PubMed Health⌕ Search

Biomedical subjects

W E Fisher

Publications and source records attributed to W E Fisher.

At least 19 recordsLinked to original sources
PubMed2006

Gastrotomy with anvil "dunk": a novel technique for gastrojejunostomy in the patient undergoing laparoscopic Roux-en-Y gastric bypass.

BACKGROUND: Many techniques for performing the gastrojejunostomy required in the laparoscopic roux-en-Y gastric bypass (LRYGB) have been described. The current study presents the results of a previously unreported method. METHODS: A total of 21 patients (2 men and 19 women) with morbid obesity underwent LRYGB over a period of 5 months. The gastrojejunostomy was created by performing a gastric transection to form a 20- to 30-ml pouch using a linear stapler. This was followed by gastrotomy using an ultrasonic scalpel along the anterior surface of the pouch. A purse-string suture then was placed circumferentially using standard laparoscopic intracorporeal suturing with an Endo-stitch device. Finally, a 25-mm circular stapler anvil was placed within the abdomen via the 15-mm left lower quadrant port site. The shaft of the anvil was grasped; the head of the anvil was "dunked" into the gastrotomy; and the purse-string suture was tied intracorporeally. RESULTS: A total of 21 patients have undergone LRYGB at the authors' institution using this technique. The early results have been excellent in all cases, with no leaks, no strictures, and no obstructions. CONCLUSION: Gastrotomy with anvil dunk is a reproducible and safe method for constructing the gastrojejunostomy. It is an advanced laparoscopic technique that closely resembles open surgical techniques and provides a safe alternative to existing methods.

Adult↗
PubMed2002

Laparoscopic ventral hernia repair during the learning curve.

Large series of laparoscopic ventral hernia repair have shown excellent results. However, published comparative studies have had conflicting outcomes. We retrospectively reviewed the first 29 laparoscopic ventral hernia repairs performed at a VA Medical Center from January 2000 to June 2001. The outcome was compared to that of open repairs performed during the same time period. Outcomes between the groups were similar in all respects, except for the length of stay. The conversion rate for the laparoscopic approach was 13.8%. There was one death in the laparoscopic group due to an unrecognized enterotomy. There were three recurrences in the open group and one in the laparoscopic group with a mean follow up of 13 months. In our series, laparoscopic hernia repair resulted in a shorter hospital stay but no other significant benefits, along with a risk of missed enterotomy. The risk-benefit ratio for this procedure may be high during the learning curve.

Clinical Competence↗
PubMed2001

Diabetes: risk factor for the development of pancreatic cancer or manifestation of the disease?

The objective of this study was to summarize the English-language literature that addresses diabetes mellitus as a potential risk factor for the development of pancreatic cancer. Studies exploring the relation between diabetes and pancreatic cancer published between 1970 and 1999 were identified from a MEDLINE search and are summarized. They showed that diabetes mellitus occurs more frequently in patients with pancreatic cancer than in the general population. Most of the literature supports the view that diabetes of at least 5 years' duration increases the risk of subsequently developing pancreatic cancer. In addition, experimental forms of diabetes clearly affect the induction and growth of pancreatic cancer. The currently available literature thus suggests that diabetes is a risk factor for the subsequent development of pancreatic cancer.

Animals↗
PubMed2001

Unique cause of duodenal obstruction by an abdominal aortic aneurysm.

We report herein a unique cause of duodenal obstruction secondary to expansion of an abdominal aortic aneurysm in a 75-year-old man with congenital malrotation of the intestines. The duodenum was found to be compressed between the abdominal aortic aneurysm inferiorly and the peritoneal band superiorly. The patient underwent uncomplicated lysis of peritoneal bands relieving the duodenal obstruction, followed by repair of the abdominal aortic aneurysm.

Abdominal Pain↗
PubMed2001

Spread of a pharyngeal cancer to the abdominal wall after percutaneous endoscopic gastrostomy.

Percutaneous endoscopic gastrostomy is frequently used in patients with head and neck cancer to establish enteral access for feeding. Spread of head and neck cancer to the gastrostomy site is a rare but increasingly reported complication after percutaneous endoscopic placement. We report the 13th such case in the literature, occurring in a 51-year-old black man with squamous cell carcinoma of the hypopharynx. The mode of tumor spread to the gastrostomy site remains debatable. Evidence exists for hematogenous dissemination and direct implantation. We think percutaneous endoscopic techniques for enteral access in this patient population are contraindicated, and we advocate a laparoscopic approach for gastrostomy placement.

Abdominal Muscles↗
PubMed1998

Genetic alterations in gastrinomas and nonfunctioning pancreatic neuroendocrine tumors: an analysis of p16/MTS1 tumor suppressor gene inactivation.

Neoplasms of the endocrine pancreas are extremely rare, and molecular mechanisms influencing their development are poorly understood. Nevertheless, gastrinomas have become a paradigm for the study of hormonally active tumors. In the present study, 12 gastrinoma and nonfunctioning pancreatic neuroendocrine tumor specimens were evaluated for genetic alterations of the p16/MTS1 tumor suppressor gene. DNA extracted from microdissected portions of paraffin-embedded tumor sections were examined for mutations and homozygous deletions using "Cold" single-strand conformation polymorphism and semiquantitative PCR-based analyses, respectively. Samples were also analyzed for the presence of 5' CpG island hypermethylation using methylation-specific PCR. The p16/MTS1 gene was found to be homozygously deleted in 41.7% of tumors and methylated in 58.3%, but no mutations were identified by single-strand conformation polymorphism analyses. Overall, 91.7% of the specimens demonstrated inactivating alterations in p16/MTS1. These data suggest that transcriptional silencing of p16/MTS1 is a frequent event in these rare and poorly understood tumors.

CpG Islands↗
PubMed1998

Oral dehydroepiandrosterone inhibits the growth of human pancreatic cancer in nude mice.

BACKGROUND: Dehydroepiandrosterone (DHEA), an androgen precursor, inhibits the induction of pancreatic cancer in some animal models. Our laboratory has previously demonstrated that the sulfated form of DHEA (DHAS), when administered by intraperitoneal injection, inhibits the growth of pancreatic cancer xenografts in nude mice. In the present study, we hypothesize that DHEA-mediated pancreatic cancer growth inhibition is associated with alterations in plasma sex hormone concentrations. MATERIALS AND METHODS: Forty male, nude, athymic mice were fed either Teklad 22/5 rodent diet or diet supplemented with 0.6% DHEA ad libitum. Four weeks following the institution of the experimental diets, 1 x 10(6) MiaPaCa-2 cells were injected into the right flank of each animal. Tumor area was recorded weekly and tumor weights were measured after 5 weeks. Plasma DHAS, testosterone, and progesterone concentrations were determined by radioimmunoassay. RESULTS: Plasma DHAS, testosterone, and progesterone concentrations were all significantly elevated in the DHEA-treated group. DHEA-treated mouse plasma DHAS concentrations were approximately 50-fold higher than controls. Mean tumor weight was significantly reduced in the DHEA group (68.9 +/- 39.1 vs 121.0 +/- 64.3). DHEA treatment did not result in significant animal weight reductions and toxic side effects were not observed. CONCLUSIONS: Dietary supplementation with 0.6% DHEA causes significant elevations in plasma DHAS concentration. DHEA administration significantly inhibits pancreatic cancer cell growth at plasma concentrations 1 x 10(5)-fold lower than previously reported. The mechanism of action may involve elevated concentrations of sex hormones.

Adjuvants, Immunologic↗
PubMed1998

Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma.

CONCLUSION: Gastrointestinal hormones and their antagonists can alter the growth of pancreatic adenocarcinoma in vitro and in vivo. The potential clinical benefit of this approach deserves further study. BACKGROUND: Epithelial cell growth is normally under hormonal control. Hormones also affect the growth of many epithelial cancers, and this fact is used to modify tumor growth. Pancreatic epithelial cell growth is under the influence of gastrointestinal hormones. This article reviews experiments designed to determine the effect of gastrointestinal hormones on the growth of pancreatic adenocarcinoma. METHODS: Eighty-eight articles were identified from a Medline search using the terms pancreatic adenocarcinoma and the individual names of gastrointestinal hormones. The experimental design and results of these studies are reviewed. RESULTS: In general, somatostatin, vasoactive intestinal polypeptide, pancreatic polypeptide, and pancreastatin inhibit pancreatic adenocarcinoma growth. Cholecystokinin, secretin, bombesin, gastrin, EGF, TGF-alpha, insulin, and IGF-1 have a growth-promoting effect.

Adenocarcinoma↗
PubMed1998

Seated-popliteal weight bearing prosthesis for a bilateral amputee.

Bilateral lower limb amputees suffer from a lack of stability when seated without prostheses due to lack of ground reaction forces through the stumps. In patients for whom ambulation is not a realistic goal, the seated-popliteal weight bearing prosthesis provides a solution for stability when seated in a wheelchair, without the problem of tibial pressure experienced with patellar-tendon-bearing prostheses.

Activities of Daily Living↗
PubMed1998

Variable effect of streptozotocin-diabetes on the growth of hamster pancreatic cancer (H2T) in the Syrian hamster and nude mouse.

BACKGROUND: Streptozotocin-diabetes prevents induction of pancreatic tumors in several animal models and inhibits the growth of established human pancreatic cancer implants in nude mice. However, it also promotes growth of the hamster pancreatic cancer cell line, H2T, in the Syrian hamster. To test the hypothesis that these contradictory effects are due to tumor host differences, the growth of the H2T cell line was examined in the streptozotocin-diabetic nude mouse. METHODS: H2T cells were implanted subcutaneously into streptozotocin-diabetic nude mice (n = 10) and untreated control mice (n = 10). After 21 days, tumors were excised and weighed. Plasma insulin and somatostatin were determined by radioimmunoassay. RESULTS: After 3 weeks, tumors in the control group weighed 118 mg and tumors in the diabetic group weighed 28 mg (p < 0.001). Plasma insulin was significantly decreased in the streptozotocin-treated animals compared with control animals (insulin, 23 microU/ml vs 31 microU/ml; p < 0.001). In contrast, somatostatin was significantly elevated in the streptozotocin-diabetic group compared with the control group (somatostatin, 179 pg/ml versus 54 pg/ml, p < 0.001). Competitive binding studies revealed specific cell surface receptors for insulin (Kd, 15.5 nmol/L), and somatostatin (Kd, 2.5 nmol/L) on the H2T cells. In an in vitro cell proliferation assay, cell division was promoted by insulin (p < 0.01, maximum +11%) and inhibited by somatostatin (p < 0.01, maximum -18%). CONCLUSIONS: The variable effect of streptozotocin-diabetes on pancreatic cancer growth is due to differences in the tumor host. The growth of pancreatic cancer, particularly in streptozotocin-diabetic nude mice, may be influenced by gut peptides in a receptor-dependent fashion.

Animals↗
PubMed1997

Dehydroepiandrosterone-sulfate inhibits pancreatic carcinoma cell proliferation in vitro and in vivo.

BACKGROUND: Dehydroepiandrosterone-sulfate (DHEA-S) is a potent inhibitor of glucose-6 phosphate dehydrogenase, the rate limiting enzyme of the hexose monophosphate shunt, a biochemical pathway that provides substrate for DNA synthesis in neoplastic tissue. DHEA-S has been shown to inhibit the growth of neoplasms arriving from human skin, lung, colon, and mammary tissue. This study evaluates the effect of DHEA-S on human pancreatic cancer cell lines in vitro and in vivo. METHODS: In vitro, the human pancreatic adenocarcinoma cell lines MiaPaCa-2, Capan-1, Capan-2, CAV and Panc-1 were treated with concentrations of 1.9 mumol/L to 1000 mumol/L DHEA-S in 1% dimethylsulfoxide (DMSO) for 5 consecutive days. Cell proliferation was determined by a nonradioactive cell proliferation assay and compared with DMSO treated controls. In vivo testing was performed by inoculating two cell lines, MiaPaCa-2 and Panc-I, into the flank of 40 male nude athymic mice in four study groups. After 1 week of growth, 667 mg/kg DHEA-S in 1% DMSO or 0.2 ml 1% DMSO alone in the control group was administered by daily intraperitoneal injection. Body weight and tumor size was recorded weekly, and tumor weight was measured after 3 weeks of treatment. RESULTS: In vitro cell proliferation was decreased in the five cell lines by 36% to 62% of controls (p < 0.001) at 500 mumol/L DHEA-S. In vivo, after 2 weeks, tumor size was only 76% (p < 0.008) and 67% (p < 0.005) of the controls. After 3 weeks of treatment, tumor size was 73% (p < 0.001) and 53% (p < 0.001) of controls, and tumor weight was decreased by 73% in MiaPaCa-2 (p < 0.001) and 66% in Panc-1 (p < 0.001). Radioimmunoassay measurements of DHEA-S and testosterone from DHEA-S treated mouse plasma showed a significant increase in circulating levels of these hormones. CONCLUSIONS: DHEA-S achieves high serum levels after intraperitoneal injection without elevation of serum testosterone levels and produces no significant toxicity. Treatment with DHEA-S results in a significant reduction of proliferation of human pancreatic cancer cells in culture and when grown as subcutaneous tumors in athymic nude mice.

Adenocarcinoma↗
PubMed1996

Insulin promotes pancreatic cancer: evidence for endocrine influence on exocrine pancreatic tumors.

Type-II diabetes is a risk factor for pancreatic cancer. In addition, diabetic patients present with more advanced tumors and have shortened survival compared to stage-matched counterparts. We hypothesize that the diabetic endocrine milieu, particularly elevated plasma insulin, favors pancreatic cancer growth. This study examines six human pancreatic cancer cell lines for the presence of insulin receptors and the influence of insulin on tumor proliferation. Classical competitive binding assays are performed using [125I insulin. Cell proliferation assays are conducted over 3 days on cultured cell lines (n = 6 replicates) with increasing concentrations of insulin. Insulin receptors are demonstrated on all six cell lines and dose dependent increases in cell proliferation (15-120% of control) are demonstrated in response to insulin. Patients with type-II diabetes hypersecrete insulin. The presence of high-affinity insulin receptors and dose dependent increases in pancreatic cancer cell proliferation with insulin supports the hypothesis that insulin may be an important tumor growth promoter in diabetes, particularly if paracrine mechanisms are involved. Additional study is required to determine whether other islet peptides altered in diabetes influence tumor growth and whether elevated plasma insulin favors pancreatic cancer induction.

Adenocarcinoma↗
PubMed1996

Expression of the somatostatin receptor subtype-2 gene predicts response of human pancreatic cancer to octreotide.

BACKGROUND: Somatostatin inhibits proliferation of many solid tumors. The current study examines whether inhibition of the growth of pancreatic cancer by the somatostatin analog, octreotide, requires tumor expression of somatostatin receptors. METHODS: We studied five human pancreatic cancer cell lines, Capan-1, Capan-2, CAV, MIA PaCa-2, and Panc-1. Solid tumors were established in nude mice (n = 20/cell line) by flank injection of tumor cells. Subcutaneous octreotide (500 micrograms/kg/day) was administered by osmotic pumps to 10 of the animals in each group, and the other 10 received control infusions of saline solution. On day 36, the tumors were excised and weighed. Plasma levels of the putative trophic peptides cholecystokinin, epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), and insulin were assessed by radioimmunoassay. Each of the five cell lines was assayed for the presence of cell surface somatostatin receptors by using whole cell competitive binding assays with 125I-somatostatin. Expression of the somatostatin receptor subtype-2 (SSR2) gene was determined with reverse transcriptase-polymerase chain reactions. Southern blot hybridization was used to assess the presence of the SSR2 gene. RESULTS: Octreotide inhibited tumor growth in the MIA PaCa-2 group (512 +/- 75 mg control versus 285 +/- 71 mg treated; p < 0.05) but had no significant effect on tumor weight in the other four cell lines. Plasma levels of cholecystokinin, epidermal growth factor, insulin-like growth factor-1, and insulin were not altered by chronic octreotide infusion. Cell surface somatostatin receptors and SSR2 gene expression were detected only in the MIA PaCa-2 tumors. The gene for the SSR2 receptor was found in all five tumor lines. CONCLUSIONS: Octreotide-mediated inhibition of pancreatic cancer growth is dependent on expression of somatostatin receptors. The expression of somatostatin receptors should be considered in the design and interpretation of clinical trials with somatostatin analogs for treatment of pancreatic cancer.

Adenocarcinoma↗
PubMed1995

GI hormonal changes in diabetes influence pancreatic cancer growth.

Streptozotocin diabetes prevents induction of pancreatic tumors in several animal models, suggesting a pivotal role for islet cell products in the pathogenesis of pancreatic cancer. To test the hypothesis that altered gastrointestinal peptide levels in streptozotocin diabetes influence tumor growth, human pancreatic cancer cells (MIA PaCa-2) were implanted subcutaneously into streptozotocin diabetic nude mice. After 3 weeks, tumors in the control group weighed 43 mg and tumors in the diabetic group weighed 12 mg (P < 0.001). Plasma insulin and IGF-1 levels were significantly decreased in the streptozotocin-treated animals compared to those of control (insulin: 23 microU/ml vs 31 microU/ml, P < 0.001; IGF-1: 254 ng/ml vs 324 ng/ml, P < 0.001). In contrast, somatostatin and glucagon were significantly elevated in the streptozotocin diabetic group relative to control levels (somatostatin: 179 pg/ml vs 54 pg/ml, P < 0.001; glucagon: 290 pg/ml vs 134 pg/ml, P < 0.001). Competitive binding studies revealed specific cell surface receptors for insulin (Kd = 15.5 nM), IGF-1 (Kd = 30.0 nM), and somatostatin (Kd = 2.5 nM) on the MIA PaCa-2 cells. Receptors for glucagon were absent. In an in vitro cell proliferation assay, cell division was promoted by insulin (P < 0.01, max + 11%) and IGF-1 (P < 0.01, max + 10%). Somatostatin inhibited cell division (P < 0.01, max - 18%). No effect was seen with glucagon. The growth of pancreatic cancer, particularly in diabetes, may be influenced by gut peptides in a receptor-dependent fashion.

Animals↗
PubMed1995

Reversal of enhanced pancreatic cancer growth in diabetes by insulin.

BACKGROUND: Epidemiologic and animal studies have linked pancreatic cancer growth with both diabetes and fat intake. This study examined the influence of insulin treatment on pancreatic cancer growth in diabetes. Diabetes-induced elevations in levels of glucose and free fatty acids were correlated with enhanced tumor growth both in vivo and in vitro. METHODS: Hamsters were divided into three groups: control (n = 15), streptozocin-diabetic (n = 20), or insulin-treated diabetic (n = 20). Diabetes was induced with streptozocin and treated with a continuous subcutaneous infusion of insulin delivered via osmotic pumps. Five x 10(5) H2T hamster pancreatic cancer cells were implanted into the cheek pouch. Levels of plasma glucose and fatty acids were measured, and their effect on H2T cell division was assessed in vitro with a spectrophotometric cell proliferation assay. RESULTS: Levels of plasma glucose and fatty acids were elevated in streptozocin-diabetic animals and normalized with insulin treatment. After 21 days of growth, tumor weight was 36 mg in the control group, 156 mg in the diabetic group (p < 0.01 versus other groups), and 33 mg in the insulin-treated diabetic group. In vitro dose-dependent promotion of cell growth was shown for glucose (250%), linoleic acid (287%), linolenic acid (169%), and oleic acid (98%). CONCLUSIONS: Insulin ameliorated enhanced tumor growth in this model of diabetes. Glucose and free fatty acids mobilized during diabetes may serve as fuel for established pancreatic cancers.

Animals↗