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Basic medical research
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Personal Statement “As a well-spent day brings happy sleep, so life well-used brings happy death”, quoted from Leonardo da Vinci’s will, is my motto since I entered the Second Military Medical University. His remark always reminds me to live life to the fullest and engage in basic medical research which has fascinated me a lot since I was a little child. When I was only 6 years old, my father, a researcher in molecular biology, often brought me to his laboratory and I was deeply impressed by the advanced equipment which aroused my curiosity. After having grown up, I was always touched by my father’s attitude towards research because he often stayed up late at night in the lab even though he had already been a chief director of the department. …show more content…
After that, I read lots of background materials about nitroglycerin and I noticed that nitric oxide is the effective constituent of nitroglycerin. Nitric oxide, a simple nitrogen oxide gas, plays a vital role in cardio-protection. From my point of view, some other kinds of gas might also have the same effect and methane, the simplest alkane, came into my thought. Methane, the most common organic gas in the atmosphere, can be synthesized biologically and a recent study showed that methane could confer protective effects on oxidative stress and inflammation in ischemic and reperfusion-induced intestinal injury. So it was meaningful for us to investigate the myocardial protective effects of methane. At that time, I got in touch with Prof. Xuejun Sun coincidently who had focused on medical gas research for more than 5 years and he offered me a chance to explore the cardio-protection of methane. It proved to be a really important start for me to pursue my dream of getting in basic medical research and curing more and more …show more content…
It was difficult for me to explore the certain molecular mechanism of methane’s protection alone, so I chose to focus on the hydrogen which had been studied for nearly ten years. Even though previous studies showed that hydrogen protects against myocardial ischemia/reperfusion (I/R) injury in rats, the effects of high-concentration hydrogen gas (HCH) on myocardial I/R injury remain unclear and the mechanism underlying this protection should be explored. In this study, I tried to explain the vital role of the specific protein in the pathway of hydrogen cardioprotection. In this study, firstly, we examined several traditional protective pathways in HCH treated mice and PI3K-Akt signaling pathway is the most relevant one. In addition, pretreatment with pharmacological inhibitors of PI3K (LY294002 and wortmannin) abrogated the cardioprotective effects of HCH in mice with I/R injury, which demonstrated that PI3K/Akt pathway mediates the cardioprotective effects of HCH in myocardial I/R injuries. We observed the results in the present study that the phosphorylation level of GSK-3β was significantly up-regulated by hydrogen, which has a high correlation of Akt1 phosphorylation. In vivo and cultured neonatal mouse cardiomyocytes experiments were conducted to reveal the important role of Akt1 during the hydrogen treatment with the application of pharmacological inhibitors. In the process of this
Retrieved on March 2014 from world wide web at http://www.webmd.com/heart-disease/guide/heart-disease-heart-attacks Wolf, Zane Robinson & Hughes, Ronda G (n.d.). Error Reporting and Disclosure. Retrieved on March 2014 from world wide web at http://www.ncbi.nlm.nih.gov/books/NBK2652
On a cellular lever, HCM can cause the cells to become disorganised and lost. Under a microscope, a normal Cardiac Muscle cell appears parallel and organised, while a cell affected by HCM will appear irregular and disorganised. This disorganisation can create changes and altercations in the signals sent and received through the lower chambers of the heart, which in turn can lead to an abnormal heart rhythm, known as ventricular
Nitric oxide is a gaseous, diatomic molecule that plays an important role as a mediator of cardiac function, working largely as a vasodilator in the cardiovascular system. Nitric oxide is synthesized by a family of enzymes known as nitric oxide synthases (...
Also, I further study Ph.D in medical physiology at Khon Kaen University to continue my research. My main point of study is to test the hypothesis taurine supplementation improves cardiac injury and arterial pressure control dysfunction after cardiac ischemia/reperfusion via renin-angiotensin system in adult female rats perinatally depleted of taurine followed by high sugar intake since weaning. My results demonstrate that taurine supplementation prevents or improves the adverse effects of cardiac cardiac ischemia/reperfusion on cardiac function and arterial pressure control via inhibition of both systemic and cardiac renin-angiotensin system
The AMGEN Summer Scholars research experience will contribute to my plans to become a M.D./Ph.D. candidate, and ultimately an Oncologist, by helping me develop critical and independent thinking as well as creative skills as they relate to the field of medicine. It will also help me develop a more thorough understanding of biological concepts, how they directly apply to medical treatment, and the ways in which biotechnology fuses multiple fields of science to create technologies to care for others. The opportunity to assist in creation of the technologies that will be used on my future patients will ultimately improve my ability to treat their illnesses in adaptive ways. The opportunity I would have to read, interpret, and be a part of creating
Hypertrophic cardiomyopathy is a genetic disease of the heart, making the cardiac muscle is thick and strong. The thick muscle causes a decrease in cavity size, forcing the heart to pump less blood. Hypertrophic cardiomyopathy is one of the primary causes of sudden death as the prevention of blood flow causes cardiac arrest. More successful research is being conducted on HCM, including research on the genetics associated and the heredity of the genes. Unfortunately this disorder effects many young athletes due to their increased stresses of training on their heart. However, despite the use of new technology such as the electrocardiogram and transthoracic echocardiogram, the strategies are limited, restricting new answers.
The term, ischemia, denotes inadequate blood supply to tissues due to blockage of the arterial inflow, while, reperfusion injury is defined as the injury caused by the restitution of blood flow after an ischemic peroid, leading to death of cells that were only reversibly injured at the time of blood flow restitution. [63]. The final infarct size after an MI event is therefore the result of the ischemic and reperfusion damage. For this reason, the term that best describes this process of myocyte death in reperfused MI is myocardial ischemia/reperfusion (I/R) injury [64]. In the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which activate the G protein signaling pathways therefore promoting myocardial survival. While in the late phase, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF and SDF-1, in the injured myocardium, hence promoting a cardio-protective state. The liver also participates in cardioprotection through the up regulation and release of secretory proteins, including FGF21 and TFF3, which also promote cardiomyocyte survival. [65]. Foundational studies performed about three decades ago with animal models demonstrated that an early reperfusion was able to limit infarct size [66]. Then fibrinolysis was indisputably associated with a decrease in mortality in patients with STEMI [67].A decade later; primary angioplasty was shown to be more superior than fibrinolysis [68]. Currently primary coronary angioplasty (PCI) has been established as the backbone treatment for STEMI patients. The period from the onset of symptoms of MI (representative of the time of coronary occlusion) and reperfusio...
Humphrey Davy was an English chemist who was the head of the Pneumatic Institute in Bristol, UK. Humphry was trying to find a way to rid people of tuberculosis using various gases. H...
[13] "Hypertrophic Cardiomyopathy." The Cleveland Clinic Foundation for Continuing Education. © 2000-2014 The Cleveland Clinic Foundation, Jan. 2009. Web. 27 Mar. 2014.
Everyone on this earth has to be grateful to Paul Ehrlich because he made so many advances in medical research. Our life expectancy rate would still be around forty years if Ehrlich hadn’t been interested in chemistry and biology as a young boy. If Ehrlich hadn’t combined so many different chemicals, he would have never combined the chemical known as number 606.
...rplexed philosophers in all ages, to track to their sources the causes of disease, to correlate the vast stores of knowledge that they may be quickly available for the prevention and cure of disease- These are our ambitions. (The President’s council on Bioethics 1)
The immediate response is to buffer hydrogen ions with non-bicarbonate buffers. Bicarbonate is ineffective in this situation as it reacts with the hydrogen ions to for H2CO3, which is the original cause. In the extracellular fluid space, proteins constitute the only buffer. While within the cells, haemoglobin, phosphate, proteins, and lactate are the major non-bicarbonate buffers. Up to 97% of the buffering of H2CO3 is derived from intracellular rather than extracellular fluid buffers (Kaehny,
There are six mechanisms of cell injury; ATP depletion, reactive oxygen species (ROS), Ca2+ entry, mitochondrial damage, membrane damage, and protein misfolding/DNA damage. ATP depletion is when there is a loss of mitochondrial ATP and decreased ATP synthesis. This will result in cellular swelling, decreased protein synthesis, decreased membrane transport, and lipogenesis, all changes that contribute to loss of integrity of plasma membrane. Reactive oxygen species is when a lack of oxygen causes a progression of cell injury in ischemia. Destruction of cell membranes and cell structure is caused by activated oxygen species. Ca2+ entry is when ischemia and certain chemicals cause an increase in cytosolic Ca2+. This increase of Ca2+ causes damage
The life of a Culinologist is ever changing, much like the constant bevy of trends. I may not be a pro in my field… yet, but I’ve concluded that much. It takes a great deal of work to do what we do, but I couldn’t think of a better way to spend my life. Why? Some people might ask? It’s because in my own way I’m helping the world by simply doing what I love to do. It may not be perfect, though most things in life aren’t, but that’s what makes it so exciting.
When it comes to working in a stressful environment while maintaining efficient, human, and profession-al conduct, I’m highly competent. In addition, my communication skills are sharp, as is my abil-ity to retain information and remember people. Thanks to my schooling and my keen interest in the industry, my research skills will keep my knowledge of the industry and practices up-to-date. In fact, taking in new material is a joy. The Clinical laboratory science field is vast and ever-changing, something I’m both excited and prepared to deal with. For this reason, I intend to re-main on top of advances in the field.