Публикации о генах и старении (titles) - История изменений

Denis.s: Denis.s переименовал страницу Публикации о генах и старении в Публикации о генах и старении (titles): Не хватает места все вместить в одной статье, несмотря на увеличение лимита в LocalSettings.php, теперь кочевряжится MySQL

2021-03-26T15:03:34Z

Denis.s переименовал страницу Публикации о генах и старении в Публикации о генах и старении (titles): Не хватает места все вместить в одной статье, несмотря на увеличение лимита в LocalSettings.php, теперь кочевряжится MySQL

← Предыдущая версия	Версия от 18:03, 26 марта 2021
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Denis.s в 14:16, 26 марта 2021

2021-03-26T14:16:34Z

Внесённые изменения

Denis.s в 20:01, 25 марта 2021

2021-03-25T20:01:31Z

Внесённые изменения

Denis.s в 20:32, 22 марта 2021

2021-03-22T20:32:22Z

Внесённые изменения

Denis.s в 20:19, 22 марта 2021

2021-03-22T20:19:56Z

Внесённые изменения

Denis.s в 18:23, 22 марта 2021

2021-03-22T18:23:04Z

← Предыдущая версия		Версия от 21:23, 22 марта 2021
Строка 17:		Строка 17:
	\|title=How Does SARS-CoV-2 Affect the Central Nervous System? A Working Hypothesis.		\|title=How Does SARS-CoV-2 Affect the Central Nervous System? A Working Hypothesis.
	\|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33304284		\|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33304284
	\|abstract=Interstitial pneumonia was the first manifestation to be recognized as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); however, in just a few weeks, it became clear that the coronavirus disease-2019 (COVID-19) overrun tissues and more body organs than just the lungs, so much so that it could be considered a systemic pathology. Several studies reported the involvement of the conjunctiva, the gut, the heart and its pace, and vascular injuries such as thromboembolic complications and Kawasaki disease in children and toddlers were also described. More recently, it was reported that in a sample of 214 SARS-CoV-2 positive patients, 36.4% complained of neurological symptoms ranging from non-specific manifestations (dizziness, headache, and seizures), to more specific symptoms such hyposmia or hypogeusia, and stroke. Older individuals, especially males with comorbidities, appear to be at the highest risk of developing such severe complications related to the Central Nervous System (CNS) involvement. Neuropsychiatric manifestations in COVID-19 appear to develop in patients with and without pre-existing neurological disorders. Growing evidence suggests that SARS-CoV-2 binds to the human Angiotensin-Converting Enzyme 2 ([[ACE2]]) for the attachment and entrance inside host cells. By describing [[ACE2]] and the whole Renin Angiotensin Aldosterone System (RAAS) we may better understand whether specific cell types may be affected by SARS-CoV-2 and whether their functioning can be disrupted in case of an infection. Since clear evidences of neurological interest have already been shown, by clarifying the topographical distribution and density of [[ACE2]], we will be able to speculate how SARS-CoV-2 may affect the CNS and what is the pathogenetic mechanism by which it contributes to the specific clinical manifestations of the disease. Based on such evidences, we finally hypothesize the process of SARS-CoV-2 invasion of the CNS and provide a possible explanation for the onset or the exacerbation of some common neuropsychiatric disorders in the elderly including cognitive impairment and Alzheimer disease.		\|abstract=Interstitial pneumonia was the first manifestation to be recognized as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); however, in just a few weeks, it became clear that the coronavirus disease-2019 (COVID-19) overrun tissues and more body organs than just the lungs, so much so that it could be considered a systemic pathology. Several studies reported the involvement of the conjunctiva, the gut, the heart and its pace, and vascular injuries such as thromboembolic complications and Kawasaki disease in children and toddlers were also described. More recently, it was reported that in a sample of 214 SARS-CoV-2 positive patients, 36.4% complained of neurological symptoms ranging from non-specific manifestations (dizziness, headache, and seizures), to more specific symptoms such hyposmia or hypogeusia, and stroke. Older individuals, especially males with comorbidities, appear to be at the highest risk of developing such severe complications related to the Central Nervous System (CNS) involvement. Neuropsychiatric manifestations in COVID-19 appear to develop in patients with and without pre-existing neurological disorders. Growing evidence suggests that SARS-CoV-2 binds to the human Angiotensin-Converting Enzyme 2 ([[ACE2]]) for the attachment and entrance inside host cells. By describing [[ACE2]] and the whole Renin Angiotensin Aldosterone System (RAAS) we may better understand whether specific cell types may be affected by SARS-CoV-2 and whether their functioning can be disrupted in case of an infection. Since clear evidences of neurological interest have already been shown, by clarifying the topographical distribution and density of [[ACE2]], we will be able to speculate how SARS-CoV-2 may affect the CNS and what is the pathogenetic mechanism by which it contributes to the specific clinical manifestations of the disease. Based on such evidences, we finally hypothesize the process of SARS-CoV-2 invasion of the CNS and provide a possible explanation for the onset or the exacerbation of some common neuropsychiatric disorders in the elderly including cognitive impairment and Alzheimer disease.

	\|keywords=* ACE2		\|keywords=* ACE2
	* Alzheimer disease		* Alzheimer disease

Denis.s в 14:37, 21 марта 2021

2021-03-21T14:37:22Z

Внесённые изменения

Denis.s в 13:18, 21 марта 2021

2021-03-21T13:18:05Z

← Предыдущая версия		Версия от 16:18, 21 марта 2021
Строка 16:		Строка 16:
	\|title=Innate and Adaptive Immunity in Aging and Longevity: The Foundation of Resilience.		\|title=Innate and Adaptive Immunity in Aging and Longevity: The Foundation of Resilience.
	\|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33269094		\|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33269094
	\|abstract=The interrelation of the processes of immunity and senescence now receives an unprecedented emphasis during the COVID-19 pandemic, which brings to the fore the critical need to combat immunosenescence and improve the immune function and resilience of older persons. Here we review the historical origins and the current state of the science of innate and adaptive immunity in aging and longevity. From the modern point of view, innate and adaptive immunity are not only affected by aging but also are important parts of its underlying mechanisms. Excessive levels or activity of antimicrobial peptides, C-reactive protein, complement system, TLR/NF-κB, cGAS/STING/IFN 1,3 and AGEs/RAGE pathways, myeloid cells and [[NLRP3]] inflammasome, declined levels of NK cells in innate immunity, thymus involution and decreased amount of naive T-cells in adaptive immunity, are biomarkers of aging and predisposition factors for cellular senescence and aging-related pathologies. Long-living species, human centenarians, and women are characterized by less inflamm-aging and decelerated immunosenescence. Despite recent progress in understanding, the harmonious theory of immunosenescence is still developing. Geroprotectors targeting these mechanisms are just emerging and are comprehensively discussed in this article.		\|abstract=The interrelation of the processes of immunity and senescence now receives an unprecedented emphasis during the COVID-19 pandemic, which brings to the fore the critical need to combat immunosenescence and improve the immune function and resilience of older persons. Here we review the historical origins and the current state of the science of innate and adaptive immunity in aging and longevity. From the modern point of view, innate and adaptive immunity are not only affected by aging but also are important parts of its underlying mechanisms. Excessive levels or activity of antimicrobial peptides, C-reactive protein, complement system, TLR/NF-κB, cGAS/STING/IFN 1 and AGEs/RAGE pathways, myeloid cells and [[NLRP3]] inflammasome, declined levels of NK cells in innate immunity, thymus involution and decreased amount of naive T-cells in adaptive immunity, are biomarkers of aging and predisposition factors for cellular senescence and aging-related pathologies. Long-living species, human centenarians, and women are characterized by less inflamm-aging and decelerated immunosenescence. Despite recent progress in understanding, the harmonious theory of immunosenescence is still developing. Geroprotectors targeting these mechanisms are just emerging and are comprehensively discussed in this article.

	\|keywords=* adaptive immunity		\|keywords=* adaptive immunity

Denis.s в 13:15, 21 марта 2021

2021-03-21T13:15:19Z

← Предыдущая версия		Версия от 16:15, 21 марта 2021
Строка 1:		Строка 1:
	__NOTOC__		__NOTOC__

	{{medline-entry		{{medline-entry
	\|title=[[MYSM1]] Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.		\|title=[[MYSM1]] Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.

Denis.s в 13:12, 21 марта 2021

2021-03-21T13:12:18Z

← Предыдущая версия		Версия от 16:12, 21 марта 2021
Строка 11:		Строка 11:
	* senescence		* senescence
	* senescence‐associated secretory phenotype (SASP)		* senescence‐associated secretory phenotype (SASP)
	\|~~pmc~~-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7675055		\|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7675055
	}}		}}

Строка 24:		Строка 24:
	* longevity		* longevity
	* resilience		* resilience
	\|~~pmc~~-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673842		\|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673842
	}}		}}

Строка 42:		Строка 42:
	* red wine		* red wine
	* salt		* salt
			\|full-text-url=https://sci-hub.do/10.3233/JAD-201058
	}}		}}

Строка 55:		Строка 55:
	* Hematopoietic stem/progenitor cells		* Hematopoietic stem/progenitor cells
	* Ischemia		* Ischemia
	\|~~pmc~~-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694587		\|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694587
	}}		}}

Строка 69:		Строка 69:
	* Structural equation modelling		* Structural equation modelling
	* Telomere length		* Telomere length
	\|~~pmc~~-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713168		\|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713168
	}}		}}

Строка 83:		Строка 83:
	* resistance training		* resistance training
	* sarcopenia		* sarcopenia
			\|full-text-url=https://sci-hub.do/10.1093/gerona/glaa309
	}}		}}

Строка 95:		Строка 95:
	* European Portuguese		* European Portuguese
	* Oral vowel		* Oral vowel
			\|full-text-url=https://sci-hub.do/10.1016/j.jvoice.2020.10.021
	}}		}}

Строка 108:		Строка 108:
	* protein homeostasis		* protein homeostasis
	* senescence		* senescence
			\|full-text-url=https://sci-hub.do/10.1073/pnas.2018138117
	}}		}}

Строка 122:		Строка 122:
	* WRKY46		* WRKY46
	* WRKY6		* WRKY6
			\|full-text-url=https://sci-hub.do/10.1111/jipb.13044
	}}		}}

Строка 140:		Строка 140:
	* placenta		* placenta
	* senescence		* senescence
	\|~~pmc~~-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712261		\|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712261
	}}		}}