Massive hemothorax due to two bleeding sources with minor injury mechanism: a case report

Massive hemothorax resulting from a minor injury mechanism is considered to be rare particularly when the diaphragm is injured. We report a case of massive hemothorax with bleeding from the intercostal artery ...

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How neuraxial labor analgesia differs by approach: dural puncture epidural as a novel option

Abstract

Background and aim

Neuraxial analgesia techniques are not limited to just standard epidural and CSE blocks. A novel approach called dural puncture epidural (DPE) which is a modification of CSE in terms of practice has gained popularity after its description and use in the obstetric population.  The aim of this review is to address the practice of DPE technique as a novel option by reviewing its benefits as well as side and/or adverse effects and to understand how neuraxial labor analgesia differs by approach based on the information available in the current literature

Discussion

Despite controversies and concerns, more rapid onset of analgesia, early bilateral sacral analgesia, lower incidence of asymmetric block and fewer maternal and fetal side effects are provided with DPE when compared to epidural.

Conclusion

DPE offers a favorable risk–benefit ratio for management of neuraxial analgesia as a novel option.

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Angiotensin II-mediated suppression of synaptic proteins in mouse hippocampal neuronal HT22 cell was inhibited by propofol: role of calcium signaling pathway

Abstract

Purpose

Angiotensin II (Ang II) has been shown to be involved in neurological disorders. Propofol demonstrated neuroprotective effects in neurons.

Methods

Mouse hippocampal HT22 cells were pre-treated with propofol, followed by Ang II treatment. The expression of synaptic proteins (synapsin I and PSD95) was examined. The effects of propofol on Ang II-induced NADPH oxidase expression and superoxide anion generation were examined. The effects of propofol on intracellular calcium concentration, the activation of calcium/calmodulin-dependent protein kinase II (CaMKII), and protein kinase C (PKC) were measured.

Results

Ang II reduced the expression of synapsin I and PSD95, which was attenuated by propofol. Ang II-induced effects were blocked by Ang II type 1 receptor (AT1 receptor) blocker. Ang II induced the expression of NADPH oxidase and caused superoxide anion accumulation, which were attenuated by propofol. In addition, propofol induced intracellular calcium concentration, and activated CaMKII as well as PKCβ. Importantly, the Ang II-mediated effects were diminished by α-tocopherol, and the propofol-mediated effects were alleviated by calcium chelator, CaMKII inhibitor, and PKCβ inhibitor.

Conclusion

Ang II, via AT1 receptor, induced oxidative stress and reduced the expression of synapsin I and PSD95 in HT22 cells. Propofol may increase synapsin I and PSD95 expression by inhibiting oxidative stress and stimulating calcium signaling pathway.

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