Hericium erinaceus, an edible mushroom, has been demonstrated to potentiate the effects of numerous biological activities. The aim of this study was to investigate whether H. erinaceus mycelium could act as an anti-inflammatory agent to bring about neuroprotection using a model of global ischemic stroke and the mechanisms involved. Rats were treated with H. erinaceus mycelium and its isolated diterpenoid derivative, erinacine A, after ischemia reperfusion brain injuries caused by the occlusion of the two common carotid arteries. The production of inflammatory cytokines in serum and the infracted volume of the brain were measured. The proteins from the stroke animal model (SAM) were evaluated to determine the effect of H. erinaceus mycelium. H. erinaceus mycelium reduced the total infarcted volumes by 22% and 44% at a concentration of 50 and 300 mg/kg, respectively, compared to the SAM group. The levels of acute inflammatory cytokines, including interleukin-1β, interleukin-6 and tumor necrosis factor á, were all reduced by erinacine A. Levels of nitrotyrosine-containing proteins, phosphorylation of p38 MAPK and CCAAT enhancer-binding protein (C/EBP) and homologous protein (CHOP) expression were attenuated by erinacine A. Moreover, the modulation of ischemia injury factors present in the SAM model by erinacine A seemed to result in the suppression of reactive nitrogen species and the downregulation of inducible NO synthase (iNOS), p38 MAPK and CHOP. These findings confirm the nerve-growth properties of Hericium erinaceus mycelium, which include the prevention of ischemic injury to neurons; this protective effect seems to be involved in the in vivo activity of iNOS, p38 MAPK and CHOP.

Ischemia-reperfusion injury resulting from arterial occlusion or hypotension in patients leads to tissue hypoxia with glucose deprivation, which causes endoplasmic reticulum (ER) stress and neuronal death. A proteomic approach was used to identify the differentially expressed proteins in the brain of rats following a global ischemic stroke. The mechanisms involved the action in apoptotic and ER stress pathways. Rats were treated with ischemia-reperfusion brain injuries by the bilateral occlusion of the common carotid artery. The cortical neuron proteins from the stroke animal model (SAM) and the control rats were separated using two-dimensional gel electrophoresis (2-DE) to purify and identify the protein profiles. Our results demonstrated that the SAM rats experienced brain cell death in the ischemic core. Fifteen proteins were expressed differentially between the SAM rats and control rats, which were assayed and validated in vivo and in vitro. Interestingly, the set of differentially expressed, down-regulated proteins included catechol O-methyltransferase (COMT) and cathepsin D (CATD), which are implicated in oxidative stress, inflammatory response and apoptosis. After an ischemic stroke, one protein spot, namely the calretinin (CALB2) protein, showed increased expression. It mediated the effects of SAM administration on the apoptotic and ER stress pathways. Our results demonstrate that the ischemic injury of neuronal cells increased cell cytoxicity and apoptosis, which were accompanied by sustained activation of the IRE1-alpha/TRAF2, JNK1/2, and p38 MAPK pathways. Proteomic analysis suggested that the differential expression of CALB2 during a global ischemic stroke could be involved in the mechanisms of ER stress-induced neuronal cell apoptosis, which occurred via IRE1-alpha/TRAF2 complex formation, with activation of JNK1/2 and p38 MAPK. Based on these results, we also provide the molecular evidence supporting the ischemia-reperfusion-related neuronal injury.

Methanol poisoning (MP) often causes acute mortality and morbidities; however, the association between MP and subsequent mortality has not been well studied. We conducted a nationwide population-based cohort study by identifying 621 participants with MP from the Nationwide Poisoning Database and 6210 participants without MP from the Longitudinal Health Insurance Database 2000 by matching the index date at a 1:10 ratio between 1999 and 2012. Comparison of the mortality rate between the two cohorts was performed by following up until 2013. A total of 249 (40%) participants with MP and 154 (2.5%) participants without MP died during the follow-up (p < 0.001). Statistic analysis showed that participants with MP had a higher risk for mortality than did the participants without MP (adjusted hazard ratio [AHR]: 13.48; 95% confidence interval [CI]: 10.76–16.88). The risk of mortality was highest in the first 6 months after MP (AHR: 480.34; 95% CI: 117.55–1962.75). Hypertension, chronic obstructive pulmonary disease, liver disease, malignancy, drug abuse, and lower monthly income also predicted mortality. MP was associated with increased subsequent mortality. Close follow-up for comorbidity control and socioeconomic assistance are suggested for patients with MP.

Background/Aim: Radiation (RT) induced ERK/NF-κB in hepatocellular carcinoma (HCC) has been reported in our previous works; it weakens the toxicity of RT or triggers a radioresistance effect. Thus, combining RT with a suitable NF-κB inhibitor may sensitize HCC to RT. Magnolol, a bioactive compound, was known to have anti-inflammatory and anti-tumor functions. Here, we aimed to investigate whether magnolol may enhance anti-HCC efficacy of RT in vivo. Materials and Methods: We established a Hep3B bearing mouse to evaluate the efficacy of the combination treatment of magnolol and RT. Results: Most significantly, tumor volume and tumor weight inhibition was found in the combination group. Tumor immunohistochemistry staining also illustrated the suppression of RT-induced ERK/NF-κB-related proteins expression by magnolol. In addition, intrinsic apoptosis-related proteins, such as caspase-3 and -9, were markedly increased in the combination group. Conclusion: Magnolol may effectively enhance anti-HCC ability of RT by downregulating the expression of ERK/NF-κB-related proteins and increasing the expression of apoptosis-related proteins.

Background: Infection is the most common precipitating factor and cause of death in patients with hyperglycemic crises. Treating infection-precipitated hyperglycemic crises includes using empiric antibiotics early; correcting dehydration, hyperglycemia, and electrolyte imbalances; and frequent monitoring. Intensive care unit admission, broad-spectrum antibiotics, and even novel therapy for infection may be beneficial for patients with a high risk of mortality. However, these management options are costly and not beneficial for every patient. Selecting high-risk patients who would most likely benefit is more appropriate. We investigated the independent mortality predictors of patients with infection-precipitated hyperglycemic crises to facilitate clinical decision making. Methods: This study was conducted in a university-affiliated medical center. Consecutive adult patients (> 18 years old) visiting the Emergency Department between January 2004 and December 2010 were enrolled when they met the criteria of an infection-precipitated hyperglycemic crisis. Thirty-day mortality was the primary endpoint. Results: One hundred forty-two patients were enrolled. The infection source did not predict mortality. The presenting variables that were independently associated with 30-day mortality in a multiple logistic regression model were cancer history (odds ratio [OR], 7.4; 95% confidence interval [CI], 2.4-23.2), bandemia (OR, 7.0; 95% CI, 1.6-30.3), and serum creatinine (OR, 1.4; 95% CI, 1.1-1.8). The common sources of infection were the lower respiratory tract (30.3%), urinary tract (49.3%), skin or soft tissue (12.0%), and intra-abdominal (6.3%). Conclusions: Cancer history, bandemia, and serum creatinine level are three independent mortality predictors for patients with infection-precipitated hyperglycemic crises. These predictors are both readily available and valuable for physicians making decisions about risk stratification, treatment, and disposition.

Background/Aim: In hepatocellular carcinoma (HCC) treatment, radiotherapy (RT) stands as a pivotal approach, yet the emergence of radioresistance poses a formidable challenge. This study aimed to explore the potential synergy between quetiapine and RT for HCC treatment. Materials and Methods: A Hep3B xenograft mouse model was used, the investigation tracked tumor progression, safety parameters, and molecular mechanisms. Results: The findings revealed a synergistic anti-HCC effect when quetiapine was coupled with RT that prolonged tumor growth time and a significantly higher growth inhibition rate compared to the control group. Safety assessments indicated minimal pathological changes, suggesting potential of quetiapine in mitigating RT-induced alterations in liver and kidney functions. Mechanistically, the combination suppressed metastasis and angiogenesis-related proteins, while triggering the activation of apoptosis-related proteins via targeting Epidermal growth factor receptor (EGFR)-mediated signaling. Conclusion: The potential of the quetiapine and RT combination is emphasized, offering enhanced anti-HCC efficacy, a safety profile, and positioning quetiapine as a radiosensitizer for HCC treatment.