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1.
Cureus ; 13(12): e20737, 2021 Dec.
Article in English | MEDLINE | ID: mdl-34984161

ABSTRACT

Additional anatomical structures are rare but can be mistaken for other conditions, causing misdiagnoses and poor outcomes for patients. The presence of concurrent anomalies within the extra structures further complicates a rare situation. We present a case of a patient with two gallbladders and a choledochal cyst diagnosed via radiography and confirmed by exploratory laparotomy. He underwent a cholecystectomy, choledochal cyst resection, and hepaticojejunostomy, and he was doing well as of his last follow-up. This case highlights the need to consider radiological imaging in patients with choledochal cysts carefully.

3.
Am J Surg ; 214(6): 1048-1052, 2017 Dec.
Article in English | MEDLINE | ID: mdl-29017731

ABSTRACT

INTRODUCTION: The elderly account for a large proportion of morbidity and mortality secondary to trauma, despite lower-energy mechanisms of injury and fewer trauma admissions. The benefit of geriatric trauma consultation services (GTCS) to this population remains unclear. METHODS: We performed a retrospective cohort analysis of a GTCS, which was established in January 2015. Patients over 60 admitted to the trauma service from January of 2014 to February 2016 were eligible. RESULTS: There were no significant differences in 30-day and in-hospital mortalities, mean ICU and total lengths of stay, or complication rates. However, if a single complication was experienced, post-GTCS patients were nearly three times more likely to experience multiple complications. More patients in the GTCS group were discharged home, but were readmitted four times more often. CONCLUSIONS: A mandatory GTCS was not associated with improved patient outcomes, suggesting that management exclusively by the trauma team is at least equally effective in treatment of geriatric trauma.


Subject(s)
Geriatric Assessment , Hospital Mortality , Wounds and Injuries/mortality , Wounds and Injuries/therapy , Aged , Aged, 80 and over , Female , Humans , Injury Severity Score , Male , Ohio , Retrospective Studies , Trauma Centers
4.
PLoS One ; 8(2): e55820, 2013.
Article in English | MEDLINE | ID: mdl-23437065

ABSTRACT

BACKGROUND: Bmi1 is an integral component of the Polycomb Repressive Complex 1 (PRC1) and is involved in the pathogenesis of multiple cancers. It also plays a key role in the functioning of endogenous stem cells and cancer stem cells. Previous work implicated a role for cancer stem cells in the pathogenesis of pancreatic cancer. We hypothesized that Bmi1 plays an integral role in enhancing pancreatic tumorigenicity and the function of cancer stem cells in pancreatic ductal adenocarcinoma. METHODS: We measured endogenous Bmi1 levels in primary human pancreatic ductal adenocarcinomas, pancreatic intraepithelial neoplasias (PanINs) and normal pancreas by immunohistochemistry and Western blotting. The function of Bmi1 in pancreatic cancer was assessed by alteration of Bmi1 expression in several cell model systems by measuring cell proliferation, cell apoptosis, in vitro invasion, chemotherapy resistance, and in vivo growth and metastasis in an orthotopic model of pancreatic cancer. We also assessed the cancer stem cell frequency, tumorsphere formation, and in vivo growth of human pancreatic cancer xenografts after Bmi1 silencing. RESULTS: Bmi1 was overexpressed in human PanINs, pancreatic cancers, and in several pancreatic cancer cell lines. Overexpression of Bmi1 in MiaPaCa2 cells resulted in increased proliferation, in vitro invasion, larger in vivo tumors, more metastases, and gemcitabine resistance while opposite results were seen when Bmi1 was silenced in Panc-1 cells. Bmi1 was overexpressed in the cancer stem cell compartment of primary human pancreatic cancer xenografts. Pancreatic tumorspheres also demonstrated high levels of Bmi1. Silencing of Bmi1 inhibited secondary and tertiary tumorsphere formation, decreased primary pancreatic xenograft growth, and lowered the proportion of cancer stem cells in the xenograft tissue. CONCLUSIONS: Our results implicate Bmi1 in the invasiveness and growth of pancreatic cancer and demonstrate its key role in the regulation of pancreatic cancer stem cells.


Subject(s)
Adenocarcinoma/metabolism , Adenocarcinoma/pathology , Cell Transformation, Neoplastic/pathology , Neoplastic Stem Cells/pathology , Pancreatic Neoplasms/metabolism , Pancreatic Neoplasms/pathology , Polycomb Repressive Complex 1/metabolism , Animals , Apoptosis/drug effects , Carcinoma in Situ/drug therapy , Carcinoma in Situ/metabolism , Carcinoma in Situ/pathology , Cell Count , Cell Cycle/drug effects , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Transformation, Neoplastic/metabolism , Deoxycytidine/analogs & derivatives , Deoxycytidine/pharmacology , Deoxycytidine/therapeutic use , Drug Resistance, Neoplasm/drug effects , Gene Silencing/drug effects , Humans , Mice , Neoplasm Invasiveness , Neoplasm Metastasis , Neoplastic Stem Cells/metabolism , Pancreatic Neoplasms/drug therapy , Phenotype , Xenograft Model Antitumor Assays , Gemcitabine
5.
Cancer Cell ; 15(3): 207-19, 2009 Mar 03.
Article in English | MEDLINE | ID: mdl-19249679

ABSTRACT

Pancreatic cancer is a deadly disease characterized by late diagnosis and resistance to therapy. Much progress has been made in defining gene defects in pancreatic cancer, but a full accounting of its molecular pathogenesis remains to be provided. Here, we show that expression of the ataxia-telangiectasia group D complementing gene (ATDC), also called TRIM29, is elevated in most invasive pancreatic cancers and pancreatic cancer precursor lesions. ATDC promoted cancer cell proliferation in vitro and enhanced tumor growth and metastasis in vivo. ATDC expression correlated with elevated beta-catenin levels in pancreatic cancer, and beta-catenin function was required for ATDC's oncogenic effects. ATDC was found to stabilize beta-catenin via ATDC-induced effects on the Disheveled-2 protein, a negative regulator of glycogen synthase kinase 3beta in the Wnt/beta-catenin signaling pathway.


Subject(s)
DNA-Binding Proteins/genetics , Pancreatic Neoplasms/genetics , Signal Transduction/physiology , Transcription Factors/genetics , Wnt Proteins/metabolism , beta Catenin/metabolism , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Animals , Blotting, Western , Dishevelled Proteins , Gene Expression , Gene Expression Regulation, Neoplastic , Humans , Immunohistochemistry , Immunoprecipitation , Male , Pancreatic Neoplasms/metabolism , Phosphoproteins/genetics , Phosphoproteins/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Wnt Proteins/genetics
6.
Transplantation ; 86(11): 1560-4, 2008 Dec 15.
Article in English | MEDLINE | ID: mdl-19077890

ABSTRACT

BACKGROUND: Urologic complications cause substantial morbidity in the pediatric population after renal transplantation, but their impact on graft survival and transplant costs is poorly understood. In this retrospective review, we evaluated the records of all pediatric renal transplant recipients at our center from 1995 to 2004. METHODS: Patient demographics, presence of urinary leak, stricture, compression, or vesicoureteral reflux, and hospital costs were analyzed. Univariable analysis identified predictors of complications and of need for reoperation, and Kaplan-Meier analysis was used to assess graft survival in relation to urinary complications. RESULTS: One hundred forty-seven children received renal transplants; mean follow-up was 1478+/-965 days. Nine (6.1%) patients had urologic complications and seven (4.8%) patients developed vesicoureteral reflux requiring reoperation. Sex, ischemia time, race, previous transplant, donor type, nephrectomy technique, and stent use did not affect the incidence of urologic complications. Previous urologic reconstruction and pretransplant ureteral pathologic conditions increased the risk of urologic complication and vesicoureteral reflux. Patients with urologic complications had equivalent graft survival, but triple the hospital costs of unaffected recipients. CONCLUSIONS: Prior urologic surgery is associated with increased risk of urologic complications posttransplant. Posttransplant urologic complications are associated with substantially increased costs in the first year after transplant, but not with decreased graft survival.


Subject(s)
Kidney Transplantation/adverse effects , Kidney Transplantation/methods , Urologic Diseases/etiology , Adolescent , Child , Child, Preschool , Female , Graft Survival , Humans , Infant , Infant, Newborn , Kidney Transplantation/economics , Male , Reoperation , Retrospective Studies , Risk Factors , Treatment Outcome , Urologic Diseases/complications
7.
Liver Transpl ; 14(1): 73-80, 2008 Jan.
Article in English | MEDLINE | ID: mdl-18161843

ABSTRACT

Biliary complications remain a significant problem following liver transplantation in the Model for End-Stage Liver Disease (MELD) era. We hypothesized that donor, recipient, and technical variables may differentially affect anastomotic biliary complications in MELD era liver transplants. We reviewed 256 deceased donor liver transplants after the institution of MELD at our center and evaluated these variables' association with anastomotic biliary complications. The bile leak rate was 18%, and the stricture rate was 23%. Univariate analysis revealed that recipient age, MELD, donor age, and warm ischemia were risk factors for leak, whereas a Roux limb or stent was protective. A bile leak was a risk factor for anastomotic stricture, whereas use of histidine tryptophan ketoglutarate (HTK) versus University of Wisconsin (UW) solution was protective. Additionally, use of a transcystic tube/stent was also protective. Multivariate analysis showed that warm ischemia was the only independent risk factor for a leak, whereas development of a leak was the only independent risk factor for a stricture. HTK versus UW use and transcystic tube/stent use were the only independent protective factors against stricture. Use of an internal stent trended in the multivariate analysis toward being protective against leaks and strictures, but this was not quite statistically significant. This represents one of the first MELD era studies of deceased donor liver transplants evaluating factors affecting the incidence of anastomotic bile leaks and strictures. Donor, recipient, and technical factors appear to differentially affect the incidence of anastomotic biliary complications, with warm ischemia, use of HTK, and use of a stent emerging as the most important variables.


Subject(s)
Bile Ducts/surgery , Biliary Tract Diseases/etiology , Liver Failure/surgery , Liver Transplantation/adverse effects , Tissue Donors , Adolescent , Adult , Anastomosis, Surgical/methods , Biliary Tract Diseases/epidemiology , Biliary Tract Diseases/surgery , Child , Female , Follow-Up Studies , Humans , Incidence , Liver Transplantation/methods , Male , Postoperative Complications , Prognosis , Retrospective Studies , Risk Factors , Time Factors
9.
J Gastrointest Surg ; 11(2): 209-16, 2007 Feb.
Article in English | MEDLINE | ID: mdl-17390175

ABSTRACT

Total pancreatectomy has been used to treat both benign and malignant disease of the pancreas, but its use has been limited by concerns about management of the a-pancreatic state with its attendant total endocrine and exocrine insufficiency. Here, we review the indications for total pancreatectomy, operative technique, and improvements in the postoperative management of patients. Total pancreatectomy remains a viable option in the treatment of intractable pain associated with chronic pancreatitis, multicentric or extensive neuroendocrine tumors, patients with familial pancreatic cancer with premalignant lesions, and in patients with intraductal papillary mucinous neoplasia with diffuse ductal involvement or invasive disease. Improvements in postoperative management include auto-islet cell transplantation, advances in insulin formulations, and the use of glucagon rescue therapy which allow much tighter control of blood glucose than previously possible. This markedly lessens the risk of life-threatening hypoglycemia and decreases the risk of long-term complications, resulting in improved quality of life for these patients.


Subject(s)
Pancreatectomy , Chronic Disease , Exocrine Pancreatic Insufficiency/etiology , Exocrine Pancreatic Insufficiency/therapy , Fatty Liver/etiology , Fatty Liver/therapy , Humans , Liver Failure/etiology , Liver Failure/therapy , Pain, Intractable/etiology , Pain, Intractable/surgery , Pancreatectomy/adverse effects , Pancreatectomy/methods , Pancreatic Neoplasms/surgery , Pancreatitis/complications , Pancreatitis/surgery , Quality of Life
10.
Cancer Res ; 67(3): 1030-7, 2007 Feb 01.
Article in English | MEDLINE | ID: mdl-17283135

ABSTRACT

Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation.


Subject(s)
Adenocarcinoma/pathology , Neoplastic Stem Cells/parasitology , Pancreatic Neoplasms/pathology , Adenocarcinoma/immunology , Animals , Antigens, Neoplasm/biosynthesis , CD24 Antigen/biosynthesis , Disease Models, Animal , Humans , Hyaluronan Receptors/biosynthesis , Male , Mice , Mice, Inbred NOD , Mice, SCID , Neoplastic Stem Cells/immunology , Pancreatic Neoplasms/immunology , Signal Transduction , Transplantation, Heterologous , Up-Regulation
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