Red Blood Analysis: Presence indicates renal dysfunction. Chemistry: * Genetic Screening indicates that Mr. Newman has a mutation on Chromosome 16. * The mutation results in the formation of an abnormal membrane protein called polycystin. Cellular Defects: * A genetic mutation has resulted in the formation of cysts in Mr. Newman’s kidneys. * Cysts form when cells in a region of the nephron divide rapidly.
Vascular dementia is caused when there is a reduction in the blood flow to the brain. Over time, this can damage the parts of the brain which play a large part of a person memory, speech and attention. A stroke can play a part in this type of dementia when it narrows the blood vessels to the brain. Dementia with Lewy Bodies is caused by lumps of protein which builds up inside nerve cells inside the brain, the proteins damage the nerve cells and how they work, these nerves are responsible for thinking, memory and movement of a person. Dementia with Lewy Bodies can be closely related to Parkinsons Disease and there is a theory that Dementia with Lewy Bodies interferes with two neurotransmitters called dopamine and acetylcholine which assist in the brains functions.
The mutation tells the cells to divide rapidly and to continue living when a healthy cell would die (Mayo Clinic, 2014). The mutation causes a large number of oversized, abnormal B cells to accumulate in the lymphatic system, where they crowd out healthy cells and cause the signs and symptoms of Hodgkin’s lymphoma (Mayo Clinic, 2014). Various types of Hodgkin’s lymphoma exists (Mayo Clinic, 2014). The type is based on the types of cells involved in the disease and their behavior (Mayo Clinic.
If you have CF, one of your genes is not working correctly. This is known as a CFTR gene, and is located on chromosome 7. There are several mutations that can happen in this gene, meaning that there are different severities of cystic fibrosis that can occur. CFTR helps to control how cells handle sodium and chloride ions. The mutation in CFTR causes the cells to be unable to handle sodium and chloride correctly.
The leukodystrophies are a group of rare, progressive, metabolic, genetic disorders that can affect the brain, spinal cord and often the nerves outside the central nervous system (peripheral nerves). Each type of leukodystrophy is caused by an abnormality affecting a specific gene that results in abnormal development of one of at least 10 different chemicals that make up the white matter of the brain. The white matter is tissue composed of nerve fibers. Many of these nerve fibers are covered by a collection of fats (lipids) and proteins known as myelin. Myelin, which collectively may be referred to as the myelin sheath, protects the nerve fibers, acts as an insulator and increases the speed of transmission of nerve signals.
These also line passageways inside the major glands of the body. The gene forces the body's epithelial cells to produce a protein called CFTR (Cystic Fibrosis Transmembrane Regulator). CFTR is found in cells that line the lungs, digestive tract, sweat glands, and reproductive system. When the CFTR protein fails, epithelial cells can't regulate the way chloride (salt) passes across cell membranes. This in turn, disrupts the amount of salt and water needed
PMID: 19774932 [PubMed - indexed for MEDLINE] Related citations Select item 23183605 34. Incivility and the nurse leader. Ostrofsky D. Nurs Manage. 2012 Dec;43(12):18-22. doi: 10.1097/01.NUMA.0000422892.06958.51. No abstract available.
 It has a prevalence that ranges between 2 and 150 per 100,000.  MS was first described in 1868 by Jean-Martin Charcot.  MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are contained within an insulating substance called myelin. In MS, the body's own immune system attacks and damages the myelin.
The age-dependent reduction in the capacity of degradation of oxidized proteins may be responsible for the build-up of damaged, dysfunctional molecules in the cell (Shringarpure and Davies 2002). It has been suggested that oxidative damage may be an important source of somatic mutations at the basis of the so-called “somatic mutation theory of aging”. This theory hypothesizes that the accumulation of genetic mutations in somatic cells represents the specific cause of senescence (Beckman and Ames