Multisystemic Inflammatory Syndrome Temporally Associated with COVID-19 in a Regional Pediatric Hospital from México.

Multisystemic inflammatory syndrome (MIS-C) is an inflammatory condition temporally associated with COVID-19 in children; nevertheless, the clinical and immunologic spectrum of MIS-C is heterogeneous, and its long-term effects are unknown. During the period of August 2020 to December 2021, a total of 52 MIS-C cases were confirmed in pediatric patients from the Hospital del Niño DIF Hidalgo, diagnosed using criteria from the World Health Organization. All patients had serologic IgG confirmation of SARS-CoV2, the mean age of the patients was 7 years, and 94% of the patients did not have a previous underlying disease. In addition to the presentation of lymphopenia, neutropenia, and thrombocytopenia, elevations in D-dimer and ferritin levels were observed in all patients. There was clinical improvement with intravenous gamma globulin and corticosteroid treatment.

Early metabolic reactivation versus antioxidant therapy after a traumatic spinal cord injury in adult rats.

Disability after traumatic spinal cord injury (TSCI) results from physical trauma and from "secondary mechanisms of injury" such as low metabolic energy levels, oxidative damage and lipid peroxidation. In order to prove if early metabolic reactivation is a better therapeutic option than antioxidant therapy in the acute phase of TSCI, spinal cord contusions were performed in adult rats using a well-characterized weight drop technique at thoracic 9 level. After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control. Rats were divided into one sham group and six with TSCI; one of them received no treatment, and the rest were treated with NDC, MP, NDC + MP, NDC + ANT or ANT. The ANT group decreased lactate and creatine phosphokinase levels and increased the amount of preserved tissue (morphometric analysis) as well as functional recovery (Basso, Beattie and Bresnahan or BBB motor scale). In contrast, NDC treatment increased lipid peroxidation, measured through thiobarbituric acid reactive substances (TBARS) levels, as well as spinal cord tissue destruction and functional deficit. Early metabolic reactivation after a TSCI may be deleterious, while natural early metabolic inhibition may not be a "secondary mechanism of injury" but a "secondary neuroprotective response". While increased antioxidant defence after a TSCI may currently be an ideal therapeutic strategy, the usefulness of metabolic reactivation should be tested in the sub-acute or chronic phases of TSCI and new strategies must continue to be tested for the early ones.

Early effects of modulating nuclear factor-kappaB activation on traumatic spinal cord injury in rats.

Genes regulated by NF-kappaB play an important role on secondary damage and repair after spinal cord injury (SCI). To assess the early effects of the pharmacological inhibition and overactivation of NF-kappaB, pyrrolidine dithiocarbamate (PDTC) or lipopolysaccharide were given to rats before or after SC contusion. The amount of spared SC tissue was higher (P < 0.05) at 24 h postinjury in rats post-treated with PDTC; both PDTC-treated rats showed no significant trend to decrease polymorphonuclear infiltrate. p65 subunit was present in inflammatory cells, neurons, and astrocytes at the injury site. These data support further investigation on functional effects of NF-kappaB inhibition in acute SCI.

Spontaneous and induced aberrant sprouting at the site of injury is irrelevant to motor function outcome in rats with spinal cord injury.

In the absence of effective regeneration following spinal cord (SC) injury, sprouting from undamaged axons has been regarded as an underlying factor for functional improvement after incomplete SC injury. The influence of spontaneous and induced axonal sprouting at the injury site on motor function was tested using rats subjected to moderate SC contusion at T9 level, using megadoses of methylprednisolone (MP) and intralesion implantation of cells from sciatic nerve (PNI). Groups using MP and PNI combined, implant vehicle, and injury with no treatment were also included. Amount of sprouting at the injury sites was significantly different depending on treatment. It was abundant in PNI-treated rats, moderate in rats treated with vehicle or nontreated, and limited in rats given MP with or without PNI (chi2, p=0.0084). This sprouting showed an aberrant course and was located in proliferating tissue at the site of injury, characterized by the presence of ependymal cells, macrophages, and myelinating and nonmyelinating Schwann cells. Functional scores and amount of spared white matter were not significantly different among groups. Correlation of the amount of sprouting vs. functional outcome or vs. amount of spared tissue was not significant, while correlation of functional outcome vs. amount of spared tissue was significant (p<0.0001). In conclusion, PNI increase aberrant sprouting at the injury site, while MP limits such sprouting, in either case without impact on motor function outcome. Missing guiding channels for sprouting axons could explain the absence of any functional improvement.