27 research outputs found

    Additional file 1: Table S1. of Body surface area is a novel predictor for surgical complications following video-assisted thoracoscopic surgery for lung adenocarcinoma: a retrospective cohort study

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    Showed the details of definitions for preoperative comorbidities estimated in the current study. Table S2. showed the demographic differences between patients with BSA ≤ 1.68 m2 and patients with BSA > 1.68 m2. (DOCX 20 kb

    sj-pptx-2-dhj-10.1177_20552076221149528 - Supplemental material for A new machine learning algorithm with high interpretability for improving the safety and efficiency of thrombolysis for stroke patients: A hospital-based pilot study

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    Supplemental material, sj-pptx-2-dhj-10.1177_20552076221149528 for A new machine learning algorithm with high interpretability for improving the safety and efficiency of thrombolysis for stroke patients: A hospital-based pilot study by Huiling Shao, Wing Chi Lawrence Chan, Heng Du and Xiangyan Fiona Chen, Qilin Ma, Zhiyu Shao in Digital Health</p

    Identification of Cre expression and mTORC1 activation in the skin of <i>Tsc1ccFsp-cre+</i> mice.

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    <p>Confocal microscopy fused images (100x) are shown with nuclear (DAPI, blue), Cre (Anti-Cre antibody, green), and pS6(S235/236) (antibody, red) are shown. Multiple cells with appearance of fibroblasts are seen in the lower dermis of the mutant <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mouse skin, that stain with both red and green stains (yellow, indicated by arrow heads). Some of these cells are shown at higher magnification in the inset in the upper right corner (600x). A similar region of the control mouse skin shows no staining.</p

    sj-docx-1-dhj-10.1177_20552076221149528 - Supplemental material for A new machine learning algorithm with high interpretability for improving the safety and efficiency of thrombolysis for stroke patients: A hospital-based pilot study

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    Supplemental material, sj-docx-1-dhj-10.1177_20552076221149528 for A new machine learning algorithm with high interpretability for improving the safety and efficiency of thrombolysis for stroke patients: A hospital-based pilot study by Huiling Shao, Wing Chi Lawrence Chan, Heng Du and Xiangyan Fiona Chen, Qilin Ma, Zhiyu Shao in Digital Health</p

    Response of the skin of <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice to one month treatment with rapamycin.

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    <p>A. Low and high power images of <i>Tsc1ccFsp-cre+</i> mouse skin at age 1 year is shown. Upper panel, H&E stain, with dermis indicated. Lower panel, chloroacetate esterase stain highlights mast cells. B-D. Quantification of epidermis and dermis thickness, and mast cell count per high-powered field (400x) as assessed by dermatopathologist (SG).</p

    Increased mast cells and fat necrosis are seen in the skin of <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice.

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    <p>A. High power images (400x magnification) of <i>Tsc1cc</i> and <i>Tsc1ccFsp-cre+</i> mouse skin at age 1 year is shown. Upper panel, chloroacetate esterase stain to highlight mast cells. Bottom panel, H&E stain showing fat necrosis, inset at 1000x. B. Quantification of mast cells per high-powered field (400x) as assessed by dermatopathologist (SG). Mast cells are significantly increased in both dorsal and ventral skin of Tsc1<sup>cc</sup>FspCre1+ mice compared to Tsc1cc mice. n = 3–9 for each measurement; mice had ages 8–13 months. C. Quantification of blood vessel density per high-powered field (400x) as assessed by dermatopathologist (SG). There is a possible trend toward more vessels in the mutant mouse skin. n = 2–4 for each measurement; mice had ages 8–13 months.</p

    Skin histology in <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice.

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    <p>A. Representative skin H&E sections are shown for mice of each genotype at 1 year of age. All images shown are taken at 40x magnification. Top panel is dorsal and the bottom panel is ventral skin. Several layers are indicated in selected images, including dermis, hypodermis, and muscle layers. Note the increase in the dermal thickness and marked reduction in the hypodermis in <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice compared to <i>Tsc1</i><sup><i>cc</i></sup> mice. B, C. Quantitation of epidermis (B) and dermis (C) thickness is shown for control (solid circles) and Tsc1ccFsp-cre+ (solid squares) mice. Note the increase in both epidermal and dermal thickness, which is statistically significant in all cases except control vs. mutant dorsal epidermis. n = 10–14 for each measurement; mice had ages 8–13 months.</p

    Survival and gross skin features of <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice.

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    <p>A. Survival curve of mice of various genotypes. Note reduced survival of <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice in comparison to other genotypes (p<0.0001). The median survival of <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice is 338 days. Right, there was no major difference between the survival of female and male <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice (p = 0.2660). The median survival of females and males is 349 days and 304 days respectively. B. Pictures of mice of various genotypes are shown. Note the loose, somewhat wrinkled skin seen in the <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice in comparison to other genotypes. All mice shown had age 8 months. C. Additional pictures of mice at age 1 year, with two <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice on left and two <i>Tsc1</i><sup><i>cc</i></sup> mice on right. Note wrinkled loose skin on abdomen, blunt nose, and larger paws of the <i>Tsc1</i><sup><i>cc</i></sup><i>Fsp-cre+</i> mice in comparison to the <i>Tsc1</i><sup><i>cc</i></sup> mice.</p

    Working hypothesis.

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    <p>Aβ-Cyclphilin D mediates impairments in axonal mitochondrial transport. In the present of Aβ, there is an increase in the opening of CypD-mediated mitochondrial permeability transition pore (mPTP), leading to disruption of Ca<sup>2+</sup> balance and increase in reactive oxygen species (ROS) production/accumulation. Consequently, elevation of Ca2+ and oxidative activates downstream signal pathway p38 MAP Kinase contributing to mitochondrial dysfunction, deficits in axonal mitochondrial trafficking, eventually, synaptic damage.</p
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