Second phalanx shortening osteotomy. An innovative technique for long second toe syndrome

AbstractLong second-toe syndrome, although frequent and disabling, has been little described. Current surgical techniques often lead to loss of function. Based on anatomical and biomechanical observations, the present study reports a second phalanx shortening osteotomy technique. The procedure is relatively non-invasive, involving self-stabilizing segment resection osteotomy of the second phalanx. Results for the first 23 feet undergoing the procedure were analyzed retrospectively. Assessment comprised clinical examination, radiography and AOFAS and FAAM scores. Mean follow-up was 19±9.9months. Second phalanx shortening osteotomy proved reliable, respecting the biomechanics of the toe

Células madre pluripotenciales en el tratamiento de la isquemia de miembros inferiores. Primer caso en Paraguay y nuestra experiencia en el Hospital de Clínicas de la Universidad Nacional de Asunción

Existe un grupo de pacientes con isquemia crítica de miembros inferiores, en los cuales no es posible restablecer una adecuada perfusión sanguínea por métodos quirúrgicos o endovasculares y presentan una posibilidad elevada de amputación. En las últimas décadas se han identificado en la médula ósea la existencia de células madre del grupo CD34+, que proliferan ante la presencia de isquemia tisular y migran a través del torrente circulatorio hacia estas zonas, dando origen a arteriolas capilares y vénulas. Este mecanismo suele verse dificultado in vivo por la oclusión de las arterias que irrigan la región afectada. En este trabajo presentamos los resultados de nuestra experiencia en dos pacientes, que fueron sometidos a la extracción mecánica de tejido de su médula ósea, que posteriormente fue filtrado e implantado a lo largo de sus miembros inferiores isquémicos, con el objeto de estimular la neoformación de vasos sanguíneos para aumentar la perfusión de sangre a estas zonas, cicatrizando sus heridas, evitando de esta manera su amputación

Atividade inseticida de óleos essenciais in natura e nanoencapsulados sobre Bemisia tabaci (Hemiptera: Aleyrodidae).

O objetivo deste trabalho foi avaliar a atividade dos óleos essenciais in natura e nanoencapsulados dos frutos de ambas as espécies vegetais sobre a mortalidade de ninfas de B. tabaci

Identification of Protein Networks Involved in the Disease Course of Experimental Autoimmune Encephalomyelitis, an Animal Model of Multiple Sclerosis

A more detailed insight into disease mechanisms of multiple sclerosis (MS) is crucial for the development of new and more effective therapies. MS is a chronic inflammatory autoimmune disease of the central nervous system. The aim of this study is to identify novel disease associated proteins involved in the development of inflammatory brain lesions, to help unravel underlying disease processes. Brainstem proteins were obtained from rats with MBP induced acute experimental autoimmune encephalomyelitis (EAE), a well characterized disease model of MS. Samples were collected at different time points: just before onset of symptoms, at the top of the disease and following recovery. To analyze changes in the brainstem proteome during the disease course, a quantitative proteomics study was performed using two-dimensional difference in-gel electrophoresis (2D-DIGE) followed by mass spectrometry. We identified 75 unique proteins in 92 spots with a significant abundance difference between the experimental groups. To find disease-related networks, these regulated proteins were mapped to existing biological networks by Ingenuity Pathway Analysis (IPA). The analysis revealed that 70% of these proteins have been described to take part in neurological disease. Furthermore, some focus networks were created by IPA. These networks suggest an integrated regulation of the identified proteins with the addition of some putative regulators. Post-synaptic density protein 95 (DLG4), a key player in neuronal signalling and calcium-activated potassium channel alpha 1 (KCNMA1), involved in neurotransmitter release, are 2 putative regulators connecting 64% of the identified proteins. Functional blocking of the KCNMA1 in macrophages was able to alter myelin phagocytosis, a disease mechanism highly involved in EAE and MS pathology. Quantitative analysis of differentially expressed brainstem proteins in an animal model of MS is a first step to identify disease-associated proteins and networks that warrant further research to study their actual contribution to disease pathology

Redox regulation of mitochondrial fission, protein misfolding, synaptic damage, and neuronal cell death: potential implications for Alzheimer’s and Parkinson’s diseases

Normal mitochondrial dynamics consist of fission and fusion events giving rise to new mitochondria, a process termed mitochondrial biogenesis. However, several neurodegenerative disorders manifest aberrant mitochondrial dynamics, resulting in morphological abnormalities often associated with deficits in mitochondrial mobility and cell bioenergetics. Rarely, dysfunctional mitochondrial occur in a familial pattern due to genetic mutations, but much more commonly patients manifest sporadic forms of mitochondrial disability presumably related to a complex set of interactions of multiple genes (or their products) with environmental factors (G × E). Recent studies have shown that generation of excessive nitric oxide (NO), in part due to generation of oligomers of amyloid-β (Aβ) protein or overactivity of the NMDA-subtype of glutamate receptor, can augment mitochondrial fission, leading to frank fragmentation of the mitochondria. S-Nitrosylation, a covalent redox reaction of NO with specific protein thiol groups, represents one mechanism contributing to NO-induced mitochondrial fragmentation, bioenergetic failure, synaptic damage, and eventually neuronal apoptosis. Here, we summarize our evidence in Alzheimer’s disease (AD) patients and animal models showing that NO contributes to mitochondrial fragmentation via S-nitrosylation of dynamin-related protein 1 (Drp1), a protein involved in mitochondrial fission. These findings may provide a new target for drug development in AD. Additionally, we review emerging evidence that redox reactions triggered by excessive levels of NO can contribute to protein misfolding, the hallmark of a number of neurodegenerative disorders, including AD and Parkinson’s disease. For example, S-nitrosylation of parkin disrupts its E3 ubiquitin ligase activity, and thereby affects Lewy body formation and neuronal cell death

Roles of glial cells in synapse development

Brain function relies on communication among neurons via highly specialized contacts, the synapses, and synaptic dysfunction lies at the heart of age-, disease-, and injury-induced defects of the nervous system. For these reasons, the formation—and repair—of synaptic connections is a major focus of neuroscience research. In this review, I summarize recent evidence that synapse development is not a cell-autonomous process and that its distinct phases depend on assistance from the so-called glial cells. The results supporting this view concern synapses in the central nervous system as well as neuromuscular junctions and originate from experimental models ranging from cell cultures to living flies, worms, and mice. Peeking at the future, I will highlight recent technical advances that are likely to revolutionize our views on synapse–glia interactions in the developing, adult and diseased brain