Biomedical subjects

Whitney Jones

Publications and source records attributed to Whitney Jones.

6 recordsLinked to original sources

PubMed2006

Cyclooxygenase-2 and epithelial growth factor receptor up-regulation during progression of Barrett's esophagus to adenocarcinoma.

AIM: To investigate the expression of cyclooxygenase-2 (COX-2) and epithelial growth factor receptor (EGFR) throughout the progression of Barretts esophagus (BE). METHODS: COX-2 and EGFR protein expressions were detected by using immunohistochemical method. A detailed cytomorphological changes were determined. Areas of COX-2 and EGFR expression were quantified by using computer Imaging System. RESULTS: The expressions of both COX-2 and EGFR increased along with the progression from BE to esophagus adenocarcinoma (EAC). A positive correlation was found between COX-2 expression and EGFR expression. CONCLUSION: COX-2 and EGFR may be cooperative in the stepwise progression from BE to EAC, thereby leading to carcinogenesis.

Adenocarcinoma↗

PubMed2006

A novel external esophageal perfusion model for reflux esophageal injury.

The current animal models of esophagitis and Barrett's esophagus consist of surgeries that divert the gastroduodenal contents to the esophagus. The limitations of these models are the inability to control the amount and concentration of the refluxate and the causing of significant postoperative stress and morbidity. Eighteen adult rats were cannulated at the upper esophagus and connected to a subcutaneous osmotic micropump to perfuse the esophageal lumen with bile and acid. Animals were sacrificed after 7 days of perfusion. Histological changes were determined. Cell proliferation, apoptosis, lipid peroxidation, and glutathione were measured. Histopathological changes in the bile- or acid-perfused esophagus were consistent with the findings associated with reflux esophagitis. Enhanced proliferation and apoptosis were seen, along with increased oxidative stress. The external esophageal perfusion model enabled precise control of the injurious agent. It induced the histologic and cellular injury of reflux esophagitis after 7 days.

Acetic Acid↗

PubMed2006

Morphological transformation in esophageal submucosa by bone marrow cells: esophageal implantation under external esophageal perfusion.

Accumulating clinical and experimental studies indicate that Barrett's esophagus might arise through multipotential stem cells under the stress of gastroesophageal reflux. Previously, we have presented a novel external pump perfusion rat model and demonstrated that perfusion with both acid and bile can induce severe esophagitis in 1 week with a similarly pathological change seen in humans. The aim of this study was to investigate the histological changes of esophagus after bone marrow cell engraftment with bile and acid perfusion. The external pump perfusion procedure involved implantation of a microosmotic pump for esophageal perfusion. Bone marrow cells were obtained by flushing of the femur marrow, and the cell suspension was injected between the esophageal muscular and inner mucosa layer. Histological changes were determined after 4 weeks of perfusion. Proliferating cell nuclear antigen, 8-hydroxy-deoxyguanosine, manganese superoxide dismutase, and apoptosis were measured by immunohistochemical staining and TUNEL assay, respectively. Severe esophagitis was seen in both acid and bile perfusion. Bone marrow engraftment and potentiation was seen in both the acid and bile perfusion, when compared to saline controls. Glandular-like cells in submucosa, consistent with intestinal metaplasia, confirmed by Alcin Blue-PAS staining were observed after bone marrow esophageal implantation along with bile perfusion, but not with acid perfusion and controls. Bone marrow implantation in conjunction with esophageal reflux injury contributes to abnormal histological changes consistent with early Barrett's esophageal changes. Engrafted bone marrow cells proliferate under oxidative stress conditions with bile perfusion.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2006

Risk factors for post-ERCP pancreatitis: a prospective multicenter study.

OBJECTIVES: Pancreatitis is the most common and serious complication of diagnostic and therapeutic ERCP. The aim of this study is to examine the potential patient- and procedure-related risk factors for post-ERCP pancreatitis in a prospective multicenter study. METHODS: A 160-variable database was prospectively collected by a defined protocol on patients undergoing diagnostic or therapeutic ERCP at 15 centers in the Midwest Pancreaticobiliary Group and participating in a randomized controlled study evaluating whether prophylactic corticosteroids will reduce the incidence of post-ERCP pancreatitis. Data were collected prior to the procedure, at the time of procedure, and 24-72 h after discharge. Post-ERCP pancreatitis was diagnosed and its severity graded according to consensus criteria. RESULTS: Of the 1,115 patients enrolled, diagnostic ERCP with or without sphincter of Oddi manometry (SOM) was performed in 536 (48.1%) and therapeutic ERCP in 579 (51.9%). Suspected sphincter of Oddi dysfunction (SOD) was the indication for the ERCP in 378 patients (33.9%). Pancreatitis developed in 168 patients (15.1%) and was graded mild in 112 (10%), moderate in 45 (4%), and severe in 11(1%). There was no difference in the incidence of pancreatitis or the frequency of investigated potential pancreatitis risk factors between the corticosteroid and placebo groups. By univariate analysis, the incidence of post-ERCP pancreatitis was significantly higher in 19 of 30 investigated variables. In the multivariate risk model, significant risk factors with adjusted odds ratios (OR) were: minor papilla sphincterotomy (OR: 3.8), suspected SOD (OR: 2.6), history of post-ERCP pancreatitis (OR: 2.0), age <60 yr (OR: 1.6), > or =2 contrast injections into the pancreatic duct (OR: 1.5), and trainee involvement (OR: 1.5). Female gender, history of recurrent idiopathic pancreatitis, pancreas divisum, SOM, difficult cannulation, and major papilla sphincterotomy (either biliary or pancreatic) were not multivariate risk factors for post-ERCP pancreatitis. CONCLUSION: This study emphasizes the role of patient factors (age, SOD, prior history of post-ERCP pancreatitis) and technical factors (number of PD injections, minor papilla sphincterotomy, and operator experience) as the determining high-risk predictors for post-ERCP pancreatitis.

Adult↗

PubMed2005

Esophageal injury with external esophageal perfusion.

BACKGROUND: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). This study is to evaluate the EEP rat model for esophagitis induced by using a micro-osmotic pump with bile perfusion. METHODS: Eighteen adult rats underwent the EEP procedure. Bile (0.5% bovine bile, pH 7.4) was used as perfusion agent and three types of perfusions were performed: 1 week perfusion, 2 weeks perfusion, and 4 weeks perfusion compared to saline perfusion and sham operation. Histological changes, cell proliferation, apoptosis, 8-hydroxy-deoxyguanosine (8-OH-dG) and Manganese superoxide dismutase (MnSOD) were observed after perfusion and compared. RESULTS: The bile perfusion for 1 week, 2 weeks, and 4 weeks induced mucosa infiltration of inflammatory cells, basal cell hyperproliferation, and papillae hypertrophy in all animals. Histopathology and cellular changes consistent with the findings associated with reflux esophagitis. The apoptotic index, the proliferating index, and expression of 8-OH-dG were significantly increased in the esophageal mucosa compared to controls. MnSOD expression was decreased with bile perfusion compared to saline controls. CONCLUSIONS: The external esophageal perfusion model enabled precise control of the injurious agent. It induced the typical histological injury and cellular changes seen in severe reflux esophagitis. The cellular changes in apoptosis, proliferation and anti-oxidant defense make this model unique for reflux esophagitis studies. Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2003

Does prophylactic administration of corticosteroid reduce the risk and severity of post-ERCP pancreatitis: a randomized, prospective, multicenter study.

BACKGROUND: Pancreatitis is the most common major complication of diagnostic and therapeutic ERCP. There have been continuing efforts to identify a pharmacologic agent capable of reducing the frequency and severity of this complication. On the basis of several case reports, experimental data, and knowledge of their mechanism of action, corticosteroids might be effective in this regard. The aim of this randomized, double-blind, controlled trial was to determine whether prophylactic, orally administered corticosteroid reduces the frequency and/or severity of post-ERCP pancreatitis. METHODS: A total of 1115 patients were randomized to receive either prednisone (40 mg) or a placebo orally 15 hours and 3 hours before ERCP. A 160 variable database was prospectively collected according to a defined protocol on patients undergoing diagnostic or therapeutic ERCP at 15 centers in the Midwest Pancreaticobiliary Group. Standardized criteria were used to diagnose and grade the severity of postprocedure pancreatitis. RESULTS: The overall frequency of pancreatitis was 15.07%. It occurred in 92 of 555 patients in the corticosteroid group (16.6%), and in 76 of 560 patients in the control group (13.6%; p = 0.19). The pancreatitis was mild in 10.04%, moderate in 4.04%, and severe in 0.99%. There was no difference between the groups with regard to the severity of pancreatitis. Moreover, the groups were similar with regard to age, gender, body mass index, frequency of prior pancreatitis, type of procedure performed (diagnostic or therapeutic), difficulty of cannulation, frequency of pre-cut sphincterotomy, pancreatic sphincterotomy, sphincter of Oddi dysfunction, sphincter of Oddi manometry, pancreatic acinarization, chronic pancreatitis, number of pancreatic duct injections, and bile duct diameter. CONCLUSION: Prophylactic orally administered corticosteroid did not reduce the frequency or severity of post-ERCP pancreatitis.

Administration, Oral↗