Background: The first years of university can be very challenging for students. Previous research has focused on the study of the prevalence of burnout and of psychological distress in medical students. The aim of this study was to investigate the prevalence of psychological symptoms and burnout reported by first-year students, the relationship between these variables and their academic performance, and the differences between health and non-health sciences students. Methods: An observational study with a cross-sectional design was performed. Students of health sciences (medicine, nursing, physiotherapy, psychology), and non-health sciences (biology, social sciences, business management, and engineering) undergraduate programs completed the Brief Symptom Inventory (BSI-18) and the Maslach Burnout Inventory-Student Survey (MBI-SS). Students’ grades for the first semester were collected. Results: A sample of 506 students participated. Prevalence of psychological distress was 27.1% and burnout was 7.3%. Academic performance was unaffected in relation to either psychological distress or burnout. Non-health sciences students showed a greater risk of depression. Conclusions: This study provides evidence of the high prevalence of psychological distress in the first year of college. Even when burnout prevalence was low, the results suggest the need to introduce prevention programs to improve the psychological wellbeing of these students.
Background and Purpose
Mu and delta opioid receptors(MOP, DOP) contribution to the manifestations of pathological pain is not understood. We used genetic approaches to investigate the opioid mechanisms modulating neuropathic pain and its comorbid manifestations.
Experimental Approach
We generated conditional knockout mice with MOP or DOP deletion in sensoryNav1.8‐positive neurons (Nav1.8), in GABAergic forebrain neurons (DLX5/6) orconstitutively (CMV). Mutant mice and wild‐type littermates were subjected topartial sciatic nerve ligation (PSNL) or sham surgery and their nociception wascompared. Anxiety‐, depressivelike behaviour and cognitive performance were also measured. Opioid receptor mRNA expression, microgliosis and astrocytosis were assessed in the dorsalroot ganglia (DRG) and/or the spinal cord (SC).
Key Results
Constitutive CMV‐MOP knockouts after PSNL displayed reduced mechanical allodynia and enhanced heat hyperalgesia. This phenotype was accompanied by increased DOP expression in DRG and SC, and reduced microgliosis and astrocytosis in deep dorsal horn laminae. Conditional MOP knockouts and control mice developed similar hypersensitivity after PSNL, except for anenhanced heat hyperalgesia by DLX5/6‐MOP male mice. Neuropathic pain‐induced anxiety was aggravated in CMV‐MOP and DLX5/6‐MOP knockouts. Nerve‐injured CMV‐DOP mice showed increased mechanical allodynia, whereas Nav1.8‐DOP and DLX5/8‐DOP mice had partial nociceptive enhancement. CMV‐DOP and DLX5/6‐DOP mutants showed increased depressive‐like behaviour after PSNL.
Conclusions and Implications
MOP activity after nerve injury increased anxiety‐like responses involving forebrain GABAergic neurons and enhanced mechanical pain sensitivity along with repression of DOP expression and spinal cord gliosis. In contrast, DOP shows a protective function limiting nociceptive and affective manifestations of neuropathic pain.
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