Effects of different selenium biofortification methods on Pleurotus eryngii polysaccharides: Structural characteristics, antioxidant activity and binding capacity in vitro.

The effects of selenium biofortification methods involving sodium selenite and selenium yeast on the structural characteristics, antioxidant activity and binding capacity of Pleurotus eryngii polysaccharides were investigated. Sodium selenite Se-enriched Pleurotus eryngii polysaccharides (Se-SPEP), selenium yeast Se-enriched Pleurotus eryngii polysaccharides (Se-YPEP), and Pleurotus eryngii polysaccharides (PEP) had Se contents of 20.548 ± 1.561, 19.822 ± 0.613, and 0.052 ± 0.016 µg/g, respectively. Compared with PEP, Se-SPEP and Se-YPEP had lower molecular weight and contained the same monosaccharides in varying molar ratios. The results of FT-IR, PS, ZP, and SEM indicated significant alterations in structural characteristics following selenium biofortification. Se-PEPs exhibited superior activity against ABTS, DPPH, and ·OH radicals, as well as the higher binding capacity for Cd2+ and Cu2+ compared to natural polysaccharides. The binding capacity of the polysaccharides for Cd2+ and Cu2+ was higher at pH 6.8 compared to pH 2.0, while the opposite was observed for Pb2+. Furthermore, Se-PEPs exhibited a significantly higher binding capacity for Cd2+ and Cu2+ at both pH levels compared to natural polysaccharides (P < 0.05). Se-YPEP displayed higher antioxidant activity than Se-SPEP, with their binding capacities reversed. These data indicated that selenium biofortification methods have different positive impacts on the structure and activity of polysaccharides compared to natural polysaccharides, making Se-PEPs promising dietary supplements for safeguarding the body against the risks posed by food-derived heavy metals.

LNC000152 Mediates Aluminum-Induced Proliferation of Reactive Astrocytes.

Aluminum is a metal element with significant neurotoxicity, and there is a substantial correlation between aluminum exposure and cognitive dysfunction. Glial fibrillary acidic protein (GFAP) is widely used as a marker of reactive astrocyte proliferation in response to pathological injury of the central nervous system. Studies of various neurodegenerative diseases have confirmed that the expression changes in GFAP are associated with nerve injury. We investigated the role of LNC000152 in the aluminum-induced reactive proliferation of astrocytes. By establishing two aluminum-exposed cell models of rat primary astrocytes and CTX-TNA2 cell lines, we examined the expression of LNC000152 and GFAP and detected cell proliferation with EdU and cell cycle changes with flow cytometry. The role of aluminum in promoting glial cell proliferation was verified; the expression levels of LNC000152 and GFAP increased with the concentration of aluminum exposure. Intervention of LNC000152 expression by siRNA technology revealed that LNC000152 affected glial cell responsive proliferation by influencing GFAP expression. These results suggest that LNC000152 plays a role in the reactive proliferation of astrocytes induced by aluminum.

Structure and immunostimulatory activity studies on two novel Flammulina velutipes polysaccharides: revealing potential impacts of →6)-α-D-Glcp(1→ on the TLR-4/MyD88/NF-κB pathway.

Two novel Flammulina velutipes (F. velutipes) polysaccharides, FVPH1 and FVPH2, were isolated and purified after hot water extraction. The structural characterization revealed that the backbone of FVPH1 consisted mainly of →6)-α-D-Glcp(1→, →3,4)-α-D-Galp(1→, →4)-α-L-Fucp(1→, and →4)-ß-D-Manp(1→, while the backbone of FVPH2 consisted of →3)-α-D-Galp(1→, →3,4)-α-D-Manp(1→,→6)-α-D-Glcp(1→. The branches of FVPH1 contained →6)-α-D-Glcp(1→ and α-D-Glcp(1→ and the branches of FVPH2 consisted of →3)-α-D-Galp(1→, →6)-α-D-Glcp(1→, and ß-L-Fucp(1→. FVPH2 exhibited significantly better immunostimulatory activity than FVPH1 (P < 0.05), as evidenced by the increased expression of NO, IL-1ß, IL-6, and TNF-α and pinocytic activity of RAW264.7 cells. As the most abundant structure in the polysaccharides of F. velutipes, the content of →6)-α-D-Glcp(1→ might play a crucial role in influencing the immunostimulatory activity of F. velutipes polysaccharides. The F. velutipes polysaccharide with a lower content of →6)-α-D-Glcp(1→ and a higher branching degree could significantly enhance the immunostimulatory activity of F. velutipes polysaccharides via activating the TLR-4/MyD88/NF-κB pathway more effectively.

Study on the physicochemical properties and antioxidant activities of Flammulina velutipes polysaccharide under controllable ultrasonic degradation based on artificial neural network.

The polysaccharide fraction (FVP2) with molecular weight of 1525.09 kDa and intrinsic viscosity of 3.43 dL/g was isolated and purified from Flammulina velutipes (F. velutipes), and the ultrasonic degradation model of FVP2 was established to predict the molecular weight and intrinsic viscosity at the same time based on artificial neural network. FVP2U1 (1149.11 kDa, 1.78 dL/g), FVP2U2 (618.91 kDa, 1.19 dL/g) and FVP2U3 (597.35 kDa, 0.48 dL/g) with different molecular weights or viscosity were produced by this model to explore the effect of ultrasound on the physicochemical properties and antioxidant activity of FVP2. The results showed that ultrasonic treatment did not change the types of characteristic functional groups, monosaccharide composition and glycosidic bond of FVP2, but changed the chemical composition ratio and the degree of polymerization. Under ultrasonic treatment, the intrinsic viscosity of FVP2 still decreased significantly when the molecular weight did not decrease. Compared to other components subjected to ultrasonic degradation, FVP2U1 demonstrated higher molecular weight and viscoelasticity, while exhibiting lower antioxidant activity. In the case of no significant difference in molecular weight and monosaccharide composition, FVP2U3 with lower intrinsic viscosity has stronger hydration ability, higher crystallization index, lower viscoelasticity and stronger antioxidant capacity than FVP2U2.

Role of the RIP3-PGAM5-Drp1 pathway in aluminum-induced PC12 cells necroptosis.

Epidemiological studies from diverse global regions suggest a correlation between the accumulation of aluminum in the brain and the onset of various neurodegenerative diseases, including Alzheimer's disease, of which, neuronal cells death happen. Our previous research has found the potential of aluminum to induce neuronal cell death. A comprehensive exploration of the regulatory pathways influenced by aluminum in neuronal cell death could contribute to the development of strategies aimed at preventing the detrimental impact of aluminum on neuronal cells. This study is dedicated to exploring the impact of aluminum on mitochondrial homeostasis through the RIP3-PGAM5-Drp1 pathway, with a specific focus on its potential role in necroptosis. We observed that the inhibition of RIP3 function and the reduction in PGAM5 protein expression both mitigate aluminum-induced necroptosis in PC12 cells and enhance mitochondrial function. However, the inhibition of PGAM5 protein expression does not exert an impact on the expression of RIP3 and MLKL proteins. In summary, our study posits that aluminum can induce necroptosis in PC12 cells through the RIP3-PGAM5-Drp1 pathway.

Nutrient recovery and recycling from fishery waste and by-products.

The circular bio-based economy offers great untapped potential for the food industry as possible valuable products and energy can be recovered from food waste. This can promote more sustainable and resilient food systems in Europe in follow-up of the European Commission's Farm to Fork strategy and support the global transition to more sustainable agri-food systems with the common agricultural and fisheries policies. With its high nutrient content, waste and by-products originating from fish and seafood industry (including aquaculture) are one of the most promising candidates to produce alternative fertilising products which can play a crucial role to replace synthetic mineral fertilisers. Whereas several studies highlighted the opportunities to recover valuable compounds from fishery waste, study towards their potential for the production of fertilising products is still scarce. This study presents an extensive overview of the characteristics of fishery waste and by-products (i.e., fish processing waste, fish sludge, seafood waste/by-products), the state-of-the-art nutrient recovery technologies and recovered nutrients as fertilising products from these waste streams. The European Commission has already adopted a revised Fertilising Products Regulation (EU) 2019/1009 providing opportunities for fertilising products from various bio-based origins. In frame of this opportunity, we address the quality and safety aspects of the fishery waste-derived fertilising products under these criteria and highlight possible obstacles on their way to the market in the future. Considering its high nutrient content and vast abundance, fish sludge has a great potential but should be treated/refined before being applied to soil. In addition to the parameters currently regulated, it is crucial to consider the salinity levels of such fertilising products as well as the possible presence of other micropollutants especially microplastics to warrant their safe use in agriculture. The agronomic performance of fishery waste-derived fertilisers is also compiled and reported in the last section of this review paper, which in most cases perform equally to that of conventional synthetic fertilisers.

Lnc001209 Participates in aluminium-induced apoptosis of PC12 cells by regulating PI3K-AKT-mTOR signalling pathway.

Aluminium (Al) is a common environmental neurotoxin, but the molecular mechanism underlying its toxic effects remains unclear. Many studies have shown that aluminium exposure leads to increased neuronal apoptosis. This study aimed to investigate the mechanisms and signalling pathways involved in aluminium exposure-induced neuronal apoptosis. The results showed a decrease in the number of PC12 cells and changes in cell morphology in the aluminium maltol exposure group. The viability of PC12 cells decreased gradually with increasing of exposure doses, and the apoptosis rate increased. The expression of Lnc001209 decreased gradually with an increase in the aluminium exposure dose. After transfection of Lnc001209 siRNA in aluminium-exposed PC12 cells, the protein expression levels of p-Akt Ser473, p-Akt Thr308, p-P85 Tyr467, p-mTOR Ser2448 and CD36 were increased. RNA pull-down MS showed that Lnc001209 interacts with the CD36 protein. Expression of the CD36 protein was increased in PC12 cells exposed to aluminium. The results of the CD36 intervention experiment showed that the protein expression levels of p-Akt Ser473, p-Akt Thr308, p-P85 Tyr467, and p-mTOR Ser2448 likely increased after CD36 overexpression. In addition, the phosphorylation level of AKT had the most significant increase. The enhancement of p-Akt activity promotes neuronal apoptosis.

Interaction between aluminum exposure and ApoEε4 gene on cognitive function of in-service workers.

The occurrence and development of cognitive impairment, the early stage of AD, may be affected both by factors of environmental (aluminum exposure) and genetic (ApoEε4 gene). But whether there is an interaction between the two factors on cognitive function is still unknown. To explore the interaction between the two factors on cognitive function of in-service workers. A total of 1121 in-service workers in a large aluminum factory were investigated in Shanxi Province. Cognitive function was assessed by the Mini-mental State Examination (MMSE), the clock-drawing test (CDT), the Digit Span Test (DST, including DSFT and DSBT), the fuld object memory evaluation (FOM), and the verbal fluency task (VFT). The plasma-Al (p-Al) concentrations were measured by inductively coupled plasma-mass spectrometry (ICP-MS) as an internal exposure indicator, and the participants were divided into four Al exposure groups according to the quartile of p-Al concentrations, namely Q1, Q2, Q3, and Q4. ApoE genotype was determined by Ligase Detection Reaction (LDR). The multiplicative model was fitted using non-conditional logistic regression and additive model was fitted using crossover analysis to analyze the interaction between p-Al concentrations and the ApoEε4 gene. Finally, a dose-response relationship between p-Al concentrations and cognitive impairment was observed, with the p-Al concentrations increased, cognitive function performance gradually becomes worse (Ptrend＜0.05), and the risk of cognitive impairment gradually increases (Ptrend＜0.05), mainly in executive/visuospatial impairment, auditory memory impairment (particularly the working memory impairment). And ApoEε4 gene may be a risk factor for cognitive impairment, while no association between the ApoEε2 gene and cognitive impairment is observed. Additionally, an additive but no multiplicative interaction between p-Al concentrations and ApoEε4 gene is observed, and when the two factors work together, the risk of cognitive impairment further increased, of which 44.2% can be attributed to the interaction effect.

miR-200a-3p Regulates PRKACB and Participates in Aluminium-Induced Tau Phosphorylation in PC12 Cells.

Aluminium (Al) is an environmental neurotoxin that humans are widely exposed to, but the molecular mechanism of its toxic effects is not fully understood. Many studies have shown that exposure to Al can cause abnormal phosphorylation of the tau protein that is believed as one of pathological features of Alzheimer's disease. Increasing evidence indicates that microRNAs (miRNAs) may be involved in the pathological processes of neurodegenerative diseases and are potential regulatory factors for related target genes. Phosphorylation at Ser-133 of cAMP response element-binding protein (CREB) is one of the major pathways of CREB activation, and phosphorylation at this site is controlled by protein kinase A (PKA). The catalytic subunit of PKA, cAMP-dependent protein kinase catalytic subunit beta (PRKACB), phosphorylates CREB. The target gene prediction software TargetScan showed that PRKACB was one of the target mRNAs of miR-200a-3p. The purpose of this study was to investigate whether miR-200a-3p regulates the PKA/CREB pathway by targeting PRKACB and leads to abnormal phosphorylation of the tau protein in nerve cells. The results showed that Al exposure increased the expression level of miR-200a-3p, and miR-200a-3p increased the expression of targeted downregulated PRKACB, and then decreased the PKA/CREB signalling pathway activity, leading to abnormal hyperphosphorylation of tau.

Chemical component analysis of the traditional Chinese medicine Guipi Tang and its effects on major depressive disorder at molecular level.

Ethnopharmacological relevance: Guipi Tang (GPT) is a widely used traditional Chinese medicine that is used to treat major depressive disorder. However, the molecular mechanisms of its effects remain unclear. Aim of the study: This study aimed to investigate the antidepressant-like effects of GPT and explore its underlying molecular mechanisms. Materials and methods: Male Sprague-Dawley rats were subjected to a chronic unpredictable mild stress (CUMS) procedure and treated with various doses of GPT, with fluoxetine treatment as a positive control. Behavioural tests (including sucrose preference test, novelty-suppressed feeding test, open-field test and forced swim test), terminal deoxynucleotidyl transferase dUTP nick end labeling and enzyme-linked immunosorbent assay were conducted. The levels of Bax, Bcl-2, cleaved caspase-3, PI3K, p-PI3K, AKT, p-AKT, BDNF, TrkB and CREB or p-CREB were assessed at the protein level using western blotting or immunofluorescence. Results: GPT consists of mainly known drugs, such as liquiritin and ginsenosides. It reversed depressive behaviours and decreased cell apoptosis in the hippocampi of CUMS rats. It significantly upregulated the protein level of Bax, p-Akt, p-PI3K, BDNF, TrkB and p-CREB and downregulated the level of cleaved caspase-3 and Bcl-2. Conclusions: GPT had anti-depressive activity as indicated by the amelioration of depression-like behaviour and the inhibition of hippocampal neuronal apoptosis in CUMS rats. This inhibition was mediated partly by modulating the PI3K/Akt and/or BDNF/TrkB/CREB pathway, in which, glycosides, the main components of GPT, might be involved.

Naoxintong Capsule for Secondary Prevention of Ischemic Stroke: A Multicenter, Randomized, and Placebo-Controlled Trial.

OBJECTIVE: To examine whether the combination of Naoxintong Capsule with standard care could further reduce the recurrence of ischemic stroke without increasing the risk of severe bleeding. METHODS: A total of 23 Chinese medical centers participated in this trial. Adult patients with a history of ischemic stroke were randomly assigned in a 1:1 ratio using a block design to receive either Naoxintong Capsule (1.2 g orally, twice a day) or placebo in addition to standard care. The primary endpoint was recurrence of ischemic stroke within 2 years. Secondary outcomes included myocardial infarction, death due to recurrent ischemic stroke, and all-cause mortality. The safety of drugs was monitored. Results were analyzed using the intention-to-treat principle. RESULTS: A total of 2,200 patients were enrolled from March 2015 to March 2016, of whom 143 and 158 in the Naoxintong and placebo groups were lost to follow-up, respectively. Compared with the placebo group, the recurrence rate of ischemic stroke within 2 years was significantly lower in the Naoxintong group [6.5% vs. 9.5%, hazard ratio (HR): 0.665, 95% confidence interval (CI): 0.492-0.899, P=0.008]. The two groups showed no significant differences in the secondary outcomes and safety, including rates of severe hemorrhage, cerebral hemorrhage and subarachnoid hemorrhage (P>0.05). CONCLUSION: The combination of Naoxintong Capsule with standard care reduced the 2-year stroke recurrence rate in patients with ischemic stroke without increasing the risk of severe hemorrhage in high-risk patients. (Trial registration No. NCT02334969).

A novel CapsNet neural network based on MobileNetV2 structure for robot image classification.

Image classification indicates that it classifies the images into a certain category according to the information in the image. Therefore, extracting image feature information is an important research content in image classification. Traditional image classification mainly uses machine learning methods to extract features. With the continuous development of deep learning, various deep learning algorithms are gradually applied to image classification. However, traditional deep learning-based image classification methods have low classification efficiency and long convergence time. The training networks are prone to over-fitting. In this paper, we present a novel CapsNet neural network based on the MobileNetV2 structure for robot image classification. Aiming at the problem that the lightweight network will sacrifice classification accuracy, the MobileNetV2 is taken as the base network architecture. CapsNet is improved by optimizing the dynamic routing algorithm to generate the feature graph. The attention module is introduced to increase the weight of the saliency feature graph learned by the convolutional layer to improve its classification accuracy. The parallel input of spatial information and channel information reduces the computation and complexity of network. Finally, the experiments are carried out in CIFAR-100 dataset. The results show that the proposed model is superior to other robot image classification models in terms of classification accuracy and robustness.

Review on the release mechanism and debittering technology of bitter peptides from protein hydrolysates.

Recent scientific evidence indicates that protein hydrolysates contain bioactive peptides that have potential benefits for human health. However, the bitter-tasting hydrophobic peptides in protein hydrolysates negatively affect the sensory quality of resulting products and limit their utilization in food and pharmaceutical industries. The approaches to reduce, mask, and remove bitter taste from protein hydrolysates have been extensively reported. This review paper focuses on the advances in the knowledge regarding the structure-bitterness relationship of peptides, the release mechanism of bitter peptides, and the debittering methods for protein hydrolysates. Bitter tastes generating with enzymatic hydrolysis of protein is influenced by the type, concentration, and bitter taste threshold of bitterness peptides. A "bell-shaped curve" is used to describe the relationship between the bitterness intensity of the hydrolysates and the degree of hydrolysis. The bitter receptor perceives bitter potencies of bitter peptides by the hydrophobicity recognition zone. The intensity of bitterness is influenced by hydrophobic and electronic properties of amino acids and the critical spatial structure of peptides. Compared to physicochemical debittering (i.e., selective separation, masking of bitter taste, encapsulation, Maillard reaction, and encapsulation) and other biological debittering (i.e., enzymatic hydrolysis, enzymatic deamidation, plastein reaction), enzymatic hydrolysis is a promising debittering approach as it combines protein hydrolyzation and debittering into a one-step process, but more work should be done to advance the knowledge on debittering mechanism of enzymatic hydrolysis and screening of suitable proteases. Further study can focus on combining physicochemical and biological approaches to achieve high debittering efficiency and produce high-quality products.

Aluminum Induced Necroptosis of PC12 Cells via TNFR1-RIP1/RIP3 Signalling Pathway.

In addition to apoptosis, it has also been reported that aluminum (Al) causes necroptosis, a new form of programmed necrosis, which has recently been discovered, in nerve cells, but its molecular mechanism is not elucidated. In order to explore the answer, in this study, we apply for this method that after PC12 cells were exposed to maltol aluminum [200 µM Al(mal)3], siRNA were used as interference technique to explore the role of Tumour necrosis factor receptor 1 (TNFR1), receptor interaction proteins 1 (RIP1) and receptor interaction proteins 3 (RIP3) in necroptosis caused by Al(mal)3. After the end of this research, we demonstrated that, initially, Al(mal)3 could trigger apoptosis and necroptosis in PC12 cells and up-regulate both mRNA and protein expressions of TNFR1, RIP1 and RIP3, also, up-regulate the phosphorylated mixed lineage kinase domain-like protein (MLKL) protein expression. Additionally, in PC12 cells treated with Al(mal)3, suppression of TNFR1 was found to enhance apoptosis and attenuate the expression of RIP1/RIP3 and phosphorylated MLKL. At last, deficiency of RIP1/RIP3 reduced the extent of necroptosis. Briefly, our results verify that the TNFR1-RIP1/RIP3 pathway could be involved in Al(mal)3 induced necroptosis.

A study on cognitive impairment of mice exposed to nano-alumina particles by nasal drip.

BACKGROUND: As an emerging nanomaterial, nano-alumina is widely used in chemical engineering, food and medicine due to its special physical and chemical properties, and its potential health hazards have attracted attention. OBJECTIVE: Aim of this study is to understanding the effect and possible mechanism of nano-alumina on cognitive function in mice. METHODS: Male healthy ICR mice were randomly assigned and given nasal drops of saline, nano-alumina (different doses) and micro-alumina for 30 days, respectively. Morris water maze test, step down test and open field test were used to detect learning and memory ability. Blood brain permeability was observed by immunofluorescence staining and lanthanum nitrate tracing, histopathological abnormalities in mice hippocampus was observed by thionine staining, the final determination of oxidative stress level in brain tissue was measured by using oxidative stress index detection kit and the level of LC3-Ⅱ and Caspase-3, 8, 9 proteins were detected by western blot. RESULTS: In the cerebral cortex of mice exposed to nano-alumina particles, lanthanum nitrate particles adhered to vascular endothelial cells, and the expression of ZO-1 and Occuldin decreased and morphology was disordered; most neurons in hippocampus CA3 region showed balloon-like swelling and degeneration, nucleoli disappeared and apical dendrites broke; mice exposed to nano-alumina, the escape latency in Morris water maze increased compared with the control group(P < 0.05),and the residence time in the original platform quadrant shortened significantly(P < 0.05);the platform latency was significantly shortened and the number of errors increased in the step down test compared with the control group; the residence time in the center of mice the nano-alumina treated was significantly increased in open field test (P < 0.05). CONCLUSION: The nano-alumina particles could be transported into the central nervous system via blood-brain barrier and olfactory bulb, impair learning and memory function in mice, which is more serious than the micro-alumina particles. The apoptosis of mice neurons caused by nano-alumina particles maybe due to the mixed neurotoxic effect of oxidative stress and the elemental toxicity of aluminum itself.

Neohesperidin Protects Angiotensin II-Induced Hypertension and Vascular Remodeling.

Vascular remodeling due to hypertension is one of the major health challenges facing countries around the world. Neohesperidin, a flavonoid glycoside found in citrus fruits, is an antioxidant. Neohesperidin has been studied for a variety of diseases in addition to hypertension. In this study, angiotensin II was used to induce hypertension in mice (490 ng/kg/min, 14 days). We used H&E, Masson, immunofluorescence, dihydroethidine and qPCR to evaluate the effect of Nehesperidin (50 mg/kg/day, 16 days) on pathological hypertension in mice. Estimating the effect of Nehesperidin on human umbilical vein endothelial cells and vascular smooth muscle cells stimulated by angiotensin II. We found that neohesperidin inhibited angiotensin II-induced hypertension in mice. Neohesperidin reduced angiotensin II-induced vascular hypertrophy, fibrosis, inflammation and oxidative stress in vivo. Neohesperidin inhibited angiotensin II-induced ROS and DNA damage in human umbilical vein endothelial cells. Neohesperidin inhibited angiotensin II-induced migration of vascular smooth muscle cells. The results showed that Nehesperidin acts as an antioxidant and could significantly inhibit angiotensin II induced hypertension and vascular remodeling in vitro and in vivo.

Roles of NOD1/Rip2 signal pathway in carotid artery remodelling in spontaneous hypertensive rats.

Nucleotide-binding and oligomerization domain (NOD) receptor is a member of inherent immunity recognition receptor family. We investigated the NOD1/Rip2 signalling pathway on carotid arterial remodelling in spontaneously hypertensive rats (SHRs). SHRs were treated with NOD1 agonist (iE-DAP), inhibitor (ML130), or normal saline. We determined the NOD1 and Rip2 expression in carotid artery tissues, serum tumour necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1). The carotid artery remodelling in 16-week SHRs was higher than that of 8-week SHRs and 16-week Wistar-Kyoto (WKY) rats. Expression of NOD1, Rip2, MCP-1 and TNF-α in 16-week SHRs was higher than that of 8-week SHRs and 16-week WKY rats. Blood pressure in iE-DAP-treated SHRs was higher than SHR-C group (no treatment), together with MCP-1, TNF-α, NOD1 and Rip2 expression, as well as carotid artery remodelling. In ML130-treated group, these aspects were completely the opposite. Taken together, inhibition of NOD1/Rip2 signalling pathway could delay the vascular remodelling process.

Malnutrition and Risk of Mortality in Ischemic Stroke Patients Treated With Intravenous Thrombolysis.

Background and Purpose: Malnutrition is highly prevalent in ischemic stroke patients. We aimed to investigate whether malnutrition indexes may be useful in predicting mortality at 90 days in ischemic stroke patients treated with intravenous thrombolysis. Methods: We retrospectively analyzed consecutive patients who underwent thrombolytic therapy at three comprehensive stroke centers. Malnutrition was assessed using the controlling nutritional status (CONUT) score, geriatric nutritional risk index (GNRI), and prognostic nutritional index (PNI). Results: Of 979 patients (mean age, 66.8 years; males, 63.6%) included in this study, 91 (9.3%; 95% confidence interval [CI]: 8.4-10.2%) died at 3-month follow up. According to the CONUT, GNRI, and PNI scores, 9.9, 33.7, and 7.0% of patients were moderately or severely malnourished, respectively; 64.0% were at least mildly malnourished by at least 1 malnutrition index. In the multivariate regression model after adjusting for potential confounders, malnutrition (severe risk versus normal nutritional status) was significantly associated with an increased risk of mortality for CONUT scores (adjusted odds ratio [OR] 16.16, 95%CI, 7.86-67.11; P < 0.001), GNRI scores (adjusted OR 9.82, 4.10-23.51; P < 0.001) and PNI scores (adjusted OR 12.74, 5.56-29.19; P < 0.001). Similar results were found when the malnutrition scores were analyzed as continuous variables. Adding the three malnutrition indexes to models containing conventional risk factors significantly improved risk reclassification for 3-month mortality. Conclusion: Our study showed that malnutrition may be associated with a higher risk of mortality at 3 months in ischemic stroke after intravenous thrombolysis.

Enhanced methane yield through sludge two-phase anaerobic digestion process with the addition of calcium hypochlorite.

This study investigated the effects of calcium hypochlorite (Ca(ClO)2) on biomethane generation from sludge two-phase anaerobic digestion system. In first (acidogenic) phase, volatile fatty acids (VFAs) were largely generated when pretreated by Ca(ClO)2, while the methane yield was severely inhibited. In second (methanogenic) phase, the methane yield was observably enhanced by Ca(ClO)2. Further calculation showed that the total methane yield from the two phases was firstly promoted from 156.0 ± 4.5 to 269.9 ± 5.2 mL when Ca(ClO)2 dosage enhanced from 0 to 1.6 g/L, which then reduced to 235.4 ± 5.5 mL when Ca(ClO)2 content reached 2.0 g/L. Mechanism analysis showed that the suppression of Ca(ClO)2 on coenzyme F420 activity was relieved in methanogenic phase, and the abundances of functional microbes in methanogenic phase were enriched when added with Ca(ClO)2. The Ca(ClO)2-based method well realized the balance between efficacy and economy, possessing outstanding potential for large-scale applications.