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Требования пользователей к количественным радиологическим отчётам при множественном склерозе.

ЦЕЛИ: Количественные радиологические отчеты (Q Reports) могут способствовать совершенствованию клинического управления множественным склерозом (MS) путем включения количественных данных, полученных в ходе сканирования МРТ. Однако отсутствие консенсуса в отношении конкретной информации для включения в нее данных о предпочтениях и предпочтениях врачей препятствует внедрению этих инструментов анализа изображений. Цель этого исследования состоит в том, чтобы облегчить клиническое внедрение QReports путем определения требований врачей в отношении их использования в управлении НР. МАТЕРИАЛЫ И МЕТОДЫ

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… Cerebellar WM volume Not Desired  Total ventricular volume Desired Desired  Thalamic volume Desired Desired  Basal ganglia volume Not Not  Hippocampus volume Not Not  Amygdala volume Not Not  Nucleus accumbens volume Not Not  Brainstem volume Desired Desired  Corpus callosum volume Desired Desired  Mesencephalon … Cerebellar WM volume Not Desired  Total ventricular volume Desired Desired  Thalamic volume Desired Desired  Basal ganglia volume Not Not  Hippocampus volume Not Not  Amygdala volume Not Not  Nucleus accumbens volume Not Not  Brainstem volume Desired Desired  Corpus callosum volume Desired Desired  Mesencephalon …

Inhibition of Cxcr4 chemokine receptor signaling improves habituation learning in a zebrafish model of neurofibromatosis.

Neurofibromatosis type 1 (NF1) is a neurogenetic disorder caused by loss-of-function mutations in the gene neurofibromin 1 (NF1). NF1 encodes neurofibromin, a multifunctional tumor-suppressing protein that regulates Ras, cAMP and dopamine signaling. NF1 predisposes patients to a wide range of symptoms, including peripheral nerve tumors, brain tumors and cognitive dysfunction. Despite considerable work using animal models to investigate the role of neurofibromin in behavior, translating research into treatment for NF1-associated cognitive dysfunction has not yet been successful. Here, we provid

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… | 206.6698 | Vglut2a-GFP | 7.5826 | Elavl3-GCaMP5G | 4.3585 | Elavl3-H2BRFP | 4.1155 Telencephalon (anterior forebrain) | 91.6901 | anti-5-HT | 5.874 | anti-tERK | 5.866 | anti-Zrf2 | 4.9997 Diencephalon (posterior forebrain) | 49.4953 | anti-Zrf2 | 1.9229 | Gad1b-GFP | 1.8527 | anti-5-HT | 1.4151 Mesencephalon … Bulb | 28.3954 | Vglut2a-GFP | 6.9219 | anti-5-HT | 2.6627 | anti-Gad67 | 2.4144 Telencephalon (anterior forebrain) | 10.7501 | Elavl3-H2BRFP | 4.1704 | anti-5-HT | 4.0196 | Vglut2a-GFP | 3.5166 Diencephalon (posterior forebrain) | 1.0461 | anti-Zrf2 | 4.6717 | anti-tERK | 4.0909 | anti-5-HT | 2.7117 Mesencephalon …

[Cerebral hydatic cyst and psychiatric disorders. Two cases].

The hydatidosis is an endemic illness in regions of the Middle Orient, Mediterranean, south of America, north Africa and the Australia. The … al scanning has been made in emergency and showed a voluminous cyst in oval foramen compressing the mesencephalon strongly. The cyst was well limited, hypodense, not taking the contrast, and without intracerebral oedema, the diagnosis of cerebral hydatic cyst has been made. The complementary exploration didn't show any other localizations, and biologic exam res …

The appearance and extension of neural differentiation tendencies in the neurectoderm of the early chick embryo.

1. Recently the direct analysis of neural induction in the early chick embryo has become possible by the perfection of a technique for mecha … tion also occurred in the more posterior 'C' and 'D' grafts, representing a part of the prospective mesencephalon and rhombencephalon. In addition, more posterior neural structures appeared in these grafts, and this became more pronounced with each successive stage. c. All the lateral grafts from all stages showed prosencephalic differentiation only, except for …

Pro-inflammatory cytokines modulate iron regulatory protein 1 expression and iron transportation through reactive oxygen/nitrogen species production in ventral mesencephalic neurons.

Both inflammatory processes associated with microglia activation and abnormal iron deposit in dopaminergic neurons are involved in the pathogenesis of Parkinson's disease (PD). However, the relationship between neuroinflammation and iron accumulation was not fully elucidated. In the present study, we aimed to investigate whether the pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) released by microglia, could affect cellular iron transportation in primary cultured ventral mesencephalic (VM) neurons. The results showed that IL-1β or TNF-α treatment led to in

A new strategic neurosurgical planning tool for brainstem cavernous malformations using interactive computer graphics with multimodal fusion images.

OBJECT: In this study, the authors used preoperative simulation employing 3D computer graphics (interactive computer graphics) to fuse all imaging data for brainstem cavernous malformations. The authors evaluated whether interactive computer graphics or 2D imaging correlated better with the actual operative field, particularly in identifying a developmental venous anomaly (DVA). METHODS: The study population consisted of 10 patients scheduled for surgical treatment of brainstem cavernous malformations. Data from preoperative imaging (MRI, CT, and 3D rotational angiography) were automatically

Engrailed protects mouse midbrain dopaminergic neurons against mitochondrial complex I insults.

Mice heterozygous for the homeobox gene Engrailed-1 (En1) display progressive loss of mesencephalic dopaminergic (mDA) neurons. We report that exogenous Engrailed-1 and Engrailed-2 (collectively Engrailed) protect mDA neurons from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a mitochondrial complex I toxin used to model Parkinson's disease in animals. Engrailed enhances the translation of nuclearly encoded mRNAs for two key complex I subunits, Ndufs1 and Ndufs3, and increases complex I activity. Accordingly, in vivo protection against MPTP by Engrailed is antagonized by Ndufs1 small in

Suppression of the morphine-induced rewarding effect and G-protein activation in the lower midbrain following nerve injury in the mouse: involvement of G-protein-coupled receptor kinase 2.

The present study was designed to investigate whether a state of neuropathic pain induced by sciatic nerve ligation could alter the rewarding effect, antinociception, and G-protein activation induced by a prototype of mu-opioid receptor agonist morphine in the mouse. The sciatic nerve ligation caused a long-lasting and profound thermal hyperalgesia. Under this neuropathic pain-like state, an i.c.v. morphine-induced place preference was observed in sham-operated mice but not in sciatic nerve-ligated mice. However, no differences in the antinociceptive effect of i.c.v.-administered morphine were

Glutathione depletion switches nitric oxide neurotrophic effects to cell death in midbrain cultures: implications for Parkinson's disease.

Nitric oxide (NO) exerts neurotrophic and neurotoxic effects on dopamine (DA) function in primary midbrain cultures. We investigate herein the role of glutathione (GSH) homeostasis in the neurotrophic effects of NO. Fetal midbrain cultures were pretreated with GSH synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO), 24 h before the addition of NO donors (diethylamine/nitric oxide-complexed sodium and S-nitroso-N-acetylpenicillamine) at doses tested previously as neurotrophic. Under these conditions, the neurotrophic effects of NO disappeared and turned on highly toxic. Reduction of GSH l

Calcium entry and α-synuclein inclusions elevate dendritic mitochondrial oxidant stress in dopaminergic neurons.

The core motor symptoms of Parkinson's disease (PD) are attributable to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc). Mitochondrial oxidant stress is widely viewed a major factor in PD pathogenesis. Previous work has shown that activity-dependent calcium entry through L-type channels elevates perinuclear mitochondrial oxidant stress in SNc dopaminergic neurons, providing a potential basis for their selective vulnerability. What is less clear is whether this physiological stress is present in dendrites and if Lewy bodies, the major neuropathological lesio

[WITHDRAWN] Overexpression of superoxide dismutase or glutathione peroxidase protects against the paraquat + maneb-induced Parkinson disease phenotype.

Oxidative stress has been implicated in the pathogenesis of Parkinson disease based on its role in the cascade of biochemical changes that lead to dopaminergic neuronal death. This study analyzed the role of oxidative stress as a mechanism of the dopaminergic neurotoxicity produced by the combined paraquat and maneb model of the Parkinson disease phenotype. Transgenic mice overexpressing either Cu,Zn superoxide dismutase or intracellular glutathione peroxidase and non-transgenic mice were exposed to saline, paraquat, or the combination of paraquat + maneb twice a week for 9 weeks. Non-transgen

Implantation of bioactive growth factor-secreting rods enhances fetal dopaminergic graft survival, outgrowth density, and functional recovery in a rat model of Parkinson's disease.

One of the drawbacks with fetal ventral mesencephalic (VM) grafts in Parkinson's disease is the limited outgrowth into the host striatum. In order to enhance graft outgrowth, epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) were administered by implantation of bioactive rods to the lateral part of the striatum to support grafted fetal VM implanted to the medial portion of the striatum. The polymer-based bioactive rods allow for a local secretion of neurotrophic factors over a time period of approximately 2 weeks. Moreover, glial cell line-derived neurotrophic factor (GDN

Axin-2 knockdown promote mitochondrial biogenesis and dopaminergic neurogenesis by regulating Wnt/β-catenin signaling in rat model of Parkinson's disease.

Wnts and the components of Wnt/β-catenin signaling are widely expressed in midbrain and required to control the fate specification of dopaminergic (DAergic) neurons, a neuronal population that specifically degenerate in Parkinson's disease (PD). Accumulating evidence suggest that mitochondrial dysfunction plays a key role in pathogenesis of PD. Axin-2, a negative regulator of Wnt/β-catenin signaling affects mitochondrial biogenesis and death/birth of new DAergic neurons is not fully explored. We investigated the functional role of Axin-2/Wnt/β-catenin signaling in mitochondrial biogenesis and

Harpagoside attenuates MPTP/MPP⁺ induced dopaminergic neurodegeneration and movement disorder via elevating glial cell line-derived neurotrophic factor.

Parkinson's disease is a chronic neurodegenerative movement disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. New therapeutic approaches aiming at delaying or reversing the neurodegenerative process are under active investigations. In this work, we found that harpagoside, an iridoid purified from the Chinese medicinal herb Scrophularia ningpoensis, could not only prevent but also rescue the dopaminergic neurodegeneration in MPTP/MPP(+) intoxication with promising efficacy. Firstly, in cultured mesencephalic neurons, harpagoside significantly atte

Neuroprotective effect of ghrelin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease by blocking microglial activation.

Ghrelin is an endogenous ligand for growth hormone (GH) secretagogue receptor 1a (GHS-R1a) and is produced and released mainly from the stomach. It was recently demonstrated that ghrelin can function as a neuroprotective factor by inhibiting apoptotic pathways. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic neurotoxicity in rodents; previous studies suggest that activated microglia actively participate in the pathogenesis of Parkinson's disease (PD) neurodegeneration. However, the role of microglia in the neuroprotective properties of ghrelin is still unk

D2 dopamine receptor activation facilitates endocannabinoid-mediated long-term synaptic depression of GABAergic synaptic transmission in midbrain dopamine neurons via cAMP-protein kinase A signaling.

Endocannabinoid (eCB) signaling mediates short-term and long-term synaptic depression (LTD) in many brain areas. In the ventral tegmental area (VTA) and striatum, D(2) dopamine receptors cooperate with group I metabotropic glutamate receptors (mGluRs) to induce eCB-mediated LTD of glutamatergic excitatory and GABAergic inhibitory (I-LTD) synaptic transmission. Because D(2) receptors and group I mGluR agonists are capable of inducing the release of eCBs, the predominant hypothesis is that the cooperation between these receptors to induce eCB-mediated synaptic depression results from the combine

Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.

Positron emission tomography (PET) and single photon emission computed tomography (SPECT) provide the means to studying in vivo the neurochemical, hemodynamic or metabolic consequences of the degeneration of the nigrostriatal dopaminergic system in Parkinson's disease (PD). The extent of striatal dopaminergic denervation can be quantified with radiotracers as [18F]FDopa for PET and [123I]tropanes for SPECT. There are other radiotracers such as [11C]Dopa and meta-tyrosines as well as PET tracers for uptake sites. Striatal uptake of [18F]FDopa and [123I]tropanes is markedly decreased in PD, more

Anatomical distribution of mu, delta, and kappa opioid- and nociceptin/orphanin FQ-stimulated [35S]guanylyl-5'-O-(gamma-thio)-triphosphate binding in guinea pig brain.

An in vitro autoradiographic technique has recently been developed to visualize receptor-activated G-proteins by using agonist-stimulated [35S]guanylyl-5'-O-(gamma-thio)-triphosphate ([35S]GTPgammaS) binding in the presence of excess guanosine 5'-diphosphate. This technique was used to localize opioid-activated G-proteins in guinea pig brain, a species that contains the three major types of opioid receptors. This study used selective mu, delta, and kappa opioid agonists as well as nociceptin or orphanin FQ (N/OFQ) peptide, an endogenous ligand for an orphan opioid receptor-like (ORL1) receptor

Неврологические последствия гипергликемии: сообщение о редком представлении о синдроме осмотической демиелинации.

Синдром осмотического обезвоживания (ОРД) представляет собой редкое, но потенциально опасное для жизни неврологическое расстройство. Она характеризуется невоспалительным обезвоживанием, которое, как правило, вызвано внезапными сменами сыворотки. Однако появляющиеся данные свидетельствуют о том, что резкие осмотические изменения, вызванные сильной гипергликемией, даже при отсутствии натриевого дисбаланса, могут также приводить к образованию ОРВ. ПРЕДОСТАВЛЕНИЕ СЛУЧАИ: А 57-year-old мужского пола с плохо управляемым типом 2 Больной диабет и хроническое употребление алкоголя сопровождаются период

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… Oligodendrocytes, which are responsible for forming and maintaining myelin, are especially vulnerable, resulting in demyelination and neurological dysfunction. 10 In ODS, demyelination predominantly affects region-specific oligodendrocytes, particularly those in the pons, basal ganglia, mesencephalon …

Progressive neurodegenerative and behavioural changes induced by AAV-mediated overexpression of α-synuclein in midbrain dopamine neurons.

Parkinson's disease (PD) is characterised by the progressive loss of nigral dopamine neurons and the presence of synucleinopathy. Overexpression of α-synuclein in vivo using viral vectors has opened interesting possibilities to model PD-like pathology in rodents. However, the attempts made so far have failed to show a consistent behavioural phenotype and pronounced dopamine neurodegeneration. Using a more efficient adeno-associated viral (AAV) vector construct, which includes a WPRE enhancer element and uses the neuron-specific synapsin-1 promoter to drive the expression of human wild-type α-s