Study on the Mechanism of Rapid Oil-Water Separation by a Fe3 O4 @PMMA@PDMS Intelligent Superhydrophobic Micro/Nanorobot.

We prepared an environmentally friendly intelligent Fe3 O4 @PMMA@PDMS superhydrophobic oil-absorbing material with simple process and excellent performance, and investigated the effects of different particle sizes of Fe3 O4 , different concentrations of PDMS, and different heating times on the superhydrophobicity of the coating. The best performance of the coating was achieved at a particle size combination of 20/500 nm for Fe3 O4 , a PDMS to Fe3 O4 @PMMA mass ratio of 6 : 1, and a heating time of 2 min at 400 °C. H2-SPSS coating not only has excellent superhydrophobicity, abrasion resistance, self-cleaning property, and chemical corrosion, but also has good flux and efficiency for separating oil-water mixture, with fluxes of 40,540, 32,432, and 37,027 Lm-2 h-1 for trichloromethane, dichloromethane and bromoethane, respectively, and separation efficiencies of 99.78 %, 99.74 % and 99.73 %, respectively. In addition, we also prepared a superhydrophobic magnetic polyurethane (SPPU) sponge using Fe3 O4 @PMMA@PDMS, which not only has a good oil absorption capacity of 18-44 g/g for different oil substances, it can also move directionally by magnet attraction and absorb oil along a fixed path. Under the control of the magnet, SPPU completes the whole oil absorption process in only 4 s, showing excellent oil absorption and intelligence.

Advances in the Research of Photo, Electrical, and Magnetic Responsive Smart Superhydrophobic Materials: Synthesis and Potential Applications.

With the rapid advancement of technology, the wettability of conventional superhydrophobic materials no longer suffice to meet the demands of practical applications. Intelligent responsive superhydrophobic materials have emerged as a highly sought-after material in various fields. The exceptional superhydrophobicity, reversible wetting, and intelligently controllable characteristics of these materials have led to extensive applications across industries, including industry, agriculture, defense, and medicine. Therefore, the development of intelligent superhydrophobic materials with superior performance, economic practicality, enhanced sensitivity, and controllability assumes utmost importance in advancing technology worldwide. This article provides a summary of the wettability principles of superhydrophobic surfaces and the mechanisms behind intelligent responsive superhydrophobicity. Furthermore, it reviews and analyzes the recent research progress on light, electric, and magnetic responsive superhydrophobic materials, encompassing aspects such as material synthesis, modification, performance, and responses under diverse external stimuli. The article also explores the challenges associated with different types of responsive superhydrophobic materials and the unique application prospects of light, electric, and magnetic responsive superhydrophobic materials. Additionally, it outlines the future directions for the development of intelligent responsive superhydrophobic materials.

Study on the mechanism of rapid degradation of Rhodamine B with Fe/Cu@antimony tailing nano catalytic particle electrode in a three dimensional electrochemical reactor.

A novel particle electrode based on antimony tailings microspheres was successfully constructed by ultrasonic immersion calcination method, and the degradation of RhB was studied in a three-dimensional electrochemical reactor (3DER). It was characterized by XRD, SEM, EDS, XPS, cyclic voltammetry and linear sweep voltammetry. When the pH value is 5.00, the dosage of Fe/Cu@antimony tailing is 1.50 g/L, the initial concentration is 100 mg/L, and the current density is 20 mA/cm2, the degradation efficiency is the best (99.40% for RhB and 98.81% for TOC) within 15 min. The results show that in the three-dimensional electrochemical oxidation system, electrochemical oxidation and electro Fenton oxidation occur at the same time to cause the increase of hydroxyl radicals. According to LC-MS analysis and EPR characterization, it can be found that the main degradation mechanism of RhB is that hydroxyl radicals continuously attack RhB, and realize rapid degradation of RhB through deethylation, deamination, dealkylation, decarboxylation, chromophore splitting, ring opening and mineralization. Fe/Cu@antimony tailing particles are both electrodes for electrochemical oxidation and catalysts for Fenton oxidation. The degradation effect of RhB remained at 94% after 6 cycles, and the leaching rates of Fe and Cu are only 1.20% and 0.79%, indicating that Fe/Cu@AT had significant stability. This work provides a new insight into the establishment of an efficient and stable three-dimensional electrocatalytic particle electrode.

Responses of applied voltages on the archaea microbial distribution in sludge digestion.

As the development of urban population led to the increase of domestic water consumption, consequently the generation of surplus sludge (SS) produced increasingly during sewage treatment processes. In order to enhance the SS resource utilization efficiency, an electricity-assisted anaerobic digestion (EAAD) system was employed to examine the alterations in the digestion broth and the characteristics of gas production. Additionally, the response of applied voltages on the distribution of archaeal community near various electrodes within the sludge was explored. The results revealed that the application of high voltages exceeding 3.0 V hindered the CH4 production but stimulated the CO2 generation. Subsequently, both CH4 and CO2 production were impeded by the applied voltages. Furthermore, the increased voltages significantly decreased the abundance of Methanomicrobia, Methanosaeta, and Methanosarcina, which were crucial determinants of CH4 content in biogas. Notably, the excessively high voltages intensities caused the AD process to halt and even inactivate the microbial flora. Interestingly, the distribution characteristics of archaeal community were influenced not only by the voltages intensity but also exhibited variations between the anode and cathode regions. Moreover, as the applied voltage intensified, the discrepancy of responses between the cathode and anode regions became more pronounced, offering novel theoretical and technical foundations for the advancement of electricity-assisted with AD technology.

Comparison of the effects of different calorie amounts of enteral nutrition in hypercatabolism associated with ghrelin-POMC in endotoxemic rats.

BACKGROUND: Hypercatabolism often occurs in critically ill patients, and it increases infection rates and mortality in these patients. Enteral nutrition (EN) is commonly used in case of hypercatabolism. However, the effect of amount of calories in EN on hypercatabolism remains unexplored. OBJECTIVE: Here, we compared the effect of low-calorie, medium-calorie and high-calorie EN on hypercatabolism in the acute phase of endotoxemia, which is associated with gastrointestinal hormones and hypothalamic neuropeptide proopiomelanocortin (POMC). METHODS: Overall 84 adult male Sprague-Dawley rats were used for research. A set of rats were divided into 5 groups, Control (NS) and lipopolysaccharide (LPS) groups were fed a standard chow diet; LPS + L (LPS + 40 kcal/kg/day EN), LPS + M (LPS + 80 kcal/kg/day EN) and LPS + H (LPS + 120 kcal/kg/day EN) groups received EN through a gastric tube for 3 days. Another set of rats were used for parallel control experiment and divided into 5 groups: NS + F (saline + fasting) and LPS + F (LPS + fasting) groups were given no food, NS + L (saline + 40 kcal/kg/day EN), NS + M (saline + 80 kcal/kg/day EN) and NS + H (saline + 120 kcal/kg/day EN) groups received EN through a gastric tube for 3 days. Hypercatabolism was evaluated by assessing skeletal muscle protein synthesis and atrophy, insulin resistance, and corticosterone levels. Moreover, serum inflammatory factors, gastrointestinal hormones, hypothalamic ghrelin, growth hormone secretagogue receptor-1α, hypothalamic neuropeptide, and intestinal injury indicators were detected. RESULTS: Low-calorie EN effectively increased serum and hypothalamic ghrelin possibly due to slight intestinal barrier damage, thereby decreasing hypothalamic POMC expression; consequently, it alleviated rat insulin resistance, reduced blood cortisol levels and muscle atrophy, and improved the survival rate of rats in the acute phase of endotoxemia. Interestingly, with an increase in calories in enteral nutrition, the aforementioned effects did not increase. CONCLUSIONS: Low-calorie EN could effectively increase gastrointestinal hormone ghrelin by reducing intestinal damage and suppressing POMC expression to ameliorate hypercatabolism when compared with medium-calorie and high-calorie EN. Therefore Low-calorie EN may be preferred for providing EN in the acute stage of endotoxemia.

Exogenous Melatonin Alleviates Skeletal Muscle Wasting by Regulating Hypothalamic Neuropeptides Expression in Endotoxemia Rats.

To investigate whether exogenous melatonin (MLT) could alleviate skeletal muscle wasting by regulating hypothalamic neuropeptides expression. Adult male Sprague Dawley rats were intraperitoneally injected with lipopolysaccharide (LPS) (10 mg/kg), followed by MLT (30 mg/kg/day) or saline for 3 days. Hypothalamic tissues and skeletal muscle were obtained on day 3. Skeletal muscle wasting was measured by the mRNA expression of two E3 ubiquitin ligases, muscle atrophy F-box and muscle ring finger 1 as well as 3-methylhistidine (3-MH) and tyrosine release. Three hypothalamic neuropeptides (POMC, AgRP, CART) expression were detected in all groups. POMC expression knockdown was achieved by ARC injection of lentiviruses containing shRNA against POMC. Two weeks after ARC viruses injection, rats were i.p. injected with LPS (10 mg/kg) followed by MLT (30 mg/kg/day) or saline for 3 days. Brain tissues were harvested for immunostaining. In septic rats, 3-MH, tyrosine release and muscle atrophic gene expression were significantly decreased in MLT treated group. POMC and CART expression were lower while AgRP expression was higher in MLT treated group. Furthermore, in septic rats treated with MLT, muscle wasting in those with lower expression of neuropeptide POMC did not differ from those with normal POMC expression. Exogenous MLT could alleviate skeletal muscle wasting in septic rats by regulating hypothalamic neuropeptides.

Application of a novel artificial perfusate based on oxygen-carrying nanoparticles in normothermic machine perfusion for porcine liver preservation after cardiac death.

OBJECTIVE: To investigate the efficacy of a novel artificial perfusate based on oxygen-carrying perfluoronaphthalene-albumin nanoparticles in normothermic machine perfusion (NMP) for preservation of porcine liver donation after cardiac death. METHODS: Artificial perfusate with perfluoronaphthalene-albumin nanoparticles was prepared at 5% albumin (w/v) and its oxygen carrying capacity was calculated. The livers of 16 Landrace pigs were isolated after 1 h of warm ischemia, and then they were divided into 4 groups and preserved continuously for 24 h with different preservation methods: cold preservation with UW solution (SCS group), NMP preservation by whole blood (blood NMP group), NMP preservation by artificial perfusate without nanoparticles (non-nanoparticles NMP group) and NMP preservation by artificial perfusate containing nanoparticles (nanoparticles NMP group). Hemodynamics, tissue metabolism, biochemical indices of perfusate and bile were monitored every 4 h after the beginning of NMP. Liver tissue samples were collected for histological examination (HE and TUNEL staining) before preservation, 12 h and 24 h after preservation. RESULTS: The oxygen carrying capacity of nanoparticles in 100 mL artificial perfusate was 6.94 µL/mmHg (1 mmHg=0.133 kPa). The hepatic artery and portal vein resistance of nanoparticles NMP group and blood NMP group remained stable during perfusion, and the vascular resistance of nanoparticles NMP group was lower than that of blood NMP group. The concentration of lactic acid in the perfusate decreased to the normal range within 8 h in both nanoparticles NMP group and blood NMP group. There were no significant differences in accumulated bile production, alanine aminotransferase and aspartate aminotransferase in perfusate between nanoparticles NMP group and blood NMP group (all P>0.05). After 24 h perfusion, the histological Suzuki score in blood NMP group and nanoparticles NMP group was lower than that in SCS group and non-nanoparticles NMP group (all P<0.05), and the quantities of TUNEL staining positive cells in blood NMP group and non-nanoparticles NMP group was higher than those in nanoparticles NMP group and SCS group 12 h and 24 h after preservation (all P<0.05). CONCLUSION: Artificial perfusate based on oxygen-carrying nanoparticles can meet the oxygen supply requirements of porcine livers donation after cardiac death during NMP preservation, and it may has superiorities in improving tissue microcirculation and alleviating ischemia-reperfusion injury.

Predictive value of transabdominal intestinal sonography in critically ill patients: a prospective observational study.

BACKGROUND: This study examined the feasibility of transabdominal intestinal ultrasonography in evaluating acute gastrointestinal injury (AGI). METHODS: A total of 116 patients were included. Intestinal ultrasonography was conducted daily within 1 week after admission to the intensive care unit. Ultrasonography indicators including intestinal diameter, changes in the intestinal folds, thickness of the intestinal wall, stratification of the intestinal wall, and intestinal peristalsis (movement of the intestinal contents) were observed to determine the acute gastrointestinal injury ultrasonography (AGIUS) score. The gastrointestinal and urinary tract sonography ultrasound (GUTS) protocol score was also calculated. During the first week of the study, the gastrointestinal failure (GIF) score was determined daily. The correlations between transabdominal intestinal scores (AGIUS and GUTS) and the GIF score were analyzed to clarify the feasibility of evaluating AGI through observation of the intestine. The utility of intestinal ultrasonography indicators in predicting feeding intolerance was investigated to improve the ability of clinicians to manage AGI. RESULTS: A total of 751 ultrasonic examinations were performed with 511 images (68%) considered to be of "good quality." AGIUS and GUTS scores differed significantly between AGI patients (GIF score 0-2) and non-AGI patients (GIF score 3-4) (p < 0.001). Both scores correlated positively with GIF score (r = 0.54, p < 0.001; r = 0.66, p < 0.001). These ultrasonography indicators could predict feeding intolerance, with an area under the receiver operating characteristic curve of 0.60 (0.48-0.71; intestinal diameter), 0.76 (0.67-0.85; intestinal folds), 0.71 (0.62-0.80; wall thickness), 0.77 (0.69-0.86; wall stratification), and 0.78 (0.68-0.88; intestinal peristalsis). Compared to patients with a normal rate of peristalsis (5-10/min), patients with abnormal peristalsis rates (< 5/min or > 10/min) have increased risk for feeding intolerance (16/83 vs. 25/33, p < 0.001). CONCLUSIONS: The transabdominal intestinal ultrasonography represents an effective means for assessing gastrointestinal injury in critically ill patients. Intestinal ultrasonography indicators, especially the degree of intestinal peristalsis, may be used to predict feeding intolerance. TRIAL REGISTRATION: ClinicalTrial.gov, NCT03589248. Registered 04 July 2018-retrospectively registered.

Constant light exposure aggravates POMC-mediated muscle wasting associated with hypothalamic alteration of circadian clock and SIRT1 in endotoxemia rats.

Constant light exposure is widespread in the intensive care unit (ICU) and could increase the rate of brain dysfunction as delirium and sleep disorders in critical patients. And the activation of hypothalamic neuropeptides is proved to play a crucial role in regulating hypercatabolism, especially skeletal muscle wasting in critical patients, which could lead to serious complications and poor prognosis. Here we investigated the hypothesis that constant light exposure could aggravate skeletal muscle wasting in endotoxemia rats and whether it was associated with alterations of circadian clock and hypothalamic proopiomelanocortin(POMC) expression. Fifty-four adult male Sprague-Dawley rats were intraperitoneally injected with lipopolysaccharide(LPS) or saline, subjected to constant light or a 12:12 h light-dark cycle for 7 days. On day 8, rats were sacrificed across six time points in 24 h and hypothalamus tissues and skeletal muscle were obtained. Rates of muscle wasting were measured by 3-methylhistidine(3-MH) and tyrosine release as well as expression of two muscle atrophic genes, muscle ring finger 1(MuRF-1) and muscle atrophy F-box(MAFbx). The expression of circadian clock genes, silent information regulator 1(SIRT1), POMC and hypothalamic inflammatory cytokines were also detected. Results showed that LPS administration significantly increased hypothalamic POMC expression, inflammatory cytokine levels and muscle wasting rates. Meanwhile constant light exposure disrupted the circadian rhythm, declined the expression of SIRT1 as well as aggravated hypothalamic POMC overexpression and skeletal muscle wasting in rats with endotoxemia. Taken together, the results demonstrated that constant light exposure could aggravate POMC-mediated skeletal muscle wasting in endotoxemia rats, which is associated with alteration of circadian clocks and SIRT1 in the hypothalamus.

Fecal Bacteriome and Mycobiome in Bats with Diverse Diets in South China.

Bats can be divided into frugivory, nectarivory, insectivory, and sanguivory based on their diets, and are therefore ideal wild animal models to study the relationship between diets and intestinal microflora. Early studies of bat gut bacteria showed that the diversity and structure of intestinal bacterial communities in bats are closely related to dietary changes. Worthy of note, intestinal microbes are composed of bacteria, fungi, protozoa, and archaea. Although the number of gut fungi is much lower than that of gut bacteria, they also play an important role in maintaining the host homeostasis. However, there are still few reports on the relationship between the gut mycobiota and the dietary habits of the host. In addition, bats have also been shown to naturally transmit pathogenic viruses and bacteria through their feces and saliva, but fungal infections from bat are less studied. Here, we used high-throughput sequencing of bacterial 16S and eukaryotic 18S rRNA genes in the V4 and V9 regions to characterize fecal bacterial and fungal microbiota in phytophagous and insectivorous bats in South China. The results show that the gut microbiota in bats were dominated by bacterial phyla Proteobacteria, Firmicutes, Tenericutes and Bacteroidetes, and fungal phyla Ascomycota and Basidiomycota. There was a significant difference in the diversity of bacterial and fungal microbiota between the groups, in addition to specific bacteria and fungi populations on each of them. Of note, the number of fungi in the feces of herbivorous bats is relatively higher. Most of these fungi are foodborne and are also pathogens of humans and other animals. Thus, bats are natural carriers of fungal pathogens. The current study expands the understanding of the bat gut bacterial and fungal mycobiota and provides further insight into the transmission of fungal pathogens.

Postoperative Interleukin-6 Predicts Intra-abdominal Septic Complications at an Early Stage After Elective Intestinal Operation for Crohn's Disease Patients.

BACKGROUND: The role of interleukin-6 (IL-6) in the prediction of intra-abdominal septic complications (IASCs) in patients with Crohn's disease (CD) remains unclear. We assessed the serum IL-6 time course and its association with postoperative IASCs in patients undergoing elective intestinal operations for CD. METHODS: In total, 118 patients who underwent intestinal operations for CD were prospectively evaluated. They were divided into an IASC group and non-IASC group. Multivariate analyses were used to identify risk factors, and receiver operating characteristic curve analysis was performed. RESULTS: Multivariate analysis showed that a high IL-6 concentration of >137.25 pg/mL on postoperative day (POD) 1 was independently associated with IASCs (odds ratio, 5.74; 95% confidence interval [CI], 1.46-22.67; P = 0.012) and a longer postoperative length of hospitalization (6 vs 9 days, P < 0.001). The median interval between surgery and IASCs (interquartile range) was 6 (4-22) days, and the IL-6 concentration was significantly different between patients with and without IASCs on PODs 1, 3, and 5. The ideal IL-6 cutoff value on POD 1 for the prediction of postoperative IASCs was 137.25 pg/mL, yielding a sensitivity of 81%, specificity of 58%, and area under the curve of 0.71 (95% CI, 0.59-0.83), with a negative predictive value of 0.93. CONCLUSIONS: A high IL-6 concentration on POD 1 is independently associated with the occurrence of postoperative IASCs in patients undergoing elective surgery for CD and could allow for earlier diagnosis and earlier intervention for IASCs compared with C-reactive protein.

Hypothalamic AMPK-induced autophagy ameliorates hypercatabolism in septic rats by regulating POMC expression.

Hypercatabolism plays a critical role in the pathogenesis of post-critical care debility in critical patients. Central nervous system may exerte a critical role in the regulation of hypercatabolism. However, little is known about the exact mechanisms of the central role. Here, we reported that actived hypothalamic AMP-activated protein kinase (AMPK)-induced autophagy modulated the expression of POMC to ameliorate hypercatabolism in septic rats. Firstly, rats were i.c.v. injected with the lentiviral vector containing shRNA against POMC. Two weeks after injections, rats were intraperitoneally injected with LPS or saline. Twenty-four hours later, blood, skeletal muscle and hypothalamus tissues were obtained. Hypercatabolism markers and neuropeptides expression were detected. Then, rats were injected with AICAR or saline into third ventricle and promptly intraperitoneally injected with LPS or saline. Twenty-four hours after infection, blood, skeletal muscle and hypothalamus tissues were obtained. Hypercatabolism, hypothalamic AMPK-induced autophagy markers and neuropeptides expression were also detected. Results showed that sepsis would decrease the level of hypothalamic autophagy accompany with the alterations of POMC expression and hypercatabolism. Knocking out hypothalamus POMC expression could significantly ameliorate hypercatabolism. Moreover, Central activation of AMPK-induced autophagy pathway via third ventricle injection of AICAR, an AMPK activator, could efficiently ameliorate hypercatabolism as well as attenuate the elevated POMC expression rather than other neuropeptides. Taken together, these results suggested that hypothalamic AMPK-autophagy pathway as a regulatory pathway for POMC expression was essential for hypercatabolism during sepsis. And hypothalamic AMPK-autophagy activation could attenuate the POMC expression to ameliorate hypercatabolism. Pharmaceuticals with the ability of activating hypothalamic AMPK-autophagy pathway may be a therapeutic potential for hypercatabolism in septic patients.

Lipid-rich enteral nutrition controls intestinal inflammation, improves intestinal motility and mucosal barrier damage in a rat model of intestinal ischemia/reperfusion injury.

BACKGROUND: It has been reported that lipid-rich enteral nutrition (EN) could ameliorate inflammation in various diseases. In this study, we investigated whether lipid-rich EN could control intestinal inflammation, improve intestinal motility and mucosal barrier injury after intestinal ischemia/reperfusion (I/R) injury. METHODS: Male adult rats received saline, conventional EN, or lipid-rich EN via gavage before and after intestinal I/R injury. The superior mesenteric artery was occluded for 60 min. The sham group underwent laparotomy without superior mesenteric artery occlusion and was administrated saline. Intestinal motility was measured 4 h after intestinal I/R injury by fluorescein isothiocyanate-dextran transit assay; the intestinal and systemic inflammation were assessed by analyzing intestinal and serum concentrations of tumor necrosis factor α, interleukin (IL)- 6, and IL-10, separately. The intestinal mucosal barrier injury was assessed by analyzing the serum levels of intestinal fatty acid-binding protein (I-FABP) and intestinal mucosal tight junction (TJ) proteins. RESULTS: The intestinal I/R injury decreased intestinal motility and intestinal mucosal TJs expression significantly when compared with the sham group (P < 0.05). The intestinal and systemic inflammatory parameters and the serum I-FABP were also significantly higher in the I/R groups than those in the sham group (P < 0.05). Both conventional and lipid-rich EN increased the intestinal motility and the intestinal mucosal TJs expression and decreased the intestinal and systemic inflammatory parameter and serum I-FABP levels to different degrees when compared with the I/R group (P < 0.05). However, lipid-rich EN significantly improved the negative alterations in these biochemical parameters when compared with the conventional EN (P < 0.05). CONCLUSIONS: These results suggest that lipid-rich EN might be able to control intestinal inflammation, improve intestinal motility and mucosal barrier injury after intestinal I/R injury. Thus, the administration of lipid-rich EN may be an effective treatment for promoting gastrointestinal function recovery after intestinal I/R injury.

Mild hypothermia ameliorates muscle wasting in septic rats associated with hypothalamic AMPK-induced autophagy and neuropeptides.

Sepsis, always developing muscle wasting, contributes to serious complications and mortality. Mild hypothermia has been reported to have protective effects on the prognosis of septic patients. However, the underlying mechanisms remain unclear. We therefore hypothesized that mild hypothermia could ameliorate muscle wasting during sepsis and whether it was associated with hypothalamus AMPK-induced autophagy and neuropeptides. Adult male Sprague-Dawley rats were intraperitoneally injected with lipopolysaccharide (LPS) (5 mg/kg) or saline. Mild hypothermia was instantly induced at 33 °C for 3h after LPS injected. Meanwhile, the control and sepsis groups were simultaneously placed on the thermal mattress to maintain the a normal temperature in control group whatever the changes induced by anesthesia. Twenty-four hours after injection, skeletal muscle and hypothalamus tissues were obtained. Muscle wasting was measured by the mRNA expression of two muscle atrophic genes, muscle ring finger 1 (MuRF-1) and muscle atrophy F-box (MAFbx), as well as 3-methylhistidine (3-MH) and tyrosine release. Hypothalamic AMPK-induced autophagy markers and neuropeptides expression were also detected. Results showed that LPS administration significantly decreased hypothalamic AMPK-induced autophagy together with muscle wasting. Also, increased hypothalamic neuropeptides, proopiomelanocortin (POMC), cocaine and amphetamine-related transcript (CART) and neuro-peptides Y (NPY) and decreased agouti-related protein (AgRP) were observed. Mild hypothermia significantly increased hypothalamic AMPK-induced autophagy and ameliorated LPS-induced muscle wasting, and attenuated the alteration of neuropeptides, POMC, CART and NPY. In conclusion, mild hypothermia could alleviate muscle wasting by LPS injection, which was associated with reversing the level of hypothalamic AMPK-induced autophagy and the alteration of neuropeptides. These results suggested that mild hypothermia could be a potential treatment concept and a novel mechanism in management of muscle wasting in critically ill patients.

Acute Colonic Pseudo-Obstruction with Feeding Intolerance in Critically Ill Patients: A Study according to Gut Wall Analysis.

Objective. To compare the differences between acute colonic pseudo-obstruction (ACPO) with and without acute gut wall thickening. Methods. ACPO patients with feeding tolerance were divided into ACPO with no obvious gut wall thickening (ACPO-NT) group and ACPO with obvious acute gut wall thickening (ACPO-T) group according to computed tomography and abdominal radiographs. Patients' condition, responses to supportive measures, pharmacologic therapy, endoscopic decompression, and surgeries and outcomes were compared. Results. Patients in ACPO-T group had a significantly higher APACHE II (11.82 versus 8.25, p = 0.008) and SOFA scores (6.47 versus 3.54, p < 0.001) and a significantly higher 28-day mortality (17.78% versus 4.16%, p = 0.032) and longer intensive care unit stage (4 versus 16 d, p < 0.001). Patients in ACPO-NT group were more likely to be responsive to supportive treatment (62.50% versus 24.44%, p < 0.001), neostigmine (77.78% versus 17.64%, p < 0.001), and colonoscopic decompression (75% versus 42.86%, p = 0.318) than those in ACPO-T group. Of the patients who underwent ileostomy, 81.25% gained benefits. Conclusions. ACPO patients with gut wall thickening are more severe and are less likely to be responsive to nonsurgical treatment. Ileostomy may be a good option for ACPO patients with gut wall thickening who are irresponsive to nonsurgical treatment.

Dexmedetomidine ameliorates muscle wasting and attenuates the alteration of hypothalamic neuropeptides and inflammation in endotoxemic rats.

Dexmedetomidine is generally used for sedaton in critically ill, it could shorten duration of mechanical ventilation, ICU stay and lower basic metabolism. However, the exact mechanism of these positive effects remains unkown. Here we investigated the hypothesis that dexmedetomidine could ameliorate muscle wasting in endotoxemic rats and whether it was related to hypothalamic neuropeptides alteration and inflammation. Fourty-eight adult male Sprague-Dawley rats were intraperitoneally injected with lipopolysaccharide (LPS) (5 mg/kg) or saline, followed by 50 µg/kg dexmedetomidine or saline administration via the femoral vein catheter (infusion at 5 µg·kg-1·hr-1). Twenty-four hours after injection, hypothalamus tissues and skeletal muscle were obtained. Muscle wasting was measured by the mRNA expression of two E3 ubiquitin ligases, muscle atrophy F-box (MAFbx) and muscle ring finger 1 (MuRF-1) as well as 3-methylhistidine (3-MH) and tyrosine release. Hypothalamic inflammatory markers and neuropeptides expression were also detected in all four groups. Results showed that LPS administration led to significant increase in hypothalamic inflammation together with muscle wasting. Increased hypothalamic neuropeptides, proopiomelanocortin (POMC), cocaine and amphetamine-related transcript (CART) and neuropeptides Y (NPY) and decreased agouti-related protein (AgRP) were also observed. Meanwhile dexmedetomidine administration ameliorated muscle wasting, hypothalamic inflammation and modulated the alteration of neuropeptides, POMC, CART and AgRP, in endotoxemic rats. In conclusion, dexmedetomidine could alleviate muscle wasting in endotoxemic rats, and it could also attenuate the alteration of hypothalamic neuropeptides and reduce hypothalamic inflammation.

Estrogen Maintains Skeletal Muscle in Septic Rats Associated with Altering Hypothalamic Inflammation and Neuropeptides.

Muscle wasting is one of the main contributors to the worse outcomes in sepsis. Whether estrogen could alleviate muscle wasting induced by sepsis remains unclear. This study was designed to test the effect of estrogen on muscle wasting and its relationship with central alteration in sepsis. Thirty Sprague-Dawley rats were divided into 3 groups: control group, sepsis group, and estrogen treated sepsis group. Animals were intraperitoneally injected with lipopolysaccharide (10 mg/kg) or saline, followed by subcutaneous injection of 17ß-estradiol (1 mg/kg) or saline. Twenty-four hours later, all animals were killed and their hypothalamus and skeletal muscles were harvested for analysis. Muscle wasting markers, hypothalamic neuropeptides, and hypothalamic inflammatory markers were measured. As a result, lipopolysaccharide administration caused a significant increase in muscle wasting, hypothalamic inflammation, and anorexigenic neuropeptides (POMC and CART) gene expression, and a significant decrease in orexigenic neuropeptides (AgRP and NPY) gene expression. Administration of estrogen signifcantl attenuated lipopolysaccharide-induced muscle wasting (body weight and extensor digitorum longus loss [52 and 62 %], tyrosine and 3-methylhistidine release [17 and 22 %], muscle ring fnger 1 [MuRF-1; 65 %], and muscle atrophy F-box [MAFbx] gene expression), hypothalamic inflammation (Tumor necrosis factor-α and interlukin-1ß [69 and 70%]) as well as alteration of POMC, CART and AgRP (61, 37, and 1008 %) expression.In conclusion, estrogen could alleviate sepsis-induced muscle wasting and it was associated with reducing hypothalamic inflammation and alteration of hypothalamic neuropeptides.

The Addition of Dexmedetomidine to Analgesia for Patients After Abdominal Operations: A Prospective Randomized Clinical Trial.

BACKGROUND: Postoperative pain and anxiety are two common factors influencing patient's recovery. Benefits and safety in the use of sedative agents after abdominal operations to improve recovery are not well known. The present study is to evaluate the efficacy and safety of dexmedetomidine use in this population. METHODS: A prospective randomized controlled trial of 145 patients undergoing abdominal operations was conducted in the Surgical Intensive Care Unit of Jinling Hospital between October and December 2015. Thirty-two patients were excluded, and 113 were included and divided into the experimental group (59 patients) receiving dexmedetomidine and analgesics for 72 h after abdominal operations, and the control group (54 patients) receiving only analgesics. Postoperative pain, inflammatory response, recovery of gastrointestinal function, adverse events, and sedation level were analyzed. RESULTS: Pain scores, assessed by Prince Henry Pain Scale (PHPS), in the experimental group were significantly lower than in the control group on the first (1.53 vs. 2.07, p ≤ 0.01), second (1.07 vs. 1.63, p ≤ 0.01), and third day (1.08 vs. 1.82, p = 0.01). Time to defecation was 0.60 days shorter in the experimental group than the control group (2.51 vs. 3.11, p = 0.01). There was no significant difference between inflammatory responses in the two groups (p > 0.05). Both groups had similar blood pressure, heart rate, prevalence of bradycardia, and hypotension requiring interventions (p > 0.05). CONCLUSIONS: The addition of dexmedetomidine to analgesia after abdominal operations is safe and could enhance gastrointestinal function recovery and pain control when monitored carefully. The capacity of dexmedetomidine to attenuate inflammatory responses requires further investigation.

Hypothalamic activation is essential for endotoxemia-induced acute muscle wasting.

Growing evidence suggests acute skeletal muscle wasting is a key factor affecting nutritional support and prognosis in critical patients. Previously, plenty of studies of muscle wasting focused on the peripheral pathway, little was known about the central role. We tested the hypothesis whether central inflammatory pathway and neuropeptides were involved in the process. In lipopolysaccharide (LPS) treated rats, hypothalamic NF-κB pathway and inflammation were highly activated, which was accompanied with severe muscle wasting. Central inhibition of nuclear factor kappa-B (NF-κB) pathway activation by infusion of an inhibitor (PS1145) can efficiently reduce muscle wasting as well as attenuate hypothalamic neuropeptides alteration. Furthermore, knockdown the expression of anorexigenic neuropeptide proopiomelanocortin (POMC) expression with a lentiviral vector containing shRNA can significantly alleviate LPS-induced muscle wasting, whereas hypothalamic inflammation or NF-κB pathway was barely affected. Taken together, these results suggest activation of hypothalamic POMC is pivotal for acute muscle wasting caused by endotoxemia. Neuropeptide POMC expression may have mediated the contribution of hypothalamic inflammation to peripheral muscle wasting. Pharmaceuticals with the ability of inhibiting hypothalamic NF-κB pathway or POMC activation may have a therapeutic potential for acute muscle wasting and nutritional therapy in septic patients.

Membrane-Bound Thrombomodulin Regulates Macrophage Inflammation in Abdominal Aortic Aneurysm.

OBJECTIVE: Thrombomodulin (TM), a glycoprotein constitutively expressed in the endothelium, is well known for its anticoagulant and anti-inflammatory properties. Paradoxically, we recently found that monocytic membrane-bound TM (ie, endogenous TM expression in monocytes) triggers lipopolysaccharide- and gram-negative bacteria-induced inflammatory responses. However, the significance of membrane-bound TM in chronic sterile vascular inflammation and the development of abdominal aortic aneurysm (AAA) remains undetermined. APPROACH AND RESULTS: Implicating a potential role for membrane-bound TM in AAA, we found that TM signals were predominantly localized to macrophages and vascular smooth muscle cells in human aneurysm specimens. Characterization of the CaCl2-induced AAA in mice revealed that during aneurysm development, TM expression was mainly localized in infiltrating macrophages and vascular smooth muscle cells. To investigate the function of membrane-bound TM in vivo, transgenic mice with myeloid- (LysMcre/TM(flox/flox)) and vascular smooth muscle cell-specific (SM22-cre(tg)/TM(flox/flox)) TM ablation and their respective wild-type controls (TM(flox/flox) and SM22-cre(tg)/TM(+/+)) were generated. In the mouse CaCl2-induced AAA model, deficiency of myeloid TM, but not vascular smooth muscle cell TM, inhibited macrophage accumulation, attenuated proinflammatory cytokine and matrix metalloproteinase-9 production, and finally mitigated elastin destruction and aortic dilatation. In vitro TM-deficient monocytes/macrophages, versus TM wild-type counterparts, exhibited attenuation of proinflammatory mediator expression, adhesion to endothelial cells, and generation of reactive oxygen species. Consistently, myeloid TM-deficient hyperlipidemic mice (ApoE(-/-)/LysMcre/TM(flox/flox)) were resistant to AAA formation induced by angiotensin II infusion, along with reduced macrophage infiltration, suppressed matrix metalloproteinase activities, and diminished oxidative stress. CONCLUSIONS: Membrane-bound TM in macrophages plays an essential role in the development of AAA by enhancing proinflammatory mediator elaboration, macrophage recruitment, and oxidative stress.