跟腱病变病人腓肠肌和比目鱼肌水肿及脂肪变性的MR成像

目的本研究目的是评价跟腱损伤病人腓肠肌和比目鱼肌的水肿与脂肪变性的发生率。方法对51例(14～84岁,平均51岁)跟腱痛病人进行小腿MRI扫描。比较正常跟腱组、跟腱病组和跟腱部分或完全撕裂组病人中腓肠肌和比目鱼肌水肿与脂肪变性的发生率。结果35%(7/20)的跟腱病     

Endoplasmic reticulum stress sensor IRE1α propels neutrophil hyperactivity in lupus

Neutrophils amplify inflammation in lupus through the release of neutrophil extracellular traps (NETs). The endoplasmic reticulum stress sensor inositol-requiring enzyme 1 α (IRE1α) has been implicated as a perpetuator of inflammation in various chronic diseases; however, IRE1α has been little studied in relation to neutrophil function or lupus pathogenesis. Here, we found that neutrophils activated by lupus-derived immune complexes demonstrated markedly increased IRE1α ribonuclease activity. Importantly, in neutrophils isolated from patients with lupus, we also detected heightened IRE1α activity that was correlated with global disease activity. Immune complex–stimulated neutrophils produced both mitochondrial ROS (mitoROS) and the activated form of caspase-2 in an IRE1α-dependent fashion, whereas inhibition of IRE1α mitigated immune complex–mediated NETosis (in both human neutrophils and a mouse model of lupus). Administration of an IRE1α inhibitor to lupus-prone MRL/lpr mice over 8 weeks reduced mitoROS levels in peripheral blood neutrophils, while also restraining plasma cell expansion and autoantibody formation. In summary, these data identify a role for IRE1α in the hyperactivity of lupus neutrophils and show that this pathway is upstream of mitochondrial dysfunction, mitoROS formation, and NETosis. We believe that inhibition of the IRE1α pathway is a novel strategy for neutralizing NETosis in lupus, and potentially other inflammatory conditions.     

Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium

The cholinergic nervous system has been demonstrated to attenuate the inflammatory response during sepsis via the inhibitory action of acetylcholine (ACh) on macrophages. These findings were largely based on experimental sepsis models using endotoxin as the inducing agent. Herein, however, we report that the specific inhibition of acetylcholinesterase (AChE) renders animals more resistant to infection by a virulent strain of Salmonella enterica serovar Typhimurium, a Gram‐negative enteric pathogen. Inhibition of AChE was induced by a subchronic exposure to paraoxon, a potent anti‐cholinesterase metabolite of the organophosphorous compound parathion. Our findings indicate that inhibition of AChE enhanced survival of infected mice in a dose‐dependent fashion and this correlated with efficient control of bacterial proliferation in target organs. Immunologically, inhibition of AChE enabled the animals to mount a more effective inflammatory anti‐microbial response, and to secrete higher levels of interleukin‐12, a key T helper type 1‐promoting cytokine. The ACh‐induced enhancement in resistance to infection was abrogated by co‐administration of an oxime which can reactivate AChE. Hence, in a model of Gram‐negative bacterial infection, cholinergic stimulation is shown to enhance the anti‐microbial immune response leading to effective control of bacterial proliferation and enhanced animal survival.     

Does the use of prophylactic antibiotics decrease implant failure?

The use of prophylactic antibiotics in implant dentistry is controversial. Given the known risks of antibiotic treatment and lack of consensus on using antibiotics at the time of implant insertion, the purpose of this article was to review available studies on use of perioperative prophylactic antibiotics at the time of implant placement and to provide evidence-based recommendations for antibiotic use. The reviewed studies suggest that a single preoperative dose of 2 g amoxicillin 1 hour before implant placement or 1 g amoxicillin 1 hour preoperatively and 500 mg 4 times daily 2 days postoperatively can reduce the rate of implant failure.     

Acute chest syndrome after splenectomy in children with sickle cell disease

Background/Purpose

The purpose of this study was to determine the incidence of acute chest syndrome (ACS) in children with sickle cell disease (SCD) undergoing laparoscopic or open splenectomy and to assess factors that may predispose to this complication.

Methods

A retrospective review of all patients with SCD undergoing splenectomy between 1999 and 2007 in our institution. Charts were screened for demographics, perioperative clinical status (vaso-occlusive crises, sequestration crises), preoperative hemoglobin electrophoresis and preoperative transfusion, postoperative development of ACS, and need for an intensive care unit (ICU) admission.

Results

Forty-three children with SCD, 17 females and 16 males (mean age 9 years), underwent splenectomy (19 laparoscopy and 24 open). Acute chest syndrome occurred in 9 patients (20%), 1 (5.2%) of 19 in the laparoscopy group, and 8 (33.3%) of the 24 in the open group. All patients with ACS were admitted to the ICU. Acute chest syndrome developed within the first 24 hours in 5 of the 9 patients, on the second postoperative day in 1 patient, and more than 1 month postoperatively in 3 patients. Six of 9 patients with ACS had been transfused preoperatively. All patients with ACS had had vaso-occlusive crises before surgery. Five of 9 patients who developed ACS had previous ACS episodes before surgery. There was no death in our series.

Conclusion

The incidence of ACS is in accordance with the literature. Preoperative transfusions did not prevent ACS . There is a clear tendency for laparoscopically operated patients to experience less ACS postoperatively. In our group of patients, there were no clear benefits for routine perioperative admission to the ICU.