Gaining Control of the Gene Responsible for Apoptosis Essay examples

Past research has said humans coincidentally evolved good traits in times of need, but jumping genes insert themselves into other parts of the genome, causing mutations. The next chapter explains epigenetics and methylation, the process of a gene changing its expression. The authors provide examples of how if a pregnant mother consumed specific vitamins, specific genes in the embryo would undergo methylation. In the final chapter, the authors tackle why we are programmed to die and why humans look this way. They explain that if we replicate too much, we run the risk of a deadly mutation or cancer, so, at around 50 replications, a cell is programmed to die, which is planned obsolescence.

It is a known fact that all measures of physiological function decline in human aging. While genetics certainly play a role in the declining of physiological function with age, it can be argued that a fundamental part of aging can be reflected by chemical processes resulting in the appearance of harmful side products of the normal metabolism over time. When enzymes speed up reactions it is harder to slow them down. At the same time side reactions are constantly occurring and more and more unwanted side products are continuously being formed.

National Institutes of Health in a study called the Hawaii Lifespan Study. The research focused on the human homologue of DAF-]6 which includes a protein group FOXO (Fork head box transcription factor) that functions as a sensor in the IIS pathway, as it has been shown to influence lifespan across a number of species. The researchers conducted a nested case control study on five candidate genes (ADIPOG, FOXO1A, FOXO3A, SIRT and COQ7), with FOXO3A found to have a significant impact in healthy human ageing and longevity. This research article is useful as it is a long term study based on finding the genetics responsible for determining longevity and healthy ageing. The author’s research is limited as it is only conducted on a homogeneous male population and more in depth data is needed by performing similar studies on other populations and

Cellular senescence has always previously thought to be an unavoidable and irreversible process wherein old cells stop dividing and undergo a series of chemical and physical changes. These bigger, flatter senescent cells do not die and accumulate in all parts of the body. Senescent cells were only associated with a body’s natural safeguard against cancer; Cells that are cancerous are often fast-tracked to senescence in hopes that it will stop dividing further. However, recent discoveries have shown that senescent cells actually pump out a variety of proteins that cause inflammation, a normally healthy immune response that damages healthy cells in the long run. Almost every discovered

The outcomes of the study, which engaged the use of a extremely accurate biomarker to evaluate biological aging, are presented in Molecular Cell.

4. Pre-osteoblasts are recruited by cytokines: transforming growth factor beta, insulin growth-like factors, fibroblast growth factors and bone morphogenetic proteins (BMPs) (Hock et al, 2004). The actions of BMPs cause pre-osteoblasts to differentiate into osteoblasts (Monolagas, 2000). Osteoblasts then secrete bone matrix proteins: type-I collagen, osteocalcin, proteoglycans, growth factors and glycoproteins into the resorption pits (Nair et al, 1996). Approximately 50% of osteoblasts then undergo apoptosis and the remaining become embedded osteocytes or bone lining cells.

The greater longevity and improved health seen at older ages in many parts of the world represent one of the crowning achievements of the last century, but also present a significant

The way God created us as humans is a life cycle where eventually late adulthood comes with the biology of aging. Santrock (2013) describes five different theories of why humans age (p. 541). The evolutionary theory explains that aging is more of a natural selection process, and diseases occur in the elderly because they “would have been eliminated” if they were in younger people (Santrock, 2013, p.541). Cellular clock theory describes how cells get tired of dividing after they have been reproducing for so long (Santrock, 2013, p.541). Free-radical theory explains when “cells metabolize energy the by-products include unstable oxygen molecules known as free radicals” (Santrock, 2013, p.541). The unstable oxygen molecules can damage DNA and other structures inside the cell (Santrock, 2013, p.541). Mitochondrial theory describes how aging occurs because of the mitochondria essentially wearing out and becoming less efficient (Santrock, 2013, p.542). Mitochondria are the cell’s “power house,” and they convert energy inside the cell (Bailey, 2008). The last theory, hormonal stress theory, illustrates the effects of stress, especially long term stress, on aging (Santrock, 2013, p.542). Stress released hormones which depress the immune system making people more susceptible to disease (Santrock, 2013, p.542). There are many theories about why human’s age, and all of them may be true, but regardless aging is inevitable and so are its effects.

According to theory of aging, free radical interferes in this case. Aging is the apparently unavoidable decrease in physiologic function that happens after some time. At least four main theories of aging have been discussed that imply to clarify much or majority of the reason of biological aging:

Aging is the process of becoming older, as we age, multiple mutations occur that concern all the processes of aging well as it compromising a number of different genes. There are many theories of biological aging, such as the Cellular Aging Theory, Immunological Theory, and the Wear and Tear Theory. The Cellular Aging theory describes the process of aging in which cells slow their number of replication, thus giving each species a “biological clock that determines its maximum life span” and how quickly one 's health will deteriorate(Hooyman, 42). After a certain number of years, each cell which follows an apparent biological clock starts to replicate itself less, thus the specific individual or species slowly deteriorates. This theory gives

In order to better understand aging-associated diseases, it is first necessary to define what aging is. Aging is a complex, multifactorial process of harmful mutations in cells and tissues that are accumulated over time and result in an increased risk of disease and, eventually, death (Tosato, Zamboni, Ferrini, & Cesari, 2007, p. 401). Contrary to the belief that aging can be cured through medical advances, it is scientifically accepted that, while human life expectancy has increased, the human life span has remained largely unchanged for the past 100,000 years (Tosato et al., p. 401). Therefore, future developments in aging research ought to focus on addressing treatment and prevention of major aging-associated diseases that will

In today's world, much gets written about combating the natural aging process. While most of the information is valid in many cases, let us examine below five, time-tested and proven methods that anyone can incorporate into their daily routine to fight advancing age. In doing so, many potential illnesses or diseases can be avoided.

The authors are thus led to conclude that “to date, no convincing evidence showing the administration of existing ‘anti-aging’ remedies can slow aging or increase longevity in humans is available.” And the SENS Research Foundation Web site admits: “No currently-available medical intervention or lifestyle choice has been shown to affect the basic human aging process.”"

Given the vital role of caspase activation in apoptotic cell death, blocking their function is a useful approach to find out whether apoptosis has a causal effect in triggering compensatory proliferation. In various species tissue regeneration was impaired if cell death was blocked with pan-caspase or effector caspase inhibitors (Fan and Bergmann 2008; Li et al. 2010; Ryoo and Bergmann 2012; Tseng et al. 2007). This approach has also been shown to ameliorate loss of neuronal cells and function after traumatic brain injury and retinal detachment (Hisatomi et al. 2001; Zacks et al. 2003). Following this approach we found that the pan-caspase inhibitor reduced the number of cleaved CASP3+ cells in cultured retina explants, but not the overall

Cell death is when a biological cell stops carrying out is function. Cell death can be due to the natural process of replacing old cells with new ones, or may result from factors such as disease, localized injury, or even death of the whole organism.