Effects of therapeutic ultrasound on the mechanical properties of skeletal muscles after contusion

CONTEXTUALIZAÇÃO: O ultra-som terapêutico (UST) é um recurso comumente aplicado na aceleração do reparo tecidual de lesões musculares. A absorção das ondas ultra-sônicas é determinada pela freqüência e pela intensidade, sendo que, em uma mesma intensidade, a profundidade atingida por 1MHz é maior quando comparada a 3MHz. OBJETIVO: Analisar o comportamento das propriedades mecânicas de músculos submetidos à lesão aguda por impacto e tratados com UST, utilizando as freqüências de 1 e 3MHz. MATERIAIS E MÉTODOS: Foram utilizadas 40 ratas Wistar (200,1±17,8g), divididas em quatro grupos: (1) controle; (2) lesão muscular sem tratamento; (3) lesão muscular tratada com UST de freqüência 1MHz (0,5W/cm²) e (4) lesão muscular tratada com UST de freqüência 3MHz (0,5W/cm²). A lesão foi provocada no músculo gastrocnêmio por mecanismo de impacto. O tratamento foi de cinco minutos diários durante seis dias consecutivos. Os músculos foram submetidos a ensaios mecânicos de tração em uma máquina universal de ensaios. RESULTADOS: As médias e desvios-padrão das propriedades mecânicas dos grupos lesionados e tratados com UST foram significativamente maiores quando comparadas ao grupo lesionado sem tratamento (p<0,05). Em destaque, a propriedade de rigidez que, com a aplicação do UST, teve acréscimo de aproximadamente 38%. CONCLUSÕES: A intervenção, por meio do UST, promoveu aumento das propriedades mecânicas nos músculos lesionados aproximando-as do grupo controle. Entretanto, não foi observada diferença significativa entre as propriedades mecânicas dos grupos tratados com ultra-som de freqüências 1MHz e 3MHz.BACKGROUND: Therapeutic ultrasound is a resource commonly applied to speed up tissue repair in muscle injuries. The absorption of the ultrasound waves is determined by their frequency and intensity. For a given intensity, the depth reached by 1MHz is greater than the depth reached by 3MHz. OBJECTIVE: To analyze the mechanical properties of muscles subjected to acute impact injury treated with therapeutic ultrasound at the frequencies of 1 and 3MHz. METHODS: Forty female Wistar rats (200.1±17.8g) were used, divided into four groups: (1) control; (2) muscle injury without treatment; (3) muscle injury treated with therapeutic ultrasound at the frequency of 1MHz (0.5W/cm²); and (4) muscle injury treated with therapeutic ultrasound at the frequency of 3MHz (0.5W/cm²). The injury was produced in the gastrocnemius muscle by means of an impact mechanism. The treatment consisted of a single five-minute session per day, for six consecutive days. The muscles were subjected to mechanical traction tests in a universal test machine. RESULTS: Means and standard deviations for the mechanical properties of the injured groups that received therapeutic ultrasound were significantly greater than those of the injured group without treatment (p<0.05). The property of stiffness should be highlighted: the application of therapeutic ultrasound increased muscle stiffness by approximately 38%. CONCLUSIONS: Therapeutic ultrasound increased the mechanical properties of the injured muscles, and brought them to a level close to the control group. However, no significant difference in mechanical properties was observed between the groups treated with ultrasound at the frequencies of 1MHz and 3MHz

A Duplication CNV That Conveys Traits Reciprocal to Metabolic Syndrome and Protects against Diet-Induced Obesity in Mice and Men

The functional contribution of CNV to human biology and disease pathophysiology has undergone limited exploration. Recent observations in humans indicate a tentative link between CNV and weight regulation. Smith-Magenis syndrome (SMS), manifesting obesity and hypercholesterolemia, results from a deletion CNV at 17p11.2, but is sometimes due to haploinsufficiency of a single gene, RAI1. The reciprocal duplication in 17p11.2 causes Potocki-Lupski syndrome (PTLS). We previously constructed mouse strains with a deletion, Df(11)17, or duplication, Dp(11)17, of the mouse genomic interval syntenic to the SMS/PTLS region. We demonstrate that Dp(11)17 is obesity-opposing; it conveys a highly penetrant, strain-independent phenotype of reduced weight, leaner body composition, lower TC/LDL, and increased insulin sensitivity that is not due to alteration in food intake or activity level. When fed with a high-fat diet, Dp(11)17/+ mice display much less weight gain and metabolic change than WT mice, demonstrating that the Dp(11)17 CNV protects against metabolic syndrome. Reciprocally, Df(11)17/+ mice with the deletion CNV have increased weight, higher fat content, decreased HDL, and reduced insulin sensitivity, manifesting a bona fide metabolic syndrome. These observations in the deficiency animal model are supported by human data from 76 SMS subjects. Further, studies on knockout/transgenic mice showed that the metabolic consequences of Dp(11)17 and Df(11)17 CNVs are not only due to dosage alterations of Rai1, the predominant dosage-sensitive gene for SMS and likely also PTLS. Our experiments in chromosome-engineered mouse CNV models for human genomic disorders demonstrate that a CNV can be causative for weight/metabolic phenotypes. Furthermore, we explored the biology underlying the contribution of CNV to the physiology of weight control and energy metabolism. The high penetrance, strain independence, and resistance to dietary influences associated with the CNVs in this study are features distinct from most SNP–associated metabolic traits and further highlight the potential importance of CNV in the etiology of both obesity and MetS as well as in the protection from these traits

Efficient Enrichment of Hepatic Cancer Stem-Like Cells from a Primary Rat HCC Model via a Density Gradient Centrifugation-Centered Method

Background: Because few definitive markers are available for hepatic cancer stem cells (HCSCs), based on physical rather than immunochemical properties, we applied a novel method to enrich HCSCs. Methodology: After hepatic tumor cells (HTCs) were first isolated from diethylinitrosamine-induced F344 rat HCC model using percoll discontinuous gradient centrifugation (PDGC) and purified via differential trypsinization and differential attachment (DTDA), they were separated into four fractions using percoll continuous gradient centrifugation (PCGC) and sequentially designated as fractions I–IV (FI–IV). Morphological characteristics, mRNA and protein levels of stem cell markers, proliferative abilities, induced differentiation, in vitro migratory capacities, in vitro chemo-resistant capacities, and in vivo malignant capacities were determined for the cells of each fraction. Findings: As the density of cells increased, 22.18%, 11.62%, 4.73 % and 61.47 % of primary cultured HTCs were segregated in FI–FIV, respectively. The cells from FIII (density between 1.041 and 1.062 g/ml) displayed a higher nuclear-cytoplasmic ratio and fewer organelles and expressed higher levels of stem cell markers (AFP, EpCAM and CD133) than cells from other fractions (P,0.01). Additionally, in vitro, the cells from FIII showed a greater capacity to self-renew, differentiate into mature HTCs, transit across membranes, close scratches, and carry resistance to chemotherapy than did cells from any other fraction; in vivo, injection of only 1610 4 cells from FIII could generate tumors not only in subcutaneous tissue but also in th