parallel ankle rehabilitation robot with joint-space force distribution Search Results


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Demographic and Baseline Characteristics of the Intent-to-Treat Population
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Demographic and Baseline Characteristics of the Intent-to-Treat Population
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Association between <t> joint space narrowing </t> <t> (JSN) </t> progression and bone marrow lesion (BML) volume change
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Association between <t> joint space narrowing </t> <t> (JSN) </t> progression and bone marrow lesion (BML) volume change
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Association between <t> joint space narrowing </t> <t> (JSN) </t> progression and bone marrow lesion (BML) volume change
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Association between <t> joint space narrowing </t> <t> (JSN) </t> progression and bone marrow lesion (BML) volume change
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PeproTech recombinant murine cxcl1 (kc)
Sdc-3 deletion reduces neutrophil recruitment in <t>CXCL1-injected</t> joints. Sdc-3 null and wild-type mice were injected intra-articularly with 3 μg per knee joint of recombinant murine CXCL1 or PBS and after 4 hours processed for histology. (A) Haematoxylin and eosin staining reveals neutrophil recruitment in the synovium following CXCL1 administration with PBS injected as control; insets show detail of synovium. Results are shown from a wild-type joint. Scale bar 500 μm (for inserts 50 μm). (B) Decrease in the number of recruited neutrophils in sdc-3−/−mice compared to wild-type animals following CXCL1 administration. Data are means ± SEM, n = 8 mice per treatment. *** P <0.0001 comparing CXCL1-injected joints. (C) Sdc-3 immunolocalises to the blood vessel in synovium of wild-type mice. (D) is the same image as (C) stained for DAPI to show cell nuclei. (E) absent staining for sdc-3 in a blood vessel in sdc-3 −/−synovium. (F) is the same image as (E) stained for DAPI to show cell nuclei. (G) is a negative control of the synovium of wild-type mouse in the absence of sdc-3 antibody and (H) is the same area stained for DAPI to show the presence of blood vessels. Bar =120 μm in C to H. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.
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Coriolis Pharma symmetric positive definite mass matrix
Sdc-3 deletion reduces neutrophil recruitment in <t>CXCL1-injected</t> joints. Sdc-3 null and wild-type mice were injected intra-articularly with 3 μg per knee joint of recombinant murine CXCL1 or PBS and after 4 hours processed for histology. (A) Haematoxylin and eosin staining reveals neutrophil recruitment in the synovium following CXCL1 administration with PBS injected as control; insets show detail of synovium. Results are shown from a wild-type joint. Scale bar 500 μm (for inserts 50 μm). (B) Decrease in the number of recruited neutrophils in sdc-3−/−mice compared to wild-type animals following CXCL1 administration. Data are means ± SEM, n = 8 mice per treatment. *** P <0.0001 comparing CXCL1-injected joints. (C) Sdc-3 immunolocalises to the blood vessel in synovium of wild-type mice. (D) is the same image as (C) stained for DAPI to show cell nuclei. (E) absent staining for sdc-3 in a blood vessel in sdc-3 −/−synovium. (F) is the same image as (E) stained for DAPI to show cell nuclei. (G) is a negative control of the synovium of wild-type mouse in the absence of sdc-3 antibody and (H) is the same area stained for DAPI to show the presence of blood vessels. Bar =120 μm in C to H. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.
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Image Search Results


Demographic and Baseline Characteristics of the Intent-to-Treat Population

Journal: JAMA

Article Title: Effect of Intra-Articular Sprifermin vs Placebo on Femorotibial Joint Cartilage Thickness in Patients With Osteoarthritis

doi: 10.1001/jama.2019.14735

Figure Lengend Snippet: Demographic and Baseline Characteristics of the Intent-to-Treat Population

Article Snippet: Knee minimum joint space width was measured in the medial and lateral femorotibial compartments using the BioClinica knee joint space width tool, which is a component of the StudyDirect reading system.

Techniques: Biomarker Discovery

Association between  joint space narrowing   (JSN)  progression and bone marrow lesion (BML) volume change

Journal: Arthritis Research & Therapy

Article Title: Evaluation of bone marrow lesion volume as a knee osteoarthritis biomarker - longitudinal relationships with pain and structural changes: data from the Osteoarthritis Initiative

doi: 10.1186/ar4292

Figure Lengend Snippet: Association between joint space narrowing (JSN) progression and bone marrow lesion (BML) volume change

Article Snippet: These JSN scores are publicly available (Files: kXR_SQ_BU03_SAS(version 3.4) and kXR_SQ_BU06_SAS (version 6.20) [ ].

Techniques:

Sdc-3 deletion reduces neutrophil recruitment in CXCL1-injected joints. Sdc-3 null and wild-type mice were injected intra-articularly with 3 μg per knee joint of recombinant murine CXCL1 or PBS and after 4 hours processed for histology. (A) Haematoxylin and eosin staining reveals neutrophil recruitment in the synovium following CXCL1 administration with PBS injected as control; insets show detail of synovium. Results are shown from a wild-type joint. Scale bar 500 μm (for inserts 50 μm). (B) Decrease in the number of recruited neutrophils in sdc-3−/−mice compared to wild-type animals following CXCL1 administration. Data are means ± SEM, n = 8 mice per treatment. *** P <0.0001 comparing CXCL1-injected joints. (C) Sdc-3 immunolocalises to the blood vessel in synovium of wild-type mice. (D) is the same image as (C) stained for DAPI to show cell nuclei. (E) absent staining for sdc-3 in a blood vessel in sdc-3 −/−synovium. (F) is the same image as (E) stained for DAPI to show cell nuclei. (G) is a negative control of the synovium of wild-type mouse in the absence of sdc-3 antibody and (H) is the same area stained for DAPI to show the presence of blood vessels. Bar =120 μm in C to H. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.

Journal: Arthritis Research & Therapy

Article Title: Syndecan-3 is selectively pro-inflammatory in the joint and contributes to antigen-induced arthritis in mice

doi: 10.1186/ar4610

Figure Lengend Snippet: Sdc-3 deletion reduces neutrophil recruitment in CXCL1-injected joints. Sdc-3 null and wild-type mice were injected intra-articularly with 3 μg per knee joint of recombinant murine CXCL1 or PBS and after 4 hours processed for histology. (A) Haematoxylin and eosin staining reveals neutrophil recruitment in the synovium following CXCL1 administration with PBS injected as control; insets show detail of synovium. Results are shown from a wild-type joint. Scale bar 500 μm (for inserts 50 μm). (B) Decrease in the number of recruited neutrophils in sdc-3−/−mice compared to wild-type animals following CXCL1 administration. Data are means ± SEM, n = 8 mice per treatment. *** P <0.0001 comparing CXCL1-injected joints. (C) Sdc-3 immunolocalises to the blood vessel in synovium of wild-type mice. (D) is the same image as (C) stained for DAPI to show cell nuclei. (E) absent staining for sdc-3 in a blood vessel in sdc-3 −/−synovium. (F) is the same image as (E) stained for DAPI to show cell nuclei. (G) is a negative control of the synovium of wild-type mouse in the absence of sdc-3 antibody and (H) is the same area stained for DAPI to show the presence of blood vessels. Bar =120 μm in C to H. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.

Article Snippet: Mice were injected intradermally or intra-articularly in the knee joint space with recombinant murine CXCL1 (KC) (PeproTech, London, UK) 3 μg/site in phosphate-buffered saline (PBS) [ ].

Techniques: Injection, Recombinant, Staining, Control, Negative Control, Saline

Reduced chemokine presentation by synovial endothelial cells in sdc-3−/−mice. In the same samples as in Figure sections of CXCL1-injected joints of wild-type and sdc-3−/−mice were stained with a CXCL1 antibody using tyramide amplification, and DAPI, and viewed by immunofluorescence. (A and B) Synovial endothelial cells of wild-type mouse joint; CXCL1 occurs as clusters with white arrows showing examples of luminal chemokine and red arrows intracellular or abluminal chemokine. The endothelial cell layer is labelled (e) and the lumen of the blood vessel (L) containing red blood cells. (C) No CXCL1 clusters are present in the endothelial cells of PBS-injected controls (arrows); this image is from a wild-type mouse. ( D ) There are less CXCL1 clusters in endothelial cells of following treatment with heparanase I and III to degrade heparan sulphate prior to immunostaining. (E) is a negative control of the synovium of wild-type mouse in the absence of CXCL1 antibody. Bar = 30 μm in A to E. (F) Quantification of CXCL1 staining shows decrease in the numbers of endothelial CXCL1 clusters per blood vessel in sdc-3−/− (n = 6) compared to wild-type (n = 6) joints. Data are mean ± SEM. *** P = 0.0003. (G) shows the data in (F) expressed as number of CXCL1 clusters at the luminal surface or intracellularly/abluminally in synovial endothelial cells. There is a reduction of the numbers of luminal CXCL1 clusters in sdc-3−/−mice compared to wild type, *** P = 0.0002. Data are means ± SEM. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.

Journal: Arthritis Research & Therapy

Article Title: Syndecan-3 is selectively pro-inflammatory in the joint and contributes to antigen-induced arthritis in mice

doi: 10.1186/ar4610

Figure Lengend Snippet: Reduced chemokine presentation by synovial endothelial cells in sdc-3−/−mice. In the same samples as in Figure sections of CXCL1-injected joints of wild-type and sdc-3−/−mice were stained with a CXCL1 antibody using tyramide amplification, and DAPI, and viewed by immunofluorescence. (A and B) Synovial endothelial cells of wild-type mouse joint; CXCL1 occurs as clusters with white arrows showing examples of luminal chemokine and red arrows intracellular or abluminal chemokine. The endothelial cell layer is labelled (e) and the lumen of the blood vessel (L) containing red blood cells. (C) No CXCL1 clusters are present in the endothelial cells of PBS-injected controls (arrows); this image is from a wild-type mouse. ( D ) There are less CXCL1 clusters in endothelial cells of following treatment with heparanase I and III to degrade heparan sulphate prior to immunostaining. (E) is a negative control of the synovium of wild-type mouse in the absence of CXCL1 antibody. Bar = 30 μm in A to E. (F) Quantification of CXCL1 staining shows decrease in the numbers of endothelial CXCL1 clusters per blood vessel in sdc-3−/− (n = 6) compared to wild-type (n = 6) joints. Data are mean ± SEM. *** P = 0.0003. (G) shows the data in (F) expressed as number of CXCL1 clusters at the luminal surface or intracellularly/abluminally in synovial endothelial cells. There is a reduction of the numbers of luminal CXCL1 clusters in sdc-3−/−mice compared to wild type, *** P = 0.0002. Data are means ± SEM. CXCL1, chemokine C-X-C ligand 1; DAPI, 4',6-diamidino-2-phenylindole; PBS, phosphate-buffered saline.

Article Snippet: Mice were injected intradermally or intra-articularly in the knee joint space with recombinant murine CXCL1 (KC) (PeproTech, London, UK) 3 μg/site in phosphate-buffered saline (PBS) [ ].

Techniques: Injection, Staining, Amplification, Immunofluorescence, Immunostaining, Negative Control, Saline

Leukocyte migration after intradermal injection of CXCL1 in sdc-3 null and wild-type mice and altered distribution of E-selectin. (A) Mice were injected intradermally with recombinant murine CXCL1 (3 μg/site in PBS) or PBS as control. After four hours the animals were sacrificed and skin biopsies were processed for light microscopy. Haematoxylin and eosin staining of skin sections show neutrophil recruitment into the dermis in sdc-3−/− (mid panel) and sdc-3+/+ (right panel) mice. The left micrograph shows skin from an sdc-3−/−mouse following PBS administration. Scale bar 50 μm. (B) Using the same samples as in (A) lysates were prepared from skin biopsies and myeloperoxidase (MPO) activity measured as a marker for the presence of neutrophils. Increased MPO activity is observed in sdc-3−/−compared to sdc-3+/+skin tissue. For sdc-3−/−mice n = 9 with CXCL1 and with PBS, and for sdc-3+/+mice n = 10 with CXCL1 and with PBS. Data are means ± SEM. * P <0.03 compared with CXCL1 injected sdc-3+/+mice. # P <0.005 compared to respective PBS control. (C and D) Sdc-3 staining of endothelial cells is shown in a dermal venule from a wild-type mouse. (E and F) E-selectin shows a luminal distribution in the endothelial cells of the dermis after PBS (E) and CXCL1 (F) administration, this section is from a sdc-3−/−mouse. Scale bar 50 μm for E-selectin and 25 μm for sdc-3 micrographs. (G) Quantification of the number of blood vessels with a luminal E-selectin distribution in the dermis of sdc-3+/+ (n = 8) compared to sdc-3−/− (n = 9) mice. Data are mean ± SEM, ** P <0.008 compared to sdc-3 wild-type mice. CXCL1, chemokine C-X-C ligand 1; PBS, phosphate-buffered saline.

Journal: Arthritis Research & Therapy

Article Title: Syndecan-3 is selectively pro-inflammatory in the joint and contributes to antigen-induced arthritis in mice

doi: 10.1186/ar4610

Figure Lengend Snippet: Leukocyte migration after intradermal injection of CXCL1 in sdc-3 null and wild-type mice and altered distribution of E-selectin. (A) Mice were injected intradermally with recombinant murine CXCL1 (3 μg/site in PBS) or PBS as control. After four hours the animals were sacrificed and skin biopsies were processed for light microscopy. Haematoxylin and eosin staining of skin sections show neutrophil recruitment into the dermis in sdc-3−/− (mid panel) and sdc-3+/+ (right panel) mice. The left micrograph shows skin from an sdc-3−/−mouse following PBS administration. Scale bar 50 μm. (B) Using the same samples as in (A) lysates were prepared from skin biopsies and myeloperoxidase (MPO) activity measured as a marker for the presence of neutrophils. Increased MPO activity is observed in sdc-3−/−compared to sdc-3+/+skin tissue. For sdc-3−/−mice n = 9 with CXCL1 and with PBS, and for sdc-3+/+mice n = 10 with CXCL1 and with PBS. Data are means ± SEM. * P <0.03 compared with CXCL1 injected sdc-3+/+mice. # P <0.005 compared to respective PBS control. (C and D) Sdc-3 staining of endothelial cells is shown in a dermal venule from a wild-type mouse. (E and F) E-selectin shows a luminal distribution in the endothelial cells of the dermis after PBS (E) and CXCL1 (F) administration, this section is from a sdc-3−/−mouse. Scale bar 50 μm for E-selectin and 25 μm for sdc-3 micrographs. (G) Quantification of the number of blood vessels with a luminal E-selectin distribution in the dermis of sdc-3+/+ (n = 8) compared to sdc-3−/− (n = 9) mice. Data are mean ± SEM, ** P <0.008 compared to sdc-3 wild-type mice. CXCL1, chemokine C-X-C ligand 1; PBS, phosphate-buffered saline.

Article Snippet: Mice were injected intradermally or intra-articularly in the knee joint space with recombinant murine CXCL1 (KC) (PeproTech, London, UK) 3 μg/site in phosphate-buffered saline (PBS) [ ].

Techniques: Migration, Injection, Recombinant, Control, Light Microscopy, Staining, Activity Assay, Marker, Saline

Increased rolling and adhesion of leukocytes in cremaster muscle post-capillary venules (PCV) in sdc-3 null mice by intravital microscopy. (A) Significant increases in leukocyte rolling are observed in TNFα-stimulated sdc-3−/−mice when compared to either TNFα-stimulated wild-type (WT) or unstimulated syn-3−/−mice. Similarly, CXCL1 stimulation induces greater rolling in sdc-3−/−mice. (B) Similar increases in leukocyte adhesion are observed in TNFα- and CXCL1-stimulated sdc-3−/−mice. Data are means ± SEM, n = 3 to 6 mice per treatment. * P <0.05; ** P <0.01. CXCL1, chemokine C-X-C ligand 1; TNFα, tumour necrosis factor alpha.

Journal: Arthritis Research & Therapy

Article Title: Syndecan-3 is selectively pro-inflammatory in the joint and contributes to antigen-induced arthritis in mice

doi: 10.1186/ar4610

Figure Lengend Snippet: Increased rolling and adhesion of leukocytes in cremaster muscle post-capillary venules (PCV) in sdc-3 null mice by intravital microscopy. (A) Significant increases in leukocyte rolling are observed in TNFα-stimulated sdc-3−/−mice when compared to either TNFα-stimulated wild-type (WT) or unstimulated syn-3−/−mice. Similarly, CXCL1 stimulation induces greater rolling in sdc-3−/−mice. (B) Similar increases in leukocyte adhesion are observed in TNFα- and CXCL1-stimulated sdc-3−/−mice. Data are means ± SEM, n = 3 to 6 mice per treatment. * P <0.05; ** P <0.01. CXCL1, chemokine C-X-C ligand 1; TNFα, tumour necrosis factor alpha.

Article Snippet: Mice were injected intradermally or intra-articularly in the knee joint space with recombinant murine CXCL1 (KC) (PeproTech, London, UK) 3 μg/site in phosphate-buffered saline (PBS) [ ].

Techniques: Intravital Microscopy