RESULTS We identified 154 deep and 53 lobar ICH patients who received TEG. Deep ICH patients were younger and had smaller admission hematoma volumes (median 16 vs 29 mL). Adjusted multivariable linear regression analysis revealed longer TEG R times (0.57 min; 95% CI 0.02-1.11; P = .04), indicating longer clot formation times, in deep compared to lobar ICH. No other TEG parameter or plasma-based coagulation differences were seen. CONCLUSION We identified longer clot formation times, suggesting relative coagulopathy in deep compared to lobar ICH confirming results from prior work. Further work is required to elucidate mechanisms for these differences and whether ICH location should be considered in future coagulopathy treatment paradigms for ICH. Copyright © 2020 by the Congress of Neurological Surgeons.Punctate midline myelotomy (PMM) is a surgical procedure that damages the ascending fibers of the postsynaptic dorsal column (PSDC) pathway to interrupt visceral pain transmission.1-3 It can offer relief to patients with chronic visceral pain conditions that are refractory to other treatments. Here, we present a surgical video of midthoracic PMM in a patient with chronic, intractable, nonmalignant visceral abdominal pain that failed over a decade of medical treatment. We choose T7-8 as the level for laminectomy in patients with pelvic or lower abdominal pain, because the postsynaptic pain fibers transmitting visceral pain sensation from the lower abdominal organs will invariably be caudal to this level. The patient developed immediate and complete relief of her visceral pain after the procedure, which was sustained through the 11-wk follow-up period to date and was able to be weaned off narcotics. Postoperatively, she remained full strength and had no impairment of light touch or proprioception of her lower extremities. Detailed physical examination showed a reduced vibratory sensation on the glabrous skin of her great toes. Regarding patient-reported sensory changes (not detected on physical examination), she reported some numbness on the insides of her feet that had resolved by 11-wk follow-up. She also reported some numbness of the vulva, but not of the vagina. However, by 11-wk follow-up, she reported this had resolved and she had normal sexual function. The only persistent sensation at 11-wk follow-up was slight tingling in her toes that was not bothersome to her.4 The patient presented in the following video consented to both the surgical procedure and the publication of her clinical history and operative video. Copyright © 2020 by the Congress of Neurological Surgeons.Resection of intra-axial tumors adjacent to the motor pathways can lead to devastating deficits; however, with an appropriate mapping technique, it can be performed safely. We present the case of a 63-yr-old woman with a diffuse glioma centered in the left supplemental motor area (SMA) and extending throughout the cingulate gyrus. In the video, we demonstrate the principles developed by the senior author for trimodal motor mapping under general anesthesia. Trimodal motor mapping includes direct stimulation of the cortex with a strip electrode, use of the bipolar stimulator for cortical and subcortical mapping, and use of the monopolar stimulator for subcortical motor mapping. We highlight technical principles required to safely resect these tumors, including the key anatomic landmarks and approach to SMA/cingulate lesions, techniques for subpial dissection, and preservation of en passage vessels. Patients with SMA tumors will almost always have a deficit after SMA resection, but if motor pathways are preserved and can be stimulated to produce movement at the end of the case, then the deficit will almost always improve, as was the case with this patient. Initially, postoperatively, she was nonverbal and hemiplegic, but by postoperative day 7 she recovered her speech significantly, was naming three of three objects, and was moving her right side. By 6 wk postoperative, she was ambulating independently and had normal speech. This case demonstrates the principles and techniques necessary for achieving maximal safe resection of tumors adjacent to the motor pathways with the patient under general anesthesia.  The patient gave written informed consent for the surgical resection of her tumor and for the publication of this video. Copyright © 2020 by the Congress of Neurological Surgeons.Excessive mitochondrial fission has been identified as the central pathogenesis of diabetic kidney disease (DKD), but the precise mechanisms remain unclear. Disulfide-bond A oxidoreductase-like protein (DsbA-L) is highly expressed in mitochondria in tubular cells of the kidney, but its pathophysiological role in DKD is unknown. Our bioinformatics analysis showed that tubular DsbA-L mRNA levels were positively associated with eGFR but negatively associated with Scr and 24h-proteinuria in CKD patients. Furthermore, the genes that were coexpressed with DsbA-L were mainly enriched in mitochondria and were involved in oxidative phosphorylation. In vivo, knockout of DsbA-L exacerbated diabetic mice tubular cell mitochondrial fragmentation, oxidative stress and renal damage. In vitro, we found that DsbA-L was localized in the mitochondria of HK-2 cells. https://www.selleckchem.com/products/terfenadine.html High glucose (HG, 30 mM) treatment decreased DsbA-L expression followed by increased mitochondrial ROS (mtROS) generation and mitochondrial fragmentation. In addition, DsbA-L knockdown exacerbated these abnormalities, but this effect was reversed by overexpression of DsbA-L. Mechanistically, under HG conditions, knockdown DsbA-L expression accentuated JNK phosphorylation in HK-2 cells. Furthermore, administration of a JNK inhibitor (SP600125) or the mtROS scavenger MitoQ significantly attenuated JNK activation and subsequent mitochondrial fragmentation in DsbA-L-knockdown HK-2 cells. Additionally, the down-regulation of DsbA-L also amplified the gene and protein expression of mitochondrial fission factor (MFF) via the JNK pathway, enhancing its ability to recruit DRP1 to mitochondria. Taken together, these results link DsbA-L to alterations in mitochondrial dynamics during tubular injury in the pathogenesis of DKD and unveil a novel mechanism by which DsbA-L modifies mtROS/JNK/MFF-related mitochondrial fission. © 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.