Preparation of Steamed Purple Sweet Potato-Based Films Containing Mandarin Essential Oil for Smart Packaging.

Anthocyanin-rich steamed purple sweet potato (SPSP) is a suitable raw material to produce smart packaging films. However, the application of SPSP-based films is restricted by the low antimicrobial activity of anthocyanins. In this study, SPSP-based smart packaging films were produced by adding mandarin essential oil (MEO) as an antimicrobial agent. The impact of MEO content (3%, 6%, and 9%) on the structures, properties, and application of SPSP-based films was measured. The results showed that MEO created several pores within films and reduced the hydrogen bonding system and crystallinity of films. The dark purple color of the SPSP films was almost unchanged by MEO. MEO significantly decreased the light transmittance, water vapor permeability, and tensile strength of the films, but remarkably increased the oxygen permeability, thermal stability, and antioxidant and antimicrobial properties of the films. The SPSP-MEO films showed intuitive color changes at different acid-base conditions. The purple-colored SPSP-MEO films turned blue when chilled shrimp and pork were not fresh. The MEO content greatly influenced the structures, physical properties, and antioxidant and antimicrobial activities of the films. However, the MEO content had no impact on the color change ability of the films. The results suggested that SPSP-MEO films have potential in the smart packaging of protein-rich foods.

[Role and mechanism of SIRT1 in regulating Nrf2/HO-1 signaling pathway in septic liver injury].

OBJECTIVE: To investigate the role and mechanism of silent information regulator 1 (SIRT1) in regulating nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in oxidative stress and inflammatory response to sepsis-induced liver injury. METHODS: A total of 24 male Sprague-Dawley (SD) rats were randomly divided into sham operation (Sham) group, cecal ligation and puncture (CLP) group, SIRT1 agonist SRT1720 pretreatment (CLP+SRT1720) group and SIRT1 inhibitor EX527 pretreatment (CLP+EX527) group, with 6 rats in each group. Two hours before operation, SRT1720 (10 mg/kg) or EX527 (10 mg/kg) were intraperitoneally injected into the CLP+SRT1720 group and CLP+EX527 group, respectively. Blood was collected from the abdominal aorta at 24 hours after modeling and the rats were sacrificed for liver tissue. The serum levels of interleukins (IL-6, IL-1ß) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA). The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by microplate method. Hematoxylin-eosin (HE) staining was used to observe the pathological injury of rats in each group. The levels of malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), glutathione (GSH) and superoxide dismutase (SOD) in liver tissue were detected by corresponding kits. The mRNA and protein expressions of SIRT1, Nrf2 and HO-1 in liver tissues were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting. RESULTS: Compared with the Sham group, the serum levels of IL-6, IL-1ß, TNF-α, ALT and AST in the CLP group were significantly increased; histopathological results showed that liver cords were disordered, hepatocytes were swollen and necrotic, and a large number of inflammatory cells infiltrated; the contents of MDA and 8-OHdG in liver tissue increased, while the contents of GSH and SOD decreased; and the mRNA and protein expressions of SIRT1, Nrf2 and HO-1 in liver tissues were significantly decreased. These results suggest that sepsis rats have liver dysfunction, and the levels of SIRT1, Nrf2, HO-1 and antioxidant protein in liver tissues were decreased, while the levels of oxidative stress and inflammation were increased. Compared with the CLP group, the levels of inflammatory factors and oxidative stress were significantly decreased in the CLP+SRT1720 group, the mRNA and protein expressions of SIRT1, Nrf2 and HO-1 were significantly increased [IL-6 (ng/L): 34.59±4.21 vs. 61.84±3.78, IL-1ß (ng/L): 41.37±2.70 vs. 72.06±3.14, TNF-α (ng/L): 76.43±5.23 vs. 130.85±5.30, ALT (U/L): 30.71±3.63 vs. 64.23±4.59, AST (U/L): 94.57±6.08 vs. 145.15±6.86, MDA (µmol/g): 6.11±0.28 vs. 9.23±0.29, 8-OHdG (ng/L): 117.43±10.38 vs. 242.37±11.71, GSH (µmol/g): 11.93±0.88 vs. 7.66±0.47, SOD (kU/g): 121.58±5.05 vs. 83.57±4.84, SIRT1 mRNA (2-ΔΔCt): 1.20±0.13 vs. 0.46±0.02, Nrf2 mRNA (2-ΔΔCt): 1.21±0.12 vs. 0.58±0.03, HO-1 mRNA (2-ΔΔCt): 1.71±0.06 vs. 0.48±0.07, SIRT1 protein (SIRT1/ß-actin): 0.89±0.04 vs. 0.58±0.03, Nrf2 protein (Nrf2/ß-actin): 0.87±0.08 vs. 0.51±0.09, HO-1 protein (HO-1/ß-actin): 0.93±0.14 vs. 0.54±0.12, all P < 0.05], these results indicated that SIRT1 agonist SRT1720 pretreatment could improve liver injury in sepsis rats. However, pretreatment with SIRT1 inhibitor EX527 showed the opposite effect [IL-6 (ng/L): 81.05±6.47 vs. 61.84±3.78, IL-1ß (ng/L): 93.89±5.83 vs. 72.06±3.14, TNF-α (ng/L): 177.67±5.12 vs. 130.85±5.30, ALT (U/L): 89.33±9.52 vs. 64.23±4.59, AST (U/L): 179.59±6.44 vs. 145.15±6.86, MDA (µmol/g): 11.39±0.51 vs. 9.23±0.29, 8-OHdG (ng/L): 328.83±11.26 vs. 242.37±11.71, GSH (µmol/g): 5.07±0.34 vs. 7.66±0.47, SOD (kU/g): 59.37±4.28 vs. 83.57±4.84, SIRT1 mRNA (2-ΔΔCt): 0.34±0.03 vs. 0.46±0.02, Nrf2 mRNA (2-ΔΔCt): 0.46±0.04 vs. 0.58±0.03, HO-1 mRNA (2-ΔΔCt): 0.21±0.03 vs. 0.48±0.07, SIRT1 protein (SIRT1/ß-actin): 0.47±0.04 vs. 0.58±0.03, Nrf2 protein (Nrf2/ß-actin): 0.32±0.07 vs. 0.51±0.09, HO-1 protein (HO-1/ß-actin): 0.19±0.09 vs. 0.54±0.12, all P < 0.05]. CONCLUSIONS: SIRT1 can inhibit the release of proinflammatory factors and alleviate the oxidative damage of hepatocytes by activating Nrf2/HO-1 signaling pathway, thus playing a protective role against CLP-induced liver injury.

Characteristics of Cephalotaxus fortunei kernel oil and its digestion behaviors.

Cephalotaxus fortunei, a potential underutilized oil resource, contains various active ingredients that exert positive effects on human health. In the present study, characteristics of C. fortunei kernel oil and its digestion properties were systematically investigated. Results indicated that C. fortunei kernels contained high oil content (64.59%), of which over 90% was triacylglycerols (TAGs). The kernel oil was rich in oleic acid (C18:1n-9, 42.88%), linoleic acid (C18:2n-6, 31.05%), and sciadonic acid (C20:3n-6, 10.78%). The kernel oil also contained some beneficial fat-soluble nutrients, such as tocopherols (143 mg/kg) and phytosterols (1474 mg/kg). Thirty-five kinds of TAGs were identified, among which O-O-L (17.96%), O-O-O (12.12%), L-L-O (11.79%), O-L-Et (8.59%), and O-O-Et (8.76%) were the most abundant. In vitro digestion experiments showed that after 120 min of small intestine digestion, the maximum FFAs release level of the kernel oil was 75.02%, which was lower than that of soybean oil (89.63%).

[Effect of SIRT1 regulating Nrf2/HO-1 signaling pathway on sepsis-induced acute lung injury].

OBJECTIVE: To investigate whether silence information regulator 1 (SIRT1) could regulate nuclear factor E2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling pathway and its role in acute lung injury (ALI) in sepsis rats. METHODS: Twenty-four male Sprague-Dawley (SD) rats were randomly divided into sham operation group (Sham group), cecal ligation and puncture (CLP) induced sepsis group (CLP group), sepsis+SIRT1 specific agonist group (CLP+SRT1720 group,10 mg/kg SRT1720 was intraperitoneally injected 2 hours before CLP), sepsis+SIRT1 specific inhibitor group (CLP+EX527 group, 10 mg/kg EX527 was intraperitoneally injected 2 hours before CLP), with 6 rats in each group. The rats were killed 24 hours after modeling and their lung tissues were taken for pathological score (Smith score), superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), interleukins (IL-6, IL-1ß), and SIRT1, Nrf2 and HO-1 mRNA and protein expression were detected. RESULTS: The lung tissue of the CLP group mice was severely damaged, the alveolar interval was widened and a large number of inflammatory cells infiltrated, and there was visible pulmonary capillary hyperemia. The Smith score, the levels of TNF-α, IL-6, IL-1ß, MDA and 8-OHdG were significantly increased, the levels of SOD, GSH, SIRT1, Nrf2 and HO-1 were significantly decreased in CLP group. After using SIRT1 specific agonist, the lung injury in CLP+SRT1720 group was significantly alleviated compared with that in CLP group, Smith score and lung tissue TNF-α, IL-6, and IL-1ß levels were significantly decreased [Smith score: 2.83±0.75 vs. 5.67±0.52, TNF-α (ng/L): 36.78±5.36 vs. 66.99±5.44, IL-6 (ng/L): 23.97±3.76 vs. 45.70±4.16, IL-1ß (ng/L): 16.76±1.39 vs. 39.64±2.59, all P < 0.05], SOD activity and GSH content increased [SOD (kU/g): 115.88±3.31 vs. 101.65±1.09, GSH (µmol/g): 8.42±0.81 vs. 5.74±0.46, both P < 0.05], MDA and 8-OHdG contents decreased [MDA (µmol/g): 5.24±0.33 vs. 9.86±0.66, 8-OHdG (ng/L): 405.76±8.54 vs. 647.12±10.64, both P < 0.05], the mRNA and protein expressions of SIRT1, Nrf2 and HO-1 were increased [SIRT1 mRNA (2-ΔΔCT): 1.49±0.15 vs. 0.64±0.03, Nrf2 mRNA (2-ΔΔCT): 1.19±0.08 vs. 0.84±0.02, HO-1 mRNA (2-ΔΔCT): 1.80±0.41 vs. 0.64±0.11, SIRT1 protein (SIRT1/ß-actin): 1.03±0.06 vs. 0.52±0.05, Nrf2 protein (Nrf2/ß-actin): 1.14±0.10 vs. 0.63±0.05, HO-1 protein (HO-1/ß-actin): 1.01±0.11 vs. 0.73±0.03, all P < 0.05]. The lung injury in CLP+EX527 group was more severe than that in CLP group, Smith score and lung tissue TNF-α, IL-6, IL-1ß levels were significantly increased [Smith score: 8.00±0.89 vs. 5.67±0.52, TNF-α (ng/L): 87.15±4.23 vs. 66.99±5.44, IL-6 (ng/L): 66.79±2.93 vs. 45.70±4.16, IL-1ß (ng/L): 58.99±2.12 vs. 39.64±2.59, all P < 0.05], SOD activity and GSH content decreased [SOD (kU/g): 72.84±3.85 vs. 101.65±1.09, GSH (µmol/g): 3.30±0.67 vs. 5.74±0.46, both P < 0.05], the contents of MDA and 8-OHdG were increased [MDA (µmol/g): 14.14±0.70 vs. 9.86±0.66, 8-OHdG (ng/L): 927.66±11.47 vs. 647.12±10.64, both P < 0.05], the mRNA and protein expressions of SIRT1, Nrf2 and HO-1 were decreased [SIRT1 mRNA (2-ΔΔCT): 0.40±0.07 vs. 0.64±0.03, Nrf2 mRNA (2-ΔΔCT): 0.48±0.07 vs. 0.84±0.02, HO-1 mRNA (2-ΔΔCT): 0.27±0.14 vs. 0.64±0.11, SIRT1 protein (SIRT1/ß-actin): 0.20±0.05 vs. 0.52±0.05, Nrf2 protein (Nrf2/ß-actin): 0.45±0.01 vs. 0.63±0.05, HO-1 protein (HO-1/ß-actin): 0.36±0.08 vs. 0.73±0.03, all P < 0.05]. CONCLUSIONS: In the rat model of ALI induced by sepsis, SIRT1 can regulate the activation of Nrf2/HO-1 signaling pathway, upregulate the expression of downstream antioxidant enzymes, reduce oxidative stress injury, and then alleviate the ALI induced by sepsis in rats.

Highly Valuable Fish Oil: Formation Process, Enrichment, Subsequent Utilization, and Storage of Eicosapentaenoic Acid Ethyl Esters.

In recent years, as the demand for precision nutrition is continuously increasing, scientific studies have shown that high-purity eicosapentaenoic acid ethyl ester (EPA-EE) functions more efficiently than mixed omega-3 polyunsaturated fatty acid preparations in diseases such as hyperlipidemia, heart disease, major depression, and heart disease; therefore, the market demand for EPA-EE is growing by the day. In this paper, we attempt to review EPA-EE from a whole-manufacturing-chain perspective. First, the extraction, refining, and ethanolysis processes (fish oil and ethanol undergo transesterification) of EPA-EE are described, emphasizing the potential of green substitute technologies. Then, the method of EPA enrichment is thoroughly detailed, the pros and cons of different methods are compared, and current developments in monomer production techniques are addressed. Finally, a summary of current advanced strategies for dealing with the low oxidative stability and low bioavailability of EPA-EE is presented. In conclusion, understanding the entire production process of EPA-EE will enable us to govern each step from a macro perspective and accomplish the best use of EPA-EE in a more cost-effective and environmentally friendly way.

Synergism of 64Cu-Labeled RGD with Anti-PD-L1 Immunotherapy for the Long-Acting Antitumor Effect.

We put forward a novel targeting-triggering-therapy (TTT) scheme that combines 64Cu-based targeted radionuclide therapy (TRT) with programmed death-ligand 1 (PD-L1)-based immunotherapy for enhancing therapeutic efficacy. The αvß3 integrin-targeted 64Cu-DOTA-EB-cRGDfK (64Cu-DER) was synthesized. Flow cytometry, immunofluorescence staining, and RT-qPCR were performed to verify PD-L1 upregulation after irradiation with 64Cu-DER. Positron emission tomography imaging was performed to investigate the prominent tumor retention property of 64Cu-DER. In the MC38 tumor model, anti-PD-L1 antibody (αPD-L1 mAb) was delivered in a concurrent or sequential manner after 64Cu-DER was injected, followed by the testing of changes in tumor microenvironment (TME). PD-L1 was upregulated in a time- and dose-dependent manner after being induced by 64Cu-DER. The combination of 64Cu-DER TRT (925 MBq/kg) and αPD-L1 mAb (10 mg/kg) resulted in significant delay in tumor growth and protected against tumor rechallenge. Blockade of PD-L1 at 4 h after 64Cu-DER TRT (64Cu-DER + αPD-L1 mAb @ 4 h combination group) was able to achieve 100% survival rate, prevent tumor relapse, and evidently prolong the survival of mice. In summary, the combination of 64Cu-DER and αPD-L1 mAb in a time-dependent manner could be a promising approach to improve therapeutic efficacy. Understandably, this strategy has the potential to extend the scope of 64Cu-based TTT and merits translation into clinical practice for the better management of immune checkpoint blockade immunotherapy.

Effect of olive polyphenols on lipid oxidation of high-fat beef during digestion.

Olive oil is one of the most important ingredients in the Mediterranean diet, in which its polyphenols adversely affect dietary lipid oxidation. In this study, the effect of olive oil polyphenols on lipid oxidation of high-fat beef during digestion was determined. Thirty-three phenolic compounds were tentatively identified, and the contents of 3,4-dihydroxyphenylethanol-elenolic acid dialdehyde (3,4-DHPEA-EDA), 3,4-dihydroxyphenylethanol-elenolic acid (3,4-DHPEA-EA), p-hydroxyphenylethanol elenolic acid (p-HPEA-EA) and hydroxytyrosol were higher than those of other compounds. In an in vitro model, the production of lipid oxidation products, including hydroperoxides, malondialdehyde, 4-hydroxy-2-hexenal and 4-hydroxy-2-nominal, were significantly inhibited by olive polyphenol in the gastrointestinal digests. Compared with the other four groups, the inhibition was better when the polyphenol content reached 600 mg GAE/kg. The 3,4-DHPEA-EDA and 3,4-DHPEA-EA played a better antioxidant role in the stomach stage, while hydroxytyrosol showed the more potent antioxidant activity in the intestinal phase. Electron spin resonance technology showed that two main free radicals, including alkyl radical and alkoxy radical, were detected during the high-fat beef digestion, and olive polyphenols could significantly reduce their formation. All these results showed that the lipid oxidation could be significantly inhibited by olive oil with higher polyphenol content, indicating that the consumption of olive oil with abundant levels of polyphenols could reduce lipid oxidation of high-fat meat during digestion.

PD-L1-Targeted Radionuclide Therapy Combined with αPD-L1 Antibody Immunotherapy Synergistically Improves the Antitumor Effect.

Immune checkpoint blockers (ICBs) targeting programmed death receptor 1 (PD-1) ligand 1 (PD-L1) for immunotherapy have radically reformed oncology. It is of great significance to enhance the response rate of ICB in cancer patients. Here, a radioiodinated anti-PD-L1 antibody (131I-αPD-L1) was developed for PD-L1-targeted single-photon emission computed tomography (SPECT) imaging and αPD-L1 immunotherapy. Flow cytometry and immunofluorescence staining were performed to identify PD-L1 upregulation in a time- and dose-dependent manner after being induced by 131I-αPD-L1. ImmunoSPECT imaging and biodistributions of 131I-αPD-L1 in CT26, MC38, 4T1, and B16F10 tumor models were conducted to visualize the high tumor uptake and low background signal. Compared to monotherapy alone, concurrent administration of αPD-L1 mAb and 131I-αPD-L1 revealed improved tumor control in murine tumor models. The combination of 11.1 MBq of 131I-αPD-L1 and 200 µg of αPD-L1 mAb resulted in significant tumor growth delay and prolonged survival. This radioligand synergized immunotherapy strategy holds great potential for cancer management.

Evans blue-modified radiolabeled fibroblast activation protein inhibitor as long-acting cancer therapeutics.

Rationale: Fibroblast activation protein (FAP) targeted molecular imaging radiotracers have shown promising preclinical and clinical results in tumor diagnosis. However, rapid clearance and inadequate tumor retention of these molecules have hindered them for further clinical translation in cancer therapy. In this study, we aimed to develop a series of albumin binder-truncated Evans blue (EB) modified FAP targeted radiotracers, and optimize the pharmacokinetic (PK) characteristics to overcome the existing limitations in order to apply in the radionuclide therapy of cancer. Methods: A series of compounds with the general structure of EB-FAPI-Bn were synthesized based on a FAP inhibitor (FAPI) variant (FAPI-02) and radiolabeled with 177LuCl3. To verify the binding affinity and FAP targeting specificity of these tracers in vitro, U87MG cell uptake and competition assays were performed. Preclinical PK was evaluated in U87MG tumor-bearing mice using SPECT imaging and biodistribution studies. The lead compound EB-FAPI-B1 was selected and cancer therapeutic efficacy of 177Lu-EB-FAPI-B1 was assessed in U87MG tumor-bearing mice. Results:177Lu-EB-FAPI-B1, B2, B3, B4 were stable in PBS (pH 7.4) and saline for at least 24 h. EB-FAPI-B1 showed high binding affinity (IC50 = 16.5 nM) to FAP in vitro, which was comparable with that of FAPI-02 (IC50 = 10.9 nM). SPECT imaging and biodistribution studies of 177Lu-EB-FAPI-B1, B2, B3, B4 have proved their prominently improved tumor accumulation and retention at 96 h post-injection, especially for 177Lu-EB-FAPI-B1, high tumor uptake and low background signal make it the optimal compound. Compared to the saline group, noteworthy tumor growth inhibitions of 177Lu-EB-FAPI-B1 have been observed after administration of different dosages. Conclusion: In this study, several EB modified FAPI-02 related radiopharmaceuticals have been synthesized successfully and evaluated. High binding affinity and FAP targeting specificity were identified in vitro and in vivo. Remarkably enhanced tumor uptake and retention of EB-FAPI-B1 were found over the unmodified FAPI-02. 177Lu-EB-FAPI-B1 showed remarkable tumor growth suppression in U87MG tumor model with negligible side effects, indicating that 177Lu-EB-FAPI-B1 is promising for clinical application and transformation.

Effect of phenolic extracts from Camellia oleifera seed cake on the formation of polar compounds, core aldehydes, and monoepoxy oleic acids during deep-fat frying.

The frying process is an excellent way to obtain food with desirable sensory. However, some harmful substances, such as aldehydes and monoepoxy oleic acids, could also be produced. This study mainly explores the inhibition of polyphenols from the Camellia oleifera seed cake extract (CSCE) on the formation of polar compounds, core aldehydes, and monoepoxy oleic acids during deep-fat frying. The results showed that the CSCE could significantly decrease peroxide, p-anisidine, total polar, and monoepoxy oleic acids compared with other groups. In addition, the CSCE could significantly inhibit the generation of oxidized triacylglycerol polymer (TGP) and oxidized triacylglycerol (ox-TG), indicating its anti-polymerization activity. The total amount of core aldehydes and glycerol ester core aldehydes (9-oxo) in soybean oil was significantly reduced. Furthermore, CSCE had a better inhibitory effect on monoepoxy fatty acids than TBHQ. Our results might be helpful to provide a basis for the search for new natural antioxidants.

Effect of palm stearin on the physicochemical characterization and capsaicinoid digestion of Sichuan hotpot oil.

Beef tallow (BT) is the common hotpot oil used in Sichuan hotpot, increasing its characteristic flavors and making it taste better. However, the cholesterol content in BT is high, which may induce cardiovascular diseases. In this study, the effect of palm stearin (PS) on Sichuan hotpot oil was evaluated. The PS: BT blends showed similar physicochemical properties to BT from the results of sensory evaluation, pulsed NMR, DSC, and polar light micrograph (PLM). Furthermore, since spiciness is the essential characteristic of Sichuan hotpot, the digestive properties of capsaicinoids in hotpot oil were used as an evaluation index. The results showed that the digestive properties of capsaicinoids in hotpot oil containing PS were consistent with those without PS. In conclusion, PS can be partially used to replace BT, which can broaden the types of oil used for hotpot and help develop a new hotpot oil.

Effect of different processing methods on physicochemical properties, chemical compositions and in vitro antioxidant activities of Paeonia lactiflora Pall seed oils.

A research was performed to determine and compare the physicochemical properties, chemical compositions and in vitro antioxidant activities of Paeonia lactiflora Pall seed oils with ultrasonic-assisted solvent extraction, pressing and supercritical fluid extraction. Paeonia lactiflora Pall seed oil contained a high percentage of polyunsaturated fatty acids and monounsaturated fatty acids, especially oleic (31.62-32.88%) and α-linolenic acids (37.55-39.95%). The beneficial multiple dietary phytochemicals (tocopherol, phytosterols and squalene) and in vitro antioxidant activity were significantly influenced by the hull and processing method (P＜0.05). However, higher tocopherol (596.67-738.76 mg/kg) and phytosterols (5775.01-6055.62 mg/kg) contents were found in supercritical fluid extraction oils. Additionally, ten individual polyphenols were quantified, and significantly influenced by the hull and processing method (P＜0.05), with the content of benzoic acid and several individual flavonoids being the higher. According to the results, pressing might be the best process for extracting oil with a high number of polyphenols.

Facile Preparation of Epoxide-Functionalized Surfaces via Photocurable Copolymer Coatings and Subsequent Immobilization of Iminodiacetic Acids.

Herein, we report a simple coat/cure preparation of epoxide-functionalized surfaces using a photocurable copolymer technology. The photocurable copolymer, poly(glycidyl methacrylate- co-butyl acrylate- co-4-benzoylphenyl methacrylate) (GBB), was synthesized by single electron transfer-living radical polymerization (SET-LRP). The epoxide content in the copolymer was tuned by controlling the content of glycidyl methacrylate. Three copolymers, GBB(1), GBB(2), and GBB(3), with epoxide contents of 22, 63, and 91 mol %, respectively, were cast onto polypropylene films and photocured by UV-light exposure. Subsequently, iminodiacetic acids (IDA) were immobilized onto the GBB-coated materials via a ring-opening reaction. The IDA-functionalized coatings GBB(1)-IDA, GBB(2)-IDA, and GBB(3)-IDA presented IDA contents of 1.47 ± 0.08, 18.67 ± 1.46, and 49.05 ± 2.88 nmol/cm2, respectively, which increased as the epoxide content increased. The IDA-functionalized GBB coatings exhibited metal chelating capability toward transition metal ions (e.g., iron and copper). The reported photocurable copolymer technology offers a facile and tunable preparation of epoxide-functionalized surfaces, with potential extended applications in biopatterning, active packaging, and nanotechnology.

Synthesis, Processing, and Characterization of Helical Polypeptide Rod-Coil Mixed Brushes.

Mixed polymer brushes of rod-type polypeptide and coil-type vinyl polymer brushes were synthesized via two sequential steps of vapor deposition surface-initiated ring-opening polymerization (SI-ROP) and surface-initiated atom transfer radical polymerization (SI-ATRP), respectively. The effect on polypeptide brushes by coil-type brushes of their surface morphology, film thickness, and orientation were investigated before and after solvent quenching processes using chloroform and acetone. Before solvent quenching, the as-grown coil-type brushes forced the polypeptide brushes to stand up from the surface, resulting in higher film thickness, but the polypeptide brushes remained randomly oriented. After solvent quenching, polypeptide brushes tended to aggregate into conical bundles with an orientation perpendicular to the substrate, but coil-type brushes restricted the free arrangement of the polypeptide brushes and lessen their upward movement. Changes in film thickness, rod orientation, morphology, and wettability were observed with increased molecular weight of the coil-type polymer in the mixed brushes.

Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation of the nutritional anti-inflammatory pathway.

Enteral administration of lipid-enriched nutrition effectively attenuates inflammation via a cholecystokinin (CCK)-mediated vagovagal anti-inflammatory reflex. Cholecystokinin release and subsequent activation of the vagus are dependent on chylomicron formation and associated with release of additional gut peptides. The current study investigates the intestinal processes underlying activation of the CCK-mediated vagal anti-inflammatory pathway by lipid-enriched nutrition. Rats and mice were subjected to hemorrhagic shock (HS) or endotoxemia, respectively. Prior to the experimental procedures, animals were fasted or fed lipid-enriched nutrition. Pluronic L-81 (L-81) was added to the feeding to investigate involvement of chylomicron formation in activation of mesenteric afferent fibers and the immune-modulating potential of lipid-enriched nutrition. Ob/Ob mice and selective receptor antagonists were used to study the role of leptin, glucagon-like peptide 1 and peptide YY in activation of the nutritional reflex. Electrophysiological analysis of mesenteric afferents in mice revealed that lipid-enriched nutrition-mediated neural activation was abrogated by L-81 (P<.05). L-81 blunted the beneficial effects of lipid-enriched nutrition on systemic inflammation and intestinal integrity in both species (all parameters, P<.01). Ob/Ob mice required a higher dose of nutrition compared with wild-type mice to attenuate plasma levels of TNF-α and ileum-lipid binding protein, a marker for enterocyte damage (both P<.01), suggesting a higher stimulation threshold in leptin-deficient mice. Administration of a glucagon-like peptide 1-receptor antagonist, but not leptin or peptide YY antagonists, suppressed the effects of lipid-enriched nutrition. These data indicate that chylomicron formation is essential and activation of the glucagon-like peptide 1-receptor is involved in activation of the nutritional anti-inflammatory pathway by lipid-enriched nutrition.

Lipid-enriched enteral nutrition controls the inflammatory response in murine Gram-negative sepsis.

OBJECTIVES: Controlling the inflammatory cascade during sepsis remains a major clinical challenge. Recently, it has become evident that the autonomic nervous system reduces inflammation through the vagus nerve. The current study investigates whether nutritional stimulation of the autonomic nervous system effectively attenuates the inflammatory response in murine Gram-negative sepsis. DESIGN: Controlled in vivo and ex vivo experimental study. SETTINGS: Research laboratory of a university hospital. SUBJECTS: Male C57bl6 mice. INTERVENTIONS: Mice were intraperitoneally challenged with lipopolysaccharide derived from Escherichia coli. Before lipopolysaccharide administration, mice were fasted or enterally fed either lipid-rich nutrition or low-lipid nutrition. Antagonists to cholecystokinin receptors or nicotinic receptors were administered before lipopolysaccharide administration. Blood and tissue samples were collected at 90 mins. Mesenteric afferent discharge was determined in ex vivo preparations in response to both nutritional compositions. MEASUREMENTS AND MAIN RESULTS: Both lipid-rich and low-lipid nutrition dose-dependently reduced lipopolysaccharide-induced tumor necrosis factor-α release (high dose: both 1.4 ± 0.4 ng/mL) compared with fasted mice (3.7 ± 0.8 ng/mL; p < .01). The anti-inflammatory effect of both nutritional compositions was mediated through cholecystokinin receptors (p < .01), activation of mesenteric vagal afferents (p < .05), and peripheral nicotinic receptors (p < .05). Lipid-rich nutrition attenuated the inflammatory response at lower dosages than low-lipid nutrition, indicating that enrichment of enteral nutrition with lipid augments the anti-inflammatory potential. Administration of lipid-rich nutrition prevented endotoxin-induced small intestinal epithelium damage and reduced inflammation in the liver and spleen compared with fasted (all p < .01) and low-lipid nutrition controls (all p < .05). CONCLUSIONS: The current study demonstrates that lipid-rich nutrition attenuates intestinal damage and systemic as well as organ-specific inflammation in murine Gram-negative sepsis through the nutritional vagal anti-inflammatory pathway. These findings implicate enteral administration of lipid-enriched nutrition as a promising intervention to modulate the inflammatory response during septic conditions.