA recombinant techniques. E. coli cells carrying the recombinant plasmid pMM-CTB have been shown to produce a large amount of CTB subunits which are secreted as extracellular proteins.

Animals↗