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Results: 1 to 10 of 11

Publication Record


Re-addressing the 2013 consensus guidelines for the diagnosis of insulitis in human type 1 diabetes: is change necessary?
Campbell-Thompson ML, Atkinson MA, Butler AE, Giepmans BN, von Herrath MG, Hyƶty H, Kay TW, Morgan NG, Powers AC, Pugliese A, Richardson SJ, In't Veld PA
(2017) Diabetologia 60: 753-755
MeSH Terms: Diabetes Mellitus, Type 1, Humans, Insulin, Islets of Langerhans, Mice, Inbred NOD, Pancreatic Diseases
Added April 26, 2017
0 Communities
1 Members
0 Resources
6 MeSH Terms
Variations of oral microbiota are associated with pancreatic diseases including pancreatic cancer.
Farrell JJ, Zhang L, Zhou H, Chia D, Elashoff D, Akin D, Paster BJ, Joshipura K, Wong DT
(2012) Gut 61: 582-8
MeSH Terms: Aged, Aged, 80 and over, Bacteria, Bacterial Typing Techniques, Biomarkers, Case-Control Studies, Female, Humans, Male, Metagenome, Middle Aged, Pancreatic Diseases, Pancreatic Neoplasms, Pancreatitis, Chronic, Phylogeny, RNA, Bacterial, RNA, Ribosomal, 16S, Real-Time Polymerase Chain Reaction, Saliva, Sensitivity and Specificity
Show Abstract · Added October 15, 2011
OBJECTIVE - The associations between oral diseases and increased risk of pancreatic cancer have been reported in several prospective cohort studies. In this study, we measured variations of salivary microbiota and evaluated their potential associations with pancreatic cancer and chronic pancreatitis.
METHODS - This study was divided into three phases: (1) microbial profiling using the Human Oral Microbe Identification Microarray to investigate salivary microbiota variation between 10 resectable patients with pancreatic cancer and 10 matched healthy controls, (2) identification and verification of bacterial candidates by real-time quantitative PCR (qPCR) and (3) validation of bacterial candidates by qPCR on an independent cohort of 28 resectable pancreatic cancer, 28 matched healthy control and 27 chronic pancreatitis samples.
RESULTS - Comprehensive comparison of the salivary microbiota between patients with pancreatic cancer and healthy control subjects revealed a significant variation of salivary microflora. Thirty-one bacterial species/clusters were increased in the saliva of patients with pancreatic cancer (n=10) in comparison to those of the healthy controls (n=10), whereas 25 bacterial species/clusters were decreased. Two out of six bacterial candidates (Neisseria elongata and Streptococcus mitis) were validated using the independent samples, showing significant variation (p<0.05, qPCR) between patients with pancreatic cancer and controls (n=56). Additionally, two bacteria (Granulicatella adiacens and S mitis) showed significant variation (p<0.05, qPCR) between chronic pancreatitis samples and controls (n=55). The combination of two bacterial biomarkers (N elongata and S mitis) yielded a receiver operating characteristic plot area under the curve value of 0.90 (95% CI 0.78 to 0.96, p<0.0001) with a 96.4% sensitivity and 82.1% specificity in distinguishing patients with pancreatic cancer from healthy subjects.
CONCLUSIONS - The authors observed associations between variations of patients' salivary microbiota with pancreatic cancer and chronic pancreatitis. This report also provides proof of salivary microbiota as an informative source for discovering non-invasive biomarkers of systemic diseases.
0 Communities
1 Members
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20 MeSH Terms
Conditional mutation of Pkd2 causes cystogenesis and upregulates beta-catenin.
Kim I, Ding T, Fu Y, Li C, Cui L, Li A, Lian P, Liang D, Wang DW, Guo C, Ma J, Zhao P, Coffey RJ, Zhan Q, Wu G
(2009) J Am Soc Nephrol 20: 2556-69
MeSH Terms: Animals, Apoptosis, Cell Line, Cell Proliferation, Cysts, Disease Models, Animal, Female, Kidney Tubules, Collecting, Liver Diseases, Male, Mice, Mice, Congenic, Mice, Inbred C57BL, Mice, Knockout, Mutation, Pancreatic Diseases, Phenotype, Polycystic Kidney, Autosomal Dominant, Pregnancy, Signal Transduction, TRPP Cation Channels, Up-Regulation, beta Catenin
Show Abstract · Added August 12, 2010
Loss of polycystin-2 (PC2) in mice (Pkd2(-/-)) results in total body edema, focal hemorrhage, structural cardiac defects, abnormal left-right axis, hepatorenal and pancreatic cysts, and embryonic lethality. The molecular mechanisms by which loss of PC2 leads to these phenotypes remain unknown. We generated a model to allow targeted Pkd2 inactivation using the Cre-loxP system. Global inactivation of Pkd2 produced a phenotype identical to Pkd2(-/-) mice with undetectable PC2 protein and perinatal lethality. Using various Cre mouse lines, we found that kidney, pancreas, or time-specific deletion of Pkd2 led to cyst formation. In addition, we developed an immortalized renal collecting duct cell line with inactive Pkd2; these cells had aberrant cell-cell contact, ciliogenesis, and tubulomorphogenesis. They also significantly upregulated beta-catenin, axin2, and cMyc. Our results suggest that loss of PC2 disrupts normal behavior of renal epithelial cells through dysregulation of beta-catenin-dependent signaling, revealing a potential role for this signaling pathway in PC2-associated ADPKD.
1 Communities
1 Members
0 Resources
23 MeSH Terms
Endocrine surgery: where are we today? A national survey of young endocrine surgeons.
Solorzano CC, Sosa JA, Lechner SC, Lew JI, Roman SA
(2010) Surgery 147: 536-41
MeSH Terms: Adrenalectomy, Adult, Career Choice, Continental Population Groups, Data Collection, Education, Medical, Graduate, Endocrine Glands, Endocrine Surgical Procedures, Fellowships and Scholarships, Female, Humans, Internship and Residency, Male, Middle Aged, Pancreatic Diseases, Thyroid Diseases, Thyroid Gland
Show Abstract · Added March 5, 2014
BACKGROUND - In recent years, there has been a growing interest in endocrine surgery. Educational objectives have been published by the American Association of Endocrine Surgeons (AAES), but data have not been collected describing the recruitment pool, fellowship, or postfellowship experiences.
METHODS - A survey was distributed to endocrine surgeons in practice <7 years and endocrine surgery fellows. Demographic, training, and practice data were collected.
RESULTS - The survey response rate was 69% (46/67); 85% were practicing endocrine surgeons and 15% were fellows. In all, 72% of respondents completed an endocrine surgery fellowship, 17% completed surgical oncology, and the remaining individuals completed no fellowship. The mean age was 38 (32-49) years; 39% were women, 67% were white, 26% were Asian, 11% were Hispanic, and 2% were black. A total of 89% completed residency at academic centers. Endocrine surgery fellows performed significantly more endocrine surgery cases in residency than the average graduating chief resident. Mentorship was a critical factor in fellows' decisions to pursue endocrine surgery. Fellows graduated with a median (range) of 150 (50-300) thyroid, 80 (35-200) parathyroid, 10 (2-50) neck dissection, 13 (0-60) laparoscopic adrenal, and 3 (0-35) endocrine-pancreas. Fellows felt the least prepared in neck dissection and pancreas. Of the respondents, 76% of endocrine surgeons in practice are at academic centers, and 75% have practices where most cases are endocrine based.
CONCLUSION - Exposure to endocrine surgery and mentorship are powerful factors that influence residents to pursue careers in endocrine surgery. Significant variation is found in the case distribution of fellowships with a relative paucity in neck dissection, pancreas procedures, and research. Recruitment to endocrine surgery should begin in residency, and the standardization of training should be a goal.
Copyright 2010 Mosby, Inc. All rights reserved.
0 Communities
1 Members
0 Resources
17 MeSH Terms
Transmembrane and soluble isoforms of heparin-binding epidermal growth factor-like growth factor regulate distinct processes in the pancreas.
Ray KC, Blaine SA, Washington MK, Braun AH, Singh AB, Harris RC, Harding PA, Coffey RJ, Means AL
(2009) Gastroenterology 137: 1785-94
MeSH Terms: Animals, Cell Culture Techniques, Cell Line, Glucose Intolerance, Heparin-binding EGF-like Growth Factor, Intercellular Signaling Peptides and Proteins, Islets of Langerhans, Membrane Proteins, Mice, Mice, Transgenic, Pancreatic Diseases, Protein Isoforms, Protein Precursors
Show Abstract · Added August 19, 2013
BACKGROUND & AIMS - Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is produced as a type-I, single-pass transmembrane protein that can be cleaved to release a diffusible peptide. HB-EGF, often overexpressed in damaged or diseased epithelium, is normally expressed in pancreatic islets, but its function is not understood.
METHODS - To understand the function of each isoform of HB-EGF, we made transgenes expressing either a constitutively transmembrane or a constitutively secreted protein.
RESULTS - The transmembrane isoform was not an inert precursor protein, but a functional molecule, downregulating the glucose-sensing apparatus of pancreatic islets. Conversely, the secreted form of HB-EGF improved islet function, but had severe fibrotic and neoplastic effects on surrounding tissues. Each isoform had a more severe phenotype than that of full-length HB-EGF, even though the full-length protein was efficiently cleaved, thus producing both isoforms, suggesting that a level of regulation was lost by separating the isoforms.
CONCLUSIONS - This work demonstrates that islet function depends on the ratio of cleaved to uncleaved HB-EGF and that the transmembrane intermediate, while deleterious to islet function, is necessary to restrict action of soluble HB-EGF away from surrounding tissue.
3 Communities
5 Members
0 Resources
13 MeSH Terms
Epidermal growth factor receptor regulates pancreatic fibrosis.
Blaine SA, Ray KC, Branch KM, Robinson PS, Whitehead RH, Means AL
(2009) Am J Physiol Gastrointest Liver Physiol 297: G434-41
MeSH Terms: Animals, Cell Line, Cell Proliferation, Chemotaxis, Disease Models, Animal, ErbB Receptors, Fibrosis, Heparin-binding EGF-like Growth Factor, Homeodomain Proteins, Intercellular Signaling Peptides and Proteins, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Pancreas, Pancreatic Diseases, Recombinant Proteins, Signal Transduction, Trans-Activators
Show Abstract · Added July 19, 2013
The development of pancreatic fibrosis has been shown to be a major component in several diseases of the pancreas including pancreatic cancer, chronic pancreatitis, and type 2 diabetes mellitus, but its actual role in the progression of these disorders is still unknown. This fibrosis is characterized by stromal expansion and the excessive deposition of extracellular matrix (ECM) that replaces pancreatic tissue. This eventually leads to dysregulation of ECM turnover, production of cytokines, restriction of blood flow, and often exocrine and endocrine insufficiencies. Activated pancreatic stellate cells (PSCs) have been identified as key mediators in the progression of pancreatic fibrosis, serving as the predominant source of excess ECM proteins. Previously, we found that overexpression of the growth factor heparin-binding epidermal growth factor-like growth factor (HB-EGF) in pancreatic islets led to intraislet fibrosis. HB-EGF binds to and activates two receptors, epidermal growth factor receptor (EGFR) and ErbB4, as well as heparin moieties and CD9/DRAP27. To understand the mechanism underlying the induction of fibrogenesis by HB-EGF, we utilized a hypomorphic allele of Egfr, the Waved-2 allele, to demonstrate that EGFR signaling regulates fibrogenesis in vivo. Using an in vitro cell migration assay, we show that HB-EGF regulates both chemoattraction and stimulation of proliferation of PSCs via EGFR activation.
1 Communities
1 Members
0 Resources
19 MeSH Terms
Left-sided pancreatectomy: a multicenter comparison of laparoscopic and open approaches.
Kooby DA, Gillespie T, Bentrem D, Nakeeb A, Schmidt MC, Merchant NB, Parikh AA, Martin RC, Scoggins CR, Ahmad S, Kim HJ, Park J, Johnston F, Strouch MJ, Menze A, Rymer J, McClaine R, Strasberg SM, Talamonti MS, Staley CA, McMasters KM, Lowy AM, Byrd-Sellers J, Wood WC, Hawkins WG
(2008) Ann Surg 248: 438-46
MeSH Terms: Adult, Aged, Cohort Studies, Female, Humans, Laparoscopy, Male, Middle Aged, Pancreatectomy, Pancreatic Diseases, Pancreatic Fistula, Retrospective Studies
Show Abstract · Added March 26, 2014
OBJECTIVES - To compare perioperative outcomes of laparoscopic left-sided pancreatectomy (LLP) with traditional open left-sided pancreatectomy (OLP) in a multicenter experience.
SUMMARY AND BACKGROUND DATA - LLP is being performed more commonly with limited data comparing results with outcomes from OLP.
METHODS - Data from 8 centers were combined for all cases performed between 2002-2006. OLP and LLP cohorts were matched by age, American Society of Anesthesiologists, resected pancreas length, tumor size, and diagnosis. Multivariate analysis was performed using binary logistic regression.
RESULTS - Six hundred sixty-seven LPs were performed, with 159 (24%) attempted laparoscopically. Indications were solid lesion in 307 (46%), cystic in 295 (44%), and pancreatitis in 65 (10%) cases. Positive margins occurred in 51 (8%) cases, 335 (50%) had complications, and significant leaks occurred in 108 (16%). Conversion to OLP occurred in 20 (13%) of the LLPs. In the matched comparison, 200 OLPs were compared with 142 LLPs. There were no differences in positive margin rates (8% vs. 7%, P = 0.8), operative times (216 vs. 230 minutes, P = 0.3), or leak rates (18% vs. 11%, P = 0.1). LLP patients had lower average blood loss (357 vs. 588 mL, P < 0.01), fewer complications (40% vs. 57%, P < 0.01), and shorter hospital stays (5.9 vs. 9.0 days, P < 0.01). By MVA, LLP was an independent factor for shorter hospital stay (P < 0.01, odds ratio 0.33, 95% confidence interval 0.19-0.56).
CONCLUSIONS - In selected patients, LLP is associated with less morbidity and shorter LOS than OLP. Pancreatic fistula rates are similar for OLP and LLP. LLP is appropriate for selected patients with left-sided pancreatic pathology.
0 Communities
2 Members
0 Resources
12 MeSH Terms
Gene expression profiling of a mouse model of pancreatic islet dysmorphogenesis.
Wilding Crawford L, Tweedie Ables E, Oh YA, Boone B, Levy S, Gannon M
(2008) PLoS One 3: e1611
MeSH Terms: Animals, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Developmental, Genomics, Hepatocyte Nuclear Factor 6, Islets of Langerhans, Mice, Mice, Transgenic, Morphogenesis, Pancreatic Diseases
Show Abstract · Added January 6, 2014
BACKGROUND - In the past decade, several transcription factors critical for pancreas organogenesis have been identified. Despite this success, many of the factors necessary for proper islet morphogenesis and function remain uncharacterized. Previous studies have shown that transgenic over-expression of the transcription factor Hnf6 specifically in the pancreatic endocrine cell lineage resulted in disruptions in islet morphogenesis, including dysfunctional endocrine cell sorting, increased individual islet size, increased number of peripheral endocrine cell types, and failure of islets to migrate away from the ductal epithelium. The mechanisms whereby maintained Hnf6 causes defects in islet morphogenesis have yet to be elucidated.
METHODOLOGY/PRINCIPAL FINDINGS - We exploited the dysmorphic islets in Hnf6 transgenic animals as a tool to identify factors important for islet morphogenesis. Genome-wide microarray analysis was used to identify differences in the gene expression profiles of late gestation and early postnatal total pancreas tissue from wild type and Hnf6 transgenic animals. Here we report the identification of genes with an altered expression in Hnf6 transgenic animals and highlight factors with potential importance in islet morphogenesis. Importantly, gene products involved in cell adhesion, cell migration, ECM remodeling and proliferation were found to be altered in Hnf6 transgenic pancreata, revealing specific candidates that can now be analyzed directly for their role in these processes during islet development.
CONCLUSIONS/SIGNIFICANCE - This study provides a unique dataset that can act as a starting point for other investigators to explore the role of the identified genes in pancreatogenesis, islet morphogenesis and mature beta cell function.
2 Communities
1 Members
0 Resources
11 MeSH Terms
Reovirus delays diabetes onset but does not prevent insulitis in nonobese diabetic mice.
Wetzel JD, Barton ES, Chappell JD, Baer GS, Mochow-Grundy M, Rodgers SE, Shyr Y, Powers AC, Thomas JW, Dermody TS
(2006) J Virol 80: 3078-82
MeSH Terms: Animals, Animals, Newborn, Autoimmune Diseases, Diabetes Mellitus, Female, Islets of Langerhans, Mammalian orthoreovirus 3, Mice, Mice, Inbred NOD, Pancreatic Diseases, Reoviridae Infections
Show Abstract · Added December 10, 2013
Mice infected with reovirus develop abnormalities in glucose homeostasis. Reovirus strain type 3 Abney (T3A) was capable of systemic infection of nonobese diabetic (NOD) mice, an experimental model of autoimmune diabetes. Reovirus antigen was detected in pancreatic islets of T3A-infected mice, and primary cultures of pancreatic islets from NOD mice supported T3A growth. Significantly fewer T3A-infected animals compared to uninfected controls developed diabetes. However, despite the alteration in diabetes penetrance, insulitis was evident in T3A-infected mice. These results suggest that viral infection of NOD mice alters autoimmune responses to beta-cell antigens and thereby delays development of diabetes.
1 Communities
1 Members
0 Resources
11 MeSH Terms
Screening asymptomatic diabetic patients for coronary artery disease prior to renal transplantation.
Ramanathan V, Goral S, Tanriover B, Feurer ID, Kazancioglu R, Shaffer D, Helderman JH
(2005) Transplantation 79: 1453-8
MeSH Terms: Adult, African Americans, Body Mass Index, Cardiac Catheterization, Coronary Artery Disease, Diabetes Complications, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Diabetic Angiopathies, Diabetic Nephropathies, European Continental Ancestry Group, Female, Humans, Kidney Transplantation, Male, Mass Screening, Middle Aged, Pancreas Transplantation, Pancreatic Diseases, Preoperative Care, Prevalence, Retrospective Studies
Show Abstract · Added March 4, 2014
BACKGROUND - Coronary artery disease (CAD) is a significant contributor to excess mortality in renal transplant candidates with diabetes mellitus (DM). Prior studies relating to risk stratification for significant CAD in diabetics are confined to Caucasian type 1 DM patients.
METHODS - To assess the prevalence of clinically silent CAD and to identify variables that are associated with CAD, we retrospectively analyzed the cardiac catheterization data of 97 asymptomatic type 1 and 2 DM kidney and kidney-pancreas transplant candidates.
RESULTS - Thirty-three percent of type 1 and 48% of type 2 DM patients had significant stenosis (> or = 70%) in 1 or more coronary arteries. On multivariate logistic regression analysis, body mass index (BMI) >25 was significantly associated with CAD (relative risk = 4.8, P = 0.002). The age of the patient (7% increase in risk/year, P = 0.01; or relative risk = 3.0 if age >47 years, P = 0.032) and smoking history (2% increase in risk/pack-year of smoking, P = 0.10) were also associated with CAD. African American patients, who comprised 30% of the sample, had a 71% lower risk compared with Caucasian patients (P = 0.03). Factors that were not significantly associated with CAD included gender, type of diabetes, and whether dialyzed for >6 months prior to catheterization.
CONCLUSIONS - We conclude that a notable proportion (approximately one-third to one-half) of asymptomatic type 1 and type 2 diabetic renal transplant candidates have significant CAD. Additionally, young African American DM patients with no smoking history and a BMI
0 Communities
1 Members
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22 MeSH Terms