首页 > 最新文献

Journal of neurobiology and physiology最新文献

英文 中文
Evaluation of chondrocyte dedifferentiation mechanisms using confocal Raman microscopy 利用共焦拉曼显微镜评估软骨细胞再分化机制
Pub Date : 2023-12-21 DOI: 10.46439/neurobiology.5.024
N’Dré Jean N’DRE, P. A. Lecor, Assoumou Aa, Blohoua Mjj
Progression to metastases remains the overriding cause of cancer-associated mortality. Metastatic cancer is not amenable to surgery and its treatment is further complicated by the development of therapy resistance often observed at advanced cancer stages. Early detection of metastases is therefore critical but has been limited by the lack of probes that can effectively localize them. Similar challenges persist with therapeutics specifically targeting metastasized cancer cells. Thus, agents that specifically target disseminating tumor cells at an early stage could produce new theranostic applications and be transformative for the survival of patients with advanced cancers. Recent studies have described new approaches for early detection and targeted eradication of metastatic cancer. Here we summarize the results from preclinical validation of the experimental probes reported to date.
癌症进展到转移灶仍然是癌症相关死亡率的首要原因。转移性癌症不适合手术治疗,而癌症晚期常出现的抗药性又使治疗变得更加复杂。因此,转移灶的早期检测至关重要,但由于缺乏能有效定位转移灶的探针,早期检测一直受到限制。专门针对转移癌细胞的疗法也面临着类似的挑战。因此,早期特异性靶向扩散肿瘤细胞的药物可产生新的治疗应用,并对晚期癌症患者的生存产生变革性影响。最近的研究描述了早期检测和靶向根除转移性癌症的新方法。在此,我们总结了迄今为止报道的实验探针的临床前验证结果。
{"title":"Evaluation of chondrocyte dedifferentiation mechanisms using confocal Raman microscopy","authors":"N’Dré Jean N’DRE, P. A. Lecor, Assoumou Aa, Blohoua Mjj","doi":"10.46439/neurobiology.5.024","DOIUrl":"https://doi.org/10.46439/neurobiology.5.024","url":null,"abstract":"Progression to metastases remains the overriding cause of cancer-associated mortality. Metastatic cancer is not amenable to surgery and its treatment is further complicated by the development of therapy resistance often observed at advanced cancer stages. Early detection of metastases is therefore critical but has been limited by the lack of probes that can effectively localize them. Similar challenges persist with therapeutics specifically targeting metastasized cancer cells. Thus, agents that specifically target disseminating tumor cells at an early stage could produce new theranostic applications and be transformative for the survival of patients with advanced cancers. Recent studies have described new approaches for early detection and targeted eradication of metastatic cancer. Here we summarize the results from preclinical validation of the experimental probes reported to date.","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"135 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138953414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Systematic evaluation of the effects of exenatide and liraglutide on neurodegenerative diseases induced by type 2 diabetes mellitus 艾塞那肽与利拉鲁肽对2型糖尿病所致神经退行性疾病疗效的系统评价
Pub Date : 2022-12-31 DOI: 10.46439/neurobiology.4.022
{"title":"Systematic evaluation of the effects of exenatide and liraglutide on neurodegenerative diseases induced by type 2 diabetes mellitus","authors":"","doi":"10.46439/neurobiology.4.022","DOIUrl":"https://doi.org/10.46439/neurobiology.4.022","url":null,"abstract":"","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43758896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The surgical philosophy for the management of rathke cleft cyst: Finding the sweet spot rathke裂囊肿治疗的手术理念:寻找最佳治疗点
Pub Date : 2022-12-31 DOI: 10.46439/neurobiology.4.019
{"title":"The surgical philosophy for the management of rathke cleft cyst: Finding the sweet spot","authors":"","doi":"10.46439/neurobiology.4.019","DOIUrl":"https://doi.org/10.46439/neurobiology.4.019","url":null,"abstract":"","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48275419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Commentary on “Calcitonin-gene related peptide and neurologic injury: An emerging target for headache management” “降钙素基因相关肽与神经损伤:头痛治疗的新靶点”评论
Pub Date : 2022-11-16 DOI: 10.46439/neurobiology.4.023
Phillip Johansen, B. Lucke-Wold
Mehkri et al. have presented a thorough review of calcitonin-gene related peptide (CGRP) and its relationship with headaches, both primary (e.g., migraine headaches) and secondary headaches (e.g., headaches secondary to subarachnoid hemorrhage (SAH) and traumatic brain injury (TBI)) [1]. They have provided an accurate depiction of the literature and the current knowledge regarding CGRP’s association with neurologic injury, as well as some of the physiologic mechanisms and therapeutic targets. This commentary aims to further discuss the veracity of this article and to add an alternative viewpoint in terms of neuromodulators influencing post-traumatic headaches (PTH). Regarding PTH, the authors accurately depict a current understanding that is grounded in literature – CGRP’s association with neurologic injury is incompletely understood. Whether it be intracellular signaling leading to a pseudo-inflammatory response or hyperstimulation of the brain, CGRP is known to exacerbate headache symptoms. However, CGRP’s interactions in the setting of secondary headaches, such as those induced by subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI), are variable depending on the timeframe. CGRP is thought to be neuroprotective in the acute setting time, CGRP levels normalize despite low-to-normal levels, patients with hypersensitized thorough
Mehkri等人对降钙素基因相关肽(CGRP)及其与头痛的关系进行了全面的综述,包括原发性头痛(如偏头痛)和继发性头痛(例如蛛网膜下腔出血(SAH)和创伤性脑损伤(TBI)引起的头痛)[1]。他们提供了关于CGRP与神经损伤的关系的文献和当前知识的准确描述,以及一些生理机制和治疗靶点。这篇评论旨在进一步讨论这篇文章的真实性,并在影响创伤后头痛(PTH)的神经调节剂方面添加另一种观点。关于PTH,作者准确地描述了目前文献中的理解——CGRP与神经损伤的关系尚不完全清楚。无论是导致假性炎症反应的细胞内信号传导还是大脑的过度刺激,CGRP都会加剧头痛症状。然而,CGRP在继发性头痛(如蛛网膜下腔出血(SAH)或创伤性脑损伤(TBI)引起的头痛)中的相互作用因时间而异。CGRP被认为在急性发作时具有神经保护作用,尽管CGRP水平较低至正常,但CGRP水平正常
{"title":"Commentary on “Calcitonin-gene related peptide and neurologic injury: An emerging target for headache management”","authors":"Phillip Johansen, B. Lucke-Wold","doi":"10.46439/neurobiology.4.023","DOIUrl":"https://doi.org/10.46439/neurobiology.4.023","url":null,"abstract":"Mehkri et al. have presented a thorough review of calcitonin-gene related peptide (CGRP) and its relationship with headaches, both primary (e.g., migraine headaches) and secondary headaches (e.g., headaches secondary to subarachnoid hemorrhage (SAH) and traumatic brain injury (TBI)) [1]. They have provided an accurate depiction of the literature and the current knowledge regarding CGRP’s association with neurologic injury, as well as some of the physiologic mechanisms and therapeutic targets. This commentary aims to further discuss the veracity of this article and to add an alternative viewpoint in terms of neuromodulators influencing post-traumatic headaches (PTH). Regarding PTH, the authors accurately depict a current understanding that is grounded in literature – CGRP’s association with neurologic injury is incompletely understood. Whether it be intracellular signaling leading to a pseudo-inflammatory response or hyperstimulation of the brain, CGRP is known to exacerbate headache symptoms. However, CGRP’s interactions in the setting of secondary headaches, such as those induced by subarachnoid hemorrhage (SAH) or traumatic brain injury (TBI), are variable depending on the timeframe. CGRP is thought to be neuroprotective in the acute setting time, CGRP levels normalize despite low-to-normal levels, patients with hypersensitized thorough","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"4 1","pages":"20 - 22"},"PeriodicalIF":0.0,"publicationDate":"2022-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44645873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology 内质网应激和线粒体功能障碍在金属诱导的神经病理
Pub Date : 2022-08-10 DOI: 10.46439/neurobiology.4.020
Sophia Cai, Min Woo Kim, Pan Chen
Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases. Taken together, to study the molecular programs of integrating ER stress with mitochondrial dysfunction should be an important area of future research for appreciating the mechanisms of as well as developing strategies and targets for metal-induced neurological diseases.
虽然人体需要必需的金属离子,但当暴露于人体无法容纳的金属浓度时,就会发生神经毒性。对于工业上很重要的非必需金属来说,这些元素即使在很小的浓度下也具有引起神经毒性的特性。当这种神经毒性长期发展时,它会导致各种神经退行性疾病,如阿尔茨海默病和帕金森病。因此,关于神经毒性与金属代谢关系的研究正在积极开展,最近的一些研究表明,金属诱导的神经毒性的机制主要涉及内质网应激和线粒体功能障碍。因此,本文将总结一些此类证据的例子,并提出新的问题,以试图解决金属诱导的内质网应激和线粒体功能障碍的神经毒性,这是金属在神经退行性疾病中影响的两个重要主题。综上所述,研究内质网应激与线粒体功能障碍整合的分子程序应该是未来研究的一个重要领域,以了解金属诱导的神经系统疾病的机制,并制定策略和靶点。
{"title":"Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology","authors":"Sophia Cai, Min Woo Kim, Pan Chen","doi":"10.46439/neurobiology.4.020","DOIUrl":"https://doi.org/10.46439/neurobiology.4.020","url":null,"abstract":"Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases. Taken together, to study the molecular programs of integrating ER stress with mitochondrial dysfunction should be an important area of future research for appreciating the mechanisms of as well as developing strategies and targets for metal-induced neurological diseases.","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"4 1","pages":"4 - 8"},"PeriodicalIF":0.0,"publicationDate":"2022-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46002647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Commentary on "Calcitonin-gene related peptide and neurologic injury: An emerging target for headache management". 关于 "降钙素基因相关肽与神经损伤:头痛治疗的新目标
Phillip Johansen, Brandon Lucke-Wold
{"title":"Commentary on \"Calcitonin-gene related peptide and neurologic injury: An emerging target for headache management\".","authors":"Phillip Johansen, Brandon Lucke-Wold","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":" ","pages":"20-22"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40491298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology. 内质网应激和线粒体功能障碍在金属诱导的神经病理。
Sophia Cai, Min Woo Kim, Pan Chen

Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases. Taken together, to study the molecular programs of integrating ER stress with mitochondrial dysfunction should be an important area of future research for appreciating the mechanisms of as well as developing strategies and targets for metal-induced neurological diseases.

虽然人体需要必需的金属离子,但当暴露于人体无法容纳的金属浓度时,就会发生神经毒性。对于工业上很重要的非必需金属来说,这些元素即使在很小的浓度下也具有引起神经毒性的特性。当这种神经毒性长期发展时,它会导致各种神经退行性疾病,如阿尔茨海默病和帕金森病。因此,关于神经毒性与金属代谢关系的研究正在积极开展,最近的一些研究表明,金属诱导的神经毒性的机制主要涉及内质网应激和线粒体功能障碍。因此,本文将总结一些此类证据的例子,并提出新的问题,以试图解决金属诱导的内质网应激和线粒体功能障碍的神经毒性,这是金属在神经退行性疾病中影响的两个重要主题。综上所述,研究内质网应激与线粒体功能障碍整合的分子程序应该是未来研究的一个重要领域,以了解金属诱导的神经系统疾病的机制,并制定策略和靶点。
{"title":"Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology.","authors":"Sophia Cai,&nbsp;Min Woo Kim,&nbsp;Pan Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases. Taken together, to study the molecular programs of integrating ER stress with mitochondrial dysfunction should be an important area of future research for appreciating the mechanisms of as well as developing strategies and targets for metal-induced neurological diseases.</p>","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":" ","pages":"4-8"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9377670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40715525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers. 蝎子毒素改进剂探测钠通道电压传感器模块间的变构相互作用。
Pub Date : 2022-01-01 DOI: 10.46439/neurobiology.4.021
Michael Gurevitz, Boris S Zhorov, Ke Dong

Gating of voltage-dependent sodium channels involves coordinated movements of the voltage sensors in the voltage-sensing modules (VSMs) of the four domains (DI-DIV) in response to membrane depolarization. Zhu et al. have recently examined the effects of charge reversal substitutions at the VSM of domain III on the action of scorpion alpha- and beta-toxins that intercept the voltage sensors in domains IV and II, respectively. The increased activity of both toxin types on the mutant channels has suggested that the VSM module at domain III interacts allosterically with the VSM modules in domains IV and II during channel gating thus affecting indirectly the action of both scorpion toxin classes.

电压依赖性钠离子通道的门控涉及四畴(DI-DIV)电压传感模块(vsm)中电压传感器响应膜去极化的协调运动。Zhu等人最近研究了III结构域VSM上的电荷反转取代对蝎子α和β毒素作用的影响,这两种毒素分别阻断了IV和II结构域的电压传感器。两种毒素在突变通道上的活性增加表明,在通道门控制期间,III结构域的VSM模块与IV和II结构域的VSM模块发生变构相互作用,从而间接影响两种蝎子毒素类的作用。
{"title":"Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers.","authors":"Michael Gurevitz,&nbsp;Boris S Zhorov,&nbsp;Ke Dong","doi":"10.46439/neurobiology.4.021","DOIUrl":"https://doi.org/10.46439/neurobiology.4.021","url":null,"abstract":"<p><p>Gating of voltage-dependent sodium channels involves coordinated movements of the voltage sensors in the voltage-sensing modules (VSMs) of the four domains (DI-DIV) in response to membrane depolarization. Zhu et al. have recently examined the effects of charge reversal substitutions at the VSM of domain III on the action of scorpion alpha- and beta-toxins that intercept the voltage sensors in domains IV and II, respectively. The increased activity of both toxin types on the mutant channels has suggested that the VSM module at domain III interacts allosterically with the VSM modules in domains IV and II during channel gating thus affecting indirectly the action of both scorpion toxin classes.</p>","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"4 1","pages":"9-12"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10081521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9336684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Surgical outcomes of the thoracic ossification of ligamentum flavum: A high incidence of combined spinal stenosis 胸椎黄韧带骨化症的手术结果:合并椎管狭窄的高发率
Pub Date : 2021-12-31 DOI: 10.46439/neurobiology.3.016
{"title":"Surgical outcomes of the thoracic ossification of ligamentum flavum: A high incidence of combined spinal stenosis","authors":"","doi":"10.46439/neurobiology.3.016","DOIUrl":"https://doi.org/10.46439/neurobiology.3.016","url":null,"abstract":"","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42533041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of fathers on HPA-axis development and activity across the lifespan: A brief review 父亲在hpa轴发育和整个生命周期活动中的作用:简要回顾
Pub Date : 2021-12-31 DOI: 10.46439/neurobiology.3.017
Erin E. Wood, Michael M. Criss, Jennifer byrd-craven
Copyright: © 2021 Wood EE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Humans are within the rare 5% of mammal species that have paternal investment [1]. The quantity and quality of paternal investment is facultative on environmental and social context [1-3]. Because paternal investment is facultative in nature, father presence is not necessarily critical for survival [4-6]. However, the presence and involvement of the father can provide sociocompetitive advantages, and indicate valuable information about the safety and predictability of the environment that can have many downstream effects on development and health [7,8]. The safety and predictability of the environment is particularly critical in early childhood during the calibration of the hypothalamic-pituitary-adrenal axis (HPA-axis) and can shape sensitivity to stressors as children age, as discussed below [9-13]. Because fathers are shown to provide unique context to environmental conditions that are important for shaping mental and physical health, more research is needed examining the role of fathers on child development outcomes to provide better accuracy in predicting developmental trajectories [7].
版权所有:©2021 Wood EE等人。这是一篇根据知识共享署名许可证条款分发的开放获取文章,该许可证允许在任何媒体上不受限制地使用、分发和复制,前提是原始作者和来源可信。在拥有父亲投资的哺乳动物物种中,人类属于罕见的5%[1]。父亲投资的数量和质量在环境和社会背景下是临时性的[1-3]。由于父亲的投资本质上是临时性的,父亲的存在对生存并不一定至关重要[4-6]。然而,父亲的存在和参与可以提供社会竞争优势,并表明有关环境安全性和可预测性的宝贵信息,这些信息可能对发展和健康产生许多下游影响[7,8]。在儿童早期,在下丘脑-垂体-肾上腺轴(HPA轴)的校准过程中,环境的安全性和可预测性尤为重要,并可能随着儿童年龄的增长而对压力源产生敏感性,如下所述[9-13]。由于父亲被证明为环境条件提供了独特的背景,而环境条件对塑造身心健康很重要,因此需要更多的研究来检验父亲在儿童发展结果中的作用,以在预测发展轨迹方面提供更好的准确性[7]。
{"title":"The role of fathers on HPA-axis development and activity across the lifespan: A brief review","authors":"Erin E. Wood, Michael M. Criss, Jennifer byrd-craven","doi":"10.46439/neurobiology.3.017","DOIUrl":"https://doi.org/10.46439/neurobiology.3.017","url":null,"abstract":"Copyright: © 2021 Wood EE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Humans are within the rare 5% of mammal species that have paternal investment [1]. The quantity and quality of paternal investment is facultative on environmental and social context [1-3]. Because paternal investment is facultative in nature, father presence is not necessarily critical for survival [4-6]. However, the presence and involvement of the father can provide sociocompetitive advantages, and indicate valuable information about the safety and predictability of the environment that can have many downstream effects on development and health [7,8]. The safety and predictability of the environment is particularly critical in early childhood during the calibration of the hypothalamic-pituitary-adrenal axis (HPA-axis) and can shape sensitivity to stressors as children age, as discussed below [9-13]. Because fathers are shown to provide unique context to environmental conditions that are important for shaping mental and physical health, more research is needed examining the role of fathers on child development outcomes to provide better accuracy in predicting developmental trajectories [7].","PeriodicalId":73855,"journal":{"name":"Journal of neurobiology and physiology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43385725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of neurobiology and physiology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1