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Langendorff Perfusion Model
Langendorff Perfusion Model
 
Research in the BioScience Center

Increasing evidence suggests that the bacteria that cause gum disease (periodontitis) may cause or promote atherosclerotic heart disease by increasing inflammation and possibly colonizing atherosclerotic plaques. The systemic inflammation from chronic infection is likely to exacerbate atherosclerosis, heart failure, diabetes, and the metabolic syndrome.

The bacteria that colonize our intestines may also contribute to obesity by increasing the extraction of calories from food and by changing our metabolism. Obesity has reached epidemic proportions in the USA and is becoming a problem worldwide.

Pathogenic infections also contribute to heart disease, especially Coxsackievirus and the parasitic protozoan that causes Chagas Disease, Trypanosoma cruzii. Chagas Disease, more commonly seen in tropical Latin America, is becoming more prevalent in the USA, possibly due to global warming and the spread of the host insect vectors that spread the trypanosomes.

It is of paramount importance to bring together cardiologists, immunologists, and microbiologists for focused research. We will also involve the School of Public Health to implement education, treatment, and prevention on a local and global basis.




Gottlieb Lab
Chengqun Huang, Hua Julie Yuan, Rick Sayen, Cynthia Perry Garza, Grant Madigan, Roberta Gottlieb
 
Roberta Gottlieb Lab

  • Cell biology of myocardial ischemia
  • Autophagy as a part of innate immunity
  • Mitochondrial biology
  • Role of stem cells in heart failure after pediatric doxorubicin exposure
  • Role of periodontal disease in atherosclerosis

Support from:
NIH P01 HL 85577
NIH R01 HL 60590
NIH R01 HL 71091
NIH R01 AG 21568
Frederick G. Henry Chair in the Life Sciences




Gustafsson Lab
Dieter Kubli, Melissa Quinsay, Åsa Gustafsson
 
Åsa Gustafsson Lab

  • Regulation of Bnip3 in myocardial ischemia
  • Role of Mcl-1 in the heart
  • Doxorubicin and cardiac stem cells

Support from:
NIH
AHA
CA TDRP




Simon Hui and Roger Davis
Simon Hui & Roger Davis
 
Roger Davis and Simon Hui Lab

Imbalanced carbohydrate and lipid metabolism has been linked to obesity, diabetes and heart disease. Using whole body and tissue-specific Thioredoxin Interacting Protein (Txnip) knockout mice, we have demonstrated that Txnip plays an important role in regulating energy metabolism. Txnip knockout mice develop hypoglycemia, hypertriglyceridemia and hyperketonemia during fasting. Txnip is a negative regulator of thioredoxin which plays an essential role in controlling cellular sulfhydryl redox status.

My research focus is on the regulation of fuel metabolism by cellular redox status. We will continue to use knockout mice as a model to elucidate the molecular mechanisms by which Txnip controls mitochondrial fuel oxidation.