Correction to: Diagnostic performance of four SARS-CoV-2 antibody assays in patients with COVID-19 or with bacterial and non-SARS-CoV-2 viral respiratory infections

European Journal of Clinical Microbiology & Infectious Diseases -     

Histological evidence concerning the osseointegration of titanium implants in the fractured rabbit femur

Stabilization of the broken bone is achieved using biocompatible materials. Since histology is still considered the gold standard technique for the assessment of bone formation around metallic implants, this report investigated the titanium implant integration in the accidentally broken bone in rabbits. The experimental protocol was reviewed and approved by the Ethical Committee of the Faculty of Medicine and Pharmacy Oradea, Romania. Holes were drilled in the diaphysis of the femur, and titanium implants were inserted in the created bone defect. In two subjects, fractures occurred on days two and three after the metallic alloy implantation. The other two rabbits presented no fractures following the surgical procedure. The rabbits were euthanized and the bones (with metallic implants) were harvested for histopathological investigation. Following decalcification, the bone samples were processed using the standard paraffin technique and stained by Goldner’s trichrome procedure. In subjects with a perfect immobilization of the titanium implants, the osseointegration occurred with minimal callus formation (i.e. primary cortical healing). In rabbits with bone fractures, the callus was more exuberant. A progressive replacement of the granulation tissue with hyaline cartilage and woven bone occurred soon after. The former aspects suggested an indirect metaplasia in the created callus. In all subjects, no inflammatory cells were identified in the created callus. The bone regeneration occurred either by primary cortical healing (in perfectly immobilized titanium implants) or by a process similar to the endochondral ossification (in poorly immobilized titanium implants following accidental post-implantation bones fracture).     

Right Ventricular Function Predicts Clinical Response to Specific Vasodilator Therapy in Patients with Pulmonary Hypertension

Introduction: We followed patients with pulmonary arterial hypertension (PAH) receiving specific vasodilator therapy and tested for predictors of clinical outcome. Methods: Thirty‐two patients (mean age 39 ± 15 years, 22 women, diagnosed with pulmonary hypertension; PH): 29 with PAH and 3 patients with inoperable chronic thromboembolic PH received therapy with either bosentan, sildenafil, or both and were evaluated with clinical parameters, biomarkers (B‐type natriuretic peptide values), and echocardiography before receiving specific medication and every 3 months thereafter. A right heart catheterization was performed at baseline. A composite endpoint of death, worsening of functional class, or the need of a second vasodilator agent was used to define the clinical nonresponders. Results: Patients were followed for 14 months (7.5–21). The endpoint was reached by 15 patients: four patients died (two idiopathic PAH and two PAH in context of Eisenmenger syndrome), seven patients showed 1 functional class worsening, and four patients needed to be switched to combination therapy. Patients who remained clinically stable or improved had at baseline a better cardiac output with a less remodeled right ventricle (RV) and better functioning RV (all P < 0.05). A RV fractional area change (RVFAC) lower than 25.7% and a RV global strain value higher than ?13.4% predict with 87% sensitivity and 83% specificity (AUC 87.3%, P = 0.001) and 73% sensitivity and 91% specificity (AUC 84.2%, P = 0.003), respectively, patients who will deteriorate clinically under specific vasodilator therapy. A multivariate model showed RVFAC to be the only independent predictor of the endpoint with a HR of 0.87 (0.8–0.96), P = 0.007. Conclusions: Over an average period of 1 year, almost half of patients showed signs of clinical deterioration despite specific vasodilator therapy. Parameters of right ventricular morphology and function had prognostic value in these patients.     

Brain temperature regulation in poor-grade subarachnoid hemorrhage patients – A multimodal neuromonitoring study

Elevated body temperature (T_core) is associated with poor outcome after subarachnoid hemorrhage (SAH). Brain temperature (T_brain) is usually higher than T_core. However, the implication of this difference (T_delta) remains unclear. We aimed to study factors associated with higher T_delta and its association with outcome. We included 46 SAH patients undergoing multimodal neuromonitoring, for a total of 7879 h of averaged data of T_core, T_brain, cerebral blood flow, cerebral perfusion pressure, intracranial pressure and cerebral metabolism (CMD). Three-months good functional outcome was defined as modified Rankin Scale ≤2. T_brain was tightly correlated with T_core (r = 0.948, p < 0.01), and was higher in 73.7% of neuromonitoring time (T_delta +0.18°C, IQR −0.01 – 0.37°C). A higher T_delta was associated with better metabolic state, indicated by lower CMD-glutamate (p = 0.003) and CMD-lactate (p < 0.001), and lower risk of mitochondrial dysfunction (MD) (OR = 0.2, p < 0.001). During MD, T_delta was significantly lower (0°C, IQR −0.2 – 0.1; p < 0.001). A higher T_delta was associated with improved outcome (OR = 7.7, p = 0.002). Our study suggests that T_brain is associated with brain metabolic activity and exceeds T_core when mitochondrial function is preserved. Further studies are needed to understand how T_delta may serve as a surrogate marker for brain function and predict clinical course and outcome after SAH.     

Parkes-Weber Syndrome and double orifice atrial septal defect as a combined rare cause of severe pulmonary hypertension

The International Journal of Cardiovascular Imaging -     

RF ablation in a patient with recurrent post-infarction ventricular tachycardia requiring multiple cardioverter-defibrillator interventions

A case of a 51 year old patient with a history of myocardial infarction (MI) and recurrent ventricular tachycardia (VT) is presented. Three months after MI the patient underwent coronary angioplasty and one year later received prophylactic implantable cardioverter-defibrillator (ICD) due to complex ventricular arrhythmias, detected on Holter ECG monitoring, and depressed left ventricular ejection fraction. Later on the patient started to experience palpitations and ICD shocks during physical activity (cycling). Interrogation of the ICD memory showed appropriate shocks due to slow (160 betas/min) VT. The device was reprogrammed and new antitachycardia pacing (ATP) algorithms were enabled, however, it occurred proarrhythmic due to the ATP-induced acceleration of VT rate. Finally, in April 2005 he received 37 appropriate ICD shocks during a few hours. The patient was selected for RF ablation and underwent successful procedure with the use of the electro-anatomical CARTO mapping system.     

LPS induces apoptosis in macrophages mostly through the autocrine production of TNF-alpha

The deleterious effects of lipopolysaccharide (LPS) during endotoxic shock are associated with the secretion of tumor necrosis factor (TNF) and the production of nitric oxide (NO), both predominantly released by tissue macrophages. We analyzed the mechanism by which LPS induces apoptosis in bone marrow-derived macrophages (BMDM). LPS-induced apoptosis reached a plateau at about 6 hours of stimulation, whereas the production of NO by the inducible NO-synthase (iNOS) required between 12 and 24 hours. Furthermore, LPS-induced early apoptosis was only moderately reduced in the presence of an inhibitor of iNOS or when using macrophages from iNOS -/-mice. In contrast, early apoptosis was paralleled by the rapid secretion of TNF and was almost absent in macrophages from mice deficient for one (p55) or both (p55 and p75) TNF-receptors. During the late phase of apoptosis (12-24 hours) NO significantly contributed to the death of macrophages even in the absence of TNF-receptor signaling. NO-mediated cell death, but not apoptosis induced by TNF, correlated with the induction of p53 and Bax genes. Thus, LPS-induced apoptosis results from 2 independent mechanisms: first and predominantly, through the autocrine secretion of TNF-alpha (early apoptotic events), and second, through the production of NO (late phase of apoptosis). (Blood. 2000;95:3823-3831)