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Although central nervous system infection following varicella zoster virus infection is relatively common, subsequent peripheral nervous system infection is comparatively rare. The present case documents a case of meningitis after varicella-zoster virus (VZV) infection, which was then followed by peripheral facial palsy. Specifically, a 54-year-old female patient was first admitted to Shengli Oilfield Central Hospital (Dongying, China) with headache and fever. Physical examination revealed herpes that formed along the intercostal nerve in the left forebreast, armpit and back. Subsequently, neurological examination found cervical resistance in more than three fingers (neck resistance of less than two transverse fingers is not evidence of meningeal irritation; the neck resistance of this patient was approximately three transverse fingers, so the patient was presumed to be positive for meningeal irritation, highly suggestive of meningitis) and Kernig sign was positive. There were no significant abnormalities according to brain MRI and lumbar puncture pressure was 330 mmH2O. In addition, the leukocyte count was 734x106/l, 50% monocyte count, 50% multinucleated cells, chloride levels of 109.1 mmol/l, protein levels of 235 mg/dl and glucose levels of 4.18 mmol/l in the cerebrospinal fluid. DNA and RNA metagenomic detection of pathogenic microorganisms in the cerebrospinal fluid revealed the presence of VZV. The patient was therefore treated with acyclovir, ceftriaxone, mannitol and methylprednisolone, but then developed right peripheral facial palsy at 10 days after treatment. This complication was not found in the literature, and the occurrence of facial neuritis was unexpected. The active period of VZV virus was 21 days, and the patient had herpes 5 days before admission. The active period of the virus was considered to have subsided and the patient was in the recovery period. Moreover, the results of lumbar puncture showed that the white blood cells, the proportion of neutrophils and the protein in cerebrospinal fluid were all decreasing, which also indicated that the patient had entered the recovery period. The patient was discharged 18 days after admission. In conclusion, observations from the present case suggested that the clinical manifestations of VZV infection can be complex and varied, requiring the clinician to have an accurate understanding of its disease progression and treatment. [ABSTRACT FROM AUTHOR]

Background Astragalus membranaceus has been clinically used in cerebral ischemia treatment in China and its main component, Astragaloside IV (Ast IV) shows anti-hypoxia activity, but the underlying mechanism has not been clearly clarified. This study was aimed to investigate the effects of Ast IV on hypoxia-induced injury in PC-12 cells as well as the underlying mechanism. Methods Relative miR-124 expression was detected by qRT-PCR. Hic-5 expression was analyzed by qRT-PCR and Western blot. To alter miR-124 and Hic-5 expressions, cells were respectively transfected with miR-124 mimic and pEX-Hic-5. Cell proliferation and apoptosis were measured by BrdU assay and Annexin V-fluorescein isothiocynate (FITC)/propidium iodide (PI) double staining method, respectively. Besides, apoptotic proteins and cell proliferation-associated factors were analyzed by Western blot. Results Ast IV alleviated hypoxia-induced injury in PC-12 cells by decreasing apoptosis ( P  <  0.01). Ast IV inhibited up-regulation of miR-124 induced by hypoxia ( P  <  0.01). miR-124 mimic impaired the anti-apoptotic effect of Ast IV on PC-12 cells ( P  <  0.01). Hic-5 expression was significantly down-regulated in miR-124 overexpressed cells ( P  <  0.001) and Hic-5 overexpression activated Sp1/Survivin signaling pathway ( P  <  0.001). Conclusion Ast IV could ameliorate hypoxia-induced injury in PC-12 cells by decreasing miR-124 expression and then up-regulating Hic-5 expression. [ABSTRACT FROM AUTHOR]