Detection and abundance of SARS-CoV-2 in wastewater in Liechtenstein, and the estimation of prevalence and impact of the B.1.1.7 variant.

The new coronavirus 2 (SARS-CoV-2) is known to be also shed through feces, which makes wastewater-based surveillance possible, independent of symptomatic cases and unbiased by any testing strategies and frequencies. We investigated the entire population of the Principality of Liechtenstein with samples from the wastewater treatment plant Bendern (serving all 39,000 inhabitants). Twenty-four-hour composite samples were taken once or twice a week over a period of 6 months from September 2020 to March 2021. Viral RNA was concentrated using the PEG centrifugation method followed by reverse transcription quantitative PCR. The aim of this research was to assess the suitability of SARS-CoV-2 fragments to relate the viral wastewater signal to the incidences and assess the impact of the emerging B.1.1.7. variant. The viral load in the wastewater peaked at almost 9 × 108 viral fragments per person equivalent (PE) and day on October 25, and showed a second peak on December 22 reaching a viral load of approximately 2 × 108 PE-1d-1. Individual testing showed a lag of 4 days and a distinct underestimation of cases at the first peak when testing frequency was low. The wastewater signal showed an immediate response to the implementation of non-pharmaceutical interventions. The new virus variant B.1.1.7. was first detected in wastewater on December 23, while it was first observed with individual testing on January 13, 2021. Further, our data indicate that the emergence of new virus variant may change the wastewater signal, probably due to different shedding patterns, which should be considered in future models.

Lung volume reduction surgery combined with cardiac interventions.

OBJECTIVE: Postoperative course and functional outcome were evaluated in patients who underwent lung volume reduction surgery (LVRS) or in combination with valve replacement (VR), percutaneous transluminal coronary angioplasty (PTCA), placement of a stent, or coronary artery bypass grafting (CABG). METHODS: Patients with severe bronchial obstruction and hyperinflation due to pulmonary emphysema were evaluated for lung volume reduction surgery. Cardiac disorders were screened by history and physical examination and assessed by coronary angiography. Nine patients were accepted for LVRS in combination with an intervention for coronary artery disease (CAD). In addition, three patients with valve disease and severe emphysema were accepted for valve replacement (two aortic-, one mitral valve) only in combination with LVRS. Functional results over the first 6 months were analysed. RESULTS: Pulmonary function testing demonstrates a significant improvement in postoperative FEV1 in patients who underwent LVRS combined with an intervention for CAD. This was reflected in reduction of overinflation (residual volume/total lung capacity (RV/TLC)), and improvement in the 12-min walking distance and dyspnea. Median hospital stay was 15 days (10-33). One patient in the CAD group died due to pulmonary edema on day 2 postoperatively. One of the three patients who underwent valve replacement and LVRS died on day 14 postoperatively following intestinal infarction. Both survivors improved in pulmonary function, dyspnea score and exercise capacity. Complications in all 12 patients included pneumothorax (n = 2), hematothorax (n = 1) and urosepsis (n = 1). CONCLUSION: Functional improvement after LVRS in patients with CAD is equal to patients without CAD. Mortality in patients who underwent LVRS after PTCA or CABG was comparable to patients without CAD. LVRS enables valve replacement in selected patients with severe emphysema otherwise inoperable.

The adrenaline-alpha 2-adrenoceptor-mediated vasoconstrictor axis.

In patients with essential hypertension plasma adrenaline concentrations have been found to be higher than in normotensive subjects and this may represent increased adrenergic activity. Adrenaline released into the circulation can be taken up by the sympathetic nerve ending and as it is re-released as a co-transmitter it enhances exocytotic noradrenaline release by stimulating prejunctional beta-adrenoceptors and as a consequence it contributes to postjunctional alpha 1-adrenoceptor-induced vasoconstriction. Adrenaline may also induce vasoconstriction via post- and extra-junctional alpha 2-adrenoceptors, as shown by a decrease in the forearm blood flow during adrenaline infusions in the postjunctional alpha 1- and beta-blocked forearm vasculature, an effect that could be antagonized by alpha 2-adrenoceptor blockade with yohimbine. alpha 2-Adrenoceptor stimulation in platelets showed an increased sensitivity to adrenaline, as determined by sensitivity in counteracting the inhibitor effect of PGI2 on intracellular free calcium concentration in untreated patients with essential hypertension, when compared with treated patients or normotensive subjects. As these effects can be normalized by antihypertensive treatment this suggests that the increased hormone sensitivity may be related to the elevated intracellular free calcium concentration. Thus adrenaline, via pre- and post-junctional adrenoceptors, may contribute to enhanced vascular smooth muscle contraction, which most likely is sensitized by the elevated intracellular calcium concentration.