First record of Neodryinus typhlocybae in Hungary (Hymenoptera: Dryinidae)

Neodryinus typhlocybae (Ashmead, 1893), a Nearctic dryinid wasp species introduced to Europe as a natural enemy of Metcalfa pruinosa (Say, 1830), is first reported here from Hungary. With 3 figures

Early phenomena following cryogenic lesion of rat brain : a preliminary study

The cerebrovascular laminin becomes detectable following lesions, whereas the lamina basalis-receptor β-dystroglycan disappears. These alterations may be indirect markers of a glio-vascular detachment which may result in the impairment of blood-brain-barrier. The present study estimates the correlations between the post-lesion exudation and the aforementioned phenomena. Lesions were performed in ketamine-xylazine anaesthesia with a copper rod cooled with dry ice. Immediately, or in 5 or 10 min brains were fixed in buffered 4% paraformaldehyde. Immunohistochemical reactions were performed in floating sections. Exudation was estimated with immunohistochemical detection of plasma-fibronectin and immunoglobulins. Glio-vascular connections were investigated with immunohistochemistry (GFAP, S100, glutamine synthetase), and electron microscopy. Laminin immunoreactivity appeared already at immediate fixation. Exudate was found only around the vessels. β-dystroglycan was still detectable. At five-ten minutes the territory of exudate became confluent and dystroglycan disappeared. Some but not all vessels were free of astrocytes. Electron microscopy demonstrated wide perivascular ’spaces’. ’In vivo’ monitoring was attempted with a multiphoton microscope in the Department of Biophysics of Semmelweis University. Astrocytes were labeled supravitally with sulforhodamine 101 so glio-vascular connections were visible. However, neither in the intact brain nor in 30-min post-lesion period astrocyte motility was observed

A kognitív funkciók változásai cukorbetegségben = Changes in Cognitive Function in Patients with Diabetes Mellitus

Patients with diabetes are approximately 1.5 times more likely to experience cognitive decline than individuals without diabetes mellitus. Most of the data suggest that patients with diabetes have reduced performance in numerous domains of cognitive function. In patients with type 1 diabetes, specific and global deficits involving speed of psychomotor efficiency, information processing, mental flexibility, attention, and visual perception seem to be present, while in patients with type 2 diabetes an increase in memory deficits, a reduction in psychomotor speed, and reduced frontal lobe (executive) functions have been found. The complex pathophysiology of changes in the central nervous system in diabetes has not yet been fully elucidated. It is important to consider the patient’s age at the onset of diabetes, the glycemic control status, and the presence of diabetic complications. Neurological consequences of diabetes appear parallel to those observed in the aging brain. Neuroimaging studies highlight several structural cerebral changes, cortical and subcortical atrophy, beside increased leukoaraiosis that occurs in association with diabetes. There is supporting evidence from many hypotheses to explain the pathophysiology of cognitive decline associated with diabetes. The main hypotheses pointing to the potential, implied mechanisms involve hyperglycemia, hypoglycemia, microvascular disease, insulin resistance, hyperinsulinism, hyperphosphorylation of tau protein, and amyloid-β deposition. Orv. Hetil., 2012, 153, 323–329.</jats:p

Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions

Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive. Here, we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. Microglia establish direct, dynamic purinergic contacts with cells in the neurovascular unit that shape CBF in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in mice, which is reiterated by chemogenetically induced microglial dysfunction associated with impaired ATP sensitivity. Hypercapnia induces rapid microglial calcium changes, P2Y12R-mediated formation of perivascular phylopodia, and microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Microglial actions modulate vascular cyclic GMP levels but are partially independent of nitric oxide. Finally, microglial dysfunction markedly impairs P2Y12R-mediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases

Thallium Labeled Citrate-Coated Prussian Blue Nanoparticles as Potential Imaging Agent

Background. The aim of this study was to develop and characterize a nanoparticle-based image-contrast platform which is biocompatible, chemically stable, and accessible for radiolabeling with 201Tl. We explored whether this nanoparticle enhanced the T1 signal which might make it an MRI contrast agent as well. Methods. The physical properties of citrate-coated Prussian blue nanoparticles (PBNPs) (iron(II);iron(III);octadecacyanide) doped with 201Tl isotope were characterized with atomic force microscopy, dynamic light scattering, and zeta potential measurement. PBNP biodistribution was determined by using SPECT and MRI following intravenous administration into C57BL6 mice. Activity concentrations (MBq/cm3) were calculated from the SPECT scans for each dedicated volume of interest (VOI) of liver, kidneys, salivary glands, heart, lungs, and brain. Results. PBNP accumulation peaked at 2 hours after injection predominantly in the kidneys and the liver followed by a gradual decrease in activity in later time points. Conclusion. We synthetized, characterized, and radiolabeled a Prussian blue-based nanoparticle platform for contrast material applications. Its in vivo radiochemical stability and biodistribution open up the way for further diagnostic applications

Evaluation of Brain Nuclear Medicine Imaging Tracers in a Murine Model of Sepsis-Associated Encephalopathy

PURPOSE: The purpose of this study was to evaluate a set of widely used nuclear medicine imaging agents as possible methods to study the early effects of systemic inflammation on the living brain in a mouse model of sepsis-associated encephalopathy (SAE). The lipopolysaccharide (LPS)-induced murine systemic inflammation model was selected as a model of SAE. PROCEDURES: C57BL/6 mice were used. A multimodal imaging protocol was carried out on each animal 4 h following the intravenous administration of LPS using the following tracers: [(99m)Tc][2,2-dimethyl-3-[(3E)-3-oxidoiminobutan-2-yl]azanidylpropyl]-[(3E)-3-hyd roxyiminobutan-2-yl]azanide ([(99m)Tc]HMPAO) and ethyl-7-[(125)I]iodo-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine-3-carbox ylate ([(125)I]iomazenil) to measure brain perfusion and neuronal damage, respectively; 2-deoxy-2-[(18)F]fluoro-D-glucose ([(18)F]FDG) to measure cerebral glucose uptake. We assessed microglia activity on another group of mice using 2-[6-chloro-2-(4-[(125)I]iodophenyl)-imidazo[1,2-a]pyridin-3-yl]-N-ethyl-N-methyl -acetamide ([(125)I]CLINME). Radiotracer uptakes were measured in different brain regions and correlated. Microglia activity was also assessed using immunohistochemistry. Brain glutathione levels were measured to investigate oxidative stress. RESULTS: Significantly reduced perfusion values and significantly enhanced [(18)F]FDG and [(125)I]CLINME uptake was measured in the LPS-treated group. Following perfusion compensation, enhanced [(125)I]iomazenil uptake was measured in the LPS-treated group's hippocampus and cerebellum. In this group, both [(18)F]FDG and [(125)I]iomazenil uptake showed highly negative correlation to perfusion measured with ([(99m)Tc]HMPAO uptake in all brain regions. No significant differences were detected in brain glutathione levels between the groups. The CD45 and P2Y12 double-labeling immunohistochemistry showed widespread microglia activation in the LPS-treated group. CONCLUSIONS: Our results suggest that [(125)I]CLINME and [(99m)Tc]HMPAO SPECT can be used to detect microglia activation and brain hypoperfusion, respectively, in the early phase (4 h post injection) of systemic inflammation. We suspect that the enhancement of [(18)F]FDG and [(125)I]iomazenil uptake in the LPS-treated group does not necessarily reflect neural hypermetabolism and the lack of neuronal damage. They are most likely caused by processes emerging during neuroinflammation, e.g., microglia activation and/or immune cell infiltration

DS_10.1369_0022155418788390 – Supplemental material for The First Postlesion Minutes: An In Vivo Study of Extravasation and Perivascular Astrocytes Following Cerebral Lesions in Various Experimental Mouse Models

<p>Supplemental material, DS_10.1369_0022155418788390 for The First Postlesion Minutes: An In Vivo Study of Extravasation and Perivascular Astrocytes Following Cerebral Lesions in Various Experimental Mouse Models by László Tóth, Dávid Szöllősi, Katalin Kis-Petik, István Adorján, Ferenc Erdélyi and Mihály Kálmán in Journal of Histochemistry & Cytochemistry</p

Intraperitoneal Glucose Transport to Micrometastasis: A Multimodal In Vivo Imaging Investigation in a Mouse Lymphoma Model

Bc-DLFL.1 is a novel spontaneous, high-grade transplantable mouse B-cell lymphoma model for selective serosal propagation. These cells attach to the omentum and mesentery and show dissemination in mesenteric lymph nodes. We aimed to investigate its early stage spread at one day post-intraperitoneal inoculation of lymphoma cells (n = 18 mice), and its advanced stage at seven days post-inoculation with in vivo [18F]FDG-PET and [18F]PET/MRI, and ex vivo by autoradiography and Cherenkov luminescence imaging (CLI). Of the early stage group, nine animals received intraperitoneal injections, and nine received intravenous [18F]FDG injections. The advanced stage group (n = 3) received intravenous FDG injections. In the early stage, using autoradiography we observed a marked accumulation in the mesentery after intraperitoneal FDG injection. Using other imaging methods and autoradiography, following the intravenous injection of FDG no accumulations were detected. At the advanced stage, tracer accumulation was clearly detected in mesenteric lymph nodes and in the peritoneum after intravenous administration using PET. We confirmed the results with immunohistochemistry. Our results in this model highlight the importance of local FDG administration during diagnostic imaging to precisely assess early peritoneal manifestations of other malignancies (colon, stomach, ovary). These findings also support the importance of applying topical therapies, in addition to systemic treatments in peritoneal cancer spread