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Introduction: Service members are exposed to ambient airborne pollutants that have been linked to adverse health effects; however, capabilities to identify and characterize exposures across multi-domain operations are currently lacking. Occupational and environmental exposure monitoring is problematic because there is not a single simple solution, and current technological limitations suggest that simultaneous deployment of multiple devices may be the most effective near-term strategy., Materials and Methods: A broad industry scan of wearable, handheld, or portable occupational and environmental exposure monitoring devices was conducted, and subject matter experts were interviewed about the state of the field., Results: This survey identified limitations including the inability to detect multiple analytes or analyte classes, size and weight, and detection limits, but multiple implementation strategies could be employed to meet a variety of combat needs. Device types could be layered, or specific device types could be deployed in acute toxic exposure environments such as dense urban population centers or subterranean spaces., Conclusions: Evolving technologies and data management strategies may advance personal exposure monitoring in the future. These new devices and methods will likely supplant current technologies, while still using the programmatic and data framework established with early implementation of current commercial off the shelf devices., (© Association of Military Surgeons of the United States 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The current studies were undertaken to determine the susceptibility of human alveolar macrophages (AMs) to influenza A virus (IAV) infection in comparison with autologous peripheral blood-derived monocytes-macrophages (PBMs). AMs and PBMs were exposed to IAV in vitro and examined for their ability to bind and internalize IAV, and synthesize viral proteins and RNA. PBMs but not AMs demonstrated binding and internalization of the virus, synthesizing viral proteins and RNA. Exposure of AMs in the presence of a sialidase inhibitor or anti-IAV antibody resulted in viral protein synthesis by the cells. Exposure of AMs to fluorescein isothiocyanate-labeled IAV in the presence of anti-fluorescein isothiocyanate antibody also resulted in viral protein synthesis. Thus, human AMs are apparently not susceptible to direct infection by a human IAV but are likely to be infected indirectly in the setting of exposure in the presence of antibody that binds the challenging strain of IAV., (© The Author 2016. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail journals.permissions@oup.com.)

Transvaginal, ultrasound-guided oocyte retrieval has become the gold standard for IVF therapy. Despite a low reported complication rate, here a case is reported of acute ureteral obstruction following seemingly uncomplicated oocyte retrieval. Prompt diagnosis and ureteral stenting led to rapid patient recovery with no long-term urinary tract sequelae. Ureteral injury needs to be included in the differential diagnosis of a patient presenting with pelvic/abdominal pain following oocyte retrieval.

Respiratory syncytial virus (RSV) infection has been shown to induce human mononuclear leukocyte (MNL) production of net interleukin-1 (IL-1)-inhibitor activity. In the current studies of IL-1-inhibitor effects, RSV-exposed cells were compared with autologous MNL that were sham-exposed or exposed to inactivated RSV or influenza virus (which induces net IL-1 activity and commonly elicits effective homotypic immunity). Exposure of MNL to influenza virus or inactivated RSV resulted in increased expression of human leukocyte antigen-DR, the IL-2 receptor, and the transferrin receptor and increased progression through the cell cycle by 3 days. In contrast, exposure to infectious RSV resulted in decreased marker expression and cell cycle arrest, with abrogation of proliferation in response to the virus or other stimuli. These data raise the possibility that a contributing mechanism for recurrence of RSV infection is early suppression of the clonal expansion of virus-specific lymphocytes due to net IL-1-inhibitor activity.

Net interleukin-1 (IL-1) inhibitor activity is induced by exposure of purified human monocytes-macrophages to respiratory syncytial virus (RSV). Furthermore, IL-1 inhibitor activity was produced by monocytes-macrophages exposed to RSV in the presence of lymphocytes, that is, by unseparated mononuclear leukocytes (MNL). Purified RSV-exposed lymphocytes, as well as the lymphocytes exposed within MNL preparations, produced net IL-1 inhibitor activity. In contrast, net IL-1 activity was produced when purified monocytes-macrophages or unseparated MNL were exposed to influenza virus. The RSV-induced IL-1 inhibitors demonstrated antiproliferative effects on mitogen-stimulated human lymphocytes as well as on the mouse thymocytes used in standard assays. The results raise the possibility that such antiproliferative activity is mediated, at least in part, by monocytes-macrophages. The data also suggest that IL-1 inhibitors produced by MNL after exposure to RSV may contribute along with other factors to the recurrence of RSV infection in immune individuals.