Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

Brain dysfunction is a common complication after sepsis and is an independent risk factor for a poor prognosis, which is partly attributed to the dysregulated inflammatory response and oxidative damage. Melatonin regulates the sleep-wake cycle and also has potent anti-inflammatory and antioxidant properties, yet the protective effects of melatonin on sepsis-induced neurobehavioral dysfunction remain to be elucidated. In the present study, melatonin was administered intraperitoneally daily at a dose of 10 mg/kg for three consecutive days immediately (early treatment) or 7 days (delayed treatment) after sham operation or cecal ligation and puncture (CLP), followed by an additional treatment in drinking water until the end of behavioral tests. The concentrations of pro-inflammatory cytokines (tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10), malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS), brain-derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF) were determined at the indicated time points. Compared with the CLP + vehicle group, we found that early melatonin treatment resulted in increased survival rate but not improvement in measures of neurobehavioral outcomes, which was accompanied by significantly lower plasma level of IL-1β. Intriguingly, delayed melatonin treatment improved neurobehavioral dysfunction by normalization of hippocampal BDNF and GDNF expressions. In conclusion, our study suggests the beneficial effects of both early and delayed melatonin treatment after sepsis development, which implicates melatonin has a potential therapeutic value in sepsis-associated organ damage including brain dysfunction.

No abstract

Memory enhancement and memory decline are two opposing cognitive performances commonly observed in clinical practice, yet the neural mechanisms underlying these two different phenomena remain poorly understood. Accumulating evidence has demonstrated that the default-mode network (DMN) is implicated in diverse cognitive, social, and affective processes. In the present study, we used the retrosplenial cortex as a seed region to study the functional connectivity within the DMN in two animal models with opposing episodic memories, of which memory enhancement was induced by footshocks to mimic posttraumatic stress disorder (PTSD) and memory decline was induced by lipopolysaccharide (LPS) challenge to mimic sepsis-associated encephalopathy (SAE). Our results showed that LPS challenge and footshocks induced opposing episodic memories. With regard to the imaging data, there were significant differences in the functional connectivity between the retrosplenial cortex and the medial prefrontal cortex (mPFC), insular lobe, left piriform cortex, left sensory cortex, and right visual cortex among the three groups. Post-hoc comparisons showed the LPS group had a significantly increased functional connectivity between the retrosplenial cortex and mPFC as compared with the control group. Compared with the LPS group, the PTSD group displayed significantly decreased functional connectivity between the retrosplenial cortex and the right visual cortex, retrosplenial cortex, insular lobe, left piriform cortex, and left sensory cortex. In summary, our study suggests that there is a significant difference in the functional connectivity within the DMN between SAE and PTSD rats.

No abstract