Case report: A case of anti-glycine receptor encephalomyelitis triggered by post-transplant or COVID-19 infection?

Even though long-term immunosuppressant drugs (ISD) are employed to inhibit immune system activity, enhancing graft functionality and patient survival in solid organ transplantation (SOT), these transplants often lead to immune complications, with post-transplant autoimmune diseases of the central nervous system (CNS) being uncommon. Here, we detail the case of a 66-year-old woman who underwent a renal transplantation 8 months prior, who was admitted with subacute onset of encephalomyelitis, accompanied by headaches, paraplegia, weakness, vomiting, and abdominal pain, with a positive COVID-19 nasopharyngeal swab test 1 month before admission. MRI scans of the brain revealed multiple lesions in the white matter of the bilateral deep frontal lobe, the left temporal lobe and insula lobe.

Radical footprinting and regularity revealing during the pyrolysis of technical lignins.

Revealing radical-mediated reactions is conducive to illustrate lignin pyrolysis and achieve subsequent regulation. Three technical lignins (hot-water-extracted lignin, kraft lignin, and soda lignin) were selected in this study and pyrolyzed from 400 °C to 700 °C, and their pyrolysis radicals in both chars and bio-oils were monitored with the electron paramagnetic resonance spectrometer. Results showed that spin concentrations of char radicals had a volcanic trend against the pyrolysis temperature, and reached the maximum values at 550-600 °C.

Elucidating radical-mediated pyrolysis behaviors of preoxidized lignins.

Effect of lignin preoxidation on subsequent radical-mediated pyrolysis was discussed in this study. Technical hot-water-extracted lignin was preoxidized by 2,3-dichloro-5,6-dicyano-1,4-benzoquinone in diverse degrees and pyrolyzed under different temperatures. Characterizations indicated that preoxidation increased lignin oxygen contents and converted α-hydroxyls to α-carbonyls.

Unmasking radical-mediated lignin pyrolysis after benzyl hydroxyl shielding.

Whether lignin benzyl hydroxyl shielding could promote its pyrolysis to phenolic compounds was investigated in this paper. Lignin benzyl hydroxyl was first preoxidized by 2,3-dichloro-5,6-dicyano-1,4-benzoquinone and stabilized by propionaldehyde respectively, then pyrolysis was conducted with milled wood lignin as a control. Organic stable radicals in pyrolytic chars were further detected to reveal lignin pyrolysis chemistry.

Genetic Creutzfeldt-Jakob disease shows fatal family insomnia phenotype.

We report a case of genetic Creutzfeldt-Jakob disease (gCJD), which has a clinical phenotype that is highly similar to Fatal Family Insomnia (FFI) and has a triad of Wernicke-Korsakoff syndrome (WKs) at the developmental stage of the disease. The 51-year-old male complained of sleep disorder and imbalance who had visited five different hospitals before diagnosed. A neurological examination revealed a triad of symptoms characteristic for WKs such as gaze paresis, ataxia of limbs and trunk, and memory disturbances.

The adenosine A receptor antagonist SCH58261 reduces macrophage/microglia activation and protects against experimental autoimmune encephalomyelitis in mice.

Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease of the central nervous system (CNS) affecting more than 2.5 million individuals worldwide. In the present study, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice were treated with adenosine receptor A antagonist SCH58261 at different periods of EAE development.

[CEMENTLESS TOTAL HIP ARTHROPLASTY FOR TREATMENT OF Crowe TYPE Ⅲ DEVELOPMENTAL DYSPLASIA OF HIP IN ADULTS].

Objective: To investigate the value of cementless total hip arthroplasty (THA) for the treatment of Crowe type Ⅲ developmental dysplasia of hip (DDH) in adults.

Methods: Between September 2013 and September 2015, 50 patients (51 hips) with Crowe type Ⅲ DDH were treated. There were 20 males (20 hips) and 30 females (31 hips), with the average age of 39 years (range, 19-55 years).

2-BFI ameliorates EAE-induced mouse spinal cord damage: effective therapeutic time window and possible mechanisms.

Our previous studies showed that ligands to type 2 imidazoline receptors (I₂R), including 2-(2-Benzofuranyl)-2-imidazoline (2-BFI) and Idazoxan, were effective in reducing spinal cord inflammation caused by experimental autoimmune encephalomyelitis (EAE). In the present study, we determined the effective therapeutic time window of 2-BFI and found that administration of 2-BFI in mice before the appearance of ascending flaccid paralysis (1-10 days post immunization), but not during the period when neurological deficits occurred (11-20 days post immunization), significantly ameliorated EAE-induced neurobehavioral deficits, reduced the infiltration of inflammatory cells into the spinal cord, and reduced the level of demyelination. More interestingly, giving 2-BFI during 1-10 days post immunization selectively suppressed IL-17 levels in the peripheral blood, which strongly suggests that IL-17 may be a good early marker to indicate EAE progression and that 2-BFI may target CD4⁺ T lymphocytes, especially Th17 cells to reduce IL-17 expression.