Advances in experimental medicine and biology最新文献

Parasitoids have an exceptional lifestyle where juvenile development is spent on or in a single host insect, but the adults are free-living. Unlike parasites, parasitoids kill the host. How parasitoids use such a limiting resource, particularly lipids, can affect chances to survive and reproduce. In part 1, we describe the parasitoid lifestyle, including typical developmental strategies. Lipid metabolism in parasitoids has been of interest to researchers since the 1960s and continues to fascinate ecologists, evolutionists, physiologists, and entomologists alike. One reason of this interest is that the majority of parasitoids do not accumulate triacylglycerols as adults. Early research revealed that some parasitoid larvae mimic the fatty acid composition of the host, which may result from a lack of de novo triacylglycerol synthesis. More recent work has focused on the evolution of lack of adult triacylglycerol accumulation and consequences for life history traits. In part 2 of this chapter, we discuss research efforts on lipid metabolism in parasitoids from the 1960s onwards. Parasitoids are also master manipulators of host physiology, including lipid metabolism, having evolved a range of mechanisms to affect the release, synthesis, transport, and take-up of lipids from the host. We lay out the effects of parasitism on host physiology in part 3 of this chapter.

Background: The most common genetic cause associated with thrombophilia is Leiden mutation (G1691A) of the coagulation factor V (FV) (F5) gene.

Materials and methods: Data collected anonymously from 355 unrelated Greeks examined for the above mutation were analyzed. Bioinformatic investigation was conducted for factor V, including phylogenetic analysis, genetic network analysis, and 3D modelling of wild-type and Leiden protein.

Results: Analysis confirmed the importance of F5 Leiden in thrombosis and the significance of a positive family history of thrombosis. In silico analysis of the F5 Leiden revealed a linkage between mammalian species and a potential functional interaction of F5 with 25 other genes, several of which have been associated with cardiovascular diseases. 3D modelling revealed that the Leiden mutation confers an H-bond network alteration in the functional region of FV, resulting in a hypercoagulable state.

Conclusions: This study highlighted the great value of a positive family history of thrombosis and the importance of testing for this common mutation as a prevention strategy component for thrombophilia, including thrombotic brain aneurysms. Bioinformatic analysis indicated the importance of the Leiden mutation in protein structure and function. The findings of this study increase understanding of molecular and clinical features of thrombophilia and may eventually lead to better prevention of thrombosis.

Acute myeloid leukemia (AML) is a heterogeneous hematological melanoma disease, which faces significant challenges in diagnosis and treatment due to its genetic complexity and variable clinical outcomes.NF342 by juxtaposition with MPO promoter/enhan In the current work, the potential of microarrays and next-generation RNA sequencing (RNA-seq) is assessed for the study of cancer and specifically to separate differences in expression that distinguish samples with AML from control ones. By using datasets derived from microarrays and RNA-seq, the study observes that there are differences in gene expression between AML samples and control. The selected probes were used as a foundation in the development of a classifier that can distinguish the AML samples. The probes then underwent cross-mapping from the microarrays platform to the RNA-seq one and vice versa. This ensured the adaptability and the reliability of the classifier on different platforms. The classifier that was trained (using probes from the same platform) showed greater reliability in the dataset from next-generation RNA-seq platform, with an accuracy of 98.9%, 98.7% sensitivity, and 100% specificity. However, when opposite platform probes were used, that underwent cross-mapping, the reliability of the classifier in the dataset from microarrays platform significantly increased. In particular, it reached an accuracy of 99.3%, 99.4% specificity, and a sensitivity of 96.4%. Lastly, the selection methods were used again with a higher number of genes and then gene set enrichment analysis was performed to find the pathways where the genes are connected. This showed the significance of multiple pathways including "Protein processing in endoplasmic reticulum Homo sapiens hsa04141" and "Proteoglycans in cancer Homo sapiens hsa05205."

Prenatal alcohol exposure (PAE) is recognized as a leading preventable cause of birth defects, giving rise to a continuum of cognitive, behavioral, and physical impairments collectively referred to as Fetal Alcohol Spectrum Disorders (FASD). While PAE affects multiple developing organ systems, the fetal brain is particularly vulnerable, exhibiting enduring structural and functional abnormalities in response to alcohol exposure. Recent research highlights mitochondrial dysfunction as an important mechanism in the pathogenesis of alcohol-related neurodevelopmental deficits. Mitochondria are highly susceptible to alcohol-induced damage, and mounting evidence demonstrates mitochondrial impairments across various organ systems following PAE-focusing growing attention on its specific effects within the developing central nervous system. This chapter explores the essential roles of mitochondria throughout key stages of neurodevelopment and evaluates how PAE disrupts mitochondrial function in different organ systems. Special emphasis is placed on the developing brain, with a focus on its three primary cellular populations: neurons, glial cells, and the cerebral vasculature. Current findings indicate that fetal mitochondria are particularly sensitive to alcohol exposure, resulting in altered mitochondrial morphology, increased production of reactive oxygen species (ROS), elevated oxidative stress, and impaired cellular respiration.Taken together, these data underscore mitochondria as a critical and vulnerable target of PAE-especially in the developing brain-where mitochondrial dysfunction contributes to the neurodevelopmental deficits' characteristic of FASD. Advancing our understanding of these mechanisms opens the door to mitochondria-targeted interventions, offering promising therapeutic avenues to protect mitochondrial function and mitigate the long-term consequences of prenatal alcohol exposure.

Fetal alcohol spectrum disorders (FASD) represent a significant global health concern and are the leading cause of preventable birth defects, intellectual disabilities, and persistent behavioral deficits. The neurodevelopmental mechanisms underlying FASD are not yet fully understood, but there is growing interest in the role of cortical development in the manifestation of these disorders. The cerebral cortex serves as the master regulator of higher-order functions, including sensory perception, motor planning, decision-making, and general intelligence-processes that are all adversely affected by prenatal alcohol exposure (PAE). Higher-level functions emerge from a complex and intricately interconnected neuronal network that develops through a series of delicate and sequential stages involving neuronal and glial cell generation, proliferation, migration, differentiation, and maturation. Recent evidence suggests that PAE disrupts these developmental processes, leading to impaired cortical structure, altered connectivity, and ultimately, to the neurobehavioral deficits observed in individuals with FASD. Rodent models, along with in vitro approaches, have proven invaluable for elucidating the consequences of PAE on cortical development and the underlying mechanisms associated with PAE-related disorders. Although gaps in knowledge remain, advancing our understanding of the neurodevelopmental basis of FASD is essential for identifying potential therapeutic targets and enhancing early intervention strategies for those affected by FASD in the future.

Background: Empathy cultivates deeper interpersonal relationships; however, frequent exposure can trigger the risk of burnout. This study aims to predict empathy, burnout, and syndrome among nursing staff in a university hospital in Central Greece.

Material and methods: This is a synchronic study on the nursing staff of the university general hospital in central Greece. The sample consisted of 210 nurses who took part in the study by completing a questionnaire that included demographic and social characteristics, the "Copenhagen Burnout Inventory" and the "Composite Empathy Scale." The Pearson correlation coefficient (r) and linear regression analysis with a statistical significance of 0.05 were used for the statistical analysis. Univariate and multiple logistic regression analyses were used to determine the potential predictive factors associated with burnout and empathy.

Results: The prevalence of burnout and empathy among nursing staff was 62.5%. A significant positive correlation between empathy with burnout was found in almost all dimensions. For burnout subscales, "Personal Burnout" was found to be at 44.1%, Operational Burnout "at 62.5%, and in" Burn related to patients "the average was 58.3%. A higher level of burnout is associated with" Workplace Burnout "for nurses on shift work. There was a significant negative correlation between "Cognitive Personal Empathy" and the "Personal Burnout." Also, 92.9% of the nursing staff reported suffering from a disease.

Conclusion: The nurses in the university hospital are "aged staff" with health problems, high levels of empathy, and burnout.

Introduction: Mental health nursing can be highly rewarding but at the same time overwhelmingly stressful or even traumatizing. Spirituality constitutes a central element of mental health nurses' resilience while personal trauma may be activated during exposure to beneficiaries' trauma.

Aim: The aim of this study is to examine the impact of sociodemographic and work-related characteristics, spirituality, and history of trauma on compassion fatigue (CF) and compassion satisfaction among psychiatric nurses in Greece.

Methods: A cross-sectional survey study with a total of 91 mental health nurses selected by convenience sampling and required to complete the Professional Quality of Life Scale (ProQOL-V), the FACIT-Spiritual Well-Being Scale-12 non-illness scale, and the Traumatic Life Events Questionnaire (TLEQ).

Results: More than a quarter (25.3%) of participants reported high compassion fatigue risk, while 76% expressed high to moderate potential for compassion satisfaction. Secondary traumatic stress (STS) as expected was found to correlate positively with traumatic life events and negatively with the spirituality dimension of meaning. Spiritual well-being, good physical health, high levels of cooperation, respect for teamwork and positive work climate were positively related to higher levels of compassion satisfaction.

Conclusion: The findings of this study shed light on the significant prevalence of compassion fatigue and personal trauma history among nursing staff, highlighting the need for targeted interventions to improve the mental health of front-line health care nurses. Mental health care organizations must recognize the importance of fostering compassionate work environments that prioritize mental health professionals' spiritual and psychological well-being.

Insects, like most animals, have intimate interactions with microorganisms that can influence the insect host's lipid metabolism. In this chapter, we describe what is known so far about the role prokaryotic microorganisms play in insect lipid metabolism. We start exploring microbe-insect lipid interactions focusing on endosymbionts, and more specifically the gut microbiota that has been predominantly studied in Drosophila melanogaster. We then move on to an overview of the work done on the common and well-studied endosymbiont Wolbachia pipientis, also in interaction with other microbes. Taking a slightly different angle, we then look at the effect of human pathogens, including dengue and other viruses, on the lipids of mosquito vectors. We extend the work on human pathogens and include interactions with the endosymbiont Wolbachia that was identified as a natural tool to reduce the spread of mosquito-borne diseases. Research on lipid metabolism of plant disease vectors is up and coming and we end this chapter by highlighting current knowledge in that field.

Lipids are essential in insects and play pleiotropic roles in energy storage, serving as a fuel for energy-driven processes such as reproduction, growth, development, locomotion, flight, starvation response, and diapause induction, maintenance, and termination. Lipids also play fundamental roles in signal transduction, hormone synthesis, forming components of the cell membrane, and thus are essential for maintenance of normal life functions. In insects, the neuroendocrine system serves as a master regulator of most life activities, including growth and development. It is thus important to pay particular attention to the regulation of lipid metabolism through the endocrine system, especially when considering the involvement of peptide hormones in the processes of lipogenesis and lipolysis. In insects, there are several lipogenic and lipolytic hormones that are involved in lipid metabolism such as insulin-like peptides (ILPs), adipokinetic hormone (AKH), 20-hydroxyecdysone (20-HE), juvenile hormone (JH), and serotonin. Other neuropeptides such as diapause hormone-pheromone biosynthesis activating neuropeptide (DH-PBAN), CCHamide-2, short neuropeptideF, and the cytokines Unpaired 1 and 2 may play a role in inducing lipogenesis. On the other hand, neuropeptides such as neuropeptide F, allatostatin-A, corazonin, leukokinin, tachykinins, limostatins, and insulin-like growth factor (ILP6) stimulate lipolysis. This chapter briefly discusses the current knowledge of the endocrine regulation of lipid metabolism in insects that could be utilized to reveal differences between insects and mammalian lipid metabolism which may help understand human diseases associated with dysregulation of lipid metabolism. Physiological similarities of insects to mammals make them valuable model systems for studying human diseases characterized by disrupted lipid metabolism, including conditions like diabetes, obesity, arteriosclerosis, and various metabolic syndromes.

While the primary function of red blood cells (RBCs) in the human body is the transport of gases (oxygen and carbon dioxide) in the vascular system, research conducted over the past few decades has demonstrated that RBCs also play a role in the active regulation of blood flow by releasing vasoactive substances (adenosine triphosphate, ATP, and nitric oxide, NO). This chapter provides an overview of the process involved in this ATP- and NO-mediated vasodilation of RBCs, and its relevance to human physiology and pathophysiology.