R. Marie, Aya Mohamed kamal Lasheen, H. Nashaat, M. Atwa
Background: Warts are viral cutaneous infections caused by human papilloma virus (HPV), presented by verrucous growth over the skin surface. The cell mediated immune response is considered to play a crucial role in HPV clearance. The viral load and number of lesions increase when there is an imbalance between the T-helper 1 and T-helper 2 immune responses. Interleukin (IL)-19 is a cytokine that belongs to interleukin 10 cytokines family and constitutes a sub-family with IL-20, IL-22 and IL-24. IL-19 is mainly produced by activated monocytes and to a lesser extent by B-cells, keratinocytes and fetal membranes. IL-19 was found to shift T-cell maturation away from the pro-inflammatory T-helper 1 cells toward the anti-inflammatory T-helper 2 cells. It induces IL-4 and IL-13 production in T cells and apoptosis in monocytes. Aim: This study aimed to measure serum level of IL-19 in patients with warts compared to healthy controls and to find out the correlation between this level and number, size and clinical types of warts. Methods: The study included 50 patients with warts and 50 control subjects. Serum concentration of IL-19 was measured by enzyme-linked immune sorbent assay. Results: Interleukin-19 serum level was significantly lower in patients with warts than in controls (P < 0.003). Moreover, there was a significant positive correlation between IL-19 serum level and the number of warts (P = 0.027). Conclusion: Serum level of IL-19 was significantly lower in patients with warts, and this low level might be crucial for an effective cell mediated immunological response to HPV.
{"title":"Assessment of serum interleukin 19 level in patients with warts","authors":"R. Marie, Aya Mohamed kamal Lasheen, H. Nashaat, M. Atwa","doi":"10.3934/molsci.2023001","DOIUrl":"https://doi.org/10.3934/molsci.2023001","url":null,"abstract":"Background: Warts are viral cutaneous infections caused by human papilloma virus (HPV), presented by verrucous growth over the skin surface. The cell mediated immune response is considered to play a crucial role in HPV clearance. The viral load and number of lesions increase when there is an imbalance between the T-helper 1 and T-helper 2 immune responses. Interleukin (IL)-19 is a cytokine that belongs to interleukin 10 cytokines family and constitutes a sub-family with IL-20, IL-22 and IL-24. IL-19 is mainly produced by activated monocytes and to a lesser extent by B-cells, keratinocytes and fetal membranes. IL-19 was found to shift T-cell maturation away from the pro-inflammatory T-helper 1 cells toward the anti-inflammatory T-helper 2 cells. It induces IL-4 and IL-13 production in T cells and apoptosis in monocytes. Aim: This study aimed to measure serum level of IL-19 in patients with warts compared to healthy controls and to find out the correlation between this level and number, size and clinical types of warts. Methods: The study included 50 patients with warts and 50 control subjects. Serum concentration of IL-19 was measured by enzyme-linked immune sorbent assay. Results: Interleukin-19 serum level was significantly lower in patients with warts than in controls (P < 0.003). Moreover, there was a significant positive correlation between IL-19 serum level and the number of warts (P = 0.027). Conclusion: Serum level of IL-19 was significantly lower in patients with warts, and this low level might be crucial for an effective cell mediated immunological response to HPV.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226818","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}
Chunzheng Li, Chenyu Wei, Gongke Zhao, Xianguang Yang
Autophagy is a normal cellular physiological process. As one of the cell degradation systems, it participates in the lysosomal pathway process of degrading damaged proteins and subcellular organelles to maintain cell metabolism and energy states. Moreover, autophagy is essential for regulating organelle quality control and cell homeostasis. In recent decades, a large number of studies have demonstrated that autophagy abnormalities are present in a variety of human malignancies and that autophagy plays a crucial role in all stages of tumor development. Multiple tumors interfere with autophagy's normal regulation and use autophagy's essential properties to restructure their proteome, reprogram their metabolism, and adapt to stress. This article primarily discusses how autophagy either promotes or inhibits cancer development, the significance of autophagy in maintaining cell genome stability, and the role of selective autophagy in the reshaping and quality control of tumor cells.
{"title":"Cancer cells remodeling and quality control are inextricably linked to autophagy","authors":"Chunzheng Li, Chenyu Wei, Gongke Zhao, Xianguang Yang","doi":"10.3934/molsci.2023009","DOIUrl":"https://doi.org/10.3934/molsci.2023009","url":null,"abstract":"Autophagy is a normal cellular physiological process. As one of the cell degradation systems, it participates in the lysosomal pathway process of degrading damaged proteins and subcellular organelles to maintain cell metabolism and energy states. Moreover, autophagy is essential for regulating organelle quality control and cell homeostasis. In recent decades, a large number of studies have demonstrated that autophagy abnormalities are present in a variety of human malignancies and that autophagy plays a crucial role in all stages of tumor development. Multiple tumors interfere with autophagy's normal regulation and use autophagy's essential properties to restructure their proteome, reprogram their metabolism, and adapt to stress. This article primarily discusses how autophagy either promotes or inhibits cancer development, the significance of autophagy in maintaining cell genome stability, and the role of selective autophagy in the reshaping and quality control of tumor cells.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226866","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}
A. Bernardini, Gaia Pellitteri, Giovanni Ermanis, G. Gigli, M. Valente, Francesco Janes
Background REM Behavior Disorder (RBD) is considered one of most powerful prodromal condition in different neurodegenerative disorders, mainly alpha-synucleinopathies. A large amount of research recently explored this relationship. Objective and Design The present critically appraised review undertakes this topic, from the perspective of the pathogenetic interplay between clinical manifestations in RBD patients and the misfolding processes that characterize neurodegeneration. In particular, evidence in favor and against the role of RBD as a biomarker of neurodegeneration is discussed. Results and Conclusion The selected papers were functional to structure the review into three main sections: 1) Protein misfolding in neurodegenerative disorders with focus on alpha-synuclein; 2) Clinical features, diagnosis, and pathophysiology of RBD; 3) RBD as a clinical biomarker of protein misfolding. Data herein highlights the current knowledge and the areas of uncertainties in the relationship between RBD and neurodegenerative disorders; we went through preclinical, prodromal and clinical stages of neurodegenerative processes as a useful reference for clinicians involved in brain pathological aging and future research in this field.
{"title":"Critically appraised topic on Rapid Eye Movement Behavior Disorder: From protein misfolding processes to clinical pathophysiology and conversion to neurodegenerative disorders","authors":"A. Bernardini, Gaia Pellitteri, Giovanni Ermanis, G. Gigli, M. Valente, Francesco Janes","doi":"10.3934/molsci.2023010","DOIUrl":"https://doi.org/10.3934/molsci.2023010","url":null,"abstract":"Background REM Behavior Disorder (RBD) is considered one of most powerful prodromal condition in different neurodegenerative disorders, mainly alpha-synucleinopathies. A large amount of research recently explored this relationship. Objective and Design The present critically appraised review undertakes this topic, from the perspective of the pathogenetic interplay between clinical manifestations in RBD patients and the misfolding processes that characterize neurodegeneration. In particular, evidence in favor and against the role of RBD as a biomarker of neurodegeneration is discussed. Results and Conclusion The selected papers were functional to structure the review into three main sections: 1) Protein misfolding in neurodegenerative disorders with focus on alpha-synuclein; 2) Clinical features, diagnosis, and pathophysiology of RBD; 3) RBD as a clinical biomarker of protein misfolding. Data herein highlights the current knowledge and the areas of uncertainties in the relationship between RBD and neurodegenerative disorders; we went through preclinical, prodromal and clinical stages of neurodegenerative processes as a useful reference for clinicians involved in brain pathological aging and future research in this field.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227380","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}
M. P. Carrera-González, M. J. Ramírez-Expósito, Carmen Guerrero-González, J. Martínez-Martos
One of the diseases more related to the continuous aging of the population is Alzheimer's disease, which is a type of dementia currently without either effective diagnosis biomarkers or treatments. Its higher prevalence in women makes it necessary to study pathways/systems that could participate and/or be involved in its development, as well as those that could be affected by hormonal factors, which, in this case, are estradiol levels. In this sense, one of the systems under study that is gaining special relevance in the scientific community is the brain renin-angiotensin system and its regulatory proteolytic enzymes. This system is strongly modulated by estrogens, and it is also connected with the cerebral glucose metabolism through the angiotensin IV receptor, also recognized as the insulin-regulated aminopeptidase (IRAP). Due to the fact that the cerebral glucose metabolism is highly compromised in patients with Alzheimer's disease, it is necessary to know the elements of the systems and their functions in this process, namely, the cerebral renin-angiotensin system, estradiol and IRAP, an enzyme and receptor co-localized in brain tissue with the insulin-dependent glucose transporter 4 (GLUT4). Knowledge of the connection between them could shed light on the molecular mechanisms of this disease and also provide new diagnostic and therapeutic targets.
{"title":"Alzheimer's disease: Is there a relationship between brain renin-angiotensin system, estradiol and glucose transporter-4 (GLUT-4)?","authors":"M. P. Carrera-González, M. J. Ramírez-Expósito, Carmen Guerrero-González, J. Martínez-Martos","doi":"10.3934/molsci.2023004","DOIUrl":"https://doi.org/10.3934/molsci.2023004","url":null,"abstract":"One of the diseases more related to the continuous aging of the population is Alzheimer's disease, which is a type of dementia currently without either effective diagnosis biomarkers or treatments. Its higher prevalence in women makes it necessary to study pathways/systems that could participate and/or be involved in its development, as well as those that could be affected by hormonal factors, which, in this case, are estradiol levels. In this sense, one of the systems under study that is gaining special relevance in the scientific community is the brain renin-angiotensin system and its regulatory proteolytic enzymes. This system is strongly modulated by estrogens, and it is also connected with the cerebral glucose metabolism through the angiotensin IV receptor, also recognized as the insulin-regulated aminopeptidase (IRAP). Due to the fact that the cerebral glucose metabolism is highly compromised in patients with Alzheimer's disease, it is necessary to know the elements of the systems and their functions in this process, namely, the cerebral renin-angiotensin system, estradiol and IRAP, an enzyme and receptor co-localized in brain tissue with the insulin-dependent glucose transporter 4 (GLUT4). Knowledge of the connection between them could shed light on the molecular mechanisms of this disease and also provide new diagnostic and therapeutic targets.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226665","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}
Sufeng Ruan, SuFei Yang, Jinrong Li, F. Xiong, D. Qie, You Lu, Zhanghui Tang, Fan Yang
Background
Iron deficiency (ID) and ID anemia are widespread in low-income countries, particularly among preterm infants. Hepcidin is a key regulator of iron metabolism, which offers the possibility of new solutions to diagnose ID in premature infants.
Objective
To explore the relationship between iron metabolism and hepcidin in premature infants.
Materials and methods
The study involved 81 preterm infants between 28+1 and 36+6 who underwent iron status indicators and hepcidin testing at 6 months of corrected gestational age. The preterm infants were divided into two groups based on iron status indicators: ID and no ID.
Results
Serum hepcidin was lower for premature infants with ID compared to those without ID (log10hepcidin, 1.18 ± 0.44 vs 1.49 ± 0.37, p = 0.002). A single-variate linear regression model was used to explore the correlation between hepcidin and other indicators of iron metabolism. A strongly positive relationship was observed between hepcidin levels and ferritin levels (p < 0.001) in the correlation analysis.
Conclusions
Hepcidin can be used as an efficient indicator of iron storage and a promising indicator for the early diagnosis of ID in premature infants.
缺铁和缺铁性贫血在低收入国家普遍存在，尤其是在早产儿中。Hepcidin是铁代谢的关键调节因子，这为早产儿ID的诊断提供了新的解决方案。目的探讨早产儿铁代谢与hepcidin的关系。材料与方法本研究纳入81例28+1 ~ 36+6岁的早产儿，在校正胎龄6个月时接受铁状态指标和hepcidin检测。根据铁状态指标将早产儿分为两组:ID组和无ID组。结果有ID早产儿血清hepcidin低于无ID早产儿(log10hepcidin, 1.18±0.44 vs 1.49±0.37,p = 0.002)。采用单变量线性回归模型探讨hepcidin与其他铁代谢指标的相关性。相关分析显示hepcidin水平与铁蛋白水平呈显著正相关(p < 0.001)。结论shepcidin可作为一种有效的铁储存指标，是早期诊断早产儿ID的一种有前景的指标。
{"title":"Hepcidin and iron metabolism in preterm infants","authors":"Sufeng Ruan, SuFei Yang, Jinrong Li, F. Xiong, D. Qie, You Lu, Zhanghui Tang, Fan Yang","doi":"10.3934/molsci.2023008","DOIUrl":"https://doi.org/10.3934/molsci.2023008","url":null,"abstract":"<abstract><sec> <title>Background</title> <p>Iron deficiency (ID) and ID anemia are widespread in low-income countries, particularly among preterm infants. Hepcidin is a key regulator of iron metabolism, which offers the possibility of new solutions to diagnose ID in premature infants.</p> </sec><sec> <title>Objective</title> <p>To explore the relationship between iron metabolism and hepcidin in premature infants.</p> </sec><sec> <title>Materials and methods</title> <p>The study involved 81 preterm infants between 28<sup>+1</sup> and 36<sup>+6</sup> who underwent iron status indicators and hepcidin testing at 6 months of corrected gestational age. The preterm infants were divided into two groups based on iron status indicators: ID and no ID.</p> </sec><sec> <title>Results</title> <p>Serum hepcidin was lower for premature infants with ID compared to those without ID (log<sub>10</sub>hepcidin, 1.18 ± 0.44 vs 1.49 ± 0.37, <italic>p</italic> = 0.002). A single-variate linear regression model was used to explore the correlation between hepcidin and other indicators of iron metabolism. A strongly positive relationship was observed between hepcidin levels and ferritin levels (<italic>p</italic> < 0.001) in the correlation analysis.</p> </sec><sec> <title>Conclusions</title> <p>Hepcidin can be used as an efficient indicator of iron storage and a promising indicator for the early diagnosis of ID in premature infants.</p> </sec></abstract>","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1197 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227123","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}
M. V. Dias-Souza, Arthur Azevedo Perpétuo, Gabriel Souza dos Santos, Luiz Felipe Carreiro Machado, R. D. dos Santos
The scenario of growing microbial resistance and of lack of interest of pharmaceutical companies in developing new antimicrobial drugs jeopardizes the present and the future of the treatment of infectious diseases. Different approaches such as antimicrobial peptides and CRISP-R have been explored to manage this situation, however, they have important limitations such as their high cost. Natural products comprise complex molecular structures for which reports of bacterial resistance are rare. They present specific and/or unspecific mechanisms of action that can be explored to provide safe and effective management of infectious diseases. In this review we assessed phytoextracts with evidence of their benefits for treating infectious diseases in humans and animals, towards the use of data for clinical and experimental purposes. Mechanisms of bacterial resistance to antimicrobials are also discussed.
{"title":"Natural products in drug discovery: meeting the urgency for new antimicrobials for human and veterinary use","authors":"M. V. Dias-Souza, Arthur Azevedo Perpétuo, Gabriel Souza dos Santos, Luiz Felipe Carreiro Machado, R. D. dos Santos","doi":"10.3934/molsci.2023002","DOIUrl":"https://doi.org/10.3934/molsci.2023002","url":null,"abstract":"The scenario of growing microbial resistance and of lack of interest of pharmaceutical companies in developing new antimicrobial drugs jeopardizes the present and the future of the treatment of infectious diseases. Different approaches such as antimicrobial peptides and CRISP-R have been explored to manage this situation, however, they have important limitations such as their high cost. Natural products comprise complex molecular structures for which reports of bacterial resistance are rare. They present specific and/or unspecific mechanisms of action that can be explored to provide safe and effective management of infectious diseases. In this review we assessed phytoextracts with evidence of their benefits for treating infectious diseases in humans and animals, towards the use of data for clinical and experimental purposes. Mechanisms of bacterial resistance to antimicrobials are also discussed.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226939","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}
Amines are abundant in natural product chemistry and are readily available chemical raw materials. The C-N bonds of amines are difficult to break due to the large C-N bond energy. In recent years, chemists have developed a variety of activation methods for amino groups of amines. Among these reported methods, to convert amines into quaternary ammonium salts is preferred, for quaternary ammonium salts are readily available and stable. In recent years, great progress has been achieved in the study of transition metal-catalyzed construction of various C-X bonds involving aromatic amines and benzyl amines-derived quaternary ammonium salts by cleavage of C-N bonds. This review describes the transition metal-catalyzed reaction of quaternary ammonium salts to construct C-X bonds by cleavage of C-N bond. Moreover, if chiral benzylamines-derived quaternary ammonium salts are used, a variety of highly enantiomeric pure chiral organic compounds can also be obtained. The chirality of quaternary ammonium salts remained good in the products and all reactions underwent SN2-type configuration inversion.
{"title":"Transition metal-catalyzed construction of C-X bonds via cleavage of C-N bond of quaternary ammonium salts","authors":"Qingle Zeng, Fuhai Li, Xianjie Yin","doi":"10.3934/molsci.2023011","DOIUrl":"https://doi.org/10.3934/molsci.2023011","url":null,"abstract":"Amines are abundant in natural product chemistry and are readily available chemical raw materials. The C-N bonds of amines are difficult to break due to the large C-N bond energy. In recent years, chemists have developed a variety of activation methods for amino groups of amines. Among these reported methods, to convert amines into quaternary ammonium salts is preferred, for quaternary ammonium salts are readily available and stable. In recent years, great progress has been achieved in the study of transition metal-catalyzed construction of various C-X bonds involving aromatic amines and benzyl amines-derived quaternary ammonium salts by cleavage of C-N bonds. This review describes the transition metal-catalyzed reaction of quaternary ammonium salts to construct C-X bonds by cleavage of C-N bond. Moreover, if chiral benzylamines-derived quaternary ammonium salts are used, a variety of highly enantiomeric pure chiral organic compounds can also be obtained. The chirality of quaternary ammonium salts remained good in the products and all reactions underwent SN2-type configuration inversion.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227447","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}
<abstract> <p>Degenerative nerve diseases affect body's balance, movement, speech, breathing and heart function. Classification of neurodegenerative disorders can be done on the basis of their molecular cause, like abnormal protein aggregation, involved cell death or loss of function of involved cell. Parkinson's disease (PD) is associated with aggregation of α-synuclein, while Alzheimer disease (AD) is associated with <italic>tau</italic>, amyloid-β42 protein aggregation. TDP-43 aggregation was found in Amyloidosis. Besides, Argyrophilic grain disease (AGD); Amyotrophic lateral sclerosis (ALS); Astrocyte plaque (AP); ALS and Parkinsonism-Dementia Complex (<italic>APDC</italic>); Aging-related tau astrogliopathy (<italic>ARTAG</italic>); Ballooned neuron (BN); Cerebral age-related TDP-43 with sclerosis (<italic>CARTS</italic>); Corticobasal degeneration (<italic>CBD</italic>); Chronic traumatic encephalopathy (<italic>CTE</italic>); Dementia with Lewy bodies (<italic>DLB</italic>); Dystrophic neuritis (<italic>DN</italic>); Facial onset sensory and motor neuronopathy (<italic>FOSMN</italic>); Glial cytoplasmic inclusions (GCI); globular glial tauopathy (<italic>GGT</italic>); Guadeloupean Parkinsonism (GP); idiopathic REM sleep behavior disorder (<italic>iRBD</italic>); Limbic-predominant age-related TDP-43 encephalopathy (<italic>LATE</italic>); Lewy bodies (<italic>LB</italic>); Lewy body diseases (<italic>LBD</italic>); Lewy neuritis (<italic>LN</italic>); muscle cells (<italic>MC</italic>); multiple system atrophy (<italic>MSA</italic>); multisystem proteinopathy (<italic>MSP</italic>); Neuronal cytoplasmic inclusions (<italic>NCI</italic>); neurofibrillary tangles (<italic>NFT</italic>); neuronal intranuclear inclusions (<italic>NII</italic>); neuropil threads (<italic>NPT</italic>); Nodding Syndrome (<italic>NS</italic>); oligodendroglial coiled bodies (<italic>OCB</italic>); oligodendroglial Pick's body-like inclusions (<italic>OPiBLI</italic>); pure autonomic failure (<italic>PAF</italic>); primary age-related tauopathy (<italic>PART</italic>); Pick's bodies (<italic>PiB</italic>); Pick's disease (<italic>PiD</italic>); Primary lateral sclerosis (<italic>PLS</italic>); Progressive muscular atrophy (<italic>PMA</italic>); progressive supranuclear palsy (<italic>PSP</italic>); pretangles (<italic>PT</italic>); tufted astrocyte (<italic>TA</italic>), are several neurodegenerative diseases name according to their involved protein factor(s).</p> <p>The cause may be genetic, may also be sporadic. Alcoholism, pesticides, a tumor, or a stroke are sometimes noticed in the disease background. Sometimes the cause remains totally unknown. Neurodegeneration, till date, cannot be cured. Only some palliative treatments may relieve some of the symptoms but temporarily. Further, some types of NDD could also be fatal.</p> <p>Our focus, in this review, is mainly on AD and PD since they vastly affect millions of people in the world, and occurs when nerve cel
{"title":"Molecular mechanisms of neurodegenerative disease (NDD)","authors":"A. Chakraborty, Anil Diwan","doi":"10.3934/molsci.2023012","DOIUrl":"https://doi.org/10.3934/molsci.2023012","url":null,"abstract":"<abstract> <p>Degenerative nerve diseases affect body's balance, movement, speech, breathing and heart function. Classification of neurodegenerative disorders can be done on the basis of their molecular cause, like abnormal protein aggregation, involved cell death or loss of function of involved cell. Parkinson's disease (PD) is associated with aggregation of α-synuclein, while Alzheimer disease (AD) is associated with <italic>tau</italic>, amyloid-β42 protein aggregation. TDP-43 aggregation was found in Amyloidosis. Besides, Argyrophilic grain disease (AGD); Amyotrophic lateral sclerosis (ALS); Astrocyte plaque (AP); ALS and Parkinsonism-Dementia Complex (<italic>APDC</italic>); Aging-related tau astrogliopathy (<italic>ARTAG</italic>); Ballooned neuron (BN); Cerebral age-related TDP-43 with sclerosis (<italic>CARTS</italic>); Corticobasal degeneration (<italic>CBD</italic>); Chronic traumatic encephalopathy (<italic>CTE</italic>); Dementia with Lewy bodies (<italic>DLB</italic>); Dystrophic neuritis (<italic>DN</italic>); Facial onset sensory and motor neuronopathy (<italic>FOSMN</italic>); Glial cytoplasmic inclusions (GCI); globular glial tauopathy (<italic>GGT</italic>); Guadeloupean Parkinsonism (GP); idiopathic REM sleep behavior disorder (<italic>iRBD</italic>); Limbic-predominant age-related TDP-43 encephalopathy (<italic>LATE</italic>); Lewy bodies (<italic>LB</italic>); Lewy body diseases (<italic>LBD</italic>); Lewy neuritis (<italic>LN</italic>); muscle cells (<italic>MC</italic>); multiple system atrophy (<italic>MSA</italic>); multisystem proteinopathy (<italic>MSP</italic>); Neuronal cytoplasmic inclusions (<italic>NCI</italic>); neurofibrillary tangles (<italic>NFT</italic>); neuronal intranuclear inclusions (<italic>NII</italic>); neuropil threads (<italic>NPT</italic>); Nodding Syndrome (<italic>NS</italic>); oligodendroglial coiled bodies (<italic>OCB</italic>); oligodendroglial Pick's body-like inclusions (<italic>OPiBLI</italic>); pure autonomic failure (<italic>PAF</italic>); primary age-related tauopathy (<italic>PART</italic>); Pick's bodies (<italic>PiB</italic>); Pick's disease (<italic>PiD</italic>); Primary lateral sclerosis (<italic>PLS</italic>); Progressive muscular atrophy (<italic>PMA</italic>); progressive supranuclear palsy (<italic>PSP</italic>); pretangles (<italic>PT</italic>); tufted astrocyte (<italic>TA</italic>), are several neurodegenerative diseases name according to their involved protein factor(s).</p> <p>The cause may be genetic, may also be sporadic. Alcoholism, pesticides, a tumor, or a stroke are sometimes noticed in the disease background. Sometimes the cause remains totally unknown. Neurodegeneration, till date, cannot be cured. Only some palliative treatments may relieve some of the symptoms but temporarily. Further, some types of NDD could also be fatal.</p> <p>Our focus, in this review, is mainly on AD and PD since they vastly affect millions of people in the world, and occurs when nerve cel","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227502","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}
Y. Takihara, Ryuji Otani, T. Ishii, Shunsuke Takaoka, Yuki Nakano, Kaori Inoue, S. Larsen, Yoko Ogino, Masashi Asai, S. Tanuma, F. Uchiumi
In cancer, the production of ATP depends mainly on glycolysis, usually accompanied by the dysfunction of the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS). Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for various biological enzymatic reactions such as those involved in the TCA cycle. To investigate the molecular mechanisms involved in carcinogenesis, the transcription system of genes associated with mitochondrial function should be elucidated. In this study, we isolated several mitochondrial function-associated bidirectional promoters and tested whether they responded to NAD+-metabolism regulating compounds, namely, trans-resveratrol (Rsv), 2-deoxy-D-glucose (2DG), 3-amino benzamide (3AB), and olaparib (OLA), in HeLa S3 cells. Transient transfection and luciferase (Luc) reporter assay showed that the IDH1 promoter was prominently activated by these compounds. The IDH1 gene, which encodes a nicotinamide adenine dinucleotide phosphate (NADP+) dependent isocitrate dehydrogenase, is frequently mutated in glioma and leukemia cells. In this study, RT-PCR showed that IDH1 gene and protein expression was induced in response to the NAD+-regulating drugs Rsv and 3AB. However, IDH1 protein amount was rather stable at control level. The result suggested that a post-transcriptional controlling system works to keep IDH1 at a stable level.
{"title":"Characterization of the human IDH1 gene promoter","authors":"Y. Takihara, Ryuji Otani, T. Ishii, Shunsuke Takaoka, Yuki Nakano, Kaori Inoue, S. Larsen, Yoko Ogino, Masashi Asai, S. Tanuma, F. Uchiumi","doi":"10.3934/molsci.2023013","DOIUrl":"https://doi.org/10.3934/molsci.2023013","url":null,"abstract":"In cancer, the production of ATP depends mainly on glycolysis, usually accompanied by the dysfunction of the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS). Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for various biological enzymatic reactions such as those involved in the TCA cycle. To investigate the molecular mechanisms involved in carcinogenesis, the transcription system of genes associated with mitochondrial function should be elucidated. In this study, we isolated several mitochondrial function-associated bidirectional promoters and tested whether they responded to NAD+-metabolism regulating compounds, namely, trans-resveratrol (Rsv), 2-deoxy-D-glucose (2DG), 3-amino benzamide (3AB), and olaparib (OLA), in HeLa S3 cells. Transient transfection and luciferase (Luc) reporter assay showed that the IDH1 promoter was prominently activated by these compounds. The IDH1 gene, which encodes a nicotinamide adenine dinucleotide phosphate (NADP+) dependent isocitrate dehydrogenase, is frequently mutated in glioma and leukemia cells. In this study, RT-PCR showed that IDH1 gene and protein expression was induced in response to the NAD+-regulating drugs Rsv and 3AB. However, IDH1 protein amount was rather stable at control level. The result suggested that a post-transcriptional controlling system works to keep IDH1 at a stable level.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227592","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}
Neurosteroids are essential endogenous compounds which modulate numerous brain-related functions. Neurosteroids affect both the excitatory (glutamate) and the inhibitory (γ-aminobutyric acid, GABA) systems in the brain allowing for the modulation of a wide array of emotions and behaviors. Their synthesis is increased in response to stress, helping the organism to return to homeostasis. Alterations of neurosteroid concentrations therefore have a role in the pathophysiology of stress and stress-related conditions, such as mood (therefore acting on sadness and anger) and anxiety (fear) disorders. Here, we summarize the action of some neuroactive compounds, such as allopregnanolone, pregnanolone, pregnenolone, pregnenolone sulfate and dehydroepiandrosterone, in regulating emotions and outline their current pharmacological use in different pathologies.
{"title":"What do we need to know about neurosteroids and emotions?","authors":"F. di Michele, E. Romeo","doi":"10.3934/molsci.2023006","DOIUrl":"https://doi.org/10.3934/molsci.2023006","url":null,"abstract":"Neurosteroids are essential endogenous compounds which modulate numerous brain-related functions. Neurosteroids affect both the excitatory (glutamate) and the inhibitory (γ-aminobutyric acid, GABA) systems in the brain allowing for the modulation of a wide array of emotions and behaviors. Their synthesis is increased in response to stress, helping the organism to return to homeostasis. Alterations of neurosteroid concentrations therefore have a role in the pathophysiology of stress and stress-related conditions, such as mood (therefore acting on sadness and anger) and anxiety (fear) disorders. Here, we summarize the action of some neuroactive compounds, such as allopregnanolone, pregnanolone, pregnenolone, pregnenolone sulfate and dehydroepiandrosterone, in regulating emotions and outline their current pharmacological use in different pathologies.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":"1 1","pages":""},"PeriodicalIF":1.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226905","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}
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