Biomedical subjects

Haibo Zhang

Publications and source records attributed to Haibo Zhang.

At least 37 records · Page 2Linked to original sources

PubMed2005

Effect of testosterone on functional recovery in a castrate male rat stroke model.

Both increased and decreased testosterone levels have been reported to correlate with poor outcome after acute ischemic stroke. The present study focused on the role of testosterone during recovery from neurological deficits in a rat focal ischemia model. Castrate male rats were subjected to behavioral tests after 90 min of middle cerebral artery occlusion (MCAO). On day 7 post-MCAO, neurological deficit-matched rats were assigned to a treatment group implanted with subcutaneous testosterone pellets or a control group implanted with sham cholesterol pellets. After 4 weeks post-MCAO, the average infarct volume was not significantly different between the two groups. Rats in the testosterone group demonstrated significantly earlier improvement in neurological deficits and shortened latency of adhesive tape removal compared with the control group as analyzed by Wilcoxon signed ranks test. Walking on parallel bars improved in both groups with a trend towards early recovery observed in the testosterone group. Biased left body swings persisted during the test period in both groups post-MCAO. Serum testosterone was within physiological levels in the treatment group but was not detectable in the control group by radioimmunoassay. GAP-43 and synaptophysin expression did not differ between groups. Less GFAP expression and reactive astrocyte hypertrophy were found around the infarct area in testosterone-treated rats compared with control rats. In conclusion, testosterone replacement post-MCAO accelerated functional recovery in castrate rats, suggesting a potential therapeutic role for testosterone replacement in stroke recovery.

Androgens↗

PubMed2005

Alternative polyadenylation of cyclooxygenase-2.

A biologically important human gene, cyclooxygenase-2 (COX-2), has been proposed to be regulated at many levels. While COX-1 is constitutively expressed in cells, COX-2 is inducible and is upregulated in response to many signals. Since increased transcriptional activity accounts for only part of the upregulation of COX-2, we chose to explore other RNA processing mechanisms in the regulation of this gene. We performed a comprehensive bioinformatics survey, the first of its kind known for human COX-2, which revealed that the human COX-2 gene has alternative polyadenylation (proximal and distal sites) and suggested that use of the alternative polyadenylation signals has tissue specificity. We experimentally established this in HepG2 and HT29 cells. We used an in vivo polyadenylation assay to examine the relative strength of the COX-2 proximal and distal polyadenylation signals, and have shown that the proximal polyadenylation signal is much weaker than the distal one. The efficiency of utilization of many suboptimal mammalian polyadenylation signals is affected by sequence elements located upstream of the AAUAAA, known as upstream efficiency elements (USEs). Here, we used in vivo polyadenylation assays in multiple cell lines to demonstrate that the COX-2 proximal polyadenylation signal contains USEs, mutation of the USEs substantially decreased usage of the proximal signal, and that USE spacing relative to the polyadenylation signal was significant. In addition, mutation of the COX-2 proximal polyadenylation signal to a more optimal sequence enhanced polyadenylation efficiency 3.5-fold. Our data suggest for the first time that alternative polyadenylation of COX-2 is an important post-transcriptional regulatory event.

3' Untranslated Regions↗

PubMed2005

A large-scale analysis of mRNA polyadenylation of human and mouse genes.

mRNA polyadenylation is a critical cellular process in eukaryotes. It involves 3' end cleavage of nascent mRNAs and addition of the poly(A) tail, which plays important roles in many aspects of the cellular metabolism of mRNA. The process is controlled by various cis-acting elements surrounding the cleavage site, and their binding factors. In this study, we surveyed genome regions containing cleavage sites [herein called poly(A) sites], for 13,942 human and 11,155 mouse genes. We found that a great proportion of human and mouse genes have alternative polyadenylation ( approximately 54 and 32%, respectively). The conservation of alternative polyadenylation type or polyadenylation configuration between human and mouse orthologs is statistically significant, indicating that alternative polyadenylation is widely employed by these two species to produce alternative gene transcripts. Genes belonging to several functional groups, indicated by their Gene Ontology annotations, are biased with respect to polyadenylation configuration. Many poly(A) sites harbor multiple cleavage sites (51.25% human and 46.97% mouse sites), leading to heterogeneous 3' end formation for transcripts. This implies that the cleavage process of polyadenylation is largely imprecise. Different types of poly(A) sites, with regard to their relative locations in a gene, are found to have distinct nucleotide composition in surrounding genomic regions. This large-scale study provides important insights into the mechanism of polyadenylation in mammalian species and represents a genomic view of the regulation of gene expression by alternative polyadenylation.

Animals↗

PubMed2005

Bench-to-bedside review: Biotrauma and modulation of the innate immune response.

The innate immune network is responsible for coordinating the initial defense against potentially noxious stimuli. This complex system includes anatomical, physical and chemical barriers, effector cells and circulating molecules that direct component and system interactions. Besides the direct effects of breaching pulmonary protective barriers, cyclic stretch generated during mechanical ventilation (MV) has been implicated in the modulation of the innate immunity. Evidence from recent human trials suggests that controlling MV-forces may significantly impact outcome in acute respiratory distress syndrome. In this paper, we explore the pertinent evidence implicating biotrauma caused by cyclic MV and its effect on innate immune responses.

Animals↗

PubMed2005

PolyA_DB: a database for mammalian mRNA polyadenylation.

Messenger RNA polyadenylation is one of the key post-transcriptional events in eukaryotic cells. A large number of genes in mammalian species can undergo alternative polyadenylation, which leads to mRNAs with variable 3' ends. As the 3' end of mRNAs often contains cis elements important for mRNA stability, mRNA localization and translation, the implications of the regulation of polyadenylation can be multifold. Alternative polyadenylation is controlled by cis elements and trans factors, and is believed to occur in a tissue- or disease-specific manner. Given the availability of many databases devoted to other aspects of mRNA metabolism, such as transcriptional initiation and splicing, systematic information on polyadenylation, including alternative polyadenylation and its regulation, is noticeably lacking. Here, we present a database named polyA_DB, through which we strive to provide several types of information regarding polyadenylation in mammalian species: (i) polyadenylation sites and their locations with respect to the genomic structure of genes; (ii) cis elements surrounding polyadenylation sites; (iii) comparison of polyadenylation configuration between orthologous genes; and (iv) tissue/organ information for alternative polyadenylation sites. Currently, polyA_DB contains 45,565 polyadenylation sites for 25,097 human and mouse genes, representing the most comprehensive polyadenylation database till date. The database is accessible via the website (http://polya.umdnj.edu/polyadb).

Animals↗

PubMed2005

Engraftment of freshly isolated or cultured human umbilical cord blood cells and the effect of cyclosporin A on the outcome.

Human umbilical cord blood (HUCB) is a potentially valuable resource for cell therapy. The present study investigated the short-term survival of intrastriatal grafts of either freshly isolated or cultured HUCB cells and the effect of the immunosuppressive agent cyclosporin A (CSA) in host rat brains. The group injected with either freshly isolated or cultured HUCB cells was subdivided into CSA or saline controls. Freshly isolated and cultured HUCB cells displayed surface markers CD33, CD44, CD45, CD51/61 and CD90/Thy-1. The hematopoietic progenitor marker CD34 was expressed only in freshly isolated cells. The majority of injected HUCB cells were localized within a 500-mum radius from the injection site in the striatum; however, a subpopulation migrated along the corpus callosum. There was no significant statistical difference in the cell count between freshly isolated and cultured HUCB cells with or without CSA. Some grafted HUCB cells expressed either a neural or microglial marker. There was weak up-regulation of major histocompatibility complex (MHC) class I antigen in rats either with or without CSA. However, there were considerably fewer positive cells labeled with an MHC class II antigen in CSA groups. These results suggest that neither freshly isolated nor cultured HUCB cells induce acute rejection after intrastriatal transplantation up to 14 days. CSA suppressed up-regulation of MHC class II antigen in the host brain.

Animals↗

PubMed2005

Mechanical ventilation exacerbates alveolar macrophage dysfunction in the lungs of ethanol-fed rats.

BACKGROUND: Patients with alcohol abuse have a two- to three-fold increased risk of acute lung injury and respiratory failure after sepsis or trauma but are also at increased risk of nosocomial pneumonia. Mechanical ventilation exacerbates lung injury during critical illnesses. In this study we tested whether mechanical ventilation of the alcoholic lung promotes on balance a proinflammatory phenotype favoring ventilator-induced lung injury or an immunosuppressive phenotype favoring ventilator-associated pneumonia. METHODS: Lungs from rats fed an isocaloric diet with or without ethanol (six weeks) were isolated and ventilated ex vivo with a low-volume (protective) or high-volume (injurious) strategy for two hours with or without prior endotoxemia (two hours). In other experiments, rats were subjected to high-volume ventilation in vivo. Airway levels of the proinflammatory cytokines tumor necrosis factor-alpha, macrophage inflammatory protein-2, and interleukin-1beta were determined after mechanical ventilation ex vivo and compared with edematous lung injury after high-volume ventilation in vivo. In parallel, alveolar macrophage phagocytosis of bacteria and secretion of interleukin-12 during ventilation ex vivo and endotoxin-stimulated alveolar macrophage phagocytosis and tumor necrosis factor-alpha secretion in vitro were determined. RESULTS: Ethanol ingestion suppressed the proinflammatory response to injurious mechanical ventilation and did not increase experimental ventilator-induced lung injury. In parallel, ethanol ingestion blunted the innate immune response of alveolar macrophages during injurious ventilation ex vivo and after endotoxin stimulation in vitro. CONCLUSIONS: Ethanol ingestion dampens ventilator-induced inflammation but exacerbates macrophage immune dysfunction. These findings could explain at least in part why alcoholic patients are at increased risk of ventilator-associated pneumonia.

Alcoholism↗

PubMed2004

Is there a place for N-acetylcysteine in the treatment of septic shock?

Excessive inflammatory responses and impaired oxygen utilization because of microcirculatory failure are implicated in septic shock. Recent studies have pointed out some beneficial effects in the treatment of septic shock of several vasodilators that exert anti-inflammatory properties. In particular, the antioxidant N-acetylcysteine has been demonstrated to enhance cardiac performance, and to improve hepatosplanchnic perfusion and liver function in patients with established septic shock. These clinical observations may lead us to examine further the role of antioxidant agents in developing novel therapies for septic shock.

Acetylcysteine↗

PubMed2004

Intercellular adhesion molecule-1 mediates cellular cross-talk between parenchymal and immune cells after lipopolysaccharide neutralization.

The mechanisms by which parenchymal cells interact with immune cells, particularly after removal of LPS, remain unknown. Lung explants from rats, mice deficient in the TNF gene, or human lung epithelial A549 cells were treated with LPS and washed, before naive alveolar macrophages, bone marrow monocytes, or PBMC, respectively, were added to the cultures. When the immune cells were cocultured with LPS-challenged explants or A549 cells, TNF production was greatly enhanced. This was not affected by neutralization of LPS with polymyxin B. The LPS-induced increase in the expression of ICAM-1 on A549 cells correlated with TNF production by PBMC. The cellular cross talk leading to the TNF response was blunted by an anti-ICAM-1 Ab and an ICAM-1 antisense oligonucleotide. In A549 cells, a persistent decrease in the concentration of intracellular cAMP was associated with colocalization of LPS into Toll-like receptor 4 and the Golgi apparatus, resulting in increased ICAM-1 expression. Inhibition of LPS internalization by cytochalasin D or treatment with dibutyryl cAMP attenuated ICAM-1 expression and TNF production by PBMC. In conclusion, lung epithelial cells are not bystanders, but possess memory of LPS through the expression of ICAM-1 that interacts with and activates leukocytes. This may provide an explanation for the failure of anti-LPS therapies in sepsis trials.

Animals↗

PubMed2004

Effect of mechanical ventilation on cytokine response to intratracheal lipopolysaccharide.

BACKGROUND: Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation. METHODS: Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP. RESULTS: In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume. CONCLUSION: Ventilation strategy can modify lung cytokine responses to lipopolysaccharide, likely through an effect on the alveolar macrophage population.

Administration, Inhalation↗

PubMed2003

Modulation of bacterial growth by tumor necrosis factor-alpha in vitro and in vivo.

Tumor necrosis factor-alpha (TNF-alpha) plays an important role in innate immunity. Recent in vitro studies have shown that TNF-alpha may also serve as a growth factor for some bacteria. We examined the physiologic relevance of this phenomenon both in vitro and in vivo. Recombinant mouse TNF-alpha increased in vitro proliferation of Escherichia coli but not Pseudomonas aeruginosa in a concentration-dependent manner, and this effect was attenuated by anti-TNF-alpha antibodies. However, in vivo, TNF-alpha gene-deficient (TNF-alpha-/-) mice showed higher mortality than wild-type (TNF-alpha+/+) mice after inoculation of intranasal bacteria. An impaired bacterial clearance in TNF-alpha-/- mice was associated with decreased systemic concentrations of chemokine macrophage inflammatory protein-2, reduced pulmonary neutrophil recruitment, and depressed expression of neutrophil CD11b and CD16/CD32, suggesting that the effect of TNF-alpha on E. coli growth was outweighed by the recruited neutrophils. We also demonstrated that neutropenic TNF-alpha+/+ mice had approximately 100-fold higher E. coli counts in their lungs than TNF-alpha-/- mice, although survival rates in both groups were similar. We conclude that TNF-alpha augments E. coli growth in vitro and in vivo. However, in vivo, this effect becomes only apparent in neutropenic animals. The relevance of these findings for immune compromised patients remains to be investigated.

Animals↗

PubMed2003

Tolerance to acute isovolemic hemodilution. Effect of anesthetic depth.

BACKGROUND: Acceptance of a lower transfusion trigger in the perioperative period requires study of the effects of anesthetic depth on the tolerance to acute isovolemic anemia. Anesthetic agents with negative effects on the cardiovascular system may exert proportionately greater depressant effects on cardiac output response than on tissue oxygen demand, reducing tolerance to acute isovolemic anemia. METHODS: In the first study, animals were anesthetized with halothane (n = 14; 23.8 +/- 4.8 kg, mean +/- SD). In a second study, animals were anesthetized with ketamine (n = 14; 24.3 +/- 4.7 kg). In each study, dogs were randomly allocated to receive either low or high concentrations of anesthetic. Oxygen delivery and oxygen consumption were determined from independent measurements during a stepwise isovolemic hemodilution protocol. In each dog, critical oxygen delivery was determined from a plot of oxygen consumption versus oxygen delivery using a least-sum-of-squares technique. Critical hemoglobin (hemoglobin) was determined from a plot of hemoglobin versus oxygen consumption using the same method. RESULTS: With both agents, the higher anesthetic concentration was associated with decreased oxygen consumption, resulting in a lower critical oxygen delivery. However, critical hemoglobin was significantly higher in the animals receiving the higher anesthetic dosage (1.5 vs. 1.0 minimum alveolar concentration of halothane: 4.1 +/- 1.3 vs. 2.3 +/- 0.5 g/dl, P < 0.05; high- vs. low-dose ketamine: 3.7 +/- 1.4 vs. 2.5 +/- 0.6 g/dl, P < 0.05). This was related to a marked blunting of the cardiac output response to hemodilution in the animals receiving the higher anesthetic dosage. CONCLUSIONS: Increased anesthetic depth with halothane or ketamine resulted in a decreased tolerance to acute anemia, as reflected by a significant increase in critical hemoglobin concentration.

Anemia↗

PubMed2003

Hemodynamic effects of glibenclamide during endotoxemia: contrasting findings in vitro versus in vivo.

The final common pathway involved in the cardiovascular alterations of septic shock is incompletely defined. The opening of KATP channels is associated with vasorelaxation and alterations in cardiac contractility. This event may be triggered during septic shock by increased nitric oxide (NO) production, by a decreased intracellular content of ATP, or by a change in the transmembrane electrical potential. In the present study, we assessed the effects of glibenclamide, an agent that blocks the opening of KATP channels in vitro, on the contractile response of rat aortic rings to norepinephrine, and in vivo in anesthetized dogs, with or without exposure to Escherichia coli endotoxin. In vitro, glibenclamide decreased the contractile response to norepinephrine in the presence of endotoxin, provided that the endothelium was intact. In vivo, administration of 0.15 mg/kg increased systemic vascular resistance (SVR) in the absence of endotoxin only, and increased myocardial performance. A higher dose of 1 mg/kg increased SVR and decreased myocardial performance, both during endotoxic shock and in control conditions. Renal and mesenteric blood flows decreased, but the respective fractional flows were unchanged. Oxygen delivery decreased in both experimental conditions, but oxygen consumption decreased only in control conditions. The in vitro observations suggest that the opening of KATP channels is involved in the regulation of vascular tone during endotoxemia, via an endothelium-dependent mechanism. As different effects of glibenclamide were observed in vivo, the importance of the opening of KATP channels in endotoxic shock may be limited.

Animals↗

PubMed2003

Comparison of polyacrylonitrile (AN69) and polysulphone membrane during hemofiltration in canine endotoxic shock.

OBJECTIVE: This study was designed to compare the effects of continuous venovenous hemofiltration (CVVH) with two different membranes, polysulphone and polyacrylonitrile (AN69), on global and regional hemodynamics, plasma lactate, tumor necrosis factor-alpha levels, and plasma nitrite/nitrate during endotoxic shock in dogs. METHODS: Fifteen pentobarbital anesthetized and mechanically ventilated dogs were randomized into three groups of five dogs each. One group served as an endotoxin alone, time matching group and, 1 hr after endotoxin administration, the two other groups received CVVH at 3 L/hr for 270 mins, with either a polysulphone membrane or an polyacrylonitrile membrane. RESULTS: At 90 mins after endotoxin administration, dogs receiving CVVH with polyacrylonitrile membranes had a higher cardiac output, stroke volume, and left-ventricular stroke work index than the endotoxin alone and the polysulphone groups. CVVH with either polyacrylonitrile or polysulphone membranes prevented the rise in pulmonary artery pressure and pulmonary vascular resistance compared with the endotoxin alone group. Plasma lactate levels were not significantly altered, but the fall in bicarbonate seen in the endotoxin alone group did not occur in the two CVVH groups. Tumor necrosis factor levels in the plasma were not significantly altered by CVVH and remained very low (<50 pg/mL) in the ultrafiltrate fluid. CONCLUSION: In this acute endotoxic shock model, CVVH with the polyacrylonitrile membrane improved cardiac performance when compared with the polysulphone membrane. These effects could be caused by a more effective adsorption of inflammatory mediators other than tumor necrosis factor. Whether the polyacrylonitrile membrane should be preferred over the polysulphone membrane for CVVH in severe sepsis warrants further experimental and clinical study.

Acrylic Resins↗

PubMed2003

Mechanical ventilation may increase susceptibility to the development of bacteremia.

OBJECTIVE: We examined the hypothesis that mechanical ventilation with a potentially injurious strategy would predispose animals to the detrimental effects of subsequent instillation of bacteria. DESIGN: Interventional animal study. SETTING: A university hospital research laboratory. SUBJECTS: Fifty Sprague-Dawley male rats. INTERVENTIONS: Rats were anesthetized and randomized to receive a protective (tidal volume 7 mL/kg, positive end-expiratory pressure 5 cm H(2)O, n = 25) or an injurious ventilatory strategy (tidal volume 21 mL/kg, zero positive end-expiratory pressure, n = 25). Hemodynamics were similar during the 1-hr ventilation period in the two groups. Animals were then disconnected from the ventilator and Pseudomonas aeruginosa was instilled intratracheally before extubation. Thereafter, animals breathed spontaneously; mortality rate was assessed up to 48 hrs, at which time the animals were killed. MEASUREMENTS AND MAIN RESULTS: The 48-hr mortality rate was 28% in the protective group and 40% in the injurious group (p = not significant). A positive bacterial culture from the lung was obtained in 56% of the surviving rats in the low tidal volume group and 67% in the high tidal volume group (p =.059). A positive blood bacterial culture was found in 11% of the low tidal volume group and 33% in the high tidal volume group (p <.05). The absolute bacterial count in the blood was lower in the low tidal volume group compared with the high tidal volume group (p <.05). Concentrations of blood tumor necrosis factor-alpha and macrophage inflammatory protein-2, and lung macrophage inflammatory protein-2 at 48 hrs were significantly higher in the low tidal volume group than in the high tidal volume group. CONCLUSIONS: An injurious ventilatory strategy predisposes animals to subsequent bacteremia associated with an impaired host defense reflected by cytokine response.

Airway Resistance↗

PubMed2003

Effects of albumin and Ringer's lactate on production of lung cytokines and hydrogen peroxide after resuscitated hemorrhage and endotoxemia in rats.

RATIONALE AND HYPOTHESIS: Acute lung injury is a frequent complication of severe sepsis or blood loss and is often associated with an excessive inflammatory response requiring mechanical ventilation. We tested the hypothesis that the types of fluids used during early resuscitation have an important effect on the evolution of lung injury. METHODS: Rats were subjected to either hemorrhage or endotoxemia for 1 hr, followed by resuscitation to a controlled mean blood pressure with Ringer's lactate, 5% albumin, or 25% albumin for 1 hr. After resuscitation, blood cytokine levels were measured. The lung was then excised and ventilated with a tidal volume of 30 mL/kg for 2 hrs. RESULTS: The volume of fluids required was significantly smaller in the albumin-treated groups than in the Ringer's lactate groups. In the hemorrhagic shock model, plasma concentrations of tumor necrosis factor-alpha, interleukin-6, and macrophage inflammatory protein-2 were significantly lower and interleukin-10 was significantly higher in the albumin-treated groups compared with the Ringer's lactate-treated group. The levels of tumor necrosis factor-alpha and macrophage inflammatory protein-2 in bronchoalveolar lavage fluid were lower and interleukin-10 was higher in the albumin-treated groups than in the Ringer's lactate group. The decreased cytokine production was associated with a reduction of hydrogen peroxide formation with albumin resuscitation. The lung wet/dry ratio was lower in the 5% albumin (0.54 +/- 0.01) and 25% albumin (0.55 +/- 0.02) groups than in the Ringer's lactate group (0.62 +/- 0.02; both p <.05). These effects of albumin seen in the hemorrhagic shock model were not observed in the endotoxic shock model. CONCLUSIONS: We conclude that resuscitation with albumin may have utility in reducing ventilator-induced lung injury after hemorrhagic shock, but not after endotoxic shock. These findings suggest that the mechanisms leading to ventilator-induced lung injury after hemorrhage differ from those after endotoxemia.

Albumins↗

PubMed2003

Hormonal and metabolic responses of fetal lamb during cardiopulmonary bypass.

OBJECTIVE: To study the hormonal and metabolic responses of fetal lamb during cardiopulmonary bypass. METHODS: Six pregnant ewes underwent fetal cardiopulmonary bypasses with artificial oxygenators and roller pumps for 30 minutes, which maintained the blood gas value at the fetal physiological level. The fetal blood pressure, heart rate, pH value and blood lactate levels were monitored. The levels of catecholamine, cortisol and insulin were measured pre-bypass and then again 30 minutes later. The blood glucose and free fatty acid levels were monitored continuously during the bypass. Fetal hepatic PAS staining was also carried out. RESULTS: There were no changes before and during the bypass in fetal blood pressure, heart rate and blood gas. However, pH values decreased and blood lactate levels increased (P < 0.05). The fetal catecholamine and cortisol levels increased significantly (P < 0.01), while the levels of insulin did not change. The blood glucose and free fatty acid levels increased at the beginning of the bypass (P < 0.01), and then gradually slowed down during the bypass. The fetal hepatic PAS staining showed that hepatic glycogen was consumed in large amounts. After 30 minutes of bypass, the fetal lamb would not survive more than 1 hour. CONCLUSION: The fetal lamb has a strong negative reaction to cardiopulmonary bypass.

Animals↗

PubMed2002

EZ-Retrieve: a web-server for batch retrieval of coordinate-specified human DNA sequences and underscoring putative transcription factor-binding sites.

The availability of a draft human genome sequence and ability to monitor the transcription of thousands of genes with DNA microarrays has necessitated the need for new computational tools that can analyze cis-regulatory elements controlling genes that display similar expression patterns. We have developed a tool designated EZ-Retrieve that can: (i) retrieve any particular region of human genome sequence from the NCBI database and (ii) analyze retrieved sequences for putative transcription factor-binding sites (TFBSs) as they appear on the TRANSFAC database. The tool is web-based, user-friendly and offers both batch sequence retrieval and batch TFBS prediction. A major application of EZ-Retrieve is the analysis of co-expressed genes that are highlighted as expression clusters in DNA microarray experiments.

Animals↗