Attributable mortality of acute kidney injury among critically ill patients with sepsis: a multicenter, retrospective cohort study.

BACKGROUND: Sepsis and acute kidney injury (AKI) are common severe diseases in the intensive care unit (ICU). This study aimed to estimate the attributable mortality of AKI among critically ill patients with sepsis and to assess whether AKI was an independent risk factor for 30-day mortality. METHODS: The information we used was derived from a multicenter prospective cohort study conducted in 18 Chinese ICUs, focusing on septic patients post ICU admission. The patients were categorized into two groups: those who developed AKI (AKI group) within seven days following a sepsis diagnosis and those who did not develop AKI (non-AKI group). Using propensity score matching (PSM), patients were matched 1:1 as AKI and non-AKI groups. We then calculated the mortality rate attributable to AKI in septic patients. Furthermore, a survival analysis was conducted comparing the matched AKI and non-AKI septic patients. The primary outcome of interest was the 30-day mortality rate following the diagnosis of sepsis. RESULTS: Out of the 2175 eligible septic patients, 61.7% developed AKI. After the application of PSM, a total of 784 septic patients who developed AKI were matched in a 1:1 ratio with 784 septic patients who did not develop AKI. The overall 30-day attributable mortality of AKI was 6.6% (95% CI 2.3 ∼ 10.9%, p = 0.002). A subgroup analysis revealed that the 30-day attributable mortality rates for stage 1, stage 2, and stage 3 AKI were 0.6% (95% CI -5.9 ∼ 7.2%, p = 0.846), 4.7% (95% CI -3.1 ∼ 12.4%, p = 0.221) and 16.8% (95% CI 8.1 ∼ 25.2%, p < 0.001), respectively. Particularly noteworthy was that stage 3 AKI emerged as an independent risk factor for 30-day mortality, possessing an adjusted hazard ratio of 1.80 (95% CI 1.31 ∼ 2.47, p < 0.001). CONCLUSIONS: The overall 30-day attributable mortality of AKI among critically ill patients with sepsis was 6.6%. Stage 3 AKI had the most significant contribution to 30-day mortality, while stage 1 and stage 2 AKI did not increase excess mortality.

E/D-Mode GaN Inverter on a 150-mm Si Wafer Based on p-GaN Gate E-Mode HEMT Technology.

AlGaN/GaN E/D-mode GaN inverters are successfully fabricated on a 150-mm Si wafer. P-GaN gate technology is applied to be compatible with the commercial E-mode GaN power device technology platform and a systematic study of E/D-mode GaN inverters has been conducted with detail. The key electrical characters have been analyzed from room temperature (RT) to 200 °C. Small variations of the inverters are observed at different temperatures. The logic swing voltage of 2.91 V and 2.89 V are observed at RT and 200 °C at a supply voltage of 3 V. Correspondingly, low/high input noise margins of 0.78 V/1.67 V and 0.68 V/1.72 V are observed at RT and 200 °C. The inverters also demonstrate small rising edge time of the output signal. The results show great potential for GaN smart power integrated circuit (IC) application.

Circ_LAS1L regulates cardiac fibroblast activation, growth, and migration through miR-125b/SFRP5 pathway.

Current studies have shown that circular RNAs (circRNAs) and microRNAs (miRNAs) are closely related in acute myocardial infarction (AMI). Previous studies have shown that miR-125b promotes fibrosis and up-regulates in cardiac fibroblasts (CFs), and further experiments showed that circ_LAS1L had multiple binding sites of miR-125b, and their expression was inversely related in AMI patients and CFs. RNA immunoprecipitation (RIP), pull down, and dual luciferase reporter gene assay all confirmed that miR-125b directly bound to circ_LAS1L. Circ_LAS1L overexpression promoted the expression of downstream target gene secreted frizzled-related protein 5 (SFRP5), inhibited the expression of alpha-SMA, collagen I, and collagen III, inhibited CF proliferation and migration, and promoted apoptosis. When cotransfected with circ_LAS1L overexpression vector and miR-125b mimics, the above gene expression and CF biological behaviours did not change significantly. But when cotransfected with circ_LAS1L overexpression vector and SFRP5 siRNA, SFRP5 expression was still down-regulated, the expression of alpha-SMA, collagen I, and collagen III was up-regulated, and the proliferation and migration of CFs were increased. Therefore, circ_LAS1L inhibits the activity of miR-125b by adsorbing it, thus promoting the expression of SFRP5 and then regulating the biological characteristics of CFs. These findings may provide an important experimental basis for the regulation of myocardial fibrosis after myocardial infarction. SIGNIFICANCE OF THE STUDY: Studies have shown that circular RNAs (circRNAs) play important roles in cardiovascular diseases, but there are few studies on their roles in the process of myocardial fibrosis. In this study, we found that circ_LAS1L was down-regulated in acute myocardial infarction (AMI) patients and cardiac fibroblasts (CFs), and could bind directly to miR-125b, thereby promoting the expression of downstream target gene secreted frizzled-related protein 5 (SFRP5), ultimately inhibiting the activation, proliferation and migration of CF, and promoting apoptosis. This suggests that circ_LAS1L/miR-125b/SFRP5 pathway can regulate the biological function of CF and may play an important role in the process of myocardial fibrosis, thus providing an important theoretical basis for the regulation of myocardial fibrosis after myocardial infarction.

Bio-based barium alginate film: Preparation, flame retardancy and thermal degradation behavior.

A bio-based barium alginate film was prepared via a facile ionic exchange and casting approach. Its flammability, thermal degradation and pyrolysis behaviors, thermal degradation mechanism were studied systemically by limiting oxygen index (LOI), vertical burning (UL-94), microscale combustion calorimetry (MCC), thermogravimetric analysis (TGA) coupled with Fourier transform infrared analysis (FTIR) and pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS). It showed that barium alginate film had much higher LOI value (52.0%) than that of sodium alginate film (24.5%). Moreover, barium alginate film passed the UL-94 V-0 rating, while the sodium alginate film showed no classification. Importantly, peak of heat release rate (PHRR) of barium alginate film in MCC test was much lower than that of sodium alginate film, suggested that introduction of barium ion into alginate film significantly decreased release of combustible gases. TG-FTIR and Py-GC-MS results indicated that barium alginate produced much less flammable products than that of sodium alginate in whole thermal degradation procedure. Finally, a possible degradation mechanism of barium alginate had been proposed.

Additive anticancer effects of chrysin and low dose cisplatin in human malignant glioma cell (U87) proliferation and evaluation of the mechanistic pathway.

PURPOSE: To evaluate the anticancer effect of chrysin and its additive combination with low-dose cisplatin in human glioma (U87) cancer cells and to study its underlying mechanism. METHODS: Inverted phase and fluorescence microscopic studies were done to demonstrate the effect of chrysin and its combination with cisplatin on cellular morphology and apoptosis. Annexin V-FITC assay was used to quantify the extent of apoptosis in chrysin and chrysin+cisplatin treated cells. Flow cytometry using propidium iodide (PI) as a staining agent was used to study the effect of chrysin and its combination with cisplatin on cell cycle phase distribution. RESULTS: The results showed chrysin brought about a potent and dose-dependent antiproliferative effect in human glioma cancer cells. However, the combination of chrysin with low dose cisplatin led to a much higher growth inhibitory effects indicating an additive effect between the two compounds. The combined effect of chrysin and cisplatin also gave rise to a greater apoptosis induction as well as cell cycle arrest in comparison to the treatment by chrysin or cisplatin alone. Fluorescence microscopy as well as inverted phase contrast microscopy also revealed that the combination of chrysin plus cisplatin resulted in greater apoptosis induction as well as cell morphology alterations. Combination treatment of chrysin and cisplatin resulted in greater percentage of cells in early as well as in late apoptotic stages. The combination effect was also seen in mitochondrial membrane potential loss. CONCLUSION: Chrysin additively potentiates the antiproliferative, cell cycle arrest and apoptotic activity of cisplatin in human glioma cancer (U87) cells.

[Construction of an acellular porcine aortic valve].

OBJECTIVE: To prepare a porcine aortic valve (PAV) free of the cellular components. METHODS: The cellular components of porcine PAV were completely removed using trypsin and Triton X-100, and the acellular PAV was examined microscopically with HE staining with its physical and chemical properties assessed. Transmission electron microscopy was used to observe the integrity of the collagen and elastin and the DNA contents in the PAV was detected to confirm the total removal of the cellular components. With the fresh PAV as the control, small pieces of the acellular PAV were implanted into the subcutaneous tissues of 4 rabbits, and 4 weeks after the implantation, the implants were harvested for microscopic observation. RESULTS: The cellular components were effectively removed from the cusps and roots of the PAV by trypsin and TritonX-100, with marked soluble protein loss [(0.24-/+0.04)% vs (0.48-/+0.12)%] and significantly increased water content [(92.2-/+1.5)% vs (89.2-/+1.6)%]. The acellular PAV still maintained good fibrous scaffold structure and the shrinkage temperature and tension at fracture underwent no significantly changes [(67.9-/+1.0) degrees celsius; vs (68.8-/+0.8) degrees celsius; and (489.3-/+19.0) g/mm2 vs (540.7-/+19.5) g/mm2, respectively]. The PAVs implanted in rabbits showed only mild tissue reaction with a few infiltrating neutrophils, lymphocytes and plasmocytes observed 4 weeks later. The accelular PAV caused obviously milder inflammatory reactions than fresh PAV. CONCLUSIONS: The acellular PAV prepared by treatment with trypsin and Triton X-100 retains good fibrous scaffold structure and mechanical strength with low antigenicity.