Proof of Aerobically Autoxidized Self-Charge Concept Based on Single Catechol-Enriched Carbon Cathode Material

The self-charging concept has drawn considerable attention due to its excellent ability to achieve environmental energy harvesting,conversion and storage without an external power supply.However,most self-charging designs assembled by multiple energy harvesting,conversion and storage materials increase the energy transfer loss;the environmental energy supply is generally limited by climate and meteorological conditions,hindering the potential application of these selfpowered devices to be available at all times.Based on aerobic autoxidation of catechol,which is similar to the electrochemical oxidation of the catechol groups on the carbon materials under an electrical charge,we proposed an air-breathing chemical self-charge concept based on the aerobic autoxidation of catechol groups on oxygen-enriched carbon materials to ortho-quinone groups.Energy harvesting,conversion and storage functions could be integrated on a single carbon material to avoid the energy transfer loss among the different materials.Moreover,the assembled Cu/oxygen-enriched carbon battery confirmed the feasibility of the air-oxidation self-charging/electrical discharging mechanism for potential applications.This air-breathing chemical self-charge concept could facilitate the exploration of high-efficiency sustainable air self-charging devices.

The Adsorption Properties of TEMPO Oxidized Cellulose against the Mixture of Methylene Blue and Rhemazol Yellow FG

TEMPO/NaOCl/NaBr treatment significantly increased the number of negative charges on the cellulose surface.Two concentrations of NaOCl,5 and 30 mmol/g of cellulose,were used in this study.The number of carboxyl groups in the two cellulosic samples oxidized using TEMPO/NaOCl/NaBr was 0.5160 and 1.8461 mmol/g of cellulose,respectively.The oxidized cellulose samples treated with 5 and 30 mmol/g NaOCl exhibited higher crystallinity,at 81.15%and 80.14%,respectively,compared to untreated cellulose,which had a crystallinity of 75.95%.The pH effect indicated that the highest adsorption capacity for methylene blue was achieved under alkaline conditions(pH 9),while the highest adsorption capacity for rhemazol yellow FG was achieved under acidic conditions.The kinetic model of TEMPO-oxidized cellulose for methylene blue and rhemazol yellow FG conformed to the pseudo-second-order model.The initial concentration parameter revealed that the isotherm model for the adsorption of methylene blue and rhemazol yellow FG by TEMPO-oxidized cellulose conformed to the Langmuir model.The dye removal efficiencies for methylene blue and rhemazol yellow FG using TEMPOoxidized cellulose(30 mmol/g)were approximately 80.17%and 59.52%,respectively.These results demonstrate that TEMPO/NaOCl/NaBr-oxidized samples can effectively separate cationic and anionic dye mixtures.Furthermore,the use of TEMPO-oxidized cellulose showed good regeneration capability,maintaining more than 95%of its adsorption capacity after 8 cycles.

Research Progress in Preparation of Oxidized Cellulose

Cellulose is the most abundant natural polymer material in the world.Cellulose is diffi-cult to dissolve because it contains a large number of inter molecular hydrogen bonds.Therefore,the modification of natural cellulose by chemical oxidation can expand its application field.The oxidation process of cellulose is focused on,the oxidation methods and research progress of cellulose are introduced,and further development direction of oxidized cellulose is prospected.

The emerging role of nitric oxide in the synaptic dysfunction of vascular dementia

With an increase in global aging,the number of people affected by cerebrovascular diseases is also increasing,and the incidence of vascular dementia-closely related to cerebrovascular risk-is increasing at an epidemic rate.However,few therapeutic options exist that can markedly improve the cognitive impairment and prognosis of vascular dementia patients.Similarly in Alzheimer’s disease and other neurological disorders,synaptic dysfunction is recognized as the main reason for cognitive decline.Nitric oxide is one of the ubiquitous gaseous cellular messengers involved in multiple physiological and pathological processes of the central nervous system.Recently,nitric oxide has been implicated in regulating synaptic plasticity and plays an important role in the pathogenesis of vascular dementia.This review introduces in detail the emerging role of nitric oxide in physiological and pathological states of vascular dementia and summarizes the diverse effects of nitric oxide on different aspects of synaptic dysfunction,neuroinflammation,oxidative stress,and blood-brain barrier dysfunction that underlie the progress of vascular dementia.Additionally,we propose that targeting the nitric oxide-sGC-cGMP pathway using certain specific approaches may provide a novel therapeutic strategy for vascular dementia.

Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Hypidone hydrochloride(YL-0919)ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation

Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary injury.In this study,we evaluated hypidone hydrochloride(YL-0919),a self-developed antidepressant with selective sigma-1 receptor agonist properties,and its associated mechanisms and targets in traumatic brain injury.Behavioral experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain edema.Next,we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in HT22 cells.Finally,the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist(BD-1047).Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury,while also decreasing neuronal mortality and reversing blood-brain barrier disruption and brain edema.Furthermore,YL-0919 effectively combated oxidative stress both in vivo and in vitro.The protective effects of YL-0919 were partially inhibited by BD-1047.These results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress,a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist BD-1047.YL-0919 may have potential as a new treatment for traumatic brain injury.

Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

Effect of alkali treatments on apatite formation of microarc-oxidized coating on titanium alloy surface

Alkali treatments with three concentrations were used to modify a microarc-oxidized(MAO) coating on titanium alloy surface in order to further improve its surface bioactivity. Morphology, chemical compositions and phase constitues, roughness, contact angle and apatite induction of the alkali-treated coatings were studied and compared. Scanning electron microscope(SEM) was applied to observe the morphologies, X-ray diffraction(XRD) and X-ray photoelectron spectroscopy(XPS) were used to detect the phase constitutes and chemical compositions, a surface topography profilometer was used to analyze the surface roughness, and contact angle was measured by liquid drop method. Alkali treatements result in the formation of Na2Ti6O13 and Na2Ti3O7 phase on the MAO coating, which leads to the increase of surface roughness and the decrease of contact angle. Experimental results showed that the apatite induction of the alkali-treated coatings was dependent on the applied alkali concentrations during treatments, and Na+concentration can promote the formation of apatite phase.

Fabrication of Silicon Condenser Microphone Using Oxidized Porous Silicon as Sacrificial Layer

A new technique to fabricate silicon condenser microphone is presented.The technique is based on the use of oxidized porous silicon as sacrificial layer for the air gap and the heavy p+-doping silicon of approximately 15μm thickness for the stiff backplate.The measured sensitivity of the microphone fabricated with this technique is in the range from -45dB(5.6mV/Pa) to -55dB(1.78mV/Pa) under the frequency from 500Hz to 10kHz,and shows a gradual increase at higher frequency.The cut-off frequency is above 20kHz.

Inhibitory Effects of Sodium Ferulate on Proliferation of Rabbit Aortic Smooth Muscle Cells Induced by Oxidized LDL

The effects of sodium ferulate(SF), a water-soluble element of Chinese medicine Angelica sinensis diels, on cell-mediated oxidative modification of human low density lipoprotein(LDL) and proliferation of rabbit aortic smooth muscle cells(SMCs) were investigated. Using experimental models of proliferation of cultured rabbit aortic SMCs induced by oxidized LDL(ox-LDL), the extent of oxidation was determined by thiobarbituric acid reactive substances(TBARS) method, MTT colorimetry and 3H-thymidine(3H-TdR) incorporation were used to observe proliferation of SMCs. It showed that SF effectively inhibited cell-mediated oxidation induced by Cu2+ in a concentration-dependent manner. At the final concentration of 40, 80, 120 gmL-1, SF could significantly inhibit 3H-TdR incorporation and cell Proliferation in a dose-dependent manner. The results indicated that SF could, in vitro protect LDL against oxidative modification and inhibit the proliferation of SMC, which might be due to its free radical scavenging capacity.

Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis

Objective PERK/elF2/CHOP is a major signaling pathway mediating endoplasmic reticulum （ER） stress related with atherosclerosis. Oxidized LDL （ox-LDL） also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis. The present study was conducted to explore the regulatory effect of ox-LDL on PERK/elF2a/CHOP signaling pathway in vascular endothelial cells. Methods The effects of ox-LDL on PERK and p-elF2a protein expression of primary human umbilical vein endothelial cells （HUVECs） were investigated by Western blot analysis. PERK gene silencing and selective elF2a phosphatase inhibitor, salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis, caspase-3 activity, and CHOP mRNA level. Results Ox-LDL treatment significantly increased the expression of PERK, PERK-mediated inactivation of elF2a phosphorylation, and the expression of CHOP, as well as the caspase-3 activity and apoptosis. The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral shRNA or by selective elF2a phosphatase inhibitor, salubrinal. Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/elF2a/CHOP ER-stress pathway. It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis.

Effect of Kovar alloy oxidized in simulated N_2/H_2O atmosphere on its sealing with glass

The effect of Kovar alloy oxidized in simulated field atmosphere on its sealing with glass was studied in this article. After Kovar plates and pins were preoxidized in N2 with 0℃, 10℃ and 20℃ dew points at 1000℃ for different times, Fe304 and Fe203 existed in the oxidation products on Kovar surface, and the quantity of Fe203 increased with increasing dew point and oxidation time. Then they were sealed with borosilicate glass insulator at 1030℃ for 20 rain. The results indicated that the type and quantity of oxidation products would directly influence the quality of glass-to-metal seals. With the increase of oxidation products, gas bubbles in the glass insulator were more serious, the climbing height of glass along the pins was higher, and corrosion of Kovar pins caused from the molten glass was transformed from uniform to the localized.

Enhanced visible-light photocatalytic degradation and disinfection performance of oxidized nanoporous g-C3N4 via decoration with graphene oxide quantum dots

Oxidized nanoporous g-C3N4(PCNO)decorated with graphene oxide quantum dots(ox-GQDs)was successfully prepared by a facile self-assembly method.As co-catalysts,the ultrasmall zero-dimensional(0 D)ox-GQDs can achieve uniform dispersion on the surface/inner channels of PCNO,as well as intimate contact with PCNO through hydrogen bonding,π-π,and chemical bonding interactions.In contrast with PCNO,the ox-GQDs/PCNO composite photocatalysts possessed improved light-harvesting ability,higher charge-transfer efficiency,enhanced photooxidation capacity,and increased amounts of reactive species due to the upconversion properties,strong electron capturing ability,and peroxidase-like activity of the ox-GQDs.Therefore,the visible-light photocatalytic degradation and disinfection performances of the ox-GQDs/PCNO composite were significantly enhanced.Remarkably,the composite with a 0.2 wt.% deposited amount of ox-GQDs(ox-GQDs-0.2%/PCNO)exhibited optimum amaranth photodegradation activity,with a corresponding rate about 3.1 times as high as that of PCNO.In addition,ox-GQDs-0.2%/PCNO could inactivate about 99.6%of Escherichia coli(E.coli)cells after 4 h of visible light irradiation,whereas only^31.9% of E.coli cells were killed by PCNO.Furthermore,h+,·O2-,and·OH were determined to be the reactive species generated in the photocatalytic process of the ox-GQDs/PCNO system;these species can thoroughly mineralize azo dyes and effectively inactivate pathogenic bacteria.

Influence of Oxidized Low Density Lipoprotein on the Proliferation of Human Artery Smooth Muscle Cells in vitro

The effects of oxidized low density lipoprotein （ox-LDL） on the proliferation of cultured human vascular smooth muscle cells （vSMC） were investigated in vitro. By using NaBr density gradient centrifugation, LDL was isolated and purified from human plasma. Ox-LDL was produced from LDL by being incubated with CuSO4. ox-LDL was then added to the culture medium at different concentrations （35, 60, 85, 110, 135 and 160μg/mL） for 7 days. The influence of ox-LDL on vSMC proliferation was observed in growth curve, mitosis index, and in situ determination of apoptosis. The data were analyzed with SPSS 10.0 software. The results showed that the ox-LDL produced in vitro had a good purity and optimal oxidative degree, which was similar to the intrinsic ox-LDL in atherosclerotic plaque, ox-LDL at a concentration of 35 μg/mL demonstrated the strongest proliferation inducement, and at a concentration of 135 μg/mL, ox-LDL could inhibit the growth of vSMC. ox-LDL at concentrations of 35 and 50 μg/mL presented powerful mitotic trigger, and with the increase of ox-LDL concentration, the mitotic index of vSMC was decreased gradually, ox-LDL at higher concentrations promoted more apoptotic vSMCs, ox-LDL at lower concentrations triggered proliferation of vSMCs, and at higher concentrations induced apoptosis in vSMCs, ox-LDL played a promotional role in the pathogenesis and development of atherosclerosis by affecting vSMC proliferation and apoptosis.

Influence of flux additives on iron ore oxidized pellets

Six additives,i.e.,limestone,lime,magnesite,magnesia,dolomite and light-burned-dolomite,were added for investigating their influences on the pellet quality.For green balls,adding lime and light-burned-dolomite makes the wet drop strength decrease firstly,and then increase with further increase of additive dosage.Ca(OH)2 affects the bentonite properties at the beginning,but the binding property of Ca(OH)2 will be main when the dosage is higher.The other four additives decrease the drop strength for their disadvantageous physical properties.For preheated pellets,no mater what kind of additive is added,the compressive strength will be decreased because of unmineralized additives.For roasted pellets,calcium additives can form binding phase of calcium-ferrite,and suitable liquid phase will improve recrystallization of hematite,but excessive liquid will destroy the structure of pellets,so the compressive strength of pellet increases firstly and then drops.When adding magnesium additives,the strength will be decreased because of the oxidation of magnetite retarded by MgO.

Resveratrol alleviates oxidative stress induced by oxidized soybean oil and improves gut function via changing gut microbiota in weaned piglets

Background Oxidized soybean oil(OSO)has been shown to impair growth and exacerbate inflammation,leading to intestinal barrier injury in animals.Recent evidence suggests important roles for resveratrol(RES)in the promoting growth performance,antioxidant capacity,anti-inflammatory,and regulate intestinal barriers in animals.Therefore,The objectives of this study are to investigate the effects of dietary RES(purity 98%)supplementation on the growth performance,antioxidant capacity,inflammatory state,and intestinal function of weaned piglets challenged with OSO.Methods A total of 28 castrated weaned male piglets with a similar body weight of 10.197 replications per treatment and±0.10 kg were randomly assigned to 4 dietary treatments for 28-d feeding trial with 1 piglet per replicate.Treatments were arranged as a 2×2 factorial with oil type[3%fresh soybean oil(FSO)vs.3%OSO]and dietary RES(0vs.300 mg/kg).Results The results showed that relative to the FSO group,OSO stress tended to decrease the average daily feed intake(ADFI),and decreased the activity levels of lipase,villus/crypt ratio(VCR),the mRNA expression of FABP1,SOD2,IL-10 and ZO-1 in the jejunum,and SOD2,GPX1,occludin and ZO-1 in the colon,the levels of acetic acid in the colonic digesta,whereas up-regulated the mRNA expression of IL-1βand TNF-αin the jejunum(P<0.05).Moreover,dietary supplementation with RES increased ether extract(EE),the activity levels of sucrase,lipase,α-amylase,villus height(VH)and VCR,the mRNA expression of FABP1,SOD2,IL-10 and occludin in the jejunum,and FABP1,PPAR-γ,GPX1,occludin and ZO-1 in the colon,and the abundance of Firmicutes,acetic and propionic acid,but decreased the levels of D-lactic acid in the plasma,the abundance of Bacteroidetes in the colonic digesta of weaned piglets compared to the non-RES group(P<0.05).Meanwhile,in the interaction effect analysis,relative to the OSO group,dietary RES supplementation in the diets supplemented with OSO increased the activity levels of trypsin,VH in the jejunum,the abundance of Actinobacteria,the levels of butyric acid of weaned piglets,but failed to influence the activity levels of trypsin and VH,Actinobacteria abundance,the levels of butyric acid when diets were supplemented with FSO(interaction,P<0.05).Relative to the OSO group,dietary RES supplementation in the diets supplemented with OSO decreased the activity levels of DAO in the plasma of weaned piglets but failed to influence the activity levels of DAO when diets were supplemented with FSO(interaction,P<0.05).Relative to the FSO group,dietary RES supplementation in the diets supplemented with FSO decreased the level of propionic acid,whereas RES supplementation failed to influence the level of propionic acid when the diet was supplemented with OSO(interaction,P<0.01).Conclusions Inclusion of OSO intensified inflammatory states and impaired the intestinal health characteristics of weaned piglets.Dietary RES supplementation improved the antioxidant capacity,anti-inflammatory activity,and intestinal morphology.Further studies showed that the protective effects of RES on gut health could be linked to the decreased abundance of Prevotella_1,Clostridium_sensu_stricto_6,and Prevotellaceae_UCG003 and increased levels of acetic and propionic acid.

Characterization of Micro-arc Oxidized Titanium

The observation of the sparkling discharges during the micro-arc oxidation process in KOH aqueous electrolyte was achieved. The change of surface morphology was progressively observed and a plausible pore formation mechanism is proposed. Cell proliferation and ALP activity of micro- arc oxidized titanium was evaluated by human body derived osteoblasts and sligtaly better than those of blasted surface.

Anti-oxidized low-density lipoprotein antibodies in chronic heart failure

Oxidative stress may play a significant role in the pathogenesis of heart failure(HF).Antibodies to oxidized low-density lipoprotein(oxLDL Abs) reflect an immune response to LDL over a prolonged period and may represent long-term oxidative stress in HF.The oxLDL plasma level is a useful predictor of mortality in HF patients,and measurement of the oxLDL Abs level may allow better management of those patients.Antibodies to oxLDL also significantly correlate with the New York Heart Association score.Hypercholesterolemia,smoking,hypertension,and obesity are risk factors for atherosclerotic coronary heart disease(CHD) leading to HF,but these factors account for only onehalf of all cases,and understanding of the pathologic process underlying HF remains incomplete.Nutrients with antioxidant properties can reduce the susceptibility of LDL to oxidation.Antioxidant therapy may be an adjunct to lipid-lowering,angiotensin converting enzyme inhibition and metformin(in diabetes) therapy for the greatest impact on CHD and HF.Observational data suggest a protective effect of antioxidant supple-mentation on the incidence of HD.This review summarizes the data on oxLDL Abs as a predictor of morbidity and mortality in HF patients.

Effect of Molecular Weight and Structure on Antitumor Activity of Oxidized Chitosan

Various low molecular weight chitosans were prepared by oxidative degradation with H2O2, and characterized by IR,13C-NMR and gel permeation chromatography. Their carboxylic contents increased with decrease in molecular weight (M w ). The antitumor test of the samples against sarcoma 180 tumors suggested that the water-soluble chitosan with higherM w have higher inhibitory ratioin vivo. The introduction of carboxylic group is advantage to water-solubility of chitosan, but more acidic groups might decrease the function of amino groups of chitosan against sarcoma 180 tumor.