Paragonimus and paragonimiasis in Asia: An update.

Radiation-induced optic neuropathy (RION) is a devastating complication following external beam radiation therapy (EBRT) that leads to acute vision loss. To date, no efficient, available treatment for this complication, due partly to the lack of understanding regarding the developmental processes behind RION. Here, we report radiation caused changes in mitochondrial dynamics by regulating the mitochondrial fission proteins dynamin-related protein 1 (Drp1) and fission-1 (Fis1). Concurrent with an excessive production of reactive oxygen species (ROS), both neuronal injury and visual dysfunction resulted. Further, our findings delineate an important mechanism by which cyclin-dependent kinase 5 (Cdk5)-mediated phosphorylation of Drp1 (Ser616) regulates defects in mitochondrial dynamics associated with neuronal injury in the development of RION. Both the pharmacological inhibition of Cdk5 by roscovitine and the inhibition of Drp1 by mdivi-1 inhibited mitochondrial fission and the production of ROS associated with radiation-induced neuronal loss. Taken together, these findings may have clinical significance in preventing the development of RION.

/pdf/cdk5-mediated-drp1-phosphorylation-drives-mitochondrial-1cjfm8p83e.pdf

Cdk5-mediated Drp1 phosphorylation drives mitochondrial defects and neuronal apoptosis in radiation-induced optic neuropathy.

Central nervous system (CNS) trauma and neurodegenerative disorders trigger a cascade of cellular and molecular events resulting in neuronal apoptosis and regenerative failure. The pathogenic mechanisms and gene expression changes associated with these detrimental events can be effectively studied using a rodent optic nerve crush (ONC) model. The purpose of this study was to use a mouse ONC model to: (a) evaluate changes in retina and optic nerve (ON) gene expression, (b) identify neurodegenerative pathogenic pathways and (c) discover potential new therapeutic targets. Only 54% of total neurons survived in the ganglion cell layer (GCL) 28 days post crush. Using Bayesian Estimation of Temporal Regulation (BETR) gene expression analysis, we identified significantly altered expression of 1,723 and 2,110 genes in the retina and ON, respectively. Meta-analysis of altered gene expression (≥1.5, ≤-1.5, p < 0.05) using Partek and DAVID demonstrated 28 up and 20 down-regulated retinal gene clusters and 57 up and 41 down-regulated optic nerve clusters. Regulated gene clusters included regenerative change, synaptic plasticity, axonogenesis, neuron projection, and neuron differentiation. Expression of selected genes (Vsnl1, Syt1, Synpr and Nrn1) from retinal and ON neuronal clusters were quantitatively and qualitatively examined for their relation to axonal neurodegeneration by immunohistochemistry and qRT-PCR. A number of detrimental gene expression changes occur that contribute to trauma-induced neurodegeneration after injury to ON axons. Nrn1 (synaptic plasticity gene), Synpr and Syt1 (synaptic vesicle fusion genes), and Vsnl1 (neuron differentiation associated gene) were a few of the potentially unique genes identified that were down-regulated spatially and temporally in our rodent ONC model. Bioinformatic meta-analysis identified significant tissue-specific and time-dependent gene clusters associated with regenerative changes, synaptic plasticity, axonogenesis, neuron projection, and neuron differentiation. These ONC induced neuronal loss and regenerative failure associated clusters can be extrapolated to changes occurring in other forms of CNS trauma or in clinical neurodegenerative pathological settings. In conclusion, this study identified potential therapeutic targets to address two key mechanisms of CNS trauma and neurodegeneration: neuronal loss and regenerative failure.

/pdf/optic-nerve-crush-induces-spatial-and-temporal-gene-2w1b7lyelw.pdf

Optic nerve crush induces spatial and temporal gene expression patterns in retina and optic nerve of BALB/cJ mice.

Purpose: Pathophysiological events in the retinal ganglion cell layer (GCL) are a prominent feature of several optic neuropathies including glaucoma. The purpose of this study was to identify and catalog genes whose expression in the human retina is restricted to the GCL. Methods: Laser capture microdissection (LCM) technology was used to isolate tissue from the perimacular retina of three human donors without retinal or optic nerve disease. RNA was isolated from the (1) retinal GCL and (2) the inner and outer nuclear layers of the same retina, and the gene expression profiles of both fractions were determined using Affymetrix Hu133Plus 2.0 GeneChips. Data were analyzed to identify those genes whose expression is substantially more prevalent in the GCL when compared to the outer retinal layers. Differential expression of selected genes was confirmed by realtime PCR and immunohistochemistry. Results: The results show that mRNA levels of previously described ganglion cell markers, e.g. the neurofilament genes (NEFH, NEF3, or NEFL) and the Brn3a transcription factor (POU4F1), were highly enriched in the isolated GCL fraction. In contrast, transcripts for genes associated with phototransduction (RHO), photoreceptor development (NR2E3), or interphotoreceptor matrix constituents (IMPG1) were nearly absent from the GCL fraction. Using bioinformatics approaches over 80 genes were identified whose expression in the human retina appears to be limited to the GCL. Conclusions: We have successfully used LCM technology to generate gene expression profiles of highly enriched GCL fractions of the normal human retina. These data not only provide clues to the normal function of retinal ganglion cells but also serve as a resource in the development of ganglion cell specific markers or transfection vectors, and the identification of candidate genes for hereditary forms of glaucoma.

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/110567/1/T200601560.pdf

Gene expression profile of the adult human retinal ganglion cell layer

Zoonotic and vector-borne parasites are important preventable risk factors for epilepsy. Three parasitic infections — cerebral malaria, Taenia solium cysticercosis and onchocerciasis — have an established association with epilepsy. Parasitoses are widely prevalent in low-income and middle-income countries, which are home to 80% of the people with epilepsy in the world. Once a parasitic infection has taken hold in the brain, therapeutic measures do not seem to influence the development of epilepsy in the long term. Consequently, strategies to control, eliminate and eradicate parasites represent the most feasible way to reduce the epilepsy burden at present. The elucidation of immune mechanisms underpinning the parasitic infections, some of which are parasite-specific, opens up new therapeutic possibilities. In this Review, we explore the pathophysiological basis of the link between parasitic infections and epilepsy, and we consider preventive and therapeutic approaches to reduce the burden of epilepsy attributable to parasitic disorders. We conclude that a concerted approach involving medical, veterinary, parasitological and ecological experts, backed by robust political support and sustainable funding, is the key to reducing this burden. Zoonotic and vector-borne parasites are important preventable risk factors for epilepsy. The authors explore the pathophysiological basis of the link between parasitic infections and epilepsy and consider preventive and therapeutic approaches to reduce the epilepsy burden associated with parasitic disorders.

/pdf/zoonotic-and-vector-borne-parasites-and-epilepsy-in-low-398bkd863u.pdf

Zoonotic and vector-borne parasites and epilepsy in low-income and middle-income countries.

OBJECT The authors retrospectively analyzed the clinical characteristics, existing problems, and treatment experiences in recently diagnosed cerebral paragonimiasis (CP) cases and sought to raise awareness of CP and to supply reference data for early diagnosis and treatment. METHODS Twenty-seven patients (22 male and 5 female; median age 20.3 years, range 4–47 years) with CP were diagnosed between September 2008 and September 2013. These diagnoses were confirmed by IgG enzyme-linked immunosorbent assays. Follow-up was performed in 24 cases for a period of 6–56 months. RESULTS Cerebral paragonimiasis accounted for 21.6% of paragonimiasis cases (27 of 125). The average duration from onset to praziquantel treatment was 69 days. All patients resided in rural areas. Twenty patients had positive lung results, which included visible lung lesions in 14 cases. The lesions were surgically removed in 8 of these cases. Twenty-four patients had high eosinophil counts (≥ 0.08 × 109/L), and eosinophilic meningitis was n...

/pdf/cerebral-paragonimiasis-a-retrospective-analysis-of-27-cases-9ooca04uan.pdf

Cerebral paragonimiasis: a retrospective analysis of 27 cases

Background and Purpose—We retrospectively analyzed the clinical and imaging characteristics, diagnosis, and treatment outcomes of 10 patients with hemorrhagic cerebral paragonimiasis (CP), and we evaluated the influence of Paragonimus infection on cerebrovascular damage. Methods—Ten patients (7 male and 3 female; median age 15.7 years, range 4–46 years) with hemorrhagic CP were diagnosed between April 2009 and January 2013. All patients underwent the head computed tomography scans and 9 patients underwent MRI examinations. Four patients underwent computed tomographic angiography, magnetic resonance angiography, and digital subtraction angiography. Liquid-based cytological examination of cerebrospinal fluid was performed in 7 patients. Follow-up examinations were performed for 9 cases for a period of 12 to 62 months. Results—Hemorrhagic CP accounted for 37% of CP cases (10/27). No patients were initially diagnosed with CP. The major symptoms of hemorrhagic CP included acute headache, vomiting, hemiparalysi...

Hemorrhagic Stroke and Cerebral Paragonimiasis

Department ofOphthalmology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, P.R. ChinaPurpose: To obtain and analyze early retinal changes at the molecular level 24 h after a radiation injury to the ipsilateralintraorbital nerve using gamma knife surgery (GKS), and to examine the morphological changes in bilateral optic nerves.Methods: Unilateral intraorbital optic nerves of three rhesus macaques were treated by GKS with irradiated doses of 15Gy, while contralateral optic nerves and retinas served as the control. Gene expression profiles of the control and affectedretinas were analyzed with Affymetrix Rhesus Macaque Genome arrays. To verify the results, a quantitative real-timepolymerase chain reaction (qRT–PCR) was performed to test the expression patterns of five function-known genes.Morphological changes in the bilateral optic nerves were examined using a transmission electron microscope (TEM) andlight microscopy. The glial cell reaction in bilateral optic nerves was studied using immunohistochemistry.Results: Of the probe sets, 1,597 (representing 1,081 genes) met the criteria for differential expression, of which 82 geneswere significantly up-or down-regulated in treated retinas. There was prominent upregulation of genes associated withglial cell activation in the treated retina. Genes related to an early inflammatory reaction and to cell death were alsosignificantly regulated in response to a radiation injury to the intraorbital optic nerve. In contrast, the messenger ribonucleicacid (mRNA) expression levels of retinal ganglion cell (RGC)-specific genes were low. Morphologically, cytoplasmicprocesses of astrocytes in treated nerves were shorter than those of the control and were not straight, while also beingaccompanied by decreased GFAP immunostaining. More oligodendrocytes and inflammatory cells were apparent intreated nerves than in the control. In addition, swollen mitochondria and slight chromation condensation could be seen inthe glial cells of treated nerves.Conclusions: We conclude that the current irradiated dose of 15 Gy was sufficient to lead to a radiation injury of the opticnerve and retina. Several transcripts deregulated in retinas after a radiation injury play a key role in radiation-inducedneurogenic visual loss, especially for genes associated with RGC, glial cell, and cell death. Glial cells in optic nervesmight be the primary target of a radiation injury in the optic nerve.

/pdf/retinal-whole-genome-microarray-analysis-and-early-16gtmyyv78.pdf

Retinal whole genome microarray analysis and early morphological changes in the optic nerves of monkeys after an intraorbital nerve irradiated injury.

Supplementary material : Characteristic CT and MR imaging findings of cerebral paragonimiasis

Characteristic CT and MR imaging findings of cerebral paragonimiasis

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