Malignant Hyperthermia-Associated Rhabdomyolysis After Succinylcholine: A Case Report.

Malignant hyperthermia-associated rhabdomyolysis is a condition that lies on the spectrum of malignant hyperthermia (MH). Unlike MH, malignant-hyperthermia-associated rhabdomyolysis is a condition which most commonly is recognized in the postoperative period by the development of discolored brown urine with notably absent rigidity, tachypnea, tachycardia, and hyperthermia. The presented case describes the subtle onset of malignant hyperthermia-associated rhabdomyolysis, along with a review of relevant literature.

Painful Post-traumatic Trigeminal Neuropathy Occurs After Third Molar Extraction.

Painful post-traumatic trigeminal neuropathy (PTTN), or anesthesia dolorosa, is a condition on the same continuum as trigeminal neuralgia. Unlike trigeminal neuralgia, trigeminal neuropathy is a more significant state of neural pathology resulting in constant pain opposed to the episodic nature of trigeminal neuralgia. This typically occurs after facial trauma or as a complication from some treatments for trigeminal neuralgia. Useful diagnostic features that can help distinguish PTTN are an identified trauma to the nerve and other clinical features such as facial swelling. The presented case describes a classic presentation after third molar (wisdom tooth) removal and a review of pertinent literature.

Senecavirus A 3C Protease Mediates Host Cell Apoptosis Late in Infection.

Senecavirus A (SVA), an oncolytic picornavirus used for cancer treatment in humans, has recently emerged as a vesicular disease (VD)-causing agent in swine worldwide. Notably, SVA-induced VD is indistinguishable from foot-and-mouth disease (FMD) and other high-consequence VDs of pigs. Here we investigated the role of apoptosis on infection and replication of SVA. Given the critical role of the nuclear factor-kappa B (NF-κB) signaling pathway on modulation of cell death, we first assessed activation of NF-κB during SVA infection. Results here show that while early during infection SVA induces activation of NF-κB, as evidenced by nuclear translocation of NF-κB-p65 and NF-κB-mediated transcription, late in infection a cleaved product corresponding to the C-terminus of NF-κB-p65 is detected in infected cells, resulting in lower NF-κB transcriptional activity. Additionally, we assessed the potential role of SVA 3C protease (3Cpro) in SVA-induced host-cell apoptosis and cleavage of NF-κB-p65. Transient expression of SVA 3Cpro was associated with cleavage of NF-κB-p65 and Poly (ADP-ribose) polymerase (PARP), suggesting its involvement in virus-induced apoptosis. Most importantly, we showed that while cleavage of NF-κB-p65 is secondary to caspase activation, the proteolytic activity of SVA 3Cpro is essential for induction of apoptosis. Experiments using the pan-caspase inhibitor Z-VAD-FMK confirmed the relevance of late apoptosis for SVA infection, indicating that SVA induces apoptosis, presumably, as a mechanism to facilitate virus release and/or spread from infected cells. Together, these results suggest an important role of apoptosis for SVA infection biology.

Generation of a CLTA reporter human induced pluripotent stem cell line, CRMi001-A-1, using the CRISPR/Cas9 system to monitor endogenous clathrin trafficking.

The most highly studied endocytic pathway, clathrin-dependent endocytosis, mediates a wide range of fundamental processes including nutrient internalization, receptor recycling, and signal transduction. In order to model tissue specific and developmental aspects of this process, CRISPR/Cas9 genomic editing was utilized to fluorescently label the C-terminus of clathrin light chain A (CLTA) within the phenotypically normal, parental CRMi001-A human induced pluripotent stem cell line. Successfully edited cells were isolated by fluorescently activated cell sorting, remained karyotypically normal, and maintained their differentiation potential. This cell line facilitates imaging of endogenous clathrin trafficking within varied cell types.