The Formation of the Electronic Tornado is the Basis of Superconductivity

The space-time ladder theory reveals that the formation of electronic tornadoes, or the formation of electronic dissipative structures, to be precise, the enhancement of electronic Energy Qi field is the basis of superconductivity. The surrounding area of the electronic tornado is expanding, which is the basis of the Meissner effect, and the center is contracting, which is the basis of the pinning force. When the attractive force of the Energy Qi field is greater than the Coulomb repulsive force, the electrons form a Cooper pair and release dark energy into virtual space-time. When the dark energy increases to a certain extent, the virtual space-time frees the Cooper pair and forms an electron-virtual space-time wave, which fluctuates freely in the superconducting material, which is the basis for the superconducting resistance to be zero. This is similar to the principle of a hot air balloon. The virtual space-time is hot air and the electron pair is a hot air balloon device. Conductor electrons are free and easy to emit dark energy, resulting in insufficient dark energy, and it is not easy to form electron-pair virtual space-time waves, so the superconducting critical temperature is very low. This is because the emission coefficient of the conductor is too high. Insulator electrons are not easy to emit dark energy and easily form electron-pair virtual space-time waves. Therefore, the superconducting critical temperature is slightly higher because of the low emission coefficient of the insulator. The solution of the Qi-space-time wave equation, that is, the coherence coefficient, is an important factor in superconductivity. In addition, the conditions under which tornadoes form are also an important basis for superconductivity. Finally, it is emphasized that the coherence coefficient and prevention of dark energy emission are the two most important elements for preparing superconducting materials

Novel Mouse Tauopathy Model for Repetitive Mild Traumatic Brain Injury: Evaluation of Long-Term Effects on Cognition and Biomarker Levels After Therapeutic Inhibition of Tau Phosphorylation

Traumatic brain injury (TBI) is a risk factor for a group of neurodegenerative diseases termed tauopathies, which includes Alzheimer's disease and chronic traumatic encephalopathy (CTE). Although TBI is stratified by impact severity as either mild (m), moderate or severe, mTBI is the most common and the most difficult to diagnose. Tauopathies are pathologically related by the accumulation of hyperphosphorylated tau (P-tau) and increased total tau (T-tau). Here we describe: (i) a novel human tau-expressing transgenic mouse model, TghTau/PS1, to study repetitive mild closed head injury (rmCHI), (ii) quantitative comparison of T-tau and P-tau from brain and plasma in TghTau/PS1 mice over a 12 month period following rmCHI (and sham), (iii) the usefulness of P-tau as an early- and late-stage blood-based biochemical biomarker for rmCHI, (iii) the influence of kinase-targeted therapeutic intervention on rmCHI-associated cognitive deficits using a combination of lithium chloride (LiCl) and R-roscovitine (ros), and (iv) correlation of behavioral and cognitive changes with concentrations of the brain and blood-based T-tau and P-tau. Compared to sham-treated mice, behavior changes and cognitive deficits of rmCHI-treated TghTau/PS1 mice correlated with increases in both cortex and plasma T-tau and P-tau levels over 12 months. In addition, T-tau, but more predominantly P-tau, levels were significantly reduced in the cortex and plasma by LiCl + ros approaching the biomarker levels in sham and drug-treated sham mice (the drugs had only modest effects on the T-tau and P-tau levels in sham mice) throughout the 12 month study period. Furthermore, although we also observed a reversal of the abnormal behavior and cognitive deficits in the drug-treated rmCHI mice (compared to the untreated rmCHI mice) throughout the time course, these drug-treated effects were most pronounced up until 10 and 12 months where the abnormal behavior and cognition deficits began to gradually increase. These studies describe: (a) a translational relevant animal model for TBI-linked tauopathies, and (b) utilization of T-tau and P-tau as rmCHI biomarkers in plasma to monitor novel therapeutic strategies and treatment regimens for these neurodegenerative diseases

Comparing Plasma Phospho Tau, Total Tau, and Phospho Tau-Total Tau Ratio as Acute and Chronic Traumatic Brain Injury Biomarkers.

Importance: Annually in the United States, at least 3.5 million people seek medical attention for traumatic brain injury (TBI). The development of therapies for TBI is limited by the absence of diagnostic and prognostic biomarkers. Microtubule-associated protein tau is an axonal phosphoprotein. To date, the presence of the hypophosphorylated tau protein (P-tau) in plasma from patients with acute TBI and chronic TBI has not been investigated. Objective: To examine the associations between plasma P-tau and total-tau (T-tau) levels and injury presence, severity, type of pathoanatomic lesion (neuroimaging), and patient outcomes in acute and chronic TBI. Design, Setting, and Participants: In the TRACK-TBI Pilot study, plasma was collected at a single time point from 196 patients with acute TBI admitted to 3 level I trauma centers (4) (AUC = 0.771 and 0.777, respectively). Plasma samples from patients with chronic TBI also showed elevated P-tau levels and a P-tau-T-tau ratio significantly higher than that of healthy controls, with both P-tau indices strongly discriminating patients with chronic TBI from healthy controls (AUC = 1.000 and 0.963, respectively). Conclusions and Relevance: Plasma P-tau levels and P-tau-T-tau ratio outperformed T-tau level as diagnostic and prognostic biomarkers for acute TBI. Compared with T-tau levels alone, P-tau levels and P-tau-T-tau ratios show more robust and sustained elevations among patients with chronic TBI.This study was supported in part by the Office of the Assistant Secretary of Defense for Health Affairs through the Department of Defense (DOD) Broad Agency Announcement under award numbers W81XWH-11-2-0069 (Dr Rubenstein) and W81XWH-14-2-0166 (Dr Rubenstein). It was also supported in part by National Institutes of Health (NIH) grant RC2 NS069409 (Dr Manley), NIH grant 1U01 NS086090-01 (Dr Manley), US DOD grant W81XWH-14-2-0176 (Dr Manley), US DOD grant W81XWH-13-1-04 (Dr Manley), NIH grant R21NS085455-01 (Dr Wang), and University of Florida McKnight Brain Institute BSCIRTF fund (Dr Wang)

Western blot analysis of PrP^Sc from vCJD-infected Tg666 mice.

<p>Ten percent brain homogenates from two vCJD-infected Tg666 mice were prepared in lysis buffer and centrifuged at 13,000×g for 10 min. Twenty µl of supernatant from each of the two mice (1, 2) was either untreated or PK-treated prior to western blotting and immunostaining with Mab 3F4 as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066352#s4" target="_blank">Materials and Methods</a>.</p

Partially purified, protease-resistant PrP^Sc titration from sCJD tissues.

<p>Homogenates of sCJD brain, spleen, tonsil, and lymph node were prepared, concentrated by ultracentrifugation and the pellets were resuspended as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066352#s4" target="_blank">Materials and Methods</a>. Undiluted (und) and two-fold serial dilutions of the PK-treated resuspended pellets were western blotted and immunostained for PrP^Sc using Mab 3F4. A PK-untreated sample is shown for each tissue to demonstrate the completeness of the PK treatment. Asterisk (*) denotes that the amount of brain tissue equivalents loaded in each lane is 1/100 the amount relative to spleen, tonsil, and lymph node.</p

Detection of PrP^Sc from sCJD by SOFIA following PASA of human CSF.

<p>PASA was carried out using normal human and sCJD CSF as the source of the seeding material. Serial PMCA was carried out individually on all of the normal human and sCJD CSF for a maximum of 200 cycles with samples collected at 0, 40, 80, 160, and 200 cycles for IP and analysis in triplicate by SOFIA. For each sample, data was calculated as the mean fluorescent signal±standard deviation and expressed as the sample to background ratio (signal intensity). Signal intensities from SOFIA were adjusted based on the dilution of samples throughout sPMCA.</p

End-Point Titrations of PrP^Sc by SOFIA in non-CNS Tissues.

*<p>Values are voltage readings expressed as the means of the sample background ratio.</p

PrP^Sc Detection by SOFIA Following PASA (sPMCA₂₀₀) in urine and blood.

<p>PASA was evaluated in human urine and blood from each sCJD case and blood from vCJD-infected Tg666 mice. Following sPMCA₂₀₀, samples were analyzed in triplicate by SOFIA for the presence of PrP^Sc. Signal intensities from SOFIA were adjusted based on the dilution of samples throughout sPMCA₂₀₀, calculated as the mean fluorescent signal±standard deviation and expressed as the signal/background ratio.</p

Effects of sCJD and vCJD brain dilution on PrP^Sc detection by SOFIA.

<p>Ten percent homogenates from all the normal human (N), vCJD (V), and sCJD brain tissues were prepared as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066352#s4" target="_blank">Materials and Methods</a>. Serial 10-fold dilutions were prepared from each brain tissue sample and analyzed in triplicate by SOFIA as described. For each sample, data was calculated as the mean fluorescent signal±standard deviation and expressed as the sample to background ratio (signal intensity).</p

Partially purified, protease-resistant PrP^Sc titration from vCJD tissues.

<p>Homogenates of vCJD brain, spleen, tonsil, and lymph node were prepared and concentrated by ultracentrifugation as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0066352#s4" target="_blank">Materials and Methods</a>. Undiluted (und) and two-fold serial dilutions of the PK-treated resuspended pellets were western blotted and immunostained for PrP^Sc using Mab 3F4. A PK-untreated sample is shown for each tissue to demonstrate the completeness of the PK treatment. Asterisk (*) denotes that the amount of brain tissue equivalents loaded in each lane is 1/100 the amount relative to spleen, tonsil, and lymph node.</p