[Moxifloxacin treatment for Mycoplasma hominis meningitis in an extremely preterm infant]. / èŽ«è¥¿æ²™æ˜Ÿæ²»ç–—è¶ æ—©äº§å„¿äººåž‹æ”¯åŽŸä½“è„‘è†œç‚Ž1例.

The patient, a male newborn, was admitted to the hospital 2 hours after birth due to prematurity (gestational age 27+5 weeks) and respiratory distress occurring 2 hours postnatally. After admission, the infant developed fever and elevated C-reactive protein levels. On the fourth day after birth, metagenomic next-generation sequencing of cerebrospinal fluid indicated a positive result for Mycoplasma hominis (9 898 reads). On the eighth day, a retest of cerebrospinal fluid metagenomics confirmed Mycoplasma hominis (56 806 reads). The diagnosis of purulent meningitis caused by Mycoplasma hominis was established, and the antibiotic treatment was switched to moxifloxacin [5 mg/(kg·day)] administered intravenously for a total of 4 weeks. After treatment, the patient's cerebrospinal fluid tests returned to normal, and he was discharged as cured on the 76th day after birth. This article focuses on the diagnosis and treatment of neonatal Mycoplasma hominis purulent meningitis, introducing the multidisciplinary diagnosis and treatment of the condition in extremely preterm infants.

Effects of delayed HIF-1α expression in astrocytes on myelination following hypoxia-ischaemia white matter injury in immature rats.

BACKGROUND: The underlying cause of neurological sequelae after immature cerebral hypoxia-ischaemia (HI) white matter injury is impaired myelination. Previous studies have indicated that astrocyte activation is closely related to impaired myelination. However, the mechanism of reactive gliosis in white matter injury post-HI remains poorly understood. METHODS: Studies using adult ischaemic animal models demonstrated that hypoxia inducible factor-1α (HIF-1α) expression was involved in the formation of reactive astrocytes. Here, we investigated the temporal expression of HIF-1α and its impact on reactive gliosis and further myelination using a perinatal HI white matter injury model induced in rats at postnatal day 3. The temporal pattern of HIF-1α expression post-HI injury was tested by western blotting and immunofluorescence. Rats were treated with a HIF-1α inhibitor at 72 hours post-HI injury. Reactive gliosis and myelination were assessed with western blotting, immunofluorescence and electron microscopy, and neurological functions were examined by behavioural testing. RESULTS: Our results showed that the expression of HIF-1α was upregulated in neurons at 24 hours and in astrocytes at 7 days post-HI. Inhibiting delayed HIF-1α expression post-HI injury could restrain reactive gliosis, ameliorate hypomyelination, and improve the performance of rats in the Morris water maze test. CONCLUSIONS: Our findings suggest that a delayed increase in HIF-1α in astrocytes is involved in glial scar formation and leads to arrested oligodendrocyte maturation, impaired myelination, and long-term neurological function after experimental white matter injury in immature rats.

[Clinical features and magnetic resonance imaging evaluation of encephalopathy in high-risk late preterm infants].

OBJECTIVE: To investigate the risk factors, clinical features, and magnetic resonance imaging (MRI) changes of encephalopathy in high-risk late preterm infants. METHODS: Head MRI scan was performed for late preterm infants with high-risk factors for brain injury who were hospitalized between January 2009 and December 2014. The risk factors, clinical features, and head MRI features of encephalopathy in late preterm infants were analyzed. RESULTS: A total of 1 007 late preterm infants underwent MRI scan, among whom 313 (31.1%) had imaging features in accordance with the features of encephalopathy of prematurity. Of all infants, 76.7% had white matter damage. There was no association between the development of encephalopathy and gestational age in late preterm infants, but the detection rate of encephalopathy gradually increased with the increasing birth weight (P<0.05). The logistic regression analysis showed that a history of resuscitation was an independent risk factor for encephalopathy of prematurity (P<0.01). CONCLUSIONS: Encephalopathy of prematurity is commonly seen in high-risk late preterm infants, especially white matter damage. A history of resuscitation is an independent risk factor for encephalopathy in late preterm infants.

[Expression of phosphorylated NMDA receptor 1 in the cerebral cortex after NMDA microinjection in vivo].

OBJECTIVE: The activation of N-methyl-D-aspartate(NMDA) receptors plays critical roles in the pathogenesis of diseases of the brain. This study aimed to examine the expression of phosphor-NR1 S897 in the cerebral cortex after NMDA microinjection in vivo. METHODS: Forty seven-day-old Sprague-Dawley rats were randomly assigned into normal control and NMDA injection groups. The rats from the NMDA injection group were injected with 10 mmol of NMDA and were sacrificed 1 hr after injection. 2, 3, 5-triphenyltetrazolium chloride (TTC) and fluorescent immunohistochemical stainings were conducted and the fluorescence intensity OD value between the two groups was compared. RESULTS: TTC staining from the two groups was normal. Expression of phosphor-NR1 S897 in the cerebral cortex of the ipsilateral hemisphere to injection in the NMDA injection group decreased significantly compared with the normal control group, with OD values of 0.366 +/- 0.087 vs 1.364 +/- 0.268 (P < 0.01). CONCLUSIONS: NMDA microinjection, as a hypoxia-ischemia (HI) insult, significantly decreased the expression of phosphor-NR1 S897. This indicates the importance of the "HI-NMDA-phospho-NR1 S897 dephosphorylation-cell damage" pathway in HI brain damage.