A history of previous exposure to surgery under GA might be associated with an increased risk of dementia, particularly in subjects who have undergone repeated exposure to GA. In addition, subjects who had received surgery under ETGA with comorbidities such as stroke, hypertension, diabetes mellitus, and atherosclerosis could have a potential relationship with dementia risk.

Casticin, a polymethoxyflavone derived from natural plants, has biological activities including induction of cell apoptosis. In this study, we showed the beneficial effects of casticin on the inhibition of prostate cancer cell metastasis. Casticin reduced total viable cell number, thus, we selected low doses of casticin for following experiments. Casticin decreased cell mobility, suppressed cell migration and invasion, and reduced cell gelatinolytic activities of MMP‐2/‐9. Furthermore, casticin inhibited the protein levels of AKT, GSK3 αβ, Snail, and MMPs (MMP‐2, ‐9, ‐13, and ‐7) at 24 and 48 hr treatment. Casticin diminished the expressions of NF‐κB p65, GRB2, SOS‐1, MEK, p‐ERK1/2, and p‐JNK1/2 at 48 hr treatment only. However, casticin reduced the level of E‐cadherin at 24 hr treatment but elevated at 48 hr. The novel findings suggest that casticin may represent a new and promising therapeutic agent for the metastatic prostate cancer. Practical applications Casticin derived from natural plants had been used for Chinese medicine in Chinese population for thousands of years. In the present study, casticin attenuated metastatic effects, including decreasing viable cell number, inhibiting the migration, invasion, and adhesion, and reducing matrix metalloproteinases activity on human prostate DU 145 cancer cells. In addition, the results also provided possible pathways involved in casticin anti‐metastasis mechanism. We conclude that casticin may be an aptitude anticancer agent or adjuvant for the metastatic prostate cancer in the future.

Cardiopulmonary bypass (CPB) induces inflammatory responses, and effective endogenous homeostasis is important for preventing systemic inflammation. We assessed whether plasma exosomal microRNAs in patients undergoing cardiac surgery with CPB are involved in the regulation of inflammatory responses. Plasma samples were isolated from CPB patients (n = 21) at 5 specified time points: pre-surgery, pre-CPB and 2 hours (h), 4 h and 24 h after CPB began. Plasma TNF-α expression was increased after CPB began compared to that in the pre-surgery samples. Plasma IL-8 and IL-6 expression peaked at 4 h after CPB began but was downregulated at 24 h. The number of plasma exosomes collected at 2 h (55.1 ± 8.3%), 4 h (63.8 ± 10.1%) and 24 h (83.5 ± 3.72%) after CPB began was significantly increased compared to that in the pre-CPB samples (42.8 ± 0.11%). These exosomes had a predominantly parental cellular origin from RBCs and platelets. Additionally, the plasma exosomal miR-223 levels were significantly increased after CPB began compared to those in the pre-CPB samples. Further, exosomal miR-223 from plasma collected after CPB began downregulated IL-6 and NLRP3 expression in the monocytes. Here, we present the novel findings that increased plasma exosomal miR-223 expression during cardiac surgery with CPB might play homeostatic roles in downregulating inflammatory responses through intercellular communication.

Prognostic/epidemiologic study, level II.

No abstract

Amniotic fluid embolism occurs rarely but is a leading cause of maternal mortality. Regardless of emergent supportive medical treatment, it is associated with a very high mortality rate. Here, we present the case of a 33-year-old pregnant woman with amniotic fluid embolism, who sustained cardiac arrest and was rescued with early application of extracorporeal membrane oxygenation. The management of amniotic fluid embolism is to initially focus on rapid cardiopulmonary stabilization. Hemodynamic decompensation may be transient and recoverable within a few hours. Early application of extracorporeal membrane oxygenation should be considered in patients who are unresponsive to medical therapy before severe organ damage supervenes.

BackgroundCancellation of surgery close to scheduled time causes a waste of healthcare resources. The current study analyzes surgery cancellations occurring after the patient has been prepared for the operating room, in order to see whether improvements in the surgery planning process may reduce the number of cancellations.MethodsIn a retrospective chart review of operating room surgery cancellations during the period from 2006 to 2011, cancellations were divided into the following categories: inadequate NPO; medical; surgical; system; airway; incomplete evaluation. The relative use of these reasons in relation to patient age and surgical department was then evaluated.ResultsForty-one percent of cancellations were for other than medical reasons. Among these, 17.7% were due to incomplete evaluation, and 8.2% were due to family issues. Sixty seven percent of cancelled cases eventually received surgery. The relative use of individual reasons for cancellation varied with patient age and surgical department. The difference between cancellations before and after anesthesia was dependent on the causes of cancellation, but not age, sex, ASA status, or follow-up procedures required.ConclusionAlmost half of the cancellations were not due to medical reasons, and these cancellations could be reduced by better administrative and surgical planning and better communication with the patient and/or his family.

Platelet activation and its interaction with leukocytes play an important role in atherothrombosis. Cardiovascular diseases resulted from atherothrombosis remain the major causes of death worldwide. Gallic acid, a major constituent of red wine and tea, has been believed to have properties of cardiovascular protection, which is likely to be related to its antioxidant effects. Nonetheless, there were few and inconsistent data regarding the effects of gallic acid on platelet function. Therefore, we designed thisin vitrostudy to determine whether gallic acid could inhibit platelet activation and the possible mechanisms. From our results, gallic acid could concentration-dependently inhibit platelet aggregation, P-selectin expression, and platelet-leukocyte aggregation. Gallic acid prevented the elevation of intracellular calcium and attenuated phosphorylation of PKCα/p38 MAPK and Akt/GSK3βon platelets stimulated by the stimulants ADP or U46619. This is the first mechanistic explanation for the inhibitory effects on platelets from gallic acid.