The Effects of Traffic Related Air Pollution and Proposed Legal Remedies

This paper intends to examine the environmental issues that accompany air pollution generated from traffic related incidents, and the implications that this mass-generated pollution has on air quality, as well as the quality of life of humans exposed chronically to airborne carcinogens. Traffic related air pollution is an environmental problem that is heightened by urban design and population demographics such as urban sprawl, spatial distribution, population density, and infrastructure design. Furthermore, this paper will scrutinize Canadian legislation that regulates traffic related air pollutants, and develop an argument for how to apply legislation going forward. As Cartier, Benmarinha, and Brousselle (2015) identify, the mechanisms of air quality intervention are overlooked, which is necessary for producing effective legislation. The objective of this paper is to gain insight on a quantifiable problem, and to prescribe solutions through legislation, in order to regulate an issue which presents heath complications on a generational level

Immunohistochemical Expression of p62 in Feline Mammary Carcinoma and Non-Neoplastic Mammary Tissue

The p62 protein, also called sequestosome 1 (SQSTM1), is a ubiquitin-binding scaffold protein. In human oncology, although the interest in the function of this protein is recent, the knowledge is now numerous, but its role in tumorigenesis is not yet clear. This preliminary study aims to evaluate the immunohistochemical expression of p62 in 38 cases of feline mammary carcinoma with different grades of differentiation and in 12 non-neoplastic mammary gland tissues, to assess the expression level and a possible correlation with malignancy. The expression of p62 was statistically higher in carcinoma compared to non-neoplastic mammary glands: 28 feline mammary carcinomas (73.7%) had a high p62 expression score, three (7.9%) had a moderate expression, while seven cases (18.4%) had a low expression. The grade of the differentiation of the carcinoma was not correlated with the p62 expression. This study represents the first approach in feline oncology that correlates p62 expression in feline mammary carcinoma. Our results, although preliminary, are similar to the results of human breast cancer, therefore, also in the cat, p62 could be considered a possible oncotarget

Recruitment of Oysters by Different Collection Devices at a Longline shellfish Farm in the Central Adriatic Sea

In 2020–2021, a trial to recruit flat oysters was implemented at a longline farm in the central Adriatic, whereby the efficiency recruitment (n. oyster/dm2) of different suspended substrates was evaluated. Two lantern nets (50 cm diameter; 145 cm h) had different substrates composed of 8 mm wide wrinkled ribbon and empty oyster shells positioned in the upper levels of the lanterns. The tumbling evaluation and the presence of mud were also considered. The efficiency recruitment was similar between the wrinkled ribbon and the oyster shell. Recruitment was in the same proportion on the external rough part of the shells as on the internal smooth part of the shells. No significant differences were shown when comparing the different substrates in terms of recruitment efficiency

Understanding the Pathogenesis of Red Mark Syndrome in Rainbow Trout (Oncorhynchus mykiss) through an Integrated Morphological and Molecular Approach

Red mark syndrome is a non-lethal widespread skin disease mainly reported in rainbow trout and caused by a Midichloria-like organism. Despite extensive research, its etiology and pathogenesis are still uncertain. In the present study, the authors used an integrated morphological and molecular approach, including gene expression, to elucidate the immune response and the complex immune interaction between the host and Midichloria-like organism. The results lead to the conclusions that the most severe skin lesions were characterized by a high level of inflammatory cytokines sustaining and modulating the severe inflammatory process. In contrast, in the moderate form, the response was driven to produce immunoglobulins and IL-10 to control the severity of the disease. Humoral immunity elicited during MLO infection appeared to have a fundamental role in controlling the severity of the skin disease, possibly through bactericidal antibody-mediated mechanisms

Comparative study of 1H-NMR metabolomic profile of canine synovial fluid in patients affected by four progressive stages of spontaneous osteoarthritis

The study aimed to assess the metabolomic profile of the synovial fluid (SF) of dogs affected by spontaneous osteoarthritis (OA) and compare any differences based on disease progression. Sixty client-owned dogs affected by spontaneous OA underwent clinical, radiographic, and cytologic evaluations to confirm the diagnosis. The affected joints were divided into four study groups based on the Kallgreen-Lawrence classification: OA1 (mild), OA2 (moderate), OA3 (severe), and OA4 (extremely severe/deforming). The osteoarthritic joint's SF was subjected to cytologic examination and H-1-NMR analysis. The metabolomic profiles of the study groups' SF samples were statistically compared using one-way ANOVA. Sixty osteoarthritic joints (45 stifles, 10 shoulders and 5 elbows) were included in the study. Fourteen, 28, and 18 joints were included in the OA1, OA2, and OA3 groups, respectively (0 joints in the OA4 group). Metabolomic analysis identified 48 metabolites, five of which were significantly different between study groups: Mannose and betaine were elevated in the OA1 group compared with the OA2 group, and the 2-hydroxyisobutyrate concentration decreased with OA progression; in contrast, isoleucine was less concentrated in mild vs. moderate OA, and lactate increased in severe OA. This study identified different H-1-NMR metabolomic profiles of canine SF in patients with progressive degrees of spontaneous OA, suggesting H-1-NMR metabolomic analysis as a potential alternative method for monitoring OA progression. In addition, the results suggest the therapeutic potentials of the metabolomic pathways that involve mannose, betaine, 2-hydroxyisobutyrate, isoleucine, and lactate

Zinc Oxide Nanoparticles (ZnO-NPs) Suppress Fertility by Activating Autophagy, Apoptosis, and Oxidative Stress in the Developing Oocytes of Female Zebrafish

In vertebrates, the core mechanisms that control gametogenesis are largely multiple, complex, successive, and orchestrated by intrinsic and extrinsic factors. However, age, health status, and hormonal activity are important factors for good fertility; other intangible intracellular molecular mechanisms that manage oocyte development are still unclear. The present study was designed to elucidate the ultrastructure changes in the ovary in response to its exposure to zinc oxide nanoparticles (ZnO-NPs) and to explore the role of autophagy and apoptosis during egg maturation and ovulation on the fertility of female zebrafish. In our study, ZnO-NPs could induce cytotoxicity in the maturing oocyte by activating autophagy and apoptosis in a caspase-dependent manner and could induce oxidative stress by generating reactive oxygen species (ROS) that elevated the mutated ovarian tP53 protein. Simultaneously, necroptosis developed, mimicking the features of apoptosis and necrosis. Collectively, ZnO-NPs created a suitable necrotic environment that led to follicular developmental retardation that altered oocyte ovulation and reduced fecundity of female zebrafish

Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.

Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poorly understood mechanisms. We performed a trans-ancestry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147 previously unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals. Serum urate showed significant genetic correlations with many cardiometabolic traits, with genetic causality analyses supporting a substantial role for pleiotropy. Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expression in 47 tissues implicated the kidney and liver as the main target organs and prioritized potentially causal genes and variants, including the transcriptional master regulators in the liver and kidney, HNF1A and HNF4A. Experimental validation showed that HNF4A transactivated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr139Ile is a functional variant. Transcriptional coregulation within and across organs may be a general mechanism underlying the observed pleiotropy between urate and cardiometabolic traits.The Genotype-Tissue Expression (GTEx) Project was supported by the Common Fund of the Office of the Director of the National Institutes of Health, and by NCI, NHGRI, NHLBI, NIDA, NIMH, and NINDS. Variant annotation was supported by software resources provided via the Caché Campus program of the InterSystems GmbH to Alexander Teumer

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries

Portfolio choice, behavioral preferences and equity home bias

We provide a plausible explanation of aggregate portfolio behavior, in a framework where economic agents have behavioral (narrow framing) preferences. The representative agent derives utility not only from consumption (standard models) but also from risky financial wealth fluctuations. Moreover, the investor frames the stock market risk narrowly and has loss averse preferences. We numerically solve, for the foreign equity share, a simple model of international portfolio choice, providing a possible explanation for the equity home bias puzzle. Only economic agents able to process correctly information deriving from stock markets exploit the diversification opportunities provided by international financial markets