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1.
J Am Coll Radiol ; 19(3): 437-445, 2022 03.
Article in English | MEDLINE | ID: mdl-34863775

ABSTRACT

OBJECTIVE: Coronavirus disease 2019 (COVID-19) vaccine mandates are being implemented in health systems across the United States, and the impact on the radiology department workforce and operations becuase of vaccine hesitancy among health care workers is currently unknown. This article discusses the potential impact of the COVID-19 vaccine mandate on a large multicenter radiology department as well as strategies to mitigate those effects. METHODS: Weekly vaccine compliance data were obtained for employees across the entire health system from August 17, 2021, through September 13, 2021, and radiology department-specific data were extracted. Vaccine compliance data was mapped to specific radiology job titles and the five different hospital locations. RESULTS: A total of 6% of radiology department employees were not fully vaccine compliant by the initial deadline of September 10, 2021. MR technologists and radiology technology assistants had the highest initial rates of noncompliance of 37% and 38%, respectively. Vaccine noncompliance rates by the mandate deadline ranged from 0.5% to 7.0% at the five hospital sites. Only one hospital required a decrease in imaging hours of operation because of the vaccine mandate. CONCLUSION: Despite initial concerns about the impact of vaccine mandate noncompliance on departmental operations, there was ultimately little effect because of improved vaccine compliance after the mandate. Understanding individual employee and locoregional differences in vaccine compliance can help leaders proactively develop mitigation strategies to manage this new challenge during the COVID-19 pandemic.


Subject(s)
COVID-19 , Radiology , COVID-19/prevention & control , COVID-19 Vaccines , Health Personnel , Humans , Pandemics/prevention & control , United States
2.
Radiol Case Rep ; 12(2): 401-404, 2017 Jun.
Article in English | MEDLINE | ID: mdl-28491197

ABSTRACT

Splenic cysts are uncommon, with large cysts and complications being rare. We describe a 6-year-old patient who initially presented 1 day after falling onto her abdomen at the playground with worsening abdominal pain and distention. An ultrasound of the abdomen demonstrated free abdominal fluid in all four quadrants. A subsequent contrast-enhanced computed tomography scan of the abdomen and pelvis was performed which showed a large splenic cyst with open communication to the peritoneal cavity. A congenital primary cyst was confirmed on pathology after partial splenectomy was performed. Although the majority of splenic cysts are asymptomatic, rupture can lead to acute peritoneal signs and mimic other significant causes of abdominal pain such as viscous injury or acute appendicitis.

3.
Biochem Biophys Res Commun ; 354(4): 955-61, 2007 Mar 23.
Article in English | MEDLINE | ID: mdl-17270147

ABSTRACT

In the present study, we examined the role of Staphylococcus aureus protein A (SpA) in inducing inflammatory response in human corneal epithelial cells (HCECs). Exposure of HCECs to SpA induces rapid NF-kappaB activation and secretion of proinflammatory cytokine/chemokines (TNF-alpha and IL-8) in both concentration and time-dependent manner. Challenge of HCECs with live SpA(-/-) mutant S. aureus strains resulted in significantly reduced production of the cytokines when compared to the wild-type S. aureus strain. SpA also elicited the activation of MAP Kinases P38, ERK, but not JNK, in HCECs. SpA-induced production of proinflammatory cytokine were completely blocked by the NF-kappaB and p38 inhibitors and partially inhibited by the Jnk inhibitor. Pretreatment with anti-TLR2 neutralizing antibody had no effect on SpA-induced inflammatory response in HCECs, suggesting that this response is independent of TLR2 signaling. Moreover, unlike TLR2 ligands, SpA failed to induce the expression of antimicrobial peptides (hBD2 and LL-37) in HCECs. These studies indicate that SpA is a S. aureus virulence factor that stimulates HCEC inflammatory response through a pathway distinct from TLR2 in HCECs.


Subject(s)
Epithelium, Corneal/drug effects , Keratitis/chemically induced , Staphylococcal Protein A/pharmacology , Enzyme Activation , Interleukin-8/metabolism , Mitogen-Activated Protein Kinases/metabolism , NF-kappa B/metabolism , Staphylococcus aureus/genetics , Toll-Like Receptor 2/drug effects , Toll-Like Receptor 2/physiology , Tumor Necrosis Factor-alpha/metabolism
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