Team:ATOMS-Turkiye

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    <li><a href="https://2014.igem.org/Team:ATOMS-Turkiye/At-a-Glance"><img src="https://static.igem.org/mediawiki/2014/4/4f/ATOMS-Turkiye_right_1.png" /></a></li>
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    <li><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Data"><img src="https://static.igem.org/mediawiki/2014/9/94/ATOMS-Turkiye_right_2.png" /></a></li>
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    <li><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Interlab-Study"><img src="https://static.igem.org/mediawiki/2014/5/58/ATOMS-Turkiye_right_3.png" /></a></li>
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    <li><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Practices-Approach"><img src="https://static.igem.org/mediawiki/2014/2/23/ATOMS-Turkiye_right_4.png" /></a></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/3/33/ATOMS-main-1.jpg/800px-ATOMS-main-1.jpg" title= "Our blood vessels  consist of three layers named as the endothelium, muscular and outer layer which allow oxygen and nutrient rich blood to flow through and diffuse into tissue cells. "></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/6/6c/ATOMS-main-2.jpg/800px-ATOMS-main-2.jpg" title= "In some cases such as excessive body weight or diabetes, accumulation of fat may occur on the surface of endothelium leading to the eventual formation of plaques."></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/8/84/ATOMS-main-3.jpg/800px-ATOMS-main-3.jpg" title= "Plaques may continue to increase in size and narrow the lumens of our vessels, decreasing and limiting the blood flow to tissues and resulting in the escalation of surface tension."></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/2/2a/ATOMS-main-4.jpg/800px-ATOMS-main-4.jpg" title= "The increase of tension in the lumen is highly likely to rupture the plaques and cause the eventual formation of the blood coagulation cascade."></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/d/d7/ATOMS-main-5.jpg/800px-ATOMS-main-5.jpg" title= "The process of coagulation results in the superfluous formation of a clot which has a tendency to grow larger. "></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/1/1b/ATOMS-main-6.jpg/800px-ATOMS-main-6.jpg" title= "If this is the case, the clot inevitably blocks the path of the bloodstream hence distrupting the oxygen and nutrient supply to tissue cells."></li>
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  <li><img src="https://static.igem.org/mediawiki/2014/thumb/1/15/ATOMS-main-7.jpg/800px-ATOMS-main-7.jpg" title= "As the blood contains oxygen and nutrients which are essential for energy production and survival of cells, tissues become oxygen and nutrient depleted which we term as Hypoxia."></li>
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  <li><img src="https://static.igem.org/mediawiki/2014/thumb/c/ca/ATOMS-main-8.jpg/800px-ATOMS-main-8.jpg" title= "Our project poses the sensing of hypoxia in early stages by using our engineered endothelial cells and activating the pathway to solve this leading cause of death worldwide."></li>
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<li><img src="https://static.igem.org/mediawiki/2014/thumb/f/fe/ATOMS-main-8a.jpg/800px-ATOMS-main-8a.jpg" title= "However as we dissolve the clot, blood supply is enabled which has a high possibility of causing an oxidative burst. We also eliminate the potential occurence of this via our engineered cells."></li>
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  <li><img src="https://static.igem.org/mediawiki/2014/thumb/a/aa/ATOMS-main-9.jpg/800px-ATOMS-main-9.jpg" title= "With our novel sensing and protective systems, evaluation of clinical presence will no longer be required to treat hypoxic conditions."></li>
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  <li><img src="https://static.igem.org/mediawiki/2014/thumb/7/78/ATOMS-main-10.jpg/800px-ATOMS-main-10.jpg" title= "Hence, our unique design of mechanism will now be a remedy to the leading cause of deaths worldwide. "></li>
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<h1 >The Change of HEART </h1>
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<p> Tissue hypoxia, or ischemia, is the condition that describes the poor conveyance of oxygen and
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other vital products to body tissues and organs which consequently results tissue death.
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<br> Up to now,the number one cause of death worldwide is caused by ischemia and related conditions such as
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heart attack or stroke. Additionally, due to the remarkable damage to tissues, these diseases end
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up with high morbidity rates. From pharmacology to biomedical industry, variety of prevention and
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treatment options have been suggested, many of them have still being applied. Nevertheless, we
 
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still have not reached the very end of cure and more novel approaches from different fields may play
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great role for this reason. One of these approaches is, of course, synthetic biology. The benefits of
 
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SynBio allow us to manipulate micro and nano scales of cell environment in order to involve in when
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<h2>Project Abstract</h2>
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<p><a href="#"></a>The condition which results in tissue death due to the poor conveyance of oxygen and other products vital for tissue cells and organs is described as tissue hypoxia or ischemia. Currently, ischemia and other related conditions such as heart attacks and strokes take the lead for being the number one cause of death worldwide. Moreover, the current treatment of ischemic attacks can intensify the damage in the tissue caused by hypoxia which is known as oxidative stress. This is due to the high oxygen concentration of the restored blood supply. Without a doubt, we need to view the bigger picture of the condition in order to solve this problem. In our project, we desire to build two different devices which work synergistically and fix these these two distinct situations, hypoxia and oxidative stress. Hence, we have decided to use "hypoxia inducible systems" and "reactive oxygen species (ROS) sensitive gene fragments". These two receptors will regulate the release of clot dissolving factors and antioxidant peptides synthesized by our engineered vessel cells. Through attaining encouraging in-vitro results, we aim to pave the way of this promising system into a lifesaving remedy.</p>
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the action starts and to interfere at the right time.  
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                <div><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Modeling" class="tit">Modeling</a><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Modeling" class="lnk"><span><strong style="font-size:15px;margin-left: 0px;margin-right: 15px;">This year we carried out mathematical modeling to comprehend how our promoter system would react against hypoxia in order to treat heart related problems. In addition to this, we have also modeled our safety experiment to show its successful outcome mathematically. For more information, click here...</strong></span></a>
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Ischemic damage is related with two different phenomena. First, the vital blood supply that carry
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                    <img src="https://static.igem.org/mediawiki/2014/thumb/6/6f/ATOMS-main-modeling.png/685px-ATOMS-main-modeling.png" alt="This year, we have carried out ..." width="210" height="220"><b>This year, we have carried out ....</b>
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oxygen, energy gathering nutrition and other minerals is cut down by an external effect, mostly by
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                </div>
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            </li>
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            <li class="two">
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                <div><a href="https://2014.igem.org/Team:ATOMS-Turkiye/BioBricks#main" class="tit">BioBricks</a><a href="https://2014.igem.org/Team:ATOMS-Turkiye/BioBricks#main" class="lnk"><span><strong>Our team proposes seven new eukaryotic cell parts to the Registry consisting of three promoters and four different enzymes with various capabilities. To get detailed information, proceed here.</strong></span></a>
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a clot. Afterwards, cells become unable to produce enough energy and start wasting their deployed
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                    <img src="https://static.igem.org/mediawiki/2014/1/16/Atoms_turkiye_main_page_diagram.jpg" alt="Our team proposes seven new eukaryotic cell parts ..." width="210" height="220"><b>Our team proposes seven new eukaryotic cell parts ...</b>
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nutrition in a different reaction cascade that results with building up toxic chemicals in the media.
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If the clot barrier is removed, excessive oxygen presence in the media may enhance this toxic
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                <div><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Achievements" class="tit">Achievements</a><a href="https://2014.igem.org/Team:ATOMS-Turkiye/Achievements" class="lnk"><span><strong>It was a long study session; but it's worth. We accomplished several of our tasks to establish a fully beneficial treatment for heart attacks. To check out what we achieve, click here.</strong></span></a>
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production because of high metabolic rate of the cells. These toxic products, also known as reactive
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oxygen species (ROS), may increase the cell damage further. Thus, it is needed to regard the big
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picture of the condition In order to solve the problem.
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In our project, our will is to build two different devices, which work synergistically, to fix these two
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distinct situations. To do this, we aim to design hypoxia inducible systems, which is the first step for
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constructing a sensitive and robust device. Hypoxia inducible promoters and their regulator proteins
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are responsible for this critical mission. Beside of this, we also want to prevent the damage caused
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by reperfusion of blood to the hypoxic environment, we also need an additional sensitive receptor
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construct. After our researches, we decided to use reactive oxygen species (ROS) sensitive promoter
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systems. These two receptors will hopefully regulate the release of clot dissolving factors synthesized
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by our engineered vessel cells. Moreover, we hope to maximize the reduction of ROS damage to the
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cells by producing antioxidant enzymes to degrade ROS within the cells. By re-providing vital oxygen
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support via bloodstream and enhancing the degradation of ROS in the tissue, this project intends to
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propose a new treatment approach for ischemia related diseases.
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In the future, following the advancements in gene therapy and cell therapy industries, we would
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like to implement our system in living models. Especially, tissue engineered heart vessel cells or
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manipulating the whole body by gene containing exosomes, this treatment option may also pose an
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alternative prevention method for ischemic heart attack or strokes.<br>We hope to bring encouraging
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results in vitro to pave the way of this promising system into the lifesaving remedy method.  </p>
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                    <img src="https://static.igem.org/mediawiki/2014/thumb/8/8a/ATOMS-main-Checklist.jpg/800px-ATOMS-main-Checklist.jpg" alt="Mechanism of ODD..." width="210" height="220"><b>It was a long study session; but...</b>
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Latest revision as of 03:55, 18 October 2014

Project Abstract

The condition which results in tissue death due to the poor conveyance of oxygen and other products vital for tissue cells and organs is described as tissue hypoxia or ischemia. Currently, ischemia and other related conditions such as heart attacks and strokes take the lead for being the number one cause of death worldwide. Moreover, the current treatment of ischemic attacks can intensify the damage in the tissue caused by hypoxia which is known as oxidative stress. This is due to the high oxygen concentration of the restored blood supply. Without a doubt, we need to view the bigger picture of the condition in order to solve this problem. In our project, we desire to build two different devices which work synergistically and fix these these two distinct situations, hypoxia and oxidative stress. Hence, we have decided to use "hypoxia inducible systems" and "reactive oxygen species (ROS) sensitive gene fragments". These two receptors will regulate the release of clot dissolving factors and antioxidant peptides synthesized by our engineered vessel cells. Through attaining encouraging in-vitro results, we aim to pave the way of this promising system into a lifesaving remedy.