目的探讨黑色素瘤缺乏因子2(absent in melanoma 2,AIM2)炎症小体介导的细胞焦亡在大鼠冷水浸泡性低体温致下丘脑损伤中的作用。方法将20只大鼠随机分为空白组(n=10)与模型组(n=10),模型组建立冷水浸泡性低体温大鼠模型,建模过程中监测...目的探讨黑色素瘤缺乏因子2(absent in melanoma 2,AIM2)炎症小体介导的细胞焦亡在大鼠冷水浸泡性低体温致下丘脑损伤中的作用。方法将20只大鼠随机分为空白组(n=10)与模型组(n=10),模型组建立冷水浸泡性低体温大鼠模型,建模过程中监测心率以评估下丘脑血供情况,应用HE染色、神经损伤评分、尼氏染色法评估下丘脑神经细胞损伤程度,Western blot、免疫荧光染色法测定下丘脑AIM2、凋亡相关斑点样蛋白(ASC)、半胱氨酸天冬氨酸蛋白酶-1(Caspase-1)、白细胞介素(IL)-1β、IL-18、焦孔素D(GSDMD)、S100钙结合蛋白β(S100β)和IL-6R等蛋白表达。结果模型组大鼠心率与核心体温变化趋势相符;模型组下丘脑神经损伤评分高于空白组(P<0.05),S100β表达高于空白组(P<0.05),脑组织病理损伤程度明显加重;与空白组比较,模型组下丘脑组织IL-1β、IL-18、IL-6R等炎症因子表达增加(P<0.05),AIM2、ASC、Caspase-1、GSDMD等焦亡相关蛋白表达增加(P<0.05)。结论冷水浸泡性低体温可诱导下丘脑损伤,该过程可能与AIM2介导的经典细胞焦亡途径有关。展开更多
Objectives:Sea sickness, a form of motion sickness, is a common condition among sailors on various sailing vessels, primarily due to their roll and pitch movements. While the exact neurobiological mechanisms remain un...Objectives:Sea sickness, a form of motion sickness, is a common condition among sailors on various sailing vessels, primarily due to their roll and pitch movements. While the exact neurobiological mechanisms remain unclear, the most widely accepted explanation is the sensory conflict theory,which identifies two main sources of conflict: discrepancies between visual and vestibular inputs and conflicts within the vestibular system itself.This study aims to evaluate otolith-mediated verticality perception in first-time seafarers on board a naval frigate ship using the Subjective Visual Vertical(SVV) test.Methods:This observational study was conducted on board a naval frigate and involved two groups. The case group consisted of50 newly recruited sailors experiencing their first sea voyage. The SVV test was conducted at three time points: prior to embarkation, during an active episode of sea sickness, and after disembarkation. A control group of 50 healthy, experienced sailors-regular seafarers with no history of vestibular symptoms underwent the same SVV testing at corresponding intervals. The results from both groups were collected and analyzed to assess changes in verticality perception related to sea exposure and sea sickness.Results:Analysis of the SVV test data from the 50 newly recruited sailors(case group) demonstrated a statistically significant difference compared to the control group of experienced sailors. During an active episode of sea sickness, the case group exhibited a notable tilt and deviation in SVV angles, indicating altered verticality perception. These deviations reduced significantly 24 hours post-disembarkation, suggesting an improvement in verticality perception once the motion stimulus was removed.Conclusion:This distinctive study assessed otolith-mediated verticality perception using the SVV test in first-time seafarers experiencing sea sickness aboard a naval frigate. Our findings emphasize the functional importance of the otolith organs in maintaining spatial orientation during maritime motion exposure. The observed SVV deviations support the subjective vertical conflict theory, highlighting the role of vestibular-visual mismatch in the development of sea sickness. However, our findings more likely reflect transient functional disturbance or overstimulation rather than a pre-existing utricular asymmetry alone. Based on the pattern of SVV deviation and recovery, we propose that the utricle may play a more significant role than the saccule in inducing sea sickness.展开更多
文摘目的探讨黑色素瘤缺乏因子2(absent in melanoma 2,AIM2)炎症小体介导的细胞焦亡在大鼠冷水浸泡性低体温致下丘脑损伤中的作用。方法将20只大鼠随机分为空白组(n=10)与模型组(n=10),模型组建立冷水浸泡性低体温大鼠模型,建模过程中监测心率以评估下丘脑血供情况,应用HE染色、神经损伤评分、尼氏染色法评估下丘脑神经细胞损伤程度,Western blot、免疫荧光染色法测定下丘脑AIM2、凋亡相关斑点样蛋白(ASC)、半胱氨酸天冬氨酸蛋白酶-1(Caspase-1)、白细胞介素(IL)-1β、IL-18、焦孔素D(GSDMD)、S100钙结合蛋白β(S100β)和IL-6R等蛋白表达。结果模型组大鼠心率与核心体温变化趋势相符;模型组下丘脑神经损伤评分高于空白组(P<0.05),S100β表达高于空白组(P<0.05),脑组织病理损伤程度明显加重;与空白组比较,模型组下丘脑组织IL-1β、IL-18、IL-6R等炎症因子表达增加(P<0.05),AIM2、ASC、Caspase-1、GSDMD等焦亡相关蛋白表达增加(P<0.05)。结论冷水浸泡性低体温可诱导下丘脑损伤,该过程可能与AIM2介导的经典细胞焦亡途径有关。
文摘Objectives:Sea sickness, a form of motion sickness, is a common condition among sailors on various sailing vessels, primarily due to their roll and pitch movements. While the exact neurobiological mechanisms remain unclear, the most widely accepted explanation is the sensory conflict theory,which identifies two main sources of conflict: discrepancies between visual and vestibular inputs and conflicts within the vestibular system itself.This study aims to evaluate otolith-mediated verticality perception in first-time seafarers on board a naval frigate ship using the Subjective Visual Vertical(SVV) test.Methods:This observational study was conducted on board a naval frigate and involved two groups. The case group consisted of50 newly recruited sailors experiencing their first sea voyage. The SVV test was conducted at three time points: prior to embarkation, during an active episode of sea sickness, and after disembarkation. A control group of 50 healthy, experienced sailors-regular seafarers with no history of vestibular symptoms underwent the same SVV testing at corresponding intervals. The results from both groups were collected and analyzed to assess changes in verticality perception related to sea exposure and sea sickness.Results:Analysis of the SVV test data from the 50 newly recruited sailors(case group) demonstrated a statistically significant difference compared to the control group of experienced sailors. During an active episode of sea sickness, the case group exhibited a notable tilt and deviation in SVV angles, indicating altered verticality perception. These deviations reduced significantly 24 hours post-disembarkation, suggesting an improvement in verticality perception once the motion stimulus was removed.Conclusion:This distinctive study assessed otolith-mediated verticality perception using the SVV test in first-time seafarers experiencing sea sickness aboard a naval frigate. Our findings emphasize the functional importance of the otolith organs in maintaining spatial orientation during maritime motion exposure. The observed SVV deviations support the subjective vertical conflict theory, highlighting the role of vestibular-visual mismatch in the development of sea sickness. However, our findings more likely reflect transient functional disturbance or overstimulation rather than a pre-existing utricular asymmetry alone. Based on the pattern of SVV deviation and recovery, we propose that the utricle may play a more significant role than the saccule in inducing sea sickness.
