Micro- and nanoplastics (MNPs) have emerged as environmental contaminants of increasing concern due to their potential to disrupt biological systems. The liver, as a key organ in detoxification and metabolism, is particularly susceptible to MNP-induced injury. This scoping review aimed to synthesize experimental evidence from preclinical animal models to identify the principal hepatotoxic mechanisms induced by MNP exposure and evaluate the implications for human health. A systematic search was conducted in PubMed, Scopus, Web of Science, and OpenAlex databases. Eligible studies included original research assessing hepatic outcomes in animal models exposed to MNPs. Data were charted for polymer type, particle size, exposure route, exposure duration, and toxicological endpoints. The review followed PRISMA-ScR guidelines and included 34 studies. Consistent hepatotoxic signatures were identified, including oxidative stress, inflammation, lipid dysregulation, and apoptosis. Polystyrene, polyethylene, and polylactic acid were the most studied polymers, with exposure via oral gavage or aquatic immersion. Mitochondrial dysfunction and genotoxic markers were also reported. The mechanistic convergence suggests shared injury pathways across particle types and models. MNPs induce liver injury through oxidative, inflammatory, and metabolic mechanisms, supporting their classification as emerging hepatotoxicants. While translational gaps persist, these findings highlight urgent research needs and inform environmental health risk frameworks.

Sudden death (SD) is a health problem worldwide affecting all strata of the population. The main cause of SD is ischemic heart disease (IHD). The aims of the study were as follows: (i) to analyze the incidence of deaths from IHD in two successive periods (1998-2006 and 2007-2015) to visualize the magnitude of the problem and (ii) to review the official reports of SD in the same lapse of time. During that period, instantaneous death (ISD) and death that occurred in the first 24 h after the onset of symptoms were analyzed according to the official databases of National Institute of Statistics and Geography (INEGI) and National Health Information System (SINAIS). There was an under-registration of SD cases in Mexico. Only 1394 cases of ISD were recorded officially in 17 years period of study, whereas it is estimated that 33,000 cases occur annually, exclusively due to sudden cardiac death. There is a serious gap in the official epidemiological information; placing the real problem in perspective would help to establish the adequate public policies for both, prevention and investigation of the causes of SD in Mexico.

Breast density (BD) is a risk factor for breast cancer.Aims. To describe BD patterns in asymptomatic Mexican women and the pathological mammographic findings.Methods and Material. Prospective, descriptive, and comparative study. Women answered a questionnaire and their mammograms were analyzed according to BI-RADS. Univariate () and conditional logistic regression analyses were performed.Results. In 300 women studied the BD patterns were fat 56.7% (170), fibroglandular 29% (87), heterogeneously dense 5.7% (17), and dense pattern 8.6% (26). Prevalence of fat pattern was significantly different in women under 50 years (37.6%, 44/117) and older than 50 (68.8%, 126/183). Patterns of high breast density (BD) (dense + heterogeneously dense) were observed in 25.6% (30/117) of women ≤50 years and 7.1% (13/183) of women >50. Asymmetry in BD was observed in 22% (66/300). Compression cone ruled out underlying disease in 56 cases. In the remaining 10, biopsy revealed one fibroadenoma, one complex cyst, and 6 invasive and 2 intraductal carcinomas. 2.6% (8/300) of patients had non-palpable carcinomas. Benign lesions were observed in 63.3% (190/300) of cases, vascular calcification in 150 cases (78.9%), and fat necrosis in 38 cases (20%).Conclusions. Mexican women have a low percentage of high-density patterns.

Background: Scarce evidence about the organic and functional abnormalities of systemic exertion intolerance disease (SEID) is found in literature and the pathophysiology is still unclear. Methods: Following the CARE Guidelines, this case report describes a patient with a 5-year history of nonspecific symptoms, lately recognized as SEID. Results: Low serum thyroid- and adrenocorticotropic stimulating hormone levels, and 24-h urinary cortisol excretion almost twice the upper limit were detected. Computed tomography scan found significant cortical atrophy. Low-dose modafinil improved the clinical outcome, added to nonpharmacologic approach. Conclusion: To ascertain an accurate SEID diagnosis and treatment are a challenge in daily clinical practice, that must be engaged based in clear methods and good practice recommendations. Thus, family practitioners should be aware of this diagnosis.

Temporal lobe epilepsy (TLE) represents a prevalent form of partial epilepsy that often requires surgical intervention and can be resistant to antiepileptic drugs. Its epidemiology varies across regions due to diagnostic challenges and underestimation of individual neurological traits. Despite these complexities, TLE accounts for a significant proportion of total epilepsies worldwide. Early discussions on TLE's forensic implications date back to the mid-20th century, highlighting its unique behavioral and mental disturbances during seizures. The international classification for epilepsies categorizes seizures based on type and onset, aiding in diagnosis and treatment planning. Neuroimaging techniques play a crucial role in identifying the epileptogenic focus within the temporal lobe. TLE's etiology involves various risk factors, including genetic predisposition and neurological insults. Clinically, TLE presents with diverse signs and symptoms across different phases. This narrative review explores the forensic implications of TLE, including legal responsibility, sudden death, and its association with criminal behavior. It examines the challenges in diagnosing TLE in court and discusses the complex interplay between TLE, psychosis, and substance use in determining legal liability. Furthermore, it addresses the risk of sudden unexpected death in epilepsy (SUDEP) and sudden unexplained death in childhood (SUDC) associated with TLE. Finally, the review underscores the need for further research to comprehensively understand TLE's forensic and medicolegal implications, considering its intricate neurobiological underpinnings and clinical manifestations.