Association between aortic coverage and spinal cord ischemia after endovascular repair of type B aortic dissection.

Objectives: To examine the association between aortic coverage and occurrence of spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection. Methods: Thirty-eight consecutive patients (mean age 52 years; 35 men) who underwent TEVAR for type B aortic dissection at our centre were included. Patients were stratified into two groups based on stent graft length (SGL): group I (≤ 200 mm; n = 19) and group II (> 200 mm; n = 19). All the procedures were performed under strict blood pressure monitoring. Preoperative cerebrospinal fluid (CSF) drain was instituted in two patients. Results: Mean SGLs were 200 mm in group I and 277 ± 27 mm in group II. The number of segmental arteries covered was significantly different between the two groups (p < 0.001). There was no significant difference in vertebral artery dominance between groups I and II (p = 0.99). One patient in group II, who also had bilateral internal iliac artery occlusion, developed postprocedural neurological deficit referrable to SCI, which resolved completely after institution of CSF drainage. However, the incidence of SCI was not significantly different between group I and group II (p = 0.5). Conclusion: Based on our experience, we recommend longer aortic coverage (beyond 200 mm) in type B aortic dissection (TBAD) for better aortic remodelling, provided that the mean arterial pressure of > 90 mm Hg is maintained perioperatively to avoid SCI.

Inhibition of pan-Aurora kinase attenuates evoked and ongoing pain in nerve injured rats via regulating KIF17-NR2B mediated signaling.

Kinesins (KIF's) are the motor proteins which are recently reported to be involved in the trafficking of nociceptors leading to chronic pain. Aurora kinases are known to be involved in the regulation of KIF proteins which are associated with the activation of N-methyl-D-aspartate (NMDA) receptors. Here, we investigated the effect of tozasertib, a pan-Aurora kinase inhibitor, on nerve injury-induced evoked and chronic ongoing pain in rats and the involvement of kinesin family member 17 (KIF17) and NMDA receptor subtype 2B (NR2B) crosstalk in the same. Rats with chronic constriction injury showed a significantly decreased pain threshold in a battery of pain behavioural assays. We found that tozasertib [10, 20, and 40 mg/kg intraperitoneally (i.p.)] treatment showed a significant and dose-dependent inhibition of both evoked and chronic ongoing pain in rats with nerve injury. Tozasertib (40 mg/kg i.p.) and gabapentin (30 mg/kg i.p.) treatment significantly inhibits spontaneous ongoing pain in nerve injured rats but did not produce any place preference behaviour in healthy naïve rats pointing towards their non-addictive analgesic potential. Moreover, tozasertib (10, 20, and 40 mg/kg i.p.) and gabapentin (30 mg/kg i.p.) treatment did not altered the normal pain threshold in healthy naïve rats and didn't produce central nervous system associated side effects as well. Western blotting and reverse transcription polymerase chain reaction studies suggested enhanced expressions of NR2B and KIF-17 along with increased nuclear factor kappa ß (NFkß), tumour necrosis factor-α (TNF-α), interleukin 1ß (IL-1ß), and interleukin 6 (IL-6) levels in dorsal root ganglion (DRG) and spinal cord of nerve injured rats which was significantly attenuated on treatment with different does of Tozasertib. Findings from the current study suggests that inhibition of pan-Aurora kinase decreased KIF-17 mediated NR2B activation which further leads to significant inhibition of evoked and chronic ongoing pain in nerve-injured rats.

Trichoderma spp. mediated induction of systemic defense response in brinjal against Sclerotinia sclerotiorum.

Induction of resistance to pathogen is associated with the colonization of root by Trichoderma spp. has been attributed as one of the major mechanisms contributing to pathogenic invasion. The present study sheds light on the defense network of brinjal plant bioprimed with Trichoderma spp. challenged with Sclerotinia sclerotiorum. Plants treated with dual inoculation of Trichoderma harzianum and Trichoderma asperellum triggered further synthesis of TPC under S. sclerotiorum challenge with maximum increment recorded at 72 hours. In consortium treated and pathogen challenged plants, a higher amount of shikimic acid was observed at 72 hours, whereas other phenolics showed little differences among the treatments. The consortium treatment showed significantly higher defense related enzymes (Phenylalanine Ammonia Lyase, Peroxidase and Polyphenol Oxidase) activity than other treatments. The study signifies how Trichoderma spp. reprograms the host's defense network to provide robust protection against S. sclerotiorum. In the present case, overall protection was provided to the brinjal plants against the attack of S. sclerotiorum.