Age- and sex-dependency of the association between systemic antioxidant potential and glaucomatous damage.
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ABSTRACT:
SUBMITTER: Asano Y
PROVIDER: S-EPMC5556047 | biostudies-other | 2017 Aug
REPOSITORIES: biostudies-other
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Project description:Local and systemic oxidative stress in intraocular pressure (IOP) elevation and optic nerve damage may be involved in the pathogenesis of glaucoma. We reported previously that a lower level of systemic antioxidative capacity is associated with IOP elevation in open-angle glaucoma (OAG). We assessed the correlation between the visual field sensitivity value, i.e., mean deviation (MD), and systemic levels of prooxidants and antioxidants by analyzing the blood biochemistry in 202 patients with glaucoma. Serum levels of lipid peroxides, ferric-reducing activity, and thiol antioxidant activity were measured using the diacron reactive oxygen metabolite (dROM), biological antioxidant potential (BAP), and sulfhydryl (SH) tests, respectively, using a free-radical analyzer. Univariate and multivariate analyses suggested a positive correlation between MD and BAP (R?=?0.005 and P?=?0.0442 by a multiple regression model adjusted for seven demographic parameters), but no significant associations between the MD and the dROM (R?=?0.002 and P?=?0.8556) and SH tests (R?=?-0.001 and P?=?0.8280). Use of more antiglaucoma medication and primary OAG rather than normal tension glaucoma also were associated significantly with worse visual field damage. This large and comprehensive assessment of the association between systemic redox status and visual field damage in OAG suggests that lower systemic antioxidant capacity measured by ferric-reducing activity is associated with more severe visual field damage in OAG that partly explained its roles in IOP elevation.
| S-EPMC4863173 | biostudies-literature
Project description:To image and analyze anatomical differences at the temporal raphe between normal and glaucomatous eyes using adaptive optics scanning laser ophthalmoscopy (AOSLO) and optical coherence tomography (OCT), and to relate these differences to visual field measurements.Nine glaucomatous eyes of 9 patients (age 54-78 years, mean deviation of visual field [MD] -5.03 to -0.20 dB) and 10 normal eyes of 10 controls (age 54-81, MD -1.13 to +1.39 dB) were enrolled. All the participants were imaged in a region that was centered approximately 9° temporal to the fovea. The size of imaging region was at least 10° vertically by 4° horizontally. The raphe gap, defined as the distance between the superior and inferior retinal nerve fiber layer (RNFL) bundles, was measured. A bundle index was computed to quantify the relative reflectivity and density of the nerve fiber bundles. We also measured thickness of the ganglion cell complex (GCC) and RNFL.The raphe gap was larger in glaucomatous eyes than control eyes. Specifically, eight glaucomatous eyes with local averaged field loss no worse than -3.5 dB had larger raphe gaps than all control eyes. The bundle index, GCC thickness, and RNFL thickness were on average reduced in glaucomatous eyes, with the first two showing statistically significant differences between the two groups.Structural changes in the temporal raphe were observed and quantified even when local functional loss was mild. These techniques open the possibility of using the raphe as a site for glaucoma research and clinical assessment.
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Project description:Increased endogenous DNA damage and type I interferon pathway activation have been implicated in systemic sclerosis (SSc) pathogenesis. Because experimental evidence suggests an interplay between DNA damage response/repair (DDR/R) and immune response, we hypothesized that deregulated DDR/R is associated with a type I interferon signature and/or fibrosis extent in SSc. DNA damage levels, oxidative stress, induction of abasic sites and the efficiency of DNA double-strand break repair (DSB/R) and nucleotide excision repair (NER) were assessed in peripheral blood mononuclear cells (PBMCs) derived from 37 SSc patients and 55 healthy controls; expression of DDR/R-associated genes and type I interferon-induced genes was also quantified. Endogenous DNA damage was significantly higher in untreated diffuse or limited SSc (Olive tail moment; 14.7 ± 7.0 and 9.5 ± 4.1, respectively) as well as in patients under cytotoxic treatment (15.0 ± 5.4) but not in very early onset SSc (5.6 ± 1.2) compared with controls (4.9 ± 2.6). Moreover, patients with pulmonary fibrosis had significantly higher DNA damage levels than those without (12.6 ± 5.8 vs. 8.8 ± 4.8, respectively). SSc patients displayed increased oxidative stress and abasic sites, defective DSB/R but not NER capacity, downregulation of genes involved in DSB/R (MRE11A, PRKDC) and base excision repair (PARP1, XRCC1), and upregulation of apoptosis-related genes (BAX, BBC3). Individual levels of DNA damage in SSc PBMCs correlated significantly with the corresponding mRNA expression of type I interferon-induced genes (IFIT1, IFI44 and MX1, r=0.419-0.490) as well as with corresponding skin involvement extent by modified Rodnan skin score (r=0.481). In conclusion, defective DDR/R may exert a fuel-on-fire effect on type I interferon pathway activation and contribute to tissue fibrosis in SSc.
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Project description:Research on sex differences in renal cancer-specific mortality (RCSM), which considered the sex effect to be constant throughout life, has yielded conflicting results. This study hypothesized the sex effect may be modified by age, which is a proxy for hormonal status. Data from the Surveillance, Epidemiology and End Results database (1988-2010) were used to identify 114,539 patients with renal cell carcinoma (RCC). The study cohort was divided into three age groups using cutoffs of 42 and 58 years, which represent the premenopausal and postmenopausal periods. The cumulative incidence function and competing risks analyses were used to examine the effect of covariates on RCSM and other-cause mortality (OCM). In premenopausal period, male sex was a significant predictor of poor RCSM for both localized (adjusted subdistribution hazard ratio [aSHR] = 1.63, P = 0.002) and advanced (aSHR = 1.20, P = 0.041) disease. In postmenopausal period, the sex disparity diminished (aSHR = 1.05, P = 0.16) and reversed (aSHR = 0.95, P = 0.017) in localized and advanced disease, respectively. On the contrary, similar trend was not found for OCM across all age groups. Our results demonstrated the sex effect on RCSM was strongly modified by age. These findings may aid in clinical practice and need further evaluation of underlying biological mechanisms.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2023-06-21 | GSE224624 | GEO
Project description:BackgroundThe relationship between smoking status or second-hand smoking and occupational injuries has been the subject of considerable study, but few have studied the relationship between nicotine dependence and occupational injuries. The objective of this study was to investigate the relationship between nicotine dependence and occupational injury among employees at a range of Korean companies.MethodsInitially, the personal and occupational characteristics and nicotine dependences of workers were measured, and 12 months later a survey was used to determine whether subjects had experienced any occupational injury. This study was conducted in several workplaces on 6,893 male workers in manufacturing and service industries that received health screening at Inha University Hospital in Incheon.ResultsThe adjusted odds ratios (ORs) of occupational injury in the low, moderate, and high nicotine dependence groups were 1.38 (95% confidence interval [CI]: 1.04-1.84), 1.52 (95% CI: 1.10-2.10), and 1.71 (95% CI: 0.92-3.19), respectively. For smokers only, adjusted ORs tended to increase linearly (p for trend < 0.05). When only smokers were included, analysis of continuous FTND (Fagerstrom Test of Nicotine Dependence) scores showed that adjusted OR increased by 1.10 (95% CI: 1.03-1.19) per FTND point. After stratifying the data by working type and working hours per week, the non-shift work group maintained this relationship (OR: 1.13, 95% CI: 1.04-1.24) and OR was higher in the group that works more than 60 hours per week with FTND score as a continuous variable (OR: 1.24, 95% CI: 1.07-1.44).ConclusionsThe study shows nicotine dependency might affect occupational injury. From a short-term perspective, addressing worker's nicotine dependence by giving an adequate break time or smoking area might reduce work-related injuries.
| S-EPMC8203833 | biostudies-literature
Project description:PurposeTo determine whether an association exists between sleep apnea and open-angle glaucoma, normal-tension glaucoma, nonarteritic ischemic optic neuropathy (NAION), papilledema, or idiopathic intracranial hypertension (IIH) and whether treatment with continuous positive airway pressure affects the development of these conditions.DesignRetrospective, longitudinal cohort study.MethodsBilling records for beneficiaries 40 years of age and older enrolled in a large United States managed care network from 2001 through 2007 were reviewed. Incidence of open-angle glaucoma, normal-tension glaucoma, NAION, papilledema, and IIH were determined for the beneficiaries and were stratified by sleep apnea status. Cox regression analyses determined the hazard of each of these conditions developing among individuals with and without sleep apnea, with adjustment for sociodemographic, ocular, and medical conditions.ResultsAmong the 2 259 061 individuals in the study, 156 336 (6.9%) had 1 or more sleep apnea diagnoses. The hazard of open-angle glaucoma was no different among persons with sleep apnea either treated (adjusted hazard ratio [HR], 0.99; 95% confidence interval [CI], 0.82 to 1.18) or untreated with continuous positive airway pressure (HR, 1.01; 95% CI, 0.98 to 1.05) and individuals without sleep apnea. Similar findings were observed when assessing the hazard of normal-tension glaucoma developing (P > .05 for both comparisons). A significantly increased hazard of NAION developing (HR, 1.16; 95% CI, 1.01 to 1.33) and IIH (HR, 2.03; 95% CI, 1.65 to 2.49) was observed among individuals with sleep apnea who were not receiving continuous positive airway pressure therapy as compared with individuals without sleep apnea, although similar increased risks could not be demonstrated among continuous positive airway pressure-treated sleep apnea patients for these conditions (P > .05 for both comparisons).ConclusionsPatients with untreated sleep apnea are at increased risk for IIH and NAION. Clinicians should consider appropriate screening for these conditions in sleep apnea patients.
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Project description:OBJECTIVE:At least half of patients with systemic lupus erythematosus (SLE) develop organ damage as a consequence of autoimmune disease or long-term therapeutic steroid use. This study synthesised evidence on the association between organ damage and mortality in patients with SLE. DESIGN:Systematic review and meta-analysis. METHODS:Electronic searches were performed in PubMed, Embase, Cochrane Library and Latin American and Caribbean Health Sciences Literature for observational (cohort, case-control and cross-sectional) studies published between January 2000 and February 2017. Included studies reported HRs or ORs on the association between organ damage (measured by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI) score) and mortality. Study quality was assessed using the modified Newcastle-Ottawa assessment. Pooled HRs were obtained using the DerSimonian and Laird random-effects model. Heterogeneity was assessed using the Cochrane Q (Q) and I2 statistics. RESULTS:The search yielded 10 420 articles, from which 21 longitudinal studies were selected. Most studies (85%) were of high quality. For 10 studies evaluating organ damage (SDI) as a continuous variable and reporting HR as a measure of association, a 1-unit increase in SDI was associated with increased mortality; pooled HR was 1.34 (95% CI: 1.24 to 1.44, p<0.001; Q p=0.027, I2=52.1%). Exclusion of one potential outlying study reduced heterogeneity with minimal impact on pooled HR (1.33 (95% CI: 1.25 to 1.42), p<0.001, Q p=0.087, I2=42.0%). The 11 remaining studies, although they could not be aggregated because of their varying patient populations and analyses, consistently demonstrated that greater SDI was associated with increased mortality. CONCLUSIONS:Organ damage in SLE is consistently associated with increased mortality across studies from various countries. Modifying the disease course with effective therapies and steroid-sparing regimens may reduce organ damage, improve outcomes and decrease mortality for patients with SLE.
| S-EPMC7247371 | biostudies-literature
Project description:ImportanceFacial recognition is a critical activity of daily living that relies on macular function. Glaucomatous macular damage may result in impaired facial recognition that may negatively affect patient quality of life.ObjectiveTo evaluate the association of patterns of glaucomatous macular damage with contrast sensitivity and facial recognition among patients with glaucoma.Design, setting, and participantsIn this prospective cohort study at a single tertiary care center, 144 eyes of 72 consecutive patients with glaucoma with good visual acuity (20/40 or better in each eye) were studied. Data were collected from March to April 2019.ExposuresEyes with macular damage were categorized as having focal, diffuse, or mixed (focal and diffuse) damage based on optic disc and macular spectral-domain optical coherence tomography and 10-2 visual field (VF) damage. Only eyes with focal or diffuse damage were included. Higher-acuity and lower-acuity eyes were determined by 10-2 VF mean deviation (MD). Facial disability was defined as facial recognition scores at the 2% level of normal participants.Main outcomes and measures(1) Monocular contrast threshold as measured by the Freiburg Visual Acuity and Contrast Test and (2) binocular facial recognition as measured by the Cambridge Face Memory Test.ResultsOf the 72 included patients, 49 (68%) were White and 41 (57%) were female, and the mean (SD) age was 67.0 (11.6) years. Eyes with diffuse damage had greater contrast impairment compared with eyes with focal damage (β = -0.5; 95% CI, -0.6 to -0.4; P < .001) after adjusting for 10-2 VF MD, 24-2 VF MD, age, presence of an early cataract, and number of drops. Similarly, Cambridge Face Memory Test scores were significantly lower in patients with diffuse rather than focal macular damage, regardless of eye (better-seeing eye: β = 10.0; 95% CI, 2.0 to 18.2; P = .001; worse-seeing eye: β = 5.5; 95% CI, 0.8 to 10.0; P = .23). Relative risk of facial disability was greater for patients with diffuse but not focal macular damage in the better-seeing eye (relative risk, 86.2; 95% CI, 2.7 to 2783.3; P = .01).Conclusions and relevanceIn this cohort study, diffuse rather than focal glaucomatous macular damage was associated with diminished facial recognition and contrast sensitivity. Evaluation of macular optical coherence tomography and 10-2 VF and resultant detection of diffuse macular damage may help minimize glaucoma-related visual disability.
| S-EPMC7645734 | biostudies-literature
Project description:Purpose:To test whether mice with microfibril deficiency due to the Tsk mutation of fibrillin-1 (Fbn1Tsk/+) have increased susceptibility to pressure-induced retinal ganglion cell (RGC) degeneration. Methods:Intraocular pressure (IOP) elevation was induced in Fbn1Tsk/+ and wild type (wt) mice by injecting microbeads into the anterior chamber. Mice were then followed up for four months, with IOP measurements every three to six days. Retinas were stained for Brn3a to determine RGC number. Optic nerve cross-sections were stained with p-phenylene diamine to determine nerve area, axon number, and caliber and thickness of the pia mater. Results:Microbead injection induced significant IOP elevation that was significantly less for Fbn1Tsk/+ mice compared with wt. The optic nerves and optic nerve axons were larger, and the elastic fiber-rich pia mater was thinner in Fbn1Tsk/+ mice. Microbead injection resulted in reduced optic nerve size, thicker pia mater, and a slight decrease in axon size. Fbn1Tsk/+ mice had significantly greater loss of RGCs and optic nerve axons compared with wt (14.8% vs. 5.8%, P = 0.002, and 17.0% vs. 7.5%, P = 0.002, respectively). Conclusions:Fbn1Tsk/+mice had altered optic nerve structure as indicated by larger optic nerves, larger optic nerve axons and thinner pia mater, consistent with our previous findings. Despite lower IOP elevation, Fbn1Tsk/+mice had greater loss of RGCs and optic nerve axons, suggesting increased susceptibility to IOP-induced optic nerve degeneration in microfibril-deficient mice.
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