Neurodegeneration, along with inflammatory demyelination, is an important component of multiple sclerosis (MS) pathogenesis. Autophagy is known to play a pivotal role in neuronal homeostasis and is implicated in several neurodegenerative disorders. However, whether autophagy is involved in the mechanisms of neuronal damage during MS remains to be investigated. Experimental autoimmune encephalomyelitis (EAE), an in vivo model of MS, was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein p35-55. After that, autophagic flux in the spinal cord of mice was evaluated by detection of LC3-II and Beclin1 protein expressions. EAE mice were then administered with rapamycin and 3-methyladenine (3-MA) for 10 days. Afterward, the changes in LC3-II, Beclin1, and p62 expression, number of infiltrated inflammatory cells, demyelinated lesion area, and neuronal damage, as well as clinical scores, were assessed. Further, apoptotic cell rate and apoptosis-related protein expressions were monitored. We observed an impaired autophagic flux and increased neuronal damage in the spinal cords of EAE mice. We also found that rapamycin, an autophagy inducer, mitigated EAE-induced autophagy decrease, inflammation, demyelination and neuronal injury, as well as the abnormal clinical score. In addition, rapamycin suppressed cell apoptosis, and decreased Bax/Bcl-2 ratio and cleaved caspase-3 expression. Conversely, the effect of autophagy inhibitor 3-MA on EAE mice resulted in completely opposite results. These results indicated that autophagy deficiency, at least in part, contributed to EAE-induced neuronal injury and that pharmacological modulation of autophagy might be a therapeutic strategy for MS.
Objective: Anti-γ-aminobutyric acid-B receptor (GABA B R) encephalitis is a rare type of autoimmune encephalitis. There are only a few, small, published studies regarding prognosis, so prediction of prognosis is of limited accuracy. We identified cases of anti-GABA B R encephalitis in China. Here, we present these patients' clinical characteristics and long-term outcomes.Methods: We collected and retrospectively analyzed the clinical data of patients with anti-GABA B R encephalitis from Beijing Fengtai You'anmen Hospital. Results:The study cohort comprised patients of anti-GABA B R encephalitis of median age years (range: -), of whom were male. The main clinical manifestations were epilepsy ( . %, / ), psychiatric disorders ( . %, / ) and cognitive impairment ( . %, / ). Tumors were identified in ( . %) patients. First-line immunotherapy was administered to patients, of whom ( . %) responded favorably. During a median follow-up of months (range: -months), patients had good outcomes [Modified Ranking Scale (mRS ≤ )],( . %) died (mRS ), and ( . %) relapsed. Age (P = .), disturbance of consciousness (P = .), admission to the Neurology Intensive Care Unit (P = .), mechanical ventilation (P = .), more numerous clinical manifestations (P = .), comorbid malignancy (P = .), multiple anti-neuronal antibodies (P = .), and hyponatremia (P = .) di ered significantly between patients with good outcomes (mRS -) and those with poor outcomes (mRS -). Conclusion:Men aged -years accounted for most of the patients with anti-GABA B R encephalitis in our case series. The main clinical manifestations were epilepsy and neuropsychiatric dysfunction. The participants often had Frontiers in Neurology frontiersin.org Feng et al. . /fneur. . concomitant lung cancer, particularly small-cell lung cancer. Patients with lung tumors and/or serious manifestations usually had a poor prognosis with high mortality. Early identification and treatment of tumors improved the poor prognosis to some extent.
Ziehl-Neelsen (Z-N) staining of cerebrospinal fluid (CSF) for acid-fast bacilli (AFB) is the cornerstone of the laboratory diagnosis of tuberculous meningitis (TBM). However, the sensitivity of conventional Z-N staining for the detection of AFB in CSF specimens is suboptimal. The present study aimed to compare the practicality of modified Z-N staining with light microscopy and fluorescence microscopy in the same smear without auramine O. A total of 155 patients with 223 CSF specimens were enrolled and grouped according to the uniform case definition. The smears of each CSF specimen were subjected to modified Z-N staining and then observed using a light microscope under transmitted light and under fluorescence with a green-excitation wavelength in the same microscopic field. The results for different groups, inspection times, and prior to and following treatment were compared. Results indicated that the fuchsin-stained AFB were visible as bright orange-red fluorescing rods under fluorescence, or as red, lightly curved rods under transmitted light. The sensitivity of fluorescence microscopy was 96.2% while that of light microscopy was 84.6%. The positive rate of fluorescence microscopy was 79.2% prior to treatment compared with 61.7% post-treatment. In the same microscopic field, a greater number of AFB were observed using fluorescence compared with transmitted light, and AFB that were not visible under transmitted light were clearly observed under fluorescence. Furthermore, transmitted light and fluorescence could be interchanged directly when equivocal smears were encountered. The combination of modified Z-N staining and fluorescence microscopy without auramine O is sensitive and convenient for the diagnosis of TBM.
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