Background Increased glucose fluctuation has been related to poor prognosis in patients with critical illnesses, while its prognostic role in patients with acute stroke remains unknown. The meta-analysis aimed to evaluate the association between the acute glycemic variation (GV) and mortality risk in patients with acute stroke. Methods Cohort studies were obtained by searching Medline, Web of Science, Embase, Wanfang and CNKI databases. A random-effect model which incorporates the intra-study heterogeneity was chosen to pool the results. Results Ten cohort studies with 1433 patients were included, and 280 (19.5%) of them died within 90 days of disease onset. Results of the meta-analyses showed that a higher acute GV was associated with an increased risk of early mortality in patients with acute stroke, as indicated by GV measured with the coefficient of variation of blood glucose (CVBG, odds ratio [OR]: 2.24, 95% CI 1.40 to 3.58, p < 0.001, I2 = 73%), the standard deviation of blood glucose (SDBG, OR: 2.31, 95% CI 1.70 to 3.13, p < 0.001, I2 = 50%), and the mean amplitude of glycemic excursion (OR: 3.57, 95% CI 1.44 to 8.85, p = 0.006, I2 = 23%). For acute GV measured with CVBG and SDBG, subgroup analyses showed consistent results in patients with acute ischemic and hemorrhagic stroke, and for studies reporting 28-day and 90-day all-cause mortality (p for subgroup analysis all > 0.05). Conclusions Higher acute GV may be an independent risk factor of early mortality in patients with acute stroke.

Pancreatic encephalopathy (Pe) is a common fatal complication of acute pancreatitis (aP). Proinflammatory cytokines such as tumor necrosis factor (TnF)-α and interleukin (il)-6 are generated during aP, and act synergistically to promote Pe and multisystem failure. caerulein-induced aP provides a convenient model to explore the role of proinflammatory cytokines in PE. The aim of the present study was to examine the effect of the TnF-α inhibitor etanercept in Pe models and elucidate the regulatory mechanisms. To model Pe in vitro, rat hippocampal H19-7/iGF-ir neuronal cells were treated with 10 nmol/ml caerulein alone or in combination with etanercept (1, 10 or 100 µmol/ml). To model Pe in vivo, rats were injected with 50 µg/kg caerulein alone or combined with 10 mg/kg etanercept. at 6 h after administration, it was noted that etanercept downregulated expression of TnF-α, il-1β and il-6 by negatively regulating nF-κB (a master regulator of cytokine expression) signaling, and prevented the accumulation of reactive oxygen species. conversely, etanercept promoted the expression of the neurotrophic and anti-inflammatory hypoxia-inducible factor 1 α . in rat hippocampus, etanercept also reduced the levels of expression and inhibited the inflammatory response to reduce edema and neural necrosis. Together, these data suggested that etanercept could attenuate caerulein-induced Pe, at least in part via suppression of nF-κB signaling and alleviation of oxidative stress.

Dysglycemia are involved in the development of functional impairment after acute ischemic stroke (AIS). The aim of the study was to evaluate the association between acute glycemic variability and functional outcome in patients with AIS. Cohort studies were obtained by search Medline, Web of Science, Embase, Wanfang, and China National Knowledge Infrastructure databases from inception to November, 2021. A random-effect model which incorporates the intra-study heterogeneity was chosen to pool the results. Ten cohort studies including 3038 patients were included, and 1319 (43.4%) had poor functional outcome (modified Rankin Scale >2) up to three months after disease onset. Pooled results showed that higher acute GV was associated with an increased risk of poor functional outcome, as evidenced by GV evaluated by the standard deviation of blood glucose (SDBG, OR: 1.91, 95% CI: 1.38 to 2.65, I2=60%, p<0.001), the coefficient of variation of blood glucose (OR: 2.03, 95% CI: 1.15 to 3.58, I2=17%, p=0.02), the range of glucose (OR: 1.43, 95% CI: 1.11 to 1.83, I2=22%, p=0.005), and the mean amplitude of glycemic excursion (OR: 1.59, 95% CI: 1.10 to 2.31, I2=0%, p=0.01). Subgroup analyses did not support that difference in study design, treatments for AIS, mean age of the patients, duration for GV measuring, or study quality would significantly affect the association between SDBG and functional outcome after AIS. In conclusion, higher acute glycemic variability may predict poor functional outcome within 3 months after AIS.

Fractional anisotropy values in diffusion tensor imaging can quantitatively reflect the consistency of nerve fibers after brain damage, where higher values generally indicate less damage to nerve fibers. Therefore, we hypothesized that diffusion tensor imaging could be used to evaluate the effect of mild hypothermia on diffuse axonal injury. A total of 102 patients with diffuse axonal injury were randomly divided into two groups: normothermic and mild hypothermic treatment groups. Patient's modified Rankin scale scores 2 months after mild hypothermia were significantly lower than those for the normothermia group. The difference in average fractional anisotropy value for each region of interest before and after mild hypothermia was 1.32-1.36 times higher than the value in the normothermia group. Quantitative assessment of diffusion tensor imaging indicates that mild hypothermia therapy may be beneficial for patients with diffuse axonal injury.