Acute osteomyelitis of the acetabulum induced by Staphylococcus capitis in a young athlete

Acute hematogenous osteomyelitis (AHOM) of the acetabulum is a rare condition in children and usually caused by Staphylococcus aureus. We present an 11-year-old soccer athlete who suffered from acute osteomyelitis involving the acetabulum caused by S. capitis, a normal flora of the human skin but never reported in this condition. The disease was associated with repetitive skin injuries of the knee and potential osseous microtrauma of the hip joint by frequent rigorous exercise. This unusual case suggests that osseous microtrauma of the acetabulum, in addition to repetitive skin injuries, allowed normal skin flora to colonize to the ipsilateral acetabulum, which served as a favorable niche and subsequently led to AHOM

Amputados transfemorais : sistema de captura de sinais eletromiográficos com interface de biomaterial látex

Monografia (graduação)—Universidade de Brasília, Faculdade UnB Gama, Curso de Engenharia Eletrônica, 2015.A amputação transfemoral, perda de um membro entre a altura do quadril e do joelho, pode ocorrer devido a doenças vasculares, neoplasias ou traumas. A rotina dos indivíduos com essa deficiência é fortemente alterada, pois geralmente há alguma dificuldade em realizar movimentos rotineiros como caminhar e subir escadas, forçando esses indivíduos a desenvolverem alguns movimentos para compensar essa adversidade. A eletromiografia de superfície (EMGs), ferramenta utilizada para captura da atividade elétrica muscular, tem sido amplamente utilizada no estudo do movimento do corpo humano. Os sinais de EMGs estão se tornando cada vez mais importantes em diversas aplicações na medicina esportiva e ocupacional. Esse sinal vem sendo utilizado para gerar comandos de controle para equipamentos de reabilitação, tais como: próteses robóticas e em interfaces homemmáquina. Também é muito utilizado em rotinas fisioterapêuticas, além de desempenhar um papel importante em pesquisas relacionadas ao sistema neuromuscular. Atualmente, é crescente o número de pesquisas que buscam melhorias na reabilitação e no controle de próteses ativas por meio de sinais de EMGs. No entanto, esses sinais são altamente contaminados por ruídos do ambiente e de artefatos mecânicos. Entretanto, a utilização de uma interface confeccionada a partir do biomaterial látex pode ajudar na redução da contaminação do sinal pelos ruídos. Nesse contexto, o desenvolvimento de um sistema de aquisição de EMG com baixo custo para captura de sinal no coto de amputados transfemorais por meio de uma interface de biomaterial látex são o foco desse trabalho onde, produzindo um sistema acessível, torna-se viável uma solução que poderia até ser implantada no Sistema Único de Saúde (SUS). Em conjunto com o Grupo de Pesquisa sobre a Saúde de Amputados Transfemorais GPSAT da UnB/FCe, foi desenvolvido esse sistema com uma interface de biomaterial látex e foram realizados testes in vivo em amputados transfemorais. _____________________________________________________________________________ ABSTRACTTransfemoral amputation, the loss of a limb between the hip and knee, can occur due to vascular diseases, neoplasms, or traumas. The routine of individuals with this handicap is severely altered, because usually there is some difficulty in performing routine movements such as walking and climbing stairs, which forces these individuals to develop some movements to compensate for this adversity. Surface electromyography (EMG), a tool used to capture electrical muscle activity, has been widely used in the study of movements of the human body. EMG is becoming increasingly important with different uses in sports and occupational medicine. EMG is being used to generate control commands for rehabilitation equipment, such as robotic prostheses and man/machine interfaces. It is also used in physical therapy routines, and also plays an important role in research related to the neuromuscular system. Currently, there is an increasing number of studies that seek improvements in rehabilitation and control of active prostheses through SEMG signals. However, these signals are severely contaminated by noises from the environment and mechanical artifacts. However, the use of an interface developed with latex biomaterial can help reduce the noise that contaminates the signal. Thus, the goal of this study was to develop a low-cost EMG acquisition system for capturing the signal from the stumps of transfemoral amputees using a latex biomaterial interface. We sought to develop an accessible system that would be a feasible solution and could even be used in the Unified Health System (SUS). Together with the Research Group on Health of Transfemoral Amputees from the GPSAT of UNB/FCe, we developed this system with a latex biomaterial interface. Tests were performed in vivo in transfemoral amputees

Molecular Interaction Between the Microenvironment and FLT3/ITD+ AML Cells Leading to the Refractory Phenotype

Internal tandem duplication mutations in the FLT3 gene (FLT3/ITD) are detected in 10–15% of children and 30% of adult patients with AML and are associated with an extremely poor prognosis. Although several antagonists against FLT3/ITD have been developed, few of them are effective for the treatment of FLT3/ITD+ AML because of the emergence of drug-resistant cells. The mechanisms responsible for drug resistance include the acquisition of additional mutations in the FLT3 gene and/or activation of other prosurvival pathways such as microenvironment-mediated resistance. Recent studies have strongly suggested that the reciprocal interaction between the microenvironment and AML cells generates specific machinery that leads to chemoresistance. This chapter describes the molecular mechanism responsible for the refractory phenotype of FLT3/ITD+ AML cells resulting from the communication between the microenvironment and FLT3/ITD+ leukemia cells. Understanding this mechanism enables the discovery of novel and innovative therapeutic interventions for resistant FLT3/ITD+ AML

A danger of induction of Brugada syndrome during pill-in-the-pocket therapy for paroxysmal atrial fibrillation

Rhythm control therapy by sodium channel blockers is widely performed for the treatment of paroxysmal atrial fibrillation. Here, we present a case of acquired Brugada syndrome by pill-in-the-pocket treatment using pilsicainide. It is important that this therapy should be applied only after confirming the drug safety to the patients

Survivin Selectively Modulates Genes Deregulated in Human Leukemia Stem Cells

ITD-Flt3 mutations are detected in leukemia stem cells (LSCs) in acute myeloid leukemia (AML) patients. While antagonizing Survivin normalizes ITD-Flt3-induced acute leukemia, it also impairs hematopoietic stem cell (HSC) function, indicating that identification of differences in signaling pathways downstream of Survivin between LSC and HSC are crucial to develop selective Survivin-based therapeutic strategies for AML. Using a Survivin-deletion model, we identified 1,096 genes regulated by Survivin in ITD-Flt3-transformed c-kit+, Sca-1+, and lineageneg (KSL) cells, of which 137 are deregulated in human LSC. Of the 137, 124 genes were regulated by Survivin exclusively in ITD-Flt3+ KSL cells but not in normal CD34neg KSL cells. Survivin-regulated genes in LSC connect through a network associated with the epidermal growth factor receptor signaling pathway and falls into various functional categories independent of effects on apoptosis. Pathways downstream of Survivin in LSC that are distinct from HSC can be potentially targeted for selective anti-LSC therapy

Internal Tandem Duplication in FLT3 Attenuates Proliferation and Regulates Resistance to the FLT3 Inhibitor AC220 by Modulating p21Cdkn1a and Pbx1 in Hematopoietic Cells

Internal tandem duplication (ITD) mutations in the Fms-related tyrosine kinase 3 (FLT3) gene (FLT3-ITD) are associated with poor prognosis in patients with acute myeloid leukemia (AML). Due to the development of drug resistance, few FLT3-ITD inhibitors are effective against FLT3-ITD+ AML. In this study, we show that FLT3-ITD activates a novel pathway involving p21Cdkn1a (p21) and pre-B cell leukemia transcription factor 1 (Pbx1) that attenuates FLT3-ITD cell proliferation and is involved in the development of drug resistance. FLT3-ITD up-regulated p21 expression in both mouse bone marrow c-kit+-Sca-1+-Lin- (KSL) cells and Ba/F3 cells. The loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of concomitantly enriching the S+G2/M phase population and significantly increasing the expression of Pbx1, but not Evi-1, in FLT3-ITD+ cells. This enhanced cell proliferation following the loss of p21 was partially abrogated when Pbx1 expression was silenced in FLT3-ITD+ primary bone marrow colony-forming cells and Ba/F3 cells. When FLT3-ITD was antagonized with AC220, a selective inhibitor of FLT3-ITD, p21 expression was decreased coincident with Pbx1 mRNA up-regulation and a rapid decline in the number of viable FLT3-ITD+ Ba/F3 cells; however, the cells eventually became refractory to AC220. Overexpressing p21 in FLT3-ITD+ Ba/F3 cells delayed the emergence of cells that were refractory to AC220, whereas p21 silencing accelerated their development. These data indicate that FLT3-ITD is capable of inhibiting FLT3-ITD+ cell proliferation through the p21/Pbx1 axis and that treatments that antagonize FLT3-ITD contribute to the subsequent development of cells that are refractory to a FLT3-ITD inhibitor by disrupting p21 expression

Survivin is Required for Mouse and Human Bone Marrow Mesenchymal Stromal Cell Function

Although mesenchymal stromal cells (MSCs) have significant potential in cell-based therapies, little is known about the factors that regulate their functions. While exploring regulatory molecules potentially involved in MSC activities, we found that the endogenous multifunctional factor Survivin is essential for MSC survival, expansion, lineage commitment, and migration. Pharmacological or genetic blockade of Survivin expression in mouse and human bone marrow MSC enhances caspase 3 and 7 expression and reduces proliferation resulting in fewer MSC and clonogenic colony-forming unit-fibroblasts (CFU-F), whereas ectopic Survivin overexpression in MSC results in their expansion. Survivin is also required for the MSC proliferative responses to basic fibroblast growth factor and platelet derived growth factor. In a wound healing model, Survivin inhibition results in suppression of MSC migration to the wound site. In addition, loss of Survivin in MSCs compromises their hematopoiesis-supporting capacity. These results demonstrate that Survivin is a key regulator of mouse and human MSC function, and suggest that targeted modulation of Survivin in MSCs may have clinical utility to enhance MSC recovery and activity following insult or stress