Proyecto FOLTRA

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Investigacion

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Lo afirmamos en 2012 y lo confirman ahora

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Correo electrónico
Jueves 03 de Marzo de 2016 00:00

En 2012 publicamos un trabajo experimental en ratas, en el que demostrábamos que la administración de GH era capaz de revertir el daño producido por la sección del nervio ciático, uno de los nervios periféricos hasta entonces imposible de reparar. Bajo estas líneas figua el abstract del trabajo entonces publicado en Muscle and Nerve. 

 2012 Mar;45(3):385-92. doi: 10.1002/mus.22303.

Growth hormone treatment enhances the functional recovery of sciatic nerves after transection and repair.

Author information

  • 1Department of Physiology, School of Medicine, University of Santiago de Compostela, San Francisco 1, 15782 Santiago de Compostela, Spain.

Abstract

INTRODUCTION: 

Although nerves can spontaneously regenerate in the peripheral nervous system without treatment, functional recovery is generally poor, and thus there is a need for strategies to improve nerve regeneration.

METHODS: 

The left sciatic nerve of adult rats was transected and immediately repaired by epineurial sutures. Rats were then assigned to one of two experimental groups treated with either growth hormone (GH) or saline for 8 weeks. Sciatic nerve regeneration was estimated by histological evaluation, nerve conduction tests, and rotarod and treadmill performance.

RESULTS: 

GH-treated rats showed increased cellularity at the lesion site together with more abundant immunoreactive axons and Schwann cells. Compound muscle action potential (CMAP) amplitude was also higher in these animals, and CMAP latency was significantly lower. Treadmill performance increased in rats receiving GH.

CONCLUSION: 

GH enhanced the functional recovery of the damaged nerves, thus supporting the use of GH treatment, alone or combined with other therapeutic approaches, in promoting nerve repair.

 

Como muchas veces se afirma que "vendemos humo", aquí está una muestra de que nadie, hasta ahora, ha rebatido ninguna de nuestras publicaciones que, desde hace ya muchos años, fueron en su día "rompedoras" del conocimiento existente. En este caso se trata de una publicación muy reciente, febrero de 2016, de neurólogos, neurocirujanos y cirujanos plásticos del Hospital Johns Hopkins de Baltimore (USA), una de las más acreditadas instituciones hospitalarias y científicas de Estados Unidos y, por ende, del mundo. Fíjense en el abstract del trabajo que publican:

 2016 Feb 11. [Epub ahead of print]

Growth Hormone Therapy Accelerates Axonal Regeneration, Promotes Motor Reinnervation, and Reduces Muscle Atrophy Following Peripheral Nerve Injury.

Author information

  • 1Department of Neurology, Johns Hopkins (Hoke) Department of Medicine, Johns Hopkins (Salvatori) Curtis National Hand Center, Baltimore, MD (Higgins, Means) Department of Plastic and Reconstructive Surgery for the rest.

Abstract

BACKGROUND: 

Therapies to improve outcomes following peripheral nerve injury are lacking. Prolonged denervation of muscle and Schwann cells (SCs) contributes to poor outcomes. In this study, we assess the effects of growth hormone (GH) therapy on axonal regeneration, SC and muscle maintenance, and end-organ reinnervation in rats.

METHODS: 

Male Sprague-Dawley rats underwent sciatic nerve transection-and-repair and femoral nerve transection-without-repair and received either daily subcutaneous GH (0.4 mg/day) or no treatment (N=8 per group). At 5 weeks, we assessed axonal regeneration within the sciatic nerve, muscle atrophy within the gastrocnemius muscle, motor endplate reinnervation within the soleus muscle, and SC proliferation within the denervated distal femoral nerve.

RESULT: 

GH-treated animals demonstrated greater percent increase in body mass (12.2 1.8 vs. 8.5 1.5, p=0.0044), greater number of regenerating myelinated axons (13876 2036 vs. 8645 3279, p=0.0018) and G-ratio (0.64 0.11 vs. 0.51 0.06, p=0.01), greater percent reinnervation of motor endplates (75.8 8.7 vs. 38.2 22.6, p=0.0008), and greater muscle myofibril cross-sectional area (731.8 157 µm vs. 545.2 144.3 µm, p=0.027).

CONCLUSIONS: 

In male rats, GH therapy accelerates axonal regeneration, reduces muscle atrophy and promotes muscle reinnervation. GH therapy may also maintain proliferating SCs in the setting of prolonged denervation. These findings suggest potential for improved outcomes with GH therapy following peripheral nerve injuries.

 

 

Brain Recovery after a Plane Crash: Treatment with Growth Hormone (GH) and Neurorehabilitation: A Case Report

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Correo electrónico
Lunes 21 de Diciembre de 2015 00:00

 Entrar en:

http://www.mdpi.com/1422-0067/16/12/26244/html 

 

Melatonina y cáncer

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Correo electrónico
Domingo 04 de Octubre de 2015 00:00

 La verdad es que no puedo resistirme a dejar sin dar a conocer lo que hay, sumamente interesante, de nuevo en relación a la melatonina y cáncer.

Para que no haya dudas de interpretación voy a copiar los abstracts de las publicaciones, en inglés, sin más que añadir alguas palabras clave.

Por ejemplo, en 2013, Reiter, un gigante como persona (buena y grande) y científico, de la Universidad de Texas escribió:

 

 2013 Dec;17(12):1483-96. doi: 10.1517/14728222.2013.834890. Epub 2013 Sep 14.

Molecular mechanisms of the pro-apoptotic actions of melatonin in cancer: a review.

Abstract

INTRODUCTION: 

Compelling evidence has highlighted the complex pleiotropic functions elicited by the melatonin in cancer cells. Melatonin behaves as a 'smart killer', i.e., modulating anti-apoptotic processes in normal cells, and triggering pro-apoptotic signals in cancer cells.

AREAS COVERED: 

Melatonin induces programmed cell death in a wide range of different tumors (breast, gastro-intestinal, hematological, prostate, osteosarcoma, melanoma, kidney, etc…). Mechanisms of action and molecular pathways involved in pro-apoptotic processes under melatonintreatment are discussed.

EXPERT OPINION: 

Melatonin involvement in apoptotic processes is a new and relevant field of investigation. Even in tumor models unresponsive to melatonin alone, this hormone can significantly amplify the cytostatic and the cytotoxic effects triggered by other compounds or conventional drugs. We are far from having a satisfactory understanding about how and when melatonin exerts its beneficial effects. Melatonin in the nanomolar range activates the intrinsic and/or the extrinsic apoptotic pathway in cancer cells, namely through an increase in the p53/MDM2p ratio and downregulation of Sirt1. This finding is of great relevance since there is intense research ongoing to identify nontoxic feasible inhibitors of MDM2 and Sirt1. Melatonin should be evaluated for the management of those cancers where both of these are overexpressed and functionally strategic.

Conceptos clave: Melatonin behaves as a "smart killer": la melatonina actúa como un asesino inteligente modulando procesos anti-apoptosis (anti muerte celular) en las células normales y "disparando señales pro-apoptóticas en las células cancerosas".

¿Cómo lo hace?: through an increase in the p53/MDM2p ratio and downregulation of Sirt1. Incrementando la relación p53 (gen pro-apoptótico)/ MDM2p y disminuyendo Sirt1. 

 

Otro trabajo, más reciente, publicado en PlOs ONe por un grupo de la Universidad de Oviedo:

 2015 Aug 7;10(8):e0135420. doi: 10.1371/journal.pone.0135420. eCollection 2015.

Melatonin Cytotoxicity Is Associated to Warburg Effect Inhibition in Ewing Sarcoma Cells.

Abstract

Melatonin kills or inhibits the proliferation of different cancer cell types, and this is associated with an increase or a decrease in reactive oxygen species, respectively. Intracellular oxidants originate mainly from oxidative metabolism, and cancer cells frequently show alterations in this metabolic pathway, such as the Warburg effect (aerobic glycolysis). Thus, we hypothesized that melatonin could also regulate differentially oxidative metabolism in cells where it is cytotoxic (Ewing sarcoma cells) and in cells where it inhibits proliferation (chondrosarcoma cells). Ewing sarcoma cells but not chondrosarcoma cells showed a metabolic profile consistent with aerobic glycolysis, i.e. increased glucose uptake, LDH activity, lactate production and HIF-1α activation. Melatonin reversed Ewing sarcoma metabolic profile and this effect was associated with its cytotoxicity. The differential regulation of metabolism by melatonin could explain why the hormone is harmless for a wide spectrum of normal and only a few tumoral cells, while it kills specific tumor cell types.

Conceptos clave: La melatonina modifica el perfil metabólico de las células cancerosas, a nivel del metabolismo oxidativo, de forma inteligente; es decir, que no actúa modificando este perfil en céluluas normales y sí "asesina" una serie de tipos celulares cancerosos específicos.... 

 
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