Gene expression changes in the skin of rats induced by prolonged 35 GHz millimeter-wave exposure.

To better understand the cellular and molecular responses to overexposure to millimeter waves, alterations in the gene expression profile and histology of skin after exposure to 35 GHz radiofrequency radiation were investigated. Rats were subjected to sham exposure, to 42 degrees C environmental heat, or to 35 GHz millimeter waves at 75 mW/cm(2). Skin samples were collected at 6 and 24 h after exposure for Affymetrix GeneChip analysis. The skin was harvested from a separate group of rats at 3-6 h or 24-48 h after exposure for histopathology analysis. Microscopic findings observed in the dermis of rats exposed to 35 GHz millimeter waves included aggregation of neutrophils in vessels, degeneration of stromal cells, and breakdown of collagen. Changes were detected in 56 genes at 6 h and 58 genes at 24 h in the millimeter-wave-exposed rats. Genes associated with regulation of transcription, protein folding, oxidative stress, immune response, and tissue matrix turnover were affected at both times. At 24 h, more genes related to extracellular matrix structure and chemokine activity were altered. Up-regulation of Hspa1a, Timp1, S100a9, Ccl2 and Angptl4 at 24 h by 35 GHz millimeter-wave exposure was confirmed by real-time RT-PCR. These results obtained from histopathology, microarrays and RT-PCR indicate that prolonged exposure to 35 GHz millimeter waves causes thermally related stress and injury in skin while triggering repair processes involving inflammation and tissue matrix recovery.

A comparison of bioabsorbable and metallic suture anchors in a dynamically loaded, intra-articular caprine model.

Little is known about the in vivo behavior of bioabsorbable suture anchors. A goat model was used to biomechanically and histologically test bioabsorbable and metallic suture anchors in an intra-articular environment at 0, 6, and 12 weeks. Significantly greater force was required to break the bioabsorbable construct than the metallic construct at 0 and 6 weeks. Failure of the metallic anchor constructs occurred at the eyelet. Histological analysis of both bone-anchor interfaces demonstrated equally good osteointegration without evidence of osteolysis. The bioabsorbable suture anchor tested is safe for use in clinical practice without concerns for the strength of the construct or bony reaction to the material.

Low-volume resuscitation with a polymerized bovine hemoglobin-based oxygen-carrying solution (HBOC-201) provides adequate tissue oxygenation for survival in a porcine model of controlled hemorrhage.

BACKGROUND: We have shown in a previous work that HBOC-201 is able to reverse anaerobic metabolism at low volumes in a porcine model of controlled hemorrhage. On the basis of these results, we hypothesize that low-volume resuscitation with HBOC-201 in a porcine model of controlled hemorrhage provides adequate tissue oxygenation to limit end-organ damage and allow for survival of the animal. METHODS: Twenty-four Yorkshire swine (55-65 kg) were rapidly hemorrhaged to a mean arterial pressure (MAP) of 30 mm Hg, maintained hypotensive for 45 minutes, and then divided into four groups. The first group, Shed Blood (BL), was resuscitated with shed blood to baseline MAP. A second group, Shed Blood (60), underwent resuscitation for four hours at an MAP of 60 mm Hg with shed blood. The third group, LR + Blood, was resuscitated with lactated Ringer's (maximum, 40 mL/kg) followed by shed blood to baseline MAP. The final group, HBOC (60), underwent resuscitation for 4 hours at an MAP of 60 mm Hg with HBOC-201. Hemodynamic variables, urine output, blood gas analyses, lactate levels, and jejunal oximetry were followed throughout the experiment. Animals were allowed to survive and underwent necropsy on postinjury day 3. Histologic comparisons were made. Data were analyzed using analysis of variance/Duncan's multiple range test. RESULTS: All animals survived the hemorrhage/resuscitation. One animal in the LR + Blood group died on postinjury day 1. Heart rate, MAP, and arterial pH were similar between groups. Cardiac output was significantly lower throughout resuscitation in the HBOC (60) group. Jejunal oximetry was similar throughout the experiment in all groups, revealing a decline in Po2 during hemorrhage and return to baseline or near baseline during resuscitation. There was no evidence of renal dysfunction. Histologically, one animal in the LR + Blood group and four of six animals in the HBOC (60) group demonstrated mild hepatocellular damage. All other tissues examined were found to have no significant abnormalities. Elevations in serum aspartate aminotransferase levels were noted when comparing the HBOC (60) group to the Shed Blood (BL) and Shed Blood (60) groups on day 2. Significant decreases in hemoglobin levels were noted in the HBOC (60) group compared with all other groups beginning on day 2. CONCLUSION: Low-volume resuscitation with HBOC-201 provides adequate tissue oxygenation for survival in a porcine model of controlled hemorrhagic shock with no long-term organ dysfunction identified. Although some animals did show mild hepatocellular damage with elevations of aspartate aminotransferase at day 2, these findings did not appear to have clinical relevance, and the enzyme elevations were trending toward normal by the third postoperative day. Decreases in hemoglobin levels at the later time points were expected, given the half-life of the product.