ABSTRACT
BACKGROUND: Although the circuit condensate, an ideal bacterial reservoir during mechanical ventilation, may flow into the humidifier reservoir, no studies have investigated if humidifier reservoir colonized bacteria colonize other circuit locations with airflow. AIMS: We aimed to prove whether the humidifier reservoir colonized bacteria colonize other circuit locations with airflow and provide some advice on the disposal of condensate in the clinical setting. STUDY DESIGN: An in vitro experiment was conducted. Mechanical ventilation simulators (n = 90) were divided into sterile water group (n = 30) and broth group (n = 60). In the sterile water group, sterile water was used for humidification, either Acinetobacter baumannii or Pseudomonas aeruginosa were inoculated to humidifier water in the humidifier reservoir, each accounted for 50% of the simulators. The broth group was performed the same as the sterile water group except for the addition of broth into the humidified water. After 24, 72, and 168 h of continuous ventilation, the humidifier water and different locations of the circuits were sampled for bacterial culture. RESULTS: All bacterial culture results of the sterile water group were negative. Bacteria in the humidifier water continued to proliferate in the broth group. With prolonged ventilation, the bacteria at the humidifier reservoir outlet increased. The bacteria at the humidifier reservoir outlet were much more in the Pseudomonas aeruginosa subgroup than in the Acinetobacter baumannii subgroup and the difference was statistically significant (p < .05). During continuous ventilation, no bacterial growth occurred at 10 cm from the humidifier reservoir outlet and the Y-piece of the ventilator circuits. CONCLUSIONS: Sterile water in the humidifier reservoir was not conducive to bacterial growth. Even if bacteria grew in the humidifier reservoir and could reach the humidifier reservoir outlet, colonization of further circuit locations with the airflow was unlikely. During a certain mechanical ventilation time, the amount of bacteria reaching the outlet of the humidifier reservoir varied due to different mobility of bacteria. RELEVANCE TO CLINICAL PRACTICE: In a clinical setting, nurses should not worry about a small amount of condensate backflow into the humidifier reservoir. Draining condensate into the humidifier reservoir can be used as a low risk and convenient method in clinical practice.
ABSTRACT
Acute myeloid leukemia (AML) is a severe hematologic malignancy that threatens human health. Long non-coding RNA (lncRNA) is emerged as a key player in human cancer. Herein, we explored the role of LINC00998 in human AML. LINC00998 was significantly decreased in human AML, which was linked to relapse and poor prognosis. Stable overexpression of LINC00998 inhibited AML cell viability, colony ability, DNA synthesis rate and increased apoptosis. LINC00998 was mainly located in the cytoplasm, in which interacted with ZFP36 ring finger protein (ZFP36), a mRNA destabilizing factor, resulting in increased decay of mammalian target of rapamycin complex 2 (mTORC2), a well-known proto-oncogene in AML. Overexpression of mTORC2 partly blocked the tumor suppressive effects of LINC00998. Importantly, LINC00998 shortened in vivo AML cell survival in xenograft tumor model. Taken together, we found that LINC00998 is a novel tumor-inhibiting lncRNA in human AML. The dysregulation of LINC00998/ZFP36/mTORC2 axis is linked to leukemogenesis and progression.
Subject(s)
Genes, Tumor Suppressor , Leukemia, Myeloid, Acute/genetics , Mechanistic Target of Rapamycin Complex 2/genetics , RNA, Long Noncoding/metabolism , Tristetraprolin/genetics , Animals , Apoptosis/genetics , Cell Line, Tumor , Cell Survival/genetics , Child , Down-Regulation/genetics , Female , Gene Expression Regulation, Leukemic , Humans , Male , Mechanistic Target of Rapamycin Complex 2/metabolism , Mice, Nude , Protein Binding/genetics , RNA Stability/genetics , RNA, Long Noncoding/genetics , Tristetraprolin/metabolismABSTRACT
UNLABELLED: The aim of this study was to evaluate the effectiveness and the safety of allopurinol in the prophylaxis of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. METHODS: : We used the method recommended by the Cochrane Collaboration to perform a meta-analysis of randomized controlled trials (RCTs) of allopurinol in the prevention of post-ERCP pancreatitis (PEP), including 6 RCTs conducted all over the world. RESULTS: : Six RCTs totaling 1554 patients undergoing ERCP were included. When the RCTs were analyzed, odds ratios of allopurinol were 0.74 (95% confidence interval [CI], 0.37-1.48; P = 0.40) for PEP, 0.87 (95% CI, 0.33-2.28; P = 0.78) for severe PEP, 0.88 (95% CI, 0.37-2.11; P = 0.78) for post-ERCP hyperamylasemia, and 0.19 (95% CI, 0.01-3.91; P = 0.28) for case-fatality ratio of PEP, thus indicating no beneficial effects of allopurinol on acute pancreatitis, PEP death rate, and hyperamylasemia. No evidence of publication bias was found. CONCLUSIONS: : Allopurinol cannot prevent the pancreatic injury after ERCP. Allopurinol is not recommended in the prophylaxis of PEP.
