Diabetes research proposal

This proposal outlines a screening program for gestational diabetes, coupled with multidisciplinary team management of this disorder through cooperative efforts of private sector medical practitioners and the public sector nutrition program for women, infants, and children (wic). The investment in this proposal is catalytic: the long-term intent is to persuade those in the medical community in the targeted geographic area to adopt the screening procedure and coordination with the wic program as a standard part of their prenatal care. 1 diabetes research proposal: degradation of c3 in subjects shows promise for a ment of forest, illinois 1 diabetes is an autoimmune disorder resulting in the destruction of beta-cells within the pancreas. Current research has outlined some improvement in the condition among individuals treated with an antibody for the complement molecule c3. It is still necessary to find a highly effective method of curing type 1 diabetes without causing destructive side-effects. This paper outlines an experimental proposal, which would hopefully lead to clinical trials and come to the market with indication for curing type 1 diabetes.

Finally, effect of treatment on type 1 diabetes would be measured through c-peptide levels, allowing for analysis of β-cell survival in the 1 diabetes is an autoimmune disorder that affects 9. The individual with the disorder is responsible for controlling their blood sugar levels, which, in a healthy individual, is taken care of naturally by the a molecular basis, the initial cause of type 1 diabetes is unknown, but there is a lot that has been found out up to this point about the development of the disease. This binding initiates the opening of glut4, a glucose transport protein (joslin diabetes center, n. Therefore, it is evident why the destruction of pancreatic islet β-cells can be dangerous and even life threatening, and thus why research for this disease is t research is working on illuminating the cellular basis for the destruction of these β-cells, as well as determining the initial cause of the auto-reactive response. The more we understand about these specifics, the better the hypotheses for cures and long-term treatment will working on treatments and therapeutic targets, researchers first needed to understand on a more molecular basis how the disease works so they can properly target further research. This focus elucidated a lot of specific immune mechanisms involved in the development of type 1 diabetes.

Researchers found this by using flow cytometry to measure the relative proportions of specific types of dendritic cells in recently diagnosed diabetes patients to that of healthy patients. It followed from qpcr of samples from mice that pdcs secrete ifn-alpha and are essential to the development of type 1 diabetes (diana, 2013). Similarly, upon examination of blood samples from recently diagnosed type 1 diabetes patients, it was discovered that pdcs use immune complexes to drive the t-cell activation, which is what perpetuates β-cell targeting by the immune system (allen, 2009). After immunohistologically analyzing the tissue, researchers found that neutrophils conjunction with b1a cells to initiate the immune response that causes β-cell death, through releasing cramp and ifn-alpha (diana, 2013). They confirmed using elisa that the most effective way to develop type 1 diabetes was with an equal mixture of b1a and neutrophil eukin-1 is another immune system molecule often implicated in diabetes. Research is being done on it and its role in the development of the disease.

Il-1β, is a molecule that has been deeply associated with the regulation of the immune system response with respect to type 1 diabetes. In preliminary experiments, 15 children with diabetes were treated with an il-1 receptor inhibitor for 28 days to see how it would impact the development and progression of their disease after recent diagnosis. Sumpter’s team of researchers did a successful initial trial on a group of children as described previously, it seemed only logical to launch clinical trials on this method with a larger sample of individuals with the condition. Thus, building off of sumpter’s research, antoinette moran and her team of researchers investigated the possibility of il-1β as a target for treatment among the masses. Though this may seem disappointing, failed results are often equally as enlightening as successful group of researchers investigated 42 recently deceased type 1 diabetes patients to determine how many of their β-cells were destroyed through programmed cell-death. One might expect that these diabetes patients would express high levels of β-cell death, as the disease functions via the destruction of pancreatic islet β-cells.

They actually found that only 5 patients had extremely high levels of β-cell death, and the levels of cell death were two times higher in those patients than the majority of the type 1 diabetes patients (meier, 2005). This interesting information lead the scientific community to further explore the way that β-cell death occurs in patients, specifically with respect to and his team of researchers did some investigation on 924 type 1 diabetes patients during which they used a c-peptide assay to measure insulin levels. After analyzing the 924 type 1 diabetes patients’ levels of c-peptide, they found that the highest c-peptide values were associated with patients who had type 1 diabetes for 5-10 years in duration (oram, 2015). Research combined with the results meier and his team found suggest that even after β-cell destruction at the onset of the disease, there is a small subset of islet β-cells that remain alive and functional. Additionally, earlier in disease progression seems to be the time period for intervention that would produce the most notable len decided to attempt to limit the β-cell death in newly diagnosed type 1 diabetes patients. His team of researchers designed an antibody for cd3, which is the molecule in the complement system that is involved in perpetuating the cycle of β-cell destruction through t-cell activation.

Therefore, it seems that the concept of protecting β-cells can be successful, but the details of the study caused adverse side effects, and over the long run didn’t produce significant enough build off of this study, harold and his team of researchers chose to study a different antibody in type 1 diabetes patients that binds cd3 as well. The mechanisms for this group of antibodies is not well known, which disables researchers from understanding how, specifically, these antibodies differ. For this round of research, 10 subjects were used to determine the efficacy of hokt3gamma1(ala-ala) (herold, 2009). Therefore, the information related to this antibody does not necessarily support its use as a potential ing from the current research and all of the recent discoveries regarding β-cell survival within the pancreatic islets of type 1 diabetes patients at different stages of their disease progression, the next step is to determine the most efficacious way of preserving β-cell function. And thus, there remains more research to be done in order to come up with an effective manner of reducing β-cell death through the immune system, while minimizing side effects for patients and maximizing the effectiveness of the treatment to salvage β- order to aid in the treatment of type 1 diabetes, it is essential to spend funding and time researching the right questions, and for them to be heavily based in a scientific hypothesis. Based on the scientific experiments outlined in the previous section, there is promising evidence for treatment of type 1 diabetes through elimination of immune system elements that promote the t-cell activation and destruction of β-cells.

Previous research has demonstrated that administration of cd3 antibodies within a month of diagnosis of the disease is a semi-efficient way of slowing disease progression, but by no means eliminates disease progression or the dependence upon synthetic insulin injections. Therefore, an experimental procedure that further investigates a way to halt the immune response to β-cells and allows for their survival would be a beneficial way to build off of current research and strive toward the end goal of curing type 1 alteration of the complement pathway within type 1 diabetes patients shows some promise, it seems logical to stick with alteration of the complement pathway as opposed to trying to alter a different part of the immune response all together. But, it is clear from the research discussed in the previous section that introduction of an antibody for c3 is not sufficient and causes too many adverse side effects to be a viable option for treatment. Therefore, it seems worthy to study the effect of increasing decay of c3 convertase, the enzyme that cleaves c4 into c3, to prevent c3 from being created in the first : before exploring how inhibiting this enzyme might affect the progression of type 1 diabetes, we would first want to test its efficacy in a nod mouse model. 2013, provides a mouse that develops type 1 diabetes in a progression analogous to that of human type 1 diabetes progression. According to previous literature, which was discussed in the current research section of this proposal, a previously confirmed and successful antibody for c3 is chaglycd3 (keymeulen, 2005).

Peptide activity in nod mice:Finally, to assess how all of this impacts the end result of developing type 1 diabetes, the obvious technique based on modern research is to analyze c-peptide release. The increase in c-peptide levels are coincidental with an increase in natural insulin production, which in turn is a signal for beta-cell activity and experiments are designed to help in addressing the question of whether decreasing the quantity of c3 within a type 1 diabetes model is a viable route for curing the disease. The research up until this point has pointed to success in relief of the dependence upon artificial insulin through muting c3’s ability to function. Researchers hypothesized that the side-effects were derived from a cytokine response to the antibody injected into the system. These human trials should consist of 10-15 recently diagnosed (which, as defined by literature, consists of diagnosis less than 30 days previous to initial experimentation) type 1 diabetes patients. From there, clinical trials should occur to show efficacy and safety of the treatment within the type 1 diabetes experiments are crucial to curing a highly prevalent disease within our society.

Population being affected by the disease, it is important to continue researching possible cures to put this horrible disease to rest. This research would be extremely beneficial to the public as well as the scientific community, and is absolutely worth the funding and time necessary to undergo experiments such as : eukaryon is published by students at lake forest college, who are solely responsible for its content. Plasmacytoid dendritic cells are proportionally expanded at diagnosis of type 1 diabetes and enhance islet autoantigen presentation to t-cells through immune complex capture. Treatment of patients with new onset type 1 diabetes with a single course of anti-cd3 mab teplizumab preserves insulin production for up to 5 years. Sustained beta cell apoptosis in patients with long-standing type 1 diabetes: indirect evidence for islet regeneration? Most people with long-duration type 1 diabetes in a large population-based study are insulin es care dia care, 38(2), 323-328.

C-peptide is the appropriate outcome measure for type 1 diabetes clinical trials to preserve -cell function: report of an ada workshop, 21-22 october 2001. Continuing to browse this site you agree to us using cookies as described in about cookies remove maintenance message to old article view ctabstracta structured written research proposal is a necessary requirement when making an application for research funding or applying to an ethics committee for approval of a research project. A proposal is built up in sections of theoretical background; aim and research questions to be answered; a description and justification of the method chosen to achieve the answer; awareness of the ethical implications of the research; experience and qualifications of the team members to perform the intended study; a budget and a paper describes the common steps taken to prepare a written proposal as attractively as possible to achieve funding.