miniature swine
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Author(s):  
Samuel G Savidge ◽  
Hossam Abdou ◽  
Joseph Edwards ◽  
Neerav Patel ◽  
Michael J Richmond ◽  
...  

Background Trans-esophageal aortic blood flow occlusion (TEABO) is an emerging technology undergoing laboratory research that offers a strategy for temporary hemorrhage control. The purpose of this study was to evaluate the anatomical relationship between the esophagus and descending thoracic aorta in two breeds of swine to support a porcine model for future TEABO investigations. Methods Thoracoabdominal CT scans were compared in Hanford miniature swine and Yorkshire swine. Measurements were taken at the five vertebral levels proximal to the gastroesophageal junction. Data collected included the distance between the center of the esophagus and the center of the descending aorta, the angle between the vertebral column, descending aorta, and esophagus, and the length the thoracic esophagus travels anteriorly to the descending aorta. Results Ten Hanford swine and ten Yorkshire swine were compared. In Hanford swine, the distal thoracic esophagus travels anteriorly to the descending aorta for a mean distance of 11.5 ± 2.3 cm. In Yorkshire swine, the thoracic esophagus travels to the right of the descending aorta. The mean angle between the vertebral body, descending aorta, and esophagus was 79.6 to 97.8 degrees higher in Hanfords compared to Yorkshires (p<0.0001 at all five vertebral levels compared). The mean distance between the esophagus and descending aorta was 0.2 to 0.6 cm higher in Hanfords compared to Yorkshires with a significant difference found at only two vertebral levels (p=0.01 and p=0.02). Conclusion Hanford miniature swine possess an aorto-esophageal relationship comparable to humans and should be the preferred animal model for TEABO studies.


Author(s):  
Lauren Ienello ◽  
Martin Kennedy ◽  
Erin Wendt-Hornickle ◽  
Caroline Baldo ◽  
Valentina Moshnikova ◽  
...  

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
John Reed ◽  
Aish Thamba ◽  
John Strobel ◽  
James Byrd ◽  
Mouhamad Alloosh ◽  
...  

Background: SIRT1 is a deacetylase that has diverse roles in intracellular Ca2+ signaling, metabolism, and cardiovascular disease. SIRT1 increases sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) activity that is essential to buffer the increase in Ca2+ induced by release from the sarcoplasmic reticulum (SR). Our lab has shown that metabolic syndrome (MetS) impairs SERCA activity in coronary smooth muscle cells and causes coronary artery disease in Ossabaw miniature swine. We hypothesized that  SIRT1 inhibition and MetS would impair Ca2+ buffering.   Methods: CRISPR/Cas9 methods delivered a leucine to proline point mutation in SIRT1 (SIRT1L100P) into the Ossabaw swine genome to compare to wild type (WT) and mimic the naturally occurring mutation in humans and decrease SIRT1 activity. Four treatment groups of juvenile swine were based on genotype and diet: WT Lean, SIRT1 Lean, WT MetS, and SIRT1 MetS. Lean swine were fed normal chow and MetS were fed a hypercaloric, atherogenic diet for 7 months. The left anterior descending coronary artery was harvested and enzymatically digested to obtain cells. Fluorescence microscopy measured the Ca2+ indicator fura-2 in single cells. The cells were exposed to 5 mM caffeine to maximally release stores of Ca2+ from the SR. Ca2+ buffering capacity of each cell was analyzed after the caffeine-induced peak increase to assess Ca2+ efflux and SERCA activity.   Results: MetS was confirmed by increased body weight, impaired glucose tolerance, hyperinsulinemia, and hypercholesterolemia. Coronary atherosclerosis was shown by angiography, intravascular ultrasound, and gross imaging. The rapid phase of Ca2+ buffering due to Ca2+ efflux was not affected by SIRT1 mutation or MetS. The slower phase of Ca2+ buffering due to SERCA activity was impaired only by SIRT1 mutation (p<0.0005), not by MetS.   Conclusion:  SIRT1 mutation alone inhibited SERCA buffering of Ca2+ in coronary smooth muscle. (Support: NIH T35HL110854, DK120240, DK09751.) 


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Aish Thamba ◽  
John Reed ◽  
John S. Strobel ◽  
James Byrd ◽  
Mouhamad Alloosh ◽  
...  

Background: Changes in Ca2+ regulation have been implicated in various pathologies such as coronary artery disease and metabolic syndrome (MetS), thereby potentiating these diseases. Our lab has shown that MetS decreases voltage-gated Ca2+ channel (VGCC) activity and sarcoplasmic reticulum (SR) Ca2+ release in coronary smooth muscle cells and increases coronary artery disease in Ossabaw miniature swine. Furthermore, decreased SIRT1 enzyme function can impair Ca2+ signaling and increase coronary disease and MetS. We hypothesized that impaired SIRT1 and MetS would decrease VGCC function and SR calcium store. Methods: CRISPR/Cas9 methods delivered a leucine to proline point mutation in SIRT1 (SIRT1L100P) into the Ossabaw swine genome to compare to wild type (WT), mimicking the naturally occurring mutation in humans which decreases SIRT1 activity. Four treatment groups of juvenile swine were based on genotype and diet: WT Lean, SIRT1 Lean, WT MetS, and SIRT1 MetS. Lean swine were fed normal chow and MetS were fed a hypercaloric, atherogenic diet for 7 months. The left anterior descending coronary artery was harvested and enzymatically digested to obtain cells. Fluorescence microscopy measured the Ca2+ indicator fura-2 in single cells. Depolarization of cells with perfusion of 80 mM K+ was used to elicit Ca2+ influx through VGCC.  Caffeine (5 mM) exposure activated the Ca2+ release channel (ryanodine receptor) on the SR. Results: MetS was confirmed by increased body weight, impaired glucose tolerance, hyperinsulinemia, and hypercholesterolemia. Coronary atherosclerosis was shown by angiography, intravascular ultrasound, and gross imaging. A two-way analysis of variance revealed statistically significant overall effects of genotype (p=0.02), diet (p<0.0001), and an interaction (p<0.0001) between these variables to decrease VGCC function. In contrast, no effect was observed on SR Ca2+ release. Conclusion and Potential Impact: SIRT1 inhibition and MetS decreased VGCC function independently, but not additively or synergistically. (Support: NIH T35HL110854, DK120240, DK09751.)


Author(s):  
Vicente Soler ◽  
Encarna Casas ◽  
Francesc Closa‐Sebastià ◽  
Albert Sanz ◽  
Jaume Martorell

Cartilage ◽  
2021 ◽  
pp. 194760352110538
Author(s):  
Akihiko Kusanagi ◽  
Eric B. Blahut ◽  
Takahiro Ogura ◽  
Akihiro Tsuchiya ◽  
Shuichi Mizuno

Objective Autologous chondrocyte implantation was the first cell-based therapy that used a tissue engineering process to repair cartilage defects. Recently improved approaches and tissue-engineered cell constructs have been developed for growing patient populations. We developed a chondrocyte construct using a collagen gel and sponge scaffold and physicochemical stimuli, implanted with a surgical adhesive. We conducted a proof-of-concept study of these improvements using a cartilage defect model in miniature swine. Design We implanted the autologous chondrocyte constructs into full-thickness chondral defects in the femoral condyle, compared those results with empty and acellular scaffold controls, and compared implantation techniques with adhesive alone and with partial adhesive with suture. Two weeks after the creation of the defects and implantation of the cellular or acellular constructs, we arthroscopically confirmed that the implanted constructs remained at the chondral defects. We evaluated the regenerated tissue macro- and microscopically 6 months after the cell constructs were implanted. The tissues were stained with Safranin-O and evaluated using Sellers’ histology grading system. Results The defects implanted with processed cell constructs and acellular scaffolds were filled with chondrocyte-like round cells and with nearly normal tissue architecture that were significantly greater degree compared to empty defect control. Even with the adhesive alone and with suture alone, the cell construct was composed of the dense cartilaginous matrix that was found in the implantation using both the sutures and the adhesive. Conclusion Implantation of cell constructs promoted regeneration and integration of articular cartilage at chondral defects in swine by 6 months.


GeroScience ◽  
2021 ◽  
Author(s):  
Kyle M. Schachtschneider ◽  
Lawrence B. Schook ◽  
Jennifer J. Meudt ◽  
Dhanansayan Shanmuganayagam ◽  
Joseph A. Zoller ◽  
...  

AbstractDNA-methylation profiles have been used successfully to develop highly accurate biomarkers of age, epigenetic clocks, for many species. Using a custom methylation array, we generated DNA methylation data from n = 238 porcine tissues including blood, bladder, frontal cortex, kidney, liver, and lung, from domestic pigs (Sus scrofa domesticus) and minipigs (Wisconsin Miniature Swine™). Samples used in this study originated from Large White X Landrace crossbred pigs, Large White X Minnesota minipig crossbred pigs, and Wisconsin Miniature Swine™. We present 4 epigenetic clocks for pigs that are distinguished by their compatibility with tissue type (pan-tissue and blood clock) and species (pig and human). Two dual-species human-pig pan-tissue clocks accurately measure chronological age and relative age, respectively. We also characterized CpGs that differ between minipigs and domestic pigs. Strikingly, several genes implicated by our epigenetic studies of minipig status overlap with genes (ADCY3, TFAP2B, SKOR1, and GPR61) implicated by genetic studies of body mass index in humans. In addition, CpGs with different levels of methylation between the two pig breeds were identified proximal to genes involved in blood LDL levels and cholesterol synthesis, of particular interest given the minipig’s increased susceptibility to cardiovascular disease compared to domestic pigs. Thus, breed-specific differences of domestic and minipigs may potentially help to identify biological mechanisms underlying weight gain and aging-associated diseases. Our porcine clocks are expected to be useful for elucidating the role of epigenetics in aging and obesity, and the testing of anti-aging interventions.


2021 ◽  
Author(s):  
Amgad S. Hanna ◽  
Daniel J. Hellenbrand ◽  
Dominic T. Schomberg ◽  
Shahriar M. Salamat ◽  
Megan Loh ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252947
Author(s):  
Han Na Suh ◽  
Young Kyu Kim ◽  
Ju Young Lee ◽  
Goo-Hwa Kang ◽  
Jeong Ho Hwang

Minipigs have remarkably similar physiology to humans, therefore, they it can be a good animal model for inflammation study. Thus, the conventional (serum chemistry, histopathology) and novel analytic tools [immune cell identification in tissue, cytokine level in peripheral blood mononuclear cells (PBMC) and serum, NF-kB target gene analysis in tissue] were applied to determine inflammation in Chicago Miniature Swine (CMS) minipig. Lipopolysaccharide (LPS)-induced acute systemic inflammation caused liver and kidney damage in serum chemistry and histopathology. Immunohistochemistry (IHC) also showed an increase of immune cell distribution in spleen and lung during inflammation. Moreover, NF-kB-target gene expression was upregulated in lung and kidney in acute inflammation and in heart, liver, and intestine in chronic inflammation. Cytokine mRNA was elevated in PBMC under acute inflammation along with elevated absolute cytokine levels in serum. Overall, LPS-mediated systemic inflammation affects the various organs, and can be detected by IHC of immune cells, gene analysis in PBMC, and measuring the absolute cytokine in serum along with conventional inflammation analytic tools.


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