Photobiomodulation for Alzheimer’s disease : translating basic research to clinical application

Abstract:One of the challenges in translating new therapeutic approaches to the patient bedside lies in bridging the gap between scientists who are conducting basic laboratory research and medical practitioners who are not exposed to highly specialized journals. This review covers the literature on photobiomodulation therapy as a novel approach to prevent and treat Alzheimer’s disease, aiming to bridge that gap by gathering together the terms and technical specifications into a single concise suggestion for a treatment protocol. In light of the predicted doubling in the number of people affected by dementia and Alzheimer’s disease within the next 30 years, a treatment option which has already shown promising results in cell culture studies and animal models, and whose safety has already been proven in humans, must not be left in the dark. This review covers the mechanistic action of photobiomodulation therapy against Alzheimer’s disease at a cellular level. Safe and effective doses have been found in animal models, and the first human case studies have provided reasons to undertake large-scale clinical trials. A brief discussion of the minimally effective and maximum tolerated dose concludes this review, and provides the basis for a successful translation from bench to bedside

On the B to D* tau nu Sensitivity to New Physics

B physics has played a prominent role in investigations of new physics effects at low-energies. Presently, the largest discrepancy between a standard model prediction and experimental measurements appears in the branching ratio of the charged current mediated B to tau nu decay, where the large tau mass lifts the helicity suppression arising in leptonic B decays. Less significant systematic deviations are also observed in the semileptonic B to D(*) tau nu rates. Due to the rich spin structure of the final state, the decay mode B to D* tau nu offers a number of tests of such possible standard model deviations. We investigate the most general set of lowest dimensional effective operators leading to helicity suppressed modifications of b to c (semi)leptonic transitions. We explore such contributions to the B to D* tau nu decay amplitudes by determining the differential decay rate, longitudinal D* polarization fraction, D* - tau opening angle asymmetry and the tau helicity asymmetry. We identify the size of possible new physics contributions constrained by the present B to D(*) tau nu rate measurements and find significant modifications are still possible in all of them. In particular, the opening angle asymmetry can be shifted by almost 30%, relative to the standard model prediction, while the tau helicity asymmetry can still deviate by as much as 80%.Comment: 10 pages, 4 figures; corrected several typos, added references, conclusions unchange

Mechanical Stimulation of Fibroblasts by Extracorporeal Shock Waves: Modulation of Cell Activation and Proliferation Through a Transient Proinflammatory Milieu

Extracorporeal shock waves (ESWTs) are \u201cmechanical\u201d waves, widely used in regenerative medicine, including soft tissue wound repair. Although already being used in the clinical practice, the mechanism of action underlying their biological activities is still not fully understood. In the present paper we tried to elucidate whether a proinflammatory effect may contribute to the regenerative potential of shock waves treatment. For this purpose, we exposed human foreskin fibroblasts (HFF1 cells) to an ESWT treatment (100 pulses using energy flux densities of 0.19 mJ/mm2 at 3 Hz), followed by cell analyses after 5 min, up to 48 h. We then evaluated cell proliferation, reactive oxygen species generation, ATP release, and cytokine production. Cells cultured in the presence of lipopolysaccharide (LPS), to induce inflammation, were used as a positive control, indicating that LPS-mediated induction of a proinflammatory pattern in HFF1 increased their proliferation. Here, we provide evidence that ESWTs affected fibroblast proliferation through the overexpression of selected cytokines involved in the establishment of a proinflammatory program, superimposable to what was observed in LPS-treated cells. The possibility that inflammatory circuits can be modulated by ESWT mechanotransduction may disclose novel hypothesis on their biological underpinning and expand the fields of their biomedical application

Mechanical Stimulation of Fibroblasts by Extracorporeal Shock Waves: Modulation of Cell Activation and Proliferation Through a Transient Proinflammatory Milieu

Extracorporeal shock waves (ESWTs) are "mechanical" waves, widely used in regenerative medicine, including soft tissue wound repair. Although already being used in the clinical practice, the mechanism of action underlying their biological activities is still not fully understood. In the present paper we tried to elucidate whether a proinflammatory effect may contribute to the regenerative potential of shock waves treatment. For this purpose, we exposed human foreskin fibroblasts (HFF1 cells) to an ESWT treatment (100 pulses using energy flux densities of 0.19 mJ/mm2 at 3 Hz), followed by cell analyses after 5 min, up to 48 h. We then evaluated cell proliferation, reactive oxygen species generation, ATP release, and cytokine production. Cells cultured in the presence of lipopolysaccharide (LPS), to induce inflammation, were used as a positive control, indicating that LPS-mediated induction of a proinflammatory pattern in HFF1 increased their proliferation. Here, we provide evidence that ESWTs affected fibroblast proliferation through the overexpression of selected cytokines involved in the establishment of a proinflammatory program, superimposable to what was observed in LPS-treated cells. The possibility that inflammatory circuits can be modulated by ESWT mechanotransduction may disclose novel hypothesis on their biological underpinning and expand the fields of their biomedical application

Search for the X(1812) in B±→K±ωϕB^{\pm} \to K^{\pm} \omega \phi

We report on a search for the X(1812) state in the decay $B^{\pm} \to K^{\pm} \omega \phi$ with a data sample of $657\times10^6$ $B\bar{B}$ pairs collected with the Belle detector at the KEKB $e^+e^-$ collider. No significant signal is observed. An upper limit ${\cal B}(B^{\pm} \to K^{\pm} X(1812),X(1812) \to \omega \phi)<3.2\times 10^{-7}$ (90% C.L.) is determined. We also constrain the three-body decay branching fraction to be ${\cal B}(B^{\pm} \to K^{\pm} \omega \phi)$ $<$ 1.9 $\times 10^{-6}$ (90% C.L.).Comment: 5pages,2 figures(3 figure files). submitted to PRD(RC