Comparison of Prognostic Performance between Procalcitonin and Procalcitonin-to-Albumin Ratio in Post Cardiac Arrest Syndrome.

(1) Background: Post-cardiac arrest syndrome (PCAS) is a type of global ischemic reperfusion injury that occurs after the return of spontaneous circulation (ROSC). The procalcitonin to albumin ratio (PAR) has been studied as an independent prognostic factor of various diseases. There are no previous studies of PAR in patients with PCAS. We assessed if PAR is more effective than procalcitonin (PCT) in predicting prognosis for patients with PCAS. (2) Methods: This retrospective cohort study included a total of 187 patients with PCAS after non-traumatic out-of-hospital cardiac arrest (OHCA) between January 2016 and December 2020. Multivariate logistic regression analysis was conducted to assess the association between PAR and PCAS prognosis. The predictive performance of PAR was compared with PCT via the receiver-operating characteristic (ROC) analysis and DeLong test.; (3) Results: PAR at 24 and 48 h after hospital admission were independently associated with one-month neurological outcome (OR: 1.167, 95% CI: 1.023-1.330; OR: 1.077, 95% CI: 1.012-1.146, p < 0.05). By ROC analysis, PAR showed better performance over PCT at 48 h after admission in predicting one-month CPC (0.763 vs. 0.772, p = 0.010). (4) Conclusions: Our findings suggest that PAR at 48 h after admission is more effective in predicting a one-month neurological outcome than PCT at 48 h after admission in patients with PCAS after OHCA.

The Effect of Therapeutic Blockades of Dust Particles-Induced Ca²âº Signaling and Proinflammatory Cytokine IL-8 in Human Bronchial Epithelial Cells.

Bronchial epithelial cells are the first barrier of defense against respiratory pathogens. Dust particles as extracellular stimuli are associated with inflammatory reactions after inhalation. It has been reported that dust particles induce intracellular Ca(2+) signal, which subsequently increases cytokines production such as interleukin- (IL-) 8. However, the study of therapeutic blockades of Ca(2+) signaling induced by dust particles in human bronchial epithelial cells is poorly understood. We investigated how to modulate dust particles-induced Ca(2+) signaling and proinflammatory cytokine IL-8 expression. Bronchial epithelial BEAS-2B cells were exposed to PM10 dust particles and subsequent mediated intracellular Ca(2+) signaling and reactive oxygen species signal. Our results show that exposure to several inhibitors of Ca(2+) pathway attenuated the PM10-induced Ca(2+) response and subsequent IL-8 mRNA expression. PM10-mediated Ca(2+) signal and IL-8 expression were attenuated by several pharmacological blockades such as antioxidants, IP3-PLC blockers, and TRPM2 inhibitors. Our results show that blockades of PLC or TRPM2 reduced both of PM10-mediated Ca(2+) signal and IL-8 expression, suggesting that treatment with these blockades should be considered for potential therapeutic trials in pulmonary epithelium for inflammation caused by environmental events such as seasonal dust storm.

Intermediate and long-term results of transcatheter closure of patent foramen ovale using the amplatzer patent foramen ovale occluder: one case of pulmonary embolism irrespective of patent foramen ovale closure.

BACKGROUND AND OBJECTIVES: Patent foramen ovale (PFO) has been implicated in the pathogenesis of cryptogenic stroke or transient ischemic attack (TIA) due to paradoxical embolism, and in the pathogenesis of migraine. This paper reports the intermediate and long-term results of transcatheter closure of PFO associated with cerebrovascular accidents (CVAs), TIAs and migraine, using the Amplatzer PFO occluder. This paper also reports a case of pulmonary embolism which developed in one patient after PFO closure. SUBJECTS AND METHODS: From January 2003 to May 2010, 16 patients with PFO (seven males and nine females) with a history of at least one episode of cryptogenic stroke/TIA, CVA, or migraine and who underwent percutaneous transcatheter closure of PFO using the Amplatzer occluder. All the procedures were performed under general anesthesia and were assisted by transesophageal echocardiography. RESULTS: The device was implanted without any significant complications in all the patients, and the PFOs were effectively closed. At an average follow-up period of 54 months, the 15 patients with TIA/CVA had no recurrence of any thromboembolic event. The symptoms in one patient with migraine subsided after occlusion of the PFO. In this study, pulmonary embolism occurred five months after PFO closure in one patient, but the cause of pulmonary embolism was not identified. However, it is believed that the pulmonary embolism occurred without stroke recurrence because occlusion of the PFO was performed when the patient had a stroke event. CONCLUSION: It can be concluded that according to the intermediate and long-term follow-up results, transcatheter PFO closure is an effective and safe therapeutic modality in the prevention of thromboembolic events, especially in the patients with cryptogenic stroke/TIA, and PFO closure is helpful in the treatment of migraine. However, this study involved a small number of patients and also the follow-up period was not long enough. Hence, randomized, controlled trials are necessary to determine if this approach is preferable to medical therapy for the prevention of recurrent stroke or as primary treatment for patients with migraine headache.

BACE inhibitor reduces APP-beta-C-terminal fragment accumulation in axonal swellings of okadaic acid-induced neurodegeneration.

Emerging evidence suggests that not only beta-amyloid but also other amyloid precursor protein (APP) fragments, such as the beta-C-terminal fragment (betaCTF), might be involved in Alzheimer's disease (AD). Treatment of neurons with okadaic acid (OA), a protein phosphatase-2A inhibitor, has been used to induce tau phosphorylation and neuronal death to create a research model of AD. In this study, we analyzed axonopathy and APP regulation in cultured rat neurons treated with OA. After OA treatment, the neurons presented with axonal swellings filled with vesicles, microtubule fragments, and transport molecules such as kinesin and synapsin-I. Western blotting showed that intracellular APP levels were increased and immunocytochemistry using antibodies against the APP C-terminus showed that APP accumulated in the axonal swellings. This APP C-terminus immunoreactivity disappeared when neurons were cotreated with a beta-secretase inhibitor, but not with alpha- or gamma-secretase inhibitors, indicating that the accumulation was primarily composed of APP-betaCTF. These findings provide the first evidence that APP-betaCTF can accumulate in the axons of OA-treated neurons, and may suggest that APP-betaCTF is involved in the pathogenesis of AD.