Rural-urban differences in the perceived impact of COVID-19 on mental health by European women.

PURPOSE: Many studies have documented an adverse impact of the pandemic on women´s mental health. This cross-sectional study aims to explore associations between women's perceived impact of lockdowns and curfews on their mental health and their residential location, along with other contextual and individual factors. METHODS: Using data from the Flash Eurobarometer 2712 "Women in times of COVID-19", conducted between January 25 and February 3, 2022, across the 27 Member States of the European Union (n = 23,671), this study applied bivariate tests and stratified models based on respondent location (rural areas, small or medium-sized towns and urban areas). The exploration sought predictors influencing the perceived mental health impact, encompassing five individual characteristics (age, disability, employment status, educational attainment, and household type), perceptions of violence against women, and country of residence. The dependent variable was assessed subjectively, measured on a scale from 1 (minor negative impact) to 5 (major negative impact). RESULTS: Women living in urban areas generally reported a higher perceived negative impact on mental health compared to women in rural areas or in small/medium-sized towns. Age and disability were significantly linked to perceiving a negative impact on mental health. Similar adjusted odds ratios for age were observed across rural areas (aOR 0.97, 95% CI = 0.97-0.98), small or medium-sized towns (aOR 0.98, 95% CI = 0.97-0.98), and urban areas (aOR 0.97, 95% CI = 0.97-0.98). In terms of disability, the odds were higher in rural areas (aOR 1.44, 95% CI = 1.20-1.73) than in urban ones (aOR 1.36, 95% CI = 1.15-1.62). Among women residing in urban areas, those in childless couples were less likely to perceive a negative impact on mental health (aOR 0.89, 95% CI = 0.80-0.99) compared to women in couples with children. Respondents perceiving increased violence against women due to COVID-19 were more likely to perceive a negative impact on mental health, with higher odds ratios in rural areas (aOR 1.56, 95% CI = 1.40-1.74) compared to urban areas (aOR 1.29, 95% CI = 1.17-1.41). Differences across countries were also found. CONCLUSION: The perceived impact of lockdowns and curfews on mental health exhibited variance between urban and rural areas. These disparities were influenced by individual characteristics such as age, disability, or household type, as well as the effects of COVID-19 on violence against women and contextual variables like country of residence.

Identification of leading hazardous waste generating industries with high improvement potential in Spain.

This paper employs Economic Input-Output Life Cycle Assessment and Data Envelopment Analysis to attribute total (direct and indirect) hazardous waste generation to the different industries and to connect total hazardous waste generation to the value added generated by each industry in Spain. In difference with previous studies we include all the industries of the economy and we focus on one specific type of environmental burden: the generation of hazardous waste. The results show that there is a very high concentration in total hazardous waste generation: only three industries accounted for almost 80% of total hazardous waste generation. This concentration also affects the type of hazardous waste generated. Thus, we find two main types of waste that account for 93% of total hazardous waste. Overall, the greatest hazardous waste generating industries are also the least efficient ones and exhibit a high improvement potential. Prevention measures directed to these industries should be implemented.

Delineation of the 9q31 deletion syndrome: Genomic microarray characterization of two patients with overlapping deletions.

Interstitial deletions of chromosome 9q31 are very rare. The deletions in most reported patients have been detected by conventional cytogenetics, with reported breakpoints ranging between 9q21 and 9q34. Therefore, an accurate description of a "9q31 deletion syndrome" could not be established. However, based on microarray studies, a small region of overlap has recently been proposed. We report clinical features of two unrelated individuals with overlapping 9q deletions identified by SNP microarray analysis. Patient 1 has a 9 Mb deletion, while Patient 2's deletion was 21.6 Mb. The clinical features common to our patients and those in the literature include developmental delay and short stature. Patient 2 shows additional features not reported in other 9q31 deletions, such as hearing loss, ventriculomegaly, cleft lip and palate, and small kidneys, which could be due to the larger size of the deletion, hence the influence of the genes in the region beyond the smallest region of overlap. Based on the comparison of these patients with the previously reported patients, we redefine the smallest region of overlap and characterize the clinical features of the 9q31 deletion syndrome.

The human and mouse SLC25A29 mitochondrial transporters rescue the deficient ornithine metabolism in fibroblasts of patients with the hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome.

The hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is a disorder of the urea cycle (UCD) and ornithine degradation pathway caused by mutations in the mitochondrial ornithine transporter (ORNT1). Unlike other UCDs, HHH syndrome is characterized by a less severe and variable phenotype that we believe may, in part, be due to genes with redundant function to ORNT1, such as the previously characterized ORNT2 gene. We reasoned that SLC25A29, a member of the same subfamily of mitochondrial carrier proteins as ORNT1 and ORNT2, might also have overlapping function with ORNT1. Here, we report that both the human and mouse SLC25A29, previously identified as mitochondrial carnitine/acyl-carnitine transporter-like, when overexpressed transiently also rescues the impaired ornithine transport in cultured HHH fibroblasts. Moreover, we observed that, in the mouse, the Slc25a29 message is more significantly expressed in the CNS and cultured astrocytes when compared with the liver and kidney. These results suggest a potential physiologic role for the SLC25A29 transporter in the oxidation of fatty acids, ornithine degradation pathway, and possibly the urea cycle. Our results show that SLC25A29 is the third human mitochondrial ornithine transporter, designated as ORNT3, which may contribute to the milder and variable phenotype seen in patients with HHH syndrome.

Clinical and functional characterization of a human ORNT1 mutation (T32R) in the hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome.

We studied two related families (HHH013 and HHH015) with the hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome, a disorder of the urea cycle and ornithine degradation pathway, who have the same novel ornithine transporter (ORNT1) genotype (T32R) but a variable phenotype. Both HHH015 patients are doing well in school and are clinically stable; conversely, the three affected HHH013 siblings had academic difficulties and one suffered recurrent episodes of hyperammonemia and ultimately died. Overexpression studies revealed that the product of the ORNT1-T32R allele has residual function. Ornithine transport studies in HHH015 fibroblasts, however, showed basal activity similar to fibroblasts carrying nonfunctional ORNT1 alleles. We also examined two potential modifying factors, the ORNT2 gene and the mitochondrial DNA lineage (haplogroup). Haplogroups, associated with specific diseases, are hypothesized to influence mitochondrial function. Results demonstrated that both HHH015 patients are heterozygous for an ORNT2 gain of function polymorphism and belong to haplogroup A whereas the HHH013 siblings carry the wild-type ORNT2 and are haplogroup H. These observations suggest that the ORNT1 genotype cannot predict the phenotype of HHH patients. The reason for the phenotypic variability is unknown, but factors such as redundant transporters and mitochondrial lineage may contribute to the neuropathophysiology of HHH patients.

Cloning and characterization of human ORNT2: a second mitochondrial ornithine transporter that can rescue a defective ORNT1 in patients with the hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, a urea cycle disorder.

We recently characterized the mitochondrial ornithine transporter (ORNT1), the gene defective in the hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome, a urea cycle disorder. Despite the apparent functional ablation of ORNT1 in 10 French-Canadian probands with the ORNT1-F188 Delta allele, these patients are mildly affected when compared to patients with other urea cycle disorders such as deficiency of ornithine transcarbamylase. Given that the inner mitochondrial membrane is impermeable to solutes, we hypothesize that other unidentified carriers have some degree of functional redundancy with ORNT1. Using conserved sequences of mammalian and fungal mitochondrial ornithine transporters, we screened the Expressed Sequence Tag database for additional transporters belonging to the ORNT subfamily. Here we identify a new intronless gene, ORNT2, located on chromosome 5. The gene product of ORNT2 is 88% identical to ORNT1, targets to the mitochondria and is expressed in human liver, pancreas, kidney, and cultured fibroblasts from control and HHH patients. When ORNT2 is overexpressed transiently in cultured fibroblasts from HHH patients, it rescues the deficient ornithine metabolism in these cells. Our results suggest that ORNT2 may in part be responsible for the milder phenotype in HHH patients secondary to a gene redundancy effect. We believe ORNT2 arose from a retrotransposition event. To our knowledge, this is the first report of a functional retroposon (ORNT2) that can rescue the disease phenotype of the gene it arose from, ORNT1. As such, ORNT2 may eventually become a candidate for pharmacological-based approaches to correct a urea cycle disorder.