The Post-Acute COVID-19-Vaccination Syndrome in the Light of Pharmacovigilance.

Clinical studies show that SARS-CoV-2 vaccination sometimes entails a severe and disabling chronic syndrome termed post-acute-COVID-19-vaccination syndrome (PACVS). PACVS shares similarities with long COVID. Today, PACVS is still not officially recognised as a disease.

Clinical and Diagnostic Features of Post-Acute COVID-19 Vaccination Syndrome (PACVS).

Post-acute COVID-19 vaccination syndrome (PACVS) is a chronic disease triggered by SARS-CoV-2 vaccination (estimated prevalence 0.02%). PACVS is discriminated from the normal post-vaccination state by altered receptor antibodies, most notably angiotensin II type 1 and alpha-2B adrenergic receptor antibodies.

Questionable Validity of Creatinine-Based eGFR in Elderly Patients but Cystatin C Is Helpful in First-Line Diagnostics.

Background: The recommended chronic kidney disease (CKD) first-line diagnostic test is based on the creatinine-derived (estimated) glomerular filtration rate (eGFR). Cystatin C use may provide a better assessment.

Methods: We compared creatinine- and cystatin C-derived eGFR determination as the first-line diagnostic test for 112 hospital patients aged > 60 years (median = 76 years).

Chronic Fatigue and Dysautonomia following COVID-19 Vaccination Is Distinguished from Normal Vaccination Response by Altered Blood Markers.

SARS-CoV-2 mRNA vaccination can entail chronic fatigue/dysautonomia tentatively termed post-acute COVID-19 vaccination syndrome (PACVS). We explored receptor autoantibodies and interleukin-6 (IL-6) as somatic correlates of PACVS. Blood markers determined before and six months after first-time SARS-CoV-2 vaccination of healthy controls ( = 89; 71 females; mean/median age: 39/49 years) were compared with corresponding values of PACVS-affected persons ( = 191; 159 females; mean/median age: 40/39 years) exhibiting chronic fatigue/dysautonomia (≥three symptoms for ≥five months after the last SARS-CoV-2 mRNA vaccination) not due to SARS-CoV-2 infection and/or confounding diseases/medications.

Ex Vivo Immune Responsiveness to SARS-CoV-2 Omicron BA.5.1 Following Vaccination with Unmodified mRNA-Vaccine.

(1) Background: The high incidence of SARS-CoV-2 infection in vaccinated persons underscores the importance of individualized re-vaccination. PanIg antibodies that act against the S1/-receptor binding domain quantified in serum by a routine diagnostic test (ECLIA, Roche) can be used to gauge the individual ex vivo capacity of SARS-CoV-2 neutralization. However, that test is not adapted to mutations in the S1/-receptor binding domain, having accumulated in SARS-CoV-2 variants.

Receptor autoantibodies: Associations with cardiac markers, histology, and function in human non-ischaemic heart failure.

Aims: A causal link between non-ischaemic heart failure (HF) and humoral autoimmunity against G-protein-coupled receptors (GPCR) remains unclear except for Chagas' cardiomyopathy. Uncertainty arises from ambiguous reports on incidences of GPCR autoantibodies, spurious correlations of autoantibody levels with disease activity, and lack of standardization and validation of measuring procedures for putatively cardio-pathogenic GPCR autoantibodies. Here, we use validated and certified immune assays presenting native receptors as binding targets.

A Diagnostic Strategy for Gauging Individual Humoral Ex Vivo Immune Responsiveness Following COVID-19 Vaccination.

Purpose: We describe a diagnostic procedure suitable for scheduling (re-)vaccination against severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) according to individual state of humoral immunization. Methods: To clarify the relation between quantitative antibody measurements and humoral ex vivo immune responsiveness, we monitored 124 individuals before, during and six months after vaccination with Spikevax (Moderna, Cambridge, MA, USA). Antibodies against SARS-CoV-2 spike (S1) protein receptor-binding domain (S1-AB) and against nucleocapsid antigens were measured by chemiluminescent immunoassay (Roche).

SARS-CoV-2 seroprevalence and determinants of infection in young adults: a population-based seroepidemiological study.

Objectives: Most SARS-CoV-2 seroprevalence studies have focussed on adults and high-risk populations, and little is known about young adults. The objective of the present study was to provide evidence on the SARS-CoV-2 seroprevalence among young adults in Germany and to explore determinants associated with seropositivity in general and, specifically, with previously undetected infections.

Study Design: This was a population-based SARS-CoV-2 seroprevalence study.

Underascertainment of COVID-19 cases among first responders: a seroepidemiological study.

Background: Providing frontline support places first responders at a high risk for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

Aims: This study was aimed to determine the anti-SARS-CoV-2 seroprevalence in a cohort of first responders (i.e.

Evaluation of Radiographic Contrast-Induced Nephropathy by Functional Diffusion Weighted Imaging.

Contrast-induced nephropathy (CIN) resembles an important complication of radiographic contrast medium (XCM) displayed by a rise in creatinine levels 48-72 h after XCM administration. The purpose of the current study was to evaluate microstructural renal changes due to CIN in high-risk patients by diffusion weighted (DWI) and diffusion tensor imaging (DTI). Fifteen patients (five CIN and ten non-CIN) scheduled for cardiological intervention were included in the study.

Sensitivity of anti-SARS-CoV-2 serological assays in a high-prevalence setting.

Evaluation and power of seroprevalence studies depend on the performed serological assays. The aim of this study was to assess four commercial serological tests from EUROIMMUN, DiaSorin, Abbott, and Roche as well as an in-house immunofluorescence and neutralization test for their capability to identify SARS-CoV-2 seropositive individuals in a high-prevalence setting. Therefore, 42 social and working contacts of a German super-spreader were tested.

Autoantibodies against M-muscarinic and beta-adrenergic receptors in periodontitis patients.

Autoantibodies against muscarinic and beta-adrenergic receptors are considered a potential cause and/or risk factor for chronic heart failure. Association of periodontitis with such autoantibodies and with impaired heart function has been observed in patients exposed to endemic Chagas' disease, which triggers by itself cardiomyopathy and receptor immunization.Here we studied the association between periodontitis, markers of cardiac injury and receptor autoimmunization in periodontitis patients (n = 147) not exposed to Chagas' disease.

Unmasking features of the auto-epitope essential for β -adrenoceptor activation by autoantibodies in chronic heart failure.

Aims: Chronic heart failure (CHF) can be caused by autoantibodies stimulating the heart via binding to first and/or second extracellular loops of cardiac β -adrenoceptors. Allosteric receptor activation depends on conformational features of the autoantibody binding site. Elucidating these features will pave the way for the development of specific diagnostics and therapeutics.

Nanodiscs Incorporating Native β1 Adrenergic Receptor as a Novel Approach for the Detection of Pathological Autoantibodies in Patients with Dilated Cardiomyopathy.

Background: Dilated cardiomyopathy (DCM) is a common cause of heart failure with high morbidity and mortality rates. The association of anti-β1 adrenergic receptor (β1AR) autoantibodies with disease progression was shown by various studies and in vivo animal experiments. The prevalence of these disease-driving autoantibodies was estimated as 25% to 75% in DCM.

Relevant effects of beta-adrenoceptor autoantibodies in chronic heart failure.

Patients suffering from chronic heart failure (CHF) caused or promoted by autoantibodies against cardiac beta-adrenergic receptors (betaAR) could benefit from specific therapies aimed at tolerance induction, removal or neutralisation of betaAR autoantibodies, provided the patients can be selected for these therapies by reliable detection and quantitation of betaAR autoantibodies in their circulation and by a valid assessment of the autoantibodies's putative cardio-pathogenic potential. Here, we discuss the current state of knowledge regarding the effects of CHF-associated (auto)antibodies on betaAR function and betaAR-mediated signal tranduction and discuss the presumed role of these effects in the development and progression of CHF. Identification of disease-relevant functional autoantibody effects and their specific assessment in medical diagnostic will be a prerequesite for the implementation of novel specific therapies not only for CHF caused or promoted by betaAR autoantibodies but alos for most other diseases involving autoantibodies that target G-protein coupled receptors.

Ultra-short laser-accelerated proton pulses have similar DNA-damaging effectiveness but produce less immediate nitroxidative stress than conventional proton beams.

Ultra-short proton pulses originating from laser-plasma accelerators can provide instantaneous dose rates at least 10(7)-fold in excess of conventional, continuous proton beams. The impact of such extremely high proton dose rates on A549 human lung cancer cells was compared with conventionally accelerated protons and 90 keV X-rays. Between 0.

Crosstalk of clock gene expression and autophagy in aging.

Autophagy and the circadian clock counteract tissue degeneration and support longevity in many organisms. Accumulating evidence indicates that aging compromises both the circadian clock and autophagy but the mechanisms involved are unknown. Here we show that the expression levels of transcriptional repressor components of the circadian oscillator, most prominently the human Period homologue , are strongly reduced in primary dermal fibroblasts from aged humans, while raising the expression of in the same cells partially restores diminished autophagy levels.

Living Long and Well: Prospects for a Personalized Approach to the Medicine of Ageing.

Research into ageing and its underlying molecular basis enables us to develop and implement targeted interventions to ameliorate or cure its consequences. However, the efficacy of interventions often differs widely between individuals, suggesting that populations should be stratified or even individualized. Large-scale cohort studies in humans, similar systematic studies in model organisms as well as detailed investigations into the biology of ageing can provide individual validated biomarkers and mechanisms, leading to recommendations for targeted interventions.

A standardised FACS assay based on native, receptor transfected cells for the clinical diagnosis and monitoring of β1-adrenergic receptor autoantibodies in human heart disease.

Background: Autoantibodies against β1-adrenergic receptors (β1AR) that stimulate cardiac cAMP-production play a causal role in the pathogenesis of human heart failure. Patients can be subjected to specific therapies, if the presence of potentially cardio-noxious β1AR-autoantibodies is reliably diagnosed. This requires assessment of IgG-interactions with the native β1AR because β1AR-autoantibodies target a conformational epitope inadequately presented by denatured receptors or linear peptides.