scholarly journals Anterior Subcapsular Cataract Secondary to Black Mold Exposure

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Katherine B Lynch ◽  
Bruce Teitelbaum
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yu Zhang ◽  
Li Hua ◽  
Quan-Hua Liu ◽  
Shu-Yuan Chu ◽  
Yue-Xin Gan ◽  
...  

Abstract Background A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. Methods A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. Results After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. Conclusions In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma.


2006 ◽  
Vol 61 (3) ◽  
pp. 101-108 ◽  
Author(s):  
Kristin J. Cummings ◽  
David Van Sickle ◽  
Carol Y. Rao ◽  
Margaret A. Riggs ◽  
Clive M. Brown ◽  
...  

Plant Disease ◽  
2002 ◽  
Vol 86 (7) ◽  
pp. 815-815 ◽  
Author(s):  
B. A. Latorre ◽  
S. C. Viertel ◽  
I. Spadaro

Severe outbreaks of bunch rots (BR) have occurred recently during harvest of table grapes (Vitis vinifera L.) in Chile. Previously, BR was almost exclusively associated with Botrytis cinerea Pers.:Fr. (2,3); however, in 2000 to 2002, BR symptoms were associated with black molds and possibly nonfilamentous yeasts and bacteria. Cvs. Thompson Seedless, Flame Seedless, Ruby Seedless, and Red Globe were severely affected. Symptoms start at the pedicels as soft, watery rots that partially or completely decay infected berries. Longitudinal cracks are produced, a black mold usually develops along the crack fissures, and the skin of the berry turns light gray. Isolations on potato dextrose agar acidified with 1 N lactic acid (APDA) at 0.5 ml/liter, consistently yielded Rhizopus stolonifer (Ehrenb. ex Fr.) Vuillemin and Aspergillus niger Tiegh. R. stolonifer on APDA produced a white-to-gray aerial and nonseptate mycelium, black and globose sporangia with an elliptical collumela, one-celled, globose to oval, striated, almost hyaline sporangiospores, rhizoids, and stolons. A. niger produced septate mycelium. Single-celled, black, rough walled, globose conidia developed on short chains on the second phialides at the tip of globose, upright conidiophores. Mature (soluble solids >16%) detached berries of cv. Thompson Seedless were inoculated with sporangiospores (≈107 spores per ml) of R. stolonifer isolates RS6, RS52, RS73, and RS79 and conidia (≈108 conidia per ml) of A. niger isolates AN12, AN69, and AN75. When berries were aseptically punctured with a sterile hypodermic syringe prior to inoculation, 60 to 86.7% and 42.5 to 100% of berries were infected with R. stolonifer and A. niger, respectively, and both developed BR symptoms (significantly different from control berries) after 48 h in humid chambers at 23°C. Injuries were needed for infection since no infection or only 23.3% of noninjured berries were infected with R. stolonifer and A. niger, respectively. For both pathogens, there was a significant (P < 0.043) interaction between isolates and the presence or absence of injuries. Both pathogens were successfully reisolated on APDA. Fungicide sensitivity tests were performed on detached cv. Thompson Seedless berries challenged by placing an ≈6 μl-drop of inoculum suspension (106 or 107 spores per ml of R. stolonifer isolate RS52 and A. niger isolate AN12, respectively) on injured berries. Pyraclostrobin (0.067 mg/ml) mixed with nicobifen at 0.134 mg/ml (BAS 516 01 F at 0.201 mg a.i./ml, BASF) and copper oxide at 1.2 mg/ml (Cuprodul 60 WP, Quimetal Chile) significantly (P < 0.01) inhibited infection (100% control) by R. stolonifer and A. niger. R. stolonifer was completely controlled by dicloran at 1.88 mg/ml (Botran 75 WP) and partially controlled by captan at 1.6 mg/ml (Captan 80 WP), but A. niger was not controlled by either fungicide. To our knowledge this is the first report of R. stolonifer causing BR of table grape in Chile (4). The severe outbreaks may be associated with warm weather conditions during harvest and injuries caused by birds, insects, or cultural practices. Infection caused by R. stolonifer or A. niger may be followed by sour rot organisms (yeasts or bacteria), as has been suggested elsewhere (1,2). References: (1) E. Gravot et al. Phytoma 543:36, 2001. (2) W. B. Hewitt Page 26 in: Compendium of Grape Diseases, American Phytopathological Society, St. Paul, MN, 1994. (3) B. A. Latorre and G. Vásquez. Aconex (Chile) 52:16, 1996. (4) F. Mujica and C. Vergara. Flora Fungosa Chilena. Universidad de Chile, Facultad de Agronomiacute;a, Santiago, Chile, 1980.


2002 ◽  
Vol 8 (2) ◽  
pp. 124-130
Author(s):  
Heung-Tae Kim ◽  
Se-Won Park ◽  
Gyung-Ja Choi ◽  
Jin-Cheol Kim ◽  
Kwang-Yun Cho

2021 ◽  
Vol 7 (9) ◽  
pp. 698
Author(s):  
Chris D. Lauruschkat ◽  
Sonja Etter ◽  
Elisabeth Schnack ◽  
Frank Ebel ◽  
Sascha Schäuble ◽  
...  

Occupational mold exposure can lead to Aspergillus-associated allergic diseases including asthma and hypersensitivity pneumonitis. Elevated IL-17 levels or disbalanced T-helper (Th) cell expansion were previously linked to Aspergillus-associated allergic diseases, whereas alterations to the Th cell repertoire in healthy occupationally exposed subjects are scarcely studied. Therefore, we employed functional immunoassays to compare Th cell responses to A. fumigatus antigens in organic farmers, a cohort frequently exposed to environmental molds, and non-occupationally exposed controls. Organic farmers harbored significantly higher A. fumigatus-specific Th-cell frequencies than controls, with comparable expansion of Th1- and Th2-cell frequencies but only slightly elevated Th17-cell frequencies. Accordingly, Aspergillus antigen-induced Th1 and Th2 cytokine levels were strongly elevated, whereas induction of IL-17A was minimal. Additionally, increased levels of some innate immune cell-derived cytokines were found in samples from organic farmers. Antigen-induced cytokine release combined with Aspergillus-specific Th-cell frequencies resulted in high classification accuracy between organic farmers and controls. Aspf22, CatB, and CipC elicited the strongest differences in Th1 and Th2 responses between the two cohorts, suggesting these antigens as potential candidates for future bio-effect monitoring approaches. Overall, we found that occupationally exposed agricultural workers display a largely balanced co-expansion of Th1 and Th2 immunity with only minor changes in Th17 responses.


2006 ◽  
Vol 20 (4) ◽  
pp. 766-785 ◽  
Author(s):  
David C. Stone ◽  
Kyle B. Boone ◽  
Carla Back-Madruga ◽  
Ira M. Lesser

2019 ◽  
Vol 45 (11) ◽  
pp. 1421-1423
Author(s):  
Laura Doerfler ◽  
C. William Hanke

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