The provision of a time-critical elective surgical service during the COVID-19 Crisis: a UK experience

IntroductionWith the emergence of the COVID-19 pandemic, all elective surgery was temporarily suspended in the UK, allowing for diversion of resource to manage the anticipated surge of critically unwell patients. Continuing to deliver time-critical surgical care is important to avoid excess morbidity and mortality from pathologies unrelated to COVID-19. We describe the implementation and short-term surgical outcomes from a system to deliver time-critical elective surgical care to patients during the COVID-19 pandemic.Materials and methodsA protocol for the prioritisation and safe delivery of time-critical surgery at a COVID-19 ‘clean’ site was implemented at the Nuffield Health Exeter Hospital, an independent sector hospital in the southwest of England. Outcomes to 30 days postoperatively were recorded, including unplanned admissions after daycase surgery, readmissions and complications, as well as the incidence of perioperative COVID-19 infection in patients and staff.ResultsA total of 128 surgical procedures were performed during a 31-day period by a range of specialties including breast, plastics, urology, gynaecology, vascular and cardiology. There was one unplanned admission and and two readmissions. Six complications were identified, and all were Clavien-Dindo grade 1 or 2. All 128 patients had preoperative COVID-19 swabs, one of which was positive and the patient had their surgery delayed. Ten patients were tested for COVID-19 postoperatively, with none testing positive.ConclusionThis study has demonstrated the implementation of a safe system for delivery of time-critical elective surgical care at a COVID-19 clean site. Other healthcare providers may benefit from implementation of similar methodology as hospitals plan to restart elective surgery.     

Gender Differences in the Amount of Gingival Display During Smiling Using Two Intraoral Dental Biometric Measurements

Purpose: The aims of this study were to compare gender differences in the width and length of the maxillary right central incisor and the horizontal and vertical overlap of the anterior teeth and to determine the relationships of these two intraoral dental biometric measurements with the amount of gingival display during smiling. Materials and Methods: A total of 61 men and 66 women were included in this study. For each participant, the gingival tissue display during smiling was judged to be either visible or not, and the maximum mesiodistal and incisogingival dimensions of the maxillary right central incisor were measured, along with the amount of horizontal and vertical overlap of anterior teeth using a digital caliper. Gender differences in these parameters and the relationship between subjects showing gingival display when smiling and the two intraoral dental biometric measurements were determined. Statistical analyses of data were performed using SPSS (V11) software. The mean scores for gender were calculated, and a Student's t‐test was used to identify significant differences between both groups. Significance level was set to 0.05. Results: The age of the participants ranged between 23 and 52, with a mean of 33.47 ± 9.07 years. A relatively small percentage of the subjects (22.05%) displayed gingiva when smiling. More women displayed gingiva when smiling than men, with a 2:1 female:male ratio. Men exhibited significantly (p < 0.05) wider (8.76 ± 0.66 mm) and longer (10.28 ± 0.88 mm) central incisors compared to women (7.92 ± 0.72 mm; 9.27 ± 0.93 mm width and length, respectively). No gender differences were found in the width‐to‐length ratio. Subjects with gingival display had significantly more horizontal (4.28 ± 1.21 mm; p < 0.001), and vertical (3.52 ± 0.66 mm; p < 0.05) overlap of anterior teeth compared to those who did not display gingiva when smiling (2.40 ± 1.03 and 2.30 ± 0.93 mm, respectively). Conclusions: Significantly more women displayed gingiva in smiling. Men had significantly wider and longer central incisors. No differences were recorded between men and women relative to both the horizontal and vertical anterior tooth overlap. Subjects who displayed gingiva when smiling had more horizontal and vertical overlap of anterior teeth.     

The pyrin inflammasome and the Yersinia effector interaction

Pyrin is a cytosolic pattern-recognition receptor that normally functions as a guard to trigger capase-1 inflammasome assembly in response to bacterial toxins and effectors that inactivate RhoA. The MEFV gene encoding human pyrin is preferentially expressed in phagocytes. Key domains in pyrin include a pyrin domain (PYD), a linker region, and a B30.2 domain. Binding of ASC to pyrin by a PYD-PYD interaction triggers inflammasome assembly. Pyrin is held in an inactive conformation by negative regulation mechanisms to avoid premature inflammasome assembly. One mechanism of negative regulation involves phosphorylation of the linker by PRK kinase which in turn is positively regulated by active RhoA. The B30.2 domain also negatively regulates pyrin. Gain of function mutations in MEFV responsible for the autoinflammatory disease Familial Mediterranean Fever (FMF) map to exon 10 encoding the B30.2 domain. Insights into pyrin regulation have come from studies of several Yersinia effectors, which are injected into phagocytes and interact with the RhoA-PRK-pyrin axis during infection. Two effectors, YopE and YopT, inactivate RhoA to disrupt phagocytic signaling. To counteract an effector-triggered immune response, a third effector, YopM, binds to and inhibits pyrin by hijacking PRK and RSK and directing linker phosphorylation. Inhibition of pyrin by YopM is required for virulence of Yersinia pestis, the agent of plague. Recent results from infection studies with human phagocytes and mice producing pyrin B30.2 FMF variants show that gain of function MEFV mutations bypass inhibition by YopM. Population genetic data suggest that MEFV mutations were selected for in individuals of Mediterranean decent during historic plague pandemics. This review discusses current concepts of pyrin regulation and its interaction with Yersinia effectors.     

Discoid lupus erythematosus

Discoid lupus erythematosus is a manifestation of chronic cutaneous lupus erythematosus with a small risk of systemic involvement. In this review article, the role of predisposing factors such as haplotype, hormones, antibodies and sunlight are discussed. The clinical features, including variants and associations, and management options are presented.     

Including emergency and acute care as a global health priority

The clinical findings of Takatsubo Cardiomyopathy and acute myocardial infarction can be very similar. While Takatsubo cardiomyopathy rarely leads to severe complications, acute myocardial infarction can be life threatening. Treatment of both these conditions is different and so it is imperative for clinicians to have a high index of suspicion for either. Several EKG differences between the two entities have been proposed. This article summarizes the EKG changes most likely seen in Takatsubo cardiomyopathy and compares them to those seen in Acute Myocardial infarction.     

胎儿和新生儿同种异体免疫性血小板减少症:进展与持续性争议

胎儿和新生儿同种异体免疫性血小板减少症(AIT)是引起胎儿和新生儿严重血小板减少的最常见原因.母亲针对源自父亲的胎儿血小板抗原的IgG抗体,在妊娠早期就可通过胎盘,通常导致胎儿严重血小板减少.由于一些血小板减少症临界值(50、100或150×109/L)的不同,他们的发生率亦各不相同.但在多数未经选择的人群中,AIT影响1/1 000到1/2 000活产数.在新生儿病房,临床确诊的重症AIT很罕见,可能只有1:10 000分娩数.     

LcrV capture enzyme-linked immunosorbent assay for detection of Yersinia pestis from human samples

In the United States, there is currently a major gap in the diagnostic capabilities with regard to plague. To address this, we developed an antigen capture assay using an essential virulence factor secreted by Yersinia spp., LcrV, as the target antigen. We generated anti-LcrV monoclonal antibodies (MAbs) and screened them for the ability to bind bacterially secreted native Yersinia pestis LcrV. Anti-LcrV MAb 19.31 was used as a capture antibody, and biotinylated MAb 40.1 was used for detection. The detection limit of this highly sensitive Yersinia LcrV capture enzyme-linked immunosorbent assay is 0.1 ng/ml. The assay detected LcrV from human sputum and blood samples treated with concentrations as low as 0.5 ng/ml of bacterially secreted native Y. pestis LcrV. This assay could be used as a tool to help confirm the diagnosis of plague in patients presenting with pneumonia.     

Interleukin-10 induction is an important virulence function of the Yersinia pseudotuberculosis type III effector YopM

Pathogenic Yersinia species modulate host immune responses through the activity of a plasmid-encoded type III secretion system and its associated effector proteins. One effector, YopM, is a leucine-rich-repeat-containing protein that is important for virulence in murine models of Yersinia infection. Although the mechanism by which YopM promotes virulence is unknown, we previously demonstrated that YopM was required for the induction of high levels of the immunosuppressive cytokine interleukin-10 (IL-10) in sera of C57BL/6J mice infected with Yersinia pseudotuberculosis. To determine if IL-10 production is important for the virulence function of YopM, C57BL/6J or congenic IL-10^−/− mice were infected intravenously with wild-type or yopM mutant Y. pseudotuberculosis strains. Analysis of cytokine levels in serum and bacterial colonization in the spleen and liver showed that YopM is required for IL-10 induction in C57BL/6J mice infected with either the IP32953 or the 32777 strain of Y. pseudotuberculosis, demonstrating that the phenotype is conserved in the species. In single-strain infections, the ability of the 32777ΔyopM mutant to colonize the liver was significantly increased by the delivery of exogenous IL-10 to C57BL/6J mice. In mixed infections, the competitive advantage of a yopM⁺ 32777 strain over an isogenic yopM mutant to colonize spleen and liver, as observed for C57BL/6J mice, was significantly reduced in IL-10^−/− animals. Thus, by experimentally controlling IL-10 levels in a mouse infection model, we obtained evidence that the induction of this cytokine is an important mechanism by which YopM contributes to Y. pseudotuberculosis virulence.