Factors That Affect The Growth Of Cells And Their Cellular Function

Cellular respiration is going on in every cell in plants. It is interesting to know there is several of factors that affects cell respiration in plants for example ph. levels, temperature, oxygen, sugars. Germinating seeds carry out cellular respiration processes in much the same way as plant and animal cells do (Jeanty). Plant seeds respiration requires enough to maintain food or nutrients. The experiment that was done is testing the rates cellular respiration of germinating lentils that were soaked in different liquids which are water, juice, cola, Gatorade and milk. The hypothesis one is the highest rate of respiration is going to be the germinating lentils in water. The second highest rate of respiration is juice. The third is Gatorade. The fourth highest is milk. The lowest rate of respiration is going to be with the germinating lentils in cola.

According to the Alzheimer’s Association, Alzheimer’s is not a disease developed with age, rather it is a disease that can start earlier in life and progress as a person ages. It starts out small. The little things that average people forget. Brain cells are damaged when the sickness begins to develop which leads to the inability to retain information or memory, according to the Alzheimer’s Association. Brain cells end up dying and normal functions disappear. Nerve cells die due to the buildup of protein within the brain. These proteins, referred to as plaques and tangles, are a normal sign of aging. An excessive amount of protein buildup

1.3: Is the lifespan extension observed in ykl∆ cells due to effects on actin cable stability? Here, the goal is to test whether reducing actin cable stability prevents the lifespan extension produced by deletion of Ykl. We will reduce actin cable stability by mutating tropomyosin. There are two tropomyosin isoforms in yeast, Tpm1 and Tpm2. Both isoforms localize to actin cables. However, Tpm1 stabilizes F-actin in actin cables. In contrast, Tpm2 regulates RACF by inhibiting the binding of myosin to actin within actin cables. Previous studies in mammalian cells indicate that mutations in the actin binding pocket of tropomyosin reduces their ability to bind to and stabilize F-actin. I will generate the same mutations in TPM1 and identify conditions that reduces actin cable abundance to wild-type levels in ykl∆ cells. Lastly, I will test whether restoring the wild-type actin cable levels in ykl∆ cells prevents the lifespan extension originally seen in ykl∆ cells.

Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Shrinkage in parts of the brain such as the cortex and hippocampus, affects functions such as remembering, planning and even thinking. The remaining tissue contains plaque, abnormal clusters of protein fragments, between surviving nerve cells. This plague can block cell-to-cell signaling at synapses and activate immune system cells that trigger inflammation while devouring disabled cells. The dead and dying nerve cells contains tangles, which are made up of twisted strands of another protein. Tangles destroy a vital cell transport made of proteins, which block nutrients and other essential supplies from reaching cells, which then die. The progression of Alzheimer’s disease follows the spreading of plaque and tangles throughout the brain. The escalation damage areas of the brain that involve speaking and understanding speech and also the sense of where a body is in relation to surrounding objects. In severe cases of Alzheimer’s, where the cortex is intensively damaged, the brain shrinks so dramatically due to widespread cell death that individuals lose the ability to communicate, recognize loved ones, and care for

Scientists believe that the combinations of genetics, environmental factors, and lifestyle play a huge part in Alzheimer’s disease. Scientists are learning that age-related changes may harm neurons. These changes include shrinking of the brain, and inflammation. In early-onset genetic mutation is usually the cause, and people thirty to sixty represent less than five percent of people with Alzheimer’s disease. In late-onset

The topics include: Alzheimer’s disease and what provokes it, amyloid-beta proteins, synapses, synaptic pruning, neurons, cognitive and microglial cells. Alzheimer’s disease affects mostly individuals in their mid-60s and is “a type of dementia that causes problems with memory, thinking and behavior” (Alzheimer 's Association). The articles reflect the discovery of the Alzheimer’s disease affects the brain by the destruction of the connection of the brain cells which causes damage in neurons and accelerate cognitive decline, and occasionally call it the earliest stage. Amyloid-beta is a term that refers to the plaques made by the proteins which interferes and cause the loss of synapses also known as synaptic pruning is the loss of connections between neurons caused microglia, that according with The Campbell Biology In Focus textbook, “microglia are immune cells that protect against pathogens” (Campbell.) The authors of the research support “microglia that prune excess synapses in development are inappropriately activated and mediate synapse loss in Alzheimer’s disease.” (Taub, 2016)

“Alzheimer’s Disease (AD) is a type of dementia, which is affecting the population that develops in the brain and can lead to problems with memory, thinking and behavior”. The Amyloid Hypothesis claims that the build up of the beta-amyloid in the brain is a cause in the development of Alzheimer disease in patients. This plaque of the beta-amyloid and its cascade of events can be linked to the deterioration and negative effects of cognitive function of the brain over time. The beta-amyloid is described to be a “sticky” protein located in the brain therefore plaques or build up of the amyloid is common. These plaques in turn can block the brain cells from communicating with each other. Which then activates an immune system, that leads to inflammation

Due to consistent improvements in healthcare over the past few years the general population lives considerably longer. Consequently, there is a considerable increase in the prevalence of non communicable diseases such as Alzheimer’s disease. It is crucial to appreciate the fact that dementia is not a normal part of ageing. Nevertheless, it is mainly associated with ageing. Studies

Alzheimer’s disease is not something we can control. The disease is a progressive, permanent, and overwhelming brain illness that causes cognitive decline, including memory, language and thinking problems. After many decades of trying to find a cure, there still isn’t one, although researchers continue to make progress. “It is unknown what causes Alzheimer’s disease but older age and family history appear to play a role” (Shu, 2011). Not only do age and family history play a factor in Alzheimer’s disease, changes to the immune system can also play a part. This could play a large role in why we do not have a cure, because we do not know, with certainty, what causes it.

Inflammation is the body’s response to infections and tissue injury. The inflammatory response is orchestrated by the cells of the immune system, both from the “adaptive” branch (including T- and B-cells with the capacity to induce long-term memory of encountered pathogens, “immunisation”) and the “innate” branch (including monocytes, macrophages, dendritic cells, and mast cells etc., that are targeted against common pathogen antigens). Inflammation was first implicated in AD pathology and development in the 1990’s with the neuropathological finding of activated inflammatory cells (microglia and astrocytes) and inflammatory proteins (e.g. cytokines and complement), surrounding the amyloid plaques and the neurofibrillary tangles [19]. In addition

The purpose of the experiment was to observe the effect of the antimitotic drug cytochalasin D on the organization of actin in human fibroblasts. The human fibroblasts were treated with increasing concentrations of the antimitotic drug and viewed using fluorescence microscopy. With each increase in concentration of cytochalasin D, we successfully observed that the presence of stress fibers decreased. The treatment of 10µM of cytochalasin D indicated that higher concentrations consistently alter actin organization. In the highest concentration treatment, the human fibroblasts no longer had stress fibers, lamellipodia, filopodia, and F-actin organization was completely disrupted. This behavior was consistent across all cells on the slide. With

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

Ageing is a natural process and part of one’s journey of life in this planet. Ageing in terms of biological process happens as the impact of the accumulation of a wide variety of molecular and cellular damage happening in the body over the period of time. This process causes gradual decrease in physical and mental capacity of a person and makes one vulnerable for getting any disease and ultimately death (World Health Organization, 2015).