Introduction: Currently, several models of stimulus-response perception have been theorized, but none have integrated second-person neuroscience with neuromaladaptive mechanisms, that is, those involving social interactions. Objective: To assist in the comprehensive multiscale understanding of cognitive function and behavior through clinical insight into the sequential phases of perceptual processes of the 5-phase multimodal model of perception. Methodology: We synthesized a 5-phase model of perception, with a generative view of perception and second-person neuroscience, in a "Bayesian" computational method, which was guided by theoretical method and robust clinical empiricism. Results and Discussion: We used the adaptation and integration of some cognitive models and presented the model based on theoretical data, combined with empirical clinical observation. Conclusion: The novel model captured nuanced patterns of functioning in dysfunctional subfunctions of perceptual neurocognition, which generate patterns of negative effects on cognition and behavior, with several neurobiological mechanisms, which were characterized as perceptual errors. Currently, this set contributes to various types of social conflicts, domestic violence, parental neglect, behavioral deviations, and addictive disorders.

Introduction: Maternal separation and neonatal paternal deprivation (PPD) have had profound and persistent effects on the physiological and behavioral development of children, with other problems neglected in professional practice, such as adverse childhood emotions and post-traumatic stress disorder (PTSD) in children, which accumulate evidence of the same cumulative effects while a harmful vicious cycle is not identified. Objective: To update the different areas of professional activity, which exert direct or indirect influence on the mental health of children, such as social workers, lawyers, judges, psychologists, psychiatrists, doctors, and educators, as well as the parents themselves, through concrete evidence from neuroscience and psychosocial neurobiology, exclusive to paternal deprivation. Methods: Review of the literature and performance of a clinical synthesis with theoretical implications, based on neurobiological and neurogenomic mechanisms, which demonstrates a concrete and harmful factor for evolutionary medicine. Results and Discussion: There are few studies on paternal deprivation in humans, and many studies in rats and mice were used to explore the mechanisms in this review, as they are equivalent to human brains. In addition to the harmful effects of deprivation, we explored other neurobiological mechanisms that are associated with paternal presence. Conclusion: This work brings together some consequences for the physical and mental health of children, as well as their future generations, which are being neglected and complicated by several professionals in medicine, law, psychology, social assistance, and politics

Introduction: Systems medicine is an approach to understanding disease through the integration of large patient data sets, integrating data with clinical measurements, which have the potential to impact our understanding of the molecular basis and management of a disease. Objective: To present a new model of Systems Medicine, which is based on neuroscience and human neurobiology, which presents the robustness of empiricism, and which addresses groups of diagnoses of chronic comorbidities, which are linked to neuropsychological symptoms, such as stress, psychosocial factors and family conflicts in an objective manner. Methods: The clinical neuroscience of family interactions and childhood adversities develops a three-level neuromaladaptive connectome through common biobehaviors, which represents a structure delimited in personality traits, which were identified in empirical observation and constructed a new model. Results: A clinical synthesis associated with organic pathophysiology, we organized a diagnostic systems medicine model, with grouping of individuals that addresses objective neuropsychological alterations associated with changes in chronic comorbidities of clinical medicine. Discussion: This method organizes the clinical approach to the family factor, which is neurodysfunctional and represents a promising tool, but is in its infancy of theoretical basis, which requires experimental evaluation. Conclusion: The model is a new instrument for new scientific research and assists in the scientific advancement of family medicine, mental health policies, and the creation of mental health care plans in primary care, which is currently lacking.

Introduction:Assessing the family context in relation to mental health involves identifying causal factors, mainly in neurodevelopment, since the temporal variation of cause and effect in the neurobiology of family interactions can be directed to develop a specific clinical assessment of the child's neurodevelopment phase, through specific clinical biomarkers of cause and effect. Objective: To reflect on the facts of mental health complications in children and adults, which are being neglected by professionals, and through clinical identification and organic dysfunctions that are present in the pre-divorce periods and are complicated as in cases of parental alienation.Methods: After the bibliographic review, we synthesized a model of neurodysfunctional personality in the family environment and the clinical assessment with a generative view of perception and second-person neuroscience, with a "Bayesian" computational method, which was guided by a theoretical method and robust clinical empiricism. We outlined theoretical implications and mechanisms of social predictive perception, neuromaladaptive predominant behaviors, and clinical syntheses that organize and clarify some situations of family conflicts in family courts and, at the same time, significantly influence the physical and mental health of children and family members. Results and Discussion: Unequivocally, we are facing a social and child health setback, through professional malpractice in Family Law courts, which not only determines certain health outcomes, but also establishes parental relationships in the next generations, in senility and in the prevention of chronic diseases. Conclusion: The current lack of care in the mental health of the family and children has an impact on occupational health, and legal professionals, social assistants, and doctors must obtain this knowledge and awareness about the child psychological abuse that is occurring. This work points out a problem and suggests organized methods in clinical and neuroscience, such as the evaluation of the microstructure of ONCs personality which identifies intrusive, externalizing, and egocentric characteristics, parental capacity, and mentalism. These are innovations in objective operationalization for forensic medicine and family law.

Introduction: The COVID-19 epidemic has highlighted another silent epidemic of mental disorders (MD) that present common symptoms and are involved with addictions and mood disorders, such as depression, anxiety, social stress, and behavioral deviations. In addition to the chronic problem with mental health, it is possible that intellectual stagnation also occurs, according to the neuroscientist specialized in human intelligence and neurogenomics. Objective: The present study aimed to fill a gap by presenting a clinical organization based on the neurobiology of intelligence and pointing out a set of maladaptive mechanisms that limit human intelligence. Methods: After reviewing the literature, we outline the theoretical implications and mechanisms of social predictive perception that limit human intelligence, with clinical and factual insights, indicating its social and mental health consequences. We used the 5-phase perception model, with a generative view of perception and second-person neuroscience, in a "Bayesian" computational method, which was guided by theoretical method and robust clinical empiricism, to explain the errors of perception that limit intelligence. Results: We outline theoretical implications related to empirical science and found that limitation intelligence by maladaptive mechanismsmay be limited since childhood Discussion: We carry out a discussion that expands the concept of limitation of intelligence with the functional and executive mechanisms of intelligence. Conclusion:We notify into this concept an improvement in depth attention and correction of systems distorted in childhood through EAI, PTSD, mainly in the issue of evaluating real values, and not learned or conditioned one.

Introduction: Notably, a phenomenon of increased early incidence of some diseases is without control and real understanding, affecting young adults and adolescents, as in the case of obesity, colon cancer, metabolic syndrome, and acute myocardial infarction (AMI). Although the mortality rate of AMI has decreased, it is currently increasingly common to find young people diagnosed with AMI; studies have already shown this increase in incidence in this age group. Objective: The integration of intricate processes of genetic pathways related to lipid metabolism, inflammation, and coagulation helps in the understanding and identification of early AMI (IAMP), in addition to guiding primary prevention strategies. Methodology: A clinical synthesis with theoretical implications was performed, based on neurobiological and neurogenomic mechanisms, which presents the integration of maladaptive neuroscience with cardiology. Results: By reviewing the data on the risk factors of IAMP, its little-known pathophysiological processes, we identified its possible relationship with psychosocial stress, which can currently be assessed through a clinic focused on clinical neuromarkers related to stress and emotional dysfunctions that are attributed to neuromaladaptivebiobehaviors. To bring better understanding, we performed the integration of the clinical and pathophysiological components related to cardiology and psychosocial neuropsychology. Discussion: Stressful factors have been involved in CVD for a long time, and there has never been a methodology to objectively assess the neuropsychological clinic, in addition to the lack of integration of the various underlying and intricate pathophysiological mechanisms, which must be assessed for the strength of the causal effect through new population research. Conclusion: We present a clinical model with an approach to stressful effects through an unprecedented clinical approach to maladaptive biobehaviors, which involves objective assessment through clinical neuromarkers and enables a new organization of research and insights, in addition to the attempt to elucidate the origins of NCDs and MI.

Sickle cell disease (SCD) is a genetic hemoglobinopathy characterized by the polymerization of hemoglobin S, leading to the formation of rigid, sickled red blood cells (RBCs). These abnormally shaped cells have an increased tendency to adhere to the vascular endothelium and aggregate, which contributes to microvascular occlusions and the onset of vaso-occlusive crises. Nitric oxide (NO), a crucial molecule for maintaining vascular homeostasis, plays a significant role in regulating RBC adhesion and aggregation. In SCD, the reduced bioavailability of NO due to hemolysis and oxidative stress exacerbates endothelial dysfunction, promoting increased RBC adhesion to the endothelium and enhancing aggregation. In healthy individuals, NO inhibits RBC-endothelial adhesion by modulating the expression of adhesion molecules and promoting vasodilation. However, in SCD, decreased NO levels lead to a pro-adhesive and pro-aggregatory state within the microvasculature. This review explores the role of NO and other nitrogen species in modulating RBC adhesion and aggregation in SCD, highlighting the biochemical mechanisms involved, including the effects of oxidative stress and the formation of peroxynitrite. These disruptions contribute significantly to the pathophysiology of SCD, leading to clinical manifestations such as pain crises, stroke, and organ damage.

Sickle cell disease (SCD) is a genetic blood disorder characterized by the presence of sickle-shaped red blood cells (RBCs), which cause impaired blood flow and lead to various systemic complications, particularly within the cardiovascular and pulmonary systems. Nitric oxide (NO), a critical vasodilator, plays a significant role in maintaining vascular homeostasis, including regulating blood vessel tone, preventing platelet aggregation, and promoting smooth muscle relaxation. In SCD, decreased NO bioavailability due to increased oxidative stress, hemolysis, and arginase activity results in endothelial dysfunction, contributing to the development of pulmonary hypertension (PH), right heart failure, and other cardiopulmonary complications. The dysregulation of NO in SCD leads to a cascade of pathophysiological changes in the vascular system, primarily affecting the pulmonary vasculature. Impaired NO signaling exacerbates pulmonary vasoconstriction and endothelial injury, which increase pulmonary vascular resistance and promote PH. Additionally, the reduction in NO levels is associated with right heart failure, as the right ventricle faces increased afterload. The combination of PH and right heart failure significantly affects the morbidity and mortality of individuals with SCD, highlighting the importance of NO in the management of these complications.