Formulation ofα-linolenic acid microemulsion free of co-surfactant

A novel class ofα-linolenic acid-in-water microemulsion free of co-surfactant was investigated as potential food delivery systems.Rough demarcation within the transparent region was deduced from the results of conductivity and polarizing optical microscopy.The microemulsion mean hydrodynamic diameter and characterization were determined by dynamic light scattering and negative-staining TEM.The location of ALA molecules in the microemulsion formulations was determined by ~1H NMR spectroscopy.

α-Linolenic acid alleviates aluminium chloride-induced toxicity in PC12 cells by activation of PKA-CREB-BDNF signaling pathway

Aluminum has been associated with neurodegenerative diseases.ALA(α-linolenic acid),an essential dietary component for human health,possesses prominent biological activities.Herein,we aim to explore the neuroprotective effects of ALA on aluminum toxicity and reveal the underlying mechanism.Results show that aluminum chloride(denoted as Al)enabled cell viability decline and apoptosis with oxidative stress and mitochondrial damage in differentiated rat pheochromocytoma cells(PC12)for 24 h incubation.Compared with Al(10 mmol/L)treatment alone,ALA(50μmol/L)pretreatment for 24 h significantly enhanced cell viability by 28.40%,and hindered cell apoptosis by 12.35%,together with recovering redox state balance and alleviating mitochondrial damage.It was measured that ALA treatment upregulated Bcl-2 expression and down-regulated Bax level,accompanied with an expression decline of caspase-3 and caspase-9.Meanwhile,ALA pretreatment was proved to increase protein kinase A(PKA)expression and to promote phosphorylation of cAMP response element-binding protein(p-CREB),resulting in elevation on the level of brain-derived neurotrophic factor(BDNF).The above results showed that ALA attenuated Al toxicity in PC12 cells by mediating the PKA-CREBBDNF signaling pathway.

Biotechnology ofα-linolenic acid in oilseed rape(Brassica napus)using FAD2 and FAD3 from chia(Salvia hispanica)

α-Linolenic acid(ALA,18:3Δ9,12,15)is an essential fatty acid for humans since it is the precursor for the biosynthesis of omega-3 long-chain polyunsaturated fatty acids(LC-PUFA).Modern people generally suffer from deficiency of ALA because most staple food oils are low or lack ALA content.Biotechnological enrichment of ALA in staple oil crops is a promising strategy.Chia(Salvia hispanica)has the highest ALA content in its seed oil among known oil crops.In this study,the FAD2 and FAD3 genes from chia were engineered into a staple oil crop,oilseed rape(Brassica napus),via Agrobaterium tumefaciens-mediated transformation of their LP4-2A fusion gene construct driven by the seed-specific promoter P_(NapA).In seeds of T0,T1,and T2 lines,the average ALA contents were 20.86,23.54,and 24.92%,respectively,which were 2.21,2.68,and 3.03 folds of the non-transformed controls(9.42,8.78,and 8.22%),respectively.The highest seed ALA levels of T0,T1,and T2 plants were 38.41,35.98,and 39.19%respectively,which were 4.10-4.77 folds of the respective controls.FA-pathway enzyme genes(BnACCD,BnFATA,BnSAD,BnSCD,BnDGAT1,BnDGAT2,and BnDGAT3)and positive regulatory genes(BnWRI1,BnLEC1,BnL1L,BnLEC2,BnABI3,BnbZIP67,and BnMYB96)were all significantly up-regulated.In contrast,BnTT1,BnTT2,BnTT8,BnTT16,BnTTG1,and BnTTG2,encoding negative oil accumulation regulators but positive secondary metabolism regulators,were all significantly down-regulated.This means the foreign ShFAD2-ShFAD3 fusion gene,directly and indirectly,remodeled both positive and negative loci of the whole FA-related network in transgenic B.napus seeds.

Palm oil protectsα-linolenic acid from rumen biohydrogenation and muscle oxidation in cashmere goat kids

Background:In ruminants,dietary C18:3n-3 can be lost through biohydrogenation in the rumen;and C18:3n-3 that by-passes the rumen still can be lost through oxidation in muscle,theoretically reducing the deposition of C18:3n-3,the substrate for synthesis of poly-unsaturated fatty acids(n-3 LCPUFA)in muscle.In vitro studies have shown that rumen hydrogenation of C18:3n-3 is reduced by supplementation with palm oil(rich in cis-9 C18:1).In addition,in hepatocytes,studies with neonatal rats have shown that cis-9 C18:1 inhibits the oxidation of C18:3n-3.It therefore seems likely that palm oil could reduce both rumen biohydrogenation of C18:3n-3 and muscle oxidation of C18:3n-3.The present experiment tested whether the addition of palm oil to a linseed oil supplement for goat kids would prevent the losses of C18:3n-3 and thus improve the FA composition in two muscles,Longissimus dorsi and Biceps femoris.To investigate the processes involved,we studied the rumen bacterial communities and measured the mRNA expression of genes related to lipid metabolism in Longissimus dorsi.Sixty 4-month-old castrated male Albas white cashmere kids were randomly allocated among three dietary treatments.All three diets contained the same ingredients in the same proportions,but differed in their fat additives:palm oil(PMO),linseed oil(LSO)or mixed oil(MIX;2 parts linseed oil plus 1 part palm oil on a weight basis).Results:Compared with the LSO diet,the MIX diet decreased the relative abuandance of Pseudobutyrivibrio,a bacterial species that is positively related to the proportional loss rate of dietary C18:3n-3 and that has been reported to generate the ATP required for biohydrogenation(reflecting a decrease in the abundance of rumen bacteria that hydrogenate C18:3n-3 in MIX kids).In muscle,the MIX diet increased concentrations of C18:3n-3,C20:5n-3,C22:6n-3,and n-3 LCPUFA,and thus decreased the n-6/n-3 ratio;decreased the mRNA expression of CPT1β(a gene associated with fatty acid oxidation)and increased the mRNA expression of FADS1 and FADS2(genes associated with n-3 LCPUFA synthesis),compared with the LSO diet.Interestingly,compared to Longissimus dorsi,Biceps femoris had greater concentrations of PUFA,greater ratios of unsaturated fatty acids/saturated fatty acids(U/S),and poly-unsaturated fatty acids/saturated fatty acids(P/S),but a lesser concentration of saturated fatty acids(SFA).Conclusions:In cashmere goat kids,a combination of linseed and palm oils in the diet increases the muscle concentration of n-3 LCPUFA,apparently by decreasing the relative abundance of rumen bacteria that are positively related to the proportional loss rate of dietary C18:3n-3,by inhibiting mRNA expression of genes related to C18:3n-3 oxidation in muscle,and by up-regulating mRNA expression of genes related to n-3 LCPUFA synthesis in muscle,especially in Longissimus dorsi.

Effects of Supplementing Various Linoleic to α-linolenic Acid Ratios and Vitamin A on Production Performance and Egg Characteristics of Laying Hens during Summer Months

In the present feeding trial,responses of laying hens that were kept at high ambient temperature and Fed with various dietary ratios of linoleic acid(LNA)toα-linolenic acid(ALA)and vitamin A levels on production performance and egg quality traits were evaluated.A total of 360 Leghorn laying hens at 40th week of age(average initial body weight;1.79±0.23 kg)were fed with various combinations of canola oil and linseed oil containing diets to achieve LNA to ALA dietary ratios of 20:1,10:1,4:1,2:1,1:1 and 1:2,each supplemented with 3000 or 10000 IU of vitamin A/kg of diet.The experiment was designed as a 6×2 factorial Completely Randomized Design that continued for 12 weeks.Feed intake,body weight gain,egg production and egg quality traits were recorded during the trial.Decreasing dietary LNA to ALA ratio or increasing poly unsaturated fatty acids(PUFA)in the diet decreased(P<0.05)body weight gain and yolk percentage in laying hens.Feed intake,hen-day and hen-housed egg production,feed conversion ratio(FCR)per dozen of eggs and shell quality remained unaffected(P>0.05)by dietary treatments.Feed conversion ratio per kg eggs,egg weight and egg-shell thickness showed a curvilinear(P<0.05)response to decreasing dietary LNA to ALA ratio.Although the dietary ratio of LNA to ALA of 4:1 or less could produce eggs by the hens with desirable quantities of n-6 and n-3 PUFA–that are characteristics of functional diets–the performance of laying hens in terms of body weight gain and egg-yolk percentage was slightly compromised.Therefore,a 4:1 or 2:1 LNA to ALA combination can make a borderline between the production traits and the feed economics.

Integrated multi-omics analysis reveals liver metabolic reprogramming by fish iridovirus and antiviral function of alpha-linolenic acid

Iridovirus poses a substantial threat to global aquaculture due to its high mortality rate;however,the molecular mechanisms underpinning its pathogenesis are not well elucidated.Here,a multi-omics approach was applied to groupers infected with Singapore grouper iridovirus(SGIV),focusing on the roles of key metabolites.Results showed that SGIV induced obvious histopathological damage and changes in metabolic enzymes within the liver.Furthermore,SGIV significantly reduced the contents of lipid droplets,triglycerides,cholesterol,and lipoproteins.Metabolomic analysis indicated that the altered metabolites were enriched in 19 pathways,with a notable down-regulation of lipid metabolites such as glycerophosphates and alpha-linolenic acid(ALA),consistent with disturbed lipid homeostasis in the liver.Integration of transcriptomic and metabolomic data revealed that the top enriched pathways were related to cell growth and death and nucleotide,carbohydrate,amino acid,and lipid metabolism,supporting the conclusion that SGIV infection induced liver metabolic reprogramming.Further integrative transcriptomic and proteomic analysis indicated that SGIV infection activated crucial molecular events in a phagosome-immune depression-metabolism dysregulation-necrosis signaling cascade.Of note,integrative multi-omics analysis demonstrated the consumption of ALA and linoleic acid(LA)metabolites,and the accumulation of L-glutamic acid(GA),accompanied by alterations in immune,inflammation,and cell death-related genes.Further experimental data showed that ALA,but not GA,suppressed SGIV replication by activating antioxidant and anti-inflammatory responses in the host.Collectively,these findings provide a comprehensive resource for understanding host response dynamics during fish iridovirus infection and highlight the antiviral potential of ALA in the prevention and treatment of iridoviral diseases.

Synthesis and characterization of medium- and long-chain structural lipid rich in α-linolenic acid and lauric acid

Medium-and long-chain triglycerides(MLCT)have been widely concerned.In this study,lauric acid(La)was incorporated into flaxseed(Linum usitatissimum L.)oil(FO,aLna-riched)by lipase-catalyzed acidolysis.The synthesis efficiency of four immobilized lipases(Lipozyme RM IM,TL IM,AOAB8 and Novozym 435)was compared,while Lipozyme AOAB8 reaction for 2 h was the best scheme.Further,the optimal conditions for synthesizing structural lipids(aLSLs,rich in aLna and La)were obtained by response surface methodology:the reaction temperature was 44.6℃,substrate molar ratio was 12(La/FO),and enzyme loading was 9.11%.After purification by molecular distillation,the triglycerides(TAGs)of aLSLs contained 75.35% of TAGs withα-linolenic acid(aLna),40.82%of MLCTs with La,and 26.75%(65.53% of the total MLCTs)of TAGs with both aLna and La(ɑ-MLCT).Meanwhile,the content of La and aLna in aLSLs were 22.38%and 39.78%,respectively.The chemical structure and microstructure of aLSLs were similar to FO.In addition,the thermo-oxidative decomposition behavior of aLSLs was significantly improved compared with physical mixture oil.This improvement might be related to the insertion of La and the structure of TAG.In all,this study firstly developed a novel thermo-oxidatively stable MLCT with high levels of aLna and La.

Anti-inflammatory Mechanism of Gamma-linolenic Acid in RAW264.7 Cells

[Objective] The aim was to investigate the anti-inflammatory effect and the mechanism of gamma-linolenic acid on lipopolysaccharide-induced RAW264.7 cells.[Method] Macrophagic system RAW 264.7 cells were cultured in vitro,when cells grew to fusion state,they were pretreated with 0,12.5,25.0,50.0 μmol/L of GLA for 4 h,and then 100 ng/ml of LPS were added to induce for 12 h or 30 min.Meanwhile,the blank control and LPS control were set.And the expression of iNOS,COX-2 and the effect of GLA on IκBα,p-JNK/SAPK（Thr183/Tyr185）,p38 MAPK,p-p38 MAPK（Thr180/Tyr182）,ERK1/2,p-ERK1/2 were detected by Western blot.[Result] GLA significantly inhibited the expression of iNOS and COX-2 in RAW264.7 cells induced by LPS,and in the range of 0-50 μmol/L of GLA,the inhibition effect was concentration-dependent（P0.05）.GLA could significantly inhibited the degradation of IκBα（P0.05）,thereby inhibited the activation of NF-κB.GLA could significantly inhibited the phosphorylation of LPS-induced JNK1/2 and ERK1/2（P0.05）,while it had not significantly effect on the phosphorylation of p38（P0.05）.[Conclusion] GLA had excellent anti-inflammation effect.The inhibition of the phosphorylation of JNK1/2,ERK1/2 and the inhibition of activation of NF-κB might be the important mechanism for the educing of its biological effect.

Production of γ-linolenic acid and stearidonic acid by Synechococcus sp.PCC7002 containing cyanobacterial fatty acid desaturase genes

Genetic modifi cation is useful for improving the nutritional qualities of cyanobacteria. To increase the total unsaturated fatty acid content, along with the ratio of ω-3/ω-6 fatty acids, genetic engineering can be used to modify fatty acid metabolism. S ynechococcus sp. PCC7002, a fast-growing cyanobacterium, does not contain a Δ6 desaturase gene and is therefore unable to synthesize γ-linolenic acid(GLA) and stearidonic acid(SDA), which are important in human health. In this work, we constructed recombinant vectors Syd6 D, Syd15 D and Syd6Dd15 D to express the Δ15 desaturase and Δ6 desaturase genes from Synechocystis PCC6803 in Synechococcus sp. PCC7002, with the aim of expressing polyunsaturated fatty acids. Overexpression of the Δ15 desaturase gene in S ynechococcus resulted in 5.4 times greater accumulation of α-linolenic acid compared with the wild-type while Δ6 desaturase gene expression produced both GLA and SDA. Co-expression of the two genes resulted in low-level accumulation of GLA but much larger amounts of SDA, accounting for as much to 11.64% of the total fatty acid content.

Decoding the nexus:branched-chain amino acids and their connection with sleep,circadian rhythms,and cardiometabolic health

The sleep-wake cycle stands as an integrative process essential for sustaining optimal brain function and,either directly or indirectly,overall body health,encompassing metabolic and cardiovascular well-being.Given the heightened metabolic activity of the brain,there exists a considerable demand for nutrients in comparison to other organs.Among these,the branched-chain amino acids,comprising leucine,isoleucine,and valine,display distinctive significance,from their contribution to protein structure to their involvement in overall metabolism,especially in cerebral processes.Among the first amino acids that are released into circulation post-food intake,branched-chain amino acids assume a pivotal role in the regulation of protein synthesis,modulating insulin secretion and the amino acid sensing pathway of target of rapamycin.Branched-chain amino acids are key players in influencing the brain's uptake of monoamine precursors,competing for a shared transporter.Beyond their involvement in protein synthesis,these amino acids contribute to the metabolic cycles ofγ-aminobutyric acid and glutamate,as well as energy metabolism.Notably,they impact GABAergic neurons and the excitation/inhibition balance.The rhythmicity of branchedchain amino acids in plasma concentrations,observed over a 24-hour cycle and conserved in rodent models,is under circadian clock control.The mechanisms underlying those rhythms and the physiological consequences of their disruption are not fully understood.Disturbed sleep,obesity,diabetes,and cardiovascular diseases can elevate branched-chain amino acid concentrations or modify their oscillatory dynamics.The mechanisms driving these effects are currently the focal point of ongoing research efforts,since normalizing branched-chain amino acid levels has the ability to alleviate the severity of these pathologies.In this context,the Drosophila model,though underutilized,holds promise in shedding new light on these mechanisms.Initial findings indicate its potential to introduce novel concepts,particularly in elucidating the intricate connections between the circadian clock,sleep/wake,and metabolism.Consequently,the use and transport of branched-chain amino acids emerge as critical components and orchestrators in the web of interactions across multiple organs throughout the sleep/wake cycle.They could represent one of the so far elusive mechanisms connecting sleep patterns to metabolic and cardiovascular health,paving the way for potential therapeutic interventions.

Increased excitatory amino acid transporter 2 levels in basolateral amygdala astrocytes mediate chronic stress–induced anxiety-like behavior

The conventional perception of astrocytes as mere supportive cells within the brain has recently been called into question by empirical evidence, which has revealed their active involvement in regulating brain function and encoding behaviors associated with emotions.Specifically, astrocytes in the basolateral amygdala have been found to play a role in the modulation of anxiety-like behaviors triggered by chronic stress. Nevertheless, the precise molecular mechanisms by which basolateral amygdala astrocytes regulate chronic stress–induced anxiety-like behaviors remain to be fully elucidated. In this study, we found that in a mouse model of anxiety triggered by unpredictable chronic mild stress, the expression of excitatory amino acid transporter 2 was upregulated in the basolateral amygdala. Interestingly, our findings indicate that the targeted knockdown of excitatory amino acid transporter 2 specifically within the basolateral amygdala astrocytes was able to rescue the anxiety-like behavior in mice subjected to stress. Furthermore, we found that the overexpression of excitatory amino acid transporter 2 in the basolateral amygdala, whether achieved through intracranial administration of excitatory amino acid transporter 2agonists or through injection of excitatory amino acid transporter 2-overexpressing viruses with GfaABC1D promoters, evoked anxiety-like behavior in mice. Our single-nucleus RNA sequencing analysis further confirmed that chronic stress induced an upregulation of excitatory amino acid transporter 2 specifically in astrocytes in the basolateral amygdala. Moreover, through in vivo calcium signal recordings, we found that the frequency of calcium activity in the basolateral amygdala of mice subjected to chronic stress was higher compared with normal mice.After knocking down the expression of excitatory amino acid transporter 2 in the basolateral amygdala, the frequency of calcium activity was not significantly increased, and anxiety-like behavior was obviously mitigated. Additionally, administration of an excitatory amino acid transporter 2 inhibitor in the basolateral amygdala yielded a notable reduction in anxiety level among mice subjected to stress. These results suggest that basolateral amygdala astrocytic excitatory amino acid transporter 2 plays a role in in the regulation of unpredictable chronic mild stress-induced anxiety-like behavior by impacting the activity of local glutamatergic neurons, and targeting excitatory amino acid transporter 2 in the basolateral amygdala holds therapeutic promise for addressing anxiety disorders.

Targeting harmful effects of non-excitatory amino acids as an alternative therapeutic strategy to reduce ischemic damage

The involvement of the excitatory amino acids glutamate and aspartate in ce rebral ischemia and excitotoxicity is well-documented.Nevertheless,the role of non-excitatory amino acids in brain damage following a stroke or brain trauma remains largely understudied.The release of amino acids by necrotic cells in the ischemic core may contribute to the expansion of the penumbra.Our findings indicated that the reversible loss of field excitato ry postsynaptic potentials caused by transient hypoxia became irreversible when exposed to a mixture of just four non-excitatory amino acids(L-alanine,glycine,L-glutamine,and L-serine)at their plasma concentrations.These amino acids induce swelling in the somas of neurons and astrocytes during hypoxia,along with permanent dendritic damage mediated by N-methyl-D-aspartate receptors.Blocking N-methyl-D-aspartate receptors prevented neuronal damage in the presence of these amino acids during hypoxia.It is likely that astroglial swelling caused by the accumulation of these amino acids via the alanine-serine-cysteine transporter 2 exchanger and system N transporters activates volume-regulated anion channels,leading to the release of excitotoxins and subsequent neuronal damage through N-methyl-D-aspartate receptor activation.Thus,previously unrecognized mechanisms involving non-excitatory amino acids may contribute to the progression and expansion of brain injury in neurological emergencies such as stroke and traumatic brain injury.Understanding these pathways co uld highlight new therapeutic targets to mitigate brain injury.

Preparation of Low Ratio Magnesium Ccement by Acid Leaching Treatment of Boron Mud

The effects of liquid-solid ratio and reaction time on the leaching rate of magnesium at room temperature were investigated,as well as the effects of the molar ratio of MgO/MgCl_(2),the amount of water added,and the amount of acid-impregnated slag dosed on the compressive strength and water resistance of LR-MOC.The results showed that the magnesium element in the boron mud could be maximally leached under the conditions of 1:1 concentration of hydrochloric acid at room temperature,liquid-solid ratio of 2.5 mL·g^(-1),and reaction time of 5 h,and the main products were amorphous SiO_(2) as well as a small amount of magnesium olivine which had not been completely reacted.The LR-MOC prepared using the acid-soaked mixture could reach a softening coefficient of 0.85 for 28 d of water immersion when the molar ratio of MgO/MgCl_(2) was 2.2,the amount of water added was 0 g,and the acid-soaked slag dosing was 40 wt%,which also led to an appreciable late-strength,with an increase of 19.4%in compressive strength at 28 d compared to that at 7 d.Unlike previous studies,LR-MOC prepared in this way has a final strength phase that is not the more easily hydrolysed 3-phase but the lath-like 5-phase.For this phenomenon,we analyzed the mechanism and found that,during the acid leaching process,a part of amorphous SiO_(2) dissolved in the acid leaching solution formed a silica sol,in which Mg^(2+)played a bridging role to make the silica sol more stable.With the addition and hydrolysis of MgO,the silica sol gel coagulation slows down,providing a capping layer to inhibit the hydrolysis of the 5-phase crystals and providing some strength after coagulation.The amorphous SiO_(2) in the other part of the acid-impregnated slag generated M-S-H gel with Mg^(2+)and OH-,which synergised with the dense structure composed of interlocking crystals to improve the water resistance of LR-MOC.

Dysregulation of genes involved in the long-chain fatty acid transport in pancreatic ductal adenocarcinoma

BACKGROUND Pancreatic ductal adenocarcinoma(PDAC)is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11%in the United States.As for other types of tumors,such as colorectal cancer,aberrant de novo lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.AIM To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid(FA)import into cell.METHODS A gene expression analysis of FASN,CD36,SLC27A1,SLC27A2,SLC27A3,SLC27A4,SLC27A5,ACSL1,and ACSL3 was performed by qRT-PCR in 24 tumoral PDAC tissues and 11 samples from non-tumoral pancreatic tissues obtained via fine needle aspiration or via surgical resection.The genes were considered significantly dysregulated between the groups when the p value was<0.05 and the fold change(FC)was≤0.5 and≥2.RESULTS We found that three FA transporters and two long-chain acyl-CoA synthetases genes were significantly upregulated in the PDAC tissue compared to the non-tumoral tissue:SLC27A2(FC=5.66;P=0.033),SLC27A3(FC=2.68;P=0.040),SLC27A4(FC=3.13;P=0.033),ACSL1(FC=4.10;P<0.001),and ACSL3(FC=2.67;P=0.012).We further investigated any possible association between the levels of the analyzed mRNAs and the specific characteristics of the tumors,including the anatomic location,the lymph node involvement,and the presence of metastasis.A significant difference in the expression of SLC27A3(FC=3.28;P=0.040)was found comparing patients with and without lymph nodes involvement with an overexpression of this transcript in 17 patients presenting tumoral cells in the lymph nodes.CONCLUSION Despite the low number of patients analyzed,these preliminary results seem to be promising.Addressing lipid metabolism through a broad strategy could be a beneficial way to treat this malignancy.Future in vitro and in vivo studies on these genes may offer important insights into the mechanisms linking PDAC with the long-chain FA import pathway.

g-C_(3)N_(4)nanosheets coupled with CoSe_(2)as co-catalyst for efficient photooxidation of xylose to xylonic acid

Photocatalysis has emerged as an effective approach to sustainably convert biomass into value-added products.CoSe_(2)is a promising nonprecious,efficient cocatalyst for photooxidation,which can facilitate the separation of photogenerated electron–holes,increase the reaction rates,and enhance photocatalytic efficiency.In this work,we synthesized a stable and efficient photocatalysis system of CoSe_(2)/g-C_(3)N_(4)through attaching CoSe_(2)on g-C_(3)N_(4)sheets,with a yield of 50.12%for the selective photooxidation of xylose to xylonic acid.Under light illumination,the photogenerated electrons were prone to migrating from g-C_(3)N_(4)to CoSe_(2)due to the higher work function of CoSe_(2),resulting in the accelerated separation of photogenerated electron–holes and the promoted photooxidation.Herein,this study reveals the unique function of CoSe_(2),which can significantly promote oxygen adsorption,work as an electron sink and accelerate the generation of ·O_(2)^(-),thereby improving the selectivity toward xylonic acid over other by-products.This work provides useful insights into the design of selective photocatalysts by engineering g-C_(3)N_(4)for biomass high-value utilization.

Flotation separation of chalcopyrite from pyrite using mineral fulvic acid as selective depressant under weakly alkaline conditions

Mineral fulvic acid(MFA)was used as an eco-friendly pyrite depressant to recover chalcopyrite by flotation with the use of the butyl xanthate as a collector.Flotation experiments showed that MFA produced a stronger inhibition effect on pyrite than on chalcopyrite.The separation of chalcopyrite from pyrite was realized by introducing 150 mg/L MFA at a pulp pH of approximately 8.0.The copper grade,copper recovery,and separation efficiency were 28.03%,84.79%,and 71.66%,respectively.Surface adsorption tests,zeta potential determinations,and localized electrochemical impedance spectroscopy tests showed that more MFA adsorbed on pyrite than on chalcopyrite,which weakened the subsequent interactions between pyrite and the collector.Atomic force microscope imaging further confirmed the adsorption of MFA on pyrite,and X-ray photoelectron spectroscopy results indicated that hydrophilic Fe-based species on the pyrite surfaces increased after exposure of pyrite to MFA,thereby decreasing the floatability of pyrite.

Additive neurorestorative effects of exercise and docosahexaenoic acid intake in a mouse model of Parkinson’s disease

There is a need to develop interventions to slow or reverse the degeneration of dopamine neurons in Parkinson’s disease after diagnosis.Given that preclinical and clinical studies suggest benefits of dietary n-3 polyunsaturated fatty acids,such as docosahexaenoic acid,and exercise in Parkinson’s disease,we investigated whether both could synergistically interact to induce recovery of the dopaminergic pathway.First,mice received a unilateral stereotactic injection of 6-hydroxydopamine into the striatum to establish an animal model of nigrostriatal denervation.Four weeks after lesion,animals were fed a docosahexaenoic acid-enriched or a control diet for the next 8 weeks.During this period,the animals had access to a running wheel,which they could use or not.Docosahexaenoic acid treatment,voluntary exercise,or the combination of both had no effect on(i)distance traveled in the open field test,(ii)the percentage of contraversive rotations in the apomorphine-induction test or(iii)the number of tyrosine-hydroxylase-positive cells in the substantia nigra pars compacta.However,the docosahexaenoic acid diet increased the number of tyrosine-hydroxylase-positive terminals and induced a rise in dopamine concentrations in the lesioned striatum.Compared to docosahexaenoic acid treatment or exercise alone,the combination of docosahexaenoic acid and exercise(i)improved forelimb balance in the stepping test,(ii)decreased the striatal DOPAC/dopamine ratio and(iii)led to increased dopamine transporter levels in the lesioned striatum.The present results suggest that the combination of exercise and docosahexaenoic acid may act synergistically in the striatum of mice with a unilateral lesion of the dopaminergic system and provide support for clinical trials combining nutrition and physical exercise in the treatment of Parkinson’s disease.

Leaching of WO_(3)from sulfuric acid converted product of scheelite in NH_(3)·H_(2)O−NH_(4)HCO_(3)solution

The leaching of sulfuric acid converted product of scheelite in NH_(3)·H_(2)O−NH_(4)HCO_(3)solution was systemically studied to improve sulfuric acid conversion−ammonium salts leaching technology route for ammonium paratungstate production.The results showed that the WO_(3)leaching efficiency was about 99%under optimal conditions of 350 r/min,liquid-to-solid ratio of 3 mL/g,1 mol/L NH_(4)HCO_(3),4 mol/L NH_(3)·H_(2)O,25℃,and 15 min.During the leaching,CaSO_(4)almost had no change and was still in a banding or rod-like shape in short leaching time,while conglobate CaCO_(3)was gradually formed on the CaSO_(4)surface.A secondary reaction might occur between CaSO_(4)and WO_(4)^(2−),which could be restrained by a certain amount of CO_(3)^(2−)in the solution.There was no CaCO_(3)phase determined by XRD in leaching residue of converted product for scheelite concentrate under optimal conditions,which was different from that for synthetic scheelite.The leaching process could be explained by neutralization reaction of H_(2)WO_(4)and solid transformation of CaSO_(4)in NH_(3)·H_(2)O−NH_(4)HCO_(3)solution.

Bile acid therapy for primary biliary cholangitis:Pathogenetic validation

Knowledge of the etiological and pathogenetic mechanisms of the development of any disease is essential for its treatment.Because the cause of primary biliary cholangitis(PBC),a chronic,slowly progressive cholestatic liver disease,is still unknown,treatment remains symptomatic.Knowledge of the physicochemical properties of various bile acids and the adaptive responses of cholangiocytes and hepatocytes to them has provided an important basis for the development of relatively effective drugs based on hydrophilic bile acids that can potentially slow the progression of the disease.Advances in the use of hydrophilic bile acids for the treatment of PBC are also associated with the discovery of pathogenetic mechanisms of the development of cholangiocyte damage and the appearance of the first signs of this disease.For 35 years,ursodeoxycholic acid(UDCA)has been the unique drug of choice for the treatment of patients with PBC.In recent years,the list of hydrophilic bile acids used to treat cholestatic liver diseases,including PBC,has expanded.In addition to UDCA,the use of obeticholic acid,tauroursodeoxycholic acid and norursodeoxycholic acid as drugs is discussed.The pathogenetic rationale for treatment of PBC with various bile acid drugs is discussed in this review.Emphasis is made on the mechanisms explaining the beneficial therapeutic effects and potential of each of the bile acid as a drug,based on the understanding of the pathogenesis of the initial stages of PBC.

Maintaining moderate levels of hypochlorous acid promotes neural stem cell proliferation and differentiation in the recovery phase of stroke

It has been shown clinically that continuous removal of ischemia/reperfusion-induced reactive oxygen species is not conducive to the recovery of late stroke.Indeed,previous studies have shown that excessive increases in hypochlorous acid after stroke can cause severe damage to brain tissue.Our previous studies have found that a small amount of hypochlorous acid still exists in the later stage of stroke,but its specific role and mechanism are currently unclear.To simulate stroke in vivo,a middle cerebral artery occlusion rat model was established,with an oxygen-glucose deprivation/reoxygenation model established in vitro to mimic stroke.We found that in the early stage(within 24 hours)of ischemic stroke,neutrophils produced a large amount of hypochlorous acid,while in the recovery phase(10 days after stroke),microglia were activated and produced a small amount of hypochlorous acid.Further,in acute stroke in rats,hypochlorous acid production was prevented using a hypochlorous acid scavenger,taurine,or myeloperoxidase inhibitor,4-aminobenzoic acid hydrazide.Our results showed that high levels of hypochlorous acid(200μM)induced neuronal apoptosis after oxygen/glucose deprivation/reoxygenation.However,in the recovery phase of the middle cerebral artery occlusion model,a moderate level of hypochlorous acid promoted the proliferation and differentiation of neural stem cells into neurons and astrocytes.This suggests that hypochlorous acid plays different roles at different phases of cerebral ischemia/reperfusion injury.Lower levels of hypochlorous acid(5 and 100μM)promoted nuclear translocation ofβ-catenin.By transfection of single-site mutation plasmids,we found that hypochlorous acid induced chlorination of theβ-catenin tyrosine 30 residue,which promoted nuclear translocation.Altogether,our study indicates that maintaining low levels of hypochlorous acid plays a key role in the recovery of neurological function.