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Discover 18,076 clinical trials near Pittsburgh, Pennsylvania. Find research studies in your area.
Showing 13241-13260 of 18,076 trials
NCT00715221
We are proposing a clinical investigation of the pathogenesis of insulin resistance (IR) in skeletal muscle and adipose tissue (AT), focusing specifically on the contributions of glucose delivery, transport and phosphorylation. The primary methodology will be dynamic PET imaging, using three tracers that respectively portray the kinetics of glucose delivery, bi-directional trans-membrane glucose transport and glucose phosphorylation. The three tracers are: 1) \[15O\]-H2O for quantifying tissue perfusion, this portrays the kinetics of glucose delivery from plasma to tissue; 2) \[11C\]-3-O-methyl glucose, a tracer constrained to bi-directional trans-membrane glucose transport; and 3) \[18F\]-fluoro-deoxy glucose, which like \[11C\]-3-OMG is transported, but adds the subsequent metabolic step, that of glucose phosphorylation. We propose 2 specific aims to apply this methodology to investigate the pathogenesis of IR. The 1st aim is to quantitatively assess the kinetics of glucose delivery, transport and phosphorylation in skeletal muscle in type 2 DM and as compared to obese and lean non-diabetic men and women. We will appraise the contribution of each step to the to the pathogenesis of IR. We postulate more severe IR in oxidative muscle, with a dual impairment of glucose transport and phosphorylation. The 2nd aim is to implement the triple-tracer dynamic PET imaging protocol in adipose tissue (AT), examining normal insulin action in non-obese volunteers and testing whether differences in AT insulin action are present in obese insulin sensitive volunteers compared to obese IR participants and the relation of AT IR to that of muscle and liver.
NCT02655068
The null hypothesis is that patients screened by PET/CT will not have detection of disease recurrence any earlier than those screened by CT alone. The alternative hypothesis is that PET/CT surveillance will lead to detection of disease recurrence 3 months earlier than CT surveillance. Furthermore, to reject the null hypothesis, earlier detection must be associated with a cause-specific survival improvement of 10%. Primary endpoints will include time from the completion of definitive therapy to diagnosis of recurrent disease, and absolute survival within 3 years after completion of initial therapy. Duration of survival between diagnosis of recurrence and subsequent death will not be a primary endpoint because the investigators expect that PET/CT will offer an opportunity for earlier recognition of recurrence and be subject to lead-time bias. Duration of survival will be measured from completion of primary treatment until death. Note: the presence of residual disease at surgical consolidation does not constitute a recurrence event.