scholarly journals Neuroimaging Biomarkers of Experimental Epileptogenesis and Refractory Epilepsy

2019 ◽  
Vol 20 (1) ◽  
pp. 220 ◽  
Author(s):  
Sandesh Reddy ◽  
Iyan Younus ◽  
Vidya Sridhar ◽  
Doodipala Reddy
Keyword(s):  
Animal Models ◽  
Refractory Epilepsy ◽  
Single Photon ◽  
Neuronal Damage ◽  
Photon Emission ◽  
Brain Magnetic Resonance Imaging ◽  
Functional Changes ◽  
Neuroimaging Biomarkers ◽  
The Brain

This article provides an overview of neuroimaging biomarkers in experimental epileptogenesis and refractory epilepsy. Neuroimaging represents a gold standard and clinically translatable technique to identify neuropathological changes in epileptogenesis and longitudinally monitor its progression after a precipitating injury. Neuroimaging studies, along with molecular studies from animal models, have greatly improved our understanding of the neuropathology of epilepsy, such as the hallmark hippocampus sclerosis. Animal models are effective for differentiating the different stages of epileptogenesis. Neuroimaging in experimental epilepsy provides unique information about anatomic, functional, and metabolic alterations linked to epileptogenesis. Recently, several in vivo biomarkers for epileptogenesis have been investigated for characterizing neuronal loss, inflammation, blood-brain barrier alterations, changes in neurotransmitter density, neurovascular coupling, cerebral blood flow and volume, network connectivity, and metabolic activity in the brain. Magnetic resonance imaging (MRI) is a sensitive method for detecting structural and functional changes in the brain, especially to identify region-specific neuronal damage patterns in epilepsy. Positron emission tomography (PET) and single-photon emission computerized tomography are helpful to elucidate key functional alterations, especially in areas of brain metabolism and molecular patterns, and can help monitor pathology of epileptic disorders. Multimodal procedures such as PET-MRI integrated systems are desired for refractory epilepsy. Validated biomarkers are warranted for early identification of people at risk for epilepsy and monitoring of the progression of medical interventions.

In vivo neuropharmacology of schizophrenia

1999 ◽  
Vol 174 (S38) ◽  
pp. 23-33 ◽  
Author(s):  
V. Bigliani ◽  
L. S. Pilowsky
Keyword(s):  
Single Photon ◽  
Photon Emission ◽  
Emission Tomography ◽  
Binding Assays ◽  
Single Photon Emission ◽  
Positron Emission ◽  
The Brain ◽  
Major Target

Since the introduction of chlorpromazine in the 1950s, followed by the discovery (with in vitro receptor binding assays), in the mid-1970s, that antipsychotic drugs block a subtype of dopamine receptor (D2/D2-like) (Creese et al, 1976) and that affinity for these receptors appears to correlate directly with clinical potency for antipsychotics (Peroutka & Synder, 1980), the study of neurotransmitters and receptors has been a major target of schizophrenia research (Owens, 1996). In 1983, the first visualisation, by positron emission tomography (PET), of the binding of D2 dopamine receptors in the brain of a living human subject was reported (Wagner et al, 1983). Following this, the number of research studies using PET and single photon emission tomography (SPET) has increased enormously.

scholarly journals Biodistribution and Acute Toxicity of Intravenous Multifunctional 125I-Radiolabeled Fe3O4-Ag Heterodimer Nanoparticles in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-6
Author(s):  
Bin Zhang ◽  
Jing Zhu ◽  
Hongwei Gu ◽  
Shengming Deng
Keyword(s):  
Acute Toxicity ◽  
Single Photon ◽  
Photon Emission ◽  
Serum Biochemistry ◽  
Imaging Agents ◽  
Control Groups ◽  
Dual Modality ◽  
Functional Changes ◽  
Dual Modality Imaging

Fe3O4-Ag125I heterostructured radionuclide nanoparticles (NPs) have been developed as a novel type of dual-modality imaging agents for single-photon emission computerized tomography (SPECT) and magnetic resonance imaging (MRI). However, the biodistribution and toxicity of Fe3O4-Ag125I NPs remain largely unknown. Therefore, we investigated the biodistribution and biological action of Fe3O4-Ag125I NPs in mice by acute toxicity experiments (exposures over 7 days). The bioaccumulation of Fe3O4-Ag125I NPs was studied via in vivo experiments. The serum biochemistry and hematology were analyzed to reveal potential functional changes. The histopathological changes were observed by using an electron microscope. Biodistribution analysis revealed that Fe3O4-Ag125I NPs were mainly accumulated in the liver and spleen. The activities of liver enzymes (ALT and AST) were increased in Fe3O4-Ag125I NP-challenged groups compared with the control groups. Collectively, liver and spleen were the major target organs for accumulation of Fe3O4-Ag125I NPs. Damage of liver tissue was observed in the Fe3O4-Ag125I NP-challenged groups compared with the control groups. Further studies on surface coating of Fe3O4-Ag with targeted materials are highly necessary for safe medical applications of Fe3O4-AgNPs as dual-modality imaging agents.

scholarly journals Brain Imaging of Nicotinic Receptors in Alzheimer's Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Jin Wu ◽  
Masatomo Ishikawa ◽  
Jichun Zhang ◽  
Kenji Hashimoto
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Single Photon ◽  
Photon Emission ◽  
Emission Computed Tomography ◽  
The Brain

Neuronal nicotinic acetylcholine receptors (nAChRs) are a family of ligand-gated ion channels which are widely distributed in the human brain. Several lines of evidence suggest that two major subtypes (α4β2 and α7) of nAChRs play an important role in the pathophysiology of Alzheimer's disease (AD). Postmortem studies demonstrated alterations in the density of these subtypes of nAChRs in the brain of patients with AD. Currently, nAChRs are one of the most attractive therapeutic targets for AD. Therefore, several researchers have made an effort to develop novel radioligands that can be used to study quantitatively the distribution of these two subtypes in the human brain with positron emission tomography (PET) and single-photon emission computed tomography (SPECT). In this paper, we discuss the current topics onin vivoimaging of two subtypes of nAChRs in the brain of patients with AD.

Correlation between in vitro and in vivo Data of Radiolabeled Peptide for Tumor Targeting

2019 ◽  
Vol 19 (12) ◽  
pp. 950-960
Author(s):  
Soghra Farzipour ◽  
Seyed Jalal Hosseinimehr
Keyword(s):  
Tumor Targeting ◽  
Single Photon ◽  
Specific Binding ◽  
Specific Interaction ◽  
Photon Emission ◽  
Emission Computed Tomography ◽  
Mixed Effect ◽  
Radiolabeled Peptides

Tumor-targeting peptides have been generally developed for the overexpression of tumor specific receptors in cancer cells. The use of specific radiolabeled peptide allows tumor visualization by single photon emission computed tomography (SPECT) and positron emission tomography (PET) tools. The high affinity and specific binding of radiolabeled peptide are focusing on tumoral receptors. The character of the peptide itself, in particular, its complex molecular structure and behaviors influence on its specific interaction with receptors which are overexpressed in tumor. This review summarizes various strategies which are applied for the expansion of radiolabeled peptides for tumor targeting based on in vitro and in vivo specific tumor data and then their data were compared to find any correlation between these experiments. With a careful look at previous studies, it can be found that in vitro unblock-block ratio was unable to correlate the tumor to muscle ratio and the success of radiolabeled peptide for in vivo tumor targeting. The introduction of modifiers’ approaches, nature of peptides, and type of chelators and co-ligands have mixed effect on the in vitro and in vivo specificity of radiolabeled peptides.

scholarly journals Dopamine D2/3 Receptor Availabilities and Evoked Dopamine Release in Striatum Differentially Predict Impulsivity and Novelty Preference in Roman High- and Low-Avoidance Rats

2020 ◽  
Author(s):  
Lidia Bellés ◽  
Andrea Dimiziani ◽  
Stergios Tsartsalis ◽  
Philippe Millet ◽  
François R Herrmann ◽  
...  
Keyword(s):  
Ventral Striatum ◽  
Single Photon ◽  
Ex Vivo ◽  
Photon Emission ◽  
Dorsal Striatum ◽  
Reaction Time Task ◽  
Emission Computed Tomography ◽  
Novelty Preference ◽  
Da Release

Abstract Background Impulsivity and novelty preference are both associated with an increased propensity to develop addiction-like behaviors, but their relationship and respective underlying dopamine (DA) underpinnings are not fully elucidated. Methods We evaluated a large cohort (n = 49) of Roman high- and low-avoidance rats using single photon emission computed tomography to concurrently measure in vivo striatal D2/3 receptor (D2/3R) availability and amphetamine (AMPH)-induced DA release in relation to impulsivity and novelty preference using a within-subject design. To further examine the DA-dependent processes related to these traits, midbrain D2/3-autoreceptor levels were measured using ex vivo autoradiography in the same animals. Results We replicated a robust inverse relationship between impulsivity, as measured with the 5-choice serial reaction time task, and D2/3R availability in ventral striatum and extended this relationship to D2/3R levels measured in dorsal striatum. Novelty preference was positively related to impulsivity and showed inverse associations with D2/3R availability in dorsal striatum and ventral striatum. A high magnitude of AMPH-induced DA release in striatum predicted both impulsivity and novelty preference, perhaps owing to the diminished midbrain D2/3-autoreceptor availability measured in high-impulsive/novelty-preferring Roman high-avoidance animals that may amplify AMPH effect on DA transmission. Mediation analyses revealed that while D2/3R availability and AMPH-induced DA release in striatum are both significant predictors of impulsivity, the effect of striatal D2/3R availability on novelty preference is fully mediated by evoked striatal DA release. Conclusions Impulsivity and novelty preference are related but mediated by overlapping, yet dissociable, DA-dependent mechanisms in striatum that may interact to promote the emergence of an addiction-prone phenotype.

scholarly journals Degradation of Drug Delivery Nanocarriers and Payload Release: A Review of Physical Methods for Tracing Nanocarrier Biological Fate

Pharmaceutics ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 770
Author(s):  
Patrick M. Perrigue ◽  
Richard A. Murray ◽  
Angelika Mielcarek ◽  
Agata Henschke ◽  
Sergio E. Moya
Keyword(s):  
Drug Delivery ◽  
Laser Scanning ◽  
Single Photon ◽  
Photon Emission ◽  
Correlation Spectroscopy ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Emission Computed Tomography ◽  
Systemic Delivery

Nanoformulations offer multiple advantages over conventional drug delivery, enhancing solubility, biocompatibility, and bioavailability of drugs. Nanocarriers can be engineered with targeting ligands for reaching specific tissue or cells, thus reducing the side effects of payloads. Following systemic delivery, nanocarriers must deliver encapsulated drugs, usually through nanocarrier degradation. A premature degradation, or the loss of the nanocarrier coating, may prevent the drug’s delivery to the targeted tissue. Despite their importance, stability and degradation of nanocarriers in biological environments are largely not studied in the literature. Here we review techniques for tracing the fate of nanocarriers, focusing on nanocarrier degradation and drug release both intracellularly and in vivo. Intracellularly, we will discuss different fluorescence techniques: confocal laser scanning microscopy, fluorescence correlation spectroscopy, lifetime imaging, flow cytometry, etc. We also consider confocal Raman microscopy as a label-free technique to trace colocalization of nanocarriers and drugs. In vivo we will consider fluorescence and nuclear imaging for tracing nanocarriers. Positron emission tomography and single-photon emission computed tomography are used for a quantitative assessment of nanocarrier and payload biodistribution. Strategies for dual radiolabelling of the nanocarriers and the payload for tracing carrier degradation, as well as the efficacy of the payload delivery in vivo, are also discussed.

scholarly journals Magnetic Resonace–Based Attenuation Correction for Micro–Single-Photon Emission Computed Tomography

2012 ◽  
Vol 11 (2) ◽  
pp. 7290.2011.00036 ◽  
Author(s):  
Vincent Keereman ◽  
Yves Fierens ◽  
Christian Vanhove ◽  
Tony Lahoutte ◽  
Stefaan Vandenberghe
Keyword(s):  
Attenuation Correction ◽  
Single Photon ◽  
Photon Emission ◽  
The Body ◽  
Emission Computed Tomography ◽  
Micro Ct ◽  
Mr Images ◽  
Brain Scans ◽  
The Brain ◽  
Photon Emission Computed Tomography

Attenuation correction is necessary for quantification in micro–single-photon emission computed tomography (micro-SPECT). In general, this is done based on micro–computed tomographic (micro-CT) images. Derivation of the attenuation map from magnetic resonance (MR) images is difficult because bone and lung are invisible in conventional MR images and hence indistinguishable from air. An ultrashort echo time (UTE) sequence yields signal in bone and lungs. Micro-SPECT, micro-CT, and MR images of 18 rats were acquired. Different tracers were used: hexamethylpropyleneamine oxime (brain), dimercaptosuccinic acid (kidney), colloids (liver and spleen), and macroaggregated albumin (lung). The micro-SPECT images were reconstructed without attenuation correction, with micro-CT-based attenuation maps, and with three MR-based attenuation maps: uniform, non-UTE-MR based (air, soft tissue), and UTE-MR based (air, lung, soft tissue, bone). The average difference with the micro-CT-based reconstruction was calculated. The UTE-MR-based attenuation correction performed best, with average errors ≤ 8% in the brain scans and ≤ 3% in the body scans. It yields nonsignificant differences for the body scans. The uniform map yields errors of ≤ 6% in the body scans. No attenuation correction yields errors ≥ 15% in the brain scans and ≥ 25% in the body scans. Attenuation correction should always be performed for quantification. The feasibility of MR-based attenuation correction was shown. When accurate quantification is necessary, a UTE-MR-based attenuation correction should be used.

scholarly journals Frontal Hypoperfusion and the Effectiveness of Perampanel in Long-Lived Patient with Lafora Disease

2021 ◽  
pp. 211-217
Author(s):  
Koji Obara ◽  
Erika Abe ◽  
Itaru Toyoshima
Keyword(s):  
Single Photon ◽  
Early Stage ◽  
Photon Emission ◽  
Cerebellar Atrophy ◽  
Brain Magnetic Resonance Imaging ◽  
Emission Computed Tomography ◽  
Homozygous Mutation ◽  
Lafora Disease ◽  
Mental Deterioration ◽  
Exon 1

We report a long-lived patient with Lafora disease (LD). A 34-year-old woman experienced onset of seizures at the age of 11 years. She was bedridden in her early twenties due to frequent generalized tonic-clonic seizures, myoclonus, and progressive mental deterioration. Her seizures occurred all the time despite administration of multiple anticonvulsants at high doses. At the age of 31, she started perampanel, which resulted in reduction of anticonvulsants after her visible myoclonus and convulsions disappeared. Brain magnetic resonance imaging showed marked cerebral and cerebellar atrophy, and single-photon emission computed tomography using N-isopropyl-p-[123I] iodoamphetamine (IMP-SPECT) revealed significant hypoperfusion of the frontal lobe and cerebellum. We identified a W219R homozygous mutation in exon 1 of the NHLRC1 gene. Because perampanel may not only control seizures but also prevent mental deterioration in LD, we propose that perampanel should be administered from the early stage of LD.

Single Photon Emission Computed Tomography of the Brain in Patients with Chemical Sensitivities

1994 ◽  
Vol 10 (4-5) ◽  
pp. 573-577
Author(s):  
Theodore R. Simon ◽  
David C. Hickey ◽  
Cynthia E. Fincher ◽  
Alfred R. Johnson ◽  
Gerald H. Ross ◽  
...  
Keyword(s):  
Psychological Symptoms ◽  
Single Photon ◽  
Single Case ◽  
Photon Emission ◽  
Clinical Syndrome ◽  
Emission Computed Tomography ◽  
Desert Storm ◽  
Petroleum Distillates ◽  
Other Substances ◽  
The Brain

Chemical sensitivities display a recurrent pattern on scintigraphic examinations of the brain. The pattern can include mismatching between early and late imaging, multiple hot and cold foci distributed throughout the cortex without regard to lobar distribution (salt and pepper pattern), temporal asymmetries, and sometimes increased activity in the basal ganglia. This study used Desert Shield/Desert Storm veterans who present with abnormal neurological and psychological symptoms as a model to exhibit abnormalities by brain scintigraphy. These are typical of those seen in patients with documented exposure to neurotoxic compounds who develop a clinical syndrome that has been termed chemical sensitivity. Exposure to cocaine, alcohol, and other substances of abuse can result in abnormal scintigrams of the brain using tracers such as [technetium 99m]hexamethylpropyleneoxime. This study used techniques combining regional cerebral blood flow data with delayed distributional data after the intracellular conversion of the tracer into a hydrophilic molecule. In addition to delayed image abnormalities, a mismatch occurs in the regional activity between the two image sets of the veterans. This degree of mismatch was not seen in control subjects who were screened for avoidance of neurotoxic agents. Patterns identified from examinations performed on patients with known exposure to petroleum distillates, pesticides and other materials linked with neurotoxicity were identified in some veterans of the Desert Shield/Desert Storm operation. A single case of repeated examinations on a veteran showed a reversion of these patterns toward normal after therapy. This reversion followed independent assessments of clinical improvement.

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