scholarly journals Interpreting the Age Dependency, Diurnal Variation, and Pathological Asymmetry of Biophoton Emission: An Analytical Hypothesis

2019 ◽  
Author(s):  
Daqing Piao
Keyword(s):  
Oxidative Stress ◽  
Steady State ◽  
Diurnal Variation ◽  
Quantitative Estimation ◽  
Pathological Condition ◽  
Alternative Form ◽  
Photon Diffusion ◽  
Spherical Domain ◽  
Pathological Conditions ◽  
Biophoton Emission

Biophoton emission has been experimented for decades. The photo-genic origin of biophoton has also been attributed to the oxidative stress or free radical production. However, there are considerable gaps in quantitative understanding of biophoton emission. In this work, I propose an analytical hypothesis for interpreting a few patterns of steady-state biophoton emission of human, including the dependency on age, the diurnal variation, and the geometric asymmetry associated with serious asymmetrical pathological conditions. The hypothesis is based on an alternative form of energy state, termed vivo-nergy, which is associated with only metabolically active organisms that are also under neuronal control. The hypothesis projects a decrease of the vivo-nergy in human during growth beyond puberty. The hypothesis also proposes a modification of the vivo-nergy by the phases of systematic or homeostatic physiology. The hypothesis further postulates that the deviation of the physiology-modified vivo-nergy from the pre-puberty level is deteriorated by acquired organ-specific pathological conditions. A temporal differential change of vivo-nergy is hypothesized to proportionally modulate oxidative stress that functions as the physical source of biophoton emission. The resulted steady-state diffusion of the photon emitted from a photo-genic source in a human geometry simplified as a homogeneous spherical domain is modeled by photon diffusion principles incorporating an extrapolated zero-boundary condition. The age and systematic physiology combined determines the intensity of the centered physiological steady-state photo-genic source. An acquired pathology sets both the intensity and the off-center position of the pathological steady-state photo-genic source. When the age-commemorated, physiology-commanded, and pathology-controlled modifications of the steady-state photo-genetic sources are implemented in the photon diffusion model, the photon fluence rate at the surface of the human-representing spherical domain reveals the patterns on age, the temporal variation corresponding to systematic physiology, and the geometric asymmetry associated with significant asymmetric pathological condition as reported for spontaneous biophoton emission. The hypothesis, as it provides conveniences for quantitative estimation of biophoton emission patterns, will be extended in future works towards interpreting the temporal characteristics of biophoton emission under stimulation.

scholarly journals Phenomenological Interpretations of Some Somatic Temporal and Spatial Patterns of Biophoton Emission in Humans

2021 ◽  
Vol 35 (2) ◽  
pp. 345-382
Author(s):  
Daqing Piao
Keyword(s):  
Oxidative Stress ◽  
Steady State ◽  
Quantitative Estimation ◽  
Pathological Condition ◽  
Energy State ◽  
Alternative Form ◽  
Photon Diffusion ◽  
Spherical Domain ◽  
Pathological Conditions ◽  
Biophoton Emission

Biophoton emission remains controversial. The photo-genic origin of biophoton has been attributed to the oxidative stress or free radical production. However, there are considerable gaps in quantitative understanding of biophoton emission. I propose an analytical hypothesis for interpreting a few patterns of steady-state biophoton emission of human, including the dependency on age, the diurnal variation, and the geometric asymmetry associated with serious asymmetrical pathological conditions. The hypothesis is based on an alternative form of energy state, termed vivo-nergy, which is associated with only metabolically active organisms that are also under neuronal control. The hypothesis projects a decrease of the vivo-nergy in human during growth beyond puberty. The hypothesis also proposes a modification of the vivo-nergy by the phases of systematic or homeostatic physiology. The hypothesis further postulates that the deviation of the physiology-modified vivo-nergy from the pre-puberty level is deteriorated by acquired organ-specific pathological conditions. A temporal differential change of vivo-nergy is hypothesized to proportionally modulate oxidative stress that functions as the physical source of biophoton emission. The resulted steady-state diffusion of the photon emitted from a photo-genic source in a human geometry simplified as a homogeneous spherical domain is modeled by photon diffusion principles incorporating an extrapolated zero-boundary condition. The age and systematic physiology combined determines the intensity of the centered physiological steady-state photo-genic source. An acquired pathology sets both the intensity and the off-center position of the pathological steady-state photo-genic source. When the age-commemorated, physiology-commanded, and pathology-controlled modifications of the steady-state photo-genetic sources are implemented in the photon diffusion model, the photon fluence rate at the surface of the human-representing spherical domain reveals the patterns on age, the temporal variation corresponding to systematic physiology, and the geometric asymmetry associated with significant asymmetric pathological condition as reported for spontaneous biophoton emission. The hypothesis, as it provides conveniences for quantitative estimation of biophoton emission patterns, will be extended in future works towards interpreting the temporal characteristics of biophoton emission under stimulation.           

scholarly journals On a Few Superficial Presentations of Ultra-Weak Photon Emission of Human: an Analytical Hypothesis

2018 ◽  
Author(s):  
Daqing Piao
Keyword(s):  
Oxidative Stress ◽  
Quantitative Estimation ◽  
Pathological Condition ◽  
Photon Emission ◽  
Critical Time ◽  
Photon Diffusion ◽  
Spherical Domain ◽  
Pathological Conditions ◽  
Age Related ◽  
Initial Objective

Ultra-weak photon emissions (UPEs) including those from human have been experimented for decades. The photo-genic origin of UPE has also been attributed to the oxidative stress or free radical production that is unique to metabolically active states of biological organisms. However, there are considerable gaps in quantitative understanding of UPE. In this work, I propose an analytical framework of hypothesis for the initial objective of modeling a few superficial presentations of UPE of human, including the systematic dependency on age, the diurnal variation, and the geometric asymmetry associated with serious asymmetrical pathological conditions. The hypothesis which is currently limited to human assumes a new form of energy state, termed vivo-nergy, which resides only in metabolically active organisms that are also under neuronal control. The hypothesis projects a decrease of the vivo-nergy in human during growth beyond puberty, with the rate of decrease dictated by a critical time-scale---the age of the first opposite-sex sexual intercourse (FOSSI). The hypothesis also proposes a modification of the vivo-nergy by the phases of systematic or homeostatic physiology. The hypothesis further postulates that the deviation of the physiology-modified vivo-nergy from the pre-puberty level is deteriorated by acquired organ-specific pathological conditions. Any reduction of vivo-nergy from the pre-puberty level is hypothesized to proportionally cause oxidative stress that functions as the physical source of UPE. The resulted steady-state diffusion of the photon emitted from a photo-genic source of UPE in a human geometry simplified as a homogeneous spherical domain is modeled by photon diffusion principles incorporating an extrapolated zero-boundary condition. The age and systematic physiology combined determines the intensity of the centered physiological photo-genic source. The acquired (single) pathology sets both the intensity and the off-center position of the (single) pathological photo-genic source. When the age-related, physiology-commanded, and pathology-controlled modifications of the photo-genetic sources are implemented in the photon diffusion model, the photon fluence rate at the surface of the simplified human-representing spherical domain reveals the dependency on age, the temporal variation corresponding to systematic physiology, and the geometric asymmetry associated with significant asymmetric pathological condition as reported previously for UPE. The hypothesis, as it provides analytical conveniences for quantitative estimation of UPE patterns, may be useful to further model-based interpretation of the spatial-temporal characteristics of UPE.           

scholarly journals Curcumin Potentiates α7 Nicotinic Acetylcholine Receptors and Alleviates Autistic-Like Social Deficits and Brain Oxidative Stress Status in Mice

2021 ◽  
Vol 22 (14) ◽  
pp. 7251
Author(s):  
Petrilla Jayaprakash ◽  
Dmytro Isaev ◽  
Waheed Shabbir ◽  
Dietrich E. Lorke ◽  
Bassem Sadek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Pathological Condition ◽  
Repetitive Behaviors ◽  
Social Deficits ◽  
Nicotinic Acetylcholine ◽  
Oxidative Stress Status ◽  
Inward Currents ◽  
Α7 Nachrs

Autistic spectrum disorder (ASD) refers to a group of neurodevelopmental disorders characterized by impaired social interaction and cognitive deficit, restricted repetitive behaviors, altered immune responses, and imbalanced oxidative stress status. In recent years, there has been a growing interest in studying the role of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in the CNS. Influence of agonists for α7-nAChRs on the cognitive behavior, learning, and memory formation has been demonstrated in neuro-pathological condition such as ASD and attention-deficit hyperactivity disorder (ADHD). Curcumin (CUR), the active compound of the spice turmeric, has been shown to act as a positive allosteric modulator of α7-nAChRs. Here we hypothesize that CUR, acting through α7-nAChRs, influences the neuropathology of ASD. In patch clamp studies, fast inward currents activated by choline, a selective agonist of α7-nAChRs, were significantly potentiated by CUR. Moreover, choline induced enhancement of spontaneous inhibitory postsynaptic currents was markedly increased in the presence of CUR. Furthermore, CUR (25, 50, and 100 mg/kg, i.p.) ameliorated dose-dependent social deficits without affecting locomotor activity or anxiety-like behaviors of tested male Black and Tan BRachyury (BTBR) mice. In addition, CUR (50 and 100 mg/kg, i.p.) mitigated oxidative stress status by restoring the decreased levels of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and the cerebellum of treated mice. Collectively, the observed results indicate that CUR potentiates α7-nAChRs in native central nervous system neurons, mitigates disturbed oxidative stress, and alleviates ASD-like features in BTBR mice used as an idiopathic rodent model of ASD, and may represent a promising novel pharmacological strategy for ASD treatment.

scholarly journals Serum Albumin Redox States: More than Oxidative Stress Biomarker

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 503
Author(s):  
Fuka Tabata ◽  
Yasuaki Wada ◽  
Satomi Kawakami ◽  
Kazuhiro Miyaji
Keyword(s):  
Oxidative Stress ◽  
Serum Albumin ◽  
Animal Studies ◽  
Redox State ◽  
Ex Vivo ◽  
Pathological Condition ◽  
Analytical Techniques ◽  
Cysteine Residue ◽  
Research Field ◽  
Systemic Oxidative Stress

Serum albumin is the most abundant circulating protein in mammals including humans. It has three isoforms according to the redox state of the free cysteine residue at position 34, named as mercaptalbumin (reduced albumin), non-mercaptalbumin-1 and -2 (oxidized albumin), respectively. The serum albumin redox state has long been viewed as a biomarker of systemic oxidative stress, as the redox state shifts to a more oxidized state in response to the severity of the pathological condition in various diseases such as liver diseases and renal failures. However, recent ex vivo studies revealed oxidized albumin per se could aggravate the pathological conditions. Furthermore, the possibility of the serum albumin redox state as a sensitive protein nutrition biomarker has also been demonstrated in a series of animal studies. A paradigm shift is thus ongoing in the research field of the serum albumin. This article provides an updated overview of analytical techniques for serum albumin redox state and its association with human health, focusing on recent findings.

scholarly journals Recent Advances in Biomarkers and Regenerative Medicine for Diabetic Neuropathy

2021 ◽  
Vol 22 (5) ◽  
pp. 2301
Author(s):  
Yoshikai Fujita ◽  
Tatsufumi Murakami ◽  
Akihiro Nakamura
Keyword(s):  
Diabetic Neuropathy ◽  
Target Gene ◽  
Pathological Condition ◽  
Nerve Fibers ◽  
Nerve Degeneration ◽  
Limb Amputation ◽  
Sensory Impairment ◽  
Mechanical Stimuli ◽  
Pathological Conditions ◽  
The Relationship

Diabetic neuropathy is one of the most common complications of diabetes. This complication is peripheral neuropathy with predominant sensory impairment, and its symptoms begin with hyperesthesia and pain and gradually become hypoesthesia with the loss of nerve fibers. In some cases, lower limb amputation occurs when hypoalgesia makes it impossible to be aware of trauma or mechanical stimuli. On the other hand, up to 50% of these complications are asymptomatic and tend to delay early detection. Therefore, sensitive and reliable biomarkers for diabetic neuropathy are needed for an early diagnosis of this condition. This review focuses on systemic biomarkers that may be useful at this time. It also describes research on the relationship between target gene polymorphisms and pathological conditions. Finally, we also introduce current information on regenerative therapy, which is expected to be a therapeutic approach when the pathological condition has progressed and nerve degeneration has been completed.

Acute Hypoxia and Exercise-Induced Blood Oxidative Stress

2014 ◽  
Vol 24 (6) ◽  
pp. 684-693 ◽  
Author(s):  
Graham McGinnis ◽  
Brian Kliszczewiscz ◽  
Matthew Barberio ◽  
Christopher Ballmann ◽  
Bridget Peters ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Steady State ◽  
Repeated Measures ◽  
Acute Hypoxia ◽  
Protein Carbonyls ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Lipid Hydroperoxides ◽  
Oxidative Stress Biomarkers ◽  
Post Exercise ◽  
Reducing Ability

Hypoxic exercise is characterized by workloads decrements. Because exercise and high altitude independently elicit redox perturbations, the study purpose was to examine hypoxic and normoxic steady-state exercise on blood oxidative stress. Active males (n = 11) completed graded cycle ergometry in normoxic (975 m) and hypoxic (3,000 m) simulated environments before programing subsequent matched intensity or workload steady-state trials. In a randomized counterbalanced crossover design, participants completed three 60-min exercise bouts to investigate the effects of hypoxia and exercise intensity on blood oxidative stress. Exercise conditions were paired as such; 60% normoxic VO2peak performed in a normoxic environment (normoxic intensity-normoxic environment, NI-NE), 60% hypoxic VO2peak performed in a normoxic environment (HI-NE), and 60% hypoxic VO2peak performed in a hypoxic environment (HI-HE). Blood plasma samples drawn pre (Pre), 0 (Post), 2 (2HR) and 4 (4HR) hr post exercise were analyzed for oxidative stress biomarkers including ferric reducing ability of plasma (FRAP), trolox equivalent antioxidant capacity (TEAC), lipid hydroperoxides (LOOH) and protein carbonyls (PCs). Repeated-measures ANOVA were performed, a priori significance of p ≤ .05. Oxygen saturation during the HI-HE trial was lower than NI-NE and HI-NE (p < .05). A Time × Trial interaction was present for LOOH (p = .013). In the HI-HE trial, LOOH were elevated for all time points post while PC (time; p = .001) decreased post exercise. As evidenced by the decrease in absolute workload during hypoxic VO2peak and LOOH increased during HI-HE versus normoxic exercise of equal absolute (HI-NE) and relative (NI-NE) intensities. Results suggest acute hypoxia elicits work decrements associated with post exercise oxidative stress.

scholarly journals AN EXPERIMENTAL STUDY OF PAROTITIS (MUMPS)

1916 ◽  
Vol 23 (3) ◽  
pp. 353-375 ◽  
Author(s):  
Martha Wollstein
Keyword(s):  
Parotid Gland ◽  
Pathological Condition ◽  
Active Material ◽  
White Blood Cells ◽  
Salivary Secretion ◽  
Human Beings ◽  
Parotid Glands ◽  
Histological Changes ◽  
Pathological Conditions ◽  
Small Series

Cats injected into the parotid gland and testicle with a bacterial sterile filtrate of the salivary secretion of children in the active stage of parotitis or mumps can be made to develop a pathological condition having several points of resemblance to the condition present in mumps in human beings. After an incubation stage of from five to eight days definite changes have been noted in the temperature, blood leukocytes, and inoculated organs. The temperature rise begins within twenty-four hours of the inoculations and reaches a maximum in from seven to fourteen days. The febrile rise fluctuates between 1° and 2.5° C. The white blood cells begin to increase on the second day following the inoculation. The first change is a polymorphonuclear leukocytosis which precedes the glandular swellings. This initial rise is followed by a decline, after which the lymphocytes increase. The increase is confined to the small lymphocytes, which increase to from 7 to 10 per cent of their initial number. The inoculated glands become swollen and tender. The swelling and tenderness become apparent from the fifth to the ninth days and persist for a variable period. The parotid changes are less constant or less obvious than are the testicular. The latter are constant and endure from eight to twelve days. The rise of temperature and the leukocytosis precede the glandular swelling, but all the changes reach the maximum at about the same time, after which they decline gradually. What may be regarded as normal conditions are reestablished in four weeks or less. The intraparotid and intratesticular injections of extracts of normal parotid gland and testicles may cause a mild rise of temperature and leukocytosis of brief duration, but swelling and tenderness are absent. The white cells increased are the polymorphonuclears and not the lymphocytes. The intraparotid and intratesticular injections of filtrates of normal saliva may cause a mild rise of temperature of very brief duration, but leukocytosis, swelling, and tenderness do not appear. The histological changes in the parotid gland when present consist chiefly of edema of the interlobular connective tissue with mononuclear interstitial infiltration about the ducts and elsewhere. In cases of long duration the ducts may be dilated. But in some instances the swollen gland while showing congestion and edema in gross showed inconspicuous changes under the microscope. The histological changes in the testicle are of two kinds: inconstant changes of cellular invasion between the tubules and swelling or even multiplication of the interstitial cells, constant ones consisting of degeneration of the epithelium and interference with spermatogenesis, a condition to which we have applied the term "spermatorrhexis." The pathological conditions set up by the filtrate derived from the salivary secretion of cases of acute parotitis are intensified by successive transfers through a small series of cats of the extract and emulsion of the parotid gland and testicle previously inoculated. The pathological changes are also prevented or reduced when the extract or emulsion is previously incubated with a quantity of blood serum obtained from a cat which has survived inoculation. Normal serum, on the other hand, has no such inhibiting effect. The deduction from these experiments is to the effect that the salivary secretion in parotitis or mumps contains a filterable substance capable of setting up a series of definite pathological conditions when inoculated into the testicle and parotid glands of cats. Whether this active material is a microorganism and if so whether it is the specific microbic cause of parotitis or mumps remains to be ascertained.

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