Humanistic Studies and Social Researches

Abstract Background: Schizophrenia is a severe psychiatric disorder characterized by a complex, multifactorial origin. While dopaminergic theories have been predominant, contemporary perspectives highlight an integrated dysfunction across genetic, molecular, and neural circuit levels, rooted in neurodevelopmental abnormalities.
Objectives: This review synthesizes recent evidence from genetics, neuroimaging, and molecular psychiatry to present an updated model of schizophrenia pathophysiology. It focuses on the interplay between synaptic pruning, interneuron dysfunction, and brain network dysconnectivity.
Methods: We conducted a narrative, integrative review. Searches in PubMed, Scopus, and Web of Science (2014-2025) utilized terms like "schizophrenia neurobiology," "dysconnectivity," "NMDA receptor hypofunction," "parvalbumin interneurons," and "genetic risk." Evidence was thematically synthesized to construct a coherent pathophysiological model.
Results: Findings outline a pathway from genetic risk (e.g., complement C4 loci) to excessive adolescent synaptic pruning, leading to impairment of parvalbumin-positive GABAergic interneurons. This results in N-methyl-D-aspartate receptor (NMDAR) hypofunction, a disrupted cortical excitation/inhibition balance, and aberrant neural oscillations. These local deficits manifest as large-scale dysconnectivity within cortico-striato-thalamo-cortical (CSTC) circuits, underpinning positive, negative, and cognitive symptoms. Dopaminergic dysregulation is positioned downstream of primary glutamatergic/GABAergic pathology.
Conclusion: Schizophrenia is best conceptualized as a neurodevelopmental disorder of synaptic connectivity. Future therapeutics should target earlier pathological stages, such as immune-mediated pruning and glutamatergic signalling, offering potential for novel treatments and preventative strategies.

Abstract Background: Emotional suppression, defined as the deliberate restraint of emotional expression, is frequently utilized by people with post-traumatic stress disorder (PTSD). While it may offer momentary relief, its persistent application is connected to negative long-term psychological and health outcomes. Examining this process through a psychophysiological lens is crucial for understanding the biological mechanisms involved.
Objective: This review consolidates contemporary research on the psychophysiological features and repercussions of chronic emotional suppression in trauma-exposed groups, with particular attention to autonomic nervous system, neuroendocrine, and central nervous system activity.
Methods: A narrative synthesis of literature published between 2000 and 2025 was performed, sourcing articles from PubMed, PsycINFO, and Web of Science. Key search terms encompassed "emotional suppression," "trauma," "PTSD," "psychophysiology," and related physiological metrics.
Results: Robust evidence demonstrates that emotional suppression in trauma patients correlates with heightened and rigid sympathetic arousal (e.g., reduced heart rate variability), dysregulated HPA axis function, and a neural pattern of excessive prefrontal effort paired with sustained limbic reactivity. These physiological markers are associated with increased PTSD symptom severity and contribute to greater allostatic load and physical health comorbidities.
Conclusion: Emotional suppression constitutes a biologically costly form of regulation that intensifies physiological stress responses and may perpetuate trauma-related pathology. Clinical interventions should prioritize helping patients replace suppression with more adaptive, antecedent-focused emotion regulation strategies to foster comprehensive resilience.

Abstract Background: Although oncology traditionally emphasizes survival rates, the patient's journey is deeply influenced by their subjective experience and psychological state. Continuity of Care (CoC)—the consistent, coordinated, and unified management of care over time—is increasingly recognized as a vital element that extends beyond its possible effects on mortality.
Objective: This review consolidates current research to explore how CoC affects patient-reported experience measures (PREMs) and mental health results in individuals with cancer.
Methods: A systematic search of databases (including PubMed, PsycINFO, CINAHL) was performed for studies published from 2000 to 2024. Search terms comprised "continuity of care," "cancer," "oncology," "patient experience," "quality of life," "anxiety," "depression," "care coordination," and "therapeutic alliance."
results: Substantial evidence shows that greater CoC is reliably linked to better patient experiences, including enhanced communication, trust, and security. Additionally, CoC serves as an important protective factor against psychological illness, lowering anxiety, depression, and sensations of abandonment, especially during care transitions and survivorship.
Conclusion: CoC is a core, adjustable component of quality cancer care that directly improves patients' care experiences and protects their mental health. Emphasizing CoC through intentional models and policies is crucial for realizing genuinely patient-focused oncology.