Racial Disparities and Other Socioeconomic Predictors of Mortality in Acute Pulmonary Embolism Treatment from the National Inpatient Sample.

PURPOSE: To explore the significance of socioeconomic factors such as race and ethnicity as predictors of mortality in sub-massive and massive acute pulmonary embolism (PE). MATERIALS AND METHODS: Hospitalizations aged > 18 years with acute, non-septic PE from 2016 to 2019 were identified in the National Inpatient Sample and divided into IR (CDT and thrombectomy) and non-IR (tPA) treatments. Statistical analyses calculated significant odds ratios via 95% confidence intervals. The primary outcome of interest was mortality rate. Comorbidities affecting mortality were examined secondarily. RESULTS: Non-Hispanic (NH) Black, Hispanic, and Asian/Pacific Islander patients were significantly less likely to undergo an IR procedure for acute, non-septic PE compared to White patients (NH Black 0.83 [0.76 - 0.90], p<0.05; Hispanic 0.78 [0.68 - 0.89], p=0.06; Asian/Pacific Islander 0.71 [0.51 - 0.98], p=0.72; OR [95% CI]); however, these differences were eliminated when propensity score matching for age, biological sex, and primary insurance-type or primary insurance-type alone. NH Black patients were significantly more likely than White patients to die regardless of undergoing non-IR or an IR treatment. Overall risk of death was 41% higher for NH Black patients compared to White patients (RR [95% CI] 1.41 [1.24 - 1.60], p<0.001). CONCLUSION: NH Black patients have a higher risk of mortality from acute, non-septic PE than White patients. Independent of race, undergoing IR management for acute, non-septic pulmonary embolisms was associated with a lower mortality rate. Matching for primary insurance-type eliminates difference in mortality between races suggest socioeconomic status (SES) may determine outcomes in acute PE.

Novel combination approaches to locoregional and systemic therapy in the management of primary and metastatic liver tumors.

Several pathways and mutations must develop or be in place for the onset of cancer. Therefore, therapies should ideally target as many of these pathways as possible to improve outcomes. Combining several agents has proven to be more effective than the use of monotherapy in the treatment of renal cell carcinoma, hepatocellular carcinoma, and other cancers. Combination therapy can also include locoregional therapies such as ablation and embolization with systemic agents for synergistic effects. This review article discusses the current literature and clinical trials covering these multifactorial combination therapies in primary and metastatic liver tumors.

Arsenate-dependent growth is independent of an ArrA mechanism of arsenate respiration in the termite hindgut isolate Citrobacter sp. strain TSA-1.

Citrobacter sp. strain TSA-1 is an enteric bacterium isolated from the hindgut of the termite. Strain TSA-1 displays anaerobic growth with selenite, fumarate, tetrathionate, nitrate, or arsenate serving as electron acceptors, and it also grows aerobically. In regards to arsenate, genome sequencing revealed that strain TSA-1 lacks a homolog for respiratory arsenate reductase, arrAB, and we were unable to obtain amplicons of arrA. This raises the question as to how strain TSA-1 achieves As(V)-dependent growth. We show that growth of strain TSA-1 on glycerol, which it cannot ferment, is linked to the electron acceptor arsenate. A series of transcriptomic experiments were conducted to discern which genes were upregulated during growth on arsenate, as opposed to those on fumarate or oxygen. For As(V), upregulation was noted for 1 of the 2 annotated arsC genes, while there was no clear upregulation for tetrathionate reductase (ttr), suggesting that this enzyme is not an alternative to arrAB as occurs in certain hyperthermophilic archaea. A gene-deletion mutant strain of TSA-1 deficient in arsC could not achieve anaerobic respiratory growth on As(V). Our results suggest that Citrobacter sp. strain TSA-1 has an unusual and as yet undefined means of achieving arsenate respiration, perhaps involving its ArsC as a respiratory reductase as well as a detoxifying agent.