Written Communication, Visitation Policies, and Awareness of Medical Issues Among Intensive Care Unit Families.

BACKGROUND: Open intensive care unit (ICU) visitation policies facilitate communication between clinicians and patients' families. Restrictive visitation policies (eg, during a pandemic) may reduce families' comprehension of information. OBJECTIVES: To determine whether written communication increased awareness of medical issues among ICU families and whether the effect size depended on the visitation policies in place when participants were enrolled. METHODS: Families of ICU patients were randomly assigned to receive usual care with or without daily written patient care updates from June 2019 to January 2021. Participants were asked whether patients had experienced 6 ICU problems at up to 2 time points during the ICU stay. Responses were compared with the study investigators' consensus. RESULTS: Of 219 participants, 131 (60%) were restricted from visiting. Participants in the written communication group were more likely than participants in the control group to correctly identify shock, renal failure, and weakness and were just as likely as participants in the control group to correctly identify respiratory failure, encephalopathy, and liver failure. Participants in the written communication group were more likely than participants in the control group to correctly identify the patient's ICU problems when all 6 were grouped as a composite outcome, with the adjusted odds ratio of correct identification tending to be higher among participants enrolled during restricted versus open visitation periods: 2.9 (95% CI, 1.9-4.2; P < .001) vs 1.8 (95% CI, 1.1-3.1; P = .02), P = .17 for difference. CONCLUSIONS: Written communication helps families correctly identify ICU issues. The benefit may be enhanced when families cannot visit the hospital. ClinicalTrials.gov Identifier: NCT03969810.

The C7orf43/TRAPPC14 component links the TRAPPII complex to Rabin8 for preciliary vesicle tethering at the mother centriole during ciliogenesis.

The primary cilium is a cellular sensor that detects light, chemicals, and movement and is important for morphogen and growth factor signaling. The small GTPase Rab11-Rab8 cascade is required for ciliogenesis. Rab11 traffics the guanine nucleotide exchange factor (GEF) Rabin8 to the centrosome to activate Rab8, needed for ciliary growth. Rabin8 also requires the transport particle protein complex (TRAPPC) proteins for centrosome recruitment during ciliogenesis. Here, using an MS-based approach for identifying Rabin8-interacting proteins, we identified C7orf43 (also known as microtubule-associated protein 11 (MAP11)) as being required for ciliation both in human cells and zebrafish embryos. We find that C7orf43 directly binds to Rabin8 and that C7orf43 knockdown diminishes Rabin8 preciliary centrosome accumulation. Interestingly, we found that C7orf43 co-sediments with TRAPPII complex subunits and directly interacts with TRAPPC proteins. Our findings establish that C7orf43 is a TRAPPII-specific complex component, referred to here as TRAPPC14. Additionally, we show that TRAPPC14 is dispensable for TRAPPII complex integrity but mediates Rabin8 association with the TRAPPII complex. Finally, we demonstrate that TRAPPC14 interacts with the distal appendage proteins Fas-binding factor 1 (FBF1) and centrosomal protein 83 (CEP83), which we show here are required for GFP-Rabin8 centrosomal accumulation, supporting a role for the TRAPPII complex in tethering preciliary vesicles to the mother centriole during ciliogenesis. In summary, our findings have revealed an uncharacterized TRAPPII-specific component, C7orf43/TRAPPC14, that regulates preciliary trafficking of Rabin8 and ciliogenesis and support previous findings that the TRAPPII complex functions as a membrane tether.

A Case of IgG4-Related Aortitis and Pericarditis: Diagnostic Challenges and Natural History.

BACKGROUND IgG4-related disease (IgG4-RD) is a systemic inflammatory condition with a myriad of presentations related to the pattern of organ involvement. Diagnostic workup for IgG4-RD requires a high index of suspicion, and further workup often includes the results of serological testing for elevated levels of IgG4. Correlation of presentation, past medical history, and histopathologic analysis are required to make a diagnosis. CASE REPORT In this case, incidental discovery of non-infectious aortitis and pulmonary mass lesions were the specific signs that led to the consideration of IgG4-RD. It was only after careful consideration of the patient's past medical history and examination of previously stored surgical specimens (pericardial tissue) that a conclusive, retrospective diagnosis of IgG4-related disease was reached. CONCLUSIONS This case demonstrates that the natural history of IgG4-related disease can be indolent and variable in presentation. Appropriate diagnosis requires consideration of all manifestations of the disease, sometimes with surveillance over several years.

Chibby promotes ciliary vesicle formation and basal body docking during airway cell differentiation.

Airway multiciliated epithelial cells play crucial roles in the mucosal defense system, but their differentiation process remains poorly understood. Mice lacking the basal body component Chibby (Cby) exhibit impaired mucociliary transport caused by defective ciliogenesis, resulting in chronic airway infection. In this paper, using primary cultures of mouse tracheal epithelial cells, we show that Cby facilitates basal body docking to the apical cell membrane through proper formation of ciliary vesicles at the distal appendage during the early stages of ciliogenesis. Cby is recruited to the distal appendages of centrioles via physical interaction with the distal appendage protein CEP164. Cby then associates with the membrane trafficking machinery component Rabin8, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rab8, to promote recruitment of Rab8 and efficient assembly of ciliary vesicles. Thus, our study identifies Cby as a key regulator of ciliary vesicle formation and basal body docking during the differentiation of airway ciliated cells.

A role for the Golgi matrix protein giantin in ciliogenesis through control of the localization of dynein-2.

The correct formation of primary cilia is central to the development and function of nearly all cells and tissues. Cilia grow from the mother centriole by extension of a microtubule core, the axoneme, which is then surrounded with a specialized ciliary membrane that is continuous with the plasma membrane. Intraflagellar transport moves particles along the length of the axoneme to direct assembly of the cilium and is also required for proper cilia function. The microtubule motor, cytoplasmic dynein-2 mediates retrograde transport along the axoneme from the tip to the base; dynein-2 is also required for some aspects of cilia formation. In most cells, the Golgi lies adjacent to the centrioles and key components of the cilia machinery localize to this organelle. Golgi-localized proteins have also been implicated in ciliogenesis and in intraflagellar transport. Here, we show that the transmembrane Golgi matrix protein giantin (GOLGB1) is required for ciliogenesis. We show that giantin is not required for the Rab11-Rabin8-Rab8 pathway that has been implicated in the early stages of ciliary membrane formation. Instead we find that suppression of giantin results in mis-localization of WDR34, the intermediate chain of dynein-2. Highly effective depletion of giantin or WDR34 leads to an inability of cells to form primary cilia. Partial depletion of giantin or of WDR34 leads to an increase in cilia length consistent with the concept that giantin acts through dynein-2. Our data implicate giantin in ciliogenesis through control of dynein-2 localization.