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Background: Undernutrition is the main reason for the use of artificial nutrition in patients with severe neurological diseases. However, the clinical and immunological outcomes of enteral nutrition supplemented with immunomodulatory nutrients in these patients remain unclear.Methods: In this single-center, randomized controlled study, 57 patients with severe neurological diseases were randomly divided into the following two groups according to the type of enteral nutrition they would receive: immune-enhancing (IE) (n = 27) and non-IE (NIE) (n = 30). The IE and NIE groups received enteral nutrition supplemented with immunomodulatory nutrients and standard enteral nutrition, respectively. We compared the nutritional status and the state of cellular immunity between the patients of the two groups. Clinical and immunological variables were evaluated following nutritional treatment.Results: Feeding intolerance was lower in the IE than that in the NIE group (P = 0.04). However, there were no significant differences between the results of the two groups in terms of length of stay in the intensive care unit or hospital, extubation time, or body mass index (P > 0.05). The CD4+ T-lymphocyte count and CD4+/CD8+ ratio in the peripheral blood increased significantly in the IE group. The expression of CD28 activated cell surface markers was higher in the IE than in the NIE group. In addition, increased plasma interferon-γ levels were recorded in the IE group, whereas the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, and IL-10 decreased.Conclusions: Immune-enhanced enteral nutrition could improve the immune status and feeding tolerance in patients with severe neurological diseases.Trial Registration:www.chictr.org.cn/index.aspx, identifier: ChiCTR-IPR-17013909.

Personalized assessment and treatment of severe patients with COVID-19 pneumonia have greatly affected the prognosis and survival of these patients. This study aimed to develop the radiomics models as the potential biomarkers to estimate the overall survival (OS) for the COVID-19 severe patients. A total of 74 COVID-19 severe patients were enrolled in this study, and 30 of them died during the follow-up period. First, the clinical risk factors of the patients were analyzed. Then, two radiomics signatures were constructed based on two segmented volumes of interest of whole lung area and lesion area. Two combination models were built depend on whether the clinic risk factors were used and/or whether two radiomics signatures were combined. Kaplan–Meier analysis were performed for validating two radiomics signatures and C-index was used to evaluated the predictive performance of all radiomics signatures and combination models. Finally, a radiomics nomogram combining radiomics signatures with clinical risk factors was developed for predicting personalized OS, and then assessed with respect to the calibration curve. Three clinical risk factors were found, included age, malignancy and highest temperature that influence OS. Both two radiomics signatures could effectively stratify the risk of OS in COVID-19 severe patients. The predictive performance of the combination model with two radiomics signatures was better than that only one radiomics signature was used, and became better when three clinical risk factors were interpolated. Calibration curves showed good agreement in both 15 d survival and 30 d survival between the estimation with the constructed nomogram and actual observation. Both two constructed radiomics signatures can act as the potential biomarkers for risk stratification of OS in COVID-19 severe patients. The radiomics+clinical nomogram generated might serve as a potential tool to guide personalized treatment and care for these patients.

Background: Equipoise exists regarding the implementation of evidence-based guidelines for nutritional therapy in critical illness because some previous cluster-randomised controlled trials (cRCTs) demonstrate patient benefits whilst others do not. We aimed to resolve this issue by initiating an appropriately powered cRCT to assess whether active implementation of an evidence-based guideline for nutrition therapy in critical illness could reduce mortality. Methods: We did a multicentre, cluster-randomised, parallel-controlled trial in 97 intensive care units (ICUs) throughout China. We developed an up-to-date, evidence-based nutrition guideline. ICUs randomly allocated to implement the guideline formed a local "intervention team", which actively implemented the guideline using standardized educational materials. ICUs assigned to the control group remained unaware of the guideline. All ICUs enroled critically ill patients who were expected to stay longer than seven days. The primary outcome was all-cause mortality within 28 days of enrolment . Findings Between March, 2018 and July, 2019, we enrolled 1,373 patients at 48 guideline ICUs and 1,399 patients at 49 control ICUs. Implementation of the nutrition guideline resulted in significantly earlier enteral nutrition (EN) initiation (1.20 vs. 1.55 mean days to initiation of EN; difference -0.40 [95% CI, -0.71 to -0.09]; P=0.01) and delayed parenteral nutrition (PN) initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI, 0.44 to 1.67]; P=0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference -1.6% [95% CI -4.3% to 1.2%]; p=0.42) between study groups. Interpretation: Active implementation of an evidence-based guideline can change practice. Our active implementation strategy improved the provision of nutrition therapy to critically ill patients. However, in our cRCT, this improvement in care did not translate to a reduction in mortality. We did not identify any safety concerns associated with the active implementation of our evidence-based guideline for nutrition therapy. Trial Registration: The study was registered in the ISRCTN registry before enrolment commenced (No. ISRCTN12233792). Funding Statement: The study was funded by the Key Research and Development Program Foundation of Jiangsu Province of China (no. BE2015685) and Nutricia, Wuxi, China. Declaration of Interests: Dr. GSD reported receiving academic research grants related to nutrition in critical illness from the Australian National Health and Medical Research Council, Fresenius Kabi Deutschland GmbH and Baxter Healthcare Pty Ltd and speakers honoraria from Fresenius Kabi Deutschland GmbH, Baxter Healthcare Australia, Pty Ltd, Nestle Healthcare, Vevy, Switzerland and Nutricia Pharmaceutical (Wuxi) Co., Ltd. China. Dr. AvZ reports personal fees from Baxter, personal fees from Nestle, personal fees from Fresenius Kabi, grants and personal fees from Nutricia, grants from Cardinal Health grants from Mermaid grants from Lyric, outside the submitted work. Dr. WqL reported receiving speakers honoraria from Nutricia Pharmaceutical (Wuxi) Co., Ltd. China. No other disclosures were reported. Ethics Approval Statement: The study was approved by the local hospital ethics committees of all the participating ICUs. At each site, informed consent was obtained from the patients or their next of kin before enrolment.

Background There is a lack of large-scale epidemiological data on the clinical practice of enteral nutrition (EN) feeding in China. This study aimed to provide such data on Chinese hospitals and to investigate factors associated with EN delivery. Methods This cross-sectional study was launched in 118 intensive care units (ICUs) of 116 mainland hospitals and conducted on April 26, 2017. At 00:00 on April 26, all patients in these ICUs were included. Demographic and clinical variables of patients on April 25 were obtained. The dates of hospitalization, ICU admission and nutrition initiation were reviewed. The outcome status 28 days after the day of investigation was obtained. Results A total of 1953 patients were included for analysis, including 1483 survivors and 312 nonsurvivors. The median study day was day 7 (IQR 2–19 days) after ICU entry. The proportions of subjects starting EN within 24, 48 and 72 h after ICU entry was 24.8% (84/352), 32.7% (150/459) and 40.0% (200/541), respectively. The proportion of subjects receiving > 80% estimated energy target within 24, 48, 72 h and 7 days after ICU entry was 10.5% (37/352), 10.9% (50/459), 11.8% (64/541) and 17.8% (162/910), respectively. Using acute gastrointestinal injury (AGI) 1 as the reference in a Cox model, patients with AGI 2–3 were associated with reduced likelihood of EN initiation (HR 0.46, 95% CI 0.353–0.599; p

Background Fucosterol has been reported to have antioxidant, antidiabetic, and anti-inflammatory effects. In this study, we investigated the protective effect and the possible mechanism of fucosterol on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Methods Lung injury was assessed by a histologic study, pulmonary edema, and inflammatory cytokines production in bronchoalveolar lavage fluid. Alveolar macrophages were stimulated with LPS in the presence or absence of fucosterol. The expressions of inflammatory cytokines were determined by enzyme-linked immunosorbant assay. Nuclear factor-kappa B (NF-κB) expression was detected by Western blotting. Results The results showed that fucosterol attenuated lung histopathologic changes, wet-to-dry ratio, and tumor necrosis factor-α, interleukin (IL)-6 and IL-1β production in LPS-induced ALI in mice. Meanwhile, fucosterol inhibited NF-κB activation and tumor necrosis factor-α, IL-6, and IL-1β production in LPS-stimulated alveolar macrophages. Conclusions In conclusion, the present study demonstrated that fucosterol exhibited a protective effect on LPS-induced acute lung injury, and the possible mechanism is involved in inhibiting NF-κB activation, thereby inhibiting LPS-induced inflammatory response.

BML-111 is a lipoxin receptor agonist that plays a vital role on inflammation. MALAT1 is reported to mediate lung injury. ALI rat model was established using the method of venous cannula. Pulmonary microvascular endothelial cells (PMVEC) of rats were isolated using immunomagnetic separation method. Hematoxylin-eosin (HE) staining was performed to observe the lung injury degree. Real-time PCR and western blot were performed to detect the genes expression. ELIAS was used to determine the level of TNF-α and IL-6. RNA pull-down and RIP were carried out to affirm the relationship between MALAT1 and TLR4. The lung injury score and lung wet/dry weight ratio was significantly increased in ALI rats, while BML-111 treatment significantly decreased it, the HE staining directly revealed the lung injury. The expression of MALAT1 was decreased, while TLR4 was increased in ALI rats, BML-111 stimulation significantly reversed it. MALAT1 targets TLR4 to regulate its expression. TLR4 regulated the inflammation and cell apoptosis of PMVEC via NF-κB and p38 MAPK signaling pathway. The down-regulated MALAT1 mediates the mechanism of ALI by regulating of NF-κB and p38 MAPK signaling pathways via TLR4, while BML-111 stimulation significantly alleviated the ALI by regulating the expression of MALAT1.

Intelligent computer image processing technology provides convenience and possibility for designers to carry out designs. Shape analysis can be achieved by extracting SURF feature. However, high dimension of SURF feature causes to lower matching speed. To solve this problem, this paper proposed a fast fabric image matching algorithm based on SURF K-means and LSH algorithm. By constructing the bag of visual words on K-Means algorithm, and forming feature histogram of each image, the dimension of SURF feature is reduced at the first step. Then with the help of LSH algorithm, the features are encoded and the dimension is further reduced. In addition, the indexes of each image and each class of image are created, and the number of matching images is decreased by LSH hash bucket. Experiments on fabric image database show that this algorithm can speed up the matching and retrieval process, the result can satisfy the requirement of dress designers with accuracy and speed.

// Hongfu Yang 1 , Rongqing Sun 1 , Ning Ma 1 , Qilong Liu 1 , Xiaoge Sun 1 , Panpan Zi 1 , Junsheng Wang 1 , Ke Chao 1 and Lei Yu 1 1 Critical Care Medical Department, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450000, P.R. China Correspondence to: Hongfu Yang, email: yanghongfu_y@yeah.net Keywords: NF-κB, acute lung injury, inflammation, oxidative stress, mitochondrial function Received: January 20, 2017 Accepted: April 11, 2017 Published: May 04, 2017 ABSTRACT This study mainly studied the effect of inhibition of nuclear factor-κB (NF-κB) signal by pyrrolidine dithiocarbamate (PDTC) on lipopolysaccharide (LPS)-induced inflammatory response, oxidative stress, and mitochondrial dysfunction in a murine acute lung injury model. The results showed that LPS exposure activated NF-κB and its upstream proteins and caused lung inflammation, oxidative stress, and mitochondrial dysfunction in mice. While inhibition of NF-κB by PDTC adminstration alleviated LPS-induced generation of lymphocytes, IL-1β, and TNF-α. Malondialdehyde, a common oxidative product, was markedly reduced after PDTC treatment in LPS-challenged mice. Furthermore, PDTC alleviated LPS-induced mitochondrial dysfunction via improving ATP synthesis and uncoupling protein 2 expression. In conclusion, inhibition of NF-κB by PDTC alleviated LPS-induced acute lung injury via maintaining inflammatory status, oxidative balance, and mitochondrial function in mice.

Background Poor inter-rater reliability in chest radiograph interpretation has been reported in the context of acute respiratory distress syndrome (ARDS), although not for the Berlin definition of ARDS. We sought to examine the effect of training material on the accuracy and consistency of intensivists’ chest radiograph interpretations for ARDS diagnosis. Methods We conducted a rater agreement study in which 286 intensivists (residents 41.3%, junior attending physicians 35.3%, and senior attending physician 23.4%) independently reviewed the same 12 chest radiographs developed by the ARDS Definition Task Force (“the panel”) before and after training. Radiographic diagnoses by the panel were classified into the consistent (n = 4), equivocal (n = 4), and inconsistent (n = 4) categories and were used as a reference. The 1.5-hour training course attended by all 286 intensivists included introduction of the diagnostic rationale, and a subsequent in-depth discussion to reach consensus for all 12 radiographs. Results Overall diagnostic accuracy, which was defined as the percentage of chest radiographs that were interpreted correctly, improved but remained poor after training (42.0 ± 14.8% before training vs. 55.3 ± 23.4% after training, p

Mechanical ventilation is an important supportive therapy in the intensive care unit (ICU) to assist the critically ill patients with respiratory failure. But longer ventilation time has been proven to contribute to the lung injury which has been recognized as ventilator-induced lung injury (VILI). Recently studies have suggested that NF-kappaB signaling pathways may play a critical role in the process of inflammation and autophagy, and autophagy can reduce the damage of VILI partly by activating the NF-kappaB pathways. Thus, we propose that autophagy may facilitate ventilator-induced lung injury partly through activation of NF-kappaB pathway, which might be a new potential therapeutic target for ventilator-induced lung injury. Although the exact mechanism of autophagy and its exact role in the VILI need to be further explored, at least it provides us a potential target in the future prevention of VILI.

Many studies have investigated the association between glutathione S-transferase T1 (GSTT1) null genotype and risk of coronary heart disease (CHD), but the impact of GSTT1 null genotype on CHD is still unclear owing to the obvious inconsistence among those studies. This study aims to quantify the strength of association between GSTT1 null genotype and risk of CHD. We searched the PubMed, Embase and Wangfang databases for studies relating the association between GSTT1 null genotype and risk of CHD. We estimated summary odds ratio (OR) with their 95 % confidence interval (95 % CI) to assess the association. 24 case–control studies with 13, 884 CHD cases and 30, 719 controls were included into this meta-analysis. Meta-analysis of total 24 studies showed GSTT1 null genotype was not associated risk of CHD (random-effects OR = 1.17, 95 % CI 0.97–1.42, P = 0.101). After adjustment for heterogeneity, meta-analysis showed GSTT1 null genotype was associated increased risk of CHD both in total population and Caucasians (for total population, fixed-effects OR = 1.12, 95 % CI 1.05–1.21, P = 0.001; for Caucasians, fixed-effects OR = 1.10, 95 % CI 1.02–1.19, P = 0.010). There was no significant association in the other populations. No evidence of publication bias was observed. Meta-analyses of available data suggest the GSTT1 null genotype contributes to increased risk of CHD in Caucasians.