The Experts below are selected from a list of 56100 Experts worldwide ranked by ideXlab platform
John P. Geibel - One of the best experts on this subject based on the ideXlab platform.
-
use of fluorescein isothiocyanate inulin as a marker for intestinal Ischemic Injury
Journal of The American College of Surgeons, 2017Co-Authors: Abedalrazaq Alkukhun, Giorgio Caturegli, Armando Salim Munozabraham, Sami S Judeeba, Roger Patronlozano, Manuel I Rodriguezdavalos, Raffaella A. Morotti, John P. GeibelAbstract:Background Intestinal ischemia is observed in conditions such as mesenteric ischemia, or during traumatic events such as intestinal transplantation. Intestinal ischemia leads to pathophysiologic disruptions that present as increased fluid secretion into the intestinal lumen. We propose a novel method to detect real-time Ischemic Injury that is used in an in vitro model applicable to intestinal transplantation. Study Design Small intestine segments from rats were procured. The segments were attached to customized perfusion chambers. Both intestines were perfused on the vascular side with a Ringer buffer solution. The experimental buffer solution was bubbled with 100% nitrogen to mimic ischemia. Both lumens were perfused with 3 mL HEPES-Ringer solution containing 50 μM fluorescein isothiocyanate (FITC)-inulin. Intraluminal samples were collected at 15-minute intervals to measure FITC-inulin concentration using a nanofluorospectrophotometer. Intestinal tissue samples were processed and evaluated by a blinded pathologist using the Park/Chiu scoring system for grading intestinal ischemia. Results Samples collected from the Ischemic intestine showed a significant decrease in FITC-inulin fluorescence compared with the control intestine, indicating enhanced fluid secretion. Histopathologic samples from the experimental arm exhibited higher scores of Ischemic Injury in comparison with the control arm, confirming the FITC-inulin as a correlation to ischemia. Conclusions Fluorescein isothiocyanate-inulin can be used as a real-time volume marker to monitor the Ischemic state of intestinal tissue. A positive correlation between the degree of fluid shift and presence of Ischemic Injury. The changes in fluorescence signal provide a potential selective method to measure real-time fluid changes inside an intestinal graft to evaluate viability.
-
use of fluorescein isothiocyanate inulin as a marker for intestinal Ischemic Injury
Journal of The American College of Surgeons, 2017Co-Authors: Abedalrazaq Alkukhun, Giorgio Caturegli, Armando Salim Munozabraham, Sami S Judeeba, Roger Patronlozano, Manuel I Rodriguezdavalos, Raffaella A. Morotti, John P. GeibelAbstract:Background Intestinal ischemia is observed in conditions such as mesenteric ischemia, or during traumatic events such as intestinal transplantation. Intestinal ischemia leads to pathophysiologic disruptions that present as increased fluid secretion into the intestinal lumen. We propose a novel method to detect real-time Ischemic Injury that is used in an in vitro model applicable to intestinal transplantation. Study Design Small intestine segments from rats were procured. The segments were attached to customized perfusion chambers. Both intestines were perfused on the vascular side with a Ringer buffer solution. The experimental buffer solution was bubbled with 100% nitrogen to mimic ischemia. Both lumens were perfused with 3 mL HEPES-Ringer solution containing 50 μM fluorescein isothiocyanate (FITC)-inulin. Intraluminal samples were collected at 15-minute intervals to measure FITC-inulin concentration using a nanofluorospectrophotometer. Intestinal tissue samples were processed and evaluated by a blinded pathologist using the Park/Chiu scoring system for grading intestinal ischemia. Results Samples collected from the Ischemic intestine showed a significant decrease in FITC-inulin fluorescence compared with the control intestine, indicating enhanced fluid secretion. Histopathologic samples from the experimental arm exhibited higher scores of Ischemic Injury in comparison with the control arm, confirming the FITC-inulin as a correlation to ischemia. Conclusions Fluorescein isothiocyanate-inulin can be used as a real-time volume marker to monitor the Ischemic state of intestinal tissue. A positive correlation between the degree of fluid shift and presence of Ischemic Injury. The changes in fluorescence signal provide a potential selective method to measure real-time fluid changes inside an intestinal graft to evaluate viability.
Kieran Clarke - One of the best experts on this subject based on the ideXlab platform.
-
thiazolidinedione treatment normalizes insulin resistance and Ischemic Injury in the zucker fatty rat heart
Diabetes, 2002Co-Authors: Robert J Sidell, Mark A Cole, Nicholas J Draper, Martine Desrois, Robin E Buckingham, Kieran ClarkeAbstract:Obesity is associated with risk factors for cardiovascular disease, including insulin resistance, and can lead to cardiac hypertrophy and congestive heart failure. Here, we used the insulin-sensitizing agent rosiglitazone to investigate the cellular mechanisms linking insulin resistance in the obese Zucker rat heart with increased susceptibility to Ischemic Injury. Rats were treated for 7 or 14 days with 3 mg/kg per os rosiglitazone. Hearts were isolated and perfused before and during insulin stimulation or during 32 min low-flow ischemia at 0.3 ml · min −1 · grams wet wt −1 and reperfusion. d[2- 3 H]glucose was used as a tracer of glucose uptake, and phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow energetics during ischemia. At 12 months of age, obese rat hearts were insulin resistant with decreased GLUT4 protein expression. During ischemia, glucose uptake was lower and depletion of ATP was greater in obese rat hearts, thereby significantly impairing recovery of contractile function during reperfusion. Rosiglitazone treatment normalized the insulin resistance and restored GLUT4 protein levels in obese rat hearts. Glucose uptake during ischemia was also normalized by rosiglitazone treatment, thereby preventing the greater loss of ATP and restoring recovery of contractile function to that of lean rat hearts. We conclude that rosiglitazone treatment, by normalizing glucose uptake, protected obese rat hearts from Ischemic Injury.
-
Thiazolidinedione Treatment Normalizes Insulin Resistance and Ischemic Injury in the Zucker Fatty Rat Heart
Diabetes, 2002Co-Authors: Robert J Sidell, Mark A Cole, Nicholas J Draper, Martine Desrois, Robin E Buckingham, Kieran ClarkeAbstract:Obesity is associated with risk factors for cardiovascular disease, including insulin resistance, and can lead to cardiac hypertrophy and congestive heart failure. Here, we used the insulin-sensitizing agent rosiglitazone to investigate the cellular mechanisms linking insulin resistance in the obese Zucker rat heart with increased susceptibility to Ischemic Injury. Rats were treated for 7 or 14 days with 3 mg/kg per os rosiglitazone. Hearts were isolated and perfused before and during insulin stimulation or during 32 min low-flow ischemia at 0.3 ml small middle dot min(-1) small middle dot grams wet wt(-1) and reperfusion. D[2-(3)H]glucose was used as a tracer of glucose uptake, and phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow energetics during ischemia. At 12 months of age, obese rat hearts were insulin resistant with decreased GLUT4 protein expression. During ischemia, glucose uptake was lower and depletion of ATP was greater in obese rat hearts, thereby significantly impairing recovery of contractile function during reperfusion. Rosiglitazone treatment normalized the insulin resistance and restored GLUT4 protein levels in obese rat hearts. Glucose uptake during ischemia was also normalized by rosiglitazone treatment, thereby preventing the greater loss of ATP and restoring recovery of contractile function to that of lean rat hearts. We conclude that rosiglitazone treatment, by normalizing glucose uptake, protected obese rat hearts from Ischemic Injury.
Harry K.w. Kim - One of the best experts on this subject based on the ideXlab platform.
-
t1ρ and t2 mapping detect acute Ischemic Injury in a piglet model of legg calve perthes disease
Journal of Orthopaedic Research, 2021Co-Authors: Casey P Johnson, Jutta M Ellermann, Ferenc Toth, Cathy S. Carlson, Harry K.w. Kim, Alexandra R Armstrong, Stefan ZbýňAbstract:This study investigated the sensitivity of T1ρ and T2 relaxation time mapping to detect acute Ischemic Injury to the secondary ossification center (SOC) and epiphyseal cartilage of the femoral head in a piglet model of Legg-Calve-Perthes disease. Six piglets underwent surgery to induce global right femoral head ischemia and were euthanized 48 hours later. Fresh operated and contralateral-control femoral heads were imaged ex vivo with T1, T2, and T1ρ mapping using a 9.4T magnetic resonance imaging scanner. The specimens were imaged a second time after a freeze/thaw cycle and then processed for histology. T1, T2, and T1ρ measurements in the SOC, epiphyseal cartilage, articular cartilage, and metaphysis were compared between operated and control femoral heads using paired t-tests. The effects of freeze/thaw, T1ρ spin-lock frequency, and fat saturation were also investigated. Five piglets with histologically-confirmed Ischemic Injury were quantitatively analyzed. T1ρ was increased in the SOC (101±15 vs. 73±16 ms, p=0.0026) and epiphyseal cartilage (84.9±9.2 vs. 74.3±3.6 ms, p=0.031) of the operated vs. control femoral heads. T2 was also increased in the SOC (28.7±2.0 vs. 22.7±1.7, p=0.0037) and epiphyseal cartilage (57.4±4.7 vs. 49.0±2.7, p=0.0041). No changes in T1 were detected. The sensitivities of T1ρ and T2 mapping in detecting Ischemic Injury were maintained after a freeze/thaw cycle, and T1ρ sensitivity was maintained after varying spin-lock frequency and applying fat saturation. In conclusion, T1ρ and T2 mapping are sensitive in detecting Ischemic Injury to the SOC and epiphyseal cartilage of the femoral head as early as 48 hours after ischemia induction. This article is protected by copyright. All rights reserved.
-
quantitative susceptibility mapping detects neovascularization of the epiphyseal cartilage after Ischemic Injury in a piglet model of legg calve perthes disease
Journal of Magnetic Resonance Imaging, 2019Co-Authors: Casey P Johnson, Luning Wang, Ferenc Toth, Cathy S. Carlson, Harry K.w. Kim, Olumide Aruwajoye, Brooke Kirkham, Jutta M EllermannAbstract:BACKGROUND Legg-Calve-Perthes disease (LCPD) is a childhood hip disorder thought to be caused by disruption of blood supply to the developing femoral head. There is potential for imaging to help assess revascularization of the femoral head. PURPOSE To investigate whether quantitative susceptibility mapping (QSM) can detect neovascularization in the epiphyseal cartilage following Ischemic Injury to the developing femoral head. STUDY TYPE Prospective. ANIMAL MODEL Right femoral head ischemia was surgically induced in 6-week-old male piglets. The animals were sacrificed 48 hours (n = 3) or 4 weeks (n = 7) following surgery, and the operated and contralateral control femoral heads were harvested for ex vivo MRI. FIELD STRENGTH/SEQUENCE Preclinical 9.4T MRI to acquire susceptibility-weighted 3D gradient echo (GRE) images with 0.1 mm isotropic spatial resolution. ASSESSMENT The 3D GRE images were used to manually segment the cartilage overlying the femoral head and were subsequently postprocessed using QSM. Vessel volume, cartilage volume, and vessel density were measured and compared between operated and control femoral heads at each timepoint. Maximum intensity projections of the QSM images were subjectively assessed to identity differences in cartilage canal appearance, location, and density. STATISTICAL TESTS Paired t-tests with Bonferroni correction were used (P < 0.008 considered significant). RESULTS Increased vascularity of the epiphyseal cartilage following Ischemic Injury was clearly identified using QSM. No changes were detected 48 hours after surgery. Vessel volume, cartilage volume, and vessel density were all increased in the operated vs. control femoral heads 4 weeks after surgery (P = 0.001, 0.002, and 0.001, respectively). Qualitatively, the increase in vessel density at 4 weeks was due to the formation of new vessels that were organized in a brush-like orientation in the epiphyseal cartilage, consistent with the histological appearance of neovascularization. DATA CONCLUSION QSM can detect neovascularization in the epiphyseal cartilage following Ischemic Injury to the femoral head. LEVEL OF EVIDENCE 1 Technical Efficacy: Stage 1 J. Magn. Reson. Imaging 2019;50:106-113.
-
hypoxia and hif 1α expression in the epiphyseal cartilage following Ischemic Injury to the immature femoral head
Bone, 2009Co-Authors: Harry K.w. Kim, Haikuo Bian, Amanda Garces, James Ayaay, Elise F Morgan, Shawn R GilbertAbstract:Abstract HIF-1α has been shown to be a central mediator of cellular response to hypoxia. The role it plays after Ischemic Injury to the immature femoral head is unknown. The purpose of this study was to determine the region of the femoral head affected by hypoxia following Ischemic Injury to the immature femoral head and to determine the site of HIF-1α activation and revascularization. We hypothesize that the epiphyseal cartilage, rather than the bony epiphysis, is the site of HIF-1α activation following Ischemic osteonecrosis and that the epiphyseal cartilage plays an important role in the revascularization process. Materials and methods Femoral head osteonecrosis was surgically induced in 56 immature pigs. Hypoxyprobe staining, cell viability assay, HIF-1α western blot, RT-qPCR of HIF-1α, VEGF, VEGFR2, and PECAM, and micro-CT assessments of microfil-infused femoral heads were performed. Results Severe hypoxia was present in the bony epiphysis and the lower part of the epiphyseal cartilage following ischemia. In the bony epiphysis, extensive cell death and tissue necrosis was observed with degradation of proteins and RNAs which precluded further analysis. In the epiphyseal cartilage, the loss of cell viability was limited to its deep layer with the remainder of the cartilage remaining viable. Furthermore, the cartilage from the Ischemic side showed a significant increase in HIF-1α protein level and HIF-1α expression. VEGF expression in the cartilage was dramatically and significantly increased at 24 h, 2 and 4 weeks ( p Conclusions Acute Ischemic Injury to the immature femoral head induced severe hypoxia and cell death in the bony epiphysis and the deep layer of the epiphyseal cartilage. Viable chondrocytes in the superficial layer of the epiphyseal cartilage showed HIF-1α activation and VEGF upregulation with subsequent revascularization occurring in the cartilage.
Abedalrazaq Alkukhun - One of the best experts on this subject based on the ideXlab platform.
-
use of fluorescein isothiocyanate inulin as a marker for intestinal Ischemic Injury
Journal of The American College of Surgeons, 2017Co-Authors: Abedalrazaq Alkukhun, Giorgio Caturegli, Armando Salim Munozabraham, Sami S Judeeba, Roger Patronlozano, Manuel I Rodriguezdavalos, Raffaella A. Morotti, John P. GeibelAbstract:Background Intestinal ischemia is observed in conditions such as mesenteric ischemia, or during traumatic events such as intestinal transplantation. Intestinal ischemia leads to pathophysiologic disruptions that present as increased fluid secretion into the intestinal lumen. We propose a novel method to detect real-time Ischemic Injury that is used in an in vitro model applicable to intestinal transplantation. Study Design Small intestine segments from rats were procured. The segments were attached to customized perfusion chambers. Both intestines were perfused on the vascular side with a Ringer buffer solution. The experimental buffer solution was bubbled with 100% nitrogen to mimic ischemia. Both lumens were perfused with 3 mL HEPES-Ringer solution containing 50 μM fluorescein isothiocyanate (FITC)-inulin. Intraluminal samples were collected at 15-minute intervals to measure FITC-inulin concentration using a nanofluorospectrophotometer. Intestinal tissue samples were processed and evaluated by a blinded pathologist using the Park/Chiu scoring system for grading intestinal ischemia. Results Samples collected from the Ischemic intestine showed a significant decrease in FITC-inulin fluorescence compared with the control intestine, indicating enhanced fluid secretion. Histopathologic samples from the experimental arm exhibited higher scores of Ischemic Injury in comparison with the control arm, confirming the FITC-inulin as a correlation to ischemia. Conclusions Fluorescein isothiocyanate-inulin can be used as a real-time volume marker to monitor the Ischemic state of intestinal tissue. A positive correlation between the degree of fluid shift and presence of Ischemic Injury. The changes in fluorescence signal provide a potential selective method to measure real-time fluid changes inside an intestinal graft to evaluate viability.
-
use of fluorescein isothiocyanate inulin as a marker for intestinal Ischemic Injury
Journal of The American College of Surgeons, 2017Co-Authors: Abedalrazaq Alkukhun, Giorgio Caturegli, Armando Salim Munozabraham, Sami S Judeeba, Roger Patronlozano, Manuel I Rodriguezdavalos, Raffaella A. Morotti, John P. GeibelAbstract:Background Intestinal ischemia is observed in conditions such as mesenteric ischemia, or during traumatic events such as intestinal transplantation. Intestinal ischemia leads to pathophysiologic disruptions that present as increased fluid secretion into the intestinal lumen. We propose a novel method to detect real-time Ischemic Injury that is used in an in vitro model applicable to intestinal transplantation. Study Design Small intestine segments from rats were procured. The segments were attached to customized perfusion chambers. Both intestines were perfused on the vascular side with a Ringer buffer solution. The experimental buffer solution was bubbled with 100% nitrogen to mimic ischemia. Both lumens were perfused with 3 mL HEPES-Ringer solution containing 50 μM fluorescein isothiocyanate (FITC)-inulin. Intraluminal samples were collected at 15-minute intervals to measure FITC-inulin concentration using a nanofluorospectrophotometer. Intestinal tissue samples were processed and evaluated by a blinded pathologist using the Park/Chiu scoring system for grading intestinal ischemia. Results Samples collected from the Ischemic intestine showed a significant decrease in FITC-inulin fluorescence compared with the control intestine, indicating enhanced fluid secretion. Histopathologic samples from the experimental arm exhibited higher scores of Ischemic Injury in comparison with the control arm, confirming the FITC-inulin as a correlation to ischemia. Conclusions Fluorescein isothiocyanate-inulin can be used as a real-time volume marker to monitor the Ischemic state of intestinal tissue. A positive correlation between the degree of fluid shift and presence of Ischemic Injury. The changes in fluorescence signal provide a potential selective method to measure real-time fluid changes inside an intestinal graft to evaluate viability.
Robert J Sidell - One of the best experts on this subject based on the ideXlab platform.
-
thiazolidinedione treatment normalizes insulin resistance and Ischemic Injury in the zucker fatty rat heart
Diabetes, 2002Co-Authors: Robert J Sidell, Mark A Cole, Nicholas J Draper, Martine Desrois, Robin E Buckingham, Kieran ClarkeAbstract:Obesity is associated with risk factors for cardiovascular disease, including insulin resistance, and can lead to cardiac hypertrophy and congestive heart failure. Here, we used the insulin-sensitizing agent rosiglitazone to investigate the cellular mechanisms linking insulin resistance in the obese Zucker rat heart with increased susceptibility to Ischemic Injury. Rats were treated for 7 or 14 days with 3 mg/kg per os rosiglitazone. Hearts were isolated and perfused before and during insulin stimulation or during 32 min low-flow ischemia at 0.3 ml · min −1 · grams wet wt −1 and reperfusion. d[2- 3 H]glucose was used as a tracer of glucose uptake, and phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow energetics during ischemia. At 12 months of age, obese rat hearts were insulin resistant with decreased GLUT4 protein expression. During ischemia, glucose uptake was lower and depletion of ATP was greater in obese rat hearts, thereby significantly impairing recovery of contractile function during reperfusion. Rosiglitazone treatment normalized the insulin resistance and restored GLUT4 protein levels in obese rat hearts. Glucose uptake during ischemia was also normalized by rosiglitazone treatment, thereby preventing the greater loss of ATP and restoring recovery of contractile function to that of lean rat hearts. We conclude that rosiglitazone treatment, by normalizing glucose uptake, protected obese rat hearts from Ischemic Injury.
-
Thiazolidinedione Treatment Normalizes Insulin Resistance and Ischemic Injury in the Zucker Fatty Rat Heart
Diabetes, 2002Co-Authors: Robert J Sidell, Mark A Cole, Nicholas J Draper, Martine Desrois, Robin E Buckingham, Kieran ClarkeAbstract:Obesity is associated with risk factors for cardiovascular disease, including insulin resistance, and can lead to cardiac hypertrophy and congestive heart failure. Here, we used the insulin-sensitizing agent rosiglitazone to investigate the cellular mechanisms linking insulin resistance in the obese Zucker rat heart with increased susceptibility to Ischemic Injury. Rats were treated for 7 or 14 days with 3 mg/kg per os rosiglitazone. Hearts were isolated and perfused before and during insulin stimulation or during 32 min low-flow ischemia at 0.3 ml small middle dot min(-1) small middle dot grams wet wt(-1) and reperfusion. D[2-(3)H]glucose was used as a tracer of glucose uptake, and phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow energetics during ischemia. At 12 months of age, obese rat hearts were insulin resistant with decreased GLUT4 protein expression. During ischemia, glucose uptake was lower and depletion of ATP was greater in obese rat hearts, thereby significantly impairing recovery of contractile function during reperfusion. Rosiglitazone treatment normalized the insulin resistance and restored GLUT4 protein levels in obese rat hearts. Glucose uptake during ischemia was also normalized by rosiglitazone treatment, thereby preventing the greater loss of ATP and restoring recovery of contractile function to that of lean rat hearts. We conclude that rosiglitazone treatment, by normalizing glucose uptake, protected obese rat hearts from Ischemic Injury.
