cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13292217
title: Quantification of Retinal Microvascular Density Using Optic Coherence Tomography Angiography in Primary Angle Closure Disease

description: <b>Purpose</b>: To evaluate the microvascular density of the peripapillary and parafoveal areas of the eyes with primary angle closure disease (PACD) using optical coherence tomography angiography (OCTA). <b>Materials and methods</b>: An observational study was conducted with 76 PACD patients (29 eyes with primary angle closure suspect, 22 eyes with primary angle closure [PAC], and 25 eyes with primary angle closure glaucoma [PACG]) and 27 control eyes. OCTA was performed for all subjects to acquire a 4.5 × 4.5 mm scanning area centered on the optic discs and a 3 × 3 mm parafoveal cubes. Peripapillary and parafoveal vessel density (VD) were compared between these four groups, and the relationship between VD values and structural and functional changes was evaluated. <b>Results</b>: Among all four groups, the peripapillary VD of the PACG eyes was the lowest in all six sections (all <i>P</i> P P = .01), while their retinal nerve fiber layer (RNFL) and ganglion cell complex thickness were not significantly different than those of the control group (all <i>P</i> &gt; .05). In addition, the stages of PACD, visual field mean deviation, and RNFL thickness were shown to be predictors of the peripapillary VD in the multiple linear regression analysis. <b>Conclusions</b>: The PAC eyes had lower peripapillary VD than normal eyes when their RNFL and GCC thickness did not differ. This suggests that a reduction in retinal VD may occur before structural loss in PAC eyes. Retinal VD measurement may be a useful tool for the assessment of PACD.
DOI: 10.6084/m9.figshare.13292217.v1
title: Quantification of Retinal Microvascular Density Using Optic Coherence Tomography Angiography in Primary Angle Closure Disease

description: <b>Purpose</b>: To evaluate the microvascular density of the peripapillary and parafoveal areas of the eyes with primary angle closure disease (PACD) using optical coherence tomography angiography (OCTA). <b>Materials and methods</b>: An observational study was conducted with 76 PACD patients (29 eyes with primary angle closure suspect, 22 eyes with primary angle closure [PAC], and 25 eyes with primary angle closure glaucoma [PACG]) and 27 control eyes. OCTA was performed for all subjects to acquire a 4.5 × 4.5 mm scanning area centered on the optic discs and a 3 × 3 mm parafoveal cubes. Peripapillary and parafoveal vessel density (VD) were compared between these four groups, and the relationship between VD values and structural and functional changes was evaluated. <b>Results</b>: Among all four groups, the peripapillary VD of the PACG eyes was the lowest in all six sections (all <i>P</i> P P = .01), while their retinal nerve fiber layer (RNFL) and ganglion cell complex thickness were not significantly different than those of the control group (all <i>P</i> &gt; .05). In addition, the stages of PACD, visual field mean deviation, and RNFL thickness were shown to be predictors of the peripapillary VD in the multiple linear regression analysis. <b>Conclusions</b>: The PAC eyes had lower peripapillary VD than normal eyes when their RNFL and GCC thickness did not differ. This suggests that a reduction in retinal VD may occur before structural loss in PAC eyes. Retinal VD measurement may be a useful tool for the assessment of PACD.
DOI: 10.6084/m9.figshare.11708487.v1
title: Cytokine and Chemokine Concentration in the Tear of Patients with Age-Related Cataract

description: The present study measured 41 soluble mediators in the tear of 19 patients with age-related cataract and 32 healthy adults as controls. This was a prospective, case–control study in which, using multiple immunoassays, we measured in tear samples the following molecules: EGF, FGF-2, Eotaxin, TGF-α, G-CSF, Flt-3L, GM-CSF, Fractalkine, IFN-α2, IFN-γ, GRO, IL-10, MCP-3, IL-12p40, MDC, IL-12p70, PDGF-AA, IL-13, PDGF-AB/BB, IL-15, sCD40L, IL-17a, IL-1ra, IL-1α, IL-9, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IP-10, MCP-1, MIP-1α, MIP-1β, RANTES, TNFα, TNFβ, VEGF. Statistical analyses were done by multiple adjusted models and <i>p</i> values were corrected by the Benjamini and Hochberg method. We did not find significant differences in the amount of the tested molecules in the tear fluid between cataract patients and controls. Correlation analyses relative to age were carried out for both groups. Analysis of MCP-1 tear levels revealed a direct correlation with age for normal healthy controls as well as for cataract patients. But IL-6 tear levels correlated with age only in the group of cataract patients. In addition, IL1-ra tear levels correlated with cataract nuclear grade; higher grades were associated with higher IL-1ra concentrations. Our results suggest that ocular aging is accompanied by increased production of IL-6 and MCP-1, which can be measured in tear fluid. AMD: Age-Related Macular Degeneration; EGF: Epidermal growth factor; Eotaxin: Eosinophil chemotactic proteins; FasL: Fas ligand; FGF-2: Basic fibroblast growth factor 2; Flt-3L: Fms related tyrosine kinase 3 ligand; G-CSF: Granulocyte colony stimulating factor; GM-CSF: Granulocyte macrophage colony stimulating factor; GRO: Growth regulated protein; HGF: Human growth factor; ICAM-1: Intercellular adhesion molecule-1; IFNα2: Interferon alpha 2; IFNγ: Interferon gamma; IL: Interleukin; IL-1ra: Interleukin-1 receptor antagonist; IL-12p40: Interleukin-12 subunit p40; IL-12p70: Interleukin-12 subunit p70; IP-10: Interferon gamma-induced protein 10; MCP-1: Monocyte chemotactic protein 1; MCP-3: Monocyte chemotactic protein 3; MDC: Macrophage derived chemokine; MIG: Monokine induced by gamma interferon; MIP-1α: Macrophage inflammatory proteins 1 alpha; MIP-1β: Macrophage inflammatory proteins 1 beta; MMPs: Matrix metalloproteinases; MMP-9: Matrix metalloproteinase 9; PAI1: Plasminogen activator inhibitor 1; PDGF-AA: Platelet-derived growth factor subunit AA; PDGF-AB/BB: Platelet-derived growth factor subunit AB and BB; PIGF: Placenta growth factor; RANTES: Regulated on activation, normal T cell expressed and secreted; SAA: Serum amyloid A; sCD40L: Soluble CD40 ligand; sTNF-RII: Soluble tumor necrosis factor receptor; TBUT Tear breakup time; TGF-α: Transforming growth factor alpha; TGF-β: Transforming growth factor beta; TNFα: Tumor necrosis factor alpha; TNFβ: Tumor necrosis factor beta; VCAM: Vascular cell adhesion molecule; VEGF: Vascular endothelium growth factor
DOI: 10.6084/m9.figshare.11708487
title: Cytokine and Chemokine Concentration in the Tear of Patients with Age-Related Cataract

description: The present study measured 41 soluble mediators in the tear of 19 patients with age-related cataract and 32 healthy adults as controls. This was a prospective, case–control study in which, using multiple immunoassays, we measured in tear samples the following molecules: EGF, FGF-2, Eotaxin, TGF-α, G-CSF, Flt-3L, GM-CSF, Fractalkine, IFN-α2, IFN-γ, GRO, IL-10, MCP-3, IL-12p40, MDC, IL-12p70, PDGF-AA, IL-13, PDGF-AB/BB, IL-15, sCD40L, IL-17a, IL-1ra, IL-1α, IL-9, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IP-10, MCP-1, MIP-1α, MIP-1β, RANTES, TNFα, TNFβ, VEGF. Statistical analyses were done by multiple adjusted models and <i>p</i> values were corrected by the Benjamini and Hochberg method. We did not find significant differences in the amount of the tested molecules in the tear fluid between cataract patients and controls. Correlation analyses relative to age were carried out for both groups. Analysis of MCP-1 tear levels revealed a direct correlation with age for normal healthy controls as well as for cataract patients. But IL-6 tear levels correlated with age only in the group of cataract patients. In addition, IL1-ra tear levels correlated with cataract nuclear grade; higher grades were associated with higher IL-1ra concentrations. Our results suggest that ocular aging is accompanied by increased production of IL-6 and MCP-1, which can be measured in tear fluid. AMD: Age-Related Macular Degeneration; EGF: Epidermal growth factor; Eotaxin: Eosinophil chemotactic proteins; FasL: Fas ligand; FGF-2: Basic fibroblast growth factor 2; Flt-3L: Fms related tyrosine kinase 3 ligand; G-CSF: Granulocyte colony stimulating factor; GM-CSF: Granulocyte macrophage colony stimulating factor; GRO: Growth regulated protein; HGF: Human growth factor; ICAM-1: Intercellular adhesion molecule-1; IFNα2: Interferon alpha 2; IFNγ: Interferon gamma; IL: Interleukin; IL-1ra: Interleukin-1 receptor antagonist; IL-12p40: Interleukin-12 subunit p40; IL-12p70: Interleukin-12 subunit p70; IP-10: Interferon gamma-induced protein 10; MCP-1: Monocyte chemotactic protein 1; MCP-3: Monocyte chemotactic protein 3; MDC: Macrophage derived chemokine; MIG: Monokine induced by gamma interferon; MIP-1α: Macrophage inflammatory proteins 1 alpha; MIP-1β: Macrophage inflammatory proteins 1 beta; MMPs: Matrix metalloproteinases; MMP-9: Matrix metalloproteinase 9; PAI1: Plasminogen activator inhibitor 1; PDGF-AA: Platelet-derived growth factor subunit AA; PDGF-AB/BB: Platelet-derived growth factor subunit AB and BB; PIGF: Placenta growth factor; RANTES: Regulated on activation, normal T cell expressed and secreted; SAA: Serum amyloid A; sCD40L: Soluble CD40 ligand; sTNF-RII: Soluble tumor necrosis factor receptor; TBUT Tear breakup time; TGF-α: Transforming growth factor alpha; TGF-β: Transforming growth factor beta; TNFα: Tumor necrosis factor alpha; TNFβ: Tumor necrosis factor beta; VCAM: Vascular cell adhesion molecule; VEGF: Vascular endothelium growth factor
DOI: 10.6084/m9.figshare.12850067
title: Transferrin isoforms analysis by capillary electrophoresis in systemic lupus erythematosus and systemic sclerosis

description: The systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are a diseases in which disturbances in plasma proteins glycosylation exist. The aim of the study was to compare the serum profile of transferrin isoforms between SLE and SSc. The study was carried out in 38 patients with SLE and 43 patients with SSc. Transferrin isoforms were analyzed by capillary electrophoresis method. Among the transferrin isoforms only the level of pentasialotransferrin in SLE patients was significantly higher than in SSc patients (<i>p</i> = .014). The median concentrations of trisialotransferrin and pentasialotransferrin were significantly lower in SLE patients (<i>p</i> p = .042; respectively) and SSc (<i>p</i> = .001, <i>p</i> p
DOI: 10.6084/m9.figshare.12850067.v1
title: Transferrin isoforms analysis by capillary electrophoresis in systemic lupus erythematosus and systemic sclerosis

description: The systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are a diseases in which disturbances in plasma proteins glycosylation exist. The aim of the study was to compare the serum profile of transferrin isoforms between SLE and SSc. The study was carried out in 38 patients with SLE and 43 patients with SSc. Transferrin isoforms were analyzed by capillary electrophoresis method. Among the transferrin isoforms only the level of pentasialotransferrin in SLE patients was significantly higher than in SSc patients (<i>p</i> = .014). The median concentrations of trisialotransferrin and pentasialotransferrin were significantly lower in SLE patients (<i>p</i> p = .042; respectively) and SSc (<i>p</i> = .001, <i>p</i> p
DOI: 10.6084/m9.figshare.12982474
title: Reproducibility of the CO rebreathing technique with a lower CO dose and a shorter rebreathing duration at sea level and at 2320 m of altitude

description: Total hemoglobin mass (Hb<sub>mass</sub>) is routinely assessed in studies by the carbon monoxide (CO) rebreathing. Its clinical application is often hindered due to the consequent rise in carboxyhemoglobin (%HbCO) and the concern of CO toxicity. We tested the reproducibility of the CO rebreathing with a CO dose of 0.5 mL/kg body mass (CO<sub>0.5</sub>) compared to 1.5 mL/kg (CO<sub>1.5</sub>) and when shortening the CO rebreathing protocol. Therefore, CO rebreathing was performed 1×/day in eight healthy individuals on four consecutive days. On each day, either CO<sub>0.5</sub> (CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2) or CO<sub>1.5</sub> (CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2) was administered. Venous blood samples to determine %HbCO and quantify Hb<sub>mass</sub> were obtained prior to, and at 6 (T<sub>6</sub>), 8 (T<sub>8</sub>) and 10 min (T<sub>10</sub>) of CO rebreathing. This protocol was tested at sea level and at 2320 m to investigate the altitude-related measurement error. At sea level, the mean difference (95% limits of agreement) in Hb<sub>mass</sub> between CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2 was 26 g (–26; 79 g) and between CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2, it was 17 g (–18; 52 g)<sub>.</sub> The respective typical error (TE) corresponded to 2.4% (CO<sub>0.5</sub>) and 1.5% (CO<sub>1.5</sub>), while it was 6.5% and 3.0% at 2320 m. With CO<sub>0.5</sub>, shortening the CO rebreathing resulted in a TE for Hb<sub>mass</sub> of 4.4% (T<sub>8</sub> vs. T<sub>10</sub>) and 14.1% (T<sub>6</sub> vs T<sub>10</sub>) and with CO<sub>1.5</sub>, TE was 1.6% and 5.8%. In conclusion, the CO dose and rebreathing time for the CO rebreathing procedure can be decreased at the cost of a measurement error ranging from 1.5-14.1%.
DOI: 10.6084/m9.figshare.12982474.v2
title: Reproducibility of the CO rebreathing technique with a lower CO dose and a shorter rebreathing duration at sea level and at 2320 m of altitude

description: Total hemoglobin mass (Hb<sub>mass</sub>) is routinely assessed in studies by the carbon monoxide (CO) rebreathing. Its clinical application is often hindered due to the consequent rise in carboxyhemoglobin (%HbCO) and the concern of CO toxicity. We tested the reproducibility of the CO rebreathing with a CO dose of 0.5 mL/kg body mass (CO<sub>0.5</sub>) compared to 1.5 mL/kg (CO<sub>1.5</sub>) and when shortening the CO rebreathing protocol. Therefore, CO rebreathing was performed 1×/day in eight healthy individuals on four consecutive days. On each day, either CO<sub>0.5</sub> (CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2) or CO<sub>1.5</sub> (CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2) was administered. Venous blood samples to determine %HbCO and quantify Hb<sub>mass</sub> were obtained prior to, and at 6 (T<sub>6</sub>), 8 (T<sub>8</sub>) and 10 min (T<sub>10</sub>) of CO rebreathing. This protocol was tested at sea level and at 2320 m to investigate the altitude-related measurement error. At sea level, the mean difference (95% limits of agreement) in Hb<sub>mass</sub> between CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2 was 26 g (–26; 79 g) and between CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2, it was 17 g (–18; 52 g)<sub>.</sub> The respective typical error (TE) corresponded to 2.4% (CO<sub>0.5</sub>) and 1.5% (CO<sub>1.5</sub>), while it was 6.5% and 3.0% at 2320 m. With CO<sub>0.5</sub>, shortening the CO rebreathing resulted in a TE for Hb<sub>mass</sub> of 4.4% (T<sub>8</sub> vs. T<sub>10</sub>) and 14.1% (T<sub>6</sub> vs T<sub>10</sub>) and with CO<sub>1.5</sub>, TE was 1.6% and 5.8%. In conclusion, the CO dose and rebreathing time for the CO rebreathing procedure can be decreased at the cost of a measurement error ranging from 1.5-14.1%.
DOI: 10.6084/m9.figshare.12982474.v1
title: Reproducibility of the CO rebreathing technique with a lower CO dose and a shorter rebreathing duration at sea level and at 2320 m of altitude

description: Total hemoglobin mass (Hb<sub>mass</sub>) is routinely assessed in studies by the carbon monoxide (CO) rebreathing. Its clinical application is often hindered due to the consequent rise in carboxyhemoglobin (%HbCO) and the concern of CO toxicity. We tested the reproducibility of the CO rebreathing with a CO dose of 0.5 mL/kg body mass (CO<sub>0.5</sub>) compared to 1.5 mL/kg (CO<sub>1.5</sub>) and when shortening the CO rebreathing protocol. Therefore, CO rebreathing was performed 1×/day in eight healthy individuals on four consecutive days. On each day, either CO<sub>0.5</sub> (CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2) or CO<sub>1.5</sub> (CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2) was administered. Venous blood samples to determine %HbCO and quantify Hb<sub>mass</sub> were obtained prior to, and at 6 (T<sub>6</sub>), 8 (T<sub>8</sub>) and 10 min (T<sub>10</sub>) of CO rebreathing. This protocol was tested at sea level and at 2320 m to investigate the altitude-related measurement error. At sea level, the mean difference (95% limits of agreement) in Hb<sub>mass</sub> between CO<sub>0.5</sub>-1 and CO<sub>0.5</sub>-2 was 26 g (–26; 79 g) and between CO<sub>1.5</sub>-1 and CO<sub>1.5</sub>-2, it was 17 g (–18; 52 g)<sub>.</sub> The respective typical error (TE) corresponded to 2.4% (CO<sub>0.5</sub>) and 1.5% (CO<sub>1.5</sub>), while it was 6.5% and 3.0% at 2320 m. With CO<sub>0.5</sub>, shortening the CO rebreathing resulted in a TE for Hb<sub>mass</sub> of 4.4% (T<sub>8</sub> vs. T<sub>10</sub>) and 14.1% (T<sub>6</sub> vs T<sub>10</sub>) and with CO<sub>1.5</sub>, TE was 1.6% and 5.8%. In conclusion, the CO dose and rebreathing time for the CO rebreathing procedure can be decreased at the cost of a measurement error ranging from 1.5-14.1%.
DOI: 10.6084/m9.figshare.9742214
title: Stanniocalcin-1 is a Modifier of Oxygen-Induced Retinopathy Severity

description: Abnormal activation of signaling pathways related to angiogenesis, inflammation, and oxidative stress has been implicated in the pathophysiology of retinopathy of prematurity (ROP), a leading cause of blindness in pre-term infants. Therapies for ROP include laser and anti-vascular endothelial growth factor agents. However, these therapies have side effects, and even with adequate treatment, visual acuity can be impaired. Novel therapeutic options are needed. Stanniocalcin-1 (STC-1) is a neuroprotective protein with anti-inflammatory and anti-oxidative stress properties. Rodent models of oxygen-induced retinopathy (OIR) were selected to determine whether STC-1 plays a role in the development of OIR. STC-1 gene and protein expression was first evaluated in the Sprague Dawley rat OIR model that is most similar to human ROP. OIR was then induced in wild-type and <i>Stc-1<sup>−/-</sup></i> mice. Retinas were isolated and evaluated for avascular and neovascular area on retinal flat mounts. Quantification of gene expression by quantitative real-time PCR was performed. VEGF was assayed by ELISA in media obtained from induced pluripotent stem-cell-derived retinal pigment epithelial (iPS-RPE) cells following treatment with recombinant STC-1. STC-1 was significantly upregulated in a rat model of OIR compared to room air controls at the gene (<i>P</i> &lt; .05) and protein (<i>P</i> &lt; .001) level. <i>Stc-1<sup>−/-</sup></i> OIR mice showed significantly worse ROP compared to wild-type mice as assessed by avascular (20.2 ± 2.4% vs 15.2 ± 2.5%; <i>P</i> = .02) and neovascular area (14.3 ± 2.7% vs 8.8 ± 3.7%; <i>P</i> &lt; .05). Transcript levels of vascular endothelial growth factor-A were significantly higher in <i>Stc-1<sup>−/-</sup></i> OIR mice compared to wild-type controls (<i>P</i> = .03). STC-1 reduced VEGF production in iPS-RPE cells (<i>P</i> = .01). STC-1 plays a role in the OIR stress response and development of pathologic vascular features in rodent OIR models by regulating VEGF levels.
DOI: 10.6084/m9.figshare.12865583
title: Strain Specific Responses in a Microbead Rat Model of Experimental Glaucoma

description: A major challenge in glaucoma research is the lack of reproducible animal models of RGC and optic nerve damage, the characteristic features of this condition. We therefore examined the glaucomatous responses of two different rat strains, the Brown Norway (BN) and Lister Hooded (LH) rats, to high intraocular pressure (IOP) induced by injection of magnetic beads into the anterior chamber. Magnetic microsphere suspensions (20 µl of 5–20 mg/ml) were injected into the anterior chamber of BN (n = 9) or LH (N = 15) rats. Animals from each strain were divided into three groups, each receiving a different dose of microspheres. IOP was measured over 4 weeks using a rebound tonometer. Retinal ganglion cell (RGC) damage and function were assessed using scotopic electroretinograms (ERGs), retinal flatmounts and optic nerve histology. ANOVA and Student’s <i>t</i>-tests were used to analyse the data. A significant elevation in IOP was observed in BN rats receiving injections of 20 mg (37.18 ± 12.28 mmHg) or 10 mg microspheres/ml (36.95 ± 13.63 mmHg) when compared with controls (19.63 ± 4.29 mmHg) (<i>p</i> p p P p p Although this model was easily reproducible in BN rats, the phenotype of injury observed in LH rats was very different from that observed in BN animals. We suggest that differences in the glaucomatous response observed in these two strains may be ascribed to anatomical and physiological differences and merits further investigation.
DOI: 10.6084/m9.figshare.12865583.v1
title: Strain Specific Responses in a Microbead Rat Model of Experimental Glaucoma

description: A major challenge in glaucoma research is the lack of reproducible animal models of RGC and optic nerve damage, the characteristic features of this condition. We therefore examined the glaucomatous responses of two different rat strains, the Brown Norway (BN) and Lister Hooded (LH) rats, to high intraocular pressure (IOP) induced by injection of magnetic beads into the anterior chamber. Magnetic microsphere suspensions (20 µl of 5–20 mg/ml) were injected into the anterior chamber of BN (n = 9) or LH (N = 15) rats. Animals from each strain were divided into three groups, each receiving a different dose of microspheres. IOP was measured over 4 weeks using a rebound tonometer. Retinal ganglion cell (RGC) damage and function were assessed using scotopic electroretinograms (ERGs), retinal flatmounts and optic nerve histology. ANOVA and Student’s <i>t</i>-tests were used to analyse the data. A significant elevation in IOP was observed in BN rats receiving injections of 20 mg (37.18 ± 12.28 mmHg) or 10 mg microspheres/ml (36.95 ± 13.63 mmHg) when compared with controls (19.63 ± 4.29 mmHg) (<i>p</i> p p P p p Although this model was easily reproducible in BN rats, the phenotype of injury observed in LH rats was very different from that observed in BN animals. We suggest that differences in the glaucomatous response observed in these two strains may be ascribed to anatomical and physiological differences and merits further investigation.