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Background: Historically, procalcitonin(PCT) has been used as a predictor of bacterial infection and to guide antibiotic therapy in hospitalized patients. The purpose of this study was to determine PCT's diagnostic utility in predicting secondary bacterial pneumonia in critically ill patients with severe COVID-19 pneumonia. Methods: A retrospective cohort study was conducted in COVID-19 adults admitted to the ICU between March 2020, and March 2021. All included patients had a PCT level within 72 h of presentation and serum creatinine of 0.05). While there was no difference in bacterial pneumonia in low versus high groups (34(26.8%) versus 12(31.6%), p = 0.562), more patients in the high PCT group had bacteremia (19(15%) versus 11(28.9%), p = 0.050). Sensitivity was 26.1% and specificity was 78.2% for PCT to predict bacterial pneumonia coinfection in ICU patients with COVID-19 pneumonia. ROC yielded an AUC 0.54 ( p = 0.415). After adjusting for LDH>350U/L and creatinine in multivariable regression, PCT did not enhance performance of the regression model. Conclusions: PCT offers little to no predictive utility in diagnosing concomitant bacterial pneumonia in critically ill patients with COVID-19 nor in predicting increased severity of disease or worse outcomes including mortality.

Hospital readmission is an important quality-of-care indicator. We sought to examine the rates and predictors of unplanned readmission for the high-risk non-trauma emergency laparotomy patient.This is a post hoc analysis of a multicenter prospective observational study. Between April 2018 and June 2019, a total of 19 centers enrolled all adult patients undergoing emergency laparotomies and systematically collected preoperative, operative, and 30-day postoperative variables. For the purpose of this study, we defined unplanned readmission as a readmission occurring within 30 days from discharge and one that was immediately preceded by an emergency department visit. Patients were excluded if they died during the index admission, were discharged to hospice, or were transferred to other hospitals. Predictors of unplanned readmission were evaluated using a multivariable logistic regression model, adjusting for patient demographics, comorbidities, laboratory variables, and preoperative acuity of disease variables.A total of 1,347 patients were included, of which 234 (17.4%) had an unplanned readmission. The median patient age was 60 y, 49.4% were male, and 71.4% were white. The most common diagnoses were hollow viscus perforation (28.1%) and small bowel obstruction (24.5%). Predictors of unplanned readmission included patient factors (eg, disseminated cancer [odds ratio: 2.22, confidence interval: 1.35-3.64, P = .002], weight loss10% in the past 6 months [odds ratio: 1.65, confidence interval: 1.07-2.54, P = .023], dyspnea at baseline [odds ratio: 1.62, confidence interval: 1.06-2.48, P = .026], wound complications [odds ratio: 2.23, confidence interval: 1.55-3.19, P.001], and discharge to nursing homes [odds ratio: 1.68, confidence interval: 1.02-2.80, P = .044]).Unplanned readmission after emergency laparotomies are common, especially for patients with wound complications or requiring nursing homes. These system factors are potential quality improvement targets to reduce readmissions.

Objective Adipose-derived stem cells (ASCs) are a potential adult mesenchymal stem cell source for restoring endothelial function in patients with critical limb ischemia. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor (VEGF) play a major role in angiogenesis and wound healing. This study evaluated the effects of FGF and VEGF on the proliferation, migration, and potential endothelial differentiation of human ASCs with regards to their use as endothelial cell substitutes. Methods ASCs were isolated from clinical lipoaspirates and cultured in M199 medium with fetal bovine serum (10%), FGF2 (10 ng/mL), VEGF (50 ng/mL), or combinations of FGF2 and VEGF. Cell proliferation rates, viability, and migration were measured by growth curves, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), and scratch assays. For cell attachment determinations, ASCs were seeded onto a scaffold of small intestinal submucosa for 5 days. Endothelial differentiation capabilities of ASCs were confirmed by expression of endothelial cell-specific markers using quantitative polymerase chain reaction, immunofluorescence staining, and cord formation on Matrigel (BD Biosciences, San Jose, Calif). PD173074, a selective inhibitor of FGF receptor, was used to confirm the importance of FGF signaling. Results ASCs treated with FGF or combinations of FGF and VEGF showed increased proliferation rates and consistent differentiation toward an endothelial cell lineage increase in platelet endothelial cell adhesion molecule (CD31), von Willebrand factor, endothelial nitric oxide synthase, and vascular endothelial cadherin message, and in protein and cord formation on Matrigel. FGF and VEGF stimulated ASC migration and increased the attachment and retention after seeding onto a matrix graft of small intestinal submucosa. Blockade of FGF signaling with PD173074 abrogated ASC endothelial cell differentiation potential. Conclusions These results indicate that FGF and VEGF are ASC promoters for proliferation, migration, attachment, and endothelial differentiation. FGF and VEGF have a costimulatory effect on ASC endotheliogenesis. These results further suggest that ASCs with enhanced FGF signaling may potentially be used for tissue engineering and cell-based therapies in patients with critical limb ischemia.

Cancer patients with chemotherapy-induced immunosuppression have poor surgical site wound healing. Prior literature supports the use of human adipose-derived stem cell (hASC) lipoinjection to improve wound healing. It has been established that multipotent hASCs facilitate neovascularization, accelerate epithelialization, and quicken wound closure in animal models. Although hASC wound therapy may benefit surgical cancer patients, the chemotherapeutic effects on hASCs are unknown. We hypothesized that paclitaxel, a chemotherapeutic agent, impairs hASC growth, multipotency, and induces apoptosis.hASCs were isolated and harvested from consented, chemotherapy and radiation naive patients. Growth curves, MTT (3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide), and EdU (5-ethynyl-2-deoxyguridine) assays measured cytotoxicity and proliferation. Oil Red O stain, Alizarin Red stain, matrigel tube formation assay, and quantitative polymerase chain reaction analyzed hASC differentiation. Annexin V assay measured apoptosis. Immunostaining and Western blot determined tumor necrosis factor α (TNF-α) expression.hASCs were selectively more sensitive to paclitaxel (0.01-30 μM) than fibroblasts (P0.05). After 12 d, paclitaxel caused hASC growth arrest, whereas control hASCs proliferated (P = 0.006). Paclitaxel caused an 80.6% reduction in new DNA synthesis (P0.001). Paclitaxel severely inhibited endothelial differentiation and capillary-like tube formation. Differentiation markers, lipoprotein lipase (adipogenic), alkaline phosphatase (osteogenic), CD31, and van Willebrand factor (endothelial), were significantly decreased (all P0.05) confirming paclitaxel impaired differentiation. Paclitaxel was also found to induce apoptosis and TNF-α was upregulated in paclitaxel-treated hASCs (P0.001).Paclitaxel is more cytotoxic to hASCs than fibroblasts. Paclitaxel inhibits hASC proliferation, differentiation, and induces apoptosis, possibly through the TNF-α pathway. Paclitaxel's severe inhibition of endothelial differentiation indicates neovascularization disruption, possibly causing poor wound healing in cancer patients receiving chemotherapy.