Conversion of positive-pressure cardiac catheterization and electrophysiology laboratories to a novel 2-zone negative-pressure system during COVID-19 pandemic.

During coronavirus disease-2019 (COVID-19) pandemic, there continues to be a need to utilize cardiac catheterization and electrophysiology laboratories for emergent and urgent procedures. Per infection prevention guidelines and hospital codes, catheterization and electrophysiology laboratories are usually built as positive-pressure ventilation rooms to minimize the infection risk. However, patients with highly transmissible airborne diseases such as COVID-19 are best caredfor in negative ventilation rooms to minimize the risk of transmission. From a mechanical and engineering perspective, positive-pressure ventilation rooms cannot be readily converted to negative-pressure ventilation rooms. In this report, we describe a novel, quick, readily implantable, and resource-friendly approach on how to secure air quality in catheterization and electrophysiology laboratories by converting a positive-pressure ventilation room to a two-zone negative ventilation system to minimize the risk of transmission.

A Division 18 conversation with the new APA Chief Executive Officer (CEO): Arthur C. Evans, PhD.

The new Chief Executive Officer of the American Psychological Association (APA) Arthur C. Evans, Jr., Ph.D., has a long-standing career in public service and an ongoing commitment to public service psychology. Leadership of APA Division 18 (Psychologists in Public Service) recently interviewed Dr. Evans about his position at APA and his vision for public service psychology and its role in the U.S. health care system. Issues for discussion were selected by the Division's sections on community and state hospitals; criminal justice; police and public safety; psychologists in Indian country; serious mental illness/severe emotional disturbance; students; and veterans affairs. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

Secretion and cell volume regulation by salivary acinar cells from mice lacking expression of the Clcn3 Cl- channel gene.

Salivary gland acinar cells shrink when Cl(-) currents are activated following cell swelling induced by exposure to a hypotonic solution or in response to calcium-mobilizing agonists. The molecular identity of the Cl(-) channel(s) in salivary cells involved in these processes is unknown, although ClC-3 has been implicated in several tissues as a cell-volume-sensitive Cl(-) channel. We found that cells isolated from mice with targeted disruption of the Clcn3 gene undergo regulatory volume decrease in a fashion similar to cells from wild-type littermates. Consistent with a normal regulatory volume decrease response, the magnitude and the kinetics of the swell-activated Cl(-) currents in cells from ClC-3-deficient mice were equivalent to those from wild-type mice. It has also been suggested that ClC-3 is activated by Ca(2+)-calmodulin-dependent protein kinase II; however, the magnitude of the Ca(2+)-dependent Cl(-) current was unchanged in the Clcn3(-/-) animals. In addition, we observed that ClC-3 appeared to be highly expressed in the smooth muscle cells of glandular blood vessels, suggesting a potential role for this channel in saliva production by regulating blood flow, yet the volume and ionic compositions of in vivo stimulated saliva from wild-type and null mutant animals were comparable. Finally, in some cells ClC-3 is an intracellular channel that is thought to be involved in vesicular acidification and secretion. Nevertheless, the protein content of saliva was unchanged in Clcn3(-/-) mice. Our results demonstrate that the ClC-3 Cl(-) channel is not a major regulator of acinar cell volume, nor is it essential for determining the secretion rate and composition of saliva.

Loss of hyperpolarization-activated Cl(-) current in salivary acinar cells from Clcn2 knockout mice.

ClC-2 is localized to the apical membranes of secretory epithelia where it has been hypothesized to play a role in fluid secretion. Although ClC-2 is clearly the inwardly rectifying anion channel in several tissues, the molecular identity of the hyperpolarization-activated Cl(-) current in other organs, including the salivary gland, is currently unknown. To determine the nature of the hyperpolarization-activated Cl(-) current and to examine the role of ClC-2 in salivary gland function, a mouse line containing a targeted disruption of the Clcn2 gene was generated. The resulting homozygous Clcn2(-/-) mice lacked detectable hyperpolarization-activated chloride currents in parotid acinar cells and, as described previously, displayed postnatal degeneration of the retina and testis. The magnitude and biophysical characteristics of the volume- and calcium-activated chloride currents in these cells were unaffected by the absence of ClC-2. Although ClC-2 appears to contribute to fluid secretion in some cell types, both the initial and sustained salivary flow rates were normal in Clcn2(-/-) mice following in vivo stimulation with pilocarpine, a cholinergic agonist. In addition, the electrolytes and protein contents of the mature secretions were normal. Because ClC-2 has been postulated to contribute to cell volume control, we also examined regulatory volume decrease following cell swelling. However, parotid acinar cells from Clcn2(-/-) mice recovered volume with similar efficiency to wild-type littermates. These data demonstrate that ClC-2 is the hyperpolarization-activated Cl(-) channel in salivary acinar cells but is not essential for maximum chloride flux during stimulated secretion of saliva or acinar cell volume regulation.