Why is Drosophila Melanogaster used in the diagnosis of ischemic stroke?
Well,for that question we should further analyse the definition of ischemic stroke, and the similarities of gene structures between humans and Drosophila Melanogaster, as well as the diagnosis of ischemic stroke itself. Before we go any further, it is understood by all biologists that all protein interactions is the base line for all the physiological systems in the human body. From cell mitosis to apoptosis, fighting off infections and developing genetic diseases, as well as the maximum age of an organism,it is determined by the interactions between proteins,as well as the sequencing on our mere genome and DNA.
Drosophila Melanogaster, also known as fruit fly, has approximately 14000 genes, which is significantly lesser than human genes,which lies on approximately 24000 genes. However,the protein interactions differ from quite a number, as humans has approximately 10 times the amount of protein interactions when compared to fruit flies. Quoted from professor Micheal Stumpf from Imperial College London Department of Life Science, ‘Scientists have believed for some time that the complexity of an organism’s protein interaction determine its biological complexity, but until now it’s been impossible to put a number on the size of one organisms; interaction network compared to another, as relatively little work has been done to identify and map these interactions.’ Understanding the human genome definitely does not come close enough to explain what makes us different than smaller and more simpler organisms, but with the understanding of protein interactions we can actually unravel how does one organism differentiate from another. Drosophila Melanogaster has been used as a model organism to understand the effects of various diseases and toxins towards an organism for the past 90 years, and has successfully proven a lot of theories and experiments,further improving the current biological advancements. Currently, with the bloom of the biological era for modern researchers, the genome sequence of Drosophila Melanogaster had been mapped out a few years ago, and was published in March 24, 2000 by a team of biologists from the University of California Berkeley, as well as researchers from the Celera Genomics Corporation. The sequence is now accessible through Genbank, the National Institutes of Health genetic sequence database. This benefits us as of 289 genetic flaws known to cause diseases in humans, it is revealed that Drosophila Melanogaster has a similarity of 60%,as well as having 70% of the genes involved in human cancers. Among these genes, the genes that is involved in Parkinsons disease and the p53 tumor suppressor gene has been identified in Drosophila Melanogaster. As a thorough conclusion, it seems that Drosophila Melanogaster has quite the potential to be a model organism reflecting human genetic diseases.
Diagnosis of Ischemic Stroke – The usage of Drosophila Melanogaster
Each year, about 800,000 people suffer from ischemic stroke. The diagnosis of ischemic stroke is the major criteria in saving the lives of ischemic stroke sufferers when first admitted to the emergency department of a hospital. The diagnosis should be done fairly fast and accurate to ensure the minimization of damage done to victims due to the lack of blood supply to the brain. Principles of classic clinical neurologic localization allow the physician to correlate particular neurologic deficits with specific lobes and deep structures. It is the possible to conclude that a focal deficit is present and to draw conclusions about its pathogenesis. Based on the localization, extent, and character of deficit, it is possible to narrow the possible sites of vascular occlusion or stenosis. This vascular localization allows an imaging evaluation to be designed that demonstrates the vascular lesion in many cases. However, there is much to none human examples having onset ischemic stroke while on close observation. This is where the used of a model organism would proof efficient in solving the diagnosis of ischemic stroke. It is discovered that some neuroprotective programs can be induced in the model of ischemic tolerance: brief exposure to sublethal ischemia produces tolerance to a subsequent, severe ischemic challenge. It is quite a discovery by modern biology to understand the effects and the outcomes regarding ischemic stroke through the usage of Drosophila Melanogaster which is easy to acquire without having moral obligations.
Further elaborations- Experiments ongoing on Drosophila Melanogaster
There are quite a number of biological experiments done on the model for quite some time now, around >100 years of biological experiments have proven useful in diagnosis,as well as in treatment fields. Multiple scientific approaches are required to understand disease etiology, progression, and management, to aid understanding of onset and risk factors, as well as treatment and intervention design. With >600 neurological disorders listed by the National Institute of Neurological Disorders and Stroke—categories include neurodevelopmental, stroke, traumatic injury, cancer, and neurodegenerative —the disease consist of a wide range of complex and unsolvable matters. An approach towards the answer to solve these complex situations is to model disease mechanisms and identify disease-modifying pathways in less complex, yet analogous, organisms. The fruit fly Drosophila melanogaster has proven to be tremendously valuable when being the model of many neurological and neurodegenerative diseases, not only providing understanding of biological pathways impaired in disease, but also the foundation for strategies for intervention approaches in mammalian systems. An example towards this statement is the so-named drop dead mutant of the fruit fly,that underwent brain deterioration and human late-onset degenerative disorder. There are quite a number to name, a few would be spongecake, eggroll and swiss cheese, and all of them are related to either gene mutation or degenerative brain diseases. From another perspective, there is also accumulating evidence that caspase-independant programmed cell death may play an important role when having delayed neuronal death following ischemic stroke. Previous research has implicated mitochondrial proteins, such as apoptosis-inducing factor (AIF) and Bcl-2/adenovirus E1B 19 kDa-interacting protein (BNIP3) being a fundemental component and key character in this interaction. As the study of caspase-independent programs has expanded, it has become increasingly apparent that this pathway is not simply an alternative to apoptosis when caspases are unavailable, but a unique process, distinct from both apoptosis and necrosis. There are a lot of experiments already conducting on the model organism stated above, and the efforts are still undergoing as the public demand and stress has increase dramatically over the years. As a continuation, endogenous neuroprotective programs has been further investigated throughout the years as its counterpart, exogenous procedures has not been showing efficiency towards the clinical trials and experiments conducted.