| 1. |
- Pérez-Maldonado, Iván N, et al.
(författare)
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Exposure assessment of polybrominated diphenyl ethers (PBDEs) in Mexican children
- 2009
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Ingår i: Chemosphere. - : Elsevier BV. - 0045-6535 .- 1879-1298. ; 75:9, s. 1215-1220
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Tidskriftsartikel (refereegranskat)abstract
- Flame retardants (FRs) constitute a group of compounds that are added to materials in order to suppress, reduce, or delay fire. At present the most used FRs are the polybrominated diphenyl ethers (PBDEs), and diverse studies have found individuals exposed to them. However, few studies have reported data in children. The objective of this report was to assess PBDEs levels in children of six communities in México. During the year 2006 we analyzed a total of 173 healthy children (aged 6-13 years old). Plasma samples were taken and quantified (gas chromatography/mass spectrometer) for PBDEs. Six PBDEs congeners (BDE-47, BDE-99, BDE-100, BDE-153, BDE-154, and BDE-209) were quantified in blood serum. We detected exposure to PBDEs in all the communities. The total PBDEs levels ranged from no detectable (nd) to 43.4 ng g(-1) lipid, the dominant PBDE congener was BDE-47, followed by BDE-100, BDE-99 and BDE-153, whereas the levels of BDE-209 were below LOD. Children living in an industrial and urban area (Cd. Juarez, Chih) had the highest levels of PBDEs, approximately two times that of children living in El Refugio, S.L.P. (a rural area) or in Milpillas, S.L.P. (municipal landfill) and 4-5 times higher than levels found in children living in San Luis Potosi, S.L.P. (urban area), in Chihuahua, Chih. (urban area), and San Juan Tilapa, Edo. Mex. (municipal landfills). Results cannot be generalized since the communities selected are not representative of the Mexican population. However, they do indicate that Mexican children are exposed to PBDEs.
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| 2. |
- Barraza-Villarreal, Albino, et al.
(författare)
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Air pollution, airway inflammation, and lung function in a cohort study of Mexico City schoolchildren.
- 2008
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Ingår i: Environmental health perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 116:6, s. 832-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The biological mechanisms involved in inflammatory response to air pollution are not clearly understood. OBJECTIVE: In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function. METHODS: We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (Fe(NO)), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models. RESULTS: An increase of 17.5 microg/m(3) in the 8-hr moving average of PM(2.5) levels (interquartile range) was associated with a 1.08-ppb increase in Fe(NO) [95% confidence interval (CI), 1.01-1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98-1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00-1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter <2.5 microm in aerodynamic diamter (PM(2.5)) was significantly inversely associated with forced expiratory volume in 1 sec (FEV(1)) (p=0.048) and forced vital capacity (FVC) (p=0.012) in asthmatic children and with FVC (p=0.021) in nonasthmatic children. Fe(NO) and FEV(1) were inversely associated (p=0.005) in asthmatic children. CONCLUSIONS: Exposure to PM(2.5) resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.
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| 3. |
- Bjurshagen, Stefan, et al.
(författare)
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Fluorescence dynamics and rate equations analysis in Er3+,Yb3+ doped double tungstates
- 2006
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Ingår i: Applied Optics. - 1559-128X .- 2155-3165. ; 45:19, s. 4715-4725
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Tidskriftsartikel (refereegranskat)abstract
- The fluorescence dynamics in Er3+ and Yb3+ doped KGd(WO4)(2) and KY(WO4)(2) has been investigated. Lifetimes have been measured for the Yb(F-2(5/2)), Er(I-4(13/2)), and Er(S-4(3/2)) levels around 1, 1.5, and 0.55 mu m, respectively. The Yb(F-2(5/2)) lifetimes show a decreasing trend toward the limiting Er(I-4(11/2)) lifetime with increasing Er-to-Yb concentration ratio, whereas the Er(I-4(13/2)) lifetimes are mostly unaffected by the doping concentrations. A rate equation analysis has been performed to explain the observed behavior and gain is calculated for a continuous-wave laser at 1.53 mu m to find the optimum doping concentrations for high gain.
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| 4. |
- Corma, Averlino, et al.
(författare)
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Synthesis and structure of polymorph B of zeolite Beta
- 2008
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Ingår i: Chemistry of Materials. - : American Chemical Society (ACS). - 0897-4756 .- 1520-5002. ; 20:9, s. 3218-3223
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Tidskriftsartikel (refereegranskat)abstract
- It was found that either polymorph B or polymorph C of zeolite beta can be obtained from the same structure directing agent: 4,4-dimethyl-4-azonia-tricyclo[5.2.2.02,6]undec-8-ene hydroxide. The synthesis occurs through a consecutive process where polymorph B is first formed and then transformed into polymorph C. It is possible to produce a zeolite highly enriched in polymorph B, provided that the transformation of this phase into polymorph C is slowed down up to the point where polymorph C is only detected at trace levels. The structure of polymorph B was determined for the first time by electron crystallography with SAED and HRTEM from areas of unfaulted polymorph B crystals.
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| 5. |
- Darai-Ramqvist, Eva, et al.
(författare)
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Array-CGH and multipoint FISH to decode complex chromosomal rearrangements
- 2006
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Ingår i: BMC Genomics. - : Springer Science and Business Media LLC. - 1471-2164. ; 7, s. 330-
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Tidskriftsartikel (refereegranskat)abstract
- Background: Recently, several high-resolution methods of chromosome analysis have been developed. It is important to compare these methods and to select reliable combinations of techniques to analyze complex chromosomal rearrangements in tumours. In this study we have compared array-CGH (comparative genomic hybridization) and multipoint FISH (mpFISH) for their ability to characterize complex rearrangements on human chromosome 3 (chr3) in tumour cell lines. We have used 179 BAC/PAC clones covering chr3 with an approximately 1 Mb resolution to analyze nine carcinoma lines. Chr3 was chosen for analysis, because of its frequent rearrangements in human solid tumours. Results: The ploidy of the tumour cell lines ranged from near-diploid to near-pentaploid. Chr3 locus copy number was assessed by interphase and metaphase mpFISH. Totally 53 chr3 fragments were identified having copy numbers from 0 to 14. MpFISH results from the BAC/PAC clones and array-CGH gave mainly corresponding results. Each copy number change on the array profile could be related to a specific chromosome aberration detected by metaphase mpFISH. The analysis of the correlation between real copy number from mpFISH and the average normalized inter-locus fluorescence ratio (ANILFR) value detected by array-CGH demonstrated that copy number is a linear function of parameters that include the variable, ANILFR, and two constants, ploidy and background normalized fluorescence ratio. Conclusion: In most cases, the changes in copy number seen on array-CGH profiles reflected cumulative chromosome rearrangements. Most of them stemmed from unbalanced translocations. Although our chr3 BAC/PAC array could identify single copy number changes even in pentaploid cells, mpFISH provided a more accurate analysis in the dissection of complex karyotypes at high ploidy levels.
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| 6. |
- Descartes, Maria, et al.
(författare)
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Distal 22q11.2 microduplication encompassing the BCR gene
- 2008
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Ingår i: American journal of medical genetics. Part A. - : Wiley. - 1552-4825 .- 1552-4833. ; 146A:23, s. 3075-3081
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Tidskriftsartikel (refereegranskat)abstract
- Chromosome 22 band q11.2 has been recognized to be highly susceptible to subtle microdeletions and microduplications, which have been attributed to the presence of several large segmental duplications; also known as low copy repeats (LCRs). These LCRs function as mediators of non-allelic homologous recombination (NAHR), which results in these chromosomal rearrangements as a result of unequal crossover. The four centromeric LCRs at proximal 22q11.2 have been previously implicated in recurrent chromosomal rearrangements including the DiGeorge/Velocardiofacial syndrome (DG/VCFs) microdeletion and its reciprocal microduplication. Recently, we and others have demonstrated that the four telomeric LCRs at distal 22q11.2 are causally implicated in a newly recognized recurrent distal 22q11.2 microdeletion syndrome in the region immediately telomeric to the DG/VCFs typically deleted region. Here we report on the clinical, cytogenetic, and array CGH studies of a 4.5-year-old girl with history of failure to thrive, developmental delay (DD), and relative macrocephaly. She carries a paternally inherited approximately 2.1 Mb microduplication at distal 22q11.2, which spans approximately 34 annotated genes, and is flanked by two of the four telomeric 22q11.2 LCRs. We conclude that the four telomeric LCRs at distal 22q11.2 can mediate both deletions and duplications in this genomic region. Both deletions and duplication of this region present with subtle clinical features including mild to moderate mental retardation, DD, and mild dysmorphic features.
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| 7. |
- Gallo, Valentina, et al.
(författare)
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Smoking and risk for amyotrophic lateral sclerosis : analysis of the EPIC cohort
- 2009
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Ingår i: Annals of Neurology. - New York : J. Wiley & Sons. - 0364-5134 .- 1531-8249. ; 65:4, s. 378-385
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrollment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.
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| 8. |
- Mikhail, Fady M., et al.
(författare)
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A previously unrecognized microdeletion syndrome on chromosome 22 band q11.2 encompassing the BCR gene
- 2007
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Ingår i: American journal of medical genetics. Part A. - : Wiley. - 1552-4825 .- 1552-4833. ; 143A:18, s. 2178-2184
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Tidskriftsartikel (refereegranskat)abstract
- Susceptibility of the chromosome 22q11.2 region to rearrangements has been recognized on the basis of common clinical disorders such as the DiGeorge/velocardiofacial syndrome (DG/VCFs). Recent evidence has implicated low-copy repeats (LCRs); also known as segmental duplications; on 22q as mediators of nonallelic homologous recombination (NAHR) that result in rearrangements of 22q11.2. It has been shown that both deletion and duplication events can occur as a result of NAHR caused by unequal crossover of LCRs. Here we report on the clinical, cytogenetic and array CGH studies of a 15-year-old Hispanic boy with history of learning and behavior problems. We suggest that he represents a previously unrecognized microdeletion syndrome on chromosome 22 band q11.2 just telomeric to the DG/VCFs typically deleted region and encompassing the BCR gene. Using a 32K BAC array CGH chip we were able to refine and precisely narrow the breakpoints of this microdeletion, which was estimated to be 1.55-1.92 Mb in size and to span approximately 20 genes. This microdeletion region is flanked by LCR clusters containing several modules with a very high degree of sequence homology (>95%), and therefore could play a causal role in its origin.
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| 9. |
- Nilsson, Kajsa E., et al.
(författare)
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Enhanced susceptibility to low-dose collagen-induced arthritis in CR1/2-deficient female mice : possible role of estrogen on CR1 expression
- 2009
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Ingår i: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 23:8, s. 2450-2458
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Tidskriftsartikel (refereegranskat)abstract
- The influence of complement receptor 1 and 2 (CR1/2) was investigated on the susceptibility to low-dose collagen-induced arthritis (CIA) in wild-type (WT) and CR1/2-deficient DBA/1 mice. Significantly enhanced CIA was observed in female CR1/2-deficient mice compared with WT female mice, while male mutant and WT mice showed similar arthritis development. The enhanced CIA was accompanied with higher complement levels and a prolonged IgM anti-collagen type II response. When investigating whether estrogen contributed to the different arthritis susceptibility, we found that ovariectomy rendered WT females more sensitive to low-dose CIA and to the same extent as CR1/2-deficient females, while CR1/2-deficient mice were unaffected by ovariectomy. Notably, the ovariectomized WT mice displayed reduced CR1(+) B220(+) B-cell numbers and CR1 expression compared with sham-operated WT mice, suggesting a stimulatory effect of estrogen on CR1. In accordance, a significant correlation was observed between reduced CR1 expression in B cells and increased age in healthy female blood donors but not in male donors. Our findings demonstrate an important role of CR1/2 in suppressing CIA in female mice under low-antigen conditions. The data suggest that estrogen promote CR1 expression in B cells. These findings provide insight to the increased frequency of rheumatoid arthritis in postmenopausal women.
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| 10. |
- Ramesh Babu, J., et al.
(författare)
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Genetic inactivation of p62 leads to accumulation of hyperphosphorylated tau and neurodegeneration
- 2008
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Ingår i: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 106:1, s. 107-120
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Tidskriftsartikel (refereegranskat)abstract
- The signaling adapter p62 plays a coordinating role in mediating phosphorylation and ubiquitin-dependent trafficking of interacting proteins. However, there is little known about the physiologic role of this protein in brain. Here, we report age-dependent constitutive activation of glycogen synthase kinase 3beta, protein kinase B, mitogen-activated protein kinase, and c-Jun-N-terminal kinase in adult p62(-/-) mice resulting in hyperphosphorylated tau, neurofibrillary tangles, and neurodegeneration. Biochemical fractionation of p62(-/-) brain led to recovery of aggregated K63-ubiquitinated tau. Loss of p62 was manifested by increased anxiety, depression, loss of working memory, and reduced serum brain-derived neurotrophic factor levels. Our findings reveal a novel role for p62 as a chaperone that regulates tau solubility thereby preventing tau aggregation. This study provides a clear demonstration of an Alzheimer-like phenotype in a mouse model in the absence of expression of human genes carrying mutations in amyloid-beta protein precursor, presenilin, or tau. Thus, these findings provide new insight into manifestation of sporadic Alzheimer disease and the impact of obesity.
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