scholarly journals Early post-ischemic glucose metabolism is dependent on function of TLR2: a study using [18F]FDG PET-CT in a mouse model of cardiac arrest and cardiopulmonary resuscitation

2021 ◽  
Author(s):  
Rika Bajorat ◽  
Jens Kurth ◽  
Jan Stenzel ◽  
Brigitte Vollmar ◽  
Bernd J. Krause ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Glucose Metabolism ◽  
Cardiopulmonary Resuscitation ◽  
Mouse Model ◽  
Fdg Pet ◽  
Mouse Strains ◽  
Whole Brain ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Abstract Purpose: An ischemic brain injury caused by cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) affects cerebral function and presumably also brain glucose metabolism. The majority of patients who survive CA suffer from cognitive deficits and physical disabilities. Toll-like receptor 2 (TLR2) plays a cruical role in inflammatory response in ischemia and reperfusion (I/R). Since deficiency of TLR2 was associated with increased survival after CA-CPR, in this study glucose metabolism was measured using non-invasive [18F]FDG PET-CT imaging before and early after CA-CPR in a mouse model comparing wild type (WT) and TLR2-deficient (TLR2-/-) mice. Methods: Two PET-CT scans using [18F]FDG tracer were carried out to measure dynamic glucose metabolism before and early after CPR. To achieve this, anesthetized and ventilated adult female WT and TLR2-/- mice were scanned in PET-CT. After recovery from the baseline scan, the same animals underwent 10-minute CA followed by CPR and approximately 90 min after CA measurements of [18F]FDG uptake were started. The [18F]FDG standardized uptake values (SUVs) were calculated using PMOD-Software on fused FDG-PET-CT images with the included 3D Mirrione-Mouse-Brain-Atlas. Results: The absolute SUV of glucose in the whole brain of WT mice was increased after CA-CPR. In contrast, the absolute glucose SUV in the whole brain of TLR2-/- mice was not significantly different between basal and measurements after CA-CPR. In comparison, basal measurements of both mouse strains show a significant difference in the whole brain absolute glucose SUVs, whereby TLR2-/- mice revealed 34.6% higher values. The altered mouse strains presented a different pattern in glucose uptake under normal and ischemic conditions. Conclusion: There is evidence that the post-ischemic differences in glucose metabolism were associated with the function of TLR2 and that PET-CT imaging could be useful as an additional methodology in assessing diagnosis and prognosis during post-cardiac arrest care. Further studies are needed.

scholarly journals Early Post-ischemic Brain Glucose Metabolism Is Dependent on Function of TLR2: a Study Using [18F]F-FDG PET-CT in a Mouse Model of Cardiac Arrest and Cardiopulmonary Resuscitation

2021 ◽  
Author(s):  
Rika Bajorat ◽  
Jens Kurth ◽  
Jan Stenzel ◽  
Brigitte Vollmar ◽  
Bernd J. Krause ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Glucose Metabolism ◽  
Fdg Pet ◽  
Mouse Strains ◽  
Whole Brain ◽  
Ischemic Brain ◽  
Brain Glucose ◽  
Pet Ct ◽  
The Absolute ◽  
Fdg Pet Ct

Abstract Purpose The mammalian brain glucose metabolism is tightly and sensitively regulated. An ischemic brain injury caused by cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) affects cerebral function and presumably also glucose metabolism. The majority of patients who survive CA suffer from cognitive deficits and physical disabilities. Toll-like receptor 2 (TLR2) plays a crucial role in inflammatory response in ischemia and reperfusion (I/R). Since deficiency of TLR2 was associated with increased survival after CA-CPR, in this study, glucose metabolism was measured using non-invasive [18F]F-FDG PET-CT imaging before and early after CA-CPR in a mouse model comparing wild-type (WT) and TLR2-deficient (TLR2−/−) mice. The investigation will evaluate whether FDG-PET could be useful as an additional methodology in assessing prognosis. Procedures Two PET-CT scans using 2-deoxy-2-[18F]fluoro-D-glucose ([18F]F-FDG) tracer were carried out to measure dynamic glucose metabolism before and early after CPR. To achieve this, anesthetized and ventilated adult female WT and TLR2−/− mice were scanned in PET-CT. After recovery from the baseline scan, the same animals underwent 10-min KCL-induced CA followed by CPR. Approximately 90 min after CA, measurements of [18F]F-FDG uptake for 60 min were started. The [18F]F-FDG standardized uptake values (SUVs) were calculated using PMOD-Software on fused FDG-PET-CT images with the included 3D Mirrione-Mouse-Brain-Atlas. Results The absolute SUVmean of glucose in the whole brain of WT mice was increased about 25.6% after CA-CPR. In contrast, the absolute glucose SUV in the whole brain of TLR2−/− mice was not significantly different between baseline and measurements post CA-CPR. In comparison, baseline measurements of both mouse strains show a highly significant difference with regard to the absolute glucose SUV in the whole brain. Values of TLR2−/− mice revealed a 34.6% higher glucose uptake. Conclusions The altered mouse strains presented a different pattern in glucose uptake under normal and ischemic conditions, whereby the post-ischemic differences in glucose metabolism were associated with the function of key immune factor TLR2. There is evidence for using early FDG-PET-CT as an additional diagnostic tool after resuscitation. Further studies are needed to use PET-CT in predicting neurological outcomes.

Change in glucose metabolism measured by 18F-FDG PET/CT as a predictor of histopathologic response to neoadjuvant treatment in rectal cancer

2009 ◽  
Vol 36 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Luca Guerra ◽  
Rita Niespolo ◽  
Giuseppe Di Pisa ◽  
Davide Ippolito ◽  
Elena De Ponti ◽  
...  
Keyword(s):  
Rectal Cancer ◽  
Glucose Metabolism ◽  
Fdg Pet ◽  
Neoadjuvant Treatment ◽  
Histopathologic Response ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Effects on 18F-FDG PET/CT Brain Glucose Metabolism in Rectal Cancer Patients Undergoing Neoadjuvant Chemotherapy

2017 ◽  
Vol 42 (12) ◽  
pp. e484-e490 ◽  
Author(s):  
Alexei M. C. Machado ◽  
Theara C. Fagundes ◽  
Arnoldo Mafra ◽  
Rodrigo G. Silva ◽  
Ana Carolina G. Castro ◽  
...  
Keyword(s):  
Rectal Cancer ◽  
Glucose Metabolism ◽  
Neoadjuvant Chemotherapy ◽  
Cancer Patients ◽  
Fdg Pet ◽  
Brain Glucose ◽  
Pet Ct ◽  
18F Fdg ◽  
Ct Brain ◽  
Fdg Pet Ct

scholarly journals TKTL1 as a Prognostic Marker in Pancreatic Ductal Adenocarcinoma and Its Correlation with FDG-PET-CT

Oncology ◽  
2020 ◽  
pp. 1-9
Author(s):  
Kaisa Ahopelto ◽  
Kapo Saukkonen ◽  
Jaana Hagström ◽  
Saila Kauhanen ◽  
Hanna Seppänen ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cancer Cells ◽  
Fdg Pet ◽  
Stage Iv ◽  
University Hospital ◽  
Ductal Adenocarcinoma ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

<b><i>Introduction:</i></b> Glucose metabolism in cancer cells differs from noncancerous cells. The expression of transketolase-like protein 1 (TKTL1), a key enzyme in the glucose metabolism of cancer cells, predicts poor prognosis in several cancer types. We studied TKTL1 as a prognostic tool and whether TKTL1 expression correlates with 18F-FDG-PET-CT among patients with pancreatic ductal adenocarcinoma (PDAC). <b><i>Methods:</i></b> This retrospective study examined two PDAC patient cohorts: 168 patients operated on at Helsinki University Hospital between 2001 and 2011, and 20 patients with FDG-PET-CT results available from the Auria Biobank. We used immunohistochemistry for TKTL1 expression, combining results with clinicopathological data. <b><i>Results:</i></b> Five-year disease-specific survival (DSS) was slightly but not significantly better in patients with a high versus low TKTL1 expression, with DSS of 28.0 versus 17.3%, respectively (<i>p</i> = 0.123). TKTL1 served as a marker of a better prognosis in patients over 65 years old (<i>p</i> = 0.012) and among those with TNM class M1 (<i>p</i> = 0.018), stage IV disease (<i>p</i> = 0.027), or perivascular invasion (<i>p</i> = 0.008). <b><i>Conclusions:</i></b> Our study shows that TKTL1 cannot be used as a prognostic factor in PDAC with the exception of elderly patients and those with advanced disease. The correlation of TKTL1 with 18F-FDG-PET-CT requires further study in a larger patient cohort.

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