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R C Burns

Publications and source records attributed to R C Burns.

At least 19 recordsLinked to original sources
PubMed2004

Requirement for fibroblast growth factor 10 or fibroblast growth factor receptor 2-IIIb signaling for cecal development in mouse.

Epithelial-mesenchymal interactions are critical for the formation of gastrointestinal buds such as the cecum from the midgut, but the mechanisms regulating this process remain unclear. To investigate this problem, we have studied the temporal and spatial expression of key genes known to orchestrate branching morphogenesis. At E10.5, Fibroblast growth factor 10 (Fgf10) is specifically expressed in the mesenchyme above the future cecal epithelial bud, whereas Fgfr2b is found throughout the gut epithelium. From E11.5 onwards, Fgf10 expression is found throughout the cecum mesenchyme. Other relevant signaling molecules such as Sonic hedgehog, Wnt2b, and Tbx4 transcripts are found throughout the gut epithelium, including the cecum. Epithelial expression is also seen for Sprouty2, but only from E14.5 onwards. By contrast, Bone morphogenetic 4 (Bmp4) and Pitx2 are specifically expressed in the mesenchyme of the cecal bud at E11.5. Abrogation of either Fgf10 or Fgfr2b leads to similar phenotypes characterized by an arrest of epithelial invasion into the cecal mesenchymal tissue. However, a bud of undifferentiated cecal mesenchymal tissue is maintained throughout development. Our results further indicate that mesenchymal FGF10 acts mostly through the epithelial FGFR2b receptor; thereby triggering invasion of the midgut epithelium into the adjacent mesenchyme via an increased rate of epithelial proliferation at the tip of the cecum. Thus, FGF10 signaling via FGFR2b appears to be critical in the extension of the epithelium into the mesenchyme during cecal development.

Actins↗
PubMed2004

A genetic mechanism for cecal atresia: the role of the Fgf10 signaling pathway.

BACKGROUND: Intestinal atresia represents a significant surgically correctable cause of intestinal obstruction in neonates. Intestinal development proceeds as a tube-like structure with differentiation along its axis. As the intestine differentiates, the cecum develops at the transition from small to large intestine. Fgf10 is known to serve a key role in budding morphogenesis; however, little is known about its role in the development of this transitional structure. Here we evaluate the effect of Fgf10/Fgfr2b invalidation on the developing cecum. MATERIALS AND METHODS: Wild-type C57Bl/6, Fgf10(-/-), and Fgfr2b(-/-) embryos harvested from timed pregnant mothers were analyzed for cecal phenotype, Fgf10 expression, and differentiation of smooth muscle actin. RESULTS: Wt cecal development is first evident at E11.5. FGF10 is discreetly expressed in the area of the developing cecum at early stages of development. One hundred percent of Fgf10(-/-) and Fgfr2b(-/-) mutant embryos demonstrate cecal atresia with absence of epithelial and muscular layers. The development of neighboring anatomical structures such as the ileocecal valve is not affected by Fgf10/Fgfr2b invalidation. CONCLUSIONS: FGF10 expression is localized to the cecum early in the normal development of the cecum. Fgf10(-/-) and Fgfr2b(-/-) mutant embryos demonstrate cecal atresia with complete penetrance. Epithelial and muscular layers of the cecum are not present in the atretic cecum. The Fgf10(-/-) and Fgfr2b(-/-) mutants represent a genetically reproducible animal model of autosomal recessive intestinal atresia.

Animals↗
PubMed2001

Pentapotassium dodecatungstoborate(III) hexadecahydrate.

The title compound, K(5)[BW(12)O(40)].16H(2)O, contains a [BW(12)O(40)](5-) polyanion of 222 crystallographic symmetry, with a central tetrahedrally coordinated B(III) atom surrounded by four groups of three edge-sharing octahedra (W(3)O(13) subunits), which are linked in turn to each other and to the central BO(4) tetrahedron by shared O atoms at the vertices. There is a crystallographically unique B-O bond of 1.554 (10) A, while the average W-O distances are 2.344 (17) A for four coordinate O atoms, 1.917 (12) and 1.89 (2) A for two coordinate O atoms within and connecting the W(3)O(13) subunits, respectively, and 1.709 (8) A for terminal O atoms. Not all of the K(+) ions and H(2)O groups were located.

Journal Article↗
PubMed2001

Electrospray characterization of perrhenate systems.

The electrospray negative ion mode (ESI-) mass spectrometry study of freshly prepared perrhenate in the ammonium and alkali metal (Na and K) solutions has been detailed. The cone voltage dependency of the negative ion abundance clearly indicates that the collision-activated dissociation (CAD) process in the cone-to-skimmer region is the source for both linear and non-linear cone voltage dependencies. The model also highlights that the [ReO2]- and [ReO3]- ions observed in the ESI- spectra are not present in the bulk, but are due to a dissociative collision, which strips a single oxygen atom from their precursor ions, namely [ReO3]- and [ReO4]- , respectively.

Algorithms↗
PubMed2001

Antibody blockade of ICAM-1 and VCAM-1 ameliorates inflammation in the SAMP-1/Yit adoptive transfer model of Crohn's disease in mice.

BACKGROUND & AIMS: Integrins (alpha(4) and beta(2)) and their endothelial ligands vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) play key roles in leukocyte recruitment to areas of inflammation. ICAM-1 and VCAM-1 are expressed in inflamed intestinal tissues. This study investigates a possible causative role of adhesion molecules ICAM-1, VCAM-1, and alpha(4) integrins in mediating the inflammatory response in a murine model of Crohn's disease (CD). METHODS: CD4+ mesenteric lymph node cells from SAMP-1/Yit donor mice were adoptively transferred into major histocompatibility complex-matched severe combined immunodeficiency disease mice. Six weeks later, these mice were left untreated or treated for 3 days with monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, or both, and alpha(4), or both ICAM-1 and alpha(4), dexamethasone, or nonblocking isotype control antibodies. On day 4 after treatment, tissues were investigated for expression of ICAM-1, VCAM-1, and for severity of inflammation using a semiquantitative inflammatory score. Dexamethasone treatment resolved all measures of intestinal inflammation. RESULTS: Blocking either ICAM-1, VCAM-1, or alpha(4) integrins had no significant beneficial effect. However, blocking ICAM-1 and alpha(4), or blocking ICAM-1 and VCAM-1, showed a 70% resolution of the active inflammation, but not chronic inflammation. CONCLUSIONS: These findings suggest that blocking ICAM-1 and VCAM-1 may have therapeutic benefit for the acute inflammatory component of Crohn's disease.

Adoptive Transfer↗
PubMed2001

Follow-up abdominal computed tomography after splenic trauma in children may not be necessary.

Nonoperative management of splenic injuries in children is well accepted. However, the need for follow-up abdominal CT to document splenic healing has not been well studied. We retrospectively reviewed initial and follow-up abdominal CT examinations of pediatric patients admitted to our institution with documented splenic trauma who were managed nonoperatively. Eighty-four patients were admitted to our pediatric surgical service with splenic injury documented by CT from 1994 through 1998. The standard approach for splenic injury was bedrest for 5 to 21 days and limited activity for up to 90 days at the discretion of the attending surgeon. Thirty-five of the 84 had follow-up CTs during outpatient follow-up to evaluate and document splenic healing by CT criteria. The initial and follow-up studies were randomized and read blindly by pediatric radiologists using a modified American Association for the Surgery of Trauma grading system (I-V). The age range of the patients was 6 months to 17 years (mean +/- SE; 11 +/- 1 years). Nineteen (54%) were male and 16 (46%) were female. Causes of splenic trauma included motor vehicle accident (22), fall (seven), assault (four), pedestrian versus vehicle (one), and sports injury (one). Eight children (23%) had grade II injuries, 14 (40%) had grade III injuries, and 13 children (37%) had grade IV injuries on initial CT scan. Seven (88%) of the grade II splenic injuries were healed by 64 +/- 11 days. The remaining grade II injury had healed by 210 days. Thirteen (93%) of the grade III splenic injuries were healed by 76 +/- 7 days. The remaining grade III injury was healed by 140 days. Spleens in 10 (77%) of the 13 patients with grade IV injuries were healed by 81 +/- 8 days. Of the three remaining grade IV injuries two were healed by 173 +/- 14 days. The remaining patient's spleen was radiologically considered to have a grade III defect 91 days from the time of injury, and no further CTs were obtained. Of the 34 patients who underwent follow-up CT imaging until splenic healing was demonstrated the mean time to complete healing was 87 +/- 8 days postinjury (range 11-217 days). These data suggest that routine follow-up abdominal CTs may not be necessary to allow children to resume their normal activities after an appropriate time of restricted activity.

Child↗
PubMed1999

The role of peritoneal drainage for intestinal perforation in infants with and without necrotizing enterocolitis.

BACKGROUND/PURPOSE: This report reviews our experience using peritoneal drainage (PD) as initial therapy for intestinal perforation in premature infants with and without necrotizing enterocolitis (NEC). METHODS: A chart review was conducted of 18 consecutive premature infants who underwent PD for intestinal perforation from 1995 to 1998. Infants were divided into two groups. Group 1 consisted of eight infants who had intestinal perforation without evidence of NEC. Group 2 consisted of 10 infants who had perforation associated with evidence of NEC. A cohort of 10 infants with intestinal perforation treated with primary laparotomy between 1990 and 1995 was identified by chart review for historical control. RESULTS: All infants improved immediately after PD. In group 1, all survived. Seven (88%) recovered systemically after PD. Of these, five (63%) never required laparotomy. Two (25%) required delayed laparotomy. One infant (12%) failed to continue to improve 48 hours after PD and underwent urgent laparotomy and recovered. In group 2, eight (80%) infants survived. Six (60%) recovered from NEC after PD, but five required delayed laparotomy for obstruction or persistent drainage. Four infants (40%) failed to progress from their initial improvement after PD. Three underwent laparotomy; two recovered and one had total intestinal necrosis and died. The fourth infant died without exploration and total intestinal necrosis was discovered during autopsy. Thus, seven of eight survivors (88%) in group 2 required laparotomy at some point in their course. CONCLUSIONS: In premature infants with intestinal perforation, PD allows acute improvement and usually systemic recovery. In infants without evidence of NEC, PD may afford definitive treatment. In contrast, infants with evidence of NEC will likely require laparotomy, but initial PD may allow systemic stabilization and recovery of much of the involved intestine before laparotomy.

Drainage↗
PubMed1998

Diminished angiotensin-II and intact vasopressin response to hemorrhage in portal hypertension.

Portal hypertension is characterized by splanchnic vasodilation and diminished arterial vasoconstrictor response to hemorrhage. Angiotensin-II and arginine vasopressin are critical modulators of the splanchnic response to hemorrhage in normal animals. We hypothesized that alterations in endogenous renin, angiotensin-II, or arginine vasopressin production or release could contribute to the abnormal response to hemorrhage in portal hypertension. Hemodynamics were studied in normal and portal hypertensive rabbits following either graded isovolumetric or single large volume hemorrhage, followed by reinfusion of blood. Hemodynamic and renin-angiotensin-II, and arginine vasopressin activities were determined. The experiments demonstrated a significantly diminished appearance in angiotensin-II (110.87+/-30 vs. 245+/-51.0 pg/mL) and aldosterone (54.2+/-9.5 vs. 119.4+/-13.5 ng/dL), and plasma renin activity (19.4+/-4.2 vs. 29.1+/-2.8 ng/mL/h) in portal hypertension compared with normal, but an appropriate rise in arginine vasopressin levels following hemorrhage in portal hypertension. These findings suggest a diminished angiotensin-II production or release in portal hypertension, which may mediate the failure of the appropriate splanchnic vasoconstrictive response to hemorrhage.

Angiotensin II↗
PubMed1995

Role of cirrhosis in the hemodynamic response to hemorrhage in portal hypertension.

BACKGROUND: We studied hemodynamic alterations in normal and three models of portal hypertension at rest, after hemorrhage, and after resuscitation to determine the role of hepatic dysfunction in the splanchnic vascular response to hemorrhage in portal hypertension. METHODS: One noncirrhotic and two cirrhotic models of portal hypertension were produced in rabbits: partial prehepatic portal vein ligation, common bile duct ligation, and carbon tetrachloride-induced cirrhosis. Animals were subjected to isovolemic hemorrhage followed by reinfusion of shed blood. Portal, central, and aortic pressures, superior mesenteric artery blood flow, and portosystemic shunt were measured. RESULTS: Histologic examination showed parenchymal damage was absent in normal and portal vein ligation, severe in common bile duct ligation, and moderate in carbon tetrachloride-induced cirrhosis. All portal hypertensive animals exhibited diminished splanchnic vasoconstrictive response to hemorrhage compared with normal. The carbon tetrachloride cirrhosis group had severe cirrhotic changes, minimal portosystemic shunt, and mildly diminished constrictive response. In contrast, the portal vein ligation and common bile duct ligation animals had larger portosystemic shunts, markedly diminished constrictive response, and less severe parenchymal damage. A direct correlation existed between magnitude of rise in portal venous pressure or degree of portosystemic shunt and the fall in mesenteric resistance or diminution of vasoconstrictive response to hemorrhage. CONCLUSIONS: We concluded that the abnormal splanchnic vascular response in portal hypertension is relatively independent of the degree of hepatic parenchymal injury, but it is related to the degree of portal hypertension and possibly to splanchnic hyperemia.

Animals↗
PubMed1995

Rectal squamous mucosectomy and ileal anal pull-through procedures: single surgeon experience in 105 patients.

BACKGROUND: The ileal anal pull-through procedure has become the most frequently used cointinence sparing procedure for patients with ulcerative colitis or familial polyposis. Areas of controversy concern the use of temporary ileostomies, and the extent of the rectal mucosectomy. The current report presents a single surgeon's experience with mucosectomy to the perianal skin (squamous mucosectomy), with ileal J-pouch reservoir construction and temporary ileostomy. METHODS: We reviewed the records of 105 consecutive patients undergoing this procedure by a single surgeon during a 5-year period. One hundred percent follow-up was achieved. RESULTS: There was 100% gross fecal continence, with 5% of patients expressing rare day time leakage, and 28% having intermittent nocturnal leakage. There were no instances of pelvic sepsis, and no pouches have been removed. The diverting ileostomy was associated with 6% morbidity. CONCLUSIONS: We conclude that the rectal mucosectomy can be safely extended to the levels of perianal skin with no loss in continence or function. We recommend that this be adopted as the standard for this procedure to ensure complete eradication of the underlying pathologic condition.

Adult↗
PubMed1995

Loss of angiotensin-II receptors in portal hypertensive rabbits.

Decreased splanchnic vascular response to exogenous angiotensin-II (A-II) infusion in portal hypertension has recently been documented. A-II receptor density and binding affinity in the mesenteric artery, portal vein, and adrenal gland of normal and portal hypertensive rabbits were studied. Portal hypertension was induced by partial portal vein ligation 3 weeks before study. There were no significant differences in serum concentrations of sodium, potassium, A-II, serum osmolality, or hematocrit between normal and portal hypertensive rabbits. The portal hypertensive portal vein exhibited a 60% fall in A-II receptor number from 65.1 +/- 0.3 fmol/mg in normal to 27.0 +/- 8 fmol/mg (P < .05) in portal hypertension. A significant decrease in receptor number occurred in the portal hypertensive mesenteric artery, 224 +/- 39 fmol/mg compared with 345 +/- 45 fmol/mg in normal rabbits, and in the adrenal cortex 6.8 +/- 1.3 pmol/mg compared with 12.1 +/- 2.5 pmol/mg in normal controls (P < .05). No significant difference in A-II receptor affinity was observed in tissues studied between normal and portal hypertensive rabbits. Autoradiographic study on A-II receptors was consistent with data from membrane binding assays. Receptor subtype analysis showed exclusive type I receptor binding in the mesenteric artery and portal vein. We conclude there is a global reduction in the A-II receptor number in portal hypertension that may mediate much of the decreased response to A-II seen in this disorder. This loss of the A-II receptor may partially explain hemodynamic derangements peculiar to portal hypertension.

Angiotensin II↗
PubMed1993

Regional chemotherapy devices: effect of experience and anatomy on complications.

PURPOSE: Regional hepatic arterial infusion (HAI) devices have been used for 17 years, but reports of unacceptably high complication rates have led to controversy about their use. Inadequate or misdirected infusion has been reported to occur in up to 45% of patients. We evaluated whether surgeon experience or presence of variant arterial anatomy related to risk of coagulation. MATERIALS AND METHODS: We reviewed 70 patients undergoing placement of HAI catheters. Surgeons were classed as experienced after 10 procedures and arterial anatomy was evaluated angiographically with confirmation at operation. Complications were categorized as technical (17%) or chemotherapy-related (16%). RESULTS: Inexperienced surgeons had a technical complication rate of 37% (80% of the patients involved had standard anatomy), while experienced surgeons had a technical complication rate of 7% (P < .01). Experienced surgeons had no complications in patients with standard anatomy, while inexperienced surgeons had a 42% (eight of 19) complication rate in similar patients (P < .01). CONCLUSION: We conclude that technical complications are closely associated with surgeon experience and arterial anatomy.

Adult↗
PubMed1993

Effects of nitric oxide and cyclooxygenase inhibition on splanchnic hemodynamics in portal hypertension.

Portal hypertension is associated with splanchnic hyperemia and increased plasma levels of prostacyclin. Recently, nitric oxide was proposed as a mediator of this arterial vasodilatation. We hypothesized that portal hypertension alters the relative contribution of prostacyclin and nitric oxide to splanchnic vasomotor control. We studied the relationship of nitric oxide and prostaglandins in normal and portal-hypertensive (3 wk after partial portal vein ligation) male rabbits at baseline and following increasing doses of indomethacin, LG-nitro-L-arginine methylester or both. L-arginine was used as the control. Aortic, central and portal venous pressures were measured directly. Blood flow in the superior mesenteric artery was measured by means of an ultrasonic flow probe, and resistance was calculated. LG-nitro-L-arginine methylester produced vasoconstriction (increased resistance and decreased blood flow in the superior mesenteric artery) in normal and portal-hypertensive rabbits, although in portal hypertensive animals resistance and superior mesenteric artery blood flow remained significantly different than that in normal rabbits because of preexisting hyperemia. L-arginine reversed the effect of LG-nitro-L-arginine methylester. Cyclooxygenase blockade induced dose-dependent vasoconstriction in normal and portal-hypertensive animals. Indomethacin induced further vasoconstriction after LG-nitro-L-arginine methylester and reduced portal venous pressure in portal-hypertensive animals. We conclude that this indicates an amplified role for some prostaglandin, probably prostacyclin, in portal hypertension hemodynamics. It also implies that the two vasodilators act by way of independent mechanisms.

Animals↗
PubMed1987

Synthetic diamonds as ionisation chamber radiation detectors in biological environments.

Synthetic diamonds with nitrogen concentrations higher than previously reported in the literature are found to operate very effectively as alpha-particle detectors, as well as detectors for gamma radiation, when operated as ionisation chambers. Certain of the specimens exhibited extensive linear response characteristics when subjected to either alpha particles or gamma radiation of various dose rates. For alpha particles, the response of the detectors at constant particle flux was also found to increase linearly with increasing alpha-particle energy. Unlike previously reported investigations, however, the variation in the response of the synthetic stones to gamma radiation as a function of time was found to be not only more rapid but also to be virtually unaffected by illumination with intense white light.

Alpha Particles↗
PubMed1986

Endodontic burnout.

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Burnout, Professional↗