Haipeng Xu, Kelin He, Rong Hu, Yanzhi Ge, Xinyun Li, F. Ni, Bei Que, Yi Chen, Ruijie Ma
Stroke is one of the leading causes of death and disability worldwide. Evidence shows that ischemic stroke (IS) accounts for nearly 80 percent of all strokes and that the etiology, risk factors, and prognosis of this disease differ by gender. Female patients may bear a greater burden than male patients. The immune system may play an important role in the pathophysiology of females with IS. Therefore, it is critical to investigate the key biomarkers and immune infiltration of female IS patients to develop effective treatment methods. Herein, we used weighted gene co-expression network analysis (WGCNA) to determine the key modules and core genes in female IS patients using the GSE22255, GSE37587, and GSE16561 datasets from the GEO database. Subsequently, we performed functional enrichment analysis and built a protein-protein interaction (PPI) network. Ten genes were selected as the true central genes for further investigation. After that, we explored the specific molecular and biological functions of these hub genes to gain a better understanding of the underlying pathogenesis of female IS patients. Moreover, the “Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)” was used to examine the distribution pattern of immune subtypes in female patients with IS and normal controls, revealing a new potential target for clinical treatment of the disease.
中风是全世界导致死亡和残疾的主要原因之一。有证据表明，缺血性中风(IS)占所有中风的近80%，其病因、危险因素和预后因性别而异。女性患者可能比男性患者承受更大的负担。免疫系统可能在IS女性的病理生理中发挥重要作用。因此，研究女性is患者的关键生物标志物和免疫浸润对制定有效的治疗方法至关重要。本文采用加权基因共表达网络分析(WGCNA)，利用GEO数据库中的GSE22255、GSE37587和GSE16561数据集，确定女性IS患者的关键模块和核心基因。随后，我们进行了功能富集分析，并建立了蛋白质-蛋白质相互作用(PPI)网络。选出10个基因作为真正的中心基因进行进一步研究。之后，我们探索了这些枢纽基因的特定分子和生物学功能，以更好地了解女性IS患者的潜在发病机制。此外，利用“Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)”检测女性IS患者和正常对照中免疫亚型的分布模式，揭示了临床治疗该疾病的新的潜在靶点。
{"title":"Identifying Key Biomarkers and Immune Infiltration in Female Patients with Ischemic Stroke Based on Weighted Gene Co-Expression Network Analysis","authors":"Haipeng Xu, Kelin He, Rong Hu, Yanzhi Ge, Xinyun Li, F. Ni, Bei Que, Yi Chen, Ruijie Ma","doi":"10.1155/2022/5379876","DOIUrl":"https://doi.org/10.1155/2022/5379876","url":null,"abstract":"Stroke is one of the leading causes of death and disability worldwide. Evidence shows that ischemic stroke (IS) accounts for nearly 80 percent of all strokes and that the etiology, risk factors, and prognosis of this disease differ by gender. Female patients may bear a greater burden than male patients. The immune system may play an important role in the pathophysiology of females with IS. Therefore, it is critical to investigate the key biomarkers and immune infiltration of female IS patients to develop effective treatment methods. Herein, we used weighted gene co-expression network analysis (WGCNA) to determine the key modules and core genes in female IS patients using the GSE22255, GSE37587, and GSE16561 datasets from the GEO database. Subsequently, we performed functional enrichment analysis and built a protein-protein interaction (PPI) network. Ten genes were selected as the true central genes for further investigation. After that, we explored the specific molecular and biological functions of these hub genes to gain a better understanding of the underlying pathogenesis of female IS patients. Moreover, the “Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)” was used to examine the distribution pattern of immune subtypes in female patients with IS and normal controls, revealing a new potential target for clinical treatment of the disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"8 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90823821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shan Xiong, Liwei Jiang, Yu Wang, T. Pan, Furong Ma
Auditory deprivation affects normal age-related changes in the central auditory maturation. Cochlear implants (CIs) have already become the best treatment strategy for severe to profound hearing impairment. However, it is still hard to evaluate the speech-language outcomes of the pediatric CI recipients because of hearing-impaired children with limited speech-language abilities. The cortical auditory evoked potential (CAEP) provides a window into the development of the auditory cortical pathways. This preliminary study is aimed at assessing electrophysical characteristics of P1-N1 of electrically CAEP in children with CIs and at exploring whether these changes could be accounted for in auditory and speech outcomes of these patients. CAEP responses were recorded in 48 children with CIs in response to electrical stimulus to determine the presence of the P1-N1 response. Speech perception and speech intelligibility of the implanted children were further evaluated with the categories of auditory performance (CAP) test and speech intelligibility rating (SIR) test, respectively, to explore the relationship between the latency of P1-N1 and auditory and speech performance. This study found that P1 and N1 of the intracochlear CAEP were reliably evoked in children fitted with CIs and that the latency of the P1 as opposed to that of N1 was negative in relation to the wearing time of the cochlear implant. Moreover, the latency of the P1 produced significantly negative scores in both CAP and SIR tests, which indicates that P1 latency may be reflective of the auditory performance and speech intelligibility of pediatric CI recipients. These results suggest that the latency of P1 could be used for the objective assessment of auditory and speech function evaluation in cochlear-implanted children, which would be helpful in clinical decision-making regarding intervention for young hearing-impaired children.
{"title":"The Role of the P1 Latency in Auditory and Speech Performance Evaluation in Cochlear Implanted Children","authors":"Shan Xiong, Liwei Jiang, Yu Wang, T. Pan, Furong Ma","doi":"10.1155/2022/6894794","DOIUrl":"https://doi.org/10.1155/2022/6894794","url":null,"abstract":"Auditory deprivation affects normal age-related changes in the central auditory maturation. Cochlear implants (CIs) have already become the best treatment strategy for severe to profound hearing impairment. However, it is still hard to evaluate the speech-language outcomes of the pediatric CI recipients because of hearing-impaired children with limited speech-language abilities. The cortical auditory evoked potential (CAEP) provides a window into the development of the auditory cortical pathways. This preliminary study is aimed at assessing electrophysical characteristics of P1-N1 of electrically CAEP in children with CIs and at exploring whether these changes could be accounted for in auditory and speech outcomes of these patients. CAEP responses were recorded in 48 children with CIs in response to electrical stimulus to determine the presence of the P1-N1 response. Speech perception and speech intelligibility of the implanted children were further evaluated with the categories of auditory performance (CAP) test and speech intelligibility rating (SIR) test, respectively, to explore the relationship between the latency of P1-N1 and auditory and speech performance. This study found that P1 and N1 of the intracochlear CAEP were reliably evoked in children fitted with CIs and that the latency of the P1 as opposed to that of N1 was negative in relation to the wearing time of the cochlear implant. Moreover, the latency of the P1 produced significantly negative scores in both CAP and SIR tests, which indicates that P1 latency may be reflective of the auditory performance and speech intelligibility of pediatric CI recipients. These results suggest that the latency of P1 could be used for the objective assessment of auditory and speech function evaluation in cochlear-implanted children, which would be helpful in clinical decision-making regarding intervention for young hearing-impaired children.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"49 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84261451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ming-hao Yang, Zhiqiang Guo, Xueyu Lv, Zhu-Qing Zhang, Wei-dong Wang, Jian Wang, L. Hong, Ying-Na Lin, ChunTing Liu
Rumination is a common symptom of major depressive disorder (MDD) and has been characterized as a vulnerability factor for the onset or recurrence of MDD. However, the neurobiological mechanisms underlying rumination and appropriate treatment strategies remain unclear. In the current study, we used resting-state functional magnetic resonance imaging to investigate the effects of body-mind relaxation meditation induction (BMRMI) intervention in MDD with rumination. To this aim, we have recruited 25 MDD and 24 healthy controls (HCs). Changes in functional connectivity (FC) of the anterior cingulate cortex (ACC) subregion and the scores of clinical measurements were examined using correlation analysis. At baseline, MDD showed stronger FC between the right dorsal ACC (dACC) and right superior frontal gyrus than did the HC group. Compared to baseline, the HC group showed a significantly enhanced FC between the right dACC and right superior frontal gyrus, and the MDD group demonstrated a significantly weaker FC between the left dACC and right middle frontal gyrus (MFG) after the intervention. Furthermore, the FC between the right dACC and right superior frontal gyrus was positively associated with rumination scores across all participants at baseline. The above results indicate that BMRMI may regulate self-referential processing and cognitive function through modulating FC of the dACC in MDD with rumination.
{"title":"BMRMI Reduces Depressive Rumination Possibly through Improving Abnormal FC of Dorsal ACC","authors":"Ming-hao Yang, Zhiqiang Guo, Xueyu Lv, Zhu-Qing Zhang, Wei-dong Wang, Jian Wang, L. Hong, Ying-Na Lin, ChunTing Liu","doi":"10.1155/2022/8068988","DOIUrl":"https://doi.org/10.1155/2022/8068988","url":null,"abstract":"Rumination is a common symptom of major depressive disorder (MDD) and has been characterized as a vulnerability factor for the onset or recurrence of MDD. However, the neurobiological mechanisms underlying rumination and appropriate treatment strategies remain unclear. In the current study, we used resting-state functional magnetic resonance imaging to investigate the effects of body-mind relaxation meditation induction (BMRMI) intervention in MDD with rumination. To this aim, we have recruited 25 MDD and 24 healthy controls (HCs). Changes in functional connectivity (FC) of the anterior cingulate cortex (ACC) subregion and the scores of clinical measurements were examined using correlation analysis. At baseline, MDD showed stronger FC between the right dorsal ACC (dACC) and right superior frontal gyrus than did the HC group. Compared to baseline, the HC group showed a significantly enhanced FC between the right dACC and right superior frontal gyrus, and the MDD group demonstrated a significantly weaker FC between the left dACC and right middle frontal gyrus (MFG) after the intervention. Furthermore, the FC between the right dACC and right superior frontal gyrus was positively associated with rumination scores across all participants at baseline. The above results indicate that BMRMI may regulate self-referential processing and cognitive function through modulating FC of the dACC in MDD with rumination.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"85 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84567711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ke Shang, Xiao Chen, Chang Cheng, Xiang Luo, Shabei Xu, Wei Wang, Chenchen Liu
Introduction The association between arterial tortuosity and acute ischemic stroke (AIS) has been reported, but showing inconsistent results. We hypothesized that tortuosity of extra- and intracranial large arteries might be higher in AIS patients. Furthermore, we explored the correlation between artery tortuosity and white matter hyperintensity (WMH) severity in AIS patients. Methods 166 AIS patients identified as large artery atherosclerosis, and 83 control subjects were enrolled. All subjects received three-dimensional computed tomography angiography (CTA). Arterial tortuosity was evaluated using the tortuosity index. WMHs were evaluated using magnetic resonance imaging in all AIS patients. Results AIS patients showed significantly increased arterial tortuosity index relative to controls, including left carotid artery (CA) (p = 0.001), right CA (p < 0.001), left common carotid artery (CCA) (p < 0.001), right CCA (p < 0.001), left internal carotid artery (p = 0.001), right internal carotid artery (p = 0.01), left extracranial internal carotid artery (EICA) (p < 0.001), right EICA (p = 0.01), and vertebral artery dominance (VAD) (p = 0.001). The tortuosity of all above arteries was associated with the presence of AIS. AIS patients with moderate or severe WMHs had a higher tortuosity index in left CA (p = 0.005), left CCA (p = 0.003), left EICA (p = 0.07), and VAD (p = 0.001). In addition, the tortuosity of left EICA and VAD was associated with WMH severity in AIS patients. Conclusions Increased extra- and intracranial large arteries tortuosity is associated with AIS. The tortuosity of left carotid artery system and vertebral artery may be the independent risk factors for WMH severity in AIS patients. Clinical Trial Registration. This trial is registered with NCT03122002 (http://www.clinicaltrials.gov).
{"title":"Arterial Tortuosity and Its Correlation with White Matter Hyperintensities in Acute Ischemic Stroke","authors":"Ke Shang, Xiao Chen, Chang Cheng, Xiang Luo, Shabei Xu, Wei Wang, Chenchen Liu","doi":"10.1155/2022/4280410","DOIUrl":"https://doi.org/10.1155/2022/4280410","url":null,"abstract":"Introduction The association between arterial tortuosity and acute ischemic stroke (AIS) has been reported, but showing inconsistent results. We hypothesized that tortuosity of extra- and intracranial large arteries might be higher in AIS patients. Furthermore, we explored the correlation between artery tortuosity and white matter hyperintensity (WMH) severity in AIS patients. Methods 166 AIS patients identified as large artery atherosclerosis, and 83 control subjects were enrolled. All subjects received three-dimensional computed tomography angiography (CTA). Arterial tortuosity was evaluated using the tortuosity index. WMHs were evaluated using magnetic resonance imaging in all AIS patients. Results AIS patients showed significantly increased arterial tortuosity index relative to controls, including left carotid artery (CA) (p = 0.001), right CA (p < 0.001), left common carotid artery (CCA) (p < 0.001), right CCA (p < 0.001), left internal carotid artery (p = 0.001), right internal carotid artery (p = 0.01), left extracranial internal carotid artery (EICA) (p < 0.001), right EICA (p = 0.01), and vertebral artery dominance (VAD) (p = 0.001). The tortuosity of all above arteries was associated with the presence of AIS. AIS patients with moderate or severe WMHs had a higher tortuosity index in left CA (p = 0.005), left CCA (p = 0.003), left EICA (p = 0.07), and VAD (p = 0.001). In addition, the tortuosity of left EICA and VAD was associated with WMH severity in AIS patients. Conclusions Increased extra- and intracranial large arteries tortuosity is associated with AIS. The tortuosity of left carotid artery system and vertebral artery may be the independent risk factors for WMH severity in AIS patients. Clinical Trial Registration. This trial is registered with NCT03122002 (http://www.clinicaltrials.gov).","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"31 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82878691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu
Recently, an increasing number of studies have highlighted the role of the cerebellum in language processing. However, the role of neural reorganization within the cerebellum as well as within the cerebrocerebellar system caused by poststroke aphasia remains unknown. To solve this problem, in the present study, we investigated regional alterations of the cerebellum as well as the functional reorganization of the cerebrocerebellar circuit by combining structural and resting-state functional magnetic resonance imaging (fMRI) techniques. Twenty patients diagnosed with aphasia following left-hemispheric stroke and 20 age-matched healthy controls (HCs) were recruited in this study. The Western Aphasia Battery (WAB) test was used to assess the participants' language ability. Gray matter volume, spontaneous brain activity, functional connectivity, and effective connectivity were examined in each participant. We discovered that gray matter volumes in right cerebellar lobule VI and right Crus I were significantly lower in the patient group, and the brain activity within these regions was significantly correlated with WAB scores. We also discovered decreased functional connectivity within the crossed cerebrocerebellar circuit, which was significantly correlated with WAB scores. Moreover, altered information flow between the cerebellum and the contralateral cerebrum was found. Together, our findings provide evidence for regional alterations within the cerebellum and the reorganization of the cerebrocerebellar system following poststroke aphasia and highlight the important role of the cerebellum in language processing within aphasic individuals after stroke.
{"title":"Regional Alteration within the Cerebellum and the Reorganization of the Cerebrocerebellar System following Poststroke Aphasia","authors":"Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu","doi":"10.1155/2022/3481423","DOIUrl":"https://doi.org/10.1155/2022/3481423","url":null,"abstract":"Recently, an increasing number of studies have highlighted the role of the cerebellum in language processing. However, the role of neural reorganization within the cerebellum as well as within the cerebrocerebellar system caused by poststroke aphasia remains unknown. To solve this problem, in the present study, we investigated regional alterations of the cerebellum as well as the functional reorganization of the cerebrocerebellar circuit by combining structural and resting-state functional magnetic resonance imaging (fMRI) techniques. Twenty patients diagnosed with aphasia following left-hemispheric stroke and 20 age-matched healthy controls (HCs) were recruited in this study. The Western Aphasia Battery (WAB) test was used to assess the participants' language ability. Gray matter volume, spontaneous brain activity, functional connectivity, and effective connectivity were examined in each participant. We discovered that gray matter volumes in right cerebellar lobule VI and right Crus I were significantly lower in the patient group, and the brain activity within these regions was significantly correlated with WAB scores. We also discovered decreased functional connectivity within the crossed cerebrocerebellar circuit, which was significantly correlated with WAB scores. Moreover, altered information flow between the cerebellum and the contralateral cerebrum was found. Together, our findings provide evidence for regional alterations within the cerebellum and the reorganization of the cerebrocerebellar system following poststroke aphasia and highlight the important role of the cerebellum in language processing within aphasic individuals after stroke.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80437744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Peripheral nerve injury can lead to partial or complete loss of limb function, and nerve transfer is an effective surgical salvage for patients with these injuries. The inability of deprived cortical regions representing damaged nerves to overcome corresponding maladaptive plasticity after the reinnervation of muscle fibers and sensory receptors is thought to be correlated with lasting and unfavorable functional recovery. However, the concept of central nervous system plasticity is rarely elucidated in classical textbooks involving peripheral nerve injury, let alone peripheral nerve transfer. This article is aimed at providing a comprehensive understanding of central nervous system plasticity involving peripheral nerve injury by reviewing studies mainly in human or nonhuman primate and by highlighting the functional and structural modifications in the central nervous system after peripheral nerve transfer. Hopefully, it will help surgeons perform successful nerve transfer under the guidance of modern concepts in neuroplasticity.
{"title":"Plasticity of the Central Nervous System Involving Peripheral Nerve Transfer","authors":"Jun Shen","doi":"10.1155/2022/5345269","DOIUrl":"https://doi.org/10.1155/2022/5345269","url":null,"abstract":"Peripheral nerve injury can lead to partial or complete loss of limb function, and nerve transfer is an effective surgical salvage for patients with these injuries. The inability of deprived cortical regions representing damaged nerves to overcome corresponding maladaptive plasticity after the reinnervation of muscle fibers and sensory receptors is thought to be correlated with lasting and unfavorable functional recovery. However, the concept of central nervous system plasticity is rarely elucidated in classical textbooks involving peripheral nerve injury, let alone peripheral nerve transfer. This article is aimed at providing a comprehensive understanding of central nervous system plasticity involving peripheral nerve injury by reviewing studies mainly in human or nonhuman primate and by highlighting the functional and structural modifications in the central nervous system after peripheral nerve transfer. Hopefully, it will help surgeons perform successful nerve transfer under the guidance of modern concepts in neuroplasticity.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"64 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89330226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua
Surround suppression (SS) is a phenomenon that a neuron's response to visual stimuli within the classical receptive field (cRF) is suppressed by a concurrent stimulation in the surrounding receptive field (sRF) beyond the cRF. Studies show that SS affects neuronal response contrast sensitivity in the primary visual cortex (V1). However, the underlying mechanisms remain unclear. Here, we examined SS effect on the contrast sensitivity of cats' V1 neurons with different preferred SFs using external noise-masked visual stimuli and perceptual template model (PTM) analysis at the system level. The contrast sensitivity was evaluated by the inverted threshold contrast of neurons in response to circular gratings of different contrasts in the cRF with or without an annular grating in the sRF. Our results showed that SS significantly reduced the contrast sensitivity of cats' V1 neurons. The SS-induced reduction of contrast sensitivity was not correlated with SS strength but was dependent on neuron's preferred SF, with a larger reduction for neurons with low preferred SFs than those with high preferred SFs. PTM analysis of threshold versus external noise contrast (TvC) functions indicated that SS decreased contrast sensitivity by increasing both the internal additive noise and impact of external noise for neurons with low preferred SFs, but improving only internal additive noise for neurons with high preferred SFs. Furthermore, the SS effect on the contrast-response function of low- and high-SF neurons also exhibited different mechanisms in contrast gain and response gain. Collectively, these results suggest that the mechanisms of SS effect on neuronal contrast sensitivity may depend on neuronal populations with different SFs.
{"title":"Mechanisms of Surround Suppression Effect on the Contrast Sensitivity of V1 Neurons in Cats","authors":"Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua","doi":"10.1155/2022/5677655","DOIUrl":"https://doi.org/10.1155/2022/5677655","url":null,"abstract":"Surround suppression (SS) is a phenomenon that a neuron's response to visual stimuli within the classical receptive field (cRF) is suppressed by a concurrent stimulation in the surrounding receptive field (sRF) beyond the cRF. Studies show that SS affects neuronal response contrast sensitivity in the primary visual cortex (V1). However, the underlying mechanisms remain unclear. Here, we examined SS effect on the contrast sensitivity of cats' V1 neurons with different preferred SFs using external noise-masked visual stimuli and perceptual template model (PTM) analysis at the system level. The contrast sensitivity was evaluated by the inverted threshold contrast of neurons in response to circular gratings of different contrasts in the cRF with or without an annular grating in the sRF. Our results showed that SS significantly reduced the contrast sensitivity of cats' V1 neurons. The SS-induced reduction of contrast sensitivity was not correlated with SS strength but was dependent on neuron's preferred SF, with a larger reduction for neurons with low preferred SFs than those with high preferred SFs. PTM analysis of threshold versus external noise contrast (TvC) functions indicated that SS decreased contrast sensitivity by increasing both the internal additive noise and impact of external noise for neurons with low preferred SFs, but improving only internal additive noise for neurons with high preferred SFs. Furthermore, the SS effect on the contrast-response function of low- and high-SF neurons also exhibited different mechanisms in contrast gain and response gain. Collectively, these results suggest that the mechanisms of SS effect on neuronal contrast sensitivity may depend on neuronal populations with different SFs.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"123 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85669508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective Muscle weakness and spasticity are common consequences of stroke, leading to a decrease in physical activity. The effective implementation of precision rehabilitation requires detailed rehabilitation evaluation. We aimed to analyze the surface electromyography (sEMG) signal features of elbow flexor muscle (biceps brachii and brachioradialis) spasticity in maximum voluntary isometric contraction (MVIC) and fast passive extension (FPE) in stroke patients and to explore the main muscle groups that affect the active movement and spasticity of the elbow flexor muscles to provide an objective reference for optimizing stroke rehabilitation. Methods Fifteen patients with elbow flexor spasticity after stroke were enrolled in this study. sEMG signals of the paretic and nonparetic elbow flexor muscles (biceps and brachioradialis) were detected during MVIC and FPE, and root mean square (RMS) values were calculated. The RMS values (mean and peak) of the biceps and brachioradialis were compared between the paretic and nonparetic sides. Additionally, the correlation between the manual muscle test (MMT) score and the RMS values (mean and peak) of the paretic elbow flexors during MVIC was analyzed, and the correlation between the modified Ashworth scale (MAS) score and the RMS values (mean and peak) of the paretic elbow flexors during FPE was analyzed. Results During MVIC exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly lower than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the bilateral biceps were significantly higher than those of the brachioradialis (p < 0.01). The MMT score was positively correlated with the mean and peak RMS values of the paretic biceps and brachioradialis (r = 0.89, r = 0.91, r = 0.82, r = 0.85; p < 0.001). During FPE exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly higher than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the brachioradialis on the paretic side were significantly higher than those of the biceps (p < 0.01). TheMAS score was positively correlated with the mean RMS of the paretic biceps and brachioradialis (r = 0.62, p = 0.021; r = 0.74, p = 0.004), and the MAS score was positively correlated with the peak RMS of the paretic brachioradialis (r = 0.59, p = 0.029) but had no significant correlation with the peak RMS of the paretic biceps (r = 0.49, p > 0.05). Conclusions The results confirm that the biceps is a vital muscle in active elbow flexion and that the brachioradialis plays an important role in elbow flexor spasticity, suggesting that the biceps should be the focus of muscle strength training of the elbow flexors and that the role of the brachioradialis should not be ignored in the treatment of elbow flexor spasticity. This study also confirmed the application value of sEMG in the objective assessment of individual
目的:肌肉无力和痉挛是中风的常见后果，导致身体活动减少。精准康复的有效实施需要详细的康复评估。我们旨在分析脑卒中患者肘关节屈肌(肱二头肌和肱桡肌)在最大自主等长收缩(MVIC)和快速被动伸展(FPE)时痉挛的肌表电(sEMG)信号特征，探讨影响肘关节屈肌主动运动和痉挛的主要肌肉群，为优化脑卒中康复提供客观参考。方法对15例脑卒中后肘关节屈肌痉挛患者进行研究。在MVIC和FPE期间检测麻痹性和非麻痹性肘关节屈肌(肱二头肌和肱桡肌)的肌电信号，并计算均方根(RMS)值。比较双亲侧和非双亲侧肱二头肌和肱桡肌的均方根值(平均值和峰值)。此外，分析MVIC过程中手工肌肉测试(MMT)评分与麻痹性屈肘肌RMS值(均值和峰值)的相关性，以及FPE过程中改良Ashworth量表(MAS)评分与麻痹性屈肘肌RMS值(均值和峰值)的相关性。结果MVIC运动时，患侧肱二头肌和肱桡肌的RMS值(平均值和峰值)显著低于非患侧(p < 0.01)，双侧肱二头肌的RMS值(平均值和峰值)显著高于肱桡肌(p < 0.01)。MMT评分与肱二头肌和肱桡肌的均方根值和峰方根值呈正相关(r = 0.89, r = 0.91, r = 0.82, r = 0.85;P < 0.001)。在FPE运动中，麻痹侧肱二头肌和肱桡肌的RMS值(平均值和峰值)显著高于非麻痹侧(p < 0.01)，麻痹侧肱桡肌的RMS值(平均值和峰值)显著高于肱二头肌(p < 0.01)。TheMAS评分与肱二头肌和肱桡肌的平均RMS呈正相关(r = 0.62, p = 0.021;r = 0.74, p = 0.004)， MAS评分与肱桡肌峰值RMS呈正相关(r = 0.59, p = 0.029)，与肱二头肌峰值RMS无显著相关(r = 0.49, p > 0.05)。结论肱二头肌是肘关节主动屈曲的重要肌肉，肱桡肌在肘关节屈曲痉挛中起着重要作用，提示肱二头肌应成为肘关节屈曲肌力量训练的重点，在肘关节屈曲痉挛的治疗中不应忽视肱桡肌的作用。本研究也证实了肌电图在脑卒中患者个体肌力和痉挛的客观评价中的应用价值。
{"title":"The Effects of the Biceps Brachii and Brachioradialis on Elbow Flexor Muscle Strength and Spasticity in Stroke Patients","authors":"Binbin Yu, Xintong Zhang, Yihui Cheng, Lingling Liu, YanJiang, Jiayue Wang, Xiao Lu","doi":"10.1155/2022/1295908","DOIUrl":"https://doi.org/10.1155/2022/1295908","url":null,"abstract":"Objective Muscle weakness and spasticity are common consequences of stroke, leading to a decrease in physical activity. The effective implementation of precision rehabilitation requires detailed rehabilitation evaluation. We aimed to analyze the surface electromyography (sEMG) signal features of elbow flexor muscle (biceps brachii and brachioradialis) spasticity in maximum voluntary isometric contraction (MVIC) and fast passive extension (FPE) in stroke patients and to explore the main muscle groups that affect the active movement and spasticity of the elbow flexor muscles to provide an objective reference for optimizing stroke rehabilitation. Methods Fifteen patients with elbow flexor spasticity after stroke were enrolled in this study. sEMG signals of the paretic and nonparetic elbow flexor muscles (biceps and brachioradialis) were detected during MVIC and FPE, and root mean square (RMS) values were calculated. The RMS values (mean and peak) of the biceps and brachioradialis were compared between the paretic and nonparetic sides. Additionally, the correlation between the manual muscle test (MMT) score and the RMS values (mean and peak) of the paretic elbow flexors during MVIC was analyzed, and the correlation between the modified Ashworth scale (MAS) score and the RMS values (mean and peak) of the paretic elbow flexors during FPE was analyzed. Results During MVIC exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly lower than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the bilateral biceps were significantly higher than those of the brachioradialis (p < 0.01). The MMT score was positively correlated with the mean and peak RMS values of the paretic biceps and brachioradialis (r = 0.89, r = 0.91, r = 0.82, r = 0.85; p < 0.001). During FPE exercise, the RMS values (mean and peak) of the biceps and brachioradialis on the paretic side were significantly higher than those on the nonparetic side (p < 0.01), and the RMS values (mean and peak) of the brachioradialis on the paretic side were significantly higher than those of the biceps (p < 0.01). TheMAS score was positively correlated with the mean RMS of the paretic biceps and brachioradialis (r = 0.62, p = 0.021; r = 0.74, p = 0.004), and the MAS score was positively correlated with the peak RMS of the paretic brachioradialis (r = 0.59, p = 0.029) but had no significant correlation with the peak RMS of the paretic biceps (r = 0.49, p > 0.05). Conclusions The results confirm that the biceps is a vital muscle in active elbow flexion and that the brachioradialis plays an important role in elbow flexor spasticity, suggesting that the biceps should be the focus of muscle strength training of the elbow flexors and that the role of the brachioradialis should not be ignored in the treatment of elbow flexor spasticity. This study also confirmed the application value of sEMG in the objective assessment of individual","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90183998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-02-22DOI: 10.21203/rs.3.rs-1344273/v1
Karina Hernández Mercado, Araceli Martínez Moreno, Luis Francisco Rodríguez Durán, M. Escobar, A. Zepeda
The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG granule cell layer (GCL) widening due to granule cell dispersion has been reported under hyperexcitation conditions in animal models as well as in patients with mesial temporal lobe epilepsy, but also in patients with no apparent relation to epilepsy. Strikingly, it is unclear whether the presence and severity of GCL widening along time affect synaptic processing arising from the PP and alter the performance in hippocampal-mediated behaviors. To evaluate the above, we injected excitotoxic kainic acid (KA) unilaterally into the DG of mice and analyzed the evolution of GCL widening at 10 and 30 days post injection (dpi), while analyzing if KA-induced GCL widening affected in vivo long-term potentiation (LTP) in the PP-DG pathway, as well as the performance in learning and memory through contextual fear conditioning. Our results show that at 10 dpi, when a subtle GCL widening was observed, LTP induction, as well as contextual fear memory, were impaired. However, at 30 dpi when a pronounced increase in GCL widening was found, LTP induction and contextual fear memory were already reestablished. These results highlight the plastic potential of the DG to recover some of its functions despite a major structural alteration such as abnormal GCL widening.
{"title":"Progression in Time of Dentate Gyrus Granule Cell Layer Widening due to Excitotoxicity Occurs along In Vivo LTP Reinstatement and Contextual Fear Memory Recovery","authors":"Karina Hernández Mercado, Araceli Martínez Moreno, Luis Francisco Rodríguez Durán, M. Escobar, A. Zepeda","doi":"10.21203/rs.3.rs-1344273/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-1344273/v1","url":null,"abstract":"The dentate gyrus (DG) is the gateway of sensory information arriving from the perforant pathway (PP) to the hippocampus. The adequate integration of incoming information into the DG is paramount in the execution of hippocampal-dependent cognitive functions. An abnormal DG granule cell layer (GCL) widening due to granule cell dispersion has been reported under hyperexcitation conditions in animal models as well as in patients with mesial temporal lobe epilepsy, but also in patients with no apparent relation to epilepsy. Strikingly, it is unclear whether the presence and severity of GCL widening along time affect synaptic processing arising from the PP and alter the performance in hippocampal-mediated behaviors. To evaluate the above, we injected excitotoxic kainic acid (KA) unilaterally into the DG of mice and analyzed the evolution of GCL widening at 10 and 30 days post injection (dpi), while analyzing if KA-induced GCL widening affected in vivo long-term potentiation (LTP) in the PP-DG pathway, as well as the performance in learning and memory through contextual fear conditioning. Our results show that at 10 dpi, when a subtle GCL widening was observed, LTP induction, as well as contextual fear memory, were impaired. However, at 30 dpi when a pronounced increase in GCL widening was found, LTP induction and contextual fear memory were already reestablished. These results highlight the plastic potential of the DG to recover some of its functions despite a major structural alteration such as abnormal GCL widening.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"32 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85590231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marcella M. Authiat, Emmanuelle Gruz-Gibelli, Julien Colas, E. Bianchi, Marta Garcia-Arauzo, P. Marin, F. Herrmann, A. Savioz
Recently, we showed that DNA double-strand breaks (DSBs) are increased by the Aβ42-amyloid peptide and decreased by all-trans retinoic acid (RA) in SH-SY5Y cells and C57BL/6J mice. The present work was aimed at investigating DSBs in cells and murine models of Alzheimer's disease carrying the preseniline-1 (PS1) P117L mutation. We observed that DSBs could hardly decrease following RA treatment in the mutated cells compared to the wild-type cells. The activation of the amyloidogenic pathway is proposed in the former case as Aβ42- and RA-dependent DSBs changes were reproduced by an α-secretase and a γ-secretase inhibitions, respectively. Unexpectedly, the PS1 P117L cells showed lower DSB levels than the controls. As the DSB repair proteins Tip60 and Fe65 were less expressed in the mutated cell nuclei, they do not appear to contribute to this difference. On the contrary, full-length BRCA1 and BARD1 proteins were significantly increased in the chromatin compartment of the mutated cells, suggesting that they decrease DSBs in the pathological situation. These Western blot data were corroborated by in situ proximity ligation assays: the numbers of BRCA1-BARD1, not of Fe65-Tip60 heterodimers, were increased only in the mutated cell nuclei. RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. The increased BRCA1 expression in the mutated cells can be related to the enhanced difficulty to inhibit this pathway by BRCA1 siRNA in these cells. Overall, our study suggests that at earlier stages of the disease, similarly to PS1 P117L cells, a compensatory mechanism exists that decreases DSB levels via an activation of the BRCA1/BARD1 pathway. This supports the importance of this pathway in neuroprotection against Alzheimer's disease.
{"title":"Preferential Involvement of BRCA1/BARD1, Not Tip60/Fe65, in DNA Double-Strand Break Repair in Presenilin-1 P117L Alzheimer Models","authors":"Marcella M. Authiat, Emmanuelle Gruz-Gibelli, Julien Colas, E. Bianchi, Marta Garcia-Arauzo, P. Marin, F. Herrmann, A. Savioz","doi":"10.1155/2022/3172861","DOIUrl":"https://doi.org/10.1155/2022/3172861","url":null,"abstract":"Recently, we showed that DNA double-strand breaks (DSBs) are increased by the Aβ42-amyloid peptide and decreased by all-trans retinoic acid (RA) in SH-SY5Y cells and C57BL/6J mice. The present work was aimed at investigating DSBs in cells and murine models of Alzheimer's disease carrying the preseniline-1 (PS1) P117L mutation. We observed that DSBs could hardly decrease following RA treatment in the mutated cells compared to the wild-type cells. The activation of the amyloidogenic pathway is proposed in the former case as Aβ42- and RA-dependent DSBs changes were reproduced by an α-secretase and a γ-secretase inhibitions, respectively. Unexpectedly, the PS1 P117L cells showed lower DSB levels than the controls. As the DSB repair proteins Tip60 and Fe65 were less expressed in the mutated cell nuclei, they do not appear to contribute to this difference. On the contrary, full-length BRCA1 and BARD1 proteins were significantly increased in the chromatin compartment of the mutated cells, suggesting that they decrease DSBs in the pathological situation. These Western blot data were corroborated by in situ proximity ligation assays: the numbers of BRCA1-BARD1, not of Fe65-Tip60 heterodimers, were increased only in the mutated cell nuclei. RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. The increased BRCA1 expression in the mutated cells can be related to the enhanced difficulty to inhibit this pathway by BRCA1 siRNA in these cells. Overall, our study suggests that at earlier stages of the disease, similarly to PS1 P117L cells, a compensatory mechanism exists that decreases DSB levels via an activation of the BRCA1/BARD1 pathway. This supports the importance of this pathway in neuroprotection against Alzheimer's disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"40 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85382143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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