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Related Concept Videos

Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

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The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
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The management of chronic pancreatitis is multifaceted, involving a comprehensive approach that includes thorough assessment, diagnostic testing, and a variety of management strategies.
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Acute Pancreatitis II: Clinical Manifestations and Management01:30

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Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
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Acute Pancreatitis I: Introduction01:27

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Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
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Calmodulin-dependent Signaling01:16

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Ca2+ signalling underlying pancreatitis.

J V Gerasimenko1, S Peng2, T Tsugorka1

  • 1Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK.

Cell Calcium
|May 30, 2017
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Summary
This summary is machine-generated.

Acute pancreatitis (AP) remains a serious disease without a cure, potentially leading to chronic pancreatitis and cancer. Research explores new causes like Asparaginase and therapeutic strategies for AP.

Keywords:
Acute pancreatitisAsparaginaseBradykininPancreatic acinar cellsPancreatic stellate cells

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Area of Science:

  • Gastroenterology and Hepatology
  • Oncology
  • Pharmacology

Background:

  • Acute pancreatitis (AP) is a severe condition with a high mortality rate and no specific cure.
  • AP can lead to chronic pancreatitis (CP) and an increased risk of pancreatic cancer (PC).
  • Premature activation of digestive pro-enzymes within pancreatic acinar cells (PACs) is a key early event in AP pathogenesis.

Purpose of the Study:

  • To review recent developments, therapeutic approaches, and potential treatments for acute pancreatitis (AP).
  • To discuss the role of Asparaginase-based drugs in triggering AP and explore potential counteracting therapies.
  • To examine the involvement of pancreatic stellate cells (PSCs) in AP, CP, and PC.

Main Methods:

  • Literature review of recent scientific progress in AP research.
  • Analysis of the mechanisms underlying AP induced by alcohol, bile acids, and Asparaginase.
  • Evaluation of the role of pancreatic stellate cells (PSCs) in pancreatic diseases.

Main Results:

  • Asparaginase-elicited AP (AAP) shares similar features with AP induced by alcohol and bile acids.
  • Emerging therapeutic strategies for AAP may offer broader applications for other AP causes.
  • Pancreatic stellate cells (PSCs) are critically involved in AP, CP, and PC, though less studied in their natural environment.

Conclusions:

  • Despite advances, AP remains a significant clinical challenge requiring novel therapeutic strategies.
  • Understanding Asparaginase-induced AP provides insights into potential treatments for various forms of AP.
  • Further research into pancreatic stellate cells (PSCs) is crucial for managing AP, CP, and PC effectively.