Collection of Dim Light for Accurate Optical Polarimetry by a Plano-Convex Spherical Lens

Author(s):  
Keith Foreman ◽  
Timothy J. Gay
Keyword(s):  
1992 ◽  
Vol 47 (11-12) ◽  
pp. 915-921 ◽  
Author(s):  
Henmg Stieve ◽  
Barbara Niemeyer ◽  
Klaus Aktories ◽  
Heidi E. Hamm

We have tested the action of three agents microinjected into the ventral nerve photoreceptor of Limulus on the electrical response to dim light. 1. A monoclonal antibody (mAb 4 A) against the Gɑ subunit of frog transducin reduces the size of the receptor current to 60%, suggesting an interaction with Gɑ in the Limulus photoreceptor. 2. Injection of Clostridium botulinum ADPribosyltransferase C 3 reduces the size to 46%; latency is not affected. The results imply that small GTP-binding proteins play a functional role in photoreception of invertebrates. 3. Injection of GD P-β-S reduces dose-dependently the size of the receptor current to 15% and prolongs the latency to 200%, presumably by reducing number and rate of G-protein activations


2021 ◽  
Vol 2 (3) ◽  
pp. 1-15
Author(s):  
Cheng Wan ◽  
Andrew W. Mchill ◽  
Elizabeth B. Klerman ◽  
Akane Sano

Circadian rhythms influence multiple essential biological activities, including sleep, performance, and mood. The dim light melatonin onset (DLMO) is the gold standard for measuring human circadian phase (i.e., timing). The collection of DLMO is expensive and time consuming since multiple saliva or blood samples are required overnight in special conditions, and the samples must then be assayed for melatonin. Recently, several computational approaches have been designed for estimating DLMO. These methods collect daily sampled data (e.g., sleep onset/offset times) or frequently sampled data (e.g., light exposure/skin temperature/physical activity collected every minute) to train learning models for estimating DLMO. One limitation of these studies is that they only leverage one time-scale data. We propose a two-step framework for estimating DLMO using data from both time scales. The first step summarizes data from before the current day, whereas the second step combines this summary with frequently sampled data of the current day. We evaluate three moving average models that input sleep timing data as the first step and use recurrent neural network models as the second step. The results using data from 207 undergraduates show that our two-step model with two time-scale features has statistically significantly lower root-mean-square errors than models that use either daily sampled data or frequently sampled data.


Diseases ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 18
Author(s):  
Rüdiger Hardeland

Melatonin has been used preclinically and clinically for different purposes. Some applications are related to readjustment of circadian oscillators, others use doses that exceed the saturation of melatonin receptors MT1 and MT2 and are unsuitable for chronobiological purposes. Conditions are outlined for appropriately applying melatonin as a chronobiotic or for protective actions at elevated levels. Circadian readjustments require doses in the lower mg range, according to receptor affinities. However, this needs consideration of the phase response curve, which contains a silent zone, a delay part, a transition point and an advance part. Notably, the dim light melatonin onset (DLMO) is found in the silent zone. In this specific phase, melatonin can induce sleep onset, but does not shift the circadian master clock. Although sleep onset is also under circadian control, sleep and circadian susceptibility are dissociated at this point. Other limits of soporific effects concern dose, duration of action and poor individual responses. The use of high melatonin doses, up to several hundred mg, for purposes of antioxidative and anti-inflammatory protection, especially in sepsis and viral diseases, have to be seen in the context of melatonin’s tissue levels, its formation in mitochondria, and detoxification of free radicals.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A45-A46
Author(s):  
Skyler Kanegi ◽  
Armen Akopian

Abstract Introduction The combination of artificial light and lack of exposure to natural light can delay the circadian clock, dysregulate the circadian cycle, and decrease alertness upon waking. This effect has been especially significant during the COVID-19 pandemic, where overexposure to artificial light at improper hours has contributed to increased rates of clinical insomnia. Artificial light may also contribute to concomitant neurological conditions such as primary headache, but the mechanisms by which light triggers sleep deprivation-induced headache are not well-understood. Methods To measure pain sensitivity, we habituated 13 wild-type male mice to von Frey filaments applied to the periorbital area until there was no response to 0.6g stimulus. We then applied 5 lux of continuous dim light to mice during their usual 12-hour dark cycle. The 12-hour light cycle remained unchanged with 200 lux continuous light. Three groups of mice experienced the dim light stimulus for one, three, or five consecutive days. Ambulation and rest activity were measured using SOF-812 Activity Monitor machines. After the experiment concluded, we waited 24 hours and measured mechanical threshold using von Frey filaments at 1, 3, 5, 8, and every 3 days subsequently until mice no longer responded to 0.6g stimulus. Results Artificial light triggered changes in circadian behavior including increased number of rest periods during 12-hour dark (dim light) cycle and shortened sleep duration during 12-hour light cycle. Following the artificial light stimulus, there was a significant decrease in mechanical threshold (P<0.05), representing allodynia. The one-day group displayed one day of significant allodynia. The three-day group displayed three days of significant allodynia. The five-day group displayed five days of significant allodynia. Conclusion Artificial light may trigger circadian dysregulation, and the duration of artificial light exposure seemed to be directly correlated to the duration of allodynia up to one week after the stimulus was removed. We will repeat these experiments and analyze CNS and PNS tissue samples to understand the underlying physiological and biochemical bases of how artificial light triggers sleep deprivation-induced headache. This knowledge could increase our understanding of the pathophysiology and comorbidity of sleep deprivation and headache. Support (if any) Funding was received from the National Institute of Health (NS104200).


2009 ◽  
Vol 10 (5) ◽  
pp. 549-555 ◽  
Author(s):  
Shadab A. Rahman ◽  
Leonid Kayumov ◽  
Ekaterina A. Tchmoutina ◽  
Colin M. Shapiro

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