Since 1998, California sea lion (Zalophus californianus) stranding events associated with domoic acid toxicosis (DAT) have consistently increased. Outside of direct measurement of domoic acid in bodily fluids at the time of stranding, there are no practical nonlethal clinical tests for the diagnosis of DAT that can be utilized in a rehabilitation facility. Proteomics analysis was conducted to discover candidate protein markers of DAT using cerebrospinal fluid from stranded California sea lions with acute DAT (n = 8), chronic DAT (n = 19), or without DAT (n = 13). A total of 2005 protein families were identified experiment-wide. A total of 83 proteins were significantly different in abundance across the three groups (adj. p < 0.05). MDH1, PLD3, ADAM22, YWHAG, VGF, and CLSTN1 could discriminate California sea lions with or without DAT (AuROC > 0.75). IGKV2D-28, PTRPF, KNG1, F2, and SNCB were able to discriminate acute DAT from chronic DAT (AuROC > 0.75). Proteins involved in alpha synuclein deposition were over-represented as classifiers of DAT, and many of these proteins have been implicated in a variety of neurodegenerative diseases. These proteins should be considered potential markers for DAT in California sea lions and should be prioritized for future validation studies as biomarkers.

Amanita phalloides poisoning is known to be the most fatal case among mushroom poisoning cases. Its main mechanism of toxicity is that it leads to cell death by the irreversible binding of its toxins to the DNA-dependent RNA polymerase II enzyme. This study was planned to analyze the effects of the CDP-choline molecule on Amanita phalloides mushroom poisoning cases. The extract of the Amanita phalloides mushroom was taken and intraperitoneally administered to male Wistar Albino rats at a dose of 0.3 g/kg. In the experiment phase, the rats were divided into three groups of CDP-choline treatment according to the doses of 100 mg/kg, 250 mg/kg, and 500 mg/kg, and one control group was administered a 1 ml/kg dose of 0.9% isotonic NaCl solution. The treatments were then administered intraperitoneally at the 2nd hour, and at the 6th hour, the rats were sacrificed. The degree of damage in the liver and kidney tissues of the rats was evaluated histopathologically. It was concluded that CDP-choline reduced or prevented the damage that occurred in the liver significantly and dose-dependently in the toxicosis picture caused by Amanita phalloides, and it showed a tendency to lower or prevent the damage in the kidney, albeit not significantly.

This article is intended to highlight toxicosis-associated pathology in horses that might be observed by a clinician in the living animal and at gross necropsy. When the clinician is aware of these pathologic changes (particularly when coupled with a suggestive environmental or herd history), then collaboration with a diagnostic laboratory can begin to help identify specific toxicants. Proper sampling and communication with the diagnostic laboratory will vastly improve the likelihood of a specific diagnosis; postmortem sampling and specimen submission are reviewed in the last section of this article.

UNASSIGNED: Domoic acid (DA) is a glutaminergic excitatory neurotoxin that causes the morbidity and mortality of California sea lions (Zalophus californianus; CSL) and other marine mammals due to a suite of effects mostly on the nervous and cardiac systems. Between 1998 and 2019, 11,737 live-stranded CSL were admitted to The Marine Mammal Center (TMMC; Sausalito, CA, USA), over 2,000 of which were intoxicated by DA. A plethora of clinical research has been performed over the past 20 years to characterize the range of toxic effects of DA exposure on CSLs, generating the largest dataset on the effects of natural exposure to this toxin in wildlife.
UNASSIGNED: In this study, we review published methods for diagnosing DA intoxication, clinical presentation, and treatment of DA-intoxicated CSL and present a practical, reproducible scoring system called the neuroscore (NS) to help assess whether a DA-affected CSL is fit for release to the wild following rehabilitation. Logistic regression models were used to assess the relationships between outcome (released vs. euthanized or died) and multiple variables to predict the outcome for a subset of 92 stranded CSLs.
UNASSIGNED: The largest proportion of DA-intoxicated CSLs was adult females (58.6%). The proportions of acute and chronic cases were 63.5 and 36.5% respectively, with 44% of affected CSL released and 56% either dying naturally or euthanized. The average time in rehabilitation was 15.9 days (range 0-169) for all outcomes. The best-performing model (85% accuracy; area under the curve = 0.90) assessing the relationship between outcome and predictor variables consisted of four variables: final NS, change in NS over time, whether the animal began eating in rehabilitation, and the state of nutrition on admission.
UNASSIGNED: Our results provide longitudinal information on the symptomatology of CSL intoxicated by domoic acid and suggest that a behavioral scoring system is a useful tool to assess the fitness for the release of DA-intoxicated CSL.

Veterinarians are often called upon to diagnose health-related issues on the farm that may be related to trace mineral deficiencies or toxicities. Trace mineral feeding rates are often not available due to the proprietary nature of the trace mineral premixes provided by nutritional consultants. The veterinarian needs to be aware of the common clinical signs of trace mineral deficiencies and toxicities, interactions between trace minerals that may result in deficiencies, clinical samples that are necessary for the proper diagnosis, and the recommended normal ranges of each trace mineral depending on the age of the animal.

Veterinarians are often called upon to diagnose health-related issues on the farm that may be related to trace mineral deficiencies or toxicities. Trace mineral feeding rates are often not available due to the proprietary nature of the trace mineral premixes provided by nutritional consultants. The veterinarian needs to be aware of the common clinical signs of trace mineral deficiencies and toxicities, interactions between trace minerals that may result in deficiencies, clinical samples that are necessary for the proper diagnosis, and the recommended normal ranges of each trace mineral depending on the age of the animal.

Introduction: In the scenario of metal toxicity, aluminum (Al) stands out as a ubiquitous type of metal that can be combined with other elements and form different compounds. Al is widely used daily as an adjuvant in vaccines, antacids, food additives (as components of AI-containing food additives), skin care products, cosmetics, and kitchenware, and can be an element or contaminant present in our daily life. Objective: To present a review of the main deleterious effects of Al on human health. Methods: The search was carried out from September 2022 to February 2023 in the Scopus, PubMed, Science Direct, Scielo, and Google Scholar databases, using scientific articles from 2012 to 2023. The quality of the studies was based on the GRADE instrument, and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusions: A total of 115 files were search returned. Further, 95 articles were evaluated, and 44 were included in this review. Based on the results, measuring Al\'s relevance to health is essential in medicine. Several studies have demonstrated clinical outcomes and metabolic alterations with Al exposure. The tolerable weekly intake established by the European Food Safety Authority (EFSA) of 1 mg Al/kg body weight can be achieved through dietary exposure alone. Proven neurotoxicity in humans is the critical adverse effect of Al. A carcinogenic effect of Al has not been proven so far. Preventive medicine advocates that exposure to Al should be kept as low as possible. Chelating agents, such as calcium disodium ethylene diamine tetraacetic acid and deferoxamine, are options for acute poisoning, and monomethysilanetriol supplementation may be a long-term strategy with chelation potential. Further studies are needed to assess the impacts of Al on human health.

A flock of 50,000 28-day-old broiler breeder chickens experienced an elevated mortality event. Chickens from that flock, five pullets and six cockerels, were submitted for diagnostic investigation. Necropsy revealed bacterial septicemia with fibrinous polyserositis in the majority of the birds while two cockerels had coccidial typhlitis. Because sulfadimethoxine was not available at the time, sulfaquinoxaline (SQ) was prescribed at label dosage with water treatment for 2 days, followed by 3 days of no medication, followed by 2 days of medication. The mortality rose dramatically 9 days after the last treatment. Lesions at that time consisted of skin discoloration, subcutaneous petechiation, and enlarged pale kidneys. Mortality remained elevated for 14 days. Analysis of blood, kidney, and liver revealed elevated levels of SQ. Recalculation of dosage, water consumption, amount of drug administered, remaining drug stock, and concentration of supplied SQ were analyzed and determined to be as predicted.
Reporte de caso- Toxicosis por sulfaquinoxalina en una parvada de reproductores de pesados jóvenes. Una parvada de 50,000 pollos de engorde de 28 días de edad experimentó un evento de mortalidad elevada. Pollos de esa parvada, cinco pollitas y seis gallitos, se enviaron para una investigación de diagnóstico. La necropsia reveló septicemia bacteriana con poliserositis fibrinosa en la mayoría de las aves, mientras que dos gallos tenían tiflitis coccidial. Debido a que la sulfadimetoxina no estaba disponible en ese momento, se prescribió sulfaquinoxalina (SQ) de acuerdo a la dosis de la etiqueta con tratamiento en el agua durante dos días, seguidos por tres días sin medicación, y por último, seguidos por dos días de medicación. La mortalidad aumentó dramáticamente nueve días después del último tratamiento. Las lesiones en ese momento consistían en decoloración de la piel, petequias subcutáneas y riñones agrandados y pálidos. La mortalidad se mantuvo elevada durante 14 días. El análisis de sangre, riñón e hígado reveló niveles elevados de sulfaquinoxalina. Se analizó el recálculo de la dosis, el consumo de agua, la cantidad de fármaco administrado, el stock de fármaco restante y la concentración de sulfaquinoxalina suministrada y se determinó que eran los previstos.

Hippocampal pathology in diabetes is constantly investigated but the resultant health impact of the concomitant presence of alcohol and combined antiretroviral therapy (cART) in diabetes requires further studies to delineate toxicities inimical to hippocampal normal function. Forty-eight male Sprague Dawley rats were divided into eight groups (n = 6): negative control (NC), alcohol (AL), cART (AV), alcohol-cART (AA), diabetic control (DB), diabetes-alcohol (DAL), diabetes-cART (DAV), and diabetes-alcohol-cART (DAA) exposure groups. Following diabetes induction and sub-chronic (90 days) treatment exposure, hippocampal homogenates were profiled for pro-inflammatory cytokines and oxidative stress (MDA and GPx) using immunoassay, while apoptotic genes (BAX, Bcl2, and Caspase-3), insulin receptor genes (INSR and IRS-1), and blood-brain barrier (BBB) junctional proteins (claudin-5, and occludin) gene expression were assessed using qPCR. Histomorphology of hippocampal neuronal number, nuclei area, and volume of dentate gyrus and neurogenesis were accessed using Giemsa stain, Ki67, and DCX histochemistry respectively. A central hippocampal effect that underpins all treatments is the reduction of DG neuronal number and antioxidant (GPx), highlighting the venerability of the hippocampal dentate gyrus neurons to diabetes, alcohol, cART, and their combinatorial interactions. Additionally, elevated BAX, Bcl2, and IRS1 mRNA levels in the DAL group, and their downregulation in AA, suggests IRS-1-regulated apoptosis due to differential modulating effects of alcohol treatment in diabetes (DAL) in contrast to alcohol with cART (AA). Although the interaction in AA therapy ameliorated the independent alcohol and cART effects on MDA levels, pro-inflammatory cytokines, and DCX, the interaction in AA exacerbated a deficiency in the expression of INSR, IRS-1 (insulin sensitivity), and BBB mRNA which are implicated in the pathogenies of diabetes. Furthermore, the diabetic comorbidity groups (DAV, DAL, and DAA) all share a central effect of elevated hippocampal oxidative stress, BAX, and Caspase-3 mRNA expression with the reduced number of hippocampal neurons, dentate gyrus volume, and neurogenesis, highlighting neurodegenerative and cognitive deficiency implication of these comorbidity treatments. Considering these findings, assessment of hippocampal well-being in patients with these comorbidities/treatment combinations is invaluable and caution is advised particularly in alcohol use with cART prophylaxis in diabetes.

Lead (Pb) was implicated in multiple genotoxic, neuroepigenotoxic, and chromosomal-toxic mechanisms and interacted with varying synaptic plasticity pathways, likely underpinning previous reports of links between Pb and cognitive impairment. Epigenetic changes have emerged as a promising biomarker for neurological disorders, including cognitive disorders, Alzheimer\'s disease (AD), and Parkinson\'s disease (PD). In the present review, special attention is paid to neural epigenetic features and mechanisms that can alter gene expression patterns upon environmental Pb exposure in rodents, primates, and zebrafish. Epigenetic modifications have also been discussed in population studies and cell experiment. Further, we explore growing evidence of potential linkage between Pb-induced disruption of regulatory pathway and neurodevelopmental and neurological disorders both in vivo and in vitro. These findings uncover how epigenome in neurons facilitates the development and function of the brain in response to Pb insult.