ObjectiveThe objective of this study was to evaluate the use of social media among healthcare workers in an attempt to identify how it affects the quality of patient care.ResultsAn anonymous survey of 35 questions was conducted in South Texas, on 366 healthcare workers. Of the 97% of people who reported owning electronic devices, 87.9% indicated that they used social media. These healthcare workers indicated that they spent approximately 1 h on social media every day. The healthcare workers below the age of 40 were more involved in social media compared to those above 40 (p < 0.05). The use of social media among physicians and nurses was noted to be identical (88% for each group), and both groups encouraged their patients to research their clinical conditions on social media (p < 0.05). A higher number of physicians reported awareness of a social media policy in their hospital compared to nurses (p < 0.05). However, a large proportion of healthcare workers (40%) were unaware of their workplace policy, which could potentially cause a privacy breach of confidential medical information. Further studies are required to evaluate specific effects of these findings on the quality of patient care.

Previous sequencing studies revealed that alterations of genes associated with DNA damage response (DDR) are enriched in men with metastatic castration-resistant prostate cancer (mCRPC). BRCA2, a DDR and cancer susceptibility gene, is frequently deleted (homozygous and heterozygous) in men with aggressive prostate cancer. Here we show that patients with prostate cancer who have lost a copy of BRCA2 frequently lose a copy of tumor suppressor gene RB1; importantly, for the first time, we demonstrate that co-loss of both genes in early prostate cancer is sufficient to induce a distinct biology that is likely associated with worse prognosis.Experimental Design: We prospectively investigated underlying molecular mechanisms and genomic consequences of co-loss of BRCA2 and RB1 in prostate cancer. We used CRISPR-Cas9 and RNAi-based methods to eliminate these two genes in prostate cancer cell lines and subjected them to in vitro studies and tran-scriptomic analyses. We developed a 3-color FISH assay to detect genomic deletions of BRCA2 and RB1 in prostate cancer cells and patient-derived mCRPC organoids.Results: In human prostate cancer cell lines (LNCaP and LAPC4), loss of BRCA2 leads to the castration-resistant phenotype. Co-loss of BRCA2-RB1 in human prostate cancer cells induces an epithelial-to-mesenchymal transition, which is associated with invasiveness and a more aggressive disease phenotype. Importantly, PARP inhibitors attenuate cell growth in human mCRPC-derived organoids and human CRPC cells harboring single-copy loss of both genes.Conclusions: Our findings suggest that early identification of this aggressive form of prostate cancer offers potential for improved outcomes with early introduction of PARP inhibitor-based therapy.See related commentary by Mandigo and Knudsen, p. 1784

Purpose: Alterations in DNA damage repair (DDR) pathway genes occur in 20-25% of men with metastatic castration-resistant prostate cancer (mCRPC). Although poly (adenosine diphosphate [ADP]-ribose) polymerase inhibitors (PARPi) have been shown to benefit men with mCRPC harboring DDR defects due to mutations in BRCA1/2 and ATM, additional treatments are necessary because the effects are not durable. Experimental Design:We performed transcriptomic analysis of publicly available mCRPC cases, comparing BRCA2-null to BRCA2 wild type. We generated BRCA2-null prostate cancer cells using CRISPR/Cas9 and treated these cells with PARPi and SRC inhibitors. We also assessed the antiproliferative effects of combination treatment in 3D prostate cancer organoids. Results:We observed significant enrichment of the SRC signaling pathway in BRCA2-altered mCRPC. BRCA2-null prostate cancer cell lines had increased SRC phosphorylation and higher

Background In heart transplantation (HT), peripheral veno‐arterial extracorporeal membranous oxygenation (VA‐ECMO) is utilized preoperatively as a direct bridge to HT or postoperatively for primary graft dysfunction (PGD). Little is known about wound complications of an arterial VA‐ECMO cannulation site which can be fatal. Methods From 2009 to 2021, outcomes of 80 HT recipients who were supported with peripheral VA‐ECMO either preoperatively or postoperatively were compared based on the site of arterial cannulation: axillary (AX: N = 49) versus femoral artery (FA: N = 31). Results Patients in the AX group were older (AX: 59 years vs. 52 years, p = .006), and less likely to have extracorporeal cardiopulmonary resuscitation (0% vs. 12.9%, p = .040). Survival to discharge (AX, 81.6% vs. FA. 90.3%, p = .460), incidence of stroke (10.2% vs. 6.5%, p = .863), VA‐ECMO cannulation‐related bleeding (6.1% vs. 12.9%, p = .522), and arm or limb ischemia (0% vs. 3.2%, p = .816) were comparable. ECMO cannulation‐related wound complications were lower in the AX group (AX, 4.1% vs. FA, 45.2%, p < .001) including the wound infections (2.0% vs. 32.3%, p < .001). In FA group, all organisms were gram‐negative species. In univariate logistic regression analysis, AX cannulation was associated with less ECMO cannulation‐related wound complications (Odds ratio, .23, p < .001). There was no difference between cutdown and percutaneous FA insertion regarding cannulation‐related complications. Conclusions Given the lower rate of wound complications and comparable hospital outcomes with femoral cannulation, axillary VA‐ECMO may be an excellent option in HT candidates or recipients when possible

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Background: Gastroparesis, a chronic disorder distinguished by delays in gastric emptying, has been a concern for both health providers and hospitals due to several of its characteristics. Gastroparesis is heterogeneous in nature and is associated with several comorbidities and increasing mortality rates. It can often be caused by underlying conditions, most of which are not well understood. This lack of knowledge regarding its underlying mechanisms creates a need to better understand the risk factors involved in this patient population. This study was undertaken to understand the risk factors involved in the mortality of patients who present with gastroparesis. Methods: This retrospective study considered data from the National Inpatient Sample for patients who were admitted with a primary diagnosis of gastroparesis from 2005 to 2014. The data were stratified according to various factors of interest to identify risk factors involved in mortality using statistical tools, including a multivariable logistic regression model with backward elimination. Results: A total of 27,000 patients were admitted emergently with a primary diagnosis of gastroparesis. The mortality rate in adult patients (0.18%, N=39) was much lower than that in elderly patients (1.27%, N=71). Females accounted for the majority of patients in both the adult (73.7%) and elderly (71%) populations. The mean age of patients in the adult and elderly groups was 43 and 75 years, respectively. The association between mortality and age was significant in both adults (OR=1.04, 95%CI=1.005-1.08, p<0.025) and the elderly (OR=1.08, 95%CI=1.04-1.12, p<0.001). The hospital length of stay (HLOS, days) in adult females (5.08, SD=5.04) was significantly longer than that in adult males (4.41, SD=5.10) (p<0.001). The association between mortality and HLOS was significant in both adults (OR=1.12, 95%CI=1.09-1.15, p<0.001) and elderly patients (OR=1.10, 95%CI=1.06-1.14, p<0.001). A lower percentage of adults (6.6%, N=1,402) underwent an operation compared to the elderly (9.6%, N=538). The mean time to operation was 4.76 days for adult patients who survived and 17.50 days for adult patients who did not survive (SD=5.37 and 9.37, respectively, p=0.006). On the other hand, this value was 5.57 and 9.10 days for elderly patients (SD=6.50 and 7.15, respectively, p=0.037). Among patients who underwent an operation, the association between mortality and time to operation was significant for both adults (OR=1.17, 95%CI=1.094-1.247, p<0.001) and elderly patients (OR=1.05, 95%CI=1.005-1.124, p<0.001). Conclusion: The risk of mortality in elderly patients with emergent gastroparesis was 7-fold greater than that in adult patients. The odds of mortality increased by 8% for every year increase in age in elderly patients and by 4% in adults.

Loss of the histone demethylase KDM5D (lysine‐specific demethylase 5D) leads to in vitro resistance of prostate cancer cells to androgen deprivation therapy (ADT) with and without docetaxel. We aimed to define downstream drivers of the KDM5D effect. Using chromatin immunoprecipitation sequencing (ChIP‐seq) of the LNCaP cell line (androgen‐sensitive human prostate adenocarcinoma) with and without silenced KDM5D, MYBL2‐binding sites were analyzed. Associations between MYBL2 mRNA expression and clinical outcomes were assessed in cohorts of men with localized and metastatic hormone‐sensitive prostate cancer. In vitro assays with silencing and overexpression of MYBL2 and KDM5D in androgen receptor (AR)‐positive hormone‐sensitive prostate cancer cell lines, LNCaP and LAPC4, were used to assess their influence on cellular proliferation, apoptosis, and cell cycle distribution, as well as sensitivity to androgen deprivation, docetaxel, and cabazitaxel. We found that silencing KDM5D increased histone H3 lysine K4 (H3K4) trimethylation and increased MYBL2 expression. KDM5D and MYBL2 were negatively correlated with some but not all clinical samples. Higher MYBL2 expression was associated with a higher rate of relapse in localized disease and poorer overall survival in men with metastatic disease in the CHAARTED trial. Lower MYBL2 levels enhanced LNCaP and LAPC4 sensitivity to androgen deprivation and taxanes. In vitro, modifications of KDM5D and MYBL2 altered cell cycle distribution and apoptosis in a cell line‐specific manner. These results show that the transcription factor MYBL2 impacts in vitro hormone‐sensitive prostate cancer sensitivity to androgen deprivation and taxanes, and lower levels are associated with better clinical outcomes in men with hormone‐sensitive prostate cancer.

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