Level IV, retrospective case series.

Polytrauma is the leading cause of death, followed by severe traumatic brain injury (sTBI). The temporal analysis of traumatic death indicates a shift from the classic "trimodal" distribution to a new "bimodal" distribution. Besides advances in road safety, prevention programs and improvement in trauma management-especially the pre-hospital phase-have the potential to significantly improve the survival rate after trauma.

MicroRNAs (miRNAs) play a pivotal role in cancerogenesis and cancer progression, but their specific role in the metastasis of clear cell renal cell carcinomas (ccRCC) is still limited. Based on microRNA microarray analyses from normal and cancerous samples of ccRCC specimens and from bone metastases of ccRCC patients, we identified a set of 57 differentially expressed microRNAs between these three sample groups of ccRCC. A selected panel of 33 miRNAs was subsequently validated by RT-qPCR on total 57 samples. Then, 30 of the 33 examined miRNAs were confirmed to be deregulated. A stepwise down-regulation of miRNA expression from normal, over primary tumor to metastatic tissue samples, was found to be typical. A total of 23 miRNAs (miR-10b/-19a/-19b/-20a/-29a/-29b/-29c/-100/-101/-126/-127/-130/-141/-143/-145/-148a/-192/-194/-200c/-210/-215/-370/-514) were down-regulated in metastatic tissue samples compared with normal tissue. This down-regulated expression in metastatic tissue in comparison with primary tumor tissue was also present in 21 miRNAs. In cell culture experiments with 5-aza-2'-deoxycytidine and trichostatin A, epigenetic modifications were shown as one reason of this down-regulation. The altered miRNA profiles, comprising newly identified metastasis-associated miRNAs, termed metastamir and the predicted miRNA-target interactions together with the significant correlations of miRNAs that were either lost or newly appeared in the studied sample groups, afford a solid basis for further functional analyses of individual miRNAs in RCC metastatic progression.

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Insufficient post-traumatic skeletal muscle regeneration with consecutive functional deficiency continues to be a serious problem in orthopedic and trauma surgery. Transplantation of autologous muscle precursor cells has shown encouraging results in muscle trauma treatment but is associated with significant donor site morbidity. In contrast to this, bone marrow-derived (BMD) cells can be obtained without any functional deficit by puncture. The goal of this study was to examine whether regular muscle regeneration can be improved by local application of autologous BMD cells in a rat model of blunt skeletal muscle trauma. One week after standardized open blunt crush injury to the left soleus muscle, 10(6) autologous BMD cells were injected into the traumatized muscle of male Sprague Dawley rats. Rats of the control group received saline solution as treatment. Three weeks after application, the fast twitch and tetanic contraction capacity of the soleus muscles was measured bilaterally by stimulating the sciatic nerves. Contraction forces of injured soleus muscles in control animals recovered to 39 +/- 10% (tetanic) and 59 +/- 12% (fast twitch) of the contralateral noninjured soleus muscles (p < 0.001). In contrast, autologous BMD cell injection significantly restored contractile forces to 53 +/- 8% (tetanic) and 72 +/- 13% (fast twitch) compared to those observed in contralateral noninjured soleus muscles. Thus, muscle function was significantly increased by BMD cell treatment (tetanic, p = 0.014; fast twitch, p = 0.05). In conclusion, autologous BMD cell grafting leads to an increase in contraction force, 14% in tetanic and 13% in fast twitch stimulation, demonstrating its potential to improve functional outcome after skeletal muscle crush injury.

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OPS imaging enabled for the first time direct in vivo visualization and quantification of the human hepatic microcirculation, providing significant insight into microvascular physiology of the human liver, to the extent that these data can be considered to represent physiologic values for human hepatic microcirculation.