Pub Date : 2022-12-07DOI: 10.3390/endocrines3040065
Woochul Kim, Ja Kyung Lee, H. Yu, J. Choi
Demand for minimally invasive surgery has driven the development of new gadgets and surgical techniques. Yet, questions about safety and skeptical views on new technology have prevented proliferation of new modes of surgery. This skepticism is perhaps due to unfamiliarity of new fields. Likewise, there are currently various remote-access techniques available for thyroid surgeons that only few regions in the world have adapted. This review will explore the history of minimally invasive techniques in thyroid surgery and introduce new technology to be implemented.
{"title":"Advancements in Thyroidectomy: A Mini Review","authors":"Woochul Kim, Ja Kyung Lee, H. Yu, J. Choi","doi":"10.3390/endocrines3040065","DOIUrl":"https://doi.org/10.3390/endocrines3040065","url":null,"abstract":"Demand for minimally invasive surgery has driven the development of new gadgets and surgical techniques. Yet, questions about safety and skeptical views on new technology have prevented proliferation of new modes of surgery. This skepticism is perhaps due to unfamiliarity of new fields. Likewise, there are currently various remote-access techniques available for thyroid surgeons that only few regions in the world have adapted. This review will explore the history of minimally invasive techniques in thyroid surgery and introduce new technology to be implemented.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43687068","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}
Pub Date : 2022-12-06DOI: 10.3390/endocrines3040064
Neeka Farnoudi, Mimi Lyang, Kees Vanderwyk, Sarah Vreeburg, Clipper F. Young
Diabetes-related distress (DRD) is defined as an emotional state experienced by people with diabetes (PWD) who are worried about their disease management, the emotional burden from the condition, and/or potential difficulties accessing care or support. The psychosocial aspect of diabetes management is a factor that directly influences patients’ well-being as well as the chronic management of the condition yet is not a primary clinical problem being addressed within the healthcare setting. This review advocates for a re-evaluation and subsequent adjustment of the current DRD screening methodology by implementing the five primary components (Intrapersonal, Interpersonal, Organizational, Community, and Public Policy) of the Socio-Ecological Model of Health (SEMH), bridging the gaps from a public-health perspective. We searched two electronic databases for studies published in the United States from 1995 to 2020 reporting the effects of social determinants of health (SDOH) on DRD. Articles that contained at least one of the five elements of the SEMH and focused on adults aged 18 years or older were included. SDOH, which include circumstances where individuals grow, work, and age, are highly influenced by external factors, such as the distribution of wealth, power, and resources. Current DRD screening tools lack the capacity to account for all major components of SDOH in a comprehensive manner. By applying the SEMH as a theory-based framework, a novel DRD screening tool addressing sex, ethnicity, and socioeconomic background should be implemented to better improve diabetes management outcomes. By exploring the relationships between each level of the SEMH and DRD, healthcare professionals will be better equipped to recognize potential stress-inducing factors for individuals managing diabetes. Further efforts should be invested with the goal of developing a novel screening tool founded on the all-encompassing SEMH in order to perpetuate a more comprehensive diabetes treatment plan to address barriers within the SDOH framework.
{"title":"Looking at Diabetes-Related Distress through a New Lens: The Socio-Ecological Health Model","authors":"Neeka Farnoudi, Mimi Lyang, Kees Vanderwyk, Sarah Vreeburg, Clipper F. Young","doi":"10.3390/endocrines3040064","DOIUrl":"https://doi.org/10.3390/endocrines3040064","url":null,"abstract":"Diabetes-related distress (DRD) is defined as an emotional state experienced by people with diabetes (PWD) who are worried about their disease management, the emotional burden from the condition, and/or potential difficulties accessing care or support. The psychosocial aspect of diabetes management is a factor that directly influences patients’ well-being as well as the chronic management of the condition yet is not a primary clinical problem being addressed within the healthcare setting. This review advocates for a re-evaluation and subsequent adjustment of the current DRD screening methodology by implementing the five primary components (Intrapersonal, Interpersonal, Organizational, Community, and Public Policy) of the Socio-Ecological Model of Health (SEMH), bridging the gaps from a public-health perspective. We searched two electronic databases for studies published in the United States from 1995 to 2020 reporting the effects of social determinants of health (SDOH) on DRD. Articles that contained at least one of the five elements of the SEMH and focused on adults aged 18 years or older were included. SDOH, which include circumstances where individuals grow, work, and age, are highly influenced by external factors, such as the distribution of wealth, power, and resources. Current DRD screening tools lack the capacity to account for all major components of SDOH in a comprehensive manner. By applying the SEMH as a theory-based framework, a novel DRD screening tool addressing sex, ethnicity, and socioeconomic background should be implemented to better improve diabetes management outcomes. By exploring the relationships between each level of the SEMH and DRD, healthcare professionals will be better equipped to recognize potential stress-inducing factors for individuals managing diabetes. Further efforts should be invested with the goal of developing a novel screening tool founded on the all-encompassing SEMH in order to perpetuate a more comprehensive diabetes treatment plan to address barriers within the SDOH framework.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41653686","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}
Pub Date : 2022-12-05DOI: 10.3390/endocrines3040063
W. Rossmanith
This review aims at defining the neuroendocrine mechanisms underlying the sport-induced restrictions of the reproductive axis in female athletes. Episodic gonadotropin release was found to be compromised, presumably a result of impaired hypothalamic pulsatile GnRH release. Any deviation from optimal gonadotropin release may result in a suboptimal function of the ovaries, leading to disorders of the menstrual cycle and ovulation. A whole spectrum of menstrual dysfunctions ranging from ovulatory eumenorrhea to luteal phase defects and amenorrhea has been reported in sportive women. As essential neuroendocrine factors underlying these observations, activation of the adrenal axis and altered central nervous neurotransmitter activity have been identified to transfer metabolic, nutritional, and stress signals into the hypothalamic GnRH release. The degree by which the neuroendocrine axis governing reproduction is impaired critically depends on the intensity and duration of exercise and the state of training. Other decisive factors may be energy expenditure and availability, nutritional components, and the maturity of the hypothalamic-pituitary-ovarian (HPO) axis when sport activity was initiated. In conclusion, the gradual cessation of reproductive function observed in female athletes may be interpreted as an adaptive mechanism in response to physical and psychological endurance during sport. This sport-induced restriction of reproductive capacity may serve as protection (endogenous contraception) to preserve a woman’s health.
{"title":"Neuroendocrine Blockade of the Reproductive Axis in Female Athletes","authors":"W. Rossmanith","doi":"10.3390/endocrines3040063","DOIUrl":"https://doi.org/10.3390/endocrines3040063","url":null,"abstract":"This review aims at defining the neuroendocrine mechanisms underlying the sport-induced restrictions of the reproductive axis in female athletes. Episodic gonadotropin release was found to be compromised, presumably a result of impaired hypothalamic pulsatile GnRH release. Any deviation from optimal gonadotropin release may result in a suboptimal function of the ovaries, leading to disorders of the menstrual cycle and ovulation. A whole spectrum of menstrual dysfunctions ranging from ovulatory eumenorrhea to luteal phase defects and amenorrhea has been reported in sportive women. As essential neuroendocrine factors underlying these observations, activation of the adrenal axis and altered central nervous neurotransmitter activity have been identified to transfer metabolic, nutritional, and stress signals into the hypothalamic GnRH release. The degree by which the neuroendocrine axis governing reproduction is impaired critically depends on the intensity and duration of exercise and the state of training. Other decisive factors may be energy expenditure and availability, nutritional components, and the maturity of the hypothalamic-pituitary-ovarian (HPO) axis when sport activity was initiated. In conclusion, the gradual cessation of reproductive function observed in female athletes may be interpreted as an adaptive mechanism in response to physical and psychological endurance during sport. This sport-induced restriction of reproductive capacity may serve as protection (endogenous contraception) to preserve a woman’s health.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41759750","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}
Pub Date : 2022-12-01DOI: 10.3390/endocrines3040050
Ettya R Fremont, Elizabeth A Friedrich, Chris Feudtner, Adda Grimberg, Victoria A Miller
Recombinant human growth hormone (rhGH) is prescribed to youth with growth hormone deficiency (GHD) to support normal growth and ensure healthy physical development, and to youth without GHD to address height concerns. Perceptions of youth involvement in rhGH treatment decisions have not been explored. This study aimed to examine perceptions of youth and parent roles in decisions around rhGH treatment. Youth (n = 22, 11.5 ± 2.0 years) who had undergone evaluation for short stature and their parents (n = 22) participated in semi-structured interviews after stimulation test results had been received. Interviews revealed the following themes: 1) parent provided youth with support; 2) parent facilitated youth's decision-making involvement; 3) youth had no role or did not remember their role; and 4) youth did not remember conversations with their parents or providers. Parents facilitated their children's involvement by sharing information and seeking their opinions. Whereas some participants described youth as having a substantial decision-making role, not all youth felt they were involved, and some youth could not recall conversations about rhGH. Parents can bolster youth involvement by having conversations using developmentally appropriate language, which is critical to youth feeling empowered and developing efficacy over their own care.
{"title":"Perceptions of Youth and Parent Decision-Making Roles Regarding Recombinant Human Growth Hormone Treatment.","authors":"Ettya R Fremont, Elizabeth A Friedrich, Chris Feudtner, Adda Grimberg, Victoria A Miller","doi":"10.3390/endocrines3040050","DOIUrl":"https://doi.org/10.3390/endocrines3040050","url":null,"abstract":"<p><p>Recombinant human growth hormone (rhGH) is prescribed to youth with growth hormone deficiency (GHD) to support normal growth and ensure healthy physical development, and to youth without GHD to address height concerns. Perceptions of youth involvement in rhGH treatment decisions have not been explored. This study aimed to examine perceptions of youth and parent roles in decisions around rhGH treatment. Youth (n = 22, 11.5 ± 2.0 years) who had undergone evaluation for short stature and their parents (n = 22) participated in semi-structured interviews after stimulation test results had been received. Interviews revealed the following themes: 1) parent provided youth with support; 2) parent facilitated youth's decision-making involvement; 3) youth had no role or did not remember their role; and 4) youth did not remember conversations with their parents or providers. Parents facilitated their children's involvement by sharing information and seeking their opinions. Whereas some participants described youth as having a substantial decision-making role, not all youth felt they were involved, and some youth could not recall conversations about rhGH. Parents can bolster youth involvement by having conversations using developmentally appropriate language, which is critical to youth feeling empowered and developing efficacy over their own care.</p>","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":"3 4","pages":"590-600"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10162591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9431174","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}
Pub Date : 2022-12-01DOI: 10.3390/endocrines3040067
Khadeja-Tul Kubra, Mohammad S Akhter, Kaitlyn Apperley, Nektarios Barabutis
Growth hormone-releasing hormone (GHRH) and its receptors are expressed in a variety of human cancers, and have been involved in malignancies. GHRH antagonists (GHRHAnt) were developed to suppress tumor progression and metastasis. Previous studies demonstrate the involvement of reactive oxygen species (ROS) in cancer progression. Herein, we investigate the effect of a commercially available GHRH antagonist, namely JV-1-36, in the redox status of the A549 human cancer cell line. Our results suggest that this peptide significantly reduces ROS production in those cells in a time-dependent manner and counteracts H2O2-induced ROS. Our study supports the anti-oxidative effects of JV-1-36 and contributes in our knowledge towards the in vitro effects of GHRHAnt in cancers.
{"title":"Growth Hormone-Releasing Hormone Antagonist JV-1-36 Suppresses Reactive Oxygen Species Generation in A549 Lung Cancer Cells.","authors":"Khadeja-Tul Kubra, Mohammad S Akhter, Kaitlyn Apperley, Nektarios Barabutis","doi":"10.3390/endocrines3040067","DOIUrl":"https://doi.org/10.3390/endocrines3040067","url":null,"abstract":"<p><p>Growth hormone-releasing hormone (GHRH) and its receptors are expressed in a variety of human cancers, and have been involved in malignancies. GHRH antagonists (GHRHAnt) were developed to suppress tumor progression and metastasis. Previous studies demonstrate the involvement of reactive oxygen species (ROS) in cancer progression. Herein, we investigate the effect of a commercially available GHRH antagonist, namely JV-1-36, in the redox status of the A549 human cancer cell line. Our results suggest that this peptide significantly reduces ROS production in those cells in a time-dependent manner and counteracts H<sub>2</sub>O<sub>2</sub>-induced ROS. Our study supports the anti-oxidative effects of JV-1-36 and contributes in our knowledge towards the in vitro effects of GHRHAnt in cancers.</p>","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":"3 4","pages":"813-820"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9762825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10413622","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}
Pub Date : 2022-12-01DOI: 10.3390/endocrines3040062
Lan Gao, Elise Tan, R. Mariño, Michelle King, Andre Priede, G. Adams, Maria Sicari, M. Moodie
Background: This study assesses the long-term cost-effectiveness of this screening protocol from a healthcare system perspective. Methods: Australians presenting to private oral healthcare practices recruited to the iDENTify study were included as the study population. A Markov model preceded by a decision tree was developed to assess the intervention’s long-term cost-effectiveness when rolled out to all eligible Australians, and measured against ‘no-intervention’ current practice. The model consisted of four health states: normoglycaemia; pre-diabetes; type 2 diabetes and death. Intervention reach of various levels (10%, 20%, 30%, and 40%) were assessed. The model adopted a 30-year lifetime horizon and a 2020 reference year. Costs and benefits were discounted at 5% per annum. Results: If the intervention reached a minimum of 10% of the target population, over the lifetime time horizon, each screened participant would incur a cost of $38,462 and a gain of 10.564 QALYs, compared to $38,469 and 10.561 QALYs for each participant under current practice. Screening was associated with lower costs and higher benefits (a saving of $8 per person and 0.003 QALYs gained), compared to current standard practice without such screening. Between 8 and 34 type 2 diabetes cases would be avoided per 10,000 patients screened if the intervention were taken up by 10% to 40% of private oral healthcare practices. Sensitivity analyses showed consistent results. Conclusions: Implementing type 2 diabetes screening in the private oral healthcare setting using a simple risk assessment tool was demonstrated to be cost-saving. The wider adoption of such screening is recommended.
{"title":"Cost-Effectiveness of Screening to Identify Pre-Diabetes and Diabetes in the Oral Healthcare Setting","authors":"Lan Gao, Elise Tan, R. Mariño, Michelle King, Andre Priede, G. Adams, Maria Sicari, M. Moodie","doi":"10.3390/endocrines3040062","DOIUrl":"https://doi.org/10.3390/endocrines3040062","url":null,"abstract":"Background: This study assesses the long-term cost-effectiveness of this screening protocol from a healthcare system perspective. Methods: Australians presenting to private oral healthcare practices recruited to the iDENTify study were included as the study population. A Markov model preceded by a decision tree was developed to assess the intervention’s long-term cost-effectiveness when rolled out to all eligible Australians, and measured against ‘no-intervention’ current practice. The model consisted of four health states: normoglycaemia; pre-diabetes; type 2 diabetes and death. Intervention reach of various levels (10%, 20%, 30%, and 40%) were assessed. The model adopted a 30-year lifetime horizon and a 2020 reference year. Costs and benefits were discounted at 5% per annum. Results: If the intervention reached a minimum of 10% of the target population, over the lifetime time horizon, each screened participant would incur a cost of $38,462 and a gain of 10.564 QALYs, compared to $38,469 and 10.561 QALYs for each participant under current practice. Screening was associated with lower costs and higher benefits (a saving of $8 per person and 0.003 QALYs gained), compared to current standard practice without such screening. Between 8 and 34 type 2 diabetes cases would be avoided per 10,000 patients screened if the intervention were taken up by 10% to 40% of private oral healthcare practices. Sensitivity analyses showed consistent results. Conclusions: Implementing type 2 diabetes screening in the private oral healthcare setting using a simple risk assessment tool was demonstrated to be cost-saving. The wider adoption of such screening is recommended.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46074070","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}
Pub Date : 2022-11-21DOI: 10.3390/endocrines3040061
S. Kong
Parathyroid carcinoma is a rare disease that needs an additional diagnostic tool and wide therapeutic options. The genomics and proteomics approach may help to find the tools to improve the prognosis of the disease by early detection and metastatic control. The findings from genomics were mainly CDC73, PRUNE2, CCND1, and genes related to PI3K/AKT/mTOR and Wnt pathways. CDC73, PRUNE2, and CCND1 were closely related to each other, and PRUNE2 and CCND1 genes are related to expression levels of parafibromin protein, which may aid in supporting the definite diagnosis of the disease. PI3K/AKT/mTOR and Wnt pathways could be a potential therapeutic target for the disease, which needs further basket trials to prove the concept. In this review, current findings from genomics and proteomics studies in parathyroid carcinoma were reviewed.
{"title":"Updates of Genomics and Proteomics of Parathyroid Carcinoma","authors":"S. Kong","doi":"10.3390/endocrines3040061","DOIUrl":"https://doi.org/10.3390/endocrines3040061","url":null,"abstract":"Parathyroid carcinoma is a rare disease that needs an additional diagnostic tool and wide therapeutic options. The genomics and proteomics approach may help to find the tools to improve the prognosis of the disease by early detection and metastatic control. The findings from genomics were mainly CDC73, PRUNE2, CCND1, and genes related to PI3K/AKT/mTOR and Wnt pathways. CDC73, PRUNE2, and CCND1 were closely related to each other, and PRUNE2 and CCND1 genes are related to expression levels of parafibromin protein, which may aid in supporting the definite diagnosis of the disease. PI3K/AKT/mTOR and Wnt pathways could be a potential therapeutic target for the disease, which needs further basket trials to prove the concept. In this review, current findings from genomics and proteomics studies in parathyroid carcinoma were reviewed.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43789419","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}
Pub Date : 2022-11-07DOI: 10.3390/endocrines3040058
A. Sfera, C. Osorio, S. Hazan, Z. Kozlakidis, J. C. Maldonado, C. M. Zapata-Martín del Campo, Jonathan J. Anton, Leah Rahman, Christina V. Andronescu, G. Nicolson
Similar to previous pandemics, COVID-19 has been succeeded by well-documented post-infectious sequelae, including chronic fatigue, cough, shortness of breath, myalgia, and concentration difficulties, which may last 5 to 12 weeks or longer after the acute phase of illness. Both the psychological stress of SARS-CoV-2 infection and being diagnosed with COVID-19 can upregulate cortisol, a stress hormone that disrupts the efferocytosis effectors, macrophages, and natural killer cells, leading to the excessive accumulation of senescent cells and disruption of biological barriers. This has been well-established in cancer patients who often experience unrelenting fatigue as well as gut and blood–brain barrier dysfunction upon treatment with senescence-inducing radiation or chemotherapy. In our previous research from 2020 and 2021, we linked COVID-19 to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) via angiotensin II upregulation, premature endothelial senescence, intestinal barrier dysfunction, and microbial translocation from the gastrointestinal tract into the systemic circulation. In 2021 and 2022, these hypotheses were validated and SARS-CoV-2-induced cellular senescence as well as microbial translocation were documented in both acute SARS-CoV-2 infection, long COVID, and ME/CFS, connecting intestinal barrier dysfunction to disabling fatigue and specific infectious events. The purpose of this narrative review is to summarize what is currently known about host immune responses to translocated gut microbes and how these responses relate to fatiguing illnesses, including long COVID. To accomplish this goal, we examine the role of intestinal and blood–brain barriers in long COVID and other illnesses typified by chronic fatigue, with a special emphasis on commensal microbes functioning as viral reservoirs. Furthermore, we discuss the role of SARS-CoV-2/Mycoplasma coinfection in dysfunctional efferocytosis, emphasizing some potential novel treatment strategies, including the use of senotherapeutic drugs, HMGB1 inhibitors, Toll-like receptor 4 (TLR4) blockers, and membrane lipid replacement.
{"title":"Long COVID and the Neuroendocrinology of Microbial Translocation Outside the GI Tract: Some Treatment Strategies","authors":"A. Sfera, C. Osorio, S. Hazan, Z. Kozlakidis, J. C. Maldonado, C. M. Zapata-Martín del Campo, Jonathan J. Anton, Leah Rahman, Christina V. Andronescu, G. Nicolson","doi":"10.3390/endocrines3040058","DOIUrl":"https://doi.org/10.3390/endocrines3040058","url":null,"abstract":"Similar to previous pandemics, COVID-19 has been succeeded by well-documented post-infectious sequelae, including chronic fatigue, cough, shortness of breath, myalgia, and concentration difficulties, which may last 5 to 12 weeks or longer after the acute phase of illness. Both the psychological stress of SARS-CoV-2 infection and being diagnosed with COVID-19 can upregulate cortisol, a stress hormone that disrupts the efferocytosis effectors, macrophages, and natural killer cells, leading to the excessive accumulation of senescent cells and disruption of biological barriers. This has been well-established in cancer patients who often experience unrelenting fatigue as well as gut and blood–brain barrier dysfunction upon treatment with senescence-inducing radiation or chemotherapy. In our previous research from 2020 and 2021, we linked COVID-19 to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) via angiotensin II upregulation, premature endothelial senescence, intestinal barrier dysfunction, and microbial translocation from the gastrointestinal tract into the systemic circulation. In 2021 and 2022, these hypotheses were validated and SARS-CoV-2-induced cellular senescence as well as microbial translocation were documented in both acute SARS-CoV-2 infection, long COVID, and ME/CFS, connecting intestinal barrier dysfunction to disabling fatigue and specific infectious events. The purpose of this narrative review is to summarize what is currently known about host immune responses to translocated gut microbes and how these responses relate to fatiguing illnesses, including long COVID. To accomplish this goal, we examine the role of intestinal and blood–brain barriers in long COVID and other illnesses typified by chronic fatigue, with a special emphasis on commensal microbes functioning as viral reservoirs. Furthermore, we discuss the role of SARS-CoV-2/Mycoplasma coinfection in dysfunctional efferocytosis, emphasizing some potential novel treatment strategies, including the use of senotherapeutic drugs, HMGB1 inhibitors, Toll-like receptor 4 (TLR4) blockers, and membrane lipid replacement.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41367845","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}
Pub Date : 2022-11-01DOI: 10.3390/endocrines3040057
J. Aseervatham
14-3-3s are a family of structurally similar proteins that bind to phosphoserine or phosphothreonine residues, forming the central signaling hub that coordinates or integrates various cellular functions, thereby controlling many pathways important in cancer, cell motility, cell death, cytoskeletal remodeling, neuro-degenerative disorders and many more. Their targets are present in all cellular compartments, and when they bind to proteins they alter their subcellular localization, stability, and molecular interactions with other proteins. Changes in environmental conditions that result in altered homeostasis trigger the interaction between 14-3-3 and other proteins to retrieve or rescue homeostasis. In circumstances where these regulatory proteins are dysregulated, it leads to pathological conditions. Therefore, deeper understanding is needed on how 14-3-3 proteins bind, and how these proteins are regulated or modified. This will help to detect disease in early stages or design inhibitors to block certain pathways. Recently, more research has been devoted to identifying the role of MicroRNAs, and long non-coding RNAs, which play an important role in regulating gene expression. Although there are many reviews on the role of 14-3-3 proteins in cancer, they do not provide a holistic view of the changes in the cell, which is the focus of this review. The unique feature of the review is that it not only focuses on how the 14-3-3 subunits associate and dissociate with their binding and regulatory proteins, but also includes the role of micro-RNAs and long non-coding RNAs and how they regulate 14-3-3 isoforms. The highlight of the review is that it focuses on the role of 14-3-3, actin, actin binding proteins and Rho GTPases in cancer, and how this complex is important for cell migration and invasion. Finally, the reader is provided with super-resolution high-clarity images of each subunit of the 14-3-3 protein family, further depicting their distribution in HeLa cells to illustrate their interactions in a cancer cell.
{"title":"Interactions between 14-3-3 Proteins and Actin Cytoskeleton and Its Regulation by microRNAs and Long Non-Coding RNAs in Cancer","authors":"J. Aseervatham","doi":"10.3390/endocrines3040057","DOIUrl":"https://doi.org/10.3390/endocrines3040057","url":null,"abstract":"14-3-3s are a family of structurally similar proteins that bind to phosphoserine or phosphothreonine residues, forming the central signaling hub that coordinates or integrates various cellular functions, thereby controlling many pathways important in cancer, cell motility, cell death, cytoskeletal remodeling, neuro-degenerative disorders and many more. Their targets are present in all cellular compartments, and when they bind to proteins they alter their subcellular localization, stability, and molecular interactions with other proteins. Changes in environmental conditions that result in altered homeostasis trigger the interaction between 14-3-3 and other proteins to retrieve or rescue homeostasis. In circumstances where these regulatory proteins are dysregulated, it leads to pathological conditions. Therefore, deeper understanding is needed on how 14-3-3 proteins bind, and how these proteins are regulated or modified. This will help to detect disease in early stages or design inhibitors to block certain pathways. Recently, more research has been devoted to identifying the role of MicroRNAs, and long non-coding RNAs, which play an important role in regulating gene expression. Although there are many reviews on the role of 14-3-3 proteins in cancer, they do not provide a holistic view of the changes in the cell, which is the focus of this review. The unique feature of the review is that it not only focuses on how the 14-3-3 subunits associate and dissociate with their binding and regulatory proteins, but also includes the role of micro-RNAs and long non-coding RNAs and how they regulate 14-3-3 isoforms. The highlight of the review is that it focuses on the role of 14-3-3, actin, actin binding proteins and Rho GTPases in cancer, and how this complex is important for cell migration and invasion. Finally, the reader is provided with super-resolution high-clarity images of each subunit of the 14-3-3 protein family, further depicting their distribution in HeLa cells to illustrate their interactions in a cancer cell.","PeriodicalId":72908,"journal":{"name":"Endocrines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41984300","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}
Pub Date : 2022-10-21DOI: 10.3390/endocrines3040056
R. Okawa, K. Nakano
X-linked hypophosphatemia (XLH) is the most common genetic form of rickets and osteomalacia and is characterized by growth retardation, deformities of the lower limbs, and bone and muscular pain. Spontaneous dental abscesses caused by endodontic infections due to dentin dysplasia are well-known dental manifestations. When dentin affected by microcracks or attrition of the enamel is exposed to oral fluids, oral bacteria are able to invade the hypomineralized dentin and pulp space, leading to pulp necrosis, followed by the formation of a periapical gingival abscess. Without appropriate dental management, this dental manifestation results in early loss of teeth and deterioration in the patient’s quality of life. Early specific dental intervention and oral management in collaboration with medical personnel are strongly recommended for XLH patients. Importantly, dental manifestations sometimes appear before the diagnosis of XLH. Dentists should be alert for this first sign of XLH and refer affected children to a pediatrician for early diagnosis. A humanized monoclonal antibody for FGF23 (burosumab) is a promising new treatment for XLH; however, the effects on the dental manifestations remain to be elucidated. The establishment of fundamental dental therapy to solve dental problems is still underway and is eagerly anticipated.
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