Reply [to “Comments on Paper by C. R. Holmes, M. Brook, P. Krehbiel, and R. McCrory, ‘On the power spectrum and mechanisms of thunder’”]

Holmes, C. R.; Brook, M.; Krehbiel, P. R.; McCrory, R.

doi:10.1029/jc076i030p07443

Cited by 18 publications

(20 citation statements)

References 3 publications

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“…The expression of these two enzymes has been confirmed in extracts of the whole rat CB (Salman et al 2016). Adenosine causes chemostimulation by either increasing type 1 cell excitability (via A 2A and/or A 2B receptors) (Conde et al 2006(Conde et al , 2008Xu et al 2006;Livermore & Nurse, 2013) or by directly activating postsynaptic sensory fibres (via A 2A receptor stimulation) (Conde et al 2006), with both mechanisms acting to increase cAMP (Nunes et al 2014;Holmes et al 2015). Alternatively, it has been proposed that adenosine may be formed in the type 1 cell and then is released directly into the synapse through the bidirectional equilibrative nucleotide transporter (ENT) (Cass et al 1998).…”

Section: Introductionmentioning

confidence: 88%

Ecto‐5′‐nucleotidase (CD73) regulates peripheral chemoreceptor activity and cardiorespiratory responses to hypoxia

Holmes

Ray

Pearson

et al. 2017

The Journal of Physiology

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Augmented sensory neuronal activity from the carotid body (CB) has emerged as a principal cause of hypertension in a number of cardiovascular related pathologies, including obstructive sleep apnoea, heart failure and diabetes. Development of new targets and pharmacological treatment strategies aiming to reduce CB sensory activity may thus improve outcomes in these key patient cohorts. The present study investigated whether ecto-5'-nucleotidase (CD73), an enzyme that generates adenosine, is functionally important in modifying CB sensory activity and cardiovascular respiratory responses to hypoxia. Inhibition of CD73 by α,β-methylene ADP (AOPCP) in the whole CB preparation in vitro reduced basal discharge frequency by 76 ± 5% and reduced sensory activity throughout graded hypoxia. AOPCP also significantly attenuated elevations in sensory activity evoked by mitochondrial inhibition. These effects were mimicked by antagonism of adenosine receptors with 8-(p-sulfophenyl) theophylline. Infusion of AOPCP in vivo significantly decreased the hypoxic ventilatory response (Δ control 74 ± 6%, Δ AOPCP 64 ± 5%, P < 0.05). AOPCP also modified cardiovascular responses to hypoxia, as indicated by reduced elevations in heart rate and exaggerated changes in femoral vascular conductance and mean arterial blood pressure. Thus we identify CD73 as a novel regulator of CB sensory activity. Future investigations are warranted to clarify whether inhibition of CD73 can effectively reduce CB activity in CB-mediated cardiovascular pathology.

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Section: Introductionmentioning

confidence: 88%

Ecto‐5′‐nucleotidase (CD73) regulates peripheral chemoreceptor activity and cardiorespiratory responses to hypoxia

Holmes

Ray

Pearson

et al. 2017

The Journal of Physiology

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“…In addition to the spatial constraint that applies to the primary image that is projected upon the celestial sphere, there is a secondary temporal constraint (applicable to both a presumed large-scale homogeneous universe with an infinite number of stars and galaxies, and a Galactic scale inhomogeneous star field) that limits the observed cumulative brightness of the night sky as recorded on the detector surface (retina) of the imaging device. The temporal constraint is manifested as a high-pass power (apparent brightness) filter, that is a result of the finite temporal summation window of the imaging device, which in the case of the fully dark-adapted unaided human eye is approximately 650 ms (Holmes et al 2017), making the fully dark-adapted human eye incapable of registering as vision any luminous astronomical object that projects an apparent brightness that is fainter than G mag 8.…”

Section: Discussionmentioning

confidence: 99%

“…The above implies that the human eye can only sum photons over a sliding temporal window of approximately 650 ms (Holmes et al 2017), and it can only register as "visible" those luminous objects that produce a photon flux that arrives at a rate (per second) that exceeds a certain minimum threshold that cannot be increased beyond the biological limits allowed by dark adaptation. As such, all photons that arrive on a specific retinal rod, but do not arrive at a rate high enough to contribute to a sum that is above the threshold during the sliding summation window of 650 ms, will be dissipated internally without registering as a sensation of vision.…”

Section: The Photochemistry Of Human Eye Visionmentioning

confidence: 99%

“…In Equation (3), the surface area a d corresponds to the surface area of the pupil through which the photons pass before being absorbed by the retinal rods. For the human eye, in scotopic vision, the temporal summation window is in the order of 650 ms for a dark-adapted pupil diameter of 6.6 mm (Holmes et al 2017). Therefore, the minimum photon flux (photons s −1 ) that is required for the unaided human eye to see a star can be computed from a knowledge of the luminosity and the distance of stars that are known to be barely visible under the best of seeing conditions.…”

Section: The Astrometric Limits Of Unaided Visionmentioning

confidence: 99%

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Analytical Resolution of the Dark Night Sky (Olbers') Paradox

Harari¹

2019

Astron Nachr

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We derive a spatiotemporal analytical resolution of the dark night sky, or Olbers' paradox, first showing that in an infinitely large universe the cumulative solid angle of the light that is projected upon the celestial sphere by an infinite population of directly observable stars is indeed finite. Using the GAIA DR2 data, we show that the number radial density of the stars that are directly visible has a radial distribution that is quasi‐unimodal, and that such a radial distribution is constrained by the inverse square law, which asymptotically limits the magnitude of the cumulative solid angle of the light that is projected upon the celestial sphere. Second, we show that the temporal summation parameter of the imaging device that samples the celestial sphere projection further limits the cumulative apparent brightness of the image formed on the detector surface of the imaging device. The unaided human eye is a biological imaging device, which in the mode of achromatic dim light sensing known as scotopic vision, has a short temporal summation window of approximately 650 ms, which is determined by retinal photochemistry (Holmes et al., Vision Res., 2017, 140, 33–43; Lamb & Pugh Jr, Prog. Retin. Eye Res., 2004, 23(3), 307–380). This short temporal summation window makes the eye act as a high‐pass power filter, making it incapable of rendering visible those stars that project an apparent brightness below a certain threshold. We show analytically that astronomical objects that individually have an apparent brightness mG > 8 will not contribute to the cumulative apparent brightness of the night sky as seen with the fully dark‐adapted unaided eye under ideal seeing conditions, even when the celestial sphere is tiled completely with an infinite number of such faint objects. Using numerical simulations, we also show that a large‐scale homogeneous star field and a Galactic‐scale inhomogeneous field project collectively a cumulative apparent brightness upon the human retina that is approximately 100 million times fainter than the apparent brightness of the Sun. We show that the cumulative solid angle projected by all the unaided eye visible stars is approximately 5.95×10−13 sr, and the asymptotic cumulative solid angle limiting distance is approximately 2 kpc, which is the radial distance beyond which no significant increase in the cumulative apparent brightness of the night sky can be detected with the unaided eye, even in a large‐scale homogeneous and infinitely large universe with an infinite number of stars.

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“…Some of them are biologically active or used as reagents and catalysts in organic reactions [8]. Several novel types of them [9] have been assembled and structurally characterized. However, organotin derivatives containing the alkyltin groups attached to organic compound through O-Sn bonds have considerable interests.…”

Section: Introductionmentioning

confidence: 99%

A Novel Tetranuclear Organotin(IV) Carboxylate with Chain Structure: Synthesis, Crystal Structure, and Characterizations

Sougoule

Balde

Keita

et al. 2015

Heteroatom Chemistry

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A new tetranuclear organotin carboxylate {[(n‐Bu2SnO)2L]2}n (complex 1) was synthesized by the reaction of di‐n‐butyltin oxide with (p‐carboxymethoxy‐phenoxy) acetic acid (LH2) and characterized by elemental analyses: IR, UV–visible, 1H, 13C, 119Sn NMR spectroscopy and single crystal X‐ray study. X‐ray crystallography diffraction data revealed that the complex 1 was polymeric fashion with a chain structure containing a ladder‐like tetranuclear organo‐oxotin cluster. In the complex 1, the ligand LH2 is coordinated to the central tin(IV) atoms via the carboxylato‐O atoms. The tetranuclear tin system is formed by the bridges through the carbonyl oxygen atom of the carboxylate moieties and making the tin atom of pentacoordinated in distorted trigonal bipyramidal geometry. Single crystal X‐ray data indicate that the complex 1 crystallized in the cubic system with the space group C2/c.

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Reply [to “Comments on Paper by C. R. Holmes, M. Brook, P. Krehbiel, and R. McCrory, ‘On the power spectrum and mechanisms of thunder’”]

Cited by 18 publications

References 3 publications

Ecto‐5′‐nucleotidase (CD73) regulates peripheral chemoreceptor activity and cardiorespiratory responses to hypoxia

Ecto‐5′‐nucleotidase (CD73) regulates peripheral chemoreceptor activity and cardiorespiratory responses to hypoxia

Analytical Resolution of the Dark Night Sky (Olbers') Paradox

A Novel Tetranuclear Organotin(IV) Carboxylate with Chain Structure: Synthesis, Crystal Structure, and Characterizations

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