In vivo imaging of the neuronal response to spinal cord injury:a narrative review

Deciphering the neuronal response to injury in the spinal cord is essential for exploring treatment strategies for spinal cord injury(SCI).However,this subject has been neglected in part because appropriate tools are lacking.Emerging in vivo imaging and labeling methods offer great potential for observing dynamic neural processes in the central nervous system in conditions of health and disease.This review first discusses in vivo imaging of the mouse spinal cord with a focus on the latest imaging techniques,and then analyzes the dynamic biological response of spinal cord sensory and motor neurons to SCI.We then summarize and compare the techniques behind these studies and clarify the advantages of in vivo imaging compared with traditional neuroscience examinations.Finally,we identify the challenges and possible solutions for spinal cord neuron imaging.

Evaluation of the long-term memory for thermosensation regulated by neuronal calcium sensor-1 in Caenorhabditis elegans

Objective To evaluate whether the thermotaxis tracking model is suitable for assessing long-term memory （LTM） in the nematode Caenorhabditis elegans. Methods Animals were trained at 20℃ overnight in presence of food. The percentage of animals performing isothermal tracking （IT） behavior was measured at different time intervals after the training. Results The percentage of animals performing IT behavior, the numbers of body bends inside and outside the training temperature, and the expression patterns of AFD and AIY neurons were similar to those in control animals at 36 and 48 h after training; whereas when extending to 60, 72, and 84 h, locomotory behavior defects were observed in the assayed animals, suggesting that this thermal tracking model is feasible for analyzing LTM at 36 and 48 h after training. Moreover, the percent-age of animals performing IT behavior was reduced at 18, 36, and 48 h after training in neuronal calcium sensor-1 gene （nsc-1） mutant animals compared with that in wild-type N2 animals. In addition, exposure to plumbum （Pb） significantly repressed the LTM at 18, 36, and 48 h after training in both wild-type N2 and ncs-1 mutant animals. Conclusion The thermotaxis tracking model is suitable for evaluating the LTM regulated by NCS-1, and can be employed for elucidating regulatory functions of specific genes or effects of stimuli on memory in C. elegans.

Potassium and calcium channels in different nerve cells act as therapeutic targets in neurological disorders

The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central nervous system, with sensory stimulation and excitation conduction functions. Astrocytes and microglia belong to the glial cell family, which is the main source of cytokines and represents the main defense system of the central nervous system. Nerve cells undergo neurotransmission or gliotransmission, which regulates neuronal activity via the ion channels, receptors, or transporters expressed on nerve cell membranes. Ion channels, composed of large transmembrane proteins, play crucial roles in maintaining nerve cell homeostasis. These channels are also important for control of the membrane potential and in the secretion of neurotransmitters. A variety of cellular functions and life activities, including functional regulation of the central nervous system, the generation and conduction of nerve excitation, the occurrence of receptor potential, heart pulsation, smooth muscle peristalsis, skeletal muscle contraction, and hormone secretion, are closely related to ion channels associated with passive transmembrane transport. Two types of ion channels in the central nervous system, potassium channels and calcium channels, are closely related to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and epilepsy. Accordingly, various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders. In this review, we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease, Alzheimer's disease, depression, epilepsy, autism, and rare disorders. We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders. We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions. Although a few novel ion-channelspecific modulators have been discovered, meaningful therapies have largely not yet been realized. The lack of target-specific drugs, their requirement to cross the blood–brain barrier, and their exact underlying mechanisms all need further attention. This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.

Regulation of specific abnormal calcium signals in the hippocampal CA1 and primary cortex M1 alleviates the progression of temporal lobe epilepsy

Temporal lobe epilepsy is a multifactorial neurological dysfunction syndrome that is refractory,resistant to antiepileptic drugs,and has a high recurrence rate.The pathogenesis of temporal lobe epilepsy is complex and is not fully understood.Intracellular calcium dynamics have been implicated in temporal lobe epilepsy.However,the effect of fluctuating calcium activity in CA1 pyramidal neurons on temporal lobe epilepsy is unknown,and no longitudinal studies have investigated calcium activity in pyramidal neurons in the hippocampal CA1 and primary motor cortex M1 of freely moving mice.In this study,we used a multichannel fiber photometry system to continuously record calcium signals in CA1 and M1 during the temporal lobe epilepsy process.We found that calcium signals varied according to the grade of temporal lobe epilepsy episodes.In particular,cortical spreading depression,which has recently been frequently used to represent the continuously and substantially increased calcium signals,was found to correspond to complex and severe behavioral characteristics of temporal lobe epilepsy ranging from gradeⅡto gradeⅤ.However,vigorous calcium oscillations and highly synchronized calcium signals in CA1 and M1 were strongly related to convulsive motor seizures.Chemogenetic inhibition of pyramidal neurons in CA1 significantly attenuated the amplitudes of the calcium signals corresponding to gradeⅠepisodes.In addition,the latency of cortical spreading depression was prolonged,and the above-mentioned abnormal calcium signals in CA1 and M1 were also significantly reduced.Intriguingly,it was possible to rescue the altered intracellular calcium dynamics.Via simultaneous analysis of calcium signals and epileptic behaviors,we found that the progression of temporal lobe epilepsy was alleviated when specific calcium signals were reduced,and that the end-point behaviors of temporal lobe epilepsy were improved.Our results indicate that the calcium dynamic between CA1 and M1 may reflect specific epileptic behaviors corresponding to different grades.Furthermore,the selective regulation of abnormal calcium signals in CA1 pyramidal neurons appears to effectively alleviate temporal lobe epilepsy,thereby providing a potential molecular mechanism for a new temporal lobe epilepsy diagnosis and treatment strategy.

Regulating Neuronal Hyper-Excitability and Hyper-Synchrony in Epileptic Patients by Using PUFA, Calcium and ATP Buffering

Epilepsy is a severe neurological disorder clinically identified by hyper-excitability and/or hyper-synchrony in the cortex and other subcortical regions of the brain. To regulate such excitability and synchrony, Hodgkin and Huxley model has been deployed with either PUFA or calcium buffering coupled with ATP modulate neurotransmitter release. We formulate and analyze a system of differential equations that describe the effects of PUFA, ATP, and calcium buffering in regulating neuronal hyper-excitability and hyper-synchrony in epileptic patients. We observed that PUFA had diverse effects on the gating variables. Specifically, there was a significant reduction in the inhibitory potency of PUFA on the m-gates which may cause a direct inhibition of the voltage-gated Na＋ channels and thus reduce neuronal excitability in epileptic patients. Also, the activation of the potassium channels by PUFA directly limited the neuronal hyper-excitability, while a small change in voltage potential coupled with PUFA restraint activated the voltage dependent ion channels which aided in lowering epileptic excitability in patients. In addition, higher ATP buffer levels in the presence of PUFA caused a significant hyperpolarization which may decrease neuronal excitability while lower ATP level initiated neuron depolarization. These results clearly suggest that PUFA coupled with calcium and ATP buffering could be used to modulate neuronal excitability excessive synchrony in epileptic patients.

Effects of Rhynchophylline on L type Calcium Channels in Isolated Rat Cortical Neurons During Acute Hypoxia

Aim: To study the effects of rhynchophylline (Rhy) on the L type calcium channels in freshly dissociated cortical neurons of Wistar rats during acute hypoxia. Methods: Cell attached configuration of patch clamp technique. L type calcium channel was activated by stepping from 40 mV to 0 mV. Results: The results showed that the L type calcium channels of cortical neurons were activated by acute hypoxia. The mean open time of the channel was increased, the mean close time decreased and the open state probability raised during acute hypoxia. Rhy (15 and 30μmol·L -1 ) in concentration dependent manner blocked activity of the channels. The drug shortened the mean open time of the channels from 8 87 ms to 3 03 ms and 2 23 ms ( P 【0 001), prolonged the mean close time from 9 23 ms to 38 84 ms and 54 43 ms ( P 【0 001), and decreased the open state probability from 0 142 to 0 031 and 0 025 ( P 【0 001) under the hypoxia condition, respectively. The effects of Rhy were similar to but weaker than those of verapamil (15 μmol·L -1 ). Conclusion: The study confirmed that Rhy has the blockade effects on L type calcium channels in cortical neurons of rats during hypoxia, by which it protects the brain from hypoxic injury.

Real-time Microwave Exposure Induces Calcium Efflux in Primary Hippocampal Neurons and Primary Cardiomyocytes

Objective To detect the effects of microwave on calcium levels in primary hippocampal neurons and primary cardiomyocytes by the real-time microwave exposure combined with laser scanning confocal microscopy. Methods The primary hippocampal neurons and primary cardiomyocytes were cultured and labeled with probes, including Fluo-4 AM, Mag-Fluo-AM, and Rhod-2, to reflect the levels of whole calcium [Ca], endoplasmic reticulum calcium [Ca]ER, and mitochondrial calcium [Ca]MIT, respectively. Then, the cells were exposed to a pulsed microwave of 2.856 GHz with specific absorption rate(SAR) values of 0, 4, and 40 W/kg for 6 min to observe the changes in calcium levels. Results The results showed that the 4 and 40 W/kg microwave radiation caused a significant decrease in the levels of [Ca], [Ca]ER, and [Ca]MIT in primary hippocampal neurons. In the primary cardiomyocytes, only the 40 W/kg microwave radiation caused the decrease in the levels of [Ca], [Ca]ER, and [Ca]MIT. Primary hippocampal neurons were more sensitive to microwave exposure than primary cardiomyocytes. The mitochondria were more sensitive to microwave exposure than the endoplasmic reticulum. Conclusion The calcium efflux was occurred during microwave exposure in primary hippocampal neurons and primary cardiomyocytes. Additionally, neurons and mitochondria were sensitive cells and organelle respectively.

Role of axon resealing in retrograde neuronal death and regeneration after spinal cord injury

Spinal cord injury leads to persistent behavioral deficits because mammalian central nervous system axons fail to regenerate. A neuron's response to axon injury results from a complex interplay of neuron-intrinsic and environmental factors. The contribution of axotomy to the death of neurons in spinal cord injury is controversial because very remote axotomy is unlikely to result in neuronal death, whereas death of neurons near an injury may reflect environmental factors such as ischemia and inflammation. In lampreys, axotomy due to spinal cord injury results in delayed apoptosis of spinal-projecting neurons in the brain, beyond the extent of these environmental factors. This retrograde apoptosis correlates with delayed resealing of the axon, and can be reversed by inducing rapid membrane resealing with polyethylene glycol. Studies in mammals also suggest that polyethylene glycol may be neuroprotective, although the mechanism(s) remain unclear. This review examines the early, mechanical, responses to axon injury in both mammals and lampreys, and the potential of polyethylene glycol to reduce injury-induced pathology. Identifying the mechanisms underlying a neuron's response to axotomy will potentially reveal new therapeutic targets to enhance regeneration and functional recovery in humans with spinal cord injury.

Recombinant AAV-mediated Expression of Human BDNF Protects Neurons against Cell Apoptosis in Aβ-induced Neuronal Damage Model

The human brain-derived neurotrophic factor (hBDNF) gene was cloned by polymerase chain reaction and the recombinant adeno-associated viral vector inserted with hBDNF gene (AAV-hBDNF) was constructed. Cultured rat hippocampal neurons were treated with Aβ25-35 and se- rued as the experimental Aβ-induced neuronal damage model (AD model), and the AD model was infected with AAV-hBDNF to explore neuroprotective effects of expression of BDNF. Cell viability was assayed by MTT. The expression of bcl-2 anti-apoptosis protein was detected by immunocyto- chemical staining. The change of intracellular free Ca ion ([Ca2+]i) was measured by laser scanning confocal microscopy. The results showed that BDNF had protective effects against Aβ-induced neu- ronal damage. The expression of the bcl-2 anti-apoptosis protein was raised significantly and the bal- ance of [Ca2+]i was maintained in the AAV-hBDNF treatment group as compared with AD model group. These data suggested that recombinant AAV mediated a stable expression of hBDNF in cul- tured hippocampal neurons and resulted in significant neuron protective effects in AD model. The BDNF may reduce neuron apoptosis through increasing the expression of the bcl-2 anti-apoptosis protein and inhibiting intracellular calcium overload. The viral vector-mediated gene expression of BDNF may pave the way of a novel therapeutic strategy for the treatment of neurodegenerative dis- eases such as Alzheimer’s disease.

Mechanism of human amylin upregulation intracellular calcium on rat primary cultured hippocampus neurons

Alzheimer disease(AD) and typeⅡdiabetes mellitus(DM2) are the most common disease in aging people,with β-amyloid and amylin accumulation respectively.Studies have shown more and more correlations between these two diseases,and amylin oligomerization in the brain provided a novel risk target for developing AD.Although cumulative studies reported that amylin aggregation induced cytotoxicity in pancreatic beta cells by altering Ca2+homeostasis,fewer studies investigated the effect of amylin on hippocampal neuron.To address this question,it was investigated the effect of amylin on primary cultured rat hippocampal neurons by calcium imaging and whole-cell patch clamp recording in this study,while the results revealed that human amylin(hAmylin) but not rat amylin or pramlintide(hAmylin analgue) produced a rapid increase in intracellular calcium in a dose dependent manner.This effect relied on extracellular calcium and not abolished by amylin receptor antagonist AC187.Additionally,the calcium increase induced by hAmylin was dependent onvoltage-gated Ca2+channels,especially L-type Ca2+channel activation.In whole-cell recording hAmylin could depolarize membrane potential and increase the cell exitability.Moreover,application of transient receptor potential vanilloid(TRPV) antagonist ruthenium red could abolish part of the intracellular calcium increase.Single cell RT-PCR revealed that TRPV4 mRNA expressed in most of the reactive neuron and selective TRPV4 antagonist HC067047 inhibited the intacellular calcium increasing.These results indicated that hAmylin aggregation precipitating on the neuron membrane activated TRPV4 channels and then triggered membrane voltage gated calcium channel opening followed by membrane depolarization,expressing that TRPV4 is a key molecular target for the cytotoxic effect of hAmylin on cultured neurons.

INTRACELLULAR SOLITARY PULSE CALCIUM WAVES IN FROG SYMPATHETIC NEURONS

In certain extracellular environments, there would appear a kind of solitary pulse calcium waves in Rana pipiens sympathetic neurons, propagating inwards along the radial direction from the plasma membrane. To gain a deeper insight into the waves, a model describing intracellular calcium waves in frog sympathetic neurons was established. In the piecewise linear approximation, the present model is identical to the Sneyd model. Thus, with (Sneyd's) method, analytical expressions for the wave speed and profiles of 1-D solitary pulse wave were obtained. A wave speed of (21.5 μm/s) was deduced, which agrees rather well with experimental data.

Effect of Interleukin-1β on the Elevation of Cytoplasmic Free Calcium of the Cultured Hippocampal Neurons Induced by L-Glutamate

To investigate the intracellular mechanism that interleukin 1β (IL 1β) facilitates epileptic seizure and neuronal damage, the effect of IL 1β alone or IL 1β plus glutamate (Glu) on the intracellular free calcium ([Ca 2+ ] i) of single cultured hippocampal neuron was examined by using EPC 9 light electricity measurement system. The results showed that IL 1β of different concentrations (5×10 3 U/L, 10×10 3 U/L, 20×10 3 U/L, 30×10 3 U/L, 50×10 3 U/L, 100×10 3 U/L) failed to affect the neuronal [Ca 2+ ] i, but IL 1β could facilitate the augmentation of neuronal [Ca 2+ ] i induced by Glu in a dose dependent pattern. MK 801 inhibited the effect of Glu on [Ca 2+ ] i, and also inhibited the effect of IL 1β on [Ca 2+ ] i induced by Glu, while verapamil did not influence the effect of Glu or IL 1β. It is concluded that IL 1β, as a neuromodulator, can facilitate the activation of NMDA receptor by Glu, induce the increase of intracellular calcium, which enhances the excitement of neuron.

Homer1b/c通过内质网功能调节由谷氨酸兴奋性毒性损伤诱发的小鼠海马神经元HT22细胞自噬

目的研究Homer1b/c蛋白在谷氨酸兴奋性毒性损伤诱发的细胞自噬中的作用及机制。方法选用小鼠海马神经元HT22细胞,通过500μmol/L L-谷氨酸处理建立细胞损伤模型。用siRNA慢病毒转染方式下调Homer1b/c表达,用10μmol/L钙离子螯合剂BAPTA-AM、10 mmol/L内质网应激抑制剂4-PBA分别抑制细胞内钙离子释放和内质网应激后,使用蛋白质印迹法检测细胞中Homer1b/c蛋白,自噬效应蛋白[beclin-1、微管相关蛋白1轻链3(LC3)]及内质网应激标志蛋白[C/EBP同源蛋白(CHOP)、葡萄糖调节蛋白78(GRP 78)]的表达水平。结果L-谷氨酸处理HT22细胞12 h后,细胞中beclin-1表达和LC3-Ⅱ/LC3-Ⅰ比值均较对照组升高(均P<0.05);与转染对照组相比,下调Homer1b/c表达可降低细胞中beclin-1表达和LC3-Ⅱ/LC3-Ⅰ比值(均P<0.05);抑制细胞内钙离子释放和内质网应激均能降低细胞中beclin-1表达和LC3-Ⅱ/LC3-Ⅰ比值(均P<0.05);下调Homer1b/c表达后,抑制细胞内钙离子释放和内质网应激未能进一步降低细胞中beclin-1表达和LC3-Ⅱ/LC3-Ⅰ比值。结论Homer1b/c能够调节谷氨酸兴奋性毒性损伤诱发的细胞自噬,其调节作用可能与内质网功能有关。

L-Type Calcium Channel Modulates Low-Intensity Pulsed Ultrasound-Induced Excitation in Cultured Hippocampal Neurons

As a noninvasive technique,ultrasound stimulation is known to modulate neuronal activity both in vitro and in vivo.The latest explanation of this phenomenon is that the acoustic wave can activate the ion channels and further impact the electrophysiological properties of targeted neurons.However,the underlying mechanism of low-intensity pulsed ultrasound(LIPUS)-induced neuro-modulation effects is still unclear.Here,we characterize the excitatory effects of LIPUS on spontaneous activity and the intracellular Ca^(2+)homeostasis in cultured hippocampal neurons.By whole-cell patch clamp recording,we found that 15 min of 1-MHz LIPUS boosts the frequency of both spontaneous action potentials and spontaneous excitatory synaptic currents(sEPSCs)and also increases the amplitude of sEPSCs in hippocampal neurons.This phenomenon lasts for>10 min after LIPUS exposure.Together with Ca^(2+)imaging,we clarified that LIPUS increases the[Ca^(2+)]cyto level by facilitating L-type Ca^(2+)channels(LTCCs).In addition,due to the[Ca^(2+)]cyto elevation by LIPUS exposure,the Ca^(2+)-dependent CaMKII-CREB pathway can be activated within 30 min to further regulate the gene transcription and protein expression.Our work suggests that LIPUS regulates neuronal activity in a Ca^(2+)-dependent manner via LTCCs.This may also explain the multi-activation effects of LIPUS beyond neurons.LIPUS stimulation potentiates spontaneous neuronal activity by increasing Ca^(2+)influx.

小鼠中缝背核向屏状核投射神经通路的形态学特征

目的探索小鼠中缝背核(DRN)向屏状核(CLA)投射神经通路的形态学特征。方法分别将逆行示踪剂594 retrobeads和顺行示踪剂生物素化的葡聚糖胺(BDA)注入CLA(n=3)和DRN(n=3),结合5-羟色胺(5-HT)免疫荧光染色,观察逆行标记神经元的分布和神经化学特征以及顺标神经纤维和终末在全脑和CLA内的分布;利用钙离子/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)-Cre、谷氨酸脱羧酶67(GAD67)-Cre动物结合狂犬逆行跨突触病毒(RV)标记,观察DRN-CLA通路的下游靶神经元类型。结果DRN的吻、中、尾段均能观察到594 retrobeads阳性神经元的胞体,中段的腹侧亚核(DRV)分布较多,且90%以上的逆行标记神经元为5-HT阳性。BDA顺标纤维密集分布于腹侧被盖区、束旁核、腹侧苍白球、杏仁中央核等区,CLA内的神经纤维和终末相对稀疏。RV跨突触逆行标记结果显示,CaMKⅡ-Cre动物的DRN中含有较多的突触前神经元,而GAD67-Cre动物DRN中突触前逆行标记神经元较少。结论DRN-CLA通路是以DRV分布为主的5-HT能投射通路,其在CLA内的纤维和终末较为稀疏,主要与CLA内的CaMKⅡ阳性神经元形成突触联系。

新生儿缺氧缺血性脑病血清miR-124与miR-126的表达及临床意义

目的探讨新生儿缺氧缺血性脑病(HIE)血清微小核糖核酸(miR)-124、miR-126的表达及临床意义。方法选取2019-01—2023-02湘南学院附属医院收治的92例HIE患儿为HIE组,根据病情严重程度分为轻度组44例,中度组27例,重度组21例,另选取同期31名健康新生儿为对照组。采用Spearman相关性分析HIE患儿血清miR-124、miR-126表达与S100B、NSE水平的相关性,采用受试者工作特征(ROC)曲线分析血清miR-124、miR-126水平对新生儿HIE的诊断价值。结果与对照组比较,HIE组血清miR-124、miR-126表达降低,S100钙结合蛋白B(S100B)、神经元特异性烯醇化酶(NSE)水平升高(P<0.05)。轻度组、中度组、重度组血清miR-124、miR-126表达依次降低,S100B、NSE水平依次升高(P<0.05)。Spearman相关性分析显示,HIE患儿血清miR-124、miR-126表达与S100B、NSE水平呈负相关(rs=—0.757、—0.781、—0.800、—0.785,P<0.001)。ROC曲线分析显示,血清miR-124、miR-126表达单独和联合诊断新生儿HIE的曲线下面积分别为0.872、0.882、0.946。结论新生儿HIE血清miR-124、miR-126低表达,可能通过神经细胞损伤参与新生儿HIE过程,血清miR-124、miR-126表达联合诊断新生儿HIE的价值较高。

血清BDNF、NSE、S100β水平对癫痫患儿治疗效果的诊断价值

目的探讨血清脑源性神经营养因子(BDNF)、神经元特异性烯醇化酶(NSE)、星形细胞钙结合蛋白β(S100β)水平对癫痫患儿治疗效果的诊断价值。方法选取2020年1月至2022年12月徐州医科大学附属徐州市立医院收治的246例癫痫患儿作为研究对象,给予其抗癫痫药物治疗,且采用酶联免疫吸附试验检测治疗前血清BDNF、NSE及S100β水平。根据治疗效果将患儿分为有效组和无效组。对比2组一般资料及血清BDNF、NSE、S100β水平;采用Cox比例风险模型分析癫痫患儿药物治疗无效的影响因素;采用受试者工作特征(ROC)曲线分析血清BDNF、NSE、S100β水平对癫痫患儿药物治疗无效的诊断价值。结果246例接受药物治疗的癫痫患儿,治疗与随访期间有9例脱落,最终有237例患儿进行了数据分析。经过疗效评估,237例患儿中有43例治疗无效,余194例患儿治疗有效,药物治疗无效占比18.14%;无效组血清NSE、S100β水平均高于有效组,差异有统计学意义(P<0.05),血清BDNF水平低于有效组,差异有统计学意义(P<0.05);多因素Cox回归分析结果显示,病程、发作次数>10次、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、NSE、S100β水平均为癫痫患儿药物治疗无效的危险因素(P<0.05),超氧化物歧化酶(SOD)、BDNF水平是其保护因素(P<0.05);ROC曲线分析结果显示血清BDNF、NSE、S100β联合诊断癫痫患儿药物治疗无效的灵敏度和曲线下面积分别为93.02%、0.895,均高于单独诊断(P<0.05),特异度(80.41%)与单独诊断基本接近。结论药物治疗无效的癫痫患儿血清NSE、S100β水平高于治疗有效患儿,BDNF水平低于有效患儿,三者均与治疗效果密切相关,对治疗效果有一定的诊断效能,但三者联合可提高诊断效能。

血清Lp-PLA2、NSE、S-100β联合检测对一氧化碳中毒患者并发急性脑梗死的诊断及预后评估

目的探究血清脂蛋白磷脂酶A2(Lp-PLA2)、神经元特异性烯醇化酶(NSE)、可溶性蛋白100β(S-100β)联合检测对一氧化碳中毒(CMP)患者并发急性脑梗死(ACI)的诊断及预后评估。方法选取2020年1月至2021年11月该院收治的CMP并发ACI患者102例为研究组,同期选择单纯CMP患者102例为对照组。对研究组患者出院后进行6个月的随访,根据随访结果分为预后良好组(60例)和预后不良组(42例)。采用酶联免疫吸附试验(ELISA)检测血清Lp-PLA2、NSE、S-100β水平;采用受试者工作特征(ROC)曲线分析血清Lp-PLA2、NSE、S-100β联合对CMP并发ACI患者的早期诊断及预后评估价值。结果与对照组比较,研究组Lp-PLA2、NSE、S-100β水平升高(P<0.05)。ROC曲线分析结果显示,血清Lp-PLA2、NSE、S-100β联合诊断CMP并发ACI的曲线下面积(AUC)大于各指标单独诊断的AUC(P<0.001)。与预后良好组比较,预后不良组Lp-PLA2、NSE、S-100β水平升高(P<0.05)。ROC曲线分析结果显示,血清Lp-PLA2、NSE、S-100β联合对CMP并发ACI患者预后预测的AUC大于各指标单独检测的AUC(P<0.05)。结论CMP并发ACI患者血清中Lp-PLA2、NSE、S-100β呈高表达,3项指标联合检测对CMP并发ACI患者具有一定诊断及预后评估价值。

胸骨上段小切口行全弓置换术后神经功能障碍的围术期预警研究

目的探讨神经元特异性烯醇化酶(NSE)和S100钙结合蛋白β(S100β)对脑损伤严重程度的预警作用。方法选取2020年6月至2021年5月北部战区总医院收治的103例经胸骨上段小切口入路并使用中度/轻度低温停循环进行全主动脉弓置换的急性A型主动脉夹层患者,男性73例,女性30例,年龄(51.5±10.6)岁,年龄范围为32~74岁。根据不同的手术策略将患者分为浅低温组(n=50)和中度低温组(n=53)。围术期检测患者血清中NSE和S100β浓度,并根据是否出现神经功能障碍进行进一步分析以评估其诊断准确性。结果两组TND和PND发生率比较,差异无统计学意义(P>0.05)。两组患者术后24 h的NSE和S100β水平比较,差异无统计学意义(P>0.05)。NSE和S100β能够准确预测低温停循环术后神经功能障碍,尤其是在术前NSE(曲线下面积为0.879,截断值为5.6,P<0.05)和体外循环停机前的S100β水平(曲线下面积为0.816,截断值为2.3,P<0.05)具有最高的预测准确性。结论微创手术方法下浅低温及中度低温显示了相似的神经系统预后,术前NSE和体外循环停机前的S100β血清水平可能是预测围术期神经功能障碍的有力指标。

热射病器官损伤及预后判断的生物标志物研究进展

近年来,随着全球气候变暖,热射病的发病率在逐年增加。热射病是一种病死率很高的致死性疾病,通常需要紧急抢救,临床上早期识别及诊断对于热射病及其引起的器官功能损伤至关重要。本文就现有研究中可能作为识别热射病器官损伤及判断预后的生物标志物进行综述,以期能够对热射病的临床救治提供一定参考。