One such candidate is MMP2, activated by MT1-MMP, which showed increased expression at nighttime in orchestrating physiologic desquamation of surface corneal epithelial cells [36]
One such candidate is MMP2, activated by MT1-MMP, which showed increased expression at nighttime in orchestrating physiologic desquamation of surface corneal epithelial cells [36]. apnea, cancer or control patients were compared for enhancement of inhibitory effects on endothelial cell survival. Size exclusion chromatography performed (in the presence or absence of a specific membrane type 1-matrix metalloproteinase inhibitor) was used to characterize the IgG autoantibody subunit(s) or fragments associated with peak neurotoxicity in diabetic obstructive sleep apnea. 1.3 Results Diabetic obstructive sleep apnea (n = 14) autoantibodies caused a significant increase (P = 0.01) in membrane depolarization in N2a mouse neuroblastoma cells compared to control diabetic patients (n = 15) not suffering with obstructive sleep apnea. Process extension in N2A mouse neuroblastoma cells was significantly inhibited (P = 0.01) by diabetic obstructive sleep apnea (n = 9) autoantibodies compared to effects from identical 10 5.5 kD putative light chain fragment. 1.4 Conclusions These results suggest that diabetic obstructive sleep apnea autoantibodies may induce strong depolarization in neuronal cells and alter Ca2+ signaling in atrial cardiomyocytes consistent with a role in pathophysiology in subsets of diabetic obstructive sleep apnea having co-morbid atrial fibrillation or another clinically significant cardiac rhythm disturbance. 13.364.6 7.70.71BMI9.330.5 6.60.008DepressionSD of triplicate determinations) compared to neurite expression in cells grown with 10 ng/mL human bFGF, but without added test protein-A-eluate fractions. 3.8 Membrane depolarization assays After cell attachment, growth medium was removed and cells were washed and then incubated in modified Tyrodes solution consisting of: 150 mM NaCl, 3 mM KCL and 30 mM HEPES, 10 mM D-glucose and 2 mM CaCL2, pH 7.4. Test fractions (human IgG fractions) were added in the presence of 97 nM DiBAC4 (Molecular Probes, Eugene, OR) – as previously reported [6]. Fluorescence was measured after 5 min or longer at room temp using a Fluoroskan Ascent FL (VWR, Inc., Franklin, MA); Ex = 485 nm, Em = 538 nm. Results are expressed as percent of change in gross fluorescence compared to cells to which no test protein-A-eluate fractions were added. 3.9 HL-1 cell culture HL-1 atrial cardiomyocytes were developed (and generously provided) by Dr. William Claycomb (Louisiana State University Medical Center, New Orleans, LA). They were maintained in 5% CO2/95% air at 37C in Claycomb media (Sigma, St. Louis, MO) containing 10% FBS (Biocell, Rancho Dominguez, CA), 100 U/mL:100 ug/mL penicillin-streptomycin (Invitrogen, Carlsbad, CA), 0.1 mM norepinephrine (Sigma, St. Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were grown in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast cancer (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open in a separate window ?T-test: comparing activity before and after storage space ??P = 0.02: in comparison to nondiabetic settings 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior research, top neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates got apparent MWs related to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. In today’s study, maximum neurotoxicity in diabetic OSA/atrial fibrillation protein-A-eluates, (we.e. Pts 1, 2) got obvious MWs of 5.5 kD (Figure 3A). Yet another neurotoxic maximum inside a third diabetic OSA/AF individual had obvious MW11 kD. 4.6 Diabetic OSA autoantibodies induce Ca2+ launch in HL-1 atrial cardiomyocytes Proteins A eluates (1 5.5 kD (Fig 5A). Protein-A-eluates subjected to NSC405020 shown a change in maximum neurotoxicity toward an increased MW varieties (43 kd) (Shape 5B). Open up in another window Shape 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two individuals having diabetes, obstructive rest apnea, and a neurodegenerative disorder, i.e. glaucoma (Pt 6), dementia and melancholy (Pt 7) pursuing incubation in the lack(A) or existence (B) of a particular MT1-MMP inhibitor. A) Maximum neurotoxicity in the autoantibodies incubated without MT1-MMP inhibitor got obvious MW of 5.5 kD. B) MT1-MMP inhibition was connected with a change in maximum neurotoxicity toward higher MW varieties, i.e. 43 kD corresponding to.Nocturnal peak (@ 2300 hours) in endothelial cell inhibitory activity was particular to autoantibody-containing fraction of plasma in type 1 diabetes having neuropsychiatric/neurodegenerative co-morbidities. with maximum neurotoxicity in diabetic obstructive rest apnea. 1.3 Outcomes Diabetic obstructive rest apnea (n = 14) autoantibodies triggered a substantial increase (P = 0.01) in membrane depolarization in N2a mouse neuroblastoma cells in comparison to control diabetics (n = 15) not battling with obstructive rest apnea. Process expansion in N2A mouse neuroblastoma cells was considerably inhibited (P = 0.01) by diabetic obstructive rest apnea (n = 9) autoantibodies in comparison to results from identical 10 5.5 kD putative light chain fragment. 1.4 Conclusions These effects claim that diabetic obstructive rest apnea autoantibodies may induce solid depolarization in neuronal cells and alter Ca2+ signaling in atrial cardiomyocytes in keeping with a job in pathophysiology in subsets of diabetic obstructive rest apnea having co-morbid atrial fibrillation or another clinically significant cardiac tempo disruption. 13.364.6 7.70.71BMI9.330.5 6.60.008DepressionSD of triplicate determinations) in comparison to neurite manifestation in cells grown with 10 ng/mL human being Abiraterone Acetate (CB7630) bFGF, but without added check protein-A-eluate fractions. 3.8 Membrane depolarization assays After cell attachment, growth moderate was removed and cells had been washed and incubated in modified Tyrodes remedy comprising: 150 mM NaCl, 3 mM KCL and 30 mM HEPES, 10 mM D-glucose and 2 mM CaCL2, pH 7.4. Check fractions (human being IgG fractions) had been added in the current presence of 97 nM DiBAC4 (Molecular Probes, Eugene, OR) – as previously reported [6]. Fluorescence was assessed after 5 min or much longer at room temperature utilizing a Fluoroskan Ascent FL (VWR, Inc., Franklin, MA); Former mate = 485 nm, Em = 538 nm. Email address details are indicated as percent of modification in gross fluorescence in comparison to cells to which no check protein-A-eluate fractions had been added. 3.9 HL-1 cell culture HL-1 atrial cardiomyocytes had been created (and generously offered) by Dr. William Claycomb (Louisiana Condition University INFIRMARY, New Orleans, LA). These were taken care of in 5% CO2/95% atmosphere at 37C in Claycomb press (Sigma, St. Louis, MO) including 10% FBS (Biocell, Rancho Dominguez, CA), 100 U/mL:100 ug/mL penicillin-streptomycin (Invitrogen, Carlsbad, CA), 0.1 mM norepinephrine (Sigma, St. Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were grown in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast tumor (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open up in another window ?T-test: looking at activity before and after storage space ??P = 0.02: in comparison to nondiabetic settings 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior research, top neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates got apparent MWs related to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. In today’s study, maximum neurotoxicity in diabetic OSA/atrial fibrillation protein-A-eluates, (we.e. Pts 1, 2) got obvious MWs of 5.5 kD (Figure 3A). Yet another neurotoxic maximum inside a third diabetic OSA/AF individual had obvious MW11 kD. 4.6 Diabetic OSA autoantibodies induce Ca2+ launch in HL-1 atrial cardiomyocytes Proteins A eluates (1 5.5 kD (Fig 5A). Protein-A-eluates subjected to NSC405020 shown a change in maximum neurotoxicity toward an increased MW varieties (43 kd) (Shape 5B). Open up in another window Shape 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two individuals having diabetes, obstructive rest apnea, and a neurodegenerative disorder, i.e. glaucoma (Pt 6), dementia and melancholy (Pt 7) pursuing incubation in the lack(A) or existence (B) of a particular MT1-MMP inhibitor..Protein-A-eluates subjected to NSC405020 displayed Abiraterone Acetate (CB7630) a change in maximum neurotoxicity toward an increased MW varieties (43 kd) (Shape 5B). Open in another window Figure 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two individuals having diabetes, obstructive rest apnea, and a neurodegenerative disorder, we.e. and IgG subunit dissociation), plasma autoantibodies from diabetic obstructive rest apnea, tumor or control individuals were likened for improvement of inhibitory results on endothelial cell success. Size exclusion chromatography performed (in the existence or lack of a particular membrane type 1-matrix metalloproteinase inhibitor) was utilized to characterize the IgG autoantibody subunit(s) or fragments connected with maximum neurotoxicity in diabetic obstructive rest apnea. 1.3 Outcomes Diabetic obstructive rest apnea (n = 14) autoantibodies triggered a substantial increase (P = 0.01) in membrane depolarization in N2a mouse neuroblastoma cells in comparison to control diabetics (n = 15) not battling with obstructive rest apnea. Process expansion in N2A mouse neuroblastoma cells was considerably inhibited (P = 0.01) by diabetic obstructive rest apnea (n = 9) autoantibodies in comparison to results from identical 10 5.5 kD putative light chain fragment. 1.4 Conclusions These effects claim that diabetic obstructive rest apnea autoantibodies may induce solid depolarization in neuronal cells and alter Ca2+ signaling in atrial cardiomyocytes in keeping with a job in pathophysiology in subsets of diabetic obstructive rest apnea having co-morbid atrial fibrillation or another clinically significant cardiac tempo disruption. 13.364.6 7.70.71BMI9.330.5 6.60.008DepressionSD of triplicate determinations) in comparison to neurite manifestation in cells grown with 10 ng/mL human being bFGF, but without added check protein-A-eluate fractions. 3.8 Membrane depolarization assays After cell attachment, growth moderate was removed and cells had been washed and incubated in modified Tyrodes remedy comprising: 150 mM NaCl, 3 mM KCL and 30 mM HEPES, 10 mM D-glucose and 2 mM CaCL2, pH 7.4. Check fractions (human being IgG fractions) were added in the presence of 97 nM DiBAC4 (Molecular Probes, Eugene, OR) – as previously reported [6]. Fluorescence was measured after 5 min or longer at room temp using a Fluoroskan Ascent FL (VWR, Inc., Franklin, MA); Ex lover = 485 nm, Em = 538 nm. Results are indicated as percent of switch in gross fluorescence compared to cells to which no test protein-A-eluate fractions were added. 3.9 HL-1 cell culture HL-1 atrial cardiomyocytes were developed (and generously offered) by Dr. William Claycomb (Louisiana State University Medical Center, New Orleans, LA). They were managed in 5% CO2/95% air flow at 37C in Claycomb press (Sigma, St. Louis, MO) comprising 10% FBS (Biocell, Rancho Dominguez, CA), 100 U/mL:100 ug/mL penicillin-streptomycin (Invitrogen, Carlsbad, CA), 0.1 mM norepinephrine (Sigma, St. Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were grown in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast malignancy (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open in a separate window ?T-test: comparing activity before and after storage ??P = 0.02: compared to nondiabetic settings 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior studies, peak neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates experienced apparent MWs related to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. In the present study, maximum neurotoxicity in diabetic OSA/atrial fibrillation protein-A-eluates, (i.e. Pts 1, 2) experienced apparent MWs of 5.5 kD (Figure 3A). An additional neurotoxic maximum inside a third diabetic OSA/AF patient had apparent MW11 kD. 4.6 Diabetic OSA autoantibodies induce Ca2+ launch in HL-1 atrial cardiomyocytes Protein A eluates (1 5.5 kD (Fig 5A). Protein-A-eluates exposed to NSC405020 displayed a shift in maximum neurotoxicity toward a higher MW varieties (43 kd) (Number 5B). Open in a separate window Number 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two individuals having diabetes, obstructive sleep apnea, and a neurodegenerative disorder, i.e. glaucoma (Pt 6), dementia and major depression (Pt 7) following incubation in the absence(A) or presence (B) of a specific MT1-MMP inhibitor. A) Maximum neurotoxicity in the autoantibodies incubated without MT1-MMP inhibitor experienced apparent MW of 5.5 kD. B) MT1-MMP inhibition was associated with a shift in maximum neurotoxicity toward higher MW varieties, i.e. 43 kD maybe related to light chain dimer(s). 4.8 Diurnal variation in plasma EC autoantibody growth activity The 25-75% ammonium sulfate pellet fraction of adult microalbuminuric diabetes plasma includes the IgG fraction and was reported to consist of FGF-like, EC growth stimulatory activity [18]. Plasma EC stimulatory activity displayed a diurnal variance: maximum activity (e.g. Pt 8, 9) occurred in the morning (0600 C 1000 hours) with much less, if any, stimulatory activity in the evening (2000-2300 hours) (Number 6ACB). Potent EC inhibitory activity was present at nighttime (2300 hours) Eptifibatide Acetate inside a 53 12 months aged, type 1 diabetic patient.B) MT1-MMP inhibition was associated with a shift in maximum neurotoxicity toward higher MW varieties, we.e. apnea, malignancy or control individuals were compared for enhancement of inhibitory effects on endothelial cell survival. Size exclusion chromatography performed (in the presence or absence of a specific membrane type 1-matrix metalloproteinase inhibitor) was used to characterize the IgG autoantibody subunit(s) or fragments associated with maximum neurotoxicity in diabetic obstructive sleep apnea. 1.3 Results Diabetic obstructive sleep apnea (n = 14) autoantibodies caused a significant increase (P = 0.01) in membrane depolarization in N2a mouse neuroblastoma cells compared to control diabetic patients (n = 15) not suffering with obstructive sleep apnea. Process expansion in N2A mouse neuroblastoma cells was considerably inhibited (P = 0.01) by diabetic obstructive rest Abiraterone Acetate (CB7630) apnea (n = 9) autoantibodies in comparison to results from identical 10 5.5 kD putative light chain fragment. 1.4 Conclusions These benefits claim that diabetic obstructive rest apnea autoantibodies may induce solid depolarization in neuronal cells and alter Ca2+ signaling in atrial cardiomyocytes in keeping with a job in pathophysiology in subsets of diabetic obstructive rest apnea having co-morbid atrial fibrillation or another clinically significant cardiac tempo disruption. 13.364.6 7.70.71BMI9.330.5 6.60.008DepressionSD of triplicate determinations) in comparison to neurite appearance in cells grown with 10 ng/mL individual bFGF, but without added check protein-A-eluate fractions. 3.8 Membrane depolarization assays After cell attachment, growth moderate was removed and cells had been washed and incubated in modified Tyrodes option comprising: 150 mM NaCl, 3 mM KCL and 30 mM HEPES, 10 mM D-glucose and 2 mM CaCL2, pH 7.4. Check fractions (individual IgG fractions) had been added in the current presence of 97 nM DiBAC4 (Molecular Probes, Eugene, OR) – as previously reported [6]. Fluorescence was assessed after 5 min or much longer at room temperature utilizing a Fluoroskan Ascent FL (VWR, Inc., Franklin, MA); Former mate = 485 nm, Em = 538 nm. Email address details are portrayed as percent of modification in gross fluorescence in comparison to cells to which no check protein-A-eluate fractions had been added. 3.9 HL-1 cell culture HL-1 atrial cardiomyocytes had been created (and generously supplied) by Dr. William Claycomb (Louisiana Condition University INFIRMARY, New Orleans, LA). These were taken care of in 5% CO2/95% atmosphere at 37C in Claycomb mass media (Sigma, St. Louis, MO) formulated with 10% FBS (Biocell, Rancho Dominguez, CA), 100 U/mL:100 ug/mL penicillin-streptomycin (Invitrogen, Carlsbad, CA), 0.1 mM norepinephrine (Sigma, St. Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were grown in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast tumor (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open up in another window ?T-test: looking at activity before and after storage space ??P = 0.02: in comparison to nondiabetic handles 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior research, top neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates got apparent MWs matching to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. In today’s study, top neurotoxicity in diabetic OSA/atrial fibrillation protein-A-eluates, (we.e. Pts 1, 2) got obvious MWs of 5.5 kD (Figure 3A). Yet another neurotoxic top within a third diabetic OSA/AF individual had obvious MW11 kD. 4.6 Diabetic OSA autoantibodies induce Ca2+ discharge in HL-1 atrial cardiomyocytes Proteins A eluates (1 5.5 kD (Fig 5A). Protein-A-eluates subjected to NSC405020 shown a change in top neurotoxicity toward an increased MW types (43 kd) (Body 5B). Open up in another window Body 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two sufferers having diabetes, obstructive rest apnea, and a neurodegenerative disorder, i.e. glaucoma (Pt 6), dementia and despair (Pt 7) pursuing incubation in the lack(A) or existence (B) of a particular MT1-MMP inhibitor. A) Top neurotoxicity in the autoantibodies incubated without MT1-MMP inhibitor got obvious MW of 5.5 kD. B) MT1-MMP inhibition was connected with a change in top neurotoxicity toward higher MW types, i.e. 43 kD probably matching to light string dimer(s). 4.8 Diurnal variation in plasma EC autoantibody growth activity The 25-75% ammonium sulfate pellet fraction of adult microalbuminuric diabetes plasma contains the IgG fraction and was reported to include FGF-like, EC growth stimulatory activity [18]. Plasma EC stimulatory activity shown a diurnal variant: top activity (e.g. Pt 8, 9) happened each day (0600 C 1000 hours) with significantly less, if any, stimulatory activity at Abiraterone Acetate (CB7630) night (2000-2300 hours) (Body 6ACB). Powerful EC inhibitory activity was present at nighttime (2300 hours) within a 53 season old, type 1 diabetic individual battling with co-morbid neuropsychiatric dementia and disorder.Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were expanded in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast tumor (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open in another window ?T-test: looking at activity before and after storage ??P = 0.02: in comparison to nondiabetic controls 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior research, peak neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates had obvious MWs matching to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. inhibitory results on endothelial cell survival. Size exclusion chromatography performed (in the existence or lack of a particular membrane type 1-matrix metalloproteinase inhibitor) was utilized to characterize the IgG autoantibody subunit(s) or fragments connected with top neurotoxicity in diabetic obstructive rest apnea. 1.3 Outcomes Diabetic obstructive rest apnea (n = 14) autoantibodies triggered a substantial increase (P = 0.01) in membrane depolarization in N2a mouse neuroblastoma cells in comparison to control diabetics (n = 15) not battling with obstructive rest apnea. Process expansion in N2A mouse neuroblastoma cells was considerably inhibited (P = 0.01) by diabetic obstructive rest apnea (n = 9) autoantibodies in comparison to results from identical 10 5.5 kD putative light chain fragment. 1.4 Conclusions These benefits claim that diabetic obstructive rest apnea autoantibodies may induce solid depolarization in neuronal cells and alter Ca2+ signaling in atrial cardiomyocytes in keeping with a job in pathophysiology in subsets of diabetic obstructive rest apnea having co-morbid atrial fibrillation or another clinically significant cardiac tempo disruption. 13.364.6 7.70.71BMI9.330.5 6.60.008DepressionSD of triplicate determinations) in comparison to neurite appearance in cells grown with 10 ng/mL individual bFGF, but without added check protein-A-eluate fractions. 3.8 Membrane depolarization assays After cell attachment, growth moderate was removed and cells had been washed and incubated in modified Tyrodes option comprising: 150 mM NaCl, 3 mM KCL and 30 mM HEPES, 10 mM D-glucose and 2 mM CaCL2, pH 7.4. Check fractions (individual IgG fractions) had been added in the current presence of 97 nM DiBAC4 (Molecular Probes, Eugene, OR) – as previously reported [6]. Fluorescence was assessed after 5 min or much longer at room temperature utilizing a Fluoroskan Ascent FL (VWR, Inc., Franklin, MA); Former mate = 485 nm, Em = 538 nm. Email address details are portrayed as percent of modification in gross fluorescence in comparison to cells to which no check protein-A-eluate fractions had been added. 3.9 HL-1 cell culture HL-1 atrial cardiomyocytes had been created (and generously supplied) by Dr. William Claycomb (Louisiana Condition University Medical Center, New Orleans, LA). They were maintained in 5% CO2/95% air at 37C in Claycomb media (Sigma, St. Louis, MO) containing 10% FBS (Biocell, Rancho Dominguez, CA), 100 U/mL:100 ug/mL penicillin-streptomycin (Invitrogen, Carlsbad, CA), 0.1 mM norepinephrine (Sigma, St. Louis, MO), and 2 mM L-glutamine (Invitrogen, Carlsbad, CA). 3.10 Intracellular calcium measurement HL-1 cells were grown in -4%8015%93 26%0.84Diabetes & Lung cancer (n=1)85 7%28 10%0.01Breast cancer (n=4)66 + 15%??NTNon-diabetic control (n=3)102 + 3%NT Open in a separate window ?T-test: comparing activity before and after storage ??P = 0.02: compared to nondiabetic controls 4.5 Peak neurite-inhibitory in diabetic OSA autoantibodies: apparent MWs In prior studies, peak neurotoxicity in cancer fatigue/depression [5] and diabetic depression protein-A-eluates had apparent MWs corresponding to IgG light chains (23 kD) or half-light chains (11.5 kD) [6]. In the present study, peak neurotoxicity in diabetic OSA/atrial fibrillation protein-A-eluates, (i.e. Pts 1, 2) had apparent MWs of 5.5 kD (Figure 3A). An additional neurotoxic peak in a third diabetic OSA/AF patient had apparent MW11 kD. 4.6 Diabetic OSA autoantibodies induce Ca2+ release in HL-1 atrial cardiomyocytes Protein A eluates (1 5.5 kD (Fig 5A). Protein-A-eluates exposed to NSC405020 displayed a shift in peak neurotoxicity toward a higher MW species (43 kd) (Figure 5B). Open in a separate window Figure 5 Size exclusion (G75 Sephacryl) chromatography of autoantibodies in two patients having diabetes, obstructive sleep apnea, and a neurodegenerative disorder, i.e. glaucoma (Pt 6), dementia and depression (Pt 7) following.