Broadband inelastic light scattering of a relaxor ferroelectric 0.71Pb(Ni1/3Nb2/3)O3-0.29PbTiO3

Brillouin and Raman scatterings of a 0.71Pb(Ni1/3Nb2/3)O3-0.29PbTiO3 single crystal have been measured to investigate broadband inelastic spectra. The two different central peaks related to fast and slow relaxation processes have been observed separately. These two processes are attributed to the thermally activated switching of polarization in polar nanoregions. By the analysis of modified superparaelectric model, the activation energies of fast and slow relaxation processes are determined to be 3.66×103 and 4.31×102 K, respectively. The fast process with the lower activation energy probably originated from 180° switching, whereas the slow one with the higher energy from non-180° switching

Oligodendrocytes Engineered with Migratory Proteins as Effective Graft Source for Cell Transplantation in Multiple Sclerosis

Multiple sclerosis (MS) is characterized by widespread immunomodulatory demyelination of the central nervous system (CNS), resulting in nerve cell dysfunction. Accordingly, treatment strategies have been centered on immunodulation and remyelination, with the former primarily focused on reducing the pathology rather than enhancing myelin repair, which the latter targets. While conceding to the emerging view of heterogeneity in the pathology of MS, which precludes variations in degree of immune response (i.e., inflammation) and demyelination, the concept of enhancing myelin repair is appealing since it is likely to provide both disease-reducing and disease-inhibiting therapeutic approaches to MS. In this regard, we and several others have proposed that cell replacement therapy is an effective strategy to repair the myelin in MS. Here we hypothesize that transplantation of mouse bone marrow-derived oligodendrocytes (BMDOs) and BMDOs transfected with ephrin proteins (BMDO + ephrin), which are known to enhance cell and axonal migratory capacity, may produce therapeutic benefits in animal models of MS

Estrogen Replacement Therapy for Stroke

Stroke is the third most common cause of death and severe disability among Western populations. Overall, the incidence of stroke is uniformly higher in men than in women. Stroke is rare in women during the reproductive years and rapidly increases after menopause, strongly suggesting that estrogen (E2) plays an important role in the prevention of stroke. Ongoing studies are currently evaluating both the benefits and the risks associated with E2 replacement therapy and hormone replacement therapy in stroke. Equally important is the role of E2 receptor (ER), as studies indicate that ER populations in several tissue sites may significantly change during stress and aging. Such changes may affect the patient\u27s susceptibility to neurological disorders including stroke and greatly affect the response to selective E2 receptor modulators (SERMs). Replacement therapies may be inefficient with low ER levels. The goal of this review paper is to discuss an animal model that will allow investigations of the potential therapeutic effects of E2 and its derivatives in stroke. We hypothesize that E2 neuroprotection is, in part, receptor mediated. This hypothesis is a proof-of-principle approach to demonstrate a role for specific ER subtypes in E2 neuroprotection. To accomplish this, we use a retroviral-mediated gene transfer strategy that expresses subtypes of the ER gene in regions of the rat brain most susceptible to neuronal damage, namely, the striatum and the cortex. The animal model is exposed to experimental stroke conditions involving middle cerebral artery occlusion (MCAo) method, and eventually the extent of neuronal damage will be evaluated. A reduction in neuronal damage is expected when E2 is administered with specific ER subtypes. From this animal model, an optimal E2 dose and treatment regimen can be determined. The animal model can help identify potential E2-like therapeutics in stroke and screen for beneficial or toxic additives present in commercial E2 preparations that are currently available. Such studies will be informative in designing drug therapies for stroke

Are the Taitao granites formed due to subduction of the Chile ridge?

The Taitao granites are distributed around the Late Miocene Taitao ophiolite (5.66 ± 0.33 Ma to 5.19 ± 0.15 Ma) exposed at the western tip of the Taitao peninsula, southern Chile, ~ 50 km southeast from the present day Chile triple junction. In thi

Adult Stem Cell Transplantation: Is Gender a Factor in Stemness?

Cell therapy now constitutes an important area of regenerative medicine. The aging of the population has mandated the discovery and development of new and innovative therapeutic modalities to combat devastating disorders such as stroke. Menstrual blood and Sertoli cells represent two sources of viable transplantable cells that are gender-specific, both of which appear to have potential as donor cells for transplantation in stroke. During the subacute phase of stroke, the use of autologous cells offers effective and practical clinical application and is suggestive of the many benefits of using the aforementioned gender-specific cells. For example, in addition to being exceptionally immunosuppressive, testis-derived Sertoli cells secrete many growth and trophic factors and have been shown to aid in the functional recovery of animals transplanted with fetal dopaminergic cells. Correspondingly, menstrual blood cells are easily obtainable and exhibit angiogenic characteristics, proliferative capability, and pluripotency. Of further interest is the ability of menstrual blood cells, following transplantation in stroke models, to migrate to the infarct site, secrete neurotrophic factors, regulate the inflammatory response, and be steered towards neural differentiation. From cell isolation to transplantation, we emphasize in this review paper the practicality and relevance of the experimental and clinical use of gender-specific stem cells, such as Sertoli cells and menstrual blood cells, in the treatment of stroke

Stem cell-paved biobridge facilitates neural repair in traumatic brain injury.

Modified mesenchymal stromal cells (MSCs) display a unique mechanism of action during the repair phase of traumatic brain injury by exhibiting the ability to build a biobridge between the neurogenic niche and the site of injury. Immunohistochemistry and laser capture assay have visualized this biobridge in the area between the neurogenic subventricular zone and the injured cortex. This biobridge expresses high levels of extracellular matrix metalloproteinases (MMPs), which are initially co-localized with a stream of transplanted MSCs, but later this region contains only few to non-detectable grafts and becomes overgrown by newly recruited host cells. We have reported that long-distance migration of host cells from the neurogenic niche to the injured brain site can be attained via these transplanted stem cell-paved biobridges, which serve as a key regenerative process for the initiation of endogenous repair mechanisms. Thus, far the two major schools of discipline in stem cell repair mechanisms support the idea of cell replacement and the bystander effects of trophic factor secretion. Our novel observation of stem cell-paved biobridges as pathways for directed migration of host cells from neurogenic niche toward the injured brain site adds another mode of action underlying stem cell therapy. More in-depth investigations on graft-host interaction will likely aid translational research focused on advancing this stem cell-paved biobridge from its current place, as an equally potent repair mechanism as cell replacement and trophic factor secretion, into a new treatment strategy for traumatic brain injury and other neurological disorders