Influence of static magnetic fields on human myoblast/mesenchymal stem cell co­cultures.

The results of surgical repair of extensive muscle tissue defects are still of primary concern, leaving patients with residual cosmetic and functional impairments. Therefore, skeletal muscle tissue engineering attempts to grow functional neo­tissue from human stem cells to promote tissue regeneration and support defect closure. Despite intensive research efforts, the goal of stable induction of myogenic differentiation in expanded human stem cells by using clinically feasible stimuli, has not yet been reached to a sufficient extent. Therefore, the present study investigated the differentiation potential of static magnetic fields (SMFs), using co­cultures of human satellite cells and human mesenchymal stem cells (MSCs). It has previously been demonstrated that SMFs may act as a promising myogenic stimulus. Tests were performed on co­cultures with and without SMF exposure, using growth medium [high growth factor concentrations (GM)] and differentiation medium [low growth factors concentrations (DM)]. AlamarBlue® assay­based cell proliferation analysis revealed no significant difference between co­cultures with, vs. without SMF stimulation, regardless of growth factor concentrations in the cell culture medium. To determine the degree of differentiation in co­cultures under stimulation with SMFs, semi­quantitative gene expression measurements of the following marker genes were performed: Desmin, myogenic factor 5, myogenic differentiation antigen 1, myogenin, adult myosin heavy chain 1 and skeletal muscle α1 actin. In neither GM nor DM was a steady, significant increase in marker gene expression detected. Verifying the gene expression findings, immunohistochemical antibody staining against differentiation markers revealed that SMF exposure did not enhance myogenic maturation. Therefore, SMF treatment of human satellite cell/MSC co­cultures did not result in the desired increase in myogenic differentiation. Further studies are required to identify a suitable stimulus for skeletal muscle tissue engineering.

The improved quality of postoperative analgesia after intrathecal morphine does not result in improved recovery and quality of life in the first 6 months after orthopedic surgery: a randomized controlled pilot study.

OBJECTIVE: In orthopedic surgery, it is well known that the use of intrathecal morphine (ITM) leads to an improved quality of postoperative analgesia. Little is known how this improved analgesia affects the long-term course after surgery. STUDY DESIGN: A randomized, double-blind trial. SETTING: Academic medical center. SUBJECTS: Forty-nine patients undergoing total hip or knee replacement surgery in spinal anesthesia. METHODS: Patients were randomly assigned to receive either 0.1 mg (n=16) or 0.2 mg (n=16) morphine sulfate intrathecally or physiological saline (n=17) added to 3 mL 0.5% isobaric bupivacaine for spinal anesthesia. As a function of the quality of the short-term postoperative analgesia, the effect on recovery and quality of life was evaluated at various time points up to 26 weeks after surgery. RESULTS: In both ITM groups, the additionally required postoperative systemic morphine dose was significantly reduced compared with the placebo group (P=0.004). One week after operation, patients with ITM reported significantly less pain at rest (P=0.01) compared to the placebo group. At discharge, in comparison with the 0.1 mg ITM and placebo group, the 0.2 mg ITM group showed a higher degree of impairment regarding pain, stiffness, and physical function of the respective joint (P=0.02). Over the further follow-up period of 6 months after surgery, recovery and the quality of life did not differ significantly between the three study groups (P>0.2). CONCLUSION: Morphine (0.1 mg) as adjunct to 0.5% bupivacaine for spinal anesthesia is effective to produce a pronounced postoperative analgesia with a beneficial analgesic effect up to 1 week after surgery. With this study design, the different quality of postoperative analgesia had no effect on quality of life and recovery in patients over the 6-month follow-up period. In the medium term, ITM may induce hyperalgesic effects.

Early alveolar and systemic mediator release in patients at different risks for ARDS after multiple trauma.

Alveolar IL-8 has been reported to early identify patients at-risk to develop ARDS. However, it remains unknown how alveolar IL-8 is related to pulmonary and systemic inflammation in patients predisposed for ARDS. We studied 24 patients 2-6h after multiple trauma. Patients with IL-8 >200 pg/ml in bronchoalveolar lavage (BAL) were assigned to the group at high risk for ARDS (H, n = 8) and patients with BAL IL-8 <200 pg/ml to the group at low risk for ARDS (L, n = 16). ARDS developed within 24h after trauma in 5 patients at high and at least after 1 week in 2 patients at low risk for ARDS (p = 0.003). High-risk patients had also increased BAL IL-6, TNF-α, IL-1ß, IL-10 and IL-1ra levels (p<0.05). BAL neutrophil counts did not differ between patient groups (H vs. L, 12% (3-73%) vs. 6% (2-32%), p = 0.1) but correlated significantly with BAL IL-8, IL-6 and IL-1ra. High-risk patients had increased plasma levels of pro- but not anti-inflammatory mediators. The enhanced alveolar and systemic inflammation associated with alveolar IL-8 release should be considered to identify high-risk patients for pulmonary complications after multiple trauma to adjust surgical and other treatment strategies to the individual risk profile.