Various animal toxins pose a significant threat to human safety, necessitating urgent attention to their treatment and research. The clinical potential of programmed cell death (PCD) is widely regarded as a target for envenomation, given its crucial role in regulating physiological and pathophysiological processes. Current research on animal toxins examines their specific components in pathomechanisms and injuries, as well as their clinical applications. This review explores the relationship between various toxins and several types of PCD, such as apoptosis, necroptosis, autophagy, ferroptosis, and pyroptosis, to provide a reference for future understanding of the pathophysiology of toxins and the development of their potential clinical value.

Selenium is an essential trace element for health that can only be obtained through food. However, the pathological processes of selenium deficiency in cattle have received little attention. This study investigated the effects of selenium deficiency on oxidative stress, apoptosis, inflammation, and necroptosis in the lungs of weaning calves compared with healthy calves as controls. The lung selenium content and the expression of 11 selenoproteins mRNA in selenium-deficient calves were substantially reduced compared with the controls. Pathological results showed engorged alveolar capillaries, thickened alveolar septa, and diffuse interstitial inflammation throughout the alveolar septa. The levels of GSH and T-AOC, as well as the CAT, SOD, and TrxR activities, were significantly decreased compared with healthy calves. MDA and H2O2 were significantly elevated. Meanwhile, the apoptosis activation in the Se-D group was validated. Next, in the Se-D group, several pro-inflammatory cytokines showed higher expression. Further research revealed that the lungs in the Se-D group experienced inflammation via hyperactive NF-κB and MAPK pathways. The high level of expression of c-FLIP, MLKL, RIPK1, and RIPK3 indicated that necroptosis also causes lung damage during selenium deficiency.

Diabetic wounds are a common complication in diabetes patients. Due to peripheral nerve damage and vascular dysfunction, diabetic wounds are prone to progress to local ulcers, wound gangrene and even to require amputation, bringing huge psychological and economic burdens to patients. However, the current treatment methods for diabetic wounds mainly include wound accessories, negative pressure drainage, skin grafting and surgery; there is still no ideal treatment to promote diabetic wound healing at present. Appropriate animal models can simulate the physiological mechanism of diabetic wounds, providing a basis for translational research in treating diabetic wound healing. Although there are no animal models that can fully mimic the pathophysiological mechanisms of diabetic wounds in humans, it is vital to explore animal simulation models used in basic research and preclinical studies of diabetic wounds. In addition, hydrogel materials are regarded as a promising treatment for diabetic wounds because of their good antimicrobial activity, biocompatibility, biodegradation and appropriate mechanical properties. Herein, we review and discuss the different animal models used to investigate the pathological mechanisms of diabetic wounds. We further discuss the promising future application of hydrogel biomaterials in diabetic wound healing.

Migraine and depression often coexist and constitute an important clinical problem. Both disorders are associated with the necessity of chronic treatment, and their mutual coexistence contributes to the phenomenon of drug resistance. Influencing the functioning of patients, they also cause numerous social consequences - affecting the quality of life and achievement of personal goals of patients. This review presents factors that may explain the common pathomechanisms of depression and migraine. Structural and functional disturbances of the central nervous system (CNS), disturbances in the neurotransmitter systems, inflammatory theories, hormonal disturbances, as well as a possible genetic basis were taken into account. Due to the fact that both depression and migraine have a multifactorial etiology and at the present stage of scientific research it is difficult to clearly determine which factor is the most important, such a broad overview has been presented. It is also difficult to determine which of the above-mentioned factors, well documented in international studies, only coexist, and which of them may have a cause-and-effect relationship in the described disorders. Further research into the comorbidity and causes of migraine and depression seems to be worth considering.

White matter lesion (WML), also known as white matter hyperintensities or leukoaraiosis, was first termed in 1986 to describe the hyperintense signals on T2-weighted imaging (T2WI) and fluid-attenuated inversion recovery (FLAIR) maps. Over the past decades, a growing body of pathophysiological findings regarding WMLs have been discovered and discussed. Currently, the generally accepted WML pathogeneses mainly include hypoxia-ischemia, endothelial dysfunction, blood-brain barrier disruption, and infiltration of inflammatory mediators or cytokines. However, none of them can explain the whole dynamics of WML formation. Herein, we primarily focus on the pathogeneses and neuroimaging features of vascular WMLs. To achieve this goal, we searched papers with any type published in PubMed from 1950 to 2020 and cross-referenced the keywords including \"leukoencephalopathy\", \"leukoaraiosis\", \"white matter hyperintensity\", \"white matter lesion\", \"pathogenesis\", \"pathology\", \"pathophysiology\", and \"neuroimaging\". Moreover, references of the selected articles were browsed and searched for additional pertinent articles. We believe this work will supply the robust references for clinicians to further understand the different WML patterns of varying vascular etiologies and thus make customized treatment.