| 1. |
- Liu, Wei, et al.
(författare)
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Household renovation before and during pregnancy in relation to preterm birth and low birthweight in China
- 2019
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Ingår i: Indoor Air. - : WILEY. - 0905-6947 .- 1600-0668. ; 29:2, s. 202-214
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Tidskriftsartikel (refereegranskat)abstract
- From October 2010 to April 2012, we conducted a cross-sectional study of associations between household environments and childhood health among preschool children in eight Chinese cities. Here, we analyze associations of early household renovation with preterm birth (PTB), low birthweight (LBW), term low birthweight (Term-LBW), and small for gestational age (SGA). Parents responded to questions about household renovation and their children's gestational age and birthweight. In the multivariate logistic regression analyses, household renovation in the year before pregnancy was significantly associated with LBW (sample size: N = 25 813; adjusted odds ratio (OR) with 95% confidence intervals (CIs): 1.23, 1.01-1.50) and Term-LBW (N = 24 823; 1.29, 1.01-1.67). Household renovation during pregnancy was significantly associated with PTB (N = 25 202; 1.28, 1.01-1.69). These significant associations were also found in the two-level (city-child) logistic regression analyses and in the sensitivity analyses among 21 009 children with complete data in all studied variates. Stronger associations were found in certain subgroups. Our findings indicate that household renovation within one year before pregnancy might be a risk factor for LBW and Term-LBW, while household renovation during pregnancy could be a risk factor for PTB.
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| 2. |
- Shi, Wenming, et al.
(författare)
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Urinary phthalate metabolites in relation to childhood asthmatic and allergic symptoms in Shanghai
- 2018
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Ingår i: Environment International. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0160-4120 .- 1873-6750. ; 121, s. 276-286
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Tidskriftsartikel (refereegranskat)abstract
- Background: Few studies can be found on phthalate exposure in relation to childhood asthma and allergic symptoms from Mainland China, where a persistent increase in prevalence of childhood asthma and allergic disease has been observed. Objectives: This study aimed to assess the exposure levels to phthalates and its relationship with asthmatic and allergic symptoms among children in Shanghai, which has the highest prevalence of childhood asthma in Mainland China. Methods: A follow-up study (2013-2014) of 434 children aged 5-10 years was conducted, based on the China, Children, Homes, Health (CCHH) study (2011-2012) in Shanghai, China. Information on asthmatic and allergic symptoms (wheeze, rhinitis, and eczema) were collected using validated questionnaires. Ten phthalate metabolites in morning urine samples were analyzed by high-performance liquid chromatography with triple quadrupole tandem mass spectrometry (HPLC-MS/MS). Multivariable logistic regression was used to estimate the associations between symptoms and urinary phthalate metabolites controlling for demographics, family history of allergic diseases and other covariates. Results: Nine out of 10 phthalate metabolites were detected in all subjects (average detection rate of 93.2%). By multivariable logistic regression analyses, the 4th quartile of Mono-n-butyl phthalate (MnBP) (reference: 1st quartile) had adjusted prevalence odds ratios (aPORs) and 95% confidence intervals (95%CIs) of 2.27(1.06-4.88), 2.14(1.02-4.46) and 2.98(1.19-7.50) for wheeze, rhinitis and eczema, respectively, while those of Mono-isobutyl phthalate (MiBP) were 2.23(1.08-4.62) and 2.96(1.02-8.60) for rhinitis and eczema, respectively. The highest quartile of mono-2-ethyl-5-hydroxyhexyl phthalate(MEHHP) and mono 2 ethyl 5 ox ohexyl phthalate(MEOHP) had aPORs and 95%CIs of 3.10(1.10-8.74) and 2.63(1.02-6.80) for eczema, respectively. By summing up the 4 low molecular weight metabolites (Sigma 4LMWP) and all 9 metabolites (Sigma(9)Total), the highest quartiles of Sigma 4LMWP and Sigma(9)Total were significantly associated with all symptoms. In most of the above associations, a significantly increasing trend from the 1st to the 4th quartile was observed. Subjects with 2 or 3 concomitant symptoms (reference: no symptoms) had significant positive associations with a higher level (the 4th quartile) of phthalate metabolites. Conclusions: Low MW metabolites such as MnBP and MiBP, high MW DEHP and the total amount of phthalate metabolites might have adverse health effects on asthma and allergic symptoms in Chinese children.
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| 3. |
- Yao, Qi, et al.
(författare)
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Unconventional Source of Neurotoxic Protein Aggregation from Organelle Off-Target Bax∆2 in Alzheimer's Disease
- 2023
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Ingår i: Biomolecules. - 2218-273X. ; 13:6
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Tidskriftsartikel (refereegranskat)abstract
- Protein aggregates are a hallmark of Alzheimer's disease (AD). Extensive studies have focused on β-amyloid plaques and Tau tangles. Here, we illustrate a novel source of protein aggregates in AD neurons from organelle off-target proteins. Bax is a mitochondrial pore-forming pro-death protein. What happens to Bax if it fails to target mitochondria? We previously showed that a mitochondrial target-deficient alternatively spliced variant, Bax∆2, formed large cytosolic protein aggregates and triggered caspase 8-mediated cell death. Bax∆2 protein levels were low in most normal organs and the proteins were quickly degraded in cancer. Here, we found that 85% of AD patients had Bax∆2 required alternative splicing. Increased Bax∆2 proteins were mostly accumulated in neurons of AD-susceptible brain regions. Intracellularly, Bax∆2 aggregates distributed independently of Tau tangles. Interestingly, Bax∆2 aggregates triggered the formation of stress granules (SGs), a large protein-RNA complex involved in AD pathogenesis. Although the functional domains required for aggregation and cell death are the same as in cancer cells, Bax∆2 relied on SGs, not caspase 8, for neuronal cell death. These results imply that the aggregation of organelle off-target proteins, such as Bax∆2, broadens the scope of traditional AD pathogenic proteins that contribute to the neuronal stress responses and AD pathogenesis.
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