scholarly journals Feasibility of TSPO-Specific Positron Emission Tomography Radiotracer for Evaluating Paracetamol-Induced Liver Injury

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1661
Author(s):  
Daehee Kim ◽  
Byung Seok Moon ◽  
Sun Mi Park ◽  
Sang Ju Lee ◽  
Seo Young Kang ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Liver Injury ◽  
Rat Model ◽  
Early Phase ◽  
Hepatic Uptake ◽  
Emission Tomography ◽  
Expression Level ◽  
Control Group ◽  
Positron Emission ◽  
Tspo Expression

Macrophages are activated during the early phase of paracetamol-induced liver injury (PLI). [18F]GE180 is a radiolabeled ligand that recognizes the macrophage translocator protein (TSPO). In this study, we evaluated the feasibility of a TSPO-specific radiotracer in a rat model of PLI. A rat model of liver injury was induced by intraperitoneal administration of paracetamol. [18F]GE180 positron emission tomography (PET) images were obtained after 24 h. The maximal and mean standardized uptake values (SUVmax and SUVav) of the liver and serum biomarker levels were examined. The TSPO expression level was examined using real-time polymerase chain reaction and Western blot analysis. [18F]GE180 hepatic uptake in the PLI group was significantly higher than that in the control group (SUVmax p = 0.001; SUVav p = 0.005). Both mRNA and protein TSPO expression levels were higher in the PLI group. The mRNA expression level of TSPO was significantly correlated with [18F]GE180 hepatic uptake in both groups (SUVmax p = 0.019; SUVav p = 0.007). [18F]GE180 hepatic uptake in the PLI group showed a significant positive correlation with ALT24 and ALT48 (ALT24 p = 0.016; ALT48 p = 0.002). [18F]GE180 enabled visualization of PLI through TSPO overexpression. Our results support the potential utility of hepatic uptake by TSPO-PET as a non-invasive imaging biomarker for the early phase of PLI.

scholarly journals Apoptotic PET Imaging of Rat Pulmonary Fibrosis With [18F]ML-8

2018 ◽  
Vol 17 ◽  
pp. 153601211879572 ◽  
Author(s):  
Ying Xiong ◽  
Dahong Nie ◽  
Shaoyu Liu ◽  
Hui Ma ◽  
Shu Su ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Pulmonary Fibrosis ◽  
Malonic Acid ◽  
Pet Imaging ◽  
Rat Model ◽  
Emission Tomography ◽  
Pathological Examination ◽  
Control Group ◽  
Positron Emission ◽  
Pet Ct

Objective: To investigate the value of 2-(3-[18F]fluoropropyl)-2-methyl-malonic acid ([18F]ML-8) positron emission tomography (PET) imaging of rat pulmonary fibrosis. Methods: Male Sprague-Dawley rats were divided into 2 groups, including pulmonary fibrosis model group and control group. The rat model was established by an intratracheal instillation of bleomycin (BLM). Control rats were treated with saline. Positron emission tomography/computed tomography (CT) with [18F]ML-8 or 18F-fluorodeoxyglucose ([18F]FDG) was performed on 2 groups. After PET/CT imaging, lung tissues were collected for histologic examination. Data were analyzed and comparisons between 2 groups were performed using Student t test. Results: Bleomycin-treated rats showed a higher lung uptake of [18F]ML-8 than control rats ( P < .05). In BLM-treated rats, the lung to muscle relative uptake ratio of [18F]ML-8 was also higher than that of [18F]FDG ( P < .05). Pathological examination showed overproliferation of fibroblasts and deposition of collagen in lungs from BLM-treated rats. Compared to control rats, BLM-treated rats had higher lung hydroxyproline content ( P < .05). Immunofluorescence staining indicated more apoptotic cells in BLM-treated rats than those in control rats. Moreover, the apoptosis rate of lung tissues obtained from BLM-treated rats was higher than that from control rats ( P < .05). Conclusions: 2-(3-[18F]fluoropropyl)-2-methyl-malonic acid PET/CT could be used for noninvasive diagnosis of pulmonary fibrosis in a rat model.

scholarly journals Positron emission tomography of cerebral angiogenesis and TSPO expression in a mouse model of chronic hypoxia

2017 ◽  
Vol 38 (4) ◽  
pp. 687-696 ◽  
Author(s):  
Iwao Kanno ◽  
Chie Seki ◽  
Hiroyuki Takuwa ◽  
Zhao-Hui Jin ◽  
Didier Boturyn ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Pet Imaging ◽  
Vascular Remodeling ◽  
Early Phase ◽  
Transient Increase ◽  
Emission Tomography ◽  
Vascular Density ◽  
Positron Emission ◽  
Imaging Results ◽  
Tspo Expression

The present study aimed to examine whether positron emission tomography (PET) could evaluate cerebral angiogenesis. Mice were housed in a hypoxic chamber with 8–9% oxygen for 4, 7, and 14 days, and the angiogenic responses were evaluated with a radiotracer, 64Cu-cyclam-RAFT-c(-RGDfK-)4, which targeted αVβ3 integrin and was imaged with PET. The PET imaging results showed little uptake during all of the hypoxic periods. Immunofluorescence staining of the β3 integrin, CD61, revealed weak expression, while the microvessel density assessed by CD31 staining increased with the hypoxic duration. These observations suggest that the increased vascular density originated from other types of vascular remodeling, unlike angiogenic sprouting. We then searched for any signs of vascular remodeling that could be detected using PET. PET imaging of 11C-PK11195, a marker of the 18-kDa translocator protein (TSPO), revealed a transient increase at day 4 of hypoxia. Because the immunofluorescence of glial markers showed unchanged staining over the early phase of hypoxia, the observed upregulation of TSPO expression probably originated from non-glial cells (e.g. vascular cells). In conclusion, a transient increase in TSPO probe uptake was detected with PET at only the early phase of hypoxia, which indicates an early sign of vascular remodeling induced by hypoxia.

scholarly journals A positron emission tomography study of cerebrovascular reserve before and after shunt surgery in patients with idiopathic chronic hydrocephalus

2000 ◽  
Vol 8 (2) ◽  
pp. 1-5 ◽  
Author(s):  
Petra M. Klinge ◽  
Georg Berding ◽  
Thomas Brinker ◽  
Wolfram H. Knapp ◽  
Madjid Samii
Keyword(s):  
Positron Emission Tomography ◽  
Clinical Outcome ◽  
Emission Tomography ◽  
Control Group ◽  
Chronic Hydrocephalus ◽  
Cerebrovascular Reserve ◽  
Shunt Placement ◽  
Positron Emission ◽  
Group A ◽  
Group B

Object In this study the authors use positron emission tomography (PET) to investigate cerebral blood flow (CBF) and cerebrovascular reserve (CVR) in chronic hydrocephalus. Methods Ten patients whose mean age was 67 ± 10 years (mean ± standard deviation [SD]) were compared with 10 healthy volunteers who were 25 ±3 years of age. Global CBF and CVR were determined using 15O–H2O and PET prior to shunt placement and 7 days and 7 months thereafter. The CVR was measured using 1 g acetazolamide. Neurological status was assessed based on a score assigned according to the methods of Stein and Langfitt. Seven months after shunt placement, five patients showed clinical improvement (Group A) and five did not (Group B). The average global CBF before shunt deployment was significantly reduced in comparison with the control group (40 ± 8 compared with 61 ± 7 ml/100 ml/minute; mean ± SD, p < 0.01). In Group A the CBF values were significantly lower than in Group B (36 ± 7 compared with 44 ± 8 ml/100 ml/minute; p < 0.05). The CVR before surgery, however, was not significantly different between groups (Group A = 43 ± 21%, Group B = 37 ± 29%). After shunt placement, there was an increase in the CVR in Group A to 52 ± 37% after 7 days and to 68 ± 47% after 7 months (p < 0.05), whereas in Group B the CVR decreased to 14 ± 18% (p < 0.05) after 7 days and returned to the preoperative level (39 ± 6%) 7 months after shunt placement. Conclusions The preliminary results indicate that a reduced baseline CBF before surgery does not indicate a poor prognosis. Baseline CBF before shunt placement and preoperative CVR are not predictive of clinical outcome. A decrease in the CVR early after shunt placement, however, is related to poor late clinical outcome, whereas early improvement in the CVR after shunt placement indicates a good prognosis.

scholarly journals [18F]FHPG Positron Emission Tomography for Detection of Herpes Simplex Virus (HSV) in Experimental HSV Encephalitis

2005 ◽  
Vol 79 (12) ◽  
pp. 7721-7727 ◽  
Author(s):  
A. R. Buursma ◽  
E. F. J. de Vries ◽  
J. Garssen ◽  
D. Kegler ◽  
A. van Waarde ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Infected Group ◽  
Emission Tomography ◽  
Saline Control ◽  
Control Group ◽  
Positron Emission ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT Herpes simplex virus type 1 (HSV-1) is one of the most common causes of sporadic encephalitis. The initial clinical course of HSV encephalitis (HSE) is highly variable, and the infection may be rapidly fatal. For effective treatment with antiviral medication, an early diagnosis of HSE is crucial. Subtle brain infections with HSV may be causally related to neuropsychiatric disorders such as Alzheimer's dementia. We investigated the feasibility of a noninvasive positron emission tomography (PET) imaging technique using [18F]FHPG as a tracer for the detection of HSE. For this purpose, rats received HSV-1 (infected group) or phosphate-buffered saline (control group) by intranasal application, and dynamic PET scans were acquired. In addition, the distribution of tracer accumulation in specific brain areas was studied with phosphor storage imaging. The PET images revealed that the overall brain uptake of [18F]FHPG was significantly higher for the infected group than for control animals. Phosphor storage images showed an enhanced accumulation of [18F]FHPG in regions known to be affected after intranasal infection with HSV. High-performance liquid chromatography metabolite analysis showed phosphorylated metabolites of [18F]FHPG in infected brains, proving that the increased [18F]FHPG uptake in infected brains was due to HSV thymidine kinase-mediated trapping. Freeze lesion experiments showed that damage to the blood-brain barrier could in principle induce elevated [18F]FHPG uptake, but this nonspecific tracer uptake could easily be discriminated from HSE-derived uptake by differences in the tracer kinetics. Our results show that [18F]FHPG PET is a promising tool for the detection of HSV encephalitis.

scholarly journals From positron emission tomography to cell analysis of the 18-kDa Translocator Protein in mild traumatic brain injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Clément Delage ◽  
Nicolas Vignal ◽  
Coralie Guerin ◽  
Toufik Taib ◽  
Clément Barboteau ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Flow Cytometry ◽  
Microglial Activation ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Flow Cytometry Analysis ◽  
Positron Emission ◽  
The Brain ◽  
Tspo Expression

AbstractTraumatic brain injury (TBI) leads to a deleterious neuroinflammation, originating from microglial activation. Monitoring microglial activation is an indispensable step to develop therapeutic strategies for TBI. In this study, we evaluated the use of the 18-kDa translocator protein (TSPO) in positron emission tomography (PET) and cellular analysis to monitor microglial activation in a mild TBI mouse model. TBI was induced on male Swiss mice. PET imaging analysis with [18F]FEPPA, a TSPO radiotracer, was performed at 1, 3 and 7 days post-TBI and flow cytometry analysis on brain at 1 and 3 days post-TBI. PET analysis showed no difference in TSPO expression between non-operated, sham-operated and TBI mice. Flow cytometry analysis demonstrated an increase in TSPO expression in ipsilateral brain 3 days post-TBI, especially in microglia, macrophages, lymphocytes and neutrophils. Moreover, microglia represent only 58.3% of TSPO+ cells in the brain. Our results raise the question of the use of TSPO radiotracer to monitor microglial activation after TBI. More broadly, flow cytometry results point the lack of specificity of TSPO for microglia and imply that microglia contribute to the overall increase in TSPO in the brain after TBI, but is not its only contributor.

scholarly journals A 18F-fluorodeoxyglucose MicroPET Imaging Study to Assess Changes in Brain Glucose Metabolism in a Rat Model of Surgery-induced Latent Pain Sensitization

2011 ◽  
Vol 115 (5) ◽  
pp. 1072-1083 ◽  
Author(s):  
Asunción Romero ◽  
Santiago Rojas ◽  
David Cabañero ◽  
Juan D. Gispert ◽  
José R. Herance ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Rat Model ◽  
Brain Metabolism ◽  
Statistical Parametric Mapping ◽  
Imaging Study ◽  
Emission Tomography ◽  
Posterior Cortex ◽  
Fdg Uptake ◽  
Positron Emission ◽  
Pain Sensitization

Background Neuroplastic changes involved in latent pain sensitization after surgery are poorly defined. We assessed temporal changes in glucose brain metabolism in a postoperative rat model using positron emission tomography. We also investigated brain metabolism after naloxone administration. Methods Rats were given remifentanil anesthetic and underwent a plantar incision, with 1 mg/kg of (-)-naloxone subcutaneously administered on postoperative days 20 and 21. Using the von Frey test, mechanical thresholds were measured pre- and postoperatively at different time points in awake animals during F-fluorodeoxyglucose (F-FDG) uptake. Brain images were also obtained the day before mechanical testing, using a positron emission tomography R4 scanner (Concorde Microsystems, Siemens, Knoxville, TN). Differences in brain activity were assessed utilizing a statistical parametric mapping. Results Surgery induced minor changes in F-FDG uptake in the cerebellum, hippocampus, and posterior cortex, which extended to the thalamus, hypothalamus, and brainstem on days 6 and 7. Changes were still present on day 21. Maximal postoperative hypersensitivity was observed on day 2. The administration of (-)-naloxone on day 21 induced significant hypersensitivity, greatly enhancing the effect on F-FDG uptake. In sham-operated rats, naloxone induced changes limited to the striatum and the cerebellum. Nonnociceptive stimulation with von Frey filaments had no effect on F-FDG uptake. Conclusions Surgery, remifentanil, and their combination induced long-lasting and significant metabolic changes in the pain brain matrix, with a positive correlation with hypersensitivity after naloxone. Changes in brain F-FDG precipitated by naloxone suggest that surgery under remifentanil anesthetic induces the greatest neuroplastic brain adaptations in opioid-related pathways involved in nociceptive processing and long-lasting pain sensitization.

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