BackgroundTo investigate the emergency treatment on facial laceration of dog bite wounds and identify whether immediate primary closure is feasible.MethodsSix hundred cases with facial laceration attacked by dog were divided into two groups randomly and evenly. After thorough debridement, the facial lacerations of group A were left open, while the lacerations of group B were undertaken immediate primary closure. Antibiotics use was administrated only after wound infected, not prophylactically given. The infection rate, infection time and healing time were analyzed.ResultsThe infection rate of group A and B was 8.3% and 6.3% respectively (P>0.05); the infection time was 26.3±11.6h and 24.9±13.8h respectively (P>0.05), the healing time was 9.12±1.30d and 6.57±0.49d respectively (P<0.05) in taintless cases, 14.24±2.63d and 10.65±1.69d respectively (P<0.05) in infected cases.Compared with group A, there was no evident tendency in increasing infection rate (8.3% in group A and 6.3% in group B respectively) and infection period (26.3±11.6h in group A and 24.9±13.8h in group B respectively) in group B. Meanwhile, in group B, the wound healing time was shorter than group A statistically in both taintless cases (9.12±1.30d in group A and 6.57±0.49d in group B respectively) and infected cases (14.24±2.63d in group A and 10.65±1.69d in group B respectively).ConclusionThe facial laceration of dog bite wounds should be primary closed immediately after formal and thoroughly debridement. And the primary closure would shorten the healing time of the dog bite wounds without increasing the rate and period of infection. There is no potentiality of increasing infection incidence and infection speed, compared immediate primary closure with the wounds left open. On the contrary, primary closure the wounds can promote its primary healing. Prophylactic antibiotics administration was not recommended. and the important facial organ or tissue injuries should be secondary reconditioned.

SummaryIn many types of tumours, especially pancreatic adenocarcinoma, miR301a is over-expressed. This over-expression results in negative regulation of the target gene of miR-301a, the nuclear factor-jB (NF-jB) repressing factor (NKRF), increasing the activation of NF-jB and production of NF-jB-responsive pro-inflammatory cytokines such as interleukin-8, interferon-b, nitric oxide synthase 2A and cytochrome oxidase subunit 2 (COX-2). However, in immune cells, mechanisms that regulate miR-301a have not been reported. Similar to tumour cells, Toll-like receptor (TLR) -activated macrophages produce NF-jB-responsive pro-inflammatory cytokines. Therefore, it is of considerable interest to determine whether miR-301a regulates the secretion of cytokines by immune cells. In the present study, we demonstrate that the expression of miR-301a was decreased in TLR-triggered macrophages. Through targeting NKRF, miR301a affected the activity of NF-jB and the expression of pro-inflammatory genes downstream of NF-jB such as COX-2, prostaglandin E 2 and interleukin-6. In addition, when lipopolysaccharide-treated macrophages were simultaneously stimulated with trichostatin A, an inhibitor of histone deacetylases, the expression of miR-301a increased, whereas NKRF and pro-inflammatory cytokine expression decreased. However, further investigation revealed that there was no correlation between the induction of miR-301a and the inhibitory effect of trichostatin A on lipopolysaccharide-induced gene expression in macrophages. In summary, our study indicates a new mechanism by which miR-301a regulates inflammatory cytokine expression in macrophages, which may clarify the regulatory role of microRNAs in immune-mediated inflammatory responses.

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