Biology subjects

Quesada-Canales, O.

Publications and source records attributed to Quesada-Canales, O..

3 recordsLinked to original sources

bioRxiv2026

Pathologies and causes of death in stranded cetaceans in the Canary Islands (2013-2018)

Cetacean pathology is a cornerstone for population and marine ecosystem health monitoring, allowing clear differentiation among natural and anthropogenic threats. Previous studies in the Canary Islands reported natural causes of death in 59.4% (1999-2005) and 81% (2006-2012) of stranded cetaceans, versus anthropogenic causes in 33.3% and 19%, respectively. This study aimed to determine the causes of death (CD), pathologic findings, and epidemiological patterns of 316 cetaceans stranded in the Canary Islands between 2013 and 2018. The CDs were classified in pathologic entities (PEs) emphasizing natural versus anthropic origins. Of 316 animals, 224 (70.9%) from 18 species were suitable for pathological investigations. Among natural PEE, natural pathology associated with good nutritional status (NP-GNS) and natural pathology associated with significant loss of nutritional status (NP-LNS) represented 43/224 (19.2%) and 36/224 (16%) cases, respectively. Natural pathology with undetermined nutritional status (NP-UNS) occurred in 19/224 (8.5%) animals. Intra- and interspecific traumatic interactions (ITI) represented 30/224 (13.4%) cases, followed by neonatal/perinatal pathology (NPN) 19/224 (8.5%) and live-stranding stress and/or capture myopathy (LS-CM) 18/224 (8%). Infectious and parasitic diseases predominated in natural PEs. Anthropogenic PEs included interaction with fishing activities (IFA) in 17/224 (7.6%) cases, vessel collisions (VC) in 9/22 (4%) cases, and foreign body-associated pathology (FBAP) in 3/224 (1.3%) animals. Overall, anthropogenic causes accounted for 12.9% of deaths, natural causes for 73.6%, and the CD could not be established in 30/194 (13.4%) cases. This study reaffirms the trends concerning recognized PEs (NP-GNS, NP-LNS, NP-UNS, ITI, NPN, LS-CM, IFA, VC, and FBAP), expands the body of knowledge on cetacean pathology in the Canary Islands, and reports novel findings including mixed infections, clostridiosis in uncommon species, uremic syndrome secondary to urethral nematodiasis, gas embolism in unusual species, epibiont stomatitis, congenital musculo-skeletal malformations, or neoplastic processes. These findings advance understanding of cetacean mortality patterns and support conservation and management strategies.

pathology↗

bioRxiv2022

Maternal age, obesity and hyperglycaemia are associated with a delay in preimplantation development in a mouse model of type 2 diabetes

Aims/hypothesisDelayed maternal age, obesity and diabetes are associated with reduced fertility. We investigated how age and obesity/metabolic syndrome impact fertility and hypothesized that its decrease is due to defects in preimplantation embryo development. MethodsThree groups of female C57Bl6 mice (12 weeks, 9 months and 1 year old) were fed either a high fat diet for 8 weeks, to induce obesity and the metabolic syndrome, or a control chow diet. Body weight and composition, glucose tolerance and insulin resistance were assessed. Fecundity was evaluated by mating and pregnancy rates, as well as number of embryos. Embryo quality was assessed morphologically, and cell fate composition was analysed in preimplantation embryos by state-of-the-art single cell quantitative confocal image analysis. ResultsThe high fat diet was associated with increased adiposity, glucose intolerance and insulin resistance, especially in the older mice. Fecundity was affected by age, more than by the diet. Both age and high fat diet were associated with reduced cell fate allocation, indicating a delay in preimplantation embryo development, and with increased expression of GATA3, an inhibitor of placentation. Conclusion/InterpretationThese results support that age and the metabolic syndrome reduce fertility through mechanisms which are present at conception very early in pregnancy. What is already known about this subject?O_LILifestyle changes in modern societies have led to an increase in obesity and type 2 diabetes, and women tend to become pregnant later than ever. These factors have a negative influence on female fecundity. C_LIO_LIIn mice, diet induced obesity is associated with poor quality oocytes that affect overall embryonic development. C_LI What is the key question?O_LIDo age and high fat diet influence cell fate differentiation during preimplantation embryo development? C_LI What are the new findings?O_LIBody composition and glucose metabolism are altered due to high fat diet even when weight is not affected in young animals. C_LIO_LIAlthough there are no differences in mating and fertilization rates, embryo quality is lower with high fat diet. C_LIO_LICells not fully committed to a cell fate (epiblast or primitive endoderm) are increased in embryos from mature dams or fed a high fat diet, indicating a delay in preimplantation embryo development. C_LI How might this impact on clinical practice in the foreseeable future?O_LIOur findings show a delay in early embryo development associated to obesity and maternal age. This delay could be responsible for the low fertility observed in women with type 2 diabetes and obesity. C_LI

developmental biology↗

bioRxiv2022

Cetacean "gas-bubble thromboembolic polycystic liver disease": "Budd-Chiari-like syndrome" in dolphins?

Nearly two decades ago, pathologic examination results suggested acoustic factors, such as mid-frequency active naval military sonar (MFAS) could be the cause of acute decompression-like sickness in stranded beaked whales. Acute systemic gas embolism in these beaked whales was published together with enigmatic cystic liver lesions (CLL), characterized by intrahepatic encapsulated gas-filled cysts, tentatively interpreted as "gas-bubble" lesions in various cetacean species. Here we provide a pathologic reinterpretation of CLL in cetaceans. From 1,200 cetaceans necropsied, CLL were only observed in striped dolphins (Stenella coeruleoalba), with a low prevalence (2%), and recapitulated pathologic features of Budd-Chiari syndrome in humans. Our results strongly suggest that CLL are the result of the combination of pre-existing or concomitant hepatic vascular disorder (e.g., severe hepatobiliary trematodiasis) superimposed and exacerbated by gas bubbles, and clearly differ from acute systemic gas embolism in stranded beaked whales linked to MFAS.

pathology↗