A Wisdom Archive on Hereditary Defect

The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. However, senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species as a mechanism to prevent the onset of cancer. In a few simple species, senescence is negligible and cannot be detected. All such species have no "post-mitotic" cells; they reduce the effect of damaging free radicals by cell division and dilution. Such species are not immortal, however ...

Read more here: » Aging senescence: Encyclopedia II - Aging senescence - Theories of aging

Evolutionary theory explains why we don't live forever, and provides a reasonable explanation for the huge variation in lifespan between (often closely related) species. The geneticist J. B. S. Haldane wondered why the dominant mutation which causes Huntington's disease remained in the population, why natural selection had not eliminated it. The onset of this neurological disease is (on average) at age 35 and is invariably fatal within 10-20 years. Haldane assumed, probably reasonably, that in human prehistory, few survived until age ...

Read more here: » Senescence: Encyclopedia II - Senescence - Evolutionary theories

It is also suggested that damage to long-lived biopolymers, such as structural proteins or DNA, caused by ubiquitous chemical agents in the body such as oxygen and sugars, are in part responsible for aging. The damage can include breakage of biopolymer chains, cross-linking of biopolymers, or chemical attachment of unnatural substituents (haptens) to biopolymers. Under normal aerobic conditions, approximately 4% of the oxygen metabolized by mitochondria is converted to superoxide ion which can subsequently be converted to hydrogen per ...

Read more here: » Aging senescence: Encyclopedia II - Aging senescence - Chemical damage

Recently, early senescence has appeared as a possible unintended outcome of early cloning experiments, notably in the case of Dolly the sheep. A set of rare hereditary (genetic) disorders, each called progeria, has been known for some time. Sufferers exhibit symptoms resembling accelerated aging, including wrinkled skin. The cause of Hutchinson–Gilford progeria syndrome was reported in the journal Nature in May 2003. This report suggests that DNA damage, not oxidative stres ...

Read more here: » Aging senescence: Encyclopedia II - Aging senescence - Miscellaneous

The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. However, senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species as a mechanism to prevent the onset of cancer. In a few simple species, senescence is negligible and cannot be detected. All such species have no "post-mitotic" cells; they reduce the effect of damaging free radicals by cell division and dilution. Such species are not immortal, however ...

Read more here: » Senescence: Encyclopedia II - Senescence - Theories of aging

A number of genetic components of aging have been identified using model organisms, ranging from the simple budding yeast Saccharomyces cerevisiae to worms such as Caenorhabditis elegans and fruit flies. Study of these organisms has revealed the presence of at least two conserved aging pathways. One of these pathways involves the gene Sir2, a NAD+-dependent histone deacetylase. In yeast, Sir2 is required for genomic silencing at three loci: the yeast mating loci, the telomeres and the ribosomal DNA (rDNA). Yeast r ...

Read more here: » Aging senescence: Encyclopedia II - Aging senescence - Gene regulation

A number of genetic components of aging have been identified using model organisms, ranging from the simple budding yeast Saccharomyces cerevisiae to worms such as Caenorhabditis elegans and fruit flies. Study of these organisms has revealed the presence of at least two conserved aging pathways. One of these pathways involves the gene Sir2, a NAD+-dependent histone deacetylase. In yeast, Sir2 is required for genomic silencing at three loci: the yeast mating loci, the telomeres and the ribosomal DNA (rDNA). Yeast r ...

Read more here: » Senescence: Encyclopedia II - Senescence - Gene regulation

As noted above, senescence is not universal, and senescence is not observed in single celled organisms that reproduce through the process of cellular mitosis. Moreover, cellular senescence is not observed in many organisms, including sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis -- i.e., cells experience replicative senescence. How and why some cells become post-mitotic in s ...

Read more here: » Senescence: Encyclopedia II - Senescence - Cellular senescence

As noted above, senescence is not universal, and senescence is not observed in single celled organisms that reproduce through the process of cellular mitosis. Moreover, cellular senescence is not observed in many organisms, including sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis -- i.e., cells experience replicative senescence. How and why some cells become post-mitotic in s ...

Read more here: » Aging senescence: Encyclopedia II - Aging senescence - Cellular senescence

The defective protein can be transmitted by human growth hormone products, corneal grafts, dural grafts or electrode implants (acquired or iatrogenic form: iCJD), it can be inherited (hereditary or familial form: fCJD) or it may appear for the first time in the patient (sporadic form: sCJD). In the hereditary form, a mutation occurs to the "PrP" gene. From 10 to 15 percent of CJD cases are inherited. (CDC) The disease has also been shown to result from usage of HGH drawn from the pituitary glands of cadavers who died from Creutzfeldt- ...

Read more here: » Creutzfeldt-Jakob disease: Encyclopedia II - Creutzfeldt-Jakob disease - Transmission

Where known, the ICD-10 code is listed below. Cephalic disorder - Anencephaly Q00.0. See anencephaly Cephalic disorder - Colpocephaly ICD10 unknown. This is a disorder in which there is an abnormal enlargement of the occipital horns - the posterior or rear portion of the lateral ventricles (cavities or chambers) of the brain. This enlargement occurs when there is an underdevelopment or lack of thickening of the white matter in the posterior cerebrum. Colpocephaly ...

Read more here: » Cephalic disorder: Encyclopedia II - Cephalic disorder - More common cephalic disorders

Four genes have been implicated in CGD (p is the weight of the protein in kDa; the g means glycoprotein): CYBB, coding the gp91-phox subunit (X-linked, accounts for 2/3 of the cases); CYBA, coding p22-phox NCF-1, coding p47-phox NCF-2, coding p67-phox A fifth gene, coding for p40-phox, has not been implicated A low level of NADPH, the cofactor required for superoxide synthesis, can lead to CGD. This has been reported in women who are homozygous for the genetic defect causing glucose-6-phosphate dehydrogenase deficien ...

Read more here: » Chronic granulomatous disease: Encyclopedia II - Chronic granulomatous disease - Genetics

A limited or excessive appetite is not necessarily pathological. Abnormal appetite could be defined as eating habits causing malnutrition on the one site or obesity and its related problems on the other. Both genetic and environmental factors may regulate appetite, and abnormalities in either may lead to abnormal appetite. Poor appetite (anorexia) may have numerous causes, but may be a result of physical (infectious, autoimmune or malignant disease) or psychological (stress, mental disorders) factors. Likely, hyperphagia (excessive eating) may be a result of hormonal imbalances, me ...

Read more here: » Appetite: Encyclopedia II - Appetite - Role in disease