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Introduction: While there has been a reduction in specific homicide categories in Sweden, the last decade has witnessed an increase in the overall rate. The escalation is predominantly linked to heightened gun violence associated with criminal gangs. As a result, Sweden faces an extreme rate of shootings and firearm-related homicides, constituting one of the most severe instances across Europe. However, comprehensive scientific studies on this phenomenon are lacking. This paper presents the design of the Violent Crimes in Skåne (ViCS) project, which aims to investigate violent crimes requiring hospitalization or causing death in Sweden's region Skåne from a medical, forensic, and criminological perspective. The project aims to examine the epidemiology and trends of violent crimes, injury profiles, treatments, patient outcomes, causes of death, and victim demographics. Methods and analysis: Using a retrospective cross-sectional design, ViCS will examine trauma by violent crimes from 2000 to 2019. Data will be sourced from several institutions, including hospital records from nine emergency hospitals, and the National Board of Forensic Medicine Agency. The project aims to study medical and criminological aspects of violent crimes, primarily focusing on assaults involving firearms, sharp weapons, blunt instruments, kicks, punches, and other types of assault like strangulation. Data analysis will involve descriptive and inferential statistics. Discussion: ViCS aims to contribute to the limited body of knowledge about victims of violent crimes in Sweden. The findings may inform evidence-based interventions in medical, forensic, and criminological fields, potentially enabling targeted prevention strategies and improvements in emergency care for victims.
RESUMO
General anesthetics are hypothesized to cause unconsciousness by interrupting communication pathways within the cerebral cortex. A correlate of this has been demonstrated in mouse neocortical slices, where anesthetics disrupt the spread of population field potential activity--resulting in a "decoupling" of activity recorded across spatial locations within the slice. In this study we investigated whether this decoupling can be explained by gap junction blockade, with a particular focus on the connexin36 (Cx36) subtype. Baseline, coupled seizure-like event (SLE) activity was recorded from two extracellular electrodes in slices perfused with no-magnesium artificial cerebrospinal fluid (aCSF). The connexin36 gap junction blocker mefloquine (25 µM) failed to decouple SLE activity in wild-type mice (median(range) decoupling rate of 0.70(0.03-3.00)%, not significantly different from controls). Slices from Cx36 knock-out mice exhibited coupled SLE activity under baseline conditions and readily decoupled when exposed to the general anesthetic etomidate. The general gap junction blocker carbenoxolone (CBX, 100 µM) strongly decoupled SLE activity compared to controls in wild-type mice (2.7(0.1-42.5) % compared to 0.03(0.0-0.5)%, p=0.0001). Taken together, the results show that Cx36 gap junction blockade does not cause decoupling of intracortical population activity, but the involvement of other gap junction subtypes cannot be ruled out.