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Purpose: COVID-19 pandemic had multiple influences on the social, industrial, and medical situation in all affected countries. Measures of obligatory medical confinement were suspensions of scheduled non-emergent surgical procedures and outpatients’ clinics as well as overall access restrictions to hospitals and medical practices. The aim of this retrospective study was to assess if the obligatory confinement (lockdown) had an effect on the number of appendectomies (during and after the period of lockdown).
Methods: This retrospective study was based on anonymized nationwide administrative claims data of the German Local General Sickness Fund (AOK). Patients admitted for diseases of the appendix (ICD-10: K35-K38) or abdominal and pelvic pain (ICD-10: R10) who underwent an appendectomy (OPS: 5-470) were included. The study period included 6 weeks of German lockdown (16 March–26 April 2020) as well as 6 weeks before (03 February–15 March 2020) and after (27 April–07 June 2020). These periods were compared to the respective one in 2018 and 2019.
Results: The overall number of appendectomies was significantly reduced during the lockdown time in 2020 compared to that in 2018 and 2019. This decrease affects only appendectomies due to acute simple (ICD-10: K35.30, K35.8) and non-acute appendicitis (ICD-10: K36-K38, R10). Numbers for appendectomies in acute complex appendicitis remained unchanged. Female patients and in the age group 1–18 years showed the strongest decrease in number of cases.
Conclusion: The lockdown in Germany resulted in a decreased number of appendectomies. This affected mainly appendectomies in simple acute and non-acute appendicitis, but not complicated acute appendicitis. The study gives no evidence that the confinement measures resulted in a deterioration of medical care for appendicitis.
Background: Alterations in the SCN5A gene encoding the cardiac sodium channel Nav1.5 have been linked to a number of arrhythmia syndromes and diseases including long-QT syndrome (LQTS), Brugada syndrome (BrS) and dilative cardiomyopathy (DCM), which may predispose to fatal arrhythmias and sudden death. We identified the heterozygous variant c.316A > G, p.(Ser106Gly) in a 35-year-old patient with survived cardiac arrest. In the present study, we aimed to investigate the functional impact of the variant to clarify the medical relevance.
Methods: Mutant as well as wild type GFP tagged Nav1.5 channels were expressed in HEK293 cells. We performed functional characterization experiments using patch-clamp technique.
Results: Electrophysiological measurements indicated, that the detected missense variant alters Nav1.5 channel functionality leading to a gain-of-function effect. Cells expressing S106G channels show an increase in Nav1.5 current over the entire voltage window.
Conclusion: The results support the assumption that the detected sequence aberration alters Nav1.5 channel function and may predispose to cardiac arrhythmias and sudden cardiac death.
Objectives: To immunohistochemically characterize and correlate macrophage M1/M2 polarization status with disease severity at peri-implantitis sites.
Materials and methods: A total of twenty patients (n = 20 implants) diagnosed with peri-implantitis (i.e., bleeding on probing with or without suppuration, probing depths ≥ 6 mm, and radiographic marginal bone loss ≥ 3 mm) were included. The severity of peri-implantitis was classified according to established criteria (i.e., slight, moderate, and advanced). Granulation tissue biopsies were obtained during surgical therapy and prepared for immunohistological assessment and macrophage polarization characterization. Macrophages, M1, and M2 phenotypes were identified through immunohistochemical markers (i.e., CD68, CD80, and CD206) and quantified through histomorphometrical analyses.
Results: Macrophages exhibiting a positive CD68 expression occupied a mean proportion of 14.36% (95% CI 11.4–17.2) of the inflammatory connective tissue (ICT) area. Positive M1 (CD80) and M2 (CD206) macrophages occupied a mean value of 7.07% (95% CI 5.9–9.4) and 5.22% (95% CI 3.8–6.6) of the ICT, respectively. The mean M1/M2 ratio was 1.56 (95% CI 1–12–1.9). Advanced peri-implantitis cases expressed a significantly higher M1 (%) when compared with M2 (%) expression. There was a significant correlation between CD68 (%) and M1 (%) expression and probing depth (PD) values.
Conclusion: The present immunohistochemical analysis suggests that macrophages constitute a considerable proportion of the inflammatory cellular composition at peri-implantitis sites, revealing a significant higher expression for M1 inflammatory phenotype at advanced peri-implantitis sites, which could possibly play a critical role in disease progression.
Clinical relevance: Macrophages have critical functions to establish homeostasis and disease. Bacteria might induce oral dysbiosis unbalancing the host’s immunological response and triggering inflammation around dental implants. M1/M2 status could possibly reveal peri-implantitis’ underlying pathogenesis.
Respiratory complex I catalyzes electron transfer from NADH to ubiquinone (Q) coupled to vectorial proton translocation across the inner mitochondrial membrane. Despite recent progress in structure determination of this very large membrane protein complex, the coupling mechanism is a matter of ongoing debate and the function of accessory subunits surrounding the canonical core subunits is essentially unknown. Concerted rearrangements within a cluster of conserved loops of central subunits NDUFS2 (β1-β2S2 loop), ND1 (TMH5-6ND1 loop) and ND3 (TMH1-2ND3 loop) were suggested to be critical for its proton pumping mechanism. Here, we show that stabilization of the TMH1-2ND3 loop by accessory subunit LYRM6 (NDUFA6) is pivotal for energy conversion by mitochondrial complex I. We determined the high-resolution structure of inactive mutant F89ALYRM6 of eukaryotic complex I from the yeast Yarrowia lipolytica and found long-range structural changes affecting the entire loop cluster. In atomistic molecular dynamics simulations of the mutant, we observed conformational transitions in the loop cluster that disrupted a putative pathway for delivery of substrate protons required in Q redox chemistry. Our results elucidate in detail the essential role of accessory subunit LYRM6 for the function of eukaryotic complex I and offer clues on its redox-linked proton pumping mechanism.
Aim: The primary aim of this study was to analyze frequency and characteristics of combined facial and peripheral trauma with consecutive hospitalization and treatment.
Materials and methods: The study included all patients with concomitant orthopedic-traumatolgical (OT) and craniomaxillofacial (CMF) injuries admitted to our level I trauma center in 2018. The data were collected by analysis of the institution’s database and radiological reviews and included age, sex, injury type, weekday and time of presentation. All patients were examined and treated by a team of surgeons specialized in OT and CMF directly after presentation.
Results: A total number of 1040 combined OT and CMF patients were identified. Mean age was 33.0 ± 26.2 years. 67.3% (n = 700) were male patients. Primary presentation happened most frequently on Sundays (n = 199) and between 7 and 8 pm (n = 74). 193 OT fractures were documented, where cervical spine injuries were most frequent (n = 30). 365 facial and skull fractures were recorded. 10.8% of the 204 patients with fractures of the viscerocranium presented with at least one fracture of the extremity, 7.8% (16/204) with cervical spine fractures, 33.3% (68/204) with signs of closed brain trauma and 9.8% (20/204) with intracranial hemorrhage.
Discussion: The study shows a high frequency of combined facial with OT-injuries and brain damage in a predominantly young and male cohort. Attendance by interdisciplinary teams of both CMF and OT surgeons specialized in cervical spine trauma surgery is highly advisable for adequate treatment.
Conclusion: Diagnostics and treatment should be performed by a highly specialized OT and CMF team, with a consulting neurosurgeon in a level-1 trauma center to avoid missed diagnoses and keep mortality low.
Background: A prototype of a noninvasive glucometer combining skin excitation by a mid-infrared quantum cascade laser with photothermal detection was evaluated in glucose correlation tests including 100 volunteers (41 people with diabetes and 59 healthy people).
Methods: Invasive reference measurements using a clinical glucometer and noninvasive measurements at a finger of the volunteer were simultaneously recorded in five-minute intervals starting from fasting glucose values for healthy subjects (low glucose values for diabetes patients) over a two-hour period. A glucose range from >50 to <350 mg/dL was covered. Machine learning algorithms were used to predict glucose values from the photothermal spectra. Data were analyzed for the average percent disagreement of the noninvasive measurements with the clinical reference measurement and visualized in consensus error grids.
Results: 98.8% (full data set) and 99.1% (improved algorithm) of glucose results were within Zones A and B of the grid, indicating the highest accuracy level. Less than 1% of the data were in Zone C, and none in Zone D or E. The mean and median percent differences between the invasive as a reference and the noninvasive method were 12.1% and 6.5%, respectively, for the full data set, and 11.3% and 6.4% with the improved algorithm.
Conclusions: Our results demonstrate that noninvasive blood glucose analysis combining mid-infrared spectroscopy and photothermal detection is feasible and comparable in accuracy with minimally invasive glucometers and finger pricking devices which use test strips. As a next step, a handheld version of the present device for diabetes patients is being developed.
Age-related diseases pose great challenges to health care systems worldwide. During aging, endothelial senescence increases the risk for cardiovascular disease. Recently, it was described that Phosphatase 1 Nuclear Targeting Subunit (PNUTS) has a central role in cardiomyocyte aging and homeostasis. Here, we determined the role of PNUTS in endothelial cell aging. We confirmed that PNUTS is repressed in senescent endothelial cells (ECs). Moreover, PNUTS silencing elicits several of the hallmarks of endothelial aging: senescence, reduced angiogenesis and loss of barrier function. To validate our findings in vivo, we generated an endothelial-specific inducible PNUTS-deficient mouse line (Cdh5-CreERT2;PNUTSfl/fl), termed PNUTSEC-KO. Two weeks after PNUTS deletion, PNUTSEC-KO mice presented severe multiorgan failure and vascular leakage. We showed that the PNUTS binding motif for protein phosphatase 1 (PP1) is essential to maintain endothelial barrier function. Transcriptomic analysis of PNUTS-silenced HUVECs and lungs of PNUTSEC-KO mice revealed that the PNUTS-PP1 axis tightly regulates the expression of semaphorin 3B (SEMA3B). Indeed, silencing of SEMA3B completely restored barrier function after PNUTS loss-of-function. These results reveal a pivotal role for PNUTS in endothelial homeostasis through a PP1-SEMA3B downstream pathway that provides a potential target against the effects of aging in ECs.