Mitochondrial Damage

Introduction: Through the second portion of the semester, we used the same DNA that we extracted from our cheek cells to amplify and analyze a region from our mitochondrial DNA instead of nuclear DNA. The DNA was amplified through Polymerase Chain Reaction (PCR) and then run on a 2% agaraose gel. The locus we looked at was the D Loop, a noncoding region that is the origin of replication for mitochondrial DNA. Mitochondrial DNA is only inherited from the mother, so our mitochondrial DNA is identical to our mothers. Mitochondrial DNA does not experience recombination but can experience mutations when replicating.

MH alters the calcium channel in the sarcoplasmic reticulum (SR) and this allows large quantity of calcium to be released from the SR creating hyper-action in skeletal muscle; this reaction increases oxygen consumption and increased heat production that ultimately leads to a hypermetabolic state after the inhaled Halothane has triggered the condition (Knies). The continuous elevation of calcium also causes excessive stimulation of anaerobic glycolytic metabolism. This creates respiratory and metabolic acidosis, rigidity (muscle contractions), and hyperkalemia (elevated potassium) and can ultimately lead to death

Glucagon acts on liver cells to promote breakdown of glycogen into glucose and formation of glucose from lactic acid and certain amino acids.

Incretin based drugs have proven to be effective glucose-lowering agents (Butler et al, 2013). But there have been concerns with respect to the long-term consequences of using such therapies. The issues raised were regarding their causal relationship with acute pancreatitis (AP). There are clearly conflicting evidence that have been presented in preclinical studies and in epidemiologic studies which suggest an association which may or may not be a causal relationship between these drugs and AP. (Butler et al, 2013)

mucus can block the ducts of the pancreas, and that prevents the enzymes from reaching the

ATPase were increased? Are there diseases or other conditions that might enhance the activity of this

In light of question number three A-B, Cystic fibrosis causes variations from the norm in almost all exocrine and numerous endocrine organs. This disturbance of organs extremely thwarts the elements of the Pancreas during absorption bringing about “…an abnormal mucous secretion that causes obstruction of single mucin-producing cells. The pancreas secretes less enzyme (ex: trypsin, lipase and amylase), so malabsorption ensues with its attendant deficiency disorders” (Walsh et al.)

* The type of proteins in the cell membrane that was involved in homeostatic imbalance of his heart cells were ATP. There was no ATP, so it affected the pumps in the membrane. The calcium levels rose, and it caused proteases to spill into the interior of the cell, attacking the cytoskeleton. This caused the lysosome enzymes to digest the plasma membranes and membranes of the organelles.

Mitochondrial Neurogastrointestinal Encephalopathy disease (MNGIE) is an extremely rare disease that affects the process of muscles and shows up in equal numbers of men and women. Only 70 cases of this disease have been reported. A mutation of the thymidine phosphorylase causes MNGIE and lowers the production of adenosine triphosphate production.

An increase in calcium inside muscle cells activates processes that generate heat and production of excess acid, leading to a continual increase in body temperature and then acidosis.

From molecular perspective, hyperforin has multidirectional mechanisms of action. It acts on ligand-gated (GABA, NMDA and AMPA receptors) (29, 30) and voltage-gated channels (Ca2+, K+, and Na+) (29, 31). In contrast to blockade of ion transport through the plasma membrane, hyperforin can increased an inward Ca2+ current. These processes are dose dependent and probably involved a few different cellular events. In the details, hyperforin in in vitro studies increased the Ca2+ intracellular level by activation of the non-selective canonical transient receptor potential 6 channels (TRPC6) or by the releasing Ca2+ from mitochondria (32–34). As has been previously shown hyperforin activates intracellular

The objective of this lab was to assess the effect that temperature and pH had on pancreatic amylase. Amylase is an enzyme involved in digestion and is secreted by both the pancreas and salivary glands (Pandol, 2010). Both salivary and pancreatic amylase display the same enzymatic activities through their role in the digestion of starch (Pandol, 2010). The goal of both salivary and pancreatic amylase is to hydrolyze starch thus breaking down the polysaccharide into a disaccharide such as maltose (Pandol, 2010). As a result, amylase breaks down these sugars making them more easily absorbed in the body during digestion (Pancreatic Cancer Action Network, 2015). Through this lab we learned about the role of pancreatic amylase and how this enzyme operates under certain conditions.

Acute Pancreatitis: Acute inflammation of the pancreas.The most common pathogenic mechanism is autodigestion of the pancreas. The etiological factor injures pancreatic cells or activates the pancreatic enzymes in the pancreas rather than in the intestine which may be due to reflux of bile acids into the pancreatic duct through an open or distended sphincter of Oddi. The result may also be caused by blockage created by a gallstone. Obstruction of pancreatic ducts results in pancreatic ischemia.The pathophysiology involvement of acute pancreatitis is

In vitro: PT shows to affect the innate immune response. It inhibits the early recruitment of neutrophils and macrophages, and interferes with the early chemokine production and the inhibition of the neutrophil chemotaxis. The effects of PT on human monocyte-derived DC (MDDC), including maturation, are mediated by cyclic adenosine monophosphate (cAMP) [1].

“Each year, acute pancreatitis sends more than 200,000 Americans to the hospital. Many of those who suffer from pancreatic problems are also heavy drinkers” (“Beyond Hangovers: Understanding Alcohol's Impact Your Health” 15). The pancreas is an important organ which aids in digestions and energy conversion. The pancreas directs enzymes to the small intestine to digest nutrients and it also secretes insulin and glucagon. The body’s main source of energy is glucose and insulin allows additional glucose to be stored away in the body properly. Too much alcohol damages cells in the pancreas, causing complications with insulin, leaving the organ open to inflammation. Alcohol causes the pancreas to discharge the enzymes intended for the small intestine back into the pancreas which can lead to inflammation and the swelling of tissues and blood vessels. Pancreatitis is the inflammation which causes the organ to malfunction and if one continues to drink, it can magnify into chronic pancreatitis when the inflammation is constant (“Beyond Hangovers: Understanding Alcohol's Impact Your Health” 15-16). Pancreatitis causing severe abdominal pain, persistent diarrhea, and is not curable. Sixty-percent of circumstances result from alcohol; although, some have been linked to gallstones (Freeman).