Effect of Negative Online Reviews and Physician Responses on Health Consumers' Choice: Experimental Study.

BACKGROUND: The COVID-19 pandemic has highlighted the importance of online medical services. Although some researchers have investigated how numerical ratings affect consumer choice, limited studies have focused on the effect of negative reviews that most concern physicians. OBJECTIVE: This study aimed to investigate how negative review features, including proportion (low/high), claim type (evaluative/factual), and physician response (absence/presence), influence consumers' physician evaluation process under conditions in which a physician's overall rating is high. METHODS: Using a 2×2×2 between-subject decision-controlled experiment, this study examined participants' judgment on physicians with different textual reviews. Collected data were analyzed using the t test and partial least squares-structural equation modeling. RESULTS: Negative reviews decreased consumers' physician selection intention. The negative review proportion (ß=-0.371, P<.001) and claim type (ß=-0.343, P<.001) had a greater effect on consumers' physician selection intention compared to the physician response (ß=0.194, P<.001). A high negative review proportion, factual negative reviews, and the absence of a physician response significantly reduced consumers' physician selection intention compared to their counterparts. Consumers' locus attributions on the negative reviews affected their evaluation process. Physician attribution mediated the effects of review proportion (ß=-0.150, P<.001), review claim type (ß=-0.068, P=.01), and physician response (ß=0.167, P<.001) on consumer choice. Reviewer attribution also mediated the effects of review proportion (ß=-0.071, P<.001), review claim type (ß=-0.025, P=.01), and physician response (ß=0.096, P<.001) on consumer choice. The moderating effects of the physician response on the relationship between review proportion and physician attribution (ß=-0.185, P<.001), review proportion and reviewer attribution (ß=-0.110, P<.001), claim type and physician attribution (ß=-0.123, P=.003), and claim type and reviewer attribution (ß=-0.074, P=.04) were all significant. CONCLUSIONS: Negative review features and the physician response significantly influence consumer choice through the causal attribution to physicians and reviewers. Physician attribution has a greater effect on consumers' physician selection intention than reviewer attribution does. The presence of a physician response decreases the influence of negative reviews through direct and moderating effects. We propose some practical implications for physicians, health care providers, and online medical service platforms.

Exogenous nanoselenium alleviates imidacloprid-induced oxidative stress toxicity by improving phenylpropanoid metabolism and antioxidant defense system in Perilla frutescens (L.) Britt.

Few studies have been conducted to investigate the impact of pesticides on the secondary metabolism of traditional Chinese medicine and strategies to mitigate the toxicity of pesticide-induced oxidative stress. The current study focuses on evaluating the potential impacts of nano selenium (NSe) and imidacloprid (IMI) on the quality, physiological biochemistry, and secondary metabolites in Perilla frutescens (L.) Britt. (P. frutescens). The study utilized metabolome analysis to explore the toxicity mechanism of IMI. The study noted that IMI-induced stress could emerge with detrimental effects by targeting the destruction of the phenylpropanoid biosynthesis pathway. IMI-induced phenylpropanoid metabolism disorder resulted in an 8%, 17%, 25%, 10%, 65%, and 29% reduction in phenylalanine, coniferyl aldehyde, ferulic acid, cafestol, p-coumaraldehyde, and p-coumaric acid levels, respectively. Under the treatment of exogenous NSe, the levels of these metabolites were increased by 16%, 32%, 22%, 22%, 92%, and 29%, respectively. The application of exogenous NSe increased the levels of these metabolites and improved the biochemical disorder and quality of P. frutescens leaves by optimizing the phenylpropanoid metabolic pathway and enhancing the antioxidant system. Overall, the results suggest that foliar application of NSe could alleviate the oxidative stress toxicity induced by IMI and improve the quality of P. frutescens.

Novel Finding on How Melatonin and Nanoselenium Alleviate 2,4-D Butylate Stress in Wheat Plants.

Nanoselenium (nano-Se) or melatonin (MT) foliar spray reduces pesticide stress by stimulating plant secondary metabolism and antioxidant capacity. However, the effects of nano-Se and MT biofortification on the interaction between plant secondary metabolic pathways and rhizosphere microbes in mitigating 2,4-D butyrate stress remain unknown. Compared to nano-Se or MT treatment alone, nano-Se and MT combined application increased the antioxidant enzyme activities and decreased the MDA (25.0%) and H2O2 (39.3%) contents with 2,4-D butylate exposure. Importantly, they enhance the soil enzymes (S-FDA by 53.1%), allelochemicals (luteolin by 164.1% and tricin by 147.3%), as well as plant secondary metabolites (JA by 63.3% and 193.3% in leaves and roots) levels. It also improved the beneficial microbial abundance of Comamonadaceae, Sphingomonadaceae, and Rhodobacteraceae in the rhizosphere soil. In conclusion, nano-Se and MT alleviate 2,4-D butylate stress in wheat plants by enabling the interaction between rhizosphere microorganisms, allelopathic substances, and secondary metabolites.

Mitigation of Acetamiprid Residue Disruption on Pea Seed Germination by Selenium Nanoparticles and Lentinans.

The use of pesticides for pest control during the storage period of legume seeds is a common practice. This study evaluated the disruptive effects on pea seed germination and the repair effects of selenium nanoparticles (SeNPs) and lentinans (LNTs) This study examined the biomass, nutrient content, antioxidant indicators, plant hormones, phenolic compounds, and metabolites associated with the lignin biosynthesis pathway in pea sprouts. The application of acetamiprid resulted in a significant decrease in yield, amino-acid content, and phenolic compound content of pea sprouts, along with observed lignin deposition. Moreover, acetamiprid residue exerted a notable level of stress on pea sprouts, as evidenced by changes in antioxidant indicators and plant hormones. During pea seed germination, separate applications of 5 mg/L SeNPs or 20 mg/L LNTs partially alleviated the negative effects induced by acetamiprid. When used in combination, these treatments restored most of the aforementioned indicators to levels comparable to the control group. Correlation analysis suggested that the regulation of lignin content in pea sprouts may involve lignin monomer levels, reactive oxygen species (ROS) metabolism, and plant hormone signaling mediation. This study provides insight into the adverse impact of acetamiprid residues on pea sprout quality and highlights the reparative mechanism of SeNPs and LNTs, offering a quality assurance method for microgreens, particularly pea sprouts. Future studies can validate the findings of this study from the perspective of gene expression.

Combined Application of Tank-mix Adjuvants, Mist Sprayer and Nano-selenium Promoted Pesticide Reduction and Enhanced Strawberry Quality.

In this paper, several technologies suitable for strawberry crops, such as armyworm boards, tank-mix adjuvants, mist sprayers combined with pesticide reduction, and biostimulant nano-selenium, were comprehensively applied and evaluated. The combined use of 60% etoxazole and bifenazate, bucket mixing additives, nano-selenium, and mist sprayers achieved an 86% prevention effect on red spiders. The prevention effect of pesticides according to the recommended dosage was 91%. Similarly, the disease index of strawberry powdery mildew in the green control group (60% carbendazim, bucket mixing additives, nano-selenium, and mist sprayer) decreased from 33.16 to 11.11, with a decrease of 22.05. The disease index of the control group decreased from 29.69 to 8.06, with a decrease of 21.63. Additionally, the combination of pesticide reduction and nano-selenium significantly improved the antioxidant activity and soluble sugar level of strawberry fruit and reduced water loss during storage. Therefore, the integrated application of green control technologies is beneficial for reducing the amount of chemical pesticides and improving their effectiveness, while enhancing the quality of strawberry fruits in disease and pest control.

Integrated non-targeted and targeted metabolomics analysis reveals the mechanism of inhibiting lignification and optimizing the quality of pea sprouts by combined application of nano-selenium and lentinans.

BACKGROUND: Lignification causes a detrimental impact on the quality of edible sprouts. However, the mechanism of inhibition of lignification of edible sprouts by nano-selenium and lentinans remains unclear. RESULTS: To reveal the mechanism of lignification regulation of sprouts by nano-selenium and lentinans, this study investigated the changes in antioxidant indicators, phytohormones, polyphenols, and metabolites in the lignin biosynthesis in pea sprouts following sprays of nano-selenium or/and lentinans twice. There was an overall increase in the aforementioned indices following treatment. In particular, the combined application of 5 mg L-1 nano-selenium and 20 mg L-1 lentinans was more effective than their individual applications in enhancing peroxidase, catalase, DPPH free-radical scavenging rate, luteolin, and sinapic acid, as well as inhibiting malondialdehyde generation and lignin accumulation. Combined with the results from correlation analysis, nano-selenium and lentinans may inhibit lignification by enhancing antioxidant systems, inducing phytohormone-mediated signaling, and enriching precursor metabolites (caffeyl alcohol, sinapyl alcohol, 4-coumaryl alcohol). In terms of the results of non-targeted metabolomics, the combined application of 5 mg L-1 nano-selenium and 20 mg L-1 lentinans mainly affected biosynthesis of plant secondary metabolites, biosynthesis of phenylpropanoids, phenylpropanoid biosynthesis, arginine and proline metabolism, and linoleic acid metabolism pathways, which supported and complemented results from targeted screenings. CONCLUSION: Overall, the combined sprays of nano-selenium and lentinans showed synergistic effects in delaying lignification and optimizing the quality of pea sprouts. This study provides a novel and practicable technology for delaying lignification in the cultivation of edible sprouts. © 2023 Society of Chemical Industry.

Metabolomic analysis on the mechanism of nanoselenium alleviating cadmium stress and improving the pepper nutritional value.

Selenium (Se) maintains soil-plant homeostasis in the rhizosphere and regulates signaling molecules to mitigate cadmium (Cd) toxicity. However, there has been no systematic investigation of the effects of nano-selenium (nano-Se) on the regulation of non-target metabolites and nutritional components in pepper plants under Cd stress. This study investigated the effects of Cd-contaminated soil stress and nano-Se (1, 5, and 20 mg/L) on the metabolic mechanism, fruit nutritional quality, and volatile organic compounds (VOCs) composition of pepper plants. The screening of differential metabolites in roots and fruit showed that most were involved in amino acid metabolism and capsaicin production. Amino acids in roots (Pro, Trp, Arg, and Gln) and fruits (Phe, Glu, Pro, Arg, Trp, and Gln) were dramatically elevated by nano-Se biofortification. The expression of genes of the phenylpropane-branched fatty acid pathway (BCAT, Fat, AT3, HCT, and Kas) was induced by nano-Se (5 mg/L), increasing the levels of capsaicin (29.6%), nordihydrocapsaicin (44.2%), and dihydrocapsaicin (45.3%). VOCs (amyl alcohol, linalool oxide, E-2-heptaldehyde, 2-hexenal, ethyl crotonate, and 2-butanone) related to crop resistance and quality were markedly increased in correspondence with the nano-Se concentration. Therefore, nano-Se can improve the health of pepper plants by regulating the capsaicin metabolic pathway and modulating both amino acid and VOC contents.

Application of insecticides on peppermint (Mentha × piperita L.) induces lignin accumulation in leaves by consuming phenolic acids and thus potentially deteriorates quality.

Irrational use of pesticides may lead to physiological and metabolic disorders in different crops. However, there are limited investigations on impacts of insecticides on physiology and biochemistry, secondary metabolic pathways, and associated quality of medicinal plants such as peppermint (Mentha × piperita L.). In this study, target metabolites in peppermint were monitored following foliar spraying of five insecticides: imidacloprid, pyriproxyfen, acetamiprid, chlorantraniliprole, and chlorfenapyr. Compared with the control, all insecticide treatments caused a significant loss of soluble protein (decreased by 22.3-38.7%) in peppermint leaves. Insecticides induced an increase in the levels of phytohormones jasmonic acid and abscisic acid in response to these chemical stresses. Among them, imidacloprid increased jasmonic acid by 388.3%, and pyriproxyfen increased abscisic acid by 98.8%. The contents of phenylpropanoid metabolites, including rutin, quercetin, apigenin, caffeic acid, 4-hydroxybenzoic acid, ferulic acid, syringic acid, and sinapic acid showed a decreasing trend, with pyriproxyfen decreasing the levels of quercetin and 4-hydroxybenzoic acid by 78.8% and 72.6%, respectively. Combined with correlation analysis, the content of lignin in leaves shows different degrees of negative correlations with several phenolic acids. It could be inferred that insecticides may trigger plant defense mechanisms that accumulate lignin (increased by 24.6-49.1%) in leaves by consuming phenolic acids to barricade absorption of insecticides. Through constructing networks between phytohormones and secondary metabolites, peppermint may regulate the contents of caffeic acid, 4-hydroxybenzoic acid, and sinapic acid by the antagonistic effect between salicylic acid and abscisic acid in response to insecticidal stresses. Principal component analysis and systemic cluster analysis revealed that the most pronounced changes in physiological indexes and metabolites were caused by the pyriproxyfen treatment. In conclusion, this study improves our understanding of the mechanism by which insecticides affect plant physiological and metabolic processes, thus potentially altering the quality and therapeutic value of peppermint as an example.

Chlorogenic Acid Prevents Hyperuricemia Nephropathy via Regulating TMAO-Related Gut Microbes and Inhibiting the PI3K/AKT/mTOR Pathway.

Hyperuricemia is an independent hazard factor of renal injury and can induce renal fibrosis, promoting the development of chronic kidney disease (CKD). This study aimed to explore the probability of chlorogenic acid (CGA) as a potential substance for preventing hyperuricemia nephropathy (HN). Pretreatment with CGA downregulated SUA, BUN, and CR levels, relieved oxidative stress and inflammatory response, alleviated kidney fibrosis, and contributed to the prevention of HN. In the gut microbiota, Blautia, Enterococcus, and Faecalibaculum related to trimethylamine N-oxide (TMAO) synthesis were significantly increased in HN rats. In addition, it showed a significant increase in serum TMAO content in HN rats. However, CGA regulated the cascade response of the microbiota-TMAO signaling to reverse the increase of serum TMAO. CGA also decreased the protein expression of protein kinase B (AKT) phosphorylation, phosphatidylinositide 3-kinase (PI3K), and mammalian target of rapamycin (mTOR) by reducing the production of TMAO. CGA delayed kidney fibrosis in HN rats as evidenced by regulating the cascade response of the microbiota-TMAO-PI3K/AKT/mTOR signaling pathway. In summary, CGA can be an excellent candidate for HN prevention.

Sub-chronic exposure to PhIP induces oxidative damage and DNA damage, and disrupts the amino acid metabolism in the colons of Wistar rats.

Heterocyclic amines (HCAs) are a group of mutagenic compounds produced during thermal processing of protein-rich foods. One of the most abundant HCAs, 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP) has potential carcinogenic and mutagenic effects on human organs, especially the colon. This study aimed to explore the toxic effects of PhIP on amino acid metabolism in the colon of Wistar rats using RNA-seq and LC-MS/MS. Exposure to PhIP for 4 weeks induced oxidative damage and DNA damage in the colons, and disrupted the expression of related genes involved in tryptophan metabolism, beta(ß)-alanine metabolism, valine, leucine, and isoleucine degradation, and glutathione metabolic pathways. Moreover, the levels of fecal metabolites related to amino acid metabolism were affected by PhIP. Cumulatively, these results indicate that PhIP can induce colonic oxidative injury and disorders related to amino acid metabolism, thereby providing a new theoretical basis for the study of PhIP toxicity.

Chlorogenic acid supplementation ameliorates hyperuricemia, relieves renal inflammation, and modulates intestinal homeostasis.

Hyperuricemia (HUA) is induced by abnormal purine metabolism and elevated serum uric acid (UA) concentrations, and it is often accompanied by inflammatory responses and intestinal disorders. This study aims to assess the protective effects of chlorogenic acid (CGA) on HUA in mice. CGA or allopurinol was given to mice with HUA induced by hypoxanthine and potassium oxonate. CGA lowered the levels of UA, blood urea nitrogen (BUN), creatinine (CR), AST, and ALT; inhibited xanthine oxidase (XOD) activity; and downregulated the mRNA expression of UA secretory proteins in HUA mice. Moreover, CGA significantly reduced serum lipopolysaccharides (LPS) levels and the mRNA expression of interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, NOD-like receptor superfamily pyrin domain containing 3 (NLRP3), and caspase-1, and it inhibited the activation of the toll-like receptor 4/myeloid differentiation factor 88/nuclear factor kappa B (TLR4/MyD88/NF-κB) signaling pathway in the kidney, resulting in inflammation relief in HUA mice. In addition, CGA treatment increased the production of fecal short-chain fatty acids (SCFAs) in HUA mice. Additional investigations showed that CGA significantly lowered the mRNA expression of ileal IL-1ß and IL-6, and it increased the mRNA expression of intestinal tight junction proteins (zonula occludens-1 (ZO-1) and occludin). Also, CGA increased the relative abundance of SCFA-producing bacteria, including Bacteroides, Prevotellaceae UGC-001, and Butyricimonas, and it reversed the purine metabolism and glutamate metabolism functions of gut microbiota. In conclusion, CGA may be a potential candidate for relieving the symptoms of HUA and regulating its associated inflammatory responses and intestinal homeostasis.