Endocavitary contrast-enhanced ultrasound: a technique whose time has come?

Endocavitary use of contrast agents in sonography (US) is a relatively new method in diagnostic imaging, competing against gray-scale US, fluoroscopy, and endoscopy. This article describes established indications, demonstrates the techniques of evolving applications, and discusses their potential benefits. These benefits include the ability to obtain precise information about the placement of drains and the extent of fluid collections, and to accurately identify the location and features of strictures in various organs, and those of complications of fluid collections or abscesses, without resorting to ionizing radiation.

[German recommendations on lung and thoracic ultrasonography in patients with COVID-19]. / Empfehlungen zur Lungen- und Thoraxsonographie bei Patienten mit COVID-19-Erkrankung.

Lung and chest ultrasound are further examination modalities in addition to computed tomography and laboratory diagnostics in patients with COVID-19. It extends the clinical-physical examination because it can examine lung surface sensitively. Lung surface pattern changes have been found in sonograms of patients with COVID-19 pneumonia and during the course of the disease. German specialist societies of clinical acute, emergency and intensive care medicine as well as imaging, which are concerned with the care of patients with SARS-CoV­2 infection and COVID-19, have coordinated recommendations for lung and thorax sonography. This document has been created within a transparent process, led by the German Society of Interdisciplinary Emergency and Acute Medicine e. V. (DGINA), and worked out by an expert panel and delegates from the societies. Sources of the first 200 cases were summarized. Typical thorax sonographic findings are presented. International sources or standards that were available in PubMed until May 24, 2020 were included. Using case studies and multimedia content, the document is intended to not only support users but also demonstrate quality features and the potential of chest and lung sonography. The German Society for Ultrasound in Medicine (DEGUM) is carrying out a multicenter study (study coordination at the TU Munich).

CaMKII is activated and translocated to the secretory apical membrane during cholinergically conveyed gastric acid secretion.

The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is thought to be activated during the cholinergic stimulation of gastric acid secretion. The carbachol-induced acid production of cultured rabbit parietal cells was dose-dependently inhibited by the CaMKII inhibitor KN-62 as measured by accumulation of the weak base [(14)C]aminopyrine ([(14)C]-AP). Inhibition by KN-62 was most efficient at concentrations of carbachol >10(-6) M. After carbachol stimulation, we observed an activation of CaMKII activity, and its translocation to the apical membrane of gastric mucosal cells. We found a doubling of the abundance of CaMKII to the stimulus-associated apical membrane (SA vesicles) compared to the apical membrane from the resting state after carbachol induction. This was shown by both an anti-CaMKII serum and the 1.8-fold increase of the CaMKII phosphotransferase activity in vitro. The SA vesicles exhibited a strong increase of autoactivated CaMKII probed with an anti-autoactivated CaMKII antibody. Additionally, we observed a colocalization of both CaMKII and the H(+)-K(+)-ATPase of SA vesicles similar to the colocalization of both enzymes to the tubulovesicles suggesting them as at least one pool for the SA vesicular CaMKII. Our data indicate that the activation of CaMKII and the carbachol-dependent redistribution of CaMKII to the SA vesicles are distinct processes that occur in parallel to regulate the activity and localization of CaMKII. These findings contribute to the model implicating an involvement for CaMKII in the intracellular dynamics of the acid secretion.

Mechanisms of secretion-associated shrinkage and volume recovery in cultured rabbit parietal cells.

We have previously shown that stimulation of acid secretion in parietal cells causes rapid initial cell shrinkage, followed by Na(+)/H(+) exchange-mediated regulatory volume increase (RVI). The factors leading to the initial cell shrinkage are unknown. We therefore monitored volume changes in cultured rabbit parietal cells by confocal measurement of the cytoplasmic calcein concentration. Although blocking the presumably apically located K(+) channel KCNQ1 with chromanol 293b reduced both the forskolin- and carbachol-induced cell shrinkage, inhibition of Ca(2+)-sensitive K(+) channels with charybdotoxin strongly inhibited the cell volume decrease after carbachol, but not after forskolin stimulation. The cell shrinkage induced by both secretagogues was partially inhibited by blocking H(+)-K(+)-ATPase with SCH28080 and completely absent after incubation with NPPB, which inhibits parietal cell anion conductances involved in acid secretion. The subsequent RVI was strongly inhibited with the Na(+)/H(+) exchanger 1 (NHE1)-specific concentration of HOE642 and completely by 500 muM dimethyl-amiloride (DMA), which also inhibits NHE4. None of the above substances induced volume changes under baseline conditions. Our results indicate that cell volume decrease associated with acid secretion is dependent on the activation of K(+) and Cl(-) channels by the respective secretagogues. K(+), Cl(-), and water secretion into the secretory canaliculi is thus one likely mechanism of stimulation-associated cell shrinkage in cultured parietal cells. The observed RVI is predominantly mediated by NHE1.