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1. Genetic defects and calcium
- Prof. Tullio Pozzan
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2. Pancreatitis and calcium signaling
- Prof. Ole Petersen
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3. Ca2+ alterations in familial Alzheimer's disease (FAD)
- Dr. Paola Pizzo
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4. Ca2+ signaling alterations in Alzheimer's disease
- Dr. Grace Stutzmann
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5. Nociception and alpha2delta3
- Dr. Greg Neely
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6. Disease hot spots of ryanodine receptors
- Dr. Filip Van Petegem
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7. Calcium channelopathies
- Dr. David Friel
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8. Ca2+, the endoplasmic reticulum and cardiac pathology
- Prof. Marek Michalak
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9. Mechanism-based therapies for heart failure and cardiac arrhythmias
- Prof. Andrew Marks
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10. Store-operated Ca2+ entry and vascular smooth muscle remodeling
- Prof. Mohamed Trebak
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11. Polycystins, calcium signaling and pathogenesis of polycystic kidney disease
- Prof. Laura del Senno
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12. Acidocalcisomes: conserved from bacterial to human cells
- Prof. Roberto Docampo
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13. Cellular signaling on host-malaria parasite interactions
- Prof. Dr. Celia Regina da Silva Garcia
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14. Ca(v)1.3 and deafness
- Dr. Amy Lee
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16. Vascular calcification location, formation and biological activity
- Dr. Diane Proudfoot
- Archived Lectures *These may not cover the latest advances in the field
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17. Ca2+ channelopathies
- Dr. David Friel
Printable Handouts
Navigable Slide Index
- Introduction
- Stimulus-secretion coupling
- Ca2+ signalling and pancreatitis
- Hyperstimulation protocol - a model for pancreatitis
- How does hyperstimulation elicit [Ca2+]i elevation?
- Effect of bile acids on pancreatic acinar cells
- Effect of alcohol on Ca2+ signal generation
- Effect of non-oxidative alcohol metabolites
- BNPP reduces the POAEE-elicited [Ca2+]i rise
- POA reduces cellular ATP content
- ATP protects against toxic Ca2+ overloading
- Action of non-oxidative alcohol metabolites
- Acute pancreatitis: potential therapeutic targets
- Caffeine is an IP3R antagonist
- Coffee has a protective effect against pancreatitis
- What caffeine can do and what it cannot do
- Mechanisms of action of FAEEs and FAs
Topics Covered
- Normal Calcium signaling events in pancreatic acinar cells
- Hyperstimulation as a cause of sustained global elevation of the cytosolic [Calcium], Calcium-dependent vacuolization and Calcium-dependent protease activation
- Bile acids causing sustained global Calcium signals and necrosis
- Calcium-dependent necrosis evoked by non-oxidative alcohol metabolites (fatty acid ethyl esters and fatty acids) but not by alcohol or acetaldehyde
- The mechanism of action of fatty acid ethyl esters and fatty acids
- The mildly protective effect of coffee (caffeine)
- A model for the initiation of alcoholic pancreatitis
Links
Series:
Categories:
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Talk Citation
Petersen, O. (2007, October 1). Pancreatitis and calcium signaling [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 26, 2024, from https://hstalks.com/bs/426/.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Ole Petersen has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.