Objective To determine the incidence of bacterial infection in neonates due to group B streptococcus(GBS) in our hospital. Methods The specimens were collected from 141 neonatal infants with infectious symptoms and maternal risk factors. 93 blood and 6 CSF samples were performed bacterial culture.141 blood sera, 65 urine and 6 CSF samples were tested for GBS antigen by countercurrent immunoelectrophoresis(CIE). Results In 141 neonatal infants, 27 cases were found GBS polysaccharide antigen positive(19.1%). Blood and CSF culture were positive only in 1 case. In 27 cases , there were 2 cases with meningitis, 6 cases with sepsis, 12 cases with infectious pneumonia , 2 cases with omphalitis, and 5 cases were only premature babies .There were 20 cases of early onset disease and 7 cases of late onset disease. There was one case that the same serotype(III/R) and DNA genes of GBS were found in the blood and CSF cultures of baby and his mother's vaginal swab culture . The antibacterial activity was found in the urine specimens of 32/34 cases in the first day on admission by micrococcus inhibition test, only 2 cases were negative. All patients were treated with Penicillin and Ampicillin. Conclusions (1)GBS is one of the pathogens in neonatal infection.(2)CIE method for identification of GBS polysaccharide antigen is sensitive and specific.(3)Penicillin was the first choice for neonatal GBS infection.

Objective To establish the cell model of intractable epilepsy and to observe its neuronal damage and morphologic change of neurites.Methods The model was established by exposing hippocampal neurons to Mg2+ -free media for 3 hours on days 10 of culture.Expression of lactic acid dehydrogenase (LDH) in supernatant was measured as an index of neuronal damage.The morphologic change of neurons and neurites was observed by optical microscope and scanning electron microscope (SEM).Results Compared to the control group, level of LDH (U/L) was significantly increased in the model group at different time points (3 hours: 4.26 ± 1.28, 6 hours: 6.56 ±2.34 and 24 hours: 16.67 ±3.57, P <0.05).With time prolonging, release of LDH in the model group was gradually increased (F = 39.316,P <0.05).Under optical microscope, neurons of model group migrated closely to each other and neurite connections appeared to be gradually "reticulated" after Mg2+ -free media treatment for 24 hours; and the "reticulated" neurites connections become more obvious after 72 hours.Under SEM, neuronal membrane was rough and had several small depressions, neurites were interlaced in cluster.Conclusions Neuronal damage and morphologic change of neurites are verified in the cell model of intractable epilepsy.

Objective:To explore the effect of rapamycin on 1-methyl-4-phenylpyridinium iodide (MPP+ )-induced activation of Nod-like receptor protein 3 (NLRP3) inflammasome in microglia.Methods:The BV2 microglia cells were divided into control group, model group and rapamycin group.The model group and rapamycin group were treated by MPP+ to activate NLRP3 inflammasome, and rapamycin group was pretreated with rapamycin.Quantitative real-time PCR (RT-qPCR) was used to detect the mRNA levels of NLRP3, apoptosis-associated speck-like protein (ASC) and caspase-1.Immunofluorescence was used to detect the protein expression of NLRP3 and interleukin-1β (IL-1β). Western blot was carried out to assess the protein expression of NLRP3, ASC, caspase-1, beclin1 and microtubule-associated protein 1 light chain 3 (LC3).Results:The mRNA levels of NLRP3, ASC and caspase-1 in model group were higher than those in control group ( t=4.825, 3.015, 5.853, all P<0.05). The mRNA levels of NLRP3 and caspase-1 in rapamycin group were lower than those in model group ( t=2.75, 2.89, both P<0.05). In model group, the protein expressions of NLRP3 (1.54±0.22), ASC (1.02±0.13) and caspase-1 (1.42±0.30) were higher than NLRP3 (0.66±0.15), ASC (0.41±0.14) and caspase-1 (0.70±0.10) in control group ( t=5.653, 5.602, 3.964, all P<0.01), while the protein expression of beclin1 (0.28±0.09) and LC3II/LC3I ratio(0.69±0.14) were lower than beclin1 (0.60±0.11) and LC3II/LC3I (1.29±0.23) in control group ( t=4.010, 3.982, both P<0.01). The protein expressions of NLRP3 (0.80±0.18) and ASC (0.68±0.14) in rapamycin group were lower than those in model group ( t=4.413, 3.077, both P<0.05), while the protein expression of beclin1 (0.65±0.20) and LC3II/LC3I ratio(1.42±0.36) were higher than those in model group ( t=2.965, 3.278, both P<0.05). Conclusion:MPP+ activates NLRP3 inflammasome and impairs autophagic function in microglia.Rapamycin inhibits MPP+ -induced activation of NLRP3 inflammasome by restoring autophagic impairment in microglia.

Humans ; Consensus ; Pancreatic Neoplasms/therapy* ; Neuroendocrine Tumors/therapy*