Atypical territorial infarction in moyamoya disease.
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Publications and source records attributed to S K Song.
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Two-dimensional (2-D) strain fields were estimated non-invasively in two simple experimental models of closed-head brain injury. In the first experimental model, shear deformation of a gel was induced by angular acceleration of its spherical container In the second model the brain of a euthanized rat pup was deformed by indentation of its skull. Tagged magnetic resonance images (MRI) were obtained by gated image acquisition during repeated motion. Harmonic phase (HARP) images corresponding to the spectral peaks of the original tagged MRI were obtained, following procedures proposed by Osman, McVeigh and Prince. Two methods of HARP strain analysis were applied, one based on the displacement of tag line intersections, and the other based on the gradient of harmonic phase. Strain analysis procedures were also validated on simulated images of deformed grids. Results show that it is possible to visualize deformation and to quantify strain efficiently in animal models of closed head injury.
This study was performed to evaluate the biodegradability of acrylonitrile wastewater, microbial inhibition effect of acrylonitrile wastewater on removal efficiency and the activity of sulphate reducing bacteria (SRB) according to COD/sulphate ratio. Acrylonitrile wastewater was hardly biodegradable in a biodegradability test, however, SRB activity was 57% for overall consumption of electron donor and it was relatively high value compared to 17% of reference test with glucose. COD removal of acrylonitrile wastewater was improved to 57% and 61% from 20% as the COD/sulphate ratio were 0.5 and 0.3 by sulphate addition to acrylonitrile wastewater. First order reaction rate constants k on organic removal of acrylonitrile wastewater were 0.001, 0.004 and 0.004 at each COD/sulphate ratio of 0.9, 0.5 and 0.3. Thus it was suggested that the activity of SRB was a significant factor for removing organics and sulphate simultaneously in acrylonitrile wastewater.
AIMS: The objective of the study was to optimize the submerged culture conditions for the production of exopolysaccharide from Paecilomyces sinclairii. METHODS AND RESULTS: The optimal temperature and initial pH for exopolysaccharide production by Paecilomyces sinclairii in shake flask culture were found to be 30 degrees C and 6.0, respectively. Sucrose (60 g l(-1)) and corn steep powder (10 g l(-1)) were the most suitable carbon and nitrogen source for exopolysaccharide production. CONCLUSIONS: Under optimal culture medium, the maximum exopolysaccharide concentration in a 5-l stirred-tank fermenter indicated 7.4 g l(-1), which was approximately three times higher than that in basal medium. The maximum specific growth rates (micro max) and yield coefficient (Y(P/S)) in the optimal culture medium was 0.16 h(-1) and 0.19, respectively. SIGNIFICANCE AND IMPACT OF THE STUDY: The optimal culture conditions reported in this article can be widely applied to the processes for submerged cultures of other mushrooms.
We previously isolated a lectin of the Korean mistletoe (Viscum album coloratum). The cDNA clones that encode the A- or the B-chain of the Korean mistletoe lectin were cloned by reverse transcriptase polymerase chain reaction (RT-PCR). The mRNAs that were extracted from the Korean mistletoe were amplified, ligated into the pGEM-T easy vector, and screened with a Korean mistletoe lectin-specific probe. The probe was prepared by PCR amplification of the Korean mistletoe DNA using a primer set designed on the basis of amino acid sequences of the Korean mistletoe lectin that we had purified and reported. Unlike a recent report, which states that the European mistletoe lectin gene has no isoforms, several different clones of the A- and B-chains of the Korean mistletoe lectin were cloned from the same primer set. Three clones of each were selected for sequencing. The sizes of the A-chains were 762, 762, and 768 bp, respectively. The B-chain sizes were 798, 789, and 789 bp, respectively. Each of the clones showed significant variation in the amino acids sequence, including the N-linked glycosylation sites of the lectin. The sequence analysis of each of the Korean lectin clones, in comparison with the European mistletoe lectin and the other type II ribosome binding proteins, is discussed in the text. In addition, Southern blot analysis of the Korean mistletoe genomic DNA, restricted by different enzymes and hybridized with the lectin DNA, showed multi-bands, supporting the existence of multicopy genes or a gene family. These data suggest that heterogeneity of the mistletoe lectin is not only introduced by post-translational modifications, but also by expression of isotypes of the lectin genes.
Tumor necrosis factor-alpha (TNF-alpha) expression has been documented extensively in animal models of traumatic spinal cord injury (SCI). However, the pathophysiological significance of TNF-alpha expression in the injured cord remains to be delineated. The TNF receptor (TNFR)-nuclear factor-kappaB (NF-kappaB) signal transduction pathway is important for maintaining cell viability. NF-kappaB exerts anti-apoptotic effects via an endogenous caspase inhibitory system mediated by cellular inhibitor of apoptosis protein 2 (c-IAP2). NF-kappaB transactivates c-IAP2 to inhibit caspase-3 activation. Progressive cell death, including morphological and biochemical features suggestive of apoptosis, has been noted after SCI. We explored the effects of TNFR1 or TNFR2 deletion on the apoptotic events downstream of NF-kappaB in relation to SCI pathology and functional recovery. Nuclear proteins from the injured cords of the TNFR1(-/-) mice had a reduced NF-kappaB binding activity compared with the wild-type controls. This decrease in NF-kappaB activation was accompanied by a reduction in c-IAP2 expression and an increase in the active form of caspase-3 protein. After SCI the TNFR1(-/-) mice had greater numbers of apoptotic cells, a larger lesion size, and worse functional recovery than wild-type mice. TNFR2-deficient mice had a similar, although not as pronounced, consequence as the TNFR1(-/-) mice. These findings support the argument that the TNFR-NF-kappaB pathway is beneficial for limiting apoptotic cell death after SCI and that a defective TNFR-NF-kappaB pathway results in a poorer neurological outcome. A worse functional outcome in TNFR(-/-) mice suggests that an endogenous apoptosis inhibitory mechanism mediated by TNFR activation, NF-kappaB, and c-IAP2 may be of pathophysiological importance.
A method employing directional correlation of the diffusion tensor, directional-correlation weighted relative anisotropy (DRA), was developed to improve the accuracy of estimated relative anisotropy (RA). The intravoxel directional correlation was established on the same voxel between two identically acquired diffusion tensor images, and the correlation coefficient derived from tensor dot product was employed as the weighting factor applied in the calculation of RA. The effect of noise influence was reduced since the random noise between repeated scans is not directionally correlated. The RA and the inter- and intravoxel DRA estimations were examined on rat brains in vivo. The background noise alters the direction of eigenvectors and the magnitude of eigenvalues. The dispersion angle between repeatedly obtained eigenvectors, representing the extent of directional alteration of eigenvectors, depends on the tissue anisotropy as well as the signal-to-noise ratio (SNR) of the source images. Current results demonstrate that the intravoxel DRA improves the accuracy of RA estimation, increases the relative contrast of gray and white matter, and avoids the partial volume effect commonly seen in the intervoxel operations.
Pb2+ accumulation by Saccharomyces cerevisiae and Aureobasidium pullulans was inhibited by the initial Pb2+ concentration. In the case of S. cerevisiae, as initial Pb2+ concentrations increased, the accumulated Pb2+ per unit cell dry weight at equilibrium and the time required to reach an equilibrium state increased at low initial Pb2+ concentration. On the contrary, the accumulated Pb2+ decreased at high initial Pb2+ concentration at all pH values. The inhibition effect of initial Pb2+ concentration was delayed by the decrease of pH. However, the maximal Pb2+ accumulation capacity of S. cerevisiae was almost constant regardless of pH values. In the case of A. pullulans, the time required to reach an equilibrium state was independent of the initial Pb2+ concentration. The maximal Pb2+ accumulation capacity of A. pullulans decreased according to the decrease of pH values. However, the initial Pb2+ concentration needed to reach maximal Pb2+ accumulation amount was almost constant.
The transcription factor early growth response protein 1 (EGR1) is overexpressed in a majority of human prostate cancers and is implicated in the regulation of several genes important for prostate tumor progression. Here we have assessed the effect of Egr1 deficiency on tumor development in two transgenic mouse models of prostate cancer (CR2-T-Ag and TRAMP). Using a combination of high-resolution magnetic resonance imaging and histopathological and survival analyses, we show that tumor progression was significantly impaired in Egr1-/- mice. Tumor initiation and tumor growth rate were not affected by the lack of Egr1; however, Egr1 deficiency significantly delayed the progression from prostatic intra-epithelial neoplasia to invasive carcinoma. These results indicate a unique role for Egr1 in regulating the transition from localized, carcinoma in situ to invasive carcinoma.
BACKGROUND: To further elucidate mechanisms of human allergic rhinosinusitis, we studied the induction, distribution and modulation of allergen-induced upper airway inflammation in a BALB/c mouse model. METHODS: Allergic inflammation induced with ovalbumin (OVA) by intraperitoneal (IP) injection in alum was compared to repeated intranasal instillation. The type and distribution of inflammatory cells was compared in the respiratory and olfactory epithelial compartments. Eosinophil distribution was assessed using Scarlet Red stain and a polyclonal antibody recognizing eosinophil major basic protein (MBP). The role of interleukin (IL)-5 in upper airway inflammation was tested by administration of polyclonal anti-IL-5 antibody during the sensitization protocol. RESULTS: Unsensitized control mice receiving saline failed to develop upper airway eosinophil infiltration. IP OVA-sensitized mice developed marked upper airway mucosal eosinophil infiltration after aerosol OVA challenge, whereas repeated intranasal instillation of OVA produced qualitatively similar, but less intense eosinophil infiltration. Using either sensitization protocol, eosinophil infiltration was seen in areas of the lower portion of the nasal septum, the floor and the lower lateral walls of the mid-caudal region of the nasal cavity. Immunofluorescence staining for MBP confirmed this distribution of eosinophils but also demonstrated some eosinophils in the maxillary sinuses and in circumscribed regions of the ethmoturbinates. All areas of eosinophil infiltration were lined by respiratory epithelium. The selective infiltration of respiratory but not olfactory epithelium by eosinophils was unassociated with a measurable induction of epithelial ICAM-1 or eotaxin expression. OVA-induced upper airway eosinophil infiltration was found to be IL-5 dependent, since administration of a polyclonal anti-IL-5 antibody (TRFK-5) during OVA sensitization resulted in a marked modulation (80% decrease) in eosinophil infiltration in response to subsequent OVA challenge. CONCLUSION: The mouse upper airway, specifically in areas containing respiratory epithelium, is a target for OVA-induced allergic inflammation. This selective infiltration of respiratory, but not olfactory, epithelium is, in part, dependent upon IL-5. This model is useful for further dissection of the inflammatory response with genetic manipulations and targeted immunological approaches.
BACKGROUND AND PURPOSE: (23)Na MRI may offer new insight into the evaluation of tissue injury. We performed a direct, longitudinal, morphological comparison of (1)H T2 relaxation, (1)H apparent diffusion coefficient (ADC), (23)Na content, and histopathology after cerebral ischemia to address the hypotheses that (a) (23)Na MRI is unique in comparison to (1)H MRI, and (b) accumulation of (23)Na is an unambiguous marker for dead tissue. METHODS: Rats underwent 30 minutes of focal ischemia. MRIs of (1)H T2, (1)H ADC, and (23)Na content were acquired from 12 hours up to 1, 2, or 14 days after reperfusion. On excision, brains were stained with triphenyltetrazolium chloride (TTC). RESULTS: In all cases, the region of abnormality increased in size for 2 days. On day 5, both (1)H T2 and ADC temporarily appeared normal despite the presence of TTC-defined infarction. By comparison, the volume of tissue exhibiting abnormally intense (23)Na signal mirrored the TTC-defined infarct at all time points. CONCLUSIONS: Regions of high (23)Na content correlate well with the TTC-defined infarct and may be a quantitative in vivo marker for dead tissue. In contrast, the dynamics of the (1)H T2 and ADC make it difficult to interpret these images without additional information because they may appear normal despite infarction. Neither type of (1)H image delineates dead tissue, and none of these methods predicts the potential infarct size at early time points.
The effect of nitric oxide (NO) on calcium current (I(Ca)) and intracellular calcium concentration ([Ca(2+)](i)) in primarily cultured dorsal root ganglion (DRG) neurons was investigated from neonatal rats. I(Ca) and [Ca(2+)](i) were simultaneously recorded using perforated-patch technique in combination with fluorescence measurement from single DRG neurons. NO donors, sodium nitroprusside (SNP) and S-nitro-N-acetylpenicillamine (SNAP), inhibited I(Ca) in small-diameter neurons without significant change in voltage-dependence of activation and activation time constants. SNP and SNAP also reduced the transient [Ca(2+)](i) peak accompanied by I(Ca). Inhibition by NO was reproducible, but gradually desensitized. In some DRG neurons, SNP and SNAP increased basal [Ca(2+)](i) in concentration of 10 microM with little effect on NO-induced inhibition of I(Ca). 8-Br-cGMP, a permeable cGMP analog, mimicked the effects of SNP and SNAP. These results suggest that, in DRG neurons, NO has inhibitory effect on I(Ca), which is independent of NO-induced increase of basal [Ca(2+)](i), through cGMP-dependent pathway.
In this study, the sensitivity of a novel fibrin-targeted contrast agent for fibrin detection was defined in vitro on human thrombus. The contrast agent was a lipid-encapsulated perfluorocarbon nanoparticle with numerous Gd-DTPA complexes incorporated into the outer surface. After binding to fibrin clots, scanning electron microscopy of treated clots revealed dense accumulation of nanoparticles on the clot surfaces. Fibrin clots with sizes ranging from 0.5-7.0 mm were imaged at 4.7 T with or without treatment with the targeted contrast agent. Regardless of sizes, untreated clots were not detectable by T(1)-weighted MRI, while targeted contrast agent dramatically improved the detectability of all clots. Decreases in T(1) and T(2) relaxation times (20-40%) were measured relative to the surrounding media and the control clots. These results suggest the potential for sensitive and specific detection of microthrombi that form on the intimal surfaces of unstable atherosclerotic plaque.
We have isolated a gene encoding a ribosome-inactivating protein (RIP) from Phytolacca insularis, designated as P. insularis antiviral protein 2 (PIP2). The PIP2 gene contained an open reading frame encoding a polypeptide of 315 amino acids. The deduced amino acid sequence of PIP2 was similar to those of other RIPs from Phytolacca plants. Recombinant PIP2 was expressed in Escherichia coli and was used to investigate its biological activities. Recombinant PIP2 inhibited protein synthesis in rabbit reticulocyte lysate by inactivating ribosomes through N-glycosidase activity. It also exhibited antiviral activity against tobacco mosaic virus (TMV). Expression of the PIP2 gene was developmentally regulated in leaves and roots of P. insularis. Furthermore, expression of the PIP2 gene was induced in leaves by mechanical wounding. The wound induction of the PIP2 gene was systemic. Expression of the PIP2 gene also increased in leaves in a systemic manner after treatment with jasmonic acid (JA) and abscisic acid (ABA), but not with salicylic acid (SA). These results imply that plants have employed the systemic synthesis of the defensive proteins to protect themselves more efficiently from infecting viruses.
Global cardiac function has been studied in small animals with methods such as echocardiography, cine-magnetic resonance imaging (MRI), and cardiac catheterization. However, these modalities make little impact on delineation of pathophysiology at the tissue level. The advantage of tagged cine-MRI technique is that the twisting motion of the ventricle, referred to as torsion, can be measured noninvasively, reflecting the underlying shearing motion of individual planes of myofibrils that generate wall thickening and ventricular ejection. Thus we sought to determine whether the mechanism of ventricular ejection, as measured by torsion, was the same in both humans and mice. Nine mice and ten healthy humans were studied with tagged cine-MRI. The magnitude and systolic time course of ventricular torsion were equivalent in mouse and humans, when normalized for heart rate and ventricular length. The end-systolic torsion angle was 12.7 +/- 1.7 degrees in humans vs. 2.0 +/- 1.5 degrees in mice unnormalized and 1.9 +/- 0.3 degrees /cm vs. 2.7 +/- 2.3 degrees /cm when normalized for ventricular length). These results support the premise that ventricular torsion may be a uniform measure of normal ventricular ejection across mammalian species and heart sizes.
Cilia have been classified as sensory or motile types on the basis of functional and structural characteristics; however, factors important for regulation of assembly of different cilia types are not well understood. Hepatocyte nuclear factor-3/forkhead homologue 4 (HFH-4) is a winged helix/forkhead transcription factor expressed in ciliated cells of the respiratory tract, oviduct, and ependyma in late development through adulthood. Targeted deletion of the Hfh4 gene resulted in defective ciliogenesis in airway epithelial cells and randomized left-right asymmetry so that half the mice had situs inversus. In HFH-4-null mice, classic motile type cilia with a 9 + 2 microtubule ultrastructure were absent in epithelial cells, including those in the airways. In other organs, sensory cilia with a 9 + 0 microtubule pattern, such as those on olfactory neuroepithelial cells, were present. Ultrastructural analysis of mutant cells with absent 9 + 2 cilia demonstrated that defective ciliogenesis was due to abnormal centriole migration and/or apical membrane docking, suggesting that HFH-4 functions to direct basal body positioning or anchoring. Evaluation of wild-type embryos at gestational days 7.0 to 7.5 revealed Hfh4 expression in embryonic node cells that have monocilium, consistent with a function for this factor at the node in early determination of left- right axis. Analysis of the node of HFH-4 mutant embryos revealed that, in contrast to absent airway cilia, node cilia were present. These observations indicate that there are independent regulatory pathways for node ciliogenesis compared with 9 + 2 type ciliogenesis in airways, and support a central role for HFH-4 in ciliogenesis and left-right axis formation.
Cytotoxic lectins (KML-C) were isolated from an extract of Korean mistletoe [Viscum album C. (coloratum)] by affinity chromatography on a hydrolysed Sepharose 4B column, and the chemical and biological properties of KML-C were examined, partly by comparing them with a lectin (EML-1) from European mistletoe[Viscum album L. (loranthaceae)]. The hemagglutinating activity of KML-C was inhibited by N-acetyl-D-galactosamine and D-galactose at the minimum concentrations of 6.3 and 12.5 microM/ml, respectively. Further biochemical analyses indicated that KML-C consists of four chains (Mr = 27.5, 30, 31 and 32.5 kDa) which, in some of the molecules, are disulfide-linked, and that the chains of KML-C are distributed over a broad range of isoelectric points (pI), 8.0 to 9.0, whereas the range for EML-1 is 6.6-7.0. A difference was also observed between the N-terminal sequences of KML-C and EML-1. The isolated lectins showed strong cytotoxicity against various human and murine tumor cells, and the cytotoxic activity of KML-C was higher than that of EML-1. Tumor cells treated with KML-C exhibited typical patterns of apoptotic cell death, such as apparent morphological changes and DNA fragmentation, and its apoptosis-inducing activity was blocked by addition of Zn2+, an inhibitor of Ca2+/Mg2+ -dependent endonucleases, in a dose-dependent manner. These results suggest that KML-C is a novel lectin related to the cytotoxicity of Korean mistletoe, and that its cytotoxic activity against tumor cells is due to apoptosis mediated by Ca2+/Mg2+ -dependent endonucleases.
Scanning electron microscopy and energy dispersive X-ray analyses were carried out in a comparative investigation of Pb(2+) accumulation in Saccharomyces cerevisiae and Aureobasidium pullulans. In S. cerevisiae, the time required to reach an equilibrium state was shortened from 100 h to 1 h as the initial Pb(2+) concentration decreased from 96.5 mg/l to 16.0 mg/l, whereas the time was almost independent of initial Pb(2+) concentration in A. pullulans. Concomitant with the Pb(2+) accumulation, the cell surface of S. cerevisiae became rough and the amounts of potassium, phosphorus and sulfur on the cell surface decreased. However, significant increase of Pb(2+) on the cell surface after Pb(2+) accumulation was not observed due to Pb(2+) penetration into the cell interior. In contrast, the Pb(2+) accumulation had no significant effect on the surface characteristics of A. pullulans and extreme Pb(2+) accumulation was observed on the cell surface because Pb(2+) could not penetrate into the cell interior due to the existence of extracellular polymeric substances.