The expression of CD86 in CD3+CD56+ NKT cells is associated with the occurrence and prognosis of sepsis-associated encephalopathy in sepsis patients: a prospective observational cohort study.

The role of CD3+CD56+ natural killer T (NKT) cells and its co-signaling molecules in patients with sepsis-associated encephalopathy (SAE) is unknown. In this prospective observational cohort study, we initially recruited 260 septic patients and eventually analyzed 90 patients, of whom 57 were in the SAE group and 37 were in the non-SAE group. Compared to the non-SAE group, 28-day mortality was significantly increased in the SAE group (33.3% vs. 12.1%, p = 0.026), while the mean fluorescence intensity (MFI) of CD86 in CD3+CD56+ NKT cells was significantly lower (2065.8 (1625.5 ~ 3198.8) vs. 3117.8 (2278.1 ~ 5349), p = 0.007). Multivariate analysis showed that MFI of CD86 in NKT cells, APACHE II score, and serum albumin were independent risk factors for SAE. Furthermore, the Kaplan-Meier survival analysis indicated that the mortality rate was significantly higher in the high-risk group than in the low-risk group (χ2 = 14.779, p < 0.001). This study showed that the decreased expression of CD86 in CD3+CD56+ NKT cells is an independent risk factor of SAE; thus, a prediction model including MFI of CD86 in NKT cells, APACHE II score, and serum albumin can be constructed for diagnosing SAE and predicting prognosis.

Computational Study of Single Metal Atom Anchored on Black Phosphorus for Methane Oxidation to Methanol by Nitrous Oxide.

Direct conversion of methane to high-value-added transportable methanol is a great challenge, which requires high energy input to break the strong C-H bond. Developing efficient catalysts for methane oxidation to methanol under mild conditions is of vital importance. In this work, single transition metal atoms (TM=Fe, Co, Ni, Cu) anchored on black phosphorus (TM@BP) were studied as catalysts to assist the methane oxidation to methanol by means of first-principles calculations. The results indicate that Cu@BP exhibits an outstanding catalytic activity through the radical reaction pathways and the formation of the Cu-O active site is rate-determining with an energy barrier of 0.48 eV. Meanwhile, electronic structure calculations and dynamic simulations show that Cu@BP offers excellent thermal stability. Our calculations provide a new approach for the rational design of single atom catalysts for methane oxidation to methanol.

Exosome-Derived lncRNA NEAT1 Exacerbates Sepsis-Associated Encephalopathy by Promoting Ferroptosis Through Regulating miR-9-5p/TFRC and GOT1 Axis.

Sepsis can cause sepsis-associated encephalopathy (SAE), but whether SAE was induced or exacerbated by ferroptosis remains unknown. In this study, the rat sepsis model was constructed using the cecal ligation and puncture method. The blood-brain barrier (BBB) permeability was measured by Evans blue dye (EBD) in vivo. The levels of ROS, Fe ion, MDA, GSH, and GPX4 were assessed by enzyme-linked immunosorbent assay (ELISA). The exosomes isolated from serum were cultured with bEnd.3 cells for the in vitro analysis. Moreover, bEnd.3 cells cultured with 100 µM FeCl3 (iron-rich) were to simulate ferroptosis stress. The cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay. A dual-luciferase reporter gene assay was performed to confirm the relationship between miR-9-5p with NEAT1, TFRC, and GOT1. In vivo, it is found that BBB permeability was damaged in model rats. Level of ROS, Fe ion, and MDA was increased, and level of GSH and GPX4 was decreased, which means ferroptosis was induced by sepsis. Exosome-packaged NEAT1 in serum was significantly upregulated in model rats. In vitro, it is found that NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro. In conclusion, these findings suggest that sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate SAE by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis.

Comparison of clinical characteristics in patients with coronavirus disease and influenza A in Guangzhou, China.

BACKGROUND: This study aims to compare the epidemiological, clinical and laboratory characteristics between patients with coronavirus disease (COVID-19) and influenza A (H1N1), and to develop a differentiating model and a simple scoring system. METHODS: We retrospectively analyzed the data from patients with COVID-19 and H1N1. The logistic regression model based on clinical and laboratory characteristics was constructed to distinguish COVID-19 from H1N1. Scores were assigned to each of independent discrimination factors based on their odds ratios. The performance of the prediction model and scoring system was assessed. RESULTS: A total of 236 patients were recruited, including 20 COVID-19 patients and 216 H1N1 patients. Logistic regression revealed that age >34 years, temperature ≤37.5 °C, no sputum or myalgia, lymphocyte ratio ≥20% and creatine kinase-myocardial band isoenzyme (CK-MB) >9.7 U/L were independent differentiating factors for COVID-19. The area under curves (AUCs) of the prediction model and scoring system in differentiating COVID-19 from H1N1 were 0.988 and 0.962, respectively. CONCLUSIONS: There are certain differences in clinical and laboratory features between patients with COVID-19 and H1N1. The simple scoring system may be a useful tool for the early identification of COVID-19 patients from H1N1 patients.

Evaluation of vitamin D storage in patients with chronic kidney disease: Detection of serum vitamin D metabolites using high performance liquid chromatography-tandem mass spectrometry.

BACKGROUND: Vitamin D (VitD) deficiency is extremely common in chronic kidney disease (CKD). However, the current clinical testing of vitamin D is based on the recommended serum 25-hydroxyvitamin D [25(OH)D]. The levels of VitD components in CKD patients are rarely reported. In this study, we tested various VitD components, and used different methods to evaluate the VitD status of CKD patients in vivo. METHODS: Totally 173 CKD patients and 111 control individuals were enrolled. Serum levels of 25(OH)D2, 25(OH)D3, C3-epimers (C3-epi) and free 25(OH)D [f-25(OH)D] were measured. The 25(OH)D2/25(OH)D3 ratio, C3-epi/25(OH)D3 ratio, total 25(OH)D [t-25(OH)D], and bioavailable vitamin D (BAVD) were calculated, respectively. RESULTS: The ratios of 25(OH)D2/25(OH)D3, C3-epi/25(OH)D3, and the level of C3-epi in CKD patients were significantly higher than those in the control group (all P < 0.05). The levels of t-25(OH)D, 25(OH)D3, C3-epi, f-25(OH)D and BAVD in patients with CKD stage 5 were significantly lower than those in stages 2, 3, and 4 (all P < 0.05). The calculated VitD storage according to Method 3 [25(OH)D2/3 + 25(OH)D3] was only 32.95 %, which was lower than the results of 53.76 % by Method 1 [25(OH)D2+ 25(OH)D3+C3-epi] and 48.56 % by Method 2 [25(OH)D2/3 + 25(OH)D3+C3-epi]. In addition, the VitD results calculated by three methods were positively correlated with f-25(OH)D and BAVD, while C3-epi levels were also positively correlated with f-25(OH)D and BAVD. CONCLUSION: Serum levels of t-25(OH)D, 25(OH)D3, C3-epi, f-25(OH)D and BAVD in CKD patients gradually decrease with the progression of CKD stages. Though the results of VitD storage in CKD patients evaluated by different methods are different, simultaneous detection of 25(OH)D2, 25(OH)D3, C3-epi and f-25(OH)D levels and fully estimation of their respective biological activities could accurately evaluate the VitD storage in vivo.

JAK/STAT signaling pathway-mediated microRNA-181b promoted blood-brain barrier impairment by targeting sphingosine-1-phosphate receptor 1 in septic rats.

BACKGROUND: Blood-brain barrier (BBB) impairment plays a significant role in the pathogenesis of sepsis-associated encephalopathy (SAE). However, the molecular mechanisms are poorly understood. In the present study, we aimed to investigate the regulatory relationship between the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway, microRNA (miR)-181b and its target genes in sepsis in vivo and in vitro. METHODS: Four rat models (sham, sepsis, sepsis plus STAT3 inhibitor (Stattic), and sepsis plus miR-181b inhibitor [sepsis + anta-miR-181b]) were established. For the in vitro experiments, rat brain microvascular endothelial cells (rBMECs) and rat brain astrocytes (rAstrocytes) were cultured with 10% serum harvested from sham, sepsis, and sepsis + anta-miR-181b rats. Chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-QPCR) analysis was carried out to detect the binding and enrichment of the JAK/STAT3 signal core transcription complex in the miR-181b promoter region. Dual-luciferase reporter gene assay was conducted to test miR-181b and its target genes. The cell adhesion rate of rBMECs was also measured. RESULTS: During our investigations, the expression levels of miR-181b, p-JAK2, p-STAT3, and C/EBPß were found to be significantly increased in the septic rats compared with the sham rats. STAT3 inhibitor halted BBB damage by downregulating the expression of miR-181b. In addition, miR-181b targeted sphingosine-1-phosphate receptor 1 (S1PR1) and neurocalcin delta (NCALD). The up-regulated miR-181b significantly decreased the cell adhesion rate of rBMECs. The administration of miR-181b inhibitor reduced damage to the BBB through increasing the expression of S1PR1 and NCALD, which again proved that miR-181b negatively regulates SIPR1 and NCALD to induce BBB damage. CONCLUSIONS: Our study demonstrated that JAK2/STAT3 signaling pathway induced expression of miR-181b, which promoted BBB impairment in rats with sepsis by downregulating S1PR1 and decreasing BBB cell adhesion. These findings strongly suggest JAK2/STAT3/miR-181b axis as therapeutic target in protecting against sepsis-induced BBB damage.

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy in hypoxemic adult rats.

BACKGROUND: Hypoxemia is a typical symptom of acute respiratory distress syndrome. To avoid pulmonary morbidity, low tidal volume ventilation is often applied. The ventilation strategy will certainly cause hypercapnia. This study aimed to explore whether hypercapnia would promote microglial pyroptosis via inhibiting mitophagy in adult rats with hypoxemia. METHODS: The cerebral oxygen extraction ratio (CERO2 ) and partial pressure of brain tissue oxygen (PbtO2 ) in a rat model of hypercapnia/hypoxemia were assessed. The reactive oxygen species (ROS) production and the expression of LC3-II/I, p62, caspase-1, gasdermin D-N domains (GSDMD-N), IL-1ß, and IL-18 in microglial cells were detected. RESULTS: Hypercapnia decreased the PbtO2 levels of the hypoxic rats, which was further evidenced by the increased levels of CERO2 . Expression levels of LC3-II were reduced, while p62 expression was increased by hypercapnia in hypoxic microglia. Hypercapnia increased the production of ROS and the expression of caspase-1, GSDMD-N, IL-1ß, and IL-18 in hypoxia-activated microglia. Scavenging ROS inhibited microglial pyroptosis and expression of IL-1ß and IL-18. CONCLUSIONS: These results suggest that hypercapnia-induced mitophagy inhibition may promote pyroptosis and enhance IL-1ß and IL-18 release in hypoxia-activated microglia.

Hypertonic saline mediates the NLRP3/IL-1ß signaling axis in microglia to alleviate ischemic blood-brain barrier permeability by downregulating astrocyte-derived VEGF in rats.

INTRODUCTION: The aim of this study was to explore whether the antibrain edema of hypertonic saline (HS) is associated with alleviating ischemic blood-brain barrier (BBB) permeability by downregulating astrocyte-derived vascular endothelial growth factor (VEGF), which is mediated by microglia-derived NOD-like receptor protein 3 (NLRP3) inflammasome. METHODS: The infarct volume and BBB permeability were detected. The protein expression level of VEGF in astrocytes in a transient focal brain ischemia model of rats was evaluated after 10% HS treatment. Changes in the NLRP3 inflammasome, IL-1ß protein expression, and the interleukin-1 receptor (IL1R1)/pNF-кBp65/VEGF signaling pathway were determined in astrocytes. RESULTS: HS alleviated the BBB permeability, reduced the infarct volume, and downregulated the expression of VEGF in astrocytes. HS downregulates IL-1ß expression by inhibiting the activation of the NLRP3 inflammasome in microglia and then downregulates VEGF expression by inhibiting the phosphorylation of NF-кBp65 mediated by IL-1ß in astrocytes. CONCLUSIONS: HS alleviated the BBB permeability, reduced the infarct volume, and downregulated the expression of VEGF in astrocytes. HS downregulated IL-1ß expression via inhibiting the activation of the NLRP3 inflammasome in microglia and then downregulated VEGF expression through inhibiting the phosphorylation of NF-кBp65 mediated by IL-1ß in astrocytes.

Hypercapnia induces IL-1ß overproduction via activation of NLRP3 inflammasome: implication in cognitive impairment in hypoxemic adult rats.

BACKGROUND: Cognitive impairment is one of common complications of acute respiratory distress syndrome (ARDS). Increasing evidence suggests that interleukin-1 beta (IL-1ß) plays a role in inducing neuronal apoptosis in cognitive dysfunction. The lung protective ventilatory strategies, which serve to reduce pulmonary morbidity for ARDS patients, almost always lead to hypercapnia. Some studies have reported that hypercapnia contributes to the risk of cognitive impairment and IL-1ß secretion outside the central nervous system (CNS). However, the underlying mechanism of hypercapnia aggravating cognitive impairment under hypoxia has remained uncertain. This study was aimed to explore whether hypercapnia would partake in increasing IL-1ß secretion via activating the NLRP3 (NLR family, pyrin domain-containing 3) inflammasome in the hypoxic CNS and in aggravating cognitive impairment. METHODS: The Sprague-Dawley (SD) rats that underwent hypercapnia/hypoxemia were used for assessment of NLRP3, caspase-1, IL-1ß, Bcl-2, Bax, and caspase-3 expression by Western blotting or double immunofluorescence, and the model was also used for Morris water maze test. In addition, Z-YVAD-FMK, a caspase-1 inhibitor, was used to treat BV-2 microglia to determine whether activation of NLRP3 inflammasome was required for the enhancing effect of hypercapnia on expressing IL-1ß by Western blotting or double immunofluorescence. The interaction effects were analyzed by factorial ANOVA. Simple effects analyses were performed when an interaction was observed. RESULTS: There were interaction effects on cognitive impairment, apoptosis of hippocampal neurons, activation of NLRP3 inflammasome, and upregulation of IL-1ß between hypercapnia treatment and hypoxia treatment. Hypercapnia + hypoxia treatment caused more serious damage to the learning and memory of rats than those subjected to hypoxia treatment alone. Expression levels of Bcl-2 were reduced, while that of Bax and caspase-3 were increased by hypercapnia in hypoxic hippocampus. Hypercapnia markedly increased the expression of NLRP3, caspase-1, and IL-1ß in hypoxia-activated microglia both in vivo and in vitro. Pharmacological inhibition of NLRP3 inflammasome activation and release of IL-1ß might ameliorate apoptosis of neurons. CONCLUSIONS: The present results suggest that hypercapnia-induced IL-1ß overproduction via activating the NLRP3 inflammasome by hypoxia-activated microglia may augment neuroinflammation, increase neuronal cell death, and contribute to the pathogenesis of cognitive impairments.

Hypertonic saline attenuates expression of Notch signaling and proinflammatory mediators in activated microglia in experimentally induced cerebral ischemia and hypoxic BV-2 microglia.

BACKGROUND: Ischemic stroke is a major disease that threatens human health in ageing population. Increasing evidence has shown that neuroinflammatory mediators play crucial roles in the pathophysiology of cerebral ischemia injury. Notch signaling is recognized as the cell fate signaling but recent evidence indicates that it may be involved in the inflammatory response in activated microglia in cerebral ischemia. Previous report in our group demonstrated hypertonic saline (HS) could reduce the release of interleukin-1 beta and tumor necrosis factor-alpha in activated microglia, but the underlying molecular and cellular mechanisms have remained uncertain. This study was aimed to explore whether HS would partake in regulating production of proinflammatory mediators through Notch signaling. RESULTS: HS markedly attenuated the expression of Notch-1, NICD, RBP-JK and Hes-1 in activated microglia both in vivo and in vitro. Remarkably, HS also reduced the expression of iNOS in vivo, while the in vitro levels of inflammatory mediators Phos-NF-κB, iNOS and ROS were reduced by HS as well. CONCLUSION: Our results suggest that HS may suppress of inflammatory mediators following ischemia/hypoxic through the Notch signaling which operates synergistically with NF-κB pathway in activated microglia. Our study has provided the morphological and biochemical evidence that HS can attenuate inflammation reaction and can be neuroprotective in cerebral ischemia, thus supporting the use of hypertonic saline by clinicians in patients with an ischemia stroke.

Hypertonic saline protects brain endothelial cells against hypoxia correlated to the levels of epidermal growth factor receptor and interleukin-1ß.

OBJECTIVE: The aim of this study was to verify the protective effect of hypertonic saline (HS) on brain endothelial cells under hypoxic conditions and the relevant underlying mechanism. METHODS: bEnd.3 cells were treated with oxygen-glucose deprivation (OGD)-induced injury. To measure HS performance, cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt assay, and cell apoptosis was assessed by flow cytometry and Terminal deoxynucleotidyl transferase UTP nick-end labeling staining. RNA-seq was performed to assess the expression profiles and screen the candidate genes that participated in OGD-induced injury and the HS protective effect. Quantitative real-time polymerase chain reaction (qPCR) and western blot analysis were used to confirm the expression of candidate genes, and enzyme-linked immunosorbent assay was used to measure the level of interleukin (IL)-1ß. Overexpression analyses were performed to confirm the functions of the differentially expressed genes. RESULTS: HS with a concentration of 40 mmol/L NaCl had an obvious protective effect on bEnd.3 cells after OGD-induced injury, resulting in increased cell viability and a smaller percentage of apoptotic cells. According to the RNA-seq results, epidermal growth factor receptor (EGFR) was chosen as the differentially expressed gene target in this study. The qPCR and western blot analyses further confirmed that the levels of EGFR/phosphorylated epidermal growth factor receptor and IL-1ß were enhanced after OGD-induced injury, but attenuated after treatment with 40 mmol/L of NaCl HS. Overexpressed EGFR reversed the protective effect of HS that caused low viability and high rates of apoptosis in cells. CONCLUSION: HS can protect endothelial cells against OGD-induced injury, but is affected by the expression of EGFR/p-EGFR and IL-1ß.

Influence of pH, inorganic anions, and dissolved organic matter on the photolysis of antimicrobial triclocarban in aqueous systems under simulated sunlight irradiation.

The photolysis of the antimicrobial triclocarban (TCC) in aqueous systems under simulated sunlight irradiation was studied. The effects of several abiotic parameters, including solution pH, initial TCC concentration, presence of natural organic matter, and most common inorganic anions in surface waters, were investigated. The results show that the photolysis of TCC followed pseudo-first-order kinetics. The TCC photolysis rate constant increased with increasing solution pH and decreasing the initial TCC concentration. Compared with the TCC photolysis in pure water, the presence of aqueous bicarbonate, nitrate, humic acids, and its sodium salt decreased the TCC photolysis rate, but fulvic acid increased the TCC photolysis rate. The electron spin resonance and reactive oxygen species scavenging experiments indicated that TCC may undergo two different types of phototransformation reactions: direct photolysis and energy transfer to generate (1)O2. The main degradation products were tentatively identified by gas chromatography interfaced with mass spectrometry (GC-MS), and a possible degradation pathway was also proposed.

Hypertonic saline alleviates cerebral edema by inhibiting microglia-derived TNF-α and IL-1ß-induced Na-K-Cl Cotransporter up-regulation.

BACKGROUND: Hypertonic saline (HS) has been successfully used clinically for treatment of various forms of cerebral edema. Up-regulated expression of Na-K-Cl Cotransporter 1 (NKCC1) and inflammatory mediators such as tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß) has been demonstrated to be closely associated with the pathogenesis of cerebral edema resulting from a variety of brain injuries. This study aimed to explore if alleviation of cerebral edema by 10% HS might be effected through down-regulation of inflammatory mediator expression in the microglia, and thus result in decreased NKCC1 expression in astrocytes in the cerebral cortex bordering the ischemic core. METHODS: The Sprague-Dawley (SD) rats that underwent right-sided middle cerebral artery occlusion (MCAO) were used for assessment of NKCC1, TNF-α and IL-1ß expression using Western blotting, double immunofluorescence and real time RT-PCR, and the model also was used for evaluation of brain water content (BWC) and infarct size. SB203580 and SP600125, specific inhibitors of the p38 and JNK signaling pathways, were used to treat primary microglia cultures to determine whether the two signaling pathways were required for the inhibition of HS on microglia expressing and secreting TNF-α and IL-1ß using Western blotting, double immunofluorescence and enzyme-linked immunosorbent assay (ELISA). The effect of TNF-α and IL-1ß on NKCC1 expression in primary astrocyte cultures was determined. In addition, the direct inhibitory effect of HS on NKCC1 expression in primary astrocytes was also investigated by Western blotting, double immunofluorescence and real time RT-PCR. RESULTS: BWC and infarct size decreased significantly after 10% HS treatment. TNF-α and IL-1ß immunoexpression in microglia was noticeably decreased. Concomitantly, NKCC1 expression in astrocytes was down-regulated. TNF-α and IL-1ß released from the primary microglia subjected to hypoxic exposure and treatment with 100 mM HS were decreased. NKCC1 expression in primary astrocytes was concurrently and progressively down-regulated with decreasing concentration of exogenous TNF-α and IL-1ß. Additionally, 100 mM HS directly inhibited NKCC1 up-regulation in astrocytes under hypoxic condition. CONCLUSIONS: The results suggest that 10% HS alleviates cerebral edema through inhibition of the NKCC1 Cotransporter, which is mediated by attenuation of TNF-α and IL-1ß stimulation on NKCC1.

[Procalcitonin change pattern in patients with septic shock and its relationship with prognosis].

OBJECTIVE: To investigate procalcitonin (PCT) change pattern in patients with septic shock and its relationship with prognosis. METHODS: Sixty-three septic shock patients were enrolled, and levels of PCT, C-reactive protein (CRP) as well as white blood cell (WBC) on 1st, 3rd, 5th,7th day after admission to intensive care unit (ICU) were checked. Patients were divided into survival group and death group according to 28-day survival result. Differences in parameters between two groups were compared. The change regulation of parameters along with in-hospital period and its relationship with prognosis were analyzed by multilevel linear model. RESULTS: There were 41 patients in survival group and 22 patients in death group. PCT and CRP level decreased in survival group with time dependency pattern, while death group increased. The PCT at 3, 5, 7 days after admission to ICU in death group were significantly higher than those in survivors (3 days: 8.7±3.7 µg/L vs. 5.6±1.7 µg/L, 5 days: 10.3±1.3 µg/L vs. 4.8±2.3 µg/L, 7 days: 12.7±2.3 µg/L vs. 0.8±0.3 µg/L, P<0.05 or P<0.01), and CRP at 5 days and 7 days was significantly higher than those in survival group (5 days: 447±63 mg/L vs. 355±91 mg/L, 7 days: 439±45 mg/L vs. 364±63 mg/L, both P<0.05). Two groups of WBC did not change significantly, and there were no statistical significance difference at each time point between the two groups. What's more, the effect analysis results showed that there were significant changes in PCT as ICU day prolonged (F=10.91, P= 0.00), and there was a significant difference between the survivor and the dead (F=7.58, P=0.00), while CRP changed only with ICU stays (F=4.17, P=0.03). CONCLUSIONS: Compared with CRP and WBC, PCT had higher sensitivity in predicting prognosis, sustainable elevation of PCT level indicates poor prognosis, serum PCT can be used as one of indexes predicting prognosis of septic shock.

Photodegradation of the antimicrobial triclocarban in aqueous systems under ultraviolet radiation.

This work aimed to investigate the effectiveness of ultraviolet (UV) radiation on the degradation of the antimicrobial triclocarban (TCC). We investigated the effects of several operational parameters, including solution pH, initial TCC concentration, photocatalyst TiO2 loading, presence of natural organic matter, and most common anions in surface waters (e.g., bicarbonate, nitrate, and sulfate). The results showed that UV radiation was very effective for TCC photodegradation and that the photolysis followed pseudo-first-order kinetics. The TCC photolysis rate was pH dependent and favored at high pH. A higher TCC photolysis rate was observed by direct photolysis than TiO2 photocatalysis. The presence of the inorganic ions bicarbonate, nitrate, and sulfate hindered TCC photolysis. Negative effects on TCC photolysis were also observed by the addition of humic acid due to competitive UV absorbance. The main degradation products of TCC were tentatively identified by gas chromatograph with mass spectrometer, and a possible degradation pathway of TCC was also proposed.

Determination of trace triclosan in environmental water by microporous bamboo-activated charcoal solid-phase extraction combined with HPLC-ESI-MS.

A sensitive and efficient analytical method for triclosan (TCS) determination in water, which involves enrichment with bamboo-activated charcoal and detection with HPLC-ESI-MS, was developed. The influence of several operational parameters, including the eluant and its volume, the flow rate, the volume andacidity of the sample, and the amount of bamboo-activated charcoal, were investigated and optimized. Under the optimum conditions, linearity of the method was observed in the range of 0.02-20 µg/L, with correlation coefficients (r(2) ) >0.9990. The limit of detection was 0.002 µg/L based on the ratio of chromatographic signal to baseline noise (S/N = 3). The spiked recoveries of TCS in real water samples were achieved in the range of 97.6-112.5%. The proposed method was applied to analyze TCS in real aqueous samples. All the surface water samples collected in Xiaoqing River had detectable levels of TCS with concentrations of 42-197 ng/L.

[Significance of serum procalcitonin levels in the evaluation of severity and prognosis of patients with systemic inflammatory response syndrome].

OBJECTIVE: To observe the dynamic changes in serum procalcitonin (PCT), C-reactive protein (CRP), and white blood cell (WBC) count in systemic inflammatory response syndrome (SIRS) and their implication in assessment of illness severity and prognosis. METHODS: A prospective case control study was conducted. Seventy-two patients with SIRS in Guangdong General Hospital were enrolled in intensive care unit (ICU) from May, 2010 to June, 2011. Parameters including PCT, CRP, and WBC count were determined on the 1st, 3rd, and 5th day after admission. The patients were divided into septic group (n=49) and non-septic group (non-infectious SIRS group, n=23) according to the presence or absence of infectious. Dynamic changes in all parameters were compared between the two groups and correlation analysis was carried out on the basis of differential indexes and sequential organ failure assessment (SOFA). The clinical outcome within 28 days after admission to ICU was observed, and the patients were divided into death group (n=19) and survival group (n=53). Dynamic changes in all parameters between the two groups were compared. Relevant parameters were analyzed with area under receiver operator characteristic curve (ROC curve, AUC) to predict 28-day survival. Logistic regression analysis of the multiple factors was used to screen independent risk factors for predicting death. RESULTS: PCT level (µg/L) on 1st, 3rd, 5th day after admission were all significantly higher in septic group than those in non-septic group (1st day: 2.5±0.3 vs. 0.9±0.2, 3rd day: 1.9±0.3 vs. 0.6±0.2, 5th day: 0.9±0.1 vs. 0.5±0.1, all P<0.05), while there was no statistically significant difference in CRP and WBC between two groups. PCT level in septic group was gradually decreased with time, there were statistically significant differences between septic group and non-septic group at the different treatment time (all P<0.05), but there was no correlation between PCT and treatment duration in non-septic group. Positive statistical correlation was found between PCT and SOFA score (r=0.979, P<0.05). PCT (µg/L) and CRP levels (mg/L) on 1st, 3rd, 5th day were significantly higher in death group than those of survival group (PCT on 1st day: 2.0±0.8 vs. 0.8±0.3, 3rd day: 2.2±0.7 vs. 0.6±0.3, 5th day: 2.4±1.0 vs. 0.4±0.1; CRP on 1st day: 422±45 vs. 411±44, 3rd day: 418±39 vs. 403±52, 5th day: 392±38 vs. 382±46, all P<0.05), but WBC count showed no statistically significant difference between two groups. PCT level in survival group showed a significant lowering along with treatment duration, and statistical difference was seen by paired comparison between every two time-points (all P<0.05). There was no correlation between PCT level and treatment duration in death group, and it maintained a rather high level. No significant difference was seen in CRP and WBC between two groups with passage of time. AUC was 0.824 and 0.720, respectively, when patient's 28-day survival was predicted by PCT and CRP (both P<0.01). Logistic regression analysis of the multiple factors revealed that PCT>2.23 µg/L was independent risk factor predicting the prognosis [odds ratio (OR) was 1.773, 95% confidence interval (95%CI) 1.033 to 3.214, P=0.015]. CONCLUSIONS: Serum PCT evaluation may be helpful in differentiating sepsis and non-sepsis at early stage of disease, and also in predicting the severity of the illness and prognosis of SIRS. PCT may be one of the independent risk factors for 28-day survival.

[Effect of hydroxyethyl starch on intracranial pressure and plasma colloid osmotic pressure in rats with cerebral ischemia/reperfusion injury].

OBJECTIVE: To investigate the regulatory effect of hydroxyethyl starch on colloidal osmotic pressure (COP), and its effect on intracranial pressure (ICP) in rats with cerebral ischemia/reperfusion (I/R) injury. METHODS: Twenty four male Sprague Dawley (SD) rats were randomly divided into sham operation group, model group and the hydroxyethyl starch group, each n =8. Cerebral I/R model was reproduced by middle cerebral artery occlusion (MCAO), followed by reperfusion after ischemia for 2 hours. Rats in hydroxyethyl starch group received hydroxyethyl starch 130/0.4206 ml × kg(-1)× d(-1) ia tail vein at the beginning of reperfusion. ICP and COP were evaluated at 0, 2, 6, 12, 18, 24 hours after the surgery. The rats were sacrificed by decapitation. The water content of the right hemisphere was measured at 24 hours after the surgery, and the ratio of apoptosis of neurons was observed by immunohistochemical method. RESULTS: Two hours after surgery the ICP (mm Hg, 1 mm Hg=0.133 kPa) of model group and hydroxyethyl starch group was significantly increased compared with sham operation group (11.50 ± 1.43, 12.48 ± 0.75 vs. 7.95 ± 0.92, both P <0.05). With prolongation of time, the ICP gradually increased and reached the peak at 24 hours (22.76 ± 0.72, 23.32 ± 0.98 vs. 8.15 ± 1.09, both P <0.05). But there was no significant difference in ICP in the hydroxyethyl starch group compared with that of the model group at all time points. The COP (mm Hg) of hydroxyethyl starch group was significantly higher than the model group and sham operation group at each time point, and peaked at 6 hours after surgery (13.49 ± 0.50 vs. 12.04 ± 0.47, 12.00 ± 0.39, both P <0.01). There was no significant difference in COP between the model group and the sham operation group at all time points. The brain water content, neuronal apoptosis of hydroxyethyl starch group and model group was significantly higher than sham operation group [brain water content: (80.16 ± 0.44)%, (80.59 ± 0.67)% vs. (78.72 ± 0.52)%; neuronal apoptosis:(44.27 ± 7.86)%,(42.82 ± 7.82)%vs. (3.26 ± 0.00)%, P <0.05 or P <0.01], but there was no significant difference between the hydroxyethyl starch group and model group (both P >0.05). CONCLUSION: Intravenous injection of hydroxyethyl starch 130/0.4 can increase the plasma COP, but it can not significantly reduce ICP and brain water content, and it also can not improve the neuronal apoptosis.

A comparative study on the efficacy of 10% hypertonic saline and equal volume of 20% mannitol in the treatment of experimentally induced cerebral edema in adult rats.

BACKGROUND: Hypertonic saline and mannitol are commonly used in the treatment of cerebral edema and elevated intracranial pressure (ICP) at present. In this connection, 10% hypertonic saline (HS) alleviates cerebral edema more effectively than the equal volume of 20% mannitol. However, the exact underlying mechanism for this remains obscure. This study aimed to explore the possible mechanism whereby 10% hypertonic saline can ameliorate cerebral edema more effectively than mannitol. RESULTS: Adult male Sprague-Dawley (SD) rats were subjected to permanent right-sided middle cerebral artery occlusion (MCAO) and treated with a continuous intravenous infusion of 10% HS, 20% mannitol or D-[1-3H(N)]-mannitol. Brain water content (BWC) as analyzed by wet-to-dry ratios in the ischemic hemisphere of SD rats decreased more significantly after 10% HS treatment compared with 20% mannitol. Concentration of serum Na+ and plasma crystal osmotic pressure of the 10% HS group at 2, 6, 12 and 18 h following permanent MCAO increased significantly when compared with 20% mannitol treated group. Moreover, there was negative correlation between the BWC of the ipsilateral ischemic hemisphere and concentration of serum Na+, plasma crystal osmotic pressure and difference value of concentration of serum Na+ and concentration of brain Na+ in ipsilateral ischemic hemisphere in the 10% HS group at the various time points after MCAO. A remarkable finding was the progressive accumulation of mannitol in the ischemic brain tissue. CONCLUSIONS: We conclude that 10% HS is more effective in alleviating cerebral edema than the equal volume of 20% mannitol. This is because 10% HS contributes to establish a higher osmotic gradient across BBB and, furthermore, the progressive accumulation of mannitol in the ischemic brain tissue counteracts its therapeutic efficacy on cerebral edema.