Role of the circulation in the systemic effects of low-light therapy

2010 ◽  
Author(s):  
M. Dyson
Keyword(s):  
Light Therapy ◽  
Systemic Effects ◽  
Low Light

Decoding the Inter-relationship between Sleep Disorders and Alzheimer’s disease Pathogenesis

2020 ◽  
Vol 19 ◽  
Author(s):  
Zeba Mueed ◽  
Pankaj Kumar Rai ◽  
Mohammad A. Kamal ◽  
Nitesh Kumar Poddar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Disorders ◽  
Sleep Disturbances ◽  
Mammalian Target Of Rapamycin ◽  
Light Therapy ◽  
Paired Helical Filaments ◽  
Bidirectional Relationship ◽  
Causative Agents

Alzheimer’s disease (AD), characterized by abnormally phosphorylated tau, paired helical filaments (PHFs), neurofibrillary tangles (NFTs), deregulated mammalian target of rapamycin (mTOR), Aβ deposits, is a multifactorial disease with sleep disorders being one of the causative agents. Therefore, we have reviewed the literature and have tried to decode the existence of positive feedback, reciprocal and a bidirectional relationship allying between sleep disturbances and AD. Much light has been thrown on the role of tau pathology and amyloid pathology in sleep pathology and its association with AD pathology. We have also discussed the role of melatonin in regulating sleep disorders and AD. The neuroprotective action of melatonin via inhibiting tau hyperphosphorylation and Aβ deposition has also been pondered upon. Moreover, astrocytes involvement in aggravating AD has also been highlighted in this review. Several therapeutic approaches aimed at improving both sleep disorders and AD have been duly discussed such as administration of antidepressants and antihistamines, immunotherapy, metal chelators, melatonin supplementation, light therapy and physical activity. Despite consistent efforts, the complete etiology concerning sleep disorder and AD is still unclear. Therefore, further research is needed to unravel the mechanism involved and also to develop strategies that may help in obstructing AD in its preclinical stage.

Cholinergic regulation of human proximal duodenal mucosal bicarbonate secretion

1991 ◽  
Vol 261 (2) ◽  
pp. G327-G331 ◽  
Author(s):  
M. A. Ballesteros ◽  
J. D. Wolosin ◽  
D. L. Hogan ◽  
M. A. Koss ◽  
J. I. Isenberg
Keyword(s):  
Vagal Stimulation ◽  
Duodenal Bulb ◽  
Cholinergic Innervation ◽  
Systemic Effects ◽  
Cholinergic Stimulation ◽  
Sham Feeding ◽  
Peak Response ◽  
Cholinergic Regulation ◽  
Upper Gastrointestinal

Cephalic-vagal stimulation affects a number of upper gastrointestinal secretory and motility events. The purpose of this study was to examine the role of vagal-cholinergic regulation on human proximal duodenal mucosal HCO-3 secretion. The duodenal bulb was isolated between balloons and perfused with 154 mM NaCl, and HCO-3 secretion was measured. Although cholinergic stimulation with bethanechol (50 micrograms.kg-1.h-1 iv) produced systemic effects, resting HCO-3 secretion was unchanged. Cephalic-vagal stimulation, induced by sham feeding, significantly increased duodenal HCO-3 secretion from a basal of 177 +/- 17 to 240 +/- 19 mumols.cm-1.h-1 (P less than 0.02). The response to sham feeding was approximately 50% of the peak response to acid-stimulated HCO-3 output. Atropine (22 micrograms/kg iv) inhibited basal HCO-3 secretion significantly (79 +/- 5%). However, the net incremental increases in duodenal mucosal HCO-3 secretion in response to luminal acidification and vagal stimulation were unaltered by atropine pretreatment. Additionally, indomethacin (100 mg po) failed to modify the response to vagal-stimulated HCO-3 secretion. These findings indicate that basal human proximal duodenal mucosal HCO-3 secretion is maintained largely by resting cholinergic innervation and is stimulated by cephalic-vagal stimulation. Furthermore, since the incremental HCO-3 responses to cephalic-vagal stimulation and luminal acidification were unaltered by atropine pretreatment, each is likely mediated by noncholinergic mechanisms.

The Sympathetic Nervous System and Pain

2018 ◽  
pp. 155-178 ◽  
Author(s):  
Judith A. Strong ◽  
Jun-Ming Zhang ◽  
Hans-Georg Schaible
Keyword(s):  
Sensory System ◽  
Sympathetic Nerves ◽  
Systemic Effects ◽  
Preclinical Studies ◽  
Preclinical Models ◽  
Immune Tissues ◽  
Sympathetic Nervous ◽  
The Many ◽  
Chronic Pain Conditions

This article reviews some of the preclinical studies of the sympathetic nervous system’s role in arthritis, inflammatory, and neuropathic pain, in light of the emerging understanding of how the immune system, sensory system, and sympathetic system markedly affect each other’s function, with many mechanisms besides sprouting. Many studies show a pro-inflammatory and pro-nociceptive role for the sympathetic nerves in preclinical models. However, these studies are sometimes conflicting, and the role of the sympathetic nerves can sometimes be anti-inflammatory or anti-nociceptive, particularly at later stages or when systemic effects on immune tissues are considered. The article discusses human correlates of these preclinical studies, as well as some possible reasons for the many conflicting studies in the literature. The article argues that sympathetic-based interventions for chronic pain conditions hold promise despite the conflicting findings in the field, especially if better ways to define appropriate subsets of patients can be developed.

The Role of Bright Light Therapy in Managing Insomnia

2013 ◽  
Vol 8 (3) ◽  
pp. 351-359 ◽  
Author(s):  
Nicole Lovato ◽  
Leon Lack
Keyword(s):  
Bright Light ◽  
Light Therapy ◽  
Bright Light Therapy

scholarly journals Regulation of Life Span by The Gut Microbiota in The Short-Lived African Turquoise Killifish

2017 ◽  
Author(s):  
Patrick Smith ◽  
David Willemsen ◽  
Miriam Popkes ◽  
Franziska Metge ◽  
Edson Gandiwa ◽  
...  
Keyword(s):  
Bacterial Community ◽  
Gut Microbiota ◽  
Life Span ◽  
Middle Age ◽  
External Environment ◽  
Systemic Effects ◽  
Life Span Extension ◽  
Nothobranchius Furzeri ◽  
Vertebrate Model

ABSTRACTGut bacteria occupy the interface between the organism and the external environment, contributing to homeostasis and disease. Yet, the causal role of the gut microbiota during host aging is largely unexplored. Here, using the African turquoise killifish (Nothobranchius furzeri), a naturally short-lived vertebrate, we show that the gut microbiota plays a key role in modulating vertebrate life span. Recolonizing the gut of middle-age individuals with bacteria from young donors resulted in life span extension and delayed behavioral decline. This intervention prevented the decrease in microbial diversity associated with host aging and maintained a young-like gut bacterial community, characterized by overrepresentation of the key genera Exiguobacterium, Planococcus, Propionigenium and Psychrobacter. Our findings demonstrate that the natural microbial gut community of young individuals can causally induce long-lasting beneficial systemic effects that lead to life span extension in a vertebrate model.

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