An Ounce of Prevention is the Only Cure: Nationwide Clinical and Financial Outcomes of Self-Inflicted Firearm Injuries.

BACKGROUND: Self-inflicted gunshot wounds (SIGSWs) remain a leading, preventable cause of death in the United States. The present study evaluated patient demographics, operative characteristics, in-hospital outcomes, and resource utilization between patients with SIGSW and other GSW. METHODS: The 2016-2020 National Inpatient Sample was queried for patients ≥16 years old admitted following gunshot wounds. Patients were categorized as SIGSW if they were injured through self-harm. Multivariable logistic regression was used to evaluate the association of SIGSW on outcomes. The primary endpoint was in-hospital mortality with complications, costs, and length of stay secondarily considered. RESULTS: Of an estimated 157,795 surviving to hospital admission, 14,670 (9.30%) were SIGSW. Self-inflicted gunshot wounds were more commonly female (18.1 vs 11.3%), insured by Medicare (21.1 vs 5.0%), and white (70.8 vs 22.3%) (all P < .001) compared to non-SIGSW. Psychiatric illness was more prevalent in SIGSW (46.0 vs 6.6%, P < .001). Additionally, SIGSW more frequently underwent neurologic (10.7 vs 2.9%) and facial operations (12.5 vs 3.2%) (both P < .001). After adjustment, SIGSW was associated with greater odds of mortality (AOR: 12.4, 95% CI: 10.4-14.7). Length of stay (ß: +1.5 days, 95% CI: .8-2.1) and costs (ß: +$3.6 K, 95% CI: 1.4-5.7) were significantly greater in SIGSW. CONCLUSIONS: Self-inflicted gunshot wounds are associated with increased mortality compared to other GSW, likely due to the increased proportion of injuries in the head and neck region. This lethality, coupled with the high prevalence of psychiatric illness in this population, indicates that efforts must be made to intervene through primary prevention, including enhanced screening and weapon safety considerations for those at risk.

Low-dose proton radiation effects in a transgenic mouse model of Alzheimer's disease - Implications for space travel.

Space radiation represents a significant health risk for astronauts. Ground-based animal studies indicate that space radiation affects neuronal functions such as excitability, synaptic transmission, and plasticity, and it may accelerate the onset of Alzheimer's disease (AD). Although protons represent the main constituent in the space radiation spectrum, their effects on AD-related pathology have not been tested. We irradiated 3 month-old APP/PSEN1 transgenic (TG) and wild type (WT) mice with protons (150 MeV; 0.1-1.0 Gy; whole body) and evaluated functional and biochemical hallmarks of AD. We performed behavioral tests in the water maze (WM) before irradiation and in the WM and Barnes maze at 3 and 6 months post-irradiation to evaluate spatial learning and memory. We also performed electrophysiological recordings in vitro in hippocampal slices prepared 6 and 9 months post-irradiation to evaluate excitatory synaptic transmission and plasticity. Next, we evaluated amyloid ß (Aß) deposition in the contralateral hippocampus and adjacent cortex using immunohistochemistry. In cortical homogenates, we analyzed the levels of the presynaptic marker synaptophysin by Western blotting and measured pro-inflammatory cytokine levels (TNFα, IL-1ß, IL-6, CXCL10 and CCL2) by bead-based multiplex assay. TG mice performed significantly worse than WT mice in the WM. Irradiation of TG mice did not affect their behavioral performance, but reduced the amplitudes of population spikes and inhibited paired-pulse facilitation in CA1 neurons. These electrophysiological alterations in the TG mice were qualitatively different from those observed in WT mice, in which irradiation increased excitability and synaptic efficacy. Irradiation increased Aß deposition in the cortex of TG mice without affecting cytokine levels and increased synaptophysin expression in WT mice (but not in the TG mice). Although irradiation with protons increased Aß deposition, the complex functional and biochemical results indicate that irradiation effects are not synergistic to AD pathology.

Transcriptional changes following long-term sensitization training and in vivo serotonin exposure in Aplysia californica.

We used Aplysia californica to compare the transcriptional changes evoked by long-term sensitization training and by a treatment meant to mimic this training, in vivo exposure to serotonin. We focused on 5 candidate plasticity genes which are rapidly up-regulated in the Aplysia genus by in vivo serotonin treatment, but which have not yet been tested for regulation during sensitization: CREB1, matrilin, antistasin, eIF3e, and BAT1 homolog. CREB1 was rapidly up-regulated by both treatments, but the regulation following training was transient, falling back to control levels 24 hours after training. This suggests some caution in interpreting the proposed role of CREB1 in consolidating long-term sensitization memory. Both matrilin and eIF3e were up-regulated by in vivo serotonin but not by long-term sensitization training. This suggests that in vivo serotonin may produce generalized transcriptional effects that are not specific to long-term sensitization learning. Finally, neither treatment produced regulation of antistasin or BAT1 homolog, transcripts regulated by in vivo serotonin in the closely related Aplysia kurodai. This suggests either that these transcripts are not regulated by experience, or that transcriptional mechanisms of memory may vary within the Aplysia genus.