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Objective:To summarize the best evidence of intracranial hypertension nursing for adult patients with severe brain injury, and to provide reference for clinical nursing practice.Methods:According to the evidence-based methodology, a systematic search of Chinese and English literature on intracranial hypertension nursing of adult patients with severe brain injury was conducted in domestic and foreign databases such as CNKI, Wanfang, PubMed, Cochrane Library and Cinahl Plus and so on, as well as related guide websites and professional association websites from the establishment of database to August 2022. Two researchers independently evaluated literature quality and screened evidence, and then the project team summarized and concluded the evidence.Results:A total of 6 009 articles were obtained through preliminary search, and 33 articles were included after screening, including 13 guidelines, 1 systematic review, 17 expert consensus, 1 evidence summary, and 1 meta-analysis. In total, 33 pieces of best evidence were obtained from 8 dimensions, including intracranial pressure related threshold, assessment and monitoring, respiratory care, circulation care, analgesic and sedative care, temperature care, nutrition care and cerebrospinal fluid care.Conclusions:This study summarizes the evidence-based basis of intracranial hypertension nursing in adult patients with severe brain injury, which provides a basis for the standardized construction of clinical nursing strategies and empirical research.
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Oxidative stress is the key determinant in the pathogenesis of noise-induced hearing loss (NIHL). Given that cellular defense against oxidative stress is an energy-consuming process, the aim of the present study was to investigate whether increasing energy availability by glucose supplementation protects cochlear hair cells against oxidative stress and attenuates NIHL. Our results revealed that glucose supplementation reduced the noise-induced formation of reactive oxygen species (ROS) and consequently attenuated noise-induced loss of outer hair cells, inner hair cell synaptic ribbons, and NIHL in CBA/J mice. In cochlear explants, glucose supplementation increased the levels of ATP and NADPH, as well as attenuating H
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Objective To investigate the effects of long non-coding RNA (SNHG1) on the autophagy and growth of human neuroblastoma cell line SH-SY5Y and their specific mechanism using a cell model of Parkinson's disease.Methods (1) After SH-SY5Y cells were cultured in vitro,the expression levels of autophagy-related proteins LC3-Ⅱ/LC3-Ⅰ and p62 were detected by Western Blotting at different time points and subjected to treatment with different dosages of 1-methyl-4-phenyl-pyridine (MPP+).The survival rate of SH-SY5Y was detected by MTT assay.(2) The expression of SNHG1 was detected by real-time quantitative PCR after SH-SY5Y treated with different concentrations of MPP+ for different time durations.(3) The expression of endogenous SNHG1 in SHSY5Y was down-regulated by specific siRNA;the expression levels ofautophagy-related proteins LC3-Ⅱ/LC3-Ⅰ and p62 were detected by Western Blotting after MPP+ treatment while the survival rate of SH-SY5Y was detected by MTT.Moreover,SH-SY5Y cells were treated with autophagy late inhibitor bafilomycin A1 (BafA1) and autophagy inducer to further clarify the role of SNHG1.(4) The expression of p27 was detected by Western blotting after treated with different concentrations of MPP+ for different time durations.In addition,after the expression of SNHG1 in SHSY5Y was down-regulated,the expression of p27 was detected by Western blotting.Results (1) The expression of LC3-Ⅱ in SH-SY5Y was significantly increased in a dose-and time-dependent manner and the expression of p62 was significantly decreased (P＜0.05).MTT results showed that MPP+ (2.5 mmol/L) significantly reduced the survival rate of SH-SY5Y (P＜0.05).(2) Compared with the control group,the expression of SNHG1 was significantly increased in SH-SY5Y cells treated with MPP+ in a dose-and time-dependent manner (P＜0.5).(3) When SNHG1 down-regulated,the expression of LC3-Ⅱ induced by MPP+ was inhibited while the expression of p62 increased (P＜0.05).In addition,when treated with Baf A 1 at the same time,the expression of LC3-Ⅱ was increased,suggesting that SNHG1 might mainly affect the autophagosome formation of SH-SY5Y.The survival rate of SH-SY5Y cells was significantly increased after SNHG1 was down-regulated,and the cell viability was further inhibited by SH-SY5Y treated with rapamycin,suggesting that SNHG1 inhibited the growth of SH-SY5Y cells through promoting the autophagy formation.(4) The expression of p27 was significantly increased in SH-SY5Y cells treated with MPP+ in a dose-and time-dependent manner (P＜0.05).Down-regulation of SNHG1 expression inhibited the expression of p27,suggesting that SNHG1 might promote the autophagy and growth of SH-SY5Y cells through the p27 signal pathway.Conclusions SNHG1 can induce the autophagy of SH-SY5Y cells and promote death of the cells,which may be related to the regulation of p27 expression.
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Objective To investigate the displacement characteristics of intraoperative and postoperative positions of electrodes on CT imaging for bilateral subthalamic nucleus-deep brain stimulation (STN-DBS) in Parkinson's disease (PD).Methods A retrospective analysis on preoperative MR imaging,intraoperative and postoperative CT images of 35 patients with PD treated with STN-DBS in our hospital from January 2014 to June 2018 was performed.A three-dimensional coordinate system was established based on preoperative MR imaging.MR imaging/CT fusion technique was used to fuse intraoperative and postoperative CT images with preoperative MR imaging to locate intraoperative and postoperative electrode positions.The displacement characteristics of intraoperative and postoperative electrodes were analyzed.Results The spatial distance between intraoperative and postoperative positions of bilateral electrodes was about 1 mm,and the depth displacement was minimal.The postoperative position of the first side electrode on lateral axis was shifted outwardly from intraopemtive position,and the second side electrode was shifted internally with a small degree;on anterior-posterior axis,the first side electrode obviously shifted backward,and the second side electrode slightly shifted backward.For bilateral electrodes,corresponding coordinate deviation of three axis between intraoperative electrode-preoperative target and postoperative electrode-preoperative target,showed a significant positive linear correlation,therefore,leading out the coordinate deviation regression function model.Conclusions The displacement of electrodes between intraoperative and postoperative positions has obvious rules after STN-DBS in PD,which can guide the adjustment of intraoperative electrode position and predict the postoperative position of electrode.
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Objective To investigate the role of long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEA T1) in regulating the activation of microglias.Methods (1) Microglias BV2 were routinely cultured in vitro and NEA T1 mRNA expression was detected by real-time PCR (RT-PCR) after 0,0.1,0.5 and 1 μg/mL lipopolysaccharide (LPS) stimulation for 6 h;NEAT1 mRNA expression was detected by RT-PCR after 1 μg/mL LPS stimulation for 0,6,12 and 24 h.(2) NEAT1 siRNA (NEA T1-si) was transfected into BV2,and RT-PCR and Western blotting were employed to detect the LC3 mRNA and protein expressions.(3) The BV2 cells were divided into control group,NEAT1-si group,LPS group and NEAT1-si+LPS group;RT-PCR was used to detect the tumor necrosis factor-α (TNF-oα) and inducible nitric oxide synthase (iNOS) mRNA expressions;morphological changes of BV2 cells were observed under inverted microscope.(4) The BV2 cells were divided into control group,negative control+Torin-1 group and NEAT1-si+Torin-1 group;Western blotting was used to detect the LC3 protein expression and LC3,TNF-α and iNOS mRNA expressions were detected by RT-PCR.Results (1) NEA T1 was significantly up-regulated in LPS-stimulated BV2 cells in dose-and time-d ependent manners;significant differences were noted between each two groups (P＜0.05).(2) The LC3-Ⅱ mRNA expression in the NEAT1-si group was significantly decreased as compared with that in the control group (P＜0.05);LC3-Ⅱ/Ⅰ protein ratio (0.7) in the NEAT1-si group was significantly lower than that in the control group (1.03,P＜0.05).(3) As compared with those in the control group,the TNF-α and iNOS mRNA expressions in the NEAT1-si group were decreased;As compared with those in the LPS group,the TNF-oα and iNOS mRNA expressions in the NEA T1-si+LPS group were significantly decreased (P＜0.05).(4) LC3-Ⅱ/Ⅰ protein ratio in the control group,Torin-1 group and Torin-l+NEAT1-si group were 0.7,1.14 and 0.97,respectively;LC3-Ⅱ,TNF-α and iNOS mRNA expressions in the Torin-1 group were significantly higher than those in the control group (P＜0.05);LC3-Ⅱ,TNF-α and iNOS mRNA expressions in the NEAT1-si+Torin-1 group were significantly higher than those in the Torin-1 group (P＜0.05).Conclusion Knockdown of long noncoding RNA NEA T1 could attenuate microglia activation through inhibiting autophagy,and NEA T1 maybe the key molecule for the mitigation and cure of the neuroinflammation related diseases.
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OBJECTIVE To explore the expression of Bcl-2, on mRNA and protein levels, in the different age of C57BL/6 mice cochleae and the expression localization in the cochleae.METHODS Using ABR to test the hearing level in C57BL/6 mice. Surface preparation of cochlear basil membrane is used to observe the morphology and amout of the outer and inner hair cells in different age of C57BL/6 mice. Fluorescent quantitative real time PCR, immunofluorescence histochemical method and western blot are used to detect the expression of Bcl-2 on the mRNA and protein levels in the C57BL/6 mice cochlea of different age groups ('young group', 'elderly group').RESULTS ABR results showed that the hearing threshold of 'older' C57BL/6 mice is much higher than that in the 'young' mice, and surface preparation of cochlear basil membrane showed the hair cell localized in the cochlear basil turn of 'old' mice arranged in a disorder station and part of hair cells were lost. Also, the spiral ganglion cells arranged sparsely and messily. Fluorescence quantitative real-time PCR results suggest the expression of Bcl-2 on/at the mRNA level of the 'old' mice cochleae decreases significantly, compared to that in the 'young' mice. The results of Immunofluorescence and Western blot suggest the expression of Bcl-2 on/at the protein levels of the 'old' mice cochlea decreased, compared to that in the 'young' mice. Also, the Bcl-2 is located in the cytoplasm, and the expression of Bcl-2 in the inner hair cells seems higher than that in the outer hair cells. CONCLUSION The expression of Bcl-2 significantly deceased in the 'old' C57BL/6 mice cochleae, both on mRNA and protein level, which may be related to the hearing loss and loss of hair cells.
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OBJECTIVE To explore the role of miR-34a on upregulating the expression of Bcl-2,which induces the apoptosis of primary auditory cortex neuron in the central mechanism of age-related hearing loss.METHODS Using C57BL/6 suckling mouse to obtain the brain tissue from auditory cortex according to the Location map,and to primary culture the neurons.After transfection on primary neurons,western blot and immunofluorescence were used to detect the expression of Bcl-2 and then hoechst staining was used to detect the apoptosis after transfection.RESULTS primary culture of auditory cortex neurons abtained from enzyme digestion were transfected with miR-34a mimic and miR-34a inhibitor to upregualte or downregulate the expression of miR-34a,the results showed that the expression of Bcl-2 was decreased after upregulation of miR-34a with the concentration of 5 nmol/L(t=5.127,P＜0.05),there was significant difference between the concentration of 10 and 20 nmol/L(t=6.379,P＜0.05),while increased after downregulation of miR-34a with concentration of 5 nmol/L(t=4.926,P＜0.05),there was significant difference between the concentration of 10 and 20 nmol/L(t=5.821,P＜0.05).Hoechst staining showed that the apoptotic neurons was increased after transfection of miR-34a mimic.CONCLUSION miR-34a induce the auditory cortex neuron apoptosis through downregulates Bcl-2,which central mechanism of age-related hearing loss.
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Objective To investigate the role of micro RNA-124 (miR-124) in regulating activation of microglias and secretion of pro-inflammation cytokines and its potential mechanism.Methods (1) BV-2 cells were exposed to different concentration oflipopolysaccharide (LPS) for different durations;relative expression level of miR-124 was detected by real time-quantitative PCR (RT-qPCR).(2) The BV-2 cells were divided into four groups:PBS group,LPS group,LPS+ctrl-simulant group and LPS+miR-124 simulant group.Protein and mRNA expressions of inflammatory factors (tumor necrosis factor [TNF]-α and interleukin [IL] 1-β) were evaluated by RT-qPCR and ELISA.Expressions of p38α,phosphorylated (p)-p38α,ERK and p-ERK were detected by Western blotting.(3) Besides the above groups,four groups were added:LPS+VX702 group,LPS+miR-124 inhibitor group,LPS+VX702+miR-124 simulant group and LPS+VX702+miR-124 inhibitor group;pretreatment with p38α specific inhibitor VX702 was given to the BV-2 cells,the latter two groups were given miR-124 simulant or miR-124 inhibitor,and LPS was used to activate the cells;the expressions of TNF-α and IL-1β were evaluated by ELISA.Results (1) As compared with control group,miR-124 was significantly down-regulated in LPS-stimulated BV-2 cells (P＜0.05),in a dose-and time-dependent manner.(2) As compared with cells in the LPS+ctrl-simulant group,cells in the LPS+miR-124 simulant group had significantly decreased TNF-α and IL-lβ mRNA and protein expressions,and p38α and p-p38α levels (P＜0.05);the ERK and p-ERK levels showed no significant difference between the two groups (P＞0.05).(3) The TNF-α and IL-1β levels between LPS+VX702 group and LPS+VX702+miR-124 simulant group were not significantly different (P＞0.05);those between the LPS+VX702+miR-124 inhibitor group and the LPS+VX702 group were not significantly different (P＞0.05).Conclusion The miR-124 is down-regulated in LPS-activated BV-2 cells and miR-124 could suppress the secretion of pro-inflammatory mediators by targeting to p38α.