Background The primary objective of this multicenter post-market study was to compare the cosmetic outcome of triclosan-coated VICRYL* Plus sutures with Chinese silk sutures for skin closure of modified radical mastectomy. A secondary objective was to assess the incidence of surgical site infection (SSI).
Methods Patients undergoing modified radical mastectomy were randomly assigned to coated VICRYL* Plus antibacterial (Polyglactin 910) suture or Chinese silk suture. Cosmetic outcomes were evaluated postoperatively at days 12 (±2) and 30 (±5), and the evidence of SSI was assessed at days 3, 5, 7, 12 (±2), 30 (±5), and 90 (±7). Cosmetic outcomes were independently assessed via visual analogue scale (VAS) score evaluations of blinded incision photographs (primary endpoint) and surgeon-assessed modified Hollander Scale (mHCS) scores (secondary endpoint). SSI assessments used both CDC criteria and ASEPSIS scores.
Results Six Chinese hospitals randomized 101 women undergoing modified radical mastectomy to closure with coated VICRYL* Plus suture (n=51) or Chinese silk suture (n=50). Mean VAS cosmetic outcome scores for antibacterial suture (67.2) were better than for Chinese silk (45.4) at day 30 (P <0.0001)). Mean mHCS cosmetic outcome total scores, were also higher for antibacterial suture (5.7) than for Chinese silk (5.0) at day 30 (P=0.002).
Conclusions Patients using coated VICRYL* Plus suture had significantly better cosmetic outcomes than those with Chinese silk sutures. Patients using coated VICRYL* Plus suture had a lower SSI incidence compared to the Chinese silk sutures, although the difference did not reach statistical significance. (ClinicalTrials.gov NCT 00768222)
Vibroacoustic disease, a progressive and systemic disease, mainly involving the central nervous system, is caused by excessive exposure to low-frequency but high-intensity noise generated by various heavy transportations and machineries. Infrasound is a type of low-frequency noise. Our previous studies demonstrated that infrasound at a certain intensity caused neuronal injury in rats but the underlying mechanism(s) is still largely unknown. Here, we showed that glial cell-expressed TRPV4, a Ca2+-permeable mechanosensitive channel, mediated infrasound-induced neuronal injury. Among different frequencies and intensities, infrasound at 16 Hz and 130 dB impaired rat learning and memory abilities most severely after 7–14 days exposure, a time during which a prominent loss of hippocampal CA1 neurons was evident. Infrasound also induced significant astrocytic and microglial activation in hippocampal regions following 1- to 7-day exposure, prior to neuronal apoptosis. Moreover, pharmacological inhibition of glial activation in vivo protected against neuronal apoptosis. In vitro, activated glial cell-released proinflammatory cytokines IL-1β and TNF-α were found to be key factors for this neuronal apoptosis. Importantly, infrasound induced an increase in the expression level of TRPV4 both in vivo and in vitro. Knockdown of TRPV4 expression by siRNA or pharmacological inhibition of TRPV4 in cultured glial cells decreased the levels of IL-1β and TNF-α, attenuated neuronal apoptosis, and reduced TRPV4-mediated Ca2+ influx and NF-κB nuclear translocation. Finally, using various antagonists we revealed that calmodulin and protein kinase C signaling pathways were involved in TRPV4-triggered NF-κB activation. Thus, our results provide the first evidence that glial cell-expressed TRPV4 is a potential key factor responsible for infrasound-induced neuronal impairment. 相似文献
