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The severity of COVID-19 is linked to excessive inflammation. Neutrophils represent a critical arm of the innate immune response and are major mediators of inflammation, but their role in COVID-19 pathophysiology remains poorly understood. We conducted transcriptomic profiling of neutrophils obtained from patients with mild and severe COVID-19, as well as from SARS-CoV-2 infected mice, in comparison to non-infected healthy controls. In addition, we investigated the inflammasome formation potential in neutrophils from patients and mice upon SARS-CoV-2 infection. Transcriptomic analysis of polymorphonuclear cells (PMNs), consisting mainly of mature neutrophils, revealed a striking type I interferon (IFN-I) gene signature in severe COVID-19 patients, contrasting with mild COVID-19 and healthy controls. Notably, low-density granulocytes (LDGs) from severe COVID-19 patients exhibited an immature neutrophil phenotype and lacked this IFN-I signature. Moreover, PMNs from severe COVID-19 patients showed heightened nigericin-induced caspase1 activation, but reduced responsiveness to exogenous inflammasome priming. Furthermore, IFN-I emerged as a priming stimulus for neutrophil inflammasomes. These findings suggest a potential role for neutrophil inflammasomes in driving inflammation during severe COVID-19. Altogether, these findings open promising avenues for targeted therapeutic interventions to mitigate the pathological processes associated with the disease. Author summary: COVID-19, caused by the SARS-CoV-2, ranges from mild "flu"-like symptoms to severe respiratory distress or even death. Neutrophils are important cells of our immune system which are strongly involved in inflammatory responses, including those occurring in COVID-19. However, despite extensive research, the precise contribution of neutrophils to the pathogenesis of COVID-19 remains elusive, and further clarification on their role is still needed. In this study, we isolated neutrophils from COVID-19 patients and healthy controls to analyze changes in their gene expression profile and inflammatory functions. These analyses revealed a distinct type I interferon (IFN-I) gene signature expressed by mature, but not immature, neutrophils from severe COVID-19 patients, which was absent in mild cases and healthy controls. Additionally, neutrophils from severe COVID-19 showed signs of increased inflammasome activation, a protein complex that contributes to inflammation by releasing inflammatory cytokines. Notably, IFN-I alone was able to promote neutrophil inflammasome formation in vitro suggesting a direct link between IFN-I response and inflammasome formation during COVID-19. Furthermore, increased neutrophil inflammasome activity was detected also in a mouse model of COVID-19. These findings suggest a potential role for neutrophils in driving excessive inflammation during severe COVID-19, and a role for IFN-I in priming the assembly of inflammasomes in these cells. [ABSTRACT FROM AUTHOR]

Introduction: Reconstruction of acetabulum in case of bone defects can be challenging. The aim of this retrospective study was to investigate the 10-year survival of trabecular tantalum metal (TM) acetabulum component in revision hip arthroplasty operations and to evaluate complications. Methods: A total of 100 consecutive acetabulum revision hip arthroplasties (100 patients) were operated on between May 2004 and October 2006 at Kuopio University Hospital. The mean follow-up time was 9.4 years and the median was 11.5 years (SD 4.118; range 0.1–13.4 years). Kaplan-Meier survival analysis was performed to study the survival of patients to re-revision surgery. Intra- and postoperative complications and reasons for re-revision were evaluated. Results: The Kaplan-Meier analysis showed a cumulative proportion of revision hip survivorship of 66% at 13.4 years (SE 0.403, 95% CI, 10.886–12.466) based on the need for further re-revision surgery for any major reason. The Kaplan-Meier survival analysis of time to re-revision surgery due acetabular component loosening showed a cumulative proportion of survivorship of 98.9% at 13.4 years (SE 0.136; 95% CI, 12.998–13.529). There were a total of 41/100 complications and the most common complication was dislocation (24/100). Re-revision for any major reason was performed on 18/100 of the revision arthroplasties. The mean time to re-revision was 4.9 years (SD 5.247; range 0.1–13.2 years). Discussion: The trabecular TM acetabular component gives excellent outcomes regarding stability and fixation to the acetabulum in acetabulum revision hip arthroplasty at a minimum of ten years of follow-up. However, acetabular component malposition and the small head size (28 mm) are risk factors for dislocation. [ABSTRACT FROM AUTHOR]

Abstract Introduction A blunt thoracic trauma may cause arterial bleeding requiring operative treatment or endovascular embolization or endovascular aortic stenting. A novel damage control technique to stop such bleeding is presented. Case presentation We present the case of an 82-year-old Caucasian man who experienced rib fractures I-VII on the left side and bleeding from damaged intercostal arteries after a blunt thoracic trauma. Emergency thoracotomy was performed. Conclusions Effective hemostasis was achieved by using a rolled surgical swab and inserting it against the chest wall next to the aorta with sutures pulled through the intercostal muscles and then sutured to the back side of the patient. The patient died four days after the surgery due to a head injury sustained in the car crash.

Abstract Background The aim of the study was to investigate expression of ADAMs (A Disintegrin and A Metalloproteinase) of host cell origin during cell-cell fusion induced by human parainfluenza virus type 2 (HPIV2). Results Induction of host cell ADAM9 was observed in GMK cells, but the applicability of this model was restricted by lack of cross-reactivity of the anti-human ADAM8 antibodies with the corresponding green monkey antigens. HSG cells were not susceptible to HPIV2 virus infection. In contrast, in human parotid gland HSY cells, a natural host cell for paramyxoviruses, HPIV2 induced ADAM8 expression. ADAM8 staining increased dramatically over time from 7.9 ± 3% at zero hours to 99.2 ± 0.8% at 72 hours (p = 0.0001). Without HPIV2 the corresponding percentages were only 7.7% and 8.8%. Moreover, ADAM8 positive cells formed bi- (16.2%) and multinuclear cells (3.5%) on day one and the corresponding percentages on day three were 15.6% for binuclear and 57.2% for multinuclear cells. Conclusion ADAM8, well recognized for participation in cell-to-cell fusion especially in osteoclast formation, is up-regulated upon formation of multinuclear giant cells after HPIV2 induction in HSY cells. The virus-HSY cell system provides a novel experimental model for study of the molecular mechanism of cell fusion events.

Introduction: Dislocation of large-diameter head (LDH) metal-on-metal (MoM) total hip arthroplasty (THA) or hip resurfacing arthroplasty (HRA) is a rare complication. This study aimed to determine the incidence and risk factors for dislocation of LDH MoM THAs and HRAs. Methods: This retrospective analysis considered 4038 cementless LDH MoM THAs and HRAs, 3207 THAs in 2912 patients and 831 HRAs in 757 patients. The end of follow-up was revision due to dislocation. Incidence of dislocation was evaluated from this study population of 4038, and study groups were formed. The study was designed as a case-control study, and a threefold stratified randomised control group was formed. Demographic data were collected and radiological analyses were performed in the study groups. Results: There were 26/3207 (0.8%) early dislocations in the THA group, and 6/831 (0.7%) in the HRA group (p = 0.9). Most LDH THA dislocations occurred in a group with head size ⩽ 38 mm (18/26) (p < 0.001). In dislocated hips, there were more dysplastic acetabula and post-traumatic hips than in the control group (p = 0.036). In the dislocation group, the mean acetabulum component anteversion angle was 19.6° (standard deviation [SD] 13.4°) and in the control group it was 23.2° (SD 10.4°) (p = 0.006); 7/32 (21.8%) of dislocated THAs needed revision surgery, and mean time to revision from the index surgery was 1.2 (SD 2.6) years. Discussion: Dislocations occurred more often in THAs of head size ⩽ 38 mm and with a smaller anteversion angle of the acetabulum component. Hip dysplasia and post-traumatic osteoarthritis were more common in patients with dislocation. [ABSTRACT FROM AUTHOR]

Background and purpose — Intraoperative periprosthetic femoral fracture is a known complication of cementless total hip arthroplasty (THA). We determined the incidence of—and risk factors for—intraoperative calcar fracture, and assessed its influence on the risk of revision. Patients and methods — This retrospective analysis included 3,207 cementless THAs (in 2,913 patients). 118 intraoperative calcar fractures were observed in these hips (3.7%). A control group of 118 patients/hips without calcar fractures was randomly selected. The mean follow-up was 4.2 (1.8–8.0) years. Demographic data, surgical data, type of implant, and proximal femur morphology were evaluated to determine risk factors for intraoperative calcar fracture. Results — The revision rates in the calcar fracture group and the control group were 10% (95% CI: 5.9–17) and 3.4% (CI: 1.3–8.4), respectively. The revision rate directly related to intraoperative calcar fracture was 7.6%. The Hardinge approach and lower age were risk factors for calcar fracture. In the fracture group, 55 of 118 patients (47%) had at least one risk factor, while only 23 of118 patients in the control group (20%) had a risk factor (p = 0.001). Radiological analysis showed that in the calcar fracture group, there were more deviated femoral anatomies and proximal femur bone cortices were thinner. Interpretation — Intraoperative calcar fracture increased the risk of revision. The Hardinge approach and lower age were risk factors for intraoperative calcar fracture. To avoid intraoperative fractures, special attention should be paid when cementless stems are used with deviant-shaped proximal femurs and with thin cortices. [ABSTRACT FROM PUBLISHER]