Comparison of the Efficiency of High-Intensity Laser Therapy and Transcutaneous Electrical Nerve Stimulation Therapy in Patients With Symptomatic Temporomandibular Joint Disc Displacement With Reduction

​

https://www.sciencedirect.com/science/article/abs/pii/S0278239121006698
https://sci-hub.se/10.1016/j.joms.2021.07.014
Abstract

Methods: Researchers conducted a prospective, single-blind, controlled clinical trial on patients with TMJ disc disease at a university's oral and maxillofacial surgery clinic. 102 patients were randomized into 3 groups (HILT, TENS and control group). The patients were evaluated in terms of maximum mouth opening (MMO), assisted MMO, Visual Analog Scale (VAS) (pain), and VAS (function). In addition, the disability status of the patients with the Jaw Functional Limitation Scale-20 (JFLS-20) and the quality-of-life with the Oral Health Impact Profile (OHIP-14) was evaluated.​

Results: At the start of the trial, in terms of socio-demographic characteristics, no significant differences existed between the groups. Significant improvements were seen in pain (VAS), MMO, total JFLS-20 and total OHIP-14 scores in the HILT and TENS groups compared to the control group. At week 4, the VAS pain score decreased significantly in the HILT group compared to the TENS group (48 and 25%, respectively), while the MMO was significantly increased (24 and 10%, respectively).​

Conclusion: It was observed that the healing effect of pulsed Nd: YAG laser therapy was significantly higher than TENS in patients with DDWR. Therefore, HILT should be a priority option over TENS therapy in patients with disc displacement.



​

 

Antiviral optical techniques as a possible novel approach to COVID-19 treatment
10.1142/S1793545821300020

https://www.researchgate.net/public...possible_novel_approach_to_COVID-19_treatment



Diagram representing a photochemical process during photodynamic therapy.

• Light (photon) with an appropriate energy is absorbed by a photosensitizer (PS0) and
  
• it moves from a ground state (low-energy ground state) to an excited state.
  
• Photophysical processes can lead to luminescence through °uorescence or phosphorescence or heat generation through thermal relaxation.
  
• Alternately, the excited singlet-state PS (1PS) may decay to a more stable triplet state through inter system crossing.
  
• Among them, the excited triplet-state PS (3PS) undergoes either a type-I or type-II photoreaction producing either reactive oxygen species or a singlet oxygen.

It has been shown that enveloped viruses are significantly more sensitive to damages caused by photodynamic therapy compared to nonenveloped viruses. Unsaturated lipids in the envelope of SARS-CoV-2 and the major envelope proteins of this virus [such as spike (S1 and S2) proteins] are important PDT targets that cause photo damage to these PS binding sites, resulting in the modication of their structure and avoiding cell infection and virus replication. Following the activation of PS localized in nucleic acid or outer structures of SARS-CoV-2 by light, sugar sections are usually photo-oxidated by radicals (generated via type-I process) and guanine residues are attacked by singlet oxygen (generated via type-II process).

The first photodynamic inactivation protocol to combat viruses was reported in 1928 followed by clinical treatment of herpes infection in the United
States in the 1970s. In recent years, this technique is increasingly employed to treat thoracic malignancies. Indeed, PDT has been approved for the
treatment of lung cancer with excellent results.
​

Note: Since the COVID "vaccines" use a nano lipid envelop technology to carry the viral code for successful human cell infestation, we may want to consider the frequecy and intensity of photodynamic therapy needed to penetrate deeply into human organs: including lungs, heart, liver, kidney and reproduction systems.

​

 

Management and Treatment Modalities in Traumatic Brain Injury -

https://sci-hub.se/10.1080/2576117X.2020.1779579

Following closed or open head trauma as well as any impact that causes a movement of the brain, there may be a wide variety of symptoms and complaints. Eye complaints, following a traumatic brain injury, range from blurriness, difficulty focusing, binocular and monocular diplopia as well as extreme photophobia to name a few.​

When we research photobiomodulation therapy for TBI, we often find the patient also has extreme photophobia. Getting the right colored glasses can help to itigate photophobia symptoms posttraumatic brain injury.

https://sci-hub.se/10.4085/1062-6050-52.4.04
​

There is more to light than just blue-blockers. Scotopic Sensitivity Syndrome https://www.scielo.br/j/anp/a/hBbLhfnC9tvVypQzknnS7hg/?lang=en
Helen Irlen over the years has identified which blend of colors help a patient.

Check out https://irlen.com/

A MAGNETOENCEPHALOGRAPHIC INVESTIGATION OF VISUAL INFORMATION PROCESSING IN IRLEN’S SCOTOPIC SENSITIVITY SYNDROME

https://irlen.com/wp-content/uploads/2013/07/lewine_new.pdf​

These three-dimensional scan using SPECT technology show the portions of the brain that are in heavey use, or ‘hot’. Both scans are of the same brain without, and then with, Irlen Filters. In the scan above, there are many parts of the brain that are ‘hot’ -many more than is the case for the ‘normal’ brain. The scan below show the brain is ‘normalized’ once the Irlen Filters are used.​

Ok, so what's the point of this post -> light is medicine -> use it wisely.

​

 

Low-Level Laser Therapy for Fibromyalgia: A Systematic Review and Meta-Analysis

https://www.researchgate.net/public...myalgia_A_Systematic_Review_and_Meta-Analysis
​

The study identified 9 RCTs that included 325 fibromyalgia patients undergoing LLLT or placebo laser treatment with or without an exercise program. The meta-analysis showed that patients receiving LLLT demonstrated significantly improvement.


Abbreviations: ACR, American College of Rheumatology; ARS, American Rheumatology Society; C, Control group; CRD, Cuaderno de recogida de datos; FIQ, Fibromyalgia Impact Questionnaire; FM, Fibromyalgia; HDRS, Hamilton Depression Rating Scale; I, Intervention group;
LED, light-emitting diode; SF-36, 36-item Short-Form Health Survey; VAS, Visual Analog Scale of pain; VSGI, global improvement as reported on a verbal scale. Age was presented as mean ± SD or mean (range). a (): % men; b stretching and aerobic exercise; c not included for our analysis; d stretching; e (): duration of outcome follow-up.

Please note: These are medical grade Ga-AS Lasers with the following specs: (850 nm; 40 mW; 2 J/cm2), (904 nm, average 11.2 mW, 2 J/cm2, 2.8 kHz)

 

Moderate-to-severe TBI treated with 665 and 810 nm laser (but not with 730 or 980 nm)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3397203/

Possible mechanisms of transcranial LLLT for TBI. Red or near-infrared light is absorbed in the mitochondria (possible by cyctochrome c oxidase in the respiratory chain) leading to release of ATP, nitric oxide, and modulation of reactive oxygen species. These second messenger molecules can lead to activation of transcription factors that migrate to the nucleus where they alter expression levels of numerous genes. These new gene products may lead to increased survival of neurons in the damaged brain, to an increase in adult neurogenesis in the hippocampus, for example, to reduced levels of inflammation and to an overall reduced level; of apoptotic and necrotic cell death in the brain.


​

Surprisingly, while all three-laser regimens gave significantly improved NSS scores, the 10 Hz pulse structure was significantly better than the other two laser regimens. Furthermore, significant improvements in mouse performance in the forced swim test and the tail suspension test suggested that psychological problems, such as depression and anxiety associated with TBI might also be helped by LLLT. There was significantly reduced lesion area at 28 days in the 10 Hz laser group.

 

From the 1950's, the benefit of light was commercialized



Now by a flip of a switch we can change it up



But what lighting is "better"; what colors work "best"; how much intensity is necessary for a "therapeutic dose"?

I have no financial incentive for withholding information on this subject -> light-water-magnetism

Have you noticed not one of Dr. @Jack Kruse clinicians whom he endorsed have ever contributed to this forum.

Perhaps, they (these clinicians) only come here (to this forum) to get answers rather than participate in dialog.

 

Well, well, the oxygen story continues
https://forum.jackkruse.com/index.p...t-a-disease-damn-it.25242/page-25#post-310496

Near infrared light decreases synaptic vulnerability to amyloid beta oligomers

https://sci-hub.se/10.1038/s41598-017-15357-x

NIR light had decreased Aβ binding at the concentrations of Aβ oligomers.​

Discussion: Synaptic function is an essential element in the maintenance and preservation of cognition. Aβ oligomer preferential binding to the synaptic region disrupts synaptic transmission and contributes to the declining functionality of the synapses during the progression of AD.
A possible mechanism that could be contributing to the protection and increased function of synapses seen in our study is increased function of the synaptic mitochondria. The 600–1000nm wavelength spectrum of the NIR light has been shown to optimally photostimulate cytochrome c oxidase, a key enzyme in the electron transport chain that is believed to result in an increase in ATP production. Cytochrome c oxidase contains 2 copper centers and 2 heme iron centers. When photostimulated, the copper centers are unable to bind nitric oxide, an inhibitor of respiration, resulting in an increase of oxygen consumption and ATP formation. Several previous studies have investigated the dysfunction of mitochondria in AD.

 

https://www.prnewswire.com/news-rel...-macular-degeneration-subjects-301507380.html

The LIGHTSITE III, a prospective, double-masked, randomized, multi-center clinical trial, was conducted at ten leading US retinal centers. The objective was to treat dry AMD subjects with PBM every four months for a duration of 24 months. The primary efficacy endpoint, best corrected visual acuity (BCVA) was evaluated at 13 months, and if statistically significant, (p < 0.025) the complete 13-month efficacy and safety endpoints would be unmasked.

Estimated Primary Completion Date : June 1, 2022​

We will "see"...

 

Published online 2019 Oct 24. doi: 10.3389/fmicb.2019.02410
PMCID: PMC6821880
PMID: 31708890

Skin Exposure to Narrow Band Ultraviolet (UVB) Light Modulates the Human Intestinal Microbiome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6821880/

Intriguingly, these repeated sub-erythemal UVB skin exposures led to a significant increase in the alpha and beta diversity of the gut microbiome in participants who had not supplemented with vitamin D prior to the study (VDS−), even though both VDS groups showed a similar increase in their serum 25(OH)D levels. This finding suggests that the modulatory effects of UVB on the microbiome were associated with the 25(OH)D insufficiency status of the VDS− group. Based on the fact that UVB light has been previously shown to modulate the immune system, we hypothesize that exposing the skin to UVB light initially leads to local changes in both innate and adaptive immune cells. These cells subsequently traffic to more systemic sites, including the gut, where their release of mediators in turn shapes the composition of the gut microbiome. Since vitamin D deficiency has been previously correlated with microbial dysbiosis in both mice and humans, this study highlights the importance of maintaining vitamin D sufficiency. Correspondingly, participants in the VDS− group started the study with a significantly lower microbial alpha diversity as compared to the VDS+ group, with UVB exposures increasing their diversity to the same level as the VDS+ group. A diverse microbiome is thought to be more resilient against stressors and is seen as a hallmark of health.​

 

Photobiomodulation in human muscle tissue: an advantage in sports performance?

https://sci-hub.se/10.1002/jbio.201600176
Performance metrics included fatigue, number of repetitions, torque, hypertrophy; measures of muscle damage and recovery such as creatine kinase and delayed onset muscle soreness. Searches retrieved 533 studies, of which 46 were included in the review (n = 1045 participants).

Based on the present literature review, the wavelengths employed have been mainly in the red (630–660 nm) and near-infrared (808–950 nm) spectral regions.

(time-response) for PBM to produce highly significant increases in mitochondrial metabolism and synthesis of ATP, with a best time occurring between 3–6 h after irradiation.

muscle performance increased more than 300–600% (compared to sham) after waiting for 3–6 h.
​

 

Low-level light therapy of the eye and brain

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436183/
The pineal gland contains pinopsin, a photoreceptor similar to rhodopsin and melanopsin. It consists of an opsin molecule sensitive to blue light (470 nm) and a retinal chromophore. Pinopsin is exclusively expressed in the pineal gland and it is not expressed in the retina or other parts of the brain. It is believed that through pinopsin, environmental light resets the endogenous circadian pacemaker that controls the rhythmic production of melatonin independently of the visual pathway.​

What I like about this article is that it explains a few things concerning photobiomodulation variables and there effect on different tissues.

Properties of low-level light. Sunlight is composed of a combination of noncoherent waves with wavelengths spanning the entire visible spectrum. In contrast, lasers emit waves of a single wavelength (monochromatic) that have spatial and temporal synchronization. This high wavelength coherence allows the transmission of energy at a high power density. Finally, low-level light consists of monochromatic or quasimonochromatic waves taking different paths leading to a common target point. While wavelength, radiant exposure, irradiance, and fractionation scheme are relevant for low-level light therapy applications, the authors introduce the possibility that noncoherence may be advantageous for some neurometabolic purposes. Noncoherence allows nervous tissue exposure at “therapeutic” wavelengths at relatively low power densities during the time necessary to modulate neural metabolism in response to activation or injury, even if this time is prolonged.
​

Note: The emphasis on non-coherent light - because coherent light is much more "powerful".

Principles of light-tissue interactions. (A) Light at short wavelengths has low tissue penetration. Light at high wavelengths displays high tissue penetration and delivers therapeutic levels of energy to deeper structures. Whereas surface structures exposed to high wavelengths may be exposed to inhibitory energy densities (eg, 100 J/cm2), light with a certain power density targeting a surface redistributes in a proportionally higher tissue volume due to diffraction (bending of waves). Multiple scattering of light allows for spreading out of waves and increases the treatment volume, so a lower applied energy can be used to achieve an effective energy density at higher depth. (B) Because radiant exposure (J/cm2) is the product of irradiance (W/cm2) and time, the energy delivered to tissues as a result of a constant irradiance can be increased by increasing exposure time. Thus, tissue penetration can also be affected by exposure time. When sources of low-level light therapy are used with high exposure times, deep structures can be treated with biomodulatory amounts of energy, while avoiding ablative effects. (C) Finally, tissues vary in their photoacceptor content, transmittance, and relaxation time. This accounts for interspecies and interregional variations in light penetration (eg, gray matter versus white matter in the brain). In addition, metabolically active tissues such as nervous tissue may exhibit variations in relaxation times, due to changes in the redox states of photoacceptors. This not only potentially affects tissue penetration, but also the susceptibility of nervous tissues to low-level light therapy depending on their activational state.
​

Hormetic effects of low-level light therapy (LLLT). LLLT does not induce classical linear dose-response pharmacological effects. LLLT effects are characterized by inverted U-shaped dose-response curves, in which linear responses may be seen only at very low doses. Whereas linear effects may be negligible, maximal stimulatory effects are typically observed at intermediate doses. However, the linear relationship does not hold at high doses, since inhibitory effects are observed instead. In fact, the inhibitory effects of very high LLLT doses might be worse than control conditions (eg, tissue destruction). A key observation concerning the modulatory effects of light in tissues is that maximal responses at intermediate doses tend to represent less than twofold increases in biological variables relative to baseline conditions. Yet these effects have been shown to have major relevance, especially when energy metabolism is involved in nervous tissue. Thus, hormesis is an essential concept for the development of neurotherapeutic applications of LLLT.


Differential effects of light on photoreceptors and photoacceptors in the retina. Light reaches the retina and travels through the different retinal layers to reach the outermost photoreceptor layer. It then excites the photoreceptor rhodopsin in rods and cones, triggering the process of phototransduction. Phototransduction causes photoreceptor cell hyperpolarization, changes in neurotransmission, and action potentials (yellow arrows) in bipolar cells and ganglion cells. These effects represent the onset of visual information processing. Light can also directly excite photoacceptors in neurons including retinal ganglion cells. The main photoacceptor in the red to near-infrared spectrum is the mitochondrial respiratory enzyme cytochrome oxidase. The effects of light on neuronal cytochrome oxidase induce modulation of cell bioenergetic mechanisms that are independent from visual processing. Yet photobiomodulation has major implications in neuronal physiology and homeostasis.
​

Due to limitations of images which can be loaded per post -> this will be continued.

​

 

Low-level light therapy of the eye and brain - continued

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436183/
​

The beneficial effects of LLLT in the eye were tested in early studies using low energy helium-neon laser irradiation in models of traumatic optic nerve injury in the rabbit and rat. The function of the injured optic nerve, as measured by compound action potentials, showed a significant improvement after two weeks of daily radiation. Optic nerve function showed more significant improvements when LLLT was started immediately after injury, and efficacy was progressively lost if onset of treatment was delayed to 2 hours, 5 hours, and 24 hours. More significantly, LLLT started immediately before injury was also effective at delaying posttraumatic nerve damage. These studies were also significant because they demonstrated that LLLT was effective on moderately injured nerves, whereas its beneficial effects were not observed in severely-injured nerves. This suggests that a physiologically viable neural substrate capable of responding to light is needed. It is less likely that LLLT worked by inducing neuronal repair; rather, light may have worked by enhancing the function of spared nerve fibers.

Transcranial effects
The ability of light to penetrate the brain and exert biological effects was first inferred after finding photoreceptor molecules present in central nervous system structures. For example, the pineal gland contains the photoreceptor pinopsin and it is believed to be sensitive to ambient light changes and be relevant for the regulation of circadian rhythms. It has been demonstrated that light is able to penetrate the cranium and reach the brain. This effect is being used for the development of optical imaging techniques using near-infrared light in humans. Although light attenuation occurs when light travels through bone, this attenuation is not of a strong magnitude. The cranium shows minimal absorption and scattering of light, with a wavelength- but not thickness-dependent attenuation of 15%–20% in the red to near-infrared spectrum. Photons at wavelengths between 630 nm and 800 nm have been shown to travel up to 28 mm even in layers of tissues with relatively low transparencies such as skin, connective tissue, muscle, bone, and spinal cord, with about 6% of the total energy density being detectable at the ventral surface of a living rat. In gray matter, red and near-infrared light penetration is governed by Beer–Lambert law, with the optical power decaying up to 80% at 1 mm from the surface. However, at this depth in solid organs, the actual power density of near-infrared light has been estimated to be up to three times higher than the power at the incident surface due to backscattering and constructive interference. As the light travels into the tissue, its intensity decreases due to absorption and scattering. Penetration of light into tissues depends not only on the wavelength but also on the optical properties of the target tissue. The maximal penetration of light in the gray and white matter of the brain occurs at wavelengths in the near-infrared spectrum. It has been shown that within the visible and near-infrared spectral range, white matter in both the central and peripheral nervous systems reflects most of the incident power and shows a low level of absorption and a short penetration depth. In contrast, the transmittance of the gray matter is approximately twice as high as that of the white matter (Figure 2 above). Finally, the penetration of light is not only contingent on the wavelength or the specific tissue, but significant interspecies differences in penetration have also been detected. For example, at 850 nm, the penetration of energy in humans is almost three times higher than that in the mouse cortex. While the cause of this significant difference of light-tissue interaction can be explained by differences in water and protein content, this observation has obvious translational implications that should be considered when LLLT data generated in animal models is applied to humans. Finally, the delivery modality of LLLT is also relevant to transcranial in vivo applications (Table 1 above). For example, noncontact delivery modalities with LEDs allow exposure of extensive surfaces, including whole-body treatments. LEDs montages can potentially be built with ergonomic considerations for whole-head and whole-body LLLT in humans. In contrast, contact modalities combined with laser sources may be ideal when localized energy delivery is needed. This may be advantageous for boosting cell functions in specific nodes within dysfunctional neural networks in which connectivity could be otherwise impaired with broad irradiation. Similarly, localized transcranial LLLT may be of use for neuroprotection of healthy tissue adjacent to tumor sites after resection, without risk of inducing photobiomodulation of residual tumor.

Compelling evidence of the in vivo neuroprotective effects of LLLT against transient ischemia has been provided by recent studies conducted by Uozumi et al; LLLT delivered transcranially was able to increase cerebral blood flow. LLLT was given at 808 nm and 0.8 W/cm2, 1.6 W/cm2, and 3.2 W/cm2 for 45 minutes over an exposure field of 3 mm in one hemisphere. Compared to sham subjects, the cerebral blood flow increased 30% with 1.6 W/cm2, whereas the lowest and highest power densities were less efficient. The increases in cerebral blood flow were accompanied by a significant increase in nitric oxide production. Treating subjects with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester hydrochloride inhibited the increases in cerebral blood flow induced by LLLT. Similarly, the late increase in cerebral blood flow elicited by LLLT was attenuated by inhibition of glutamatergic transmission with the N-Methyl-D-aspartic acid competitive antagonist MK-801. These observations support that the increases in blood flow are secondary to an increased production of nitric oxide and related to neuronal activation. The neuroprotective effects of LLLT against decreased cerebrovascular perfusion in vivo were also demonstrated using a model of bilateral common carotid artery occlusion in mice. They showed that near-infrared treatment for 15–45 minutes increased local cerebral blood flow by 30% in this mouse model of stroke. Remarkably, the cerebral blood flow in conditions of normal and decreased perfusion was increased in both the treated and nontreated hemispheres. Also, subjects pretreated with LLLT showed improved residual cerebral blood flow during the period of occlusion, with stable body temperature, heart rate, and respiratory rates. Finally, the transient cerebral ischemia induced by carotid occlusion produced cell death in 84% of cells in the CA1 field of the hippocampus and in 27% of cortical neurons 96 hours after the insult. In contrast, LLLT had a significant neuroprotective effect by decreasing the number of apoptotic cells to only 44% and 8% in the hippocampus and cortex, respectively, after transient ischemia. Of note, these experiments showed that LLLT and neuroprotection against transient ischemia were not associated with increased expression of nitric oxide synthase. This suggests that the observed increases in nitric oxide concentrations were the product of nitric oxide synthase-independent mechanisms. Mechanisms of nitric oxide synthase-independent nitric oxide formation include reduction of nitrite by xanthine oxidase or cytochromes. As mentioned before, LLLT increases brain cytochrome oxidase expression in vivo49 and the activation of intracellular signals induced by LLLT seem to be contingent upon concentrations of nitric oxide.

Parkinson’s disease
The protective effects of LLLT have also been demonstrated in paradigms of neurodegeneration. Shaw et al showed that LLLT has a potential application in the treatment of Parkinson’s disease. This group tested the neuroprotective effects if LLLT in a mouse in vivo model of dopaminergic degeneration induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). LLLT was given 15 minutes after MPTP intraperitoneal injection at 670 nm and 40 mW/cm2. A total dose of 2 J/cm2 was delivered in four fractions of 9 seconds evenly spaced over 30 hours. Approximately 10% of the power density reaching the skull reached the brain. Two days after MPTP injection, there was a 45% reduction in the number of dopaminergic cells in the substantia nigra compared to saline-treated controls. LLLT completely prevented the loss of dopaminergic cells in the substantia nigra. When the dose of MPTP was doubled, there was an even more profound decrease in dopaminergic cells of 60%. However, LLLT limited the neurodegeneration induced by this higher MPTP dose to only 30% compared to control. This study not only offered evidence that LLLT induces neuroprotective effects against dopaminergic toxins in vivo, but that its effects reach structures deep in the brain.
​

Experimental data in humans also support that LLLT may be effective in the treatment of cognitive and emotional disorders in humans. A pilot study showed that LLLT applied transcranially to the forehead was able to increase frontal cortex blood flow and induce a 63% reduction in depression scores in a group of patients with major depression. Beneficial antidepressant effects were seen 2 weeks and 4 weeks after a single treatment. LLLT was given in one fraction at 810 nm, power density of 250 mW/cm2. Additionally, LLLT to the forehead and scalp with an LED cluster at 633 nm and 870 nm has been reported to improve and maintain attention, executive function, and memory in two patients with chronic traumatic brain injury. LLLT with a power density of 22.2 mW/cm2 was applied for 10 minutes per placement weekly for 2 months or daily for 4 months prior to testing of the cognitive effects, and these patients have continued daily treatment at home for up to 5.5 years. Remarkably, no side effects have been reported so far with the use of LLLT in humans.​

 

Hi all

If I have inability to detox toxins out of my body. Does that mean if I use photobiomodulation such as Mitogen or Firestorm, my symptoms will get worse?

If I use red light but can't detox. Then the toxins won't be released out of the body and I may feel worse?

 

https://pubmed.ncbi.nlm.nih.gov/32305654/

 

Photobiomodulation effects of pulsed-NIR laser (810 nm) and LED (808 ± 3 nm) with identical treatment regimen on burn wound healing: A quantitative label-free global proteomic approach

https://www.sciencedirect.com/science/article/pii/S2666469021000099​

The findings of the present study demonstrated that both laser and LED in 810 nm wavelength range at pulsed-mode (10 Hz) are equally effective for PBM-mediated acceleration of full-thickness burn wound healing.

Our earlier studies reported that PBM with 810 nm laser at pulsed mode (10 Hz) predominantly decreased the exaggerated inflammatory response, stimulating cell proliferation, migration, neovascularisation, re-epithelialization, bioenergetics activation, collagen accumulation, ECM stabilization and tissue remodeling, which in turn accelerated dermal wound repair in immunosuppressed rats [19]. Additionally, we further explored the molecular aspects of PBM with 810 nm laser at pulsed mode (10 Hz), which positively regulate the cellular proliferation and survival through Ca2+-calmodulin, Akt, ERK, redox signaling cascades. It also mitigates oxidative stress, alleviates pain and inflammation, and inhibits apoptosis, which may ameliorate the cutaneous wound repair process in immunosuppressed rats [7]. With this development, the present study compared the tissue repair efficacy of both laser (810 nm) and LED (808 ± 3 nm) light at pulsed-mode (10 Hz) with identical irradiation parameters on full-thickness transdermal burn wound in rats by employing the comprehensive analysis of quantitative label-free global proteomics, followed by validation of the proteomics data by using biophysical, biochemical, ELISA, histopathology and immunohistochemical analyses for the markers associated with cell proliferation, cytoprotection, ECM deposition and inflammatory response.

Earlier, we have reported the cytoprotective role of pulsed 810 nm PBMT in wound tissue, which has been shown to reduced apoptosis by downregulating the expression of pro-apoptotic markers (cytochrome c and caspase 3). Sequential activation of caspase 3 has a prime role in apoptosis as it catalyzes the specific cleavage of key cellular proteins. In the present study, apoptotic cell distribution was observed via TUNEL assay. The apoptotic bodies in non-irradiated burn control group were increased in number as compared to pulsed laser and LED treated groups.

Effect of pulsed (10 Hz) laser (810 nm) and LED (808 ± 3 nm) photobiomodulation and silver sulfadiazine (SSD, reference care) on the pro-reparative markers on burn wound healing.



TUNEL analysis of DNA damage shows the distribution of apoptotic bodies on eighth day post-wounding in granulation tissue. Higher magnification (40 X) of dermal area showing higher number of TUNEL-positive cells in non-irradiated burn control group. Conversely, pulsed (10 Hz) laser (810 nm) and LED (808 ± 3 nm) irradiated groups showed lesser number of TUNEL-positive cells in wound tissue.




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By keeping glucose and insulin levels low to allow for the production of ketones,
---
Using diet it may be relatively easy to keep fasting insulin low.
but fasting glucose may still keep staying high.

Metformin to the rescue.


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View of Melatonin and the Optics of the Human Body (melatonin-research.net)

https://www.melatonin-research.net/index.php/MR/article/view/19/213

visible red or near-infrared (NIR) light has been shown to heal and stimulate damaged tissue

Note that we are mostly talking about very small amounts of melatonin produced by pineal gland.

It is about time to get interested in other (very large) sources of melatonin.
That melatonin is produced by NIR light.

So anytime one thinks of using red light
think that possibly 10 - 100 milligrams of melatonin pills may do a similar job.

@Jack Kruse

 

Higher triglyceride level was linked to a lower risk of cognitive decline, less of a reduction in the ability to perform daily tasks, less frailty, and lower risk for death.

https://www.sciencedaily.com/releases/2019/02/190204142313​

 

New Wisdom about High Cholesterol Treatment for Adults Aged 80 and Older > Health in Aging Blog > Health in Aging

 

Thank you - @JanSz - the referenced article is:

Triglycerides Paradox Among the Oldest Old: “The Lower the Better?”
https://sci-hub.se/10.1111/jgs.15733

CONCLUSION: In the oldest old, a higher concentration of TGs was associated with a lower risk of cognitive decline, ADL decline, frailty aggravation, and mortality.

​

 

​

Interesting
05/19/2022 Spectracell indicates Triglycerides =183 (desirable less than 150), Total Cholesterol =318
05/06/2022 LaCorp Triglycirides = 111(desirable less than 150), Total Cholesterol =255



05/06/2022 LaCorp Fasting Glucose =114 ( ordered Metformin, how much to take?)
Using pants 32"waist

BP 112/73 pulse 72 (how to lower pulse?

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