Thors would like to thank Ms Hong Yi of the EM core facility of Emory University.population present in monkey bone marrows treated with the drug diethylaminobenzaldehyde (DEAB). Bone marrows were treated with DEAB, an inhibitor for aldehyde dehydrogenase (ALDH), at a concentration of 1 mmol/l for two days. Cellular morphology of cells after Wright Giemsa staining was captured with a Zeiss inverted microscope. (TIF)Figure S9 Bone marrow cells pre-treated with DEAB are permissive for dengue virus infection in vitro. Monkey whole BM cell samples treated in three different ways (DEABuntreated (green), 2 day pre-treated (red) and DEAB-treated concurrently with the infection (blue) were performed as described in methods. Results from two representative monkeys are shown. The peak in genome titer was at days 2 or 3 post initiation of infection. (TIF) Figure SAuthor ContributionsConceived and designed the experiments: KBC SN NO FV AAA GCP. Performed the experiments: KBC SN NO HMH. Analyzed the data: KBC SN JR NO FV AAA GCP. Contributed reagents/materials/analysis tools: FV JB. Wrote the paper: KBC SN FV AAA GCP. Performed EM and the immunohistochemistry staining: KBC. Performed the subset of the EM: SN. Performed real time PCR and ELISA: HMH. Assisted in IRB protocol approval and obtained human bone marrow samples for the study: JR. Directed the IACUC protocol: FV. Obtained monkey bone marrow samples for the experiments: FV. Assisted in approval of IACUC protocol: AAA. Wrote the IACUC and IRB protocol: GCP.Monkey bone marrows treated with DEAB for two days are highly permissive to dengue virus infection. (A) RNA quantification was performed with the three
Myelinated axon segments have four distinct regions: the node of Ranvier, the paranode, the juxtaparanode, and the internode [1]. Each region is involved in 18325633 the activity and protection of the axon. The paranodal junction, which is a specialized axon-glia contact zone, seals the internodal periaxonal space from the outside milieu. The zone’s molecular architecture is built on axonal and glial adhesion proteins linked by scaffolding proteins [2]. Honke et al reported that mice with a disrupted cerebroside sulfotransferase (CST) gene have abnormal or nonfunctional paranodal junctions in the central and peripheral nervous Dimethylenastron supplier systems [3?]. The CST enzyme synthesizes sulfatide, a major lipid Homotaurine component of the myelin sheath [6,7]. Significantly abnormal sulfatide levels are found in patients with disorders such as metachromatic leukodystrophy and Alzheimer’s disease [8]. Therefore, paranodal junctions and the sulfatide lipid may be involved in the pathogenesis of these neurological disorders.Diffusion tensor MRI (DTI), a tool that has proven useful in the diagnosis of central nervous disorders [9?2], has recently been used to characterize 1527786 tissue structures at the microscopic level. DTI is particularly helpful in understanding the pathology of neurodegenerative disorders and injuries [13?5]. Although transgenic mice are often used to analyze the pathology of white-matter disorders, they are rarely used for in vivo MRI of the spinal cord, because their body movement and small size make it difficult to delineate the spinal cord. To overcome these problems, we applied a cryogenic quadrature radio-frequency (RF) surface probe to the mouse spinal cord to improve the sensitivity of the in vivo MRI. This cryogenic device has been used successfully to improve the MR imaging of small animals [16]. Although in vivo.Thors would like to thank Ms Hong Yi of the EM core facility of Emory University.population present in monkey bone marrows treated with the drug diethylaminobenzaldehyde (DEAB). Bone marrows were treated with DEAB, an inhibitor for aldehyde dehydrogenase (ALDH), at a concentration of 1 mmol/l for two days. Cellular morphology of cells after Wright Giemsa staining was captured with a Zeiss inverted microscope. (TIF)Figure S9 Bone marrow cells pre-treated with DEAB are permissive for dengue virus infection in vitro. Monkey whole BM cell samples treated in three different ways (DEABuntreated (green), 2 day pre-treated (red) and DEAB-treated concurrently with the infection (blue) were performed as described in methods. Results from two representative monkeys are shown. The peak in genome titer was at days 2 or 3 post initiation of infection. (TIF) Figure SAuthor ContributionsConceived and designed the experiments: KBC SN NO FV AAA GCP. Performed the experiments: KBC SN NO HMH. Analyzed the data: KBC SN JR NO FV AAA GCP. Contributed reagents/materials/analysis tools: FV JB. Wrote the paper: KBC SN FV AAA GCP. Performed EM and the immunohistochemistry staining: KBC. Performed the subset of the EM: SN. Performed real time PCR and ELISA: HMH. Assisted in IRB protocol approval and obtained human bone marrow samples for the study: JR. Directed the IACUC protocol: FV. Obtained monkey bone marrow samples for the experiments: FV. Assisted in approval of IACUC protocol: AAA. Wrote the IACUC and IRB protocol: GCP.Monkey bone marrows treated with DEAB for two days are highly permissive to dengue virus infection. (A) RNA quantification was performed with the three
Myelinated axon segments have four distinct regions: the node of Ranvier, the paranode, the juxtaparanode, and the internode [1]. Each region is involved in 18325633 the activity and protection of the axon. The paranodal junction, which is a specialized axon-glia contact zone, seals the internodal periaxonal space from the outside milieu. The zone’s molecular architecture is built on axonal and glial adhesion proteins linked by scaffolding proteins [2]. Honke et al reported that mice with a disrupted cerebroside sulfotransferase (CST) gene have abnormal or nonfunctional paranodal junctions in the central and peripheral nervous systems [3?]. The CST enzyme synthesizes sulfatide, a major lipid component of the myelin sheath [6,7]. Significantly abnormal sulfatide levels are found in patients with disorders such as metachromatic leukodystrophy and Alzheimer’s disease [8]. Therefore, paranodal junctions and the sulfatide lipid may be involved in the pathogenesis of these neurological disorders.Diffusion tensor MRI (DTI), a tool that has proven useful in the diagnosis of central nervous disorders [9?2], has recently been used to characterize 1527786 tissue structures at the microscopic level. DTI is particularly helpful in understanding the pathology of neurodegenerative disorders and injuries [13?5]. Although transgenic mice are often used to analyze the pathology of white-matter disorders, they are rarely used for in vivo MRI of the spinal cord, because their body movement and small size make it difficult to delineate the spinal cord. To overcome these problems, we applied a cryogenic quadrature radio-frequency (RF) surface probe to the mouse spinal cord to improve the sensitivity of the in vivo MRI. This cryogenic device has been used successfully to improve the MR imaging of small animals [16]. Although in vivo.
