艾灸对缺氧缺血性脑损伤新生小鼠的治疗作用*

目的: 探讨艾灸对缺氧缺血性脑损伤新生小鼠行为学表现、脑组织形态结构的影响及作用机制。方法: 将106只出生7 d小鼠随机分为三组:假手术组(23只)、模型组(46只)和艾灸组(37只)。采用左侧颈总动脉结扎后再置于37℃密闭舱内进行低氧处理(氧气浓度为8%,100 min),制备新生儿缺氧缺血性脑病动物模型。艾灸组同模型组,并于造模后2 h开始艾灸“大椎”进行治疗,以后每日1次,每次35 min,连续治疗4 d。采用行为学测试评价小鼠的行为学表现;HE染色观察小鼠脑组织形态结构;Western blot技术检测小鼠脑组织超氧化物歧化酶2(SOD2)蛋白表达;比色法测定小鼠脑组织丙二醛(MDA)含量。结果: 假手术组小鼠行为表现正常,脑组织细胞排列致密整齐,脑组织SOD2蛋白表达量和MDA含量正常。与假手术组相比,模型组小鼠翻正反射、趋地反射、悬崖躲避试验时间延长(P＜0.05),抓力试验时间缩短(P＜0.05);脑组织细胞大量坏死脱落;脑组织SOD2蛋白表达量明显减少(P＜0.05)、MDA含量增加。与模型组相比,艾灸组小鼠翻正反射、趋地反射、悬崖躲避试验时间缩短(P＜0.05),抓力试验时间增长(P＜0.05);脑组织细胞排列较致密、整齐;脑组织SOD2蛋白表达量增多(P＜0.05)、MDA含量降低(P＜0.05)。结论: 艾灸能减轻缺氧缺血性脑病新生小鼠脑损伤、改善行为学表现,这可能与其增加脑组织SOD2蛋白的表达、降低MDA含量,从而提高抗氧化应激能力有关。     

早产儿肠道菌群检测及其与脑损伤的关系CSCD

目的 对早产儿肠道菌群进行检测,并分析肠道菌群与早产儿脑损伤的关系。方法 选取2018年1月至2020年1月本院产科分娩的174例早产儿(胎龄≤34周)为研究对象,所有早产儿均于纠正胎龄40周时行颅脑MRI和早产儿肠道菌群检测,根据早产儿是否发生脑损伤,分为无脑损伤组(136例)和脑损伤组(38例)。分析无脑损伤早产儿和脑损伤早产儿的肠道菌群相对丰度、菌群物种丰富度(Chao1指数)及菌群群落多样性(Shannon指数)的差异,采用Pearson秩相关性法分析早产儿的肠道菌群相对丰度、Chao1指数、Shannon指数与脑损伤程度相关性。结果 脑损伤组早产儿的脑组织TMS评分(13.42分±1.03分)低于无脑损伤组(17.91分±1.81分),差异有统计学意义(t=19.724,P=0.000 1)。脑损伤组早产儿的双歧杆菌属丰度比(23.63%±1.24%)、乳杆菌属丰度比(16.58%±0.94%)、乳球菌属丰度比(15.73%±0.89%)和拟杆菌属丰度比(8.78%±0.64%)均低于无脑损伤组早产儿(28.43%±1.34%,22.43%±1.27%,17.81%±1.10%,9.81%±0.69%),差异均有统计学意义(t=27.163、16.871、20.764、26.917,均P<0.000 1),脑损伤组早产儿的链球菌属丰度比(13.92%±0.84%)、沙门菌属丰度比(5.74%±0.51%)、瓦氏菌属丰度比(4.86%±0.29%)、梭菌属丰度比(6.74%±0.54%)和葡萄球菌属丰度比(8.52%±0.60%)均高于无脑损伤组早产儿(5.81%±0.37%,4.28%±0.32%,3.94%±0.22%,2.18%±0.19%,1.98%±0.16%),差异均有统计学意义(t=34.261、22.914、19.084、24.807、27.043,均P<0.000 1)。脑损伤组早产儿的肠道菌群Chao1指数(281.55±17.71)和Shannon指数(2.74±0.32)均低于无脑损伤组早产儿(397.43±21.58,3.98±0.49),差异均有统计学意义(t=36.812、17.949,均P<0.000 1)。脑组织TMS评分与双歧杆菌属丰度比(r=-0.843)、乳杆菌属丰度比(r=-0.782)、乳球菌属丰度比(r=-0.815)、拟杆菌属丰度比(r=-0.708)、肠道菌群Chao1指数(r=-0.742)和肠道菌群Shannon指数(r=-0.743)呈负相关,与链球菌属丰度比(r=0.871)、沙门菌属丰度比(r=0.903)、瓦氏菌属丰度比(r=0.791)、梭菌属丰度比(r=0.782)和葡萄球菌属丰度比(r=0.793)呈正相关。结论 早产儿的脑损伤发生率仍然较高,与早产儿肠道菌群相对丰度、菌群物种丰富度和菌群群落多样性均有密切的相关性。     

Effect of IL-18 on intrauterine infection of HBV in mice on cell molecular level

ObjectiveThe objective of this study is to investigate the effect of IL-18 on intrauterine infection of HBV (Hepatitis B Virus) in mice based on cellular and molecular level, and to analyze its mechanism, as well as the relationship between IL-18 and intrauterine infection of HBV.MethodsPregnant rats are taken as the study subjects and divided into two groups according to infection and non-infection, namely the study group and the control group. Firstly, the peripheral blood of rats and the blood of newborn mice are collected for the determination of hepatitis B in two-and-a-half pairs. Then, the levels of interleukin-18 (IL-18), interferon-γ (IFN-γ) and interleukin-4 (IL-4) in peripheral serum are detected by ELISA (Enzyme Linked Immunosorbent Assay). Finally, the two groups of horizontal values are compared and analyzed. The effect of IL-18 on intrauterine infection of HBV in mice is investigated based on the level of cell and molecular.ResultsThe levels of IL-18, IFN-γ, IL-4 and IFN-γ/IL-4 in the two groups are compared and analyzed. The levels of IL-18, IFN-γ and IFN-γ/IL-4 in the study group are significantly lower than those in the control group, with statistical significance. However, the level of IL-4 in the study group is higher than that in the control group, with statistical significance.ConclusionIt is found that the decrease of HL-type specific response and the enhancement of Th2-type specific response in pregnant mice are closely related to HBV intrauterine infection. Moreover, the decrease of IL-18 secretion in peripheral blood may cause intrauterine infection of HBV. This study can make people better realize the mechanism of HBV intrauterine infection, and effectively help clinical prevention and treatment of intrauterine infection.     

胎盘Hofbauer细胞与HBV宫内感染

Hofbauer细胞起源于绒毛问质,是胎盘巨噬细胞,不仅能够吞噬入侵的病原微生物,参与母胎免疫反应;还可表达DC—SIGN、Fc等多种受体,这些受体分子可与乙肝病毒颗粒相互作用,使病毒通过跨膜转运进入细胞内。同时HofDauer细胞能够在母体间游走,当HBV感染Hofbauer细胞后,可借助HoPoauer细胞游走性介导HBV宫内感染。     

Therapeutic mechanism of intracranial infection in patients with hydrocephalus after craniocerebral injury based on decompressive craniectomy

The objective of this study is to analyze the treatment mechanism of decompressive craniectomy for intracranial infection in patients with hydrocephalus after craniocerebral injury, and to provide a treatment plan for intracranial infection in patients with hydrocephalus after craniocerebral injury. In this study, literature screening and data acquisition were carried out firstly based on the research content, and then heterogeneity analysis, Meta-analysis, sensitivity analysis, and publication bias analysis were performed using statistical methods for the unilateral and bilateral decompressive craniectomy. Heterogeneity analysis, Meta-analysis and sensitivity analysis of indiscriminate unilateral decompressive craniectomy was performed; heterogeneity analysis, Meta-analysis, cumulative Meta-analysis, and sensitivity analysis for bilateral decompressive craniectomy were performed. In this study, the order of influence on patients with hydrocephalus after brain injury was as follows: bilateral decompressive craniectomy > unilateral and bilateral decompressive decompression > indiscriminate unilateral decompressive. Intracranial infection in patients with hydrocephalus after the craniocerebral injury should be comprehensively evaluated before the surgery and given clinical treatment in time.     

Role of maternal viremia and placental infection in hepatitis B virus intrauterine transmission

The mechanism of intrauterine hepatitis B virus infection has not been established. In this study, venous blood, cord blood, and placental tissues from 171 chronic hepatitis B virus infected pregnant women were tested for hepatitis B surface antigen, hepatitis B core antigen, and hepatitis B virus DNA. We found that residence, mode of delivery, age, and number of gestational weeks of pregnant women were not correlated with intrauterine hepatitis B virus infection, while neonates of mothers who were hepatitis B s antigen positive and hepatitis B e antigen positive (P < 0.01) or who had high hepatitis B virus DNA levels (≥10⁶ copies/ml) were more likely to get an intrauterine infection (P < 0.01). The hepatitis B virus infection rate in placental cell layers gradiently decreased from the mother's side to the fetus's side of the placenta, but the odds ratio value of correlation between placental hepatitis B virus infection and intrauterine infection gradiently increased. The way of intrauterine hepatitis B virus infection may be through a layer–layer transmission pathway, although the possibility of placental leakage cannot be excluded.     

PARP-1 gene disruption in mice preferentially protects males from perinatal brain injury

Poly(ADP-ribose) polymerase-1 is over-activated in the adult brain in response to ischemia and contributes to neuronal death, but its role in perinatal brain injury remains uncertain. To address this issue, 7-day-old wild-type (wt) and PARP-1 gene deficient (parp+/- and parp-/-) Sv129/CD-1 hybrid mice were subjected to unilateral hypoxia-ischemia and histologic damage was assessed 10 days later by two evaluators. Poly(ADP-ribose) polymerase-1 knockout produced moderate but significant (p < 0.05) protection in the total group of animals, but analysis by sex revealed that males were strongly protected (p < 0.05) in contrast to females in which there was no significant effect. Separate experiments demonstrated that PARP-1 was activated over 1-24 h in both females and males after the insult in neonatal wt mice and rats using immnocytochemistry and western blotting for poly(ADP-ribose). Brain levels of NAD+ were also significantly reduced, but the decrease of NAD+ during the early post-hypoxia-ischemia (HI) phase was only seen in males. The results indicate that hypoxia-ischemia activates Poly(ADP-ribose) polymerase-1 in the neonatal brain and that the sex of the animal strongly influences its role in the pathogenesis of brain injury.     

银杏叶提取物对对乙酰氨基酚诱导的小鼠急性肝损伤的保护作用

目的：探究银杏叶提取物（GBE）对对乙酰氨基酚（APAP）诱导的小鼠急性肝损伤的保护作用及其机制。方法：30只小鼠随机分为对照组、模型组、GBE低、中、高剂量组（50,100,and 200 mg·kg^-1）,每组6只。除对照组外,剩余小鼠腹腔注射APAP （300 mg/kg）一次,随后GBE低、中、高剂量组按照相应剂量灌胃给药,治疗2 d后取材。观察各组肝脏大体情况和肝组织的病理组织学变化;取血测定各组小鼠血清中ALT、AST的活性和TNF-α、IL-6的水平;取肝检测各组肝组织中SOD、MPO的活性和GSH、MDA的含量;通过Western blot检测各组肝组织中Nrf2、HO-1蛋白的表达量。结果：与对照组相比,模型组肝脏明显肿大,病理表现差,血清中ALT、AST、TNF-α、IL-6的水平显著升高（P<0.01）,肝组织中GSH的含量和SOD的活性显著降低（P<0.01）,MDA的含量和MPO的活性显著升高（P<0.01）,Nrf2、HO-1蛋白表达明显下调（P<0.01）。与模型组相比,GBE组肝脏肿大减轻,病理表现有所改善,血清中ALT、AST、TNF-α、IL-6的水平显著降低（P<0.01）,肝组织中GSH的含量和SOD的活性显著提高（P<0.01）,MDA的含量和MPO的活性显著降低（P<0.01）,Nrf2、HO-1蛋白表达上调（P<0.05）,其中高剂量GBE组治疗效果最明显。结论：GBE可对APAP诱导的小鼠急性肝损伤具有保护作用,其作用机制可能是通过Nrf2/HO-1抗氧化途径发挥作用。     

Mitochondrial damage and dysfunction in traumatic brain injury

The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates, mitochondrial populations depending on injury severity, with the remaining population left to provide metabolic support for survival or repair in the wake of cellular pathology. With a considerable understanding of post-injury mitochondrial populations, therapeutic interventions targeted to the mitochondria may delay or prevent secondary cascades that lead to long-term cell death and neurobehavioral disability.     

无创辅助通气早产儿呼吸道感染病原菌分布 及影响因素分析

目的分析无创辅助通气早产儿呼吸道感染的病原菌及相关影响因素。方法选择2016年3月至2018年10月我院新生儿监护室收治的100例行无创辅助通气呼吸的早产儿为观察组。选择同期100例正常早产儿作为对照组。对两组患儿痰样本进行细菌鉴定,记录患儿基本情况并检测血中CD3~+、CD3~+/CD8~+、CD3~+/CD19~+和CD19~+/CD23~+水平。结果观察组患儿呼吸困难、发热、咳嗽、肺部喘鸣音及湿罗音发生率均高于对照组,差异有统计学意义(均P0.05)。观察组患儿血液中CD3~+、CD3~+/CD8~+水平明显低于对照组,CD3~+/CD19~+及CD19~+/CD23~+水平明显高于对照组,差异有统计学意义(均P0.05)。观察组患儿革兰阳性菌的感染率为17.00%,革兰阴性菌感染率为27.00%,其中金黄色葡萄球菌、大肠埃希菌和肺炎克雷伯菌的感染率占比相对较高。季节、通气时间、胎龄及出生体重是影响患儿呼吸道感染发生的独立性影响因素(P0.05)。结论无创辅助通气早产儿呼吸道感染病原菌以金黄色葡萄球菌、大肠埃希菌和肺炎克雷伯菌为主,季节、通气时间、胎龄及出生体重均是导致感染发生及发展的独立性影响因素。     

乳酸菌阴道胶囊辅助治疗对未足月胎膜早破的疗效及对其阴道微生态的影响

目的 观察乳酸菌阴道胶囊辅助治疗对未足月胎膜早破的治疗效果,并探讨其对阴道微生态的影响。 方法 86例未足月胎膜早破患者采用随机数表分为常规组与研究组,各43例。常规组予以常规治疗,研究组予以乳酸菌阴道胶囊联合常规治疗。比较治疗后两组阴道微生态、胎儿宫内感染率和分娩方式、母体和胎儿不良妊娠结局发生情况。 结果 治疗后研究组Chao1指数和Shannon指数均高于常规组(均P结论 乳酸菌阴道胶囊辅助治疗未足月胎膜早破相较于常规治疗可改善阴道微生态,还可降低胎儿宫内感染率、剖宫产率,减少母体和围产儿不良妊娠结局的发生。     

Metallothioneins I/II are involved in the neuroprotective effect of sildenafil in focal brain injury

We recently reported that administration of the non-selective cyclic GMP-phosphodiesterase (cGMP-PDE) inhibitor zaprinast to cortically cryoinjured rats results three days post-lesion in reduced neuronal cell death that was associated to decreased macrophage/microglial activation and oxidative stress and increased astrogliosis and angiogenesis. Similar effects have been observed in cryoinjured animals overexpressing metallothioneins I/II (MT-I/II), metal-binding cysteine-rich proteins that are up-regulated in response to injury. In this work we have examined the effect of administration of the selective PDE5 inhibitor sildenafil (10 mg/kg, sc) 2 h before and 24 and 48 h after induction of cortical cryolesion in wild-type and MT-I/II-deficient mice. Our results show that in wild-type animals sildenafil induces similar changes in glial reactivity, angiogenesis and antioxidant and antiapoptotic effects in the cryolesioned cortex as those observed in rats with zaprinast, indicating that inhibition of PDE5 is responsible for the neuroprotective actions. However, these effects were not observed in mice deficient in MT-I/II. We further show that sildenafil significantly increases MT-I/II protein levels in homogenates of lesioned cortex and MT-I/II immunostaining in glial cells around the lesion. Taken together these results indicate that cGMP-mediated pathways regulate expression of MT-I/II and support the involvement of these proteins in the neuroprotective effects of sildenafil in focal brain lesion.     

Intrinsic and extrinsic erythropoietin enhances neuroprotection against ischemia and reperfusion injury in vitro

This study was designed to investigate the neuroprotective effect of intrinsic and extrinsic erythropoietin (EPO) against hypoxia/ischemia, and determine the optimal time-window with respect to the EPO-induced neuroprotection. Experiments were conducted using primary mixed neuronal/astrocytic cultures and neuron-rich cultures. Hypoxia (2%) induces hypoxia-inducible factor-1alpha (HIF-1alpha) activity followed by strong EPO expression in mixed cultures and weak expression in neuron-rich cultures as documented by both western blot and RT-PCR. Immunoreactive EPO was strongly detected in astrocytes, whereas EPOR was only detected in neurons. Neurons were significantly damaged in neuron-rich cultures but were distinctly rescued in mixed cultures. Application of recombinant human EPO (rhEPO) (0.1 U/mL) within 6 h before or after hypoxia significantly increased neuronal survival compared with no rhEPO treatment. Application of rhEPO after onset of reoxygenation achieved the maximal neuronal protection against ischemia/reperfusion injury (6 h hypoxia followed 24 h reoxygenation). Our results indicate that HIF-1alpha induces EPO gene released by astrocytes and acts as an essential mediator of neuroprotection, prove the protective role of intrinsic astrocytic-neuronal signaling pathway in hypoxic/ischemic injury and demonstrate an optimal therapeutic time-window of extrinsic rhEPO in ischemia/reperfusion injury in vitro. The results point to the potential beneficial effects of HIF-1alpha and EPO for the possible treatment of stroke.     

Therapeutic inducers of the HSP70/HSP110 protect mice against traumatic brain injury

Traumatic brain injury (TBI) induces severe harm and disability in many accident victims and combat‐related activities. The heat‐shock proteins Hsp70/Hsp110 protect cells against death and ischemic damage. In this study, we used mice deficient in Hsp110 or Hsp70 to examine their potential requirement following TBI. Data indicate that loss of Hsp110 or Hsp70 increases brain injury and death of neurons. One of the mechanisms underlying the increased cell death observed in the absence of Hsp110 and Hsp70 following TBI is the increased expression of reactive oxygen species‐induced p53 target genes Pig1, Pig8, and Pig12. To examine whether drugs that increase the levels of Hsp70/Hsp110 can protect cells against TBI, we subjected mice to TBI and administered Celastrol or BGP‐15. In contrast to Hsp110‐ or Hsp70i‐deficient mice that were not protected following TBI and Celastrol treatment, there was a significant improvement of wild‐type mice following administration of these drugs during the first week following TBI. In addition, assessment of neurological injury shows significant improvement in contextual and cued fear conditioning tests and beam balance in wild‐type mice that were treated with Celastrol or BGP‐15 following TBI compared to TBI‐treated mice. These studies indicate a significant role of Hsp70/Hsp110 in neuronal survival following TBI and the beneficial effects of Hsp70/Hsp110 inducers toward reducing the pathological consequences of TBI.

     

不同浓度中药怀牛膝加黄芪煎液对重型颅脑损伤大鼠脑组织含水量及AQP4表达的影响

目的观察低、中、高不同浓度中药怀牛膝加黄芪煎液对重型颅脑损伤大鼠脑组织含水量及水通道蛋白4(AQP4)表达的影响,探讨其治疗重型脑损伤性脑水肿最佳用药浓度及机制。方法将SD大鼠65只随机分为假手术组(5只),模型组(15只),低浓度怀牛膝加黄芪组(A组)15只,中浓度怀牛膝加黄芪组(B组)15只,高浓度怀牛膝加黄芪组(C组)15只,采用改良后Feency’s方法建立大鼠重型颅脑损伤模型。分别在1、3、7天3个时间点每组各取5只大鼠测定脑组织含水量,HE染色观察脑组织变化情况,并采用免疫组化方法检测脑组织AQP4的表达。结果模型组大鼠重型颅脑损伤后各时间点脑组织含水量、损伤灶周围AQP4的表达均高于假手术组(P0.05),HE染色观察发现模型组的脑组织肿胀水肿明显;A、B组各时间点脑组织含水量、AQP4表达水平与模型组相比较无明显降低(P0.05),HE染色观察发现与模型组基本一致;C组各时间点脑组织含水量、AQP4表达水平均较模型组降低(P0.05),HE染色观察发现与模型组比较,脑组织水肿情况有所改善。结论 C组改善重型颅脑损伤后引起的脑水肿效果最明显,其作用机制可能与减少AQP4在损伤脑组织中的表达、减轻脑细胞损害有关。     

急性低氧暴露小鼠外周血代谢组变化分析

目的：探讨急性低氧对小鼠外周血代谢组的影响。方法：将14只小鼠随机分为正常组和低氧组。用基础饲料喂养2周后,将低氧组减压至6000m模拟高度停留8h,实验结束后,采集静脉血制备血浆待测。在核磁共振波谱仪进行^1H NMR检测,采用模式识别分析方法处理数据。结果：与正常组相比,低氧组乳酸含量明显增加,肉碱水平明显降低;脂类、丙氨酸、丙酮酸、谷氨酰胺、胆碱、牛磺酸和葡萄糖含量升高,缬氨酸、肛羟丁酸、谷氨酸、甘油、甘氨酸和丝氨酸含量下降。结论：急性低氧暴露使小鼠血浆碳水化合物、脂肪代谢和氨基酸代谢谱发生变化,表明低氧后能量代谢以及相关物质含量发生改变。     

体外循环心脏手术围术期脑损伤监测进展

脑损伤是体外循环心脏手术的严重并发症之一,目前患病人数在全球范围内呈逐年增高的趋势,并且临床上应用的脑保护措施效果并不确切,因此有效的神经系统监测关系到外科手术的成败和病人的预后。本文从术中脑组织氧供需平衡、栓子的监测、生化标志物和术后神经功能监测四个方面综述目前脑损伤监测的新进展。     

促红细胞生成素对脑损伤早产儿NBNA评分、肝肾功能以及脑干听觉诱发电位的影响

目的:探讨促红细胞生成素(EPO)对脑损伤早产儿新生儿神经行为测定(NBNA)评分、肝肾功能以及脑干听觉诱发电位的影响。方法:选取2015年2月~2018年7月期间我院收治的脑损伤早产儿117例,将上述研究对象根据随机数字表法将其分为对照组(n=58)和观察组(n=59),对照组患儿给予常规对症治疗,观察组在对照组的基础上联合EPO治疗,比较两组NBNA评分、肝肾功能以及脑干听觉诱发电位,记录两组患儿治疗期间并发症发生情况。结果:观察组纠正胎龄40周时NBNA评分高于对照组(P<0.05)。两组患儿治疗后峰间期(Ⅰ~Ⅲ波、Ⅲ~Ⅳ波、Ⅰ~Ⅳ波)、潜伏期(Ⅰ波、Ⅲ波、Ⅳ波)均较治疗前降低,且观察组低于对照组(P<0.05)。两组患儿治疗前、后尿素氮(BUN)、肌酐(Cr)、血清谷丙转氨酶(SGPT)、总胆红素(TBIL)比较差异均无统计学意义(P>0.05)。两组患儿动脉导管未闭、新生儿败血症发生率比较差异无统计学意义(P>0.05),而观察组支气管肺发育不良、颅内出血、脑干听觉诱发电位异常等发生率低于对照组(P<0.05)。结论:EPO对脑损伤早产儿具有一定的神经保护作用,能够有效保护受损神经细胞与听觉神经通路,降低脑损伤并发症的发生率,且不影响患儿的肝肾功能。     

Biomechanical analysis of fluid percussion model of brain injury

Fluid percussion injury (FPI) is a widely used experimental model for studying traumatic brain injury (TBI). However, little is known about how the brain mechanically responds to fluid impacts and how the mechanical pressures/strains of the brain correlate to subsequent brain damage for rodents during FPI. Hence, we developed a numerical approach to simulate FPI experiments on rats and characterize rat brain pressure/strain responses at a high resolution. A previous rat brain model was improved with a new hexahedral elements-based skull model and a new cerebrospinal fluid (CSF) layer. We validated the numerical model against experimentally measured pressures from FPI. Our results indicated that brain tissues under FPI experienced high pressures, which were slightly lower (10–20%) than input saline pressure. Interestingly, FPI was a mixed focus- and diffuse-type injury model with highest strains (12%) being concentrated in the ipsilateral cortex under the fluid-impact site and diffuse strains (5–10%) being spread to the entire brain, which was different from controlled cortical impact in which high strains decreased gradually away from the impact site.     

血清HBP和PTX3在重度脑损伤继发性肺部细菌性感染诊断中的应用价值

目的 探讨血清肝素结合蛋白（HBP）与正五聚蛋白3（PTX3）对重度脑损伤继发性肺部细菌性感染的诊断价值。方法 选择2015年3月至2019年1月我院重症医学科收治的重型颅脑损伤患者96例,对所有患者进行肺部感染情况判断,将出现继发性肺部细菌感染的患者纳入感染组,未出现继发性肺部细菌感染的患者纳入未感染组。分别检测两组患者入院后第1、3、5、7天的HBP、PTX3、白细胞（WBC）和C反应蛋白（CRP）水平,探讨其对于重度脑损伤患者继发肺部细菌感染的诊断价值,并对HBP、PTX3与WBC、CRP的相关性进行分析。结果 共有39例重度脑损患者纳入感染组,57例患者纳入未感染组,患者肺部细菌感染的发生率为40.6%。入院第1天感染组患者HBP、WBC及CRP水平明显高于未感染组,同时入院后第3、5、7天时感染组患者HBP、PTX3、WBC、CRP水平均显著高于未感染组,差异均具有统计学意义（均P<0.05）。单独采用HBP或PTX3对重度脑损伤继发性肺部细菌性感染进行诊断的约登指数为0.586和0.655,诊断的敏感性、特异性、阳性预测值、阴性预测值为74.3%、84.2%、76.3%、82.7%和79.5%、86.0%、79.5%、86.0%。联合检测的约登指数为0.776,诊断的敏感性、特异性、阳性预测值、阴性预测值为84.6%、93.4%、89.2%、89.8%。Spearman相关性分析显示HBP、PTX3水平与CRP水平均呈正线性相关（r=0.362、0.284,均P<0.05）。结论 HBP和PTX3均为重度脑损伤患者继发肺部细菌感染诊断的敏感指标,联合检测能够提高其检测价值,对重度脑损伤患者肺部感染的早期诊断具有一定临床意义。