188 research outputs found
Ectopic Cilia: A Histopathological Study
Cilia are normally found at the eyelid margin, while ectopic cilia are one or more lash follicles appearing in an abnormal position within the eyelid. We herein report two cases of cilia located in the palpebral conjunctiva. A 31-year-old female and a 46-year-old male presented with ectopic cilia in the superior palpebral conjunctiva. Histopathological study of the excised ectopic cilia and related lesions showed the cilia-related lesion to be located in the epithelial pit that contains goblet cells, which is consistent with the crypts of Henle. The hair follicle was surrounded by granulation tissue, while a dermal papilla and a hair matrix, which are known to produce hair follicles, did not exist in the excised tissue. While anterior ectopic cilia are congenital, ectopic cilia in the palpebral conjunctiva may be acquired, and these aberrant cilia are associated with crypts of Henle and chronic inflammation
Nuclear localization of beta-catenin involved in precancerous change in oral leukoplakia
<p>Abstract</p> <p>Background</p> <p>Oral leukoplakia is a precancerous change developed in the oral mucosa, and the mechanism that oral leukoplakia becomes malignant through atypical epithelium is not known. Here we compared the β-catenin expression detected by immunohistochemical staining in the normal oral epithelium and in the oral leukoplakia with or without dysplasia.</p> <p>Results</p> <p>The normal oral epithelium showed β-catenin expression only in the cell membrane, but not in the nuclei. In the oral leukoplakia without dysplasia, 7 out of 17 samples (41%) showed β-catenin expression in the cell membrane, and 5 samples (29%) showed expression in the nuclei. In the oral leukoplakia with dysplasia, nuclear expression of β-catenin was shown in 11 out of 12 samples (92%). Incidence of nuclear β-catenin expression was significantly different between dysplasia and normal oral epithelium (P < 0.01), and also between oral leukoplakia with dysplasia and those without dysplasia (P < 0.01). Wnt3 expression was detected in the epithelial cell membrane or cytoplasm in oral leukoplakia where nuclear expression of β-catenin was evident, but not in epithelial cells without nuclear expression of β-catenin.</p> <p>Conclusion</p> <p>The components of canonical Wnt pathway, such as Wnt3, β-catenin, and cyclin D1, were detected, implying that this pathway is potentially involved in the progression of dysplasia in oral leukoplakia.</p
Study of hadron interactions in a lead-emulsion target
Topological and kinematical characteristics of hadron interactions have been
studied using a lead-emulsion target exposed to 2, 4 and 10 GeV/c hadron beams.
A total length of 60 m tracks was followed using a high speed automated
emulsion scanning system. A total of 318 hadron interaction vertices and their
secondary charged particle tracks were reconstructed. Measurement results of
interaction lengths, charged particle multiplicity, emission angles and momenta
of secondary charged particles are compared with a Monte Carlo simulation and
appear to be consistent. Nuclear fragments emitted from interaction vertices
were also detected by a newly developed emulsion scanning system with
wide-angle acceptance. Their emission angle distributions are in good agreement
with the simulated distributions. Probabilities of an event being associated
with at least one fragment track are found to be greater than 50% for beam
momentum GeV/c and are well reproduced by the simulation. These
experimental results validate estimation of the background due to hadron
interactions in the sample of decay candidates in the OPERA oscillation experiment.Comment: 14 pages, 11 figure
Tissue factor expression in human pterygium
Purpose: A pterygium shows tumor-like characteristics, such as proliferation, invasion, and epithelial–mesenchymal transition (EMT). Previous reports suggest that tissue factor (TF) expression is closely related to the EMT of tumor cells, and subsequent tumor development. In this study, we analyzed the expression and immunolocalization of TF in pterygial and normal conjunctival tissues of humans. Methods: Eight pterygia and three normal bulbar conjunctivas, surgically removed, were used in this study. Formalinfixed, paraffin-embedded tissues were submitted for immunohistochemical analysis with anti-TF antibody. Double staining immunohistochemistry was performed to assess TF and alpha-smooth muscle actin (α-SMA) or epidermal growth factor receptor (EGFR) expression in the pterygia. Results: Immunoreactivity for TF was detected in all pterygial tissues examined. TF immunoreactivity was localized in the cytoplasm of basal, suprabasal, and superficial epithelial cells. The number of TF-immunopositive cells in pterygial epithelial cells was significantly higher than in normal conjunctival epithelial cells (p<0.001). TF immunoreactivity was detected in α-SMA-positive or -negative pterygial epithelial cells. EGFR immunoreactivity was detected in pterygial epithelium, which was colocalized with TF. Conclusions: These results suggest that TF plays a potential role in the pathogenesis and development of a pterygium, and that TF expression might be involved through EMT-dependent and -independent pathways
Systematic characterization of upper critical fields for MgB thin films using the two-band superconducting theory
We present experimental results of the upper critical fields of
various MgB thin films prepared by the molecular beam epitaxy,
multiple-targets sputtering, and co-evaporation deposition apparatus.
Experimental data of the are successfully analyzed by applying
the Gurevich theory of dirty two-band superconductivity in the case of
, where and are the intraband
electron diffusivities for and bands, respectively. We find that
the parameters obtained from the analysis are strongly correlated to the
superconducting transition temperature of the films. We also
discuss the anormalous narrowing of the transition width at intermediate
temperatures confirmed by the magnetoresistance measurements.Comment: 7 pages, 7 figures, submitted to Phys. Rev.
Magnetization plateau in a two-dimensional multiple-spin exchange model
We study a multiple-spin exchange model on a triangular lattice, which is a
possible model for low-density solid 3He films. Due to strong competitions
between ferromagnetic three-spin exchange and antiferromagnetic four-spin one,
the ground states are highly degenerate in the classical limit. At least
2^{L/2}-fold degeneracy exists on the L*L triangular lattice except for the
SO(3) symmetry. In the magnetization process, we found a plateau at
m/m_{sat}=1/2, in which the ground state is "uuud state" (a collinear state
with four sublattices). The 1/2-plateau appears due to the strong four-spin
exchange interaction. This plateau survives against both quantum and thermal
fluctuations. Under a magnetic field which realizes the "uuud" ordered state, a
phase transition occurs at a finite temperature. We predict that low-density
solid 3He thin films may show the 1/2-plateau in the magnetization process.
Experimental observation of the plateau will verify strength of the four-spin
exchange. It is also discussed that this magnetization plateau can be
understood as an insulating-conducting transition in a particle picture.Comment: 10 pages, RevTeX, 12 figures, added a reference and corrected typos,
to be published in Phys.Rev.B (01 APR 99
DIDS, a chemical compound that inhibits RAD51-mediated homologous pairing and strand exchange
RAD51, an essential eukaryotic DNA recombinase, promotes homologous pairing and strand exchange during homologous recombination and the recombinational repair of double strand breaks. Mutations that up- or down-regulate RAD51 gene expression have been identified in several tumors, suggesting that inappropriate expression of the RAD51 activity may cause tumorigenesis. To identify chemical compounds that affect the RAD51 activity, in the present study, we performed the RAD51-mediated strand exchange assay in the presence of 185 chemical compounds. We found that 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) efficiently inhibited the RAD51-mediated strand exchange. DIDS also inhibited the RAD51-mediated homologous pairing in the absence of RPA. A surface plasmon resonance analysis revealed that DIDS directly binds to RAD51. A gel mobility shift assay showed that DIDS significantly inhibited the DNA-binding activity of RAD51. Therefore, DIDS may bind near the DNA binding site(s) of RAD51 and compete with DNA for RAD51 binding
Display of both N- and C-terminal target fusion proteins on the Aspergillus oryzae cell surface using a chitin-binding module
A novel cell surface display system in Aspergillus oryzae was established by using a chitin-binding module (CBM) from Saccharomyces cerevisiae as an anchor protein. CBM was fused to the N or C terminus of green fluorescent protein (GFP) and the fusion proteins (GFP-CBM and CBM-GFP) were expressed using A. oryzae as a host. Western blotting and fluorescence microscopy analysis showed that both GFP-CBM and CBM-GFP were successfully expressed on the cell surface. In addition, cell surface display of triacylglycerol lipase from A. oryzae (tglA), while retaining its activity, was also successfully demonstrated using CBM as an anchor protein. The activity of tglA was significantly higher when tglA was fused to the C terminus than N terminus of CBM. Together, these results show that CBM used as a first anchor protein enables the fusion of both the N and/or C terminus of a target protein
RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS
Repulsive guidance molecule A (RGMa) was originally identified as a neuronal growth cone–collapsing factor. Previous reports have demonstrated the multifunctional roles of RGMa mediated by neogenin1. However, the pathogenic involvement of RGMa in amyotrophic lateral sclerosis (ALS) remains unclear. Here, we demonstrated that RGMa concentration was elevated in the cerebrospinal fluid of both patients with ALS and transgenic mice overexpressing the mutant human superoxide dismutase1 (mSOD1 mice). Treatment with humanized anti-RGMa monoclonal antibody ameliorated the clinical symptoms in mSOD1 mice. Histochemical analysis revealed that the anti-RGMa antibody significantly decreased mutant SOD1 protein accumulation in the motor neurons of mSOD1 mice via inhibition of actin depolymerization. In vitro analysis revealed that the anti-RGMa antibody inhibited the cellular uptake of the mutant SOD1 protein, presumably by reinforcing the neuronal actin barrier. Collectively, these data suggest that RGMa leads to the collapse of the neuronal actin barrier and promotes aberrant protein deposition, resulting in exacerbation of the ALS pathology.Shimizu Mikito, Shiraishi Naoyuki, Tada Satoru, et al. RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS. Science Advances 9, 686 (2023); https://doi.org/10.1126/sciadv.adg3193
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