BK Viremia as a Predictor of Hemorrhagic Cystitis in Adults During the First 100 Days After Allogeneic Hematopoietic Stem Cell Transplantation.

In a retrospective case-control study, we aimed to assess the utility of plasma BK viral load value to predict hemorrhagic cystitis (HC) symptoms after allogeneic hematopoietic stem cell transplantation (alloHSCT). During first 100 post-transplantation days of all adult AlloHSCT recipients at the University of Nebraska Medical Center from October 1, 2011, to June 30, 2014, 8 unexcluded cases of HC were identified and matched with 88 unexcluded unaffected control cases. Viral loads were determined for archived DNA extracted from plasma collected within 3 weeks before transplantation until ∼100 days after transplantation. Clinical factors, time of onset of BK viremia, and BK viral load were compared between case and control subjects to identify risks for HC. Symptomatic HC occurred in 8/96 (8.3%) of patients at a median of 34 days after transplantation. BK viremia either before or during symptoms was detected in all 8 (100%) HC patients and in 20/88 (22.7%) of control subjects. BK viremia was detected at a median of 8 days before HC clinical symptoms. The log of first positive viral load was not a statistically significant predictor (P = .17) of symptomatic BK. Median BK viral load peak was significantly higher for 8 patients with HC versus 20 viremic patients without HC (6.66 vs 5.06; P < .052). Further study is required to evaluate the predictive value of the BK viral load for HC.

Resveratrol protects spinal cord dorsal column from hypoxic injury by activating Nrf-2.

Damage from oxidative stress plays a critical role in spinal cord injury. Nuclear factor erythroid 2-related factor (Nrf-2) signaling pathway can be activated by cellular oxidative stress. Resveratrol, a plant-derived polyphenolic compound found in red wine, has antioxidant properties. In the present study, we have examined the neuroprotective effect of resveratrol and the role of Nrf-2 in spinal cord hypoxic injury. The spinal cord was removed from adult male Wistar rats from T2-T10 and the dorsal column was used to induce hypoxic injury in vitro with and without treatment with resveratrol (50µM). Significant changes were found in the compound action potential (CAP) of spinal cord dorsal column, and hematoxyline and eosin (H&E) staining showed that resveratrol significantly improved neuronal injury. The biochemical assays showed significant changes in lipid peroxidase (LPO), reduced glutathione (GSH), superoxide dismutase (SOD), protein carbonyl (PC), mitochondrial ATP content, and mitochondrial Ca(++). Furthermore, using immunohistochemistry and Western blot, we found that after resveratrol treatment during hypoxic injury there was a significant activation of NrF-2 and down regulation of the glial fibrillary acidic protein (GFAP) content. The results show that resveratrol treatment has neuroprotective effects on CAP, Ca(++) loading, and biochemical parameters after hypoxic injury. The neuroprotective effect is likely to be exerted by increased activation of transcription factor Nrf-2 by resveratrol along with its direct antioxidant effect to ameliorate the oxidative damage and preserve mitochondrial function.

Effect of sodium hydrosulphide after acute compression injury of spinal cord.

BACKGROUND: Early treatment of spinal cord white matter injury has been found beneficial. H2S, a neurotransmitter is neuroprotective at lower doses. PURPOSE: In the present study the effect of NaHS after clip compression injury of spinal cord white matter in vivo was studied. METHODS: The injury was induced in 8-10 weeks old Wistar rats by exposing the spinal cord at T8-T10 level by laminectomy and applying 35 g clip for 1 min. A dose of 50 µM NaHS was given intraperitoneally after 1h of injury. 0.5mm Spinal cord tissues were collected 8h after injury from both sides including epicenter and dorsal column was microdissected and used for further study. RESULTS: NaHS treatment decreases nitric oxide (NO) by 27% and lipid peroxide (LPO) by 18% as compared to injury, which are hallmark of attenuation in oxidative stress. Western blots shows significant changes in Myeloperoxidase (MPO) level went down by 10%. GSH contents increased 44% in treated group as compared to the injury group. NaHS treatment increased Nrf-2 expression 1.8 times. We found NaHS treatment reduced the GFAP expression 8%, there was no significant changes in NF-200 after treatment and no evident morphological changes with H and E staining. CONCLUSIONS: With the above data we conclude that NaHS at 50 µM dose at 1h after injury reduces the NO, LPO, GFAP and MPO level at injury site by increasing the expression of Nrf-2. We expect that a decrease in these parameters during acute phase of spinal cord injury would be helpful in neuroprotection and regeneration.