BACKGROUND This study aimed to analyze fluid management standards in 2 high-volume, enhanced recovery after surgery institutions 7 years after implementation. METHODS Retrospective analysis of consecutive patients undergoing elective, segmental colonic and extensive colorectal resections for benign and malignant pathology (2011-2017). Administration and composition of intravenous fluids, postoperative weight gain, and factors impeding compliance to preidentified fluid thresholds (3L fluid administration, 2.5 kg weight gain) were assessed. Multivariable logistic regression was performed to identify risk factors for postoperative adverse events. RESULTS A total of 5,155 patients were included. Among them, 2,320 patients (45.1%) received >3 L intravenous fluids at postoperative day 0. Fluid totals remained unchanged over the 7-year observation period. Fluid overload was independently associated with postoperative weight gain ≥2.5 kg at postoperative day 2 (odds ratio 1.34, P less then .001). Patients with high American Society of Anesthesiologists score (≥3) undergoing open and longer (≥180 minutes) procedures were more likely to exceed both thresholds according to multivariable analysis (all P less then .001). Other than open surgery, American Society of Anesthesiologists score ≥3, contamination class ≥3, and malignancy, both thresholds (≥3 L odds ratio 1.76, 95% confidence interval 1.44-2.15, ≥ 2.5 kg odds ratio 1.62, 95% confidence interval 1.33-1.97) were independent risk factors for postoperative adverse outcomes (occurring in 28.1% of patients). CONCLUSION Compliance with fluid thresholds appears to be challenging in patients with comorbidities undergoing open and long procedures. Efforts are encouraged because both thresholds are linked to adverse outcomes and appear to be potentially modifiable in selected patients. BACKGROUND Neuroblastoma is the most common pediatric extracranial solid malignancy with limited effective treatment. We have shown that sustained-release, single drugs delivered locally through a silk-based biomaterial are effective in decreasing orthotopic neuroblastoma xenograft growth. We further optimized this approach and hypothesized that increasing doses of local chemotherapy or delivering 2 chemotherapeutic agents simultaneously inhibit additional tumor growth. METHODS MYCN-amplified and non-MYCN-amplified neuroblastoma cells were treated with combinations of cisplatin, vincristine, doxorubicin, and etoposide to determine cytotoxicity and synergy. Drug-loaded silk material was created, and the amounts of drug released from the material over time were recorded. Murine orthotopic neuroblastoma xenografts were generated; tumors were implanted with single- or dual-agent chemotherapy-loaded silk. Ultrasound was used to monitor tumor growth, and tumor histology was evaluated. RESULTS In vitro, vincristine/cisplatin combination was synergistic and significantly decreased cell viability relative to other combinations. Both drugs loaded into silk could be released effectively for over 2 weeks. Locally implanted vincristine/cisplatin silk induced increased tumor growth suppression compared with either agent alone in MYCN-amplified tumors (P 50 μg to 500 μg for vincristine-cisplatin, respectively. Tumor histology demonstrated tumor cell necrosis adjacent to drug-loaded silk material and presence of large cell neuroblastoma. CONCLUSION Local delivery of sustained release chemotherapy can suppress tumor growth especially at high doses or with 2 synergistic drugs. Locally delivered dual therapy is a promising approach for future clinical testing. It has been documented that Helicobacter hepaticus (H. hepaticus) infection is linked to hepatic inflammation and fibrosis. Interleukin 33 (IL-33) is a cytokine involved in inflammatory and fibrotic diseases, but its relevance to H. hepaticus infection-induced liver inflammation and fibrosis is unknown. In this study, we found that the expression of IL-33 in mice liver was significantly induced by H. hepaticus infection at 24 weeks post infection (WPI). Immunohistochemistry analysis revealed that IL-33 was transferred from the nucleus to the cytoplasm due to infection. The quantitation of inflammatory cytokine and histopathology evaluation showed that IL-33 knockdown attenuated the H. hepaticus-induced hepatic inflammation and fibrosis. More importantly, H. hepaticus promoted the expression of the IL-33 receptor ST2 on cell surfaces, and the expression of ST2 then activated the expression nuclear factor-κB (p65), α-SMA, and Erk1/2. These observations provide novel insights into the pathogenic mechanism of hepatic inflammation and fibrosis during H. hepaticus infection. This study is aimed to examine the association between umbilical cord blood (UCB) derived exosomal microRNA (miRNA) with preeclampsia (PE) and to further explore the mechanism of a key differential gene (hsa-miR-125a-5p) in preeclampsia. Umbilical cord blood exosomal miRNA(exo-miRNA) from normal pregnant women and pregnant women with preeclampsia was processed via miRNA sequencing. Quantitative real-time polymerase chain reaction (QRT-PCR) was performed to assess the expression of miR-125a-5p in normal and PE placental tissues and peripheral blood derived exosomes in the third trimester.  https://www.selleckchem.com/btk.html  Human trophoblast cell line HTR8/SVneo was assigned as the negative control and miR-125a-5p mimics. QRT-PCR and Western blot were performed to identify the expressions of miR-125a-5p and vascular endothelial growth factor A (VEGFA). CCK8, flow cytometry, wound-healing and Transwell assays were used to analyze the effect of miR-125a-5p on HTR8/SVneo cell migration, proliferation, and cycle distribution. Tube formation was performed to estimate the angiogenesis ability of miR-125a-5p on HUVECs. In conclusion, miR-125a-5p expression in PE placental tissues was higher than in normal subjects, while the expression of VEGFA was lower in PE placental tissues. We then compared the miR-125a-5p mimics group with the negative control group and found that in the mimics group, the cell migration, proliferation and angiogenesis abilities were decreased, and more cells were arrested in the S stage. Our study systematically profiled the UCB exo-miRNA in normal and PE pregnant women and demonstrated that dysregulation of miR-125a-5p might affect HTR8/SVneo cell proliferation and migration and inhibit angiogenesis by regulating VEGFA, indicating that miR-125a-5p is involved in the progression of PE.