Browse Ideas with tag 'biomarker':

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  DIABETIC NEPHROPATHY »

  Will systems biology discover new pathways and targets for DN?

  There has been an explosion of new genetic, biochemical, and cell biologic techniques. Appropriate systems biology tools are needed to facilitate integration of genotyping information, mRNA expression, microRNA expression, promoter analysis, proteome expression, and metabolome profiles in order to identify key biological processes and their interactions. In addition to better computational tools, a deeper understanding ...more »

  There has been an explosion of new genetic, biochemical, and cell biologic techniques. Appropriate systems biology tools are needed to facilitate integration of genotyping information, mRNA expression, microRNA expression, promoter analysis, proteome expression, and metabolome profiles in order to identify key biological processes and their interactions. In addition to better computational tools, a deeper understanding is needed of the control mechanisms of mRNA and protein expression levels in the diabetic state, such as ubiquitination, sumoylation, DNA methylation, histone modifications, and non-coding RNAs. Ultimately, this knowledge needs to be applied to clinical diabetes through better access and techniques for understanding pathobiology in individuals with DN. Large scale, longitudinal collection of CKD patients’ genetic, serum, tissue, and urine samples are required to allow use of these technologies to define the relationships between phenotype and multiple biomarkers. What is the best way to acquire tissue samples for these types of studies? Is their value in applying these approaches to human cadaveric tissue or from patients with End Stage Renal Disease?

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  Submitted by KUH Moderator 1 year ago

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  How will personalized medicine alter patient care in DN?

  One explanation for the discordant response of agents that treat complications in rodents versus humans is that deleterious pathways that are responsive to a certain drug may be widely expressed in inbred animal models, but expressed in only a small number of individuals. Should some agents be tested in primates or some other larger mammal? Pharmacogenomic, pharmacometabolomic, and pharmacoproteomic approaches could ...more »

  One explanation for the discordant response of agents that treat complications in rodents versus humans is that deleterious pathways that are responsive to a certain drug may be widely expressed in inbred animal models, but expressed in only a small number of individuals. Should some agents be tested in primates or some other larger mammal? Pharmacogenomic, pharmacometabolomic, and pharmacoproteomic approaches could be used to identify markers for people who would be responsive to specific agents, such as the case for haptoglobin genotypes and responses to vitamin E therapy. In addition, genotyping of individuals participating in clinical trials through networks such as the DRCR.net can provide information on the relationship between a genetic profile and the likely response to a particular therapy. Individually-tailored therapy for DN is a goal with enormous public health and patient benefit. Do dietary maneuvers or treatments that prevent the development of DN also prevent the progression of DN? What is the impact of diabetes duration and pre-existing tissue damage on the ability to respond to therapies? What behavioral interventions improve nutrition, diabetes adherence and self-management, and prevent DN? Will combination therapies be more effective than single therapies? Can mechanisms for efficient testing combination therapies be developed? What approaches will lead to individualizing therapies? Should therapies be targeted to specific tissues or should systemic therapies be emphasized?

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  Submitted by KUH Moderator 1 year ago

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  What new technologies will lead the field of DN forward?

  Translation of the knowledge of the molecular consequences of diabetes to effective therapies requires better measures of disease progression, faithful models of the molecular and cellular pathology, and application of cutting-edge technologies. Validated biomarkers and surrogate end points will allow rapid screening of clinical interventions prior to larger clinical trials, and can assess risk factors and treatment adequacy ...more »

  Translation of the knowledge of the molecular consequences of diabetes to effective therapies requires better measures of disease progression, faithful models of the molecular and cellular pathology, and application of cutting-edge technologies. Validated biomarkers and surrogate end points will allow rapid screening of clinical interventions prior to larger clinical trials, and can assess risk factors and treatment adequacy for patients. Surrogate end points, if adequately validated as predictors, could enable shorter randomized clinical trials and require smaller sample sizes, factors that would accelerate acquisition of clinical information. The challenge is finding biomarkers that reliably characterize risk or the disease state among numerous biomarker candidates. Animal models exist or can be developed for specific aspects of DN, but cannot completely replicate the human clinical disease. Ready access to human samples and noninvasive imaging would allow testing hypotheses within the complexity of real people with diabetes. Without question, future advances in DN will come from emerging technologies and those not yet imagined. Will the artificial pancreas or other technologies that control the blood sugar prevent the systemic complications of diabetes? Currently, the field is poised to benefit from new imaging methods, systems biology approaches, and bioinformatics tools. Can early diabetes-induced changes in tissues and organs be detected by noninvasive imaging? Will computational models that incorporate several biomarkers and imaging results create a composite analysis that is a better measure of disease progression than the individual components? What are the indicators that predict an irreversible step in the progression of DN? How can the large amount of data generated by genomic, epigenomic, and high-throughput screening experiments be synthesized into new, testable hypotheses? DN arises at the molecular, cell, and tissue level, so novel high-throughput assays are needed to encompass these interactions. Is this an area where model organisms like C. elegans, drosophila and zebrafish could be exploited?

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  Submitted by KUH Moderator 1 year ago

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