Physicochemical and Structural Properties of Gluten-Konjac glucomannan Conjugates Prepared by Maillard Reaction.

Gluten (Glu) is important to wheat products by forming a three-dimensional matrix. This study aimed to investigate the physicochemical and structural properties of gluten after conjugation with konjac glucomannan (KGM) through the Maillard reaction. The study revealed that the degree of graft increased with the prolonged reaction time. The Glu-KGM conjugates were possessed of increased ß-sheet but decreased α-helix and ß-turn, as well as unfolding and loose tertiary structures as the reaction proceeded. Among three different proportions, the Glu-KGM 1:1 conjugate was proved to have the most excellent foaming and emulsifying properties, and could form more rigid and firm gelation structures, which could be related to the decreased particle size and increased zeta potential of the conjugate. Overall, the physicochemical and structural properties of gluten were significantly related to the KGM ratios as well as the reaction period.

Photodynamic Effect of Riboflavin on Chitosan Coatings and the Application in Pork Preservation.

Riboflavin (RF) was considered to be possessed of photoactivity to generate reactive oxygen species (ROS) under ultraviolet (UV) light, which is thought to be a favorable antibacterial candidate. Herein, RF was incorporated into chitosan (CS) coatings and treated under UV with different exposure times (2, 4, and 6 h) to improve the physicochemical and antibacterial properties. The results showed that the light transmittance and antibacterial performance of chitosan coatings gradually increased with the extension of the UV irradiation time. The antibacterial ability of chitosan coatings correlated with the generation of ROS: ∙OH and H2O2, which achieved 1549.08 and 95.48 µg/g, respectively, after 6 h irradiation. Furthermore, the chitosan coatings with UV irradiation also reduced the pH value, total volatile basic nitrogen (TVB-N), ΔE, and total viable counts (TVC) and improved sensory attributes of pork. In conclusion, the UV irradiated chitosan coatings could be used as an environmentally friendly antimicrobial packaging material to effectively delay the spoilage of pork, maintain its sensory quality and prolong its shelf life.

Public Space Satisfaction Evaluation of New Centralized Communities in Urban Fringe Areas-A Study of Suzhou, China.

The fast and pronounced changes in dwelling space in urban fringe areas, caused by rapid urbanization, has led to the appearance of new centralized communities. These communities possess characteristics of both urban and rural communities and have been facing great pressure related to the reconstruction of social network relations and the cultivation of a community identity. The outcomes of public space satisfaction evaluations are related to the social functions they fulfill, such as motivating social interaction, cultivating community identity, and integrating social relationships. This study evaluates public space satisfaction based on the study of six new centralized communities in an urban fringe area of Suzhou, using grey relational analysis. The results show that the overall satisfaction value is a standard level. Moreover, public space satisfaction is related to patterns of centralization and factors of social culture; especially the latter has great influence on public space satisfaction. Factors related to public space satisfaction can generally be divided into quadrants of "Low Satisfaction-High Significance" and "High Satisfaction-Low Significance." According to the inverse correlation between satisfaction level with public space and significance of indexes, we propose that indexes of public space satisfaction in the "Low Satisfaction-High Significance" quadrant should be improved greatly during the process of the optimization and construction of public spaces in new centralized communities.

The application of photodynamic inactivation to microorganisms in food.

Nowadays, food safety issues have drawn increased attention due to the continual occurrence of infectious diseases caused by foodborne pathogens, which is an important factor causing food safety hazard. Meanwhile, the emergence of an increasing number of antibiotic-resistant pathogens is a worrisome phenomenon. Therefore, it is imperative to find new technologies with low-cost to inactivate pathogenic microorganisms and prevent cross-contamination. Compared with traditional preservatives, photodynamic inactivation (PDI) has emerged as a novel and promising strategy to eliminate foodborne pathogens with advantages such as non-toxic and low microbial resistance, which also meets the demand of current consumers for green treatment. Over the past few years, reports of using this technology for food safety have increased rapidly. This review summarizes recent progresses in the development of photodynamic inactivation of foodborne microorganisms. The mechanisms, factors influencing PDI and the application of different photosensitizers (PSs) in different food substrates are reviewed.

Use of the modified Glasgow Coma Scale score to guide sequential invasive-noninvasive mechanical ventilation weaning in patients with AECOPD and respiratory failure.

Sequential invasive-noninvasive ventilation (NIV) improves the outcomes of patients with respiratory failure caused by acute exacerbation of chronic obstructive pulmonary disease (AECOPD); however, there is no clear consensus on the optimal timing of the switch to sequential invasive-NIV in these patients. In the present study, a potential role for the modified Glasgow Coma Scale (GCS) score to guide sequential weaning was investigated. Patients with AECOPD and respiratory failure were prospectively recruited from three study centers (Wenling Hospital Affiliated to Wenzhou Medical University, the First Affiliated Hospital of Wenzhou Medical University and Changsha Central Hospital) between January 1st 2016 and December 31st 2018. Patients were randomly assigned to group A and B, with the switching point for sequential weaning strategy in the two groups being a modified GCS score ≥13 and 10 points, respectively. Each group included 240 patients. Baseline demographic characteristics were comparable in the two groups. The duration of invasive mechanical ventilation (IMV) in group A was significantly shorter than that in group B. However, there were no significant between-group differences with respect to the incidence of re-intubation, ventilator-associated pneumonia, in-hospital mortality or the length of hospital stay. Use of a modified GCS score ≥13 as the switching point for sequential invasive-NIV may help decrease the duration of IMV in patients with AECOPD and respiratory failure.

Productive transcription of miR-124-3p by RelA and RNA polymerase II directs RIP1 ubiquitination-dependent apoptosis resistance during hypoxia.

The K63-linked ubiquitination of RIP1 coordinates survival/death homeostasis by driving transcription of genes downstream of RelA. Previously, we demonstrated that EGF-dependent RelA transactivation overcomes hypoxia-initiated apoptosis, yet the underlying mechanisms remain mysterious. We report here that UBXN1 deficiency empowers apoptosis resistance against hypoxia through triggering IκBα degradation, for which K63-linked ubiquitination of RIP1 is required. MiR-124-3p is a bona fide inhibitor upstream of UBXN1, thereby antagonizing the hypoxia-initiated apoptosis. UBXN1 repression by miR-124-3p restores the K63-linked ubiquitination of RIP1, IKKß phosphorylation, IκBα-RelA disassembly, RelA nuclear localization and transactivation of EGF gene as well as EGF secretion under hypoxia. Reconstitution of wild-type UBXN1, but not a truncated UBXN1ΔUBA mutant, or pharmacological inhibition of RelA transactivation in miR-124-3p-replete cells compromises the apoptosis-resistant phenotypes of miR-124-3p. Hypoxia transcriptionally downregulates miR-124-3p by disassociating RelA and RNAP II from its promoter. EGFR activation renders the K63-linked ubiquitination of RIP1 and hypoxic tolerance in conjunction with miR-124-3p. Our findings identify a pivotal role of miR-124-3p in ubiquitin conjugation of RIP1 against hypoxic damage and underscore that productive transcription of miR-124-3p by RelA and RNAP II might be a switching mechanism for this process.

Blocking CXCR1/2 contributes to amelioration of lipopolysaccharide-induced sepsis by downregulating substance P.

OBJECTIVES: C-X-C chemokine receptor types 1/2 (CXCR1/2) is known to be activated in liver damage in acute-on-chronic liver failure; however, the role in lipopolysaccharide (LPS)-induced sepsis is unknown. The current study was designed to determine whether or not CXCR1/2 blockade with reparixin ameliorates acute lung injury (ALI) by affecting neuropeptides in a LPS-induced sepsis mouse model. MATERIALS AND METHODS: Male C57BL/6 mice (10 to 14-week old) were divided into sham, LPS, sham-R, and LPS-R groups. Bronchoalveolar lavage fluid (BALF) was collected and evaluated. The lung histopathology was assessed by immunocytochemistry staining. Western blot analysis was used to measure myeloperoxidase, substance P (SP), and vasoactive intestinal peptide. RESULTS: LPS-induced animal models were ameliorated by cotreatment with a CXCR1/2 antagonist. Moreover, the protective effects of CXCR1/2 antagonists were attributed to the increased secretion of pro-opiomelanocortin and decreased the secretion of SP. Reparixin decreased the expression of necroptosis cell death markers induced by LPS. CONCLUSION: The results of this study indicate that blockade of CXCR1/2 may represent a promising therapeutic strategy for the treatment of sepsis-associated ALI through regulation of neuropeptides and necroptosis.

Ulinastatin attenuates liver injury and inflammation in a cecal ligation and puncture induced sepsis mouse model.

Sepsis is a syndrome of life-threatening multiorgan dysfunction caused by host response dysregulation to infection. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory properties and has been suggested to modulate lipopolysaccharide-induced sepsis. However, little is known about the mechanism underlying its effects on sepsis. In the current study, we investigated the protective effect of UTI on liver injury in a cecal ligation and puncture (CLP)-induced sepsis of C57BL/6 mouse model and explored the possible mechanisms. Mice underwent CLP as sepsis models and were randomized into five groups including the sham group, UTI group, CLP group, UTI-L group, and UTI-H group. UTI was intraperitoneally administered at doses of UTI 1500 U/100 g (UTI-L group) or 3000 U/100 g (UTI-H group), before CLP. The mice were killed, and immunohistochemical changes, cytokine levels, and antioxidant enzyme activities were detected. Our results showed that UTI ameliorated CLP-mediated increases in serum aspartate aminotransferase and alanine aminotransferase activities, histological activity index, degenerative region ratio, and infiltrated inflammatory cell numbers. Moreover, UTI also decreased nitrotyrosine and 4-hydroxynonenal, activated caspase-3, and activated poly (ADP-ribose) polymerase (PARP) levels and inhibited the mitogen-activated protein kinase pathway activation in liver tissues. Our results indicated that UTI could inhibit CLP-induced liver injury by suppressing inflammation and oxidation. Our results indicated that UTI may serve as a potential therapeutic agent for sepsis.

Gastric Adenocarcinoma Predictive Long Intergenic Non-Coding RNA Promotes Tumor Occurrence and Progression in Non-Small Cell Lung Cancer via Regulation of the miR-661/eEF2K Signaling Pathway.

BACKGROUND/AIMS: Long non-coding RNAs (lncRNAs) play vital roles in carcinogenesis as oncogenes or tumor suppressor genes. This study explored the biological function of lncRNA gastric adenocarcinoma predictive long intergenic non-coding RNA (GAPLINC) in human non-small cell lung cancer (NSCLC). METHODS: GAPLINC expression in NSCLC specimens and cell lines was detected by qRT-PCR and Western blot. The effect of GAPLINC on cell proliferation was investigated using CCK8-assay, colony formation assay, and xenograft model. The effects of GAPLINC on apoptosis and cell cycle were determined using flow cytometry. The mechanism of GAPLINC involved in NSCLC was explored using Western blot, luciferase reporter assay, and RNA fluorescence in situ hybridization. RESULTS: We found that GAPLINC expression was up-regulated in NSCLC tissues and cell lines. Overexpression of GAPLINC was associated with poor prognosis in patients with NSCLC. Silencing of GAPLINC significantly inhibited cell proliferation, promoted apoptosis, and induced cell cycle arrest in the G0/G1 phase. Results from xenograft transplantation showed that GAPLINC silencing inhibited the tumor growth in vivo. Interestingly, GAPLINC silencing decreased the expression of eukaryotic elongation factor-2 kinase (eEF2K) protein both in vivo and in vitro. Bioinformatic analysis and luciferase reporter confirmed that miR-661 targeted GAPLINC and eEF2K 3'-UTR and was negatively correlated with the expression of GAPLINC and eEF2K. CONCLUSION: Our findings indicate that GAPLINC promotes NSCLC tumorigenesis by regulating miR-661/eEF2K cascade and provide new insights for the pathogenesis underlying NSCLC and potential targets for therapeutic strategy.

microRNA-300/NAMPT regulates inflammatory responses through activation of AMPK/mTOR signaling pathway in neonatal sepsis.

AIM: Rapid and accurate diagnosis of neonatal sepsis (NS) is highly warranted because of high associated morbidity and mortality. The study aims to evaluate the effects of miR-300 on inflammatory responses in a septic neonate mouse model. METHODS: A septic mouse model was established by intraperitoneal (i.p.) cecal slurry (CS) injection in order to validate the effect of miR-300 on the inflammatory response in endothelial cells. Bioinformatics tools and luciferase activity were employed to detect the target of miR-300. Serum inflammatory factors were determined by ELISA assay. RT-qPCR and western blot analysis were used to determine the gene expressions. Flow cytometry was employed to evaluate cell apoptosis. RESULTS: Gain- and loss-of-function studies revealed that miR-300 overexpression augmented autophagy, inhibited cell apoptosis, enhanced cell cycle entry in endothelial cells, and decreased inflammatory response through the regulation of pro- and anti-apoptotic factors in endothelial cells. The effect of miR-300on endothelial cells was upregulated after nicotinamide phosphoribosyltransferase (NAMPT) silencing and AMPK/mTOR signaling pathway activation, indicating that miR-300 influences sepsis via suppressing NAMPT and triggering the AMPK/mTOR signaling pathway. CONCLUSIONS: Our study provides evidence indicating that overexpressedmiR-300 enhances autophagy by targeting NAMPT through activation of the AMPK/mTOR signaling pathway in septic mouse models, indicating it may serve as a potential therapeutic target for sepsis.

Transient receptor potential ankyrin 1 protects against sepsis-induced kidney injury by modulating mitochondrial biogenesis and mitophagy.

This study was undertaken to investigate the cytoprotective role of transient receptor potential ankyrin 1 (TRPA1) in sepsis-induced kidney injury. The Cecal ligation and puncture (CLP) was employed to induce septic kidney injury in C57BL/6 mice. Six hours before CLP or a sham procedure, mice were injected intraperitoneally with 10 mg/kg hemin or 30 mg/kg of the TRPA1 antagonist A-967079. Our study showed that mice treated with A-967079 exhibited less sepsis-induced mortality and kidney injury compared with those in the sham group. Moreover, A-967079 prevented multiple organ dysfunction, pathological changes, and increased secretion of in proinflammatory cytokines. In addition, A-967079 decreased the levels of mitochondrial lipid peroxidation and mitochondrial dysfunction in kidney tissues. The protein levels of mitochondrial biogenesis markers, including Sirt1, nuclear respiratory factor 1, and mitochondrial transcription factor A, were decreased in the A-967079 treatment group. Additionally, A-967079 treatment attenuated mitochondrial mitophagy. The levels of PTEN-induced putative kinase 1 increased and parkin levels decreased compared to the untreated CLP group. Our findings suggest that TRPA1 prevents septic injury by modulating mitochondrial biogenesis and mitophagy.