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Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Lipid droplet (LD) is a metabolically active organelle, which changes dynamically with the metabolic state and energy requirements of cells. Proteins that either insert into the LD phospholipid monolayer or are present in the cytoplasm, playing a crucial role in lipid homeostasis and signaling regulation, are known as LD-associated proteins. Methods: The keywords "lipid droplets" and "metabolic diseases" were used to obtain literature on LD metabolism and pathological mechanism. After searching databases including Scopus, OVID, Web of Science, and PubMed from 2013 to 2024 using terms like "lipid droplets", "lipid droplet-associated proteins", "fatty liver disease", "diabetes", "diabetic kidney disease", "obesity", "atherosclerosis", "hyperlipidemia", "natural drug monomers" and "natural compounds", the most common natural compounds were identified in about 954 articles. Eventually, a total of 91 studies of 10 natural compounds reporting in vitro or in vivo studies were refined and summarized. Results: The most frequently used natural compounds include Berberine, Mangostin, Capsaicin, Caffeine, Genistein, Epigallocatechin-3-gallate, Chlorogenic acid, Betaine, Ginsenoside, Resveratrol. These natural compounds interact with LD-associated proteins and help ameliorate abnormal LDs in various metabolic diseases. Conclusion: Natural compounds involved in the regulation of LDs and LD-associated proteins hold promise for treating metabolic diseases. Further research into these interactions may lead to new therapeutic applications. [ABSTRACT FROM AUTHOR]

Mitochondrial damage is an early and key marker of neuronal damage in prion diseases. As a process involved in mitochondrial quality control, mitochondrial biogenesis regulates mitochondrial homeostasis in neurons and promotes neuron health by increasing the number of effective mitochondria in the cytoplasm. Sirtuin 1 (SIRT1) is a NAD+-dependent deacetylase that regulates neuronal mitochondrial biogenesis and quality control in neurodegenerative diseases via deacetylation of a variety of substrates. In a cellular model of prion diseases, we found that both SIRT1 protein levels and deacetylase activity decreased, and SIRT1 overexpression and activation significantly ameliorated mitochondrial morphological damage and dysfunction caused by the neurotoxic peptide PrP106–126. Moreover, we found that mitochondrial biogenesis was impaired, and SIRT1 overexpression and activation alleviated PrP106–126-induced impairment of mitochondrial biogenesis in N2a cells. Further studies in PrP106–126-treated N2a cells revealed that SIRT1 regulates mitochondrial biogenesis through the PGC-1α-TFAM pathway. Finally, we showed that resveratrol resolved PrP106–126-induced mitochondrial dysfunction and cell apoptosis by promoting mitochondrial biogenesis through activation of the SIRT1-dependent PGC-1α/TFAM signaling pathway in N2a cells. Taken together, our findings further describe SIRT1 regulation of mitochondrial biogenesis and improve our understanding of mitochondria-related pathogenesis in prion diseases. Our findings support further investigation of SIRT1 as a potential target for therapeutic intervention of prion diseases. [ABSTRACT FROM AUTHOR]

The process of apoptotic cell clearance by phagocytes, known as efferocytosis, plays an essential role in maintaining homeostasis. Defects in efferocytosis can lead to inflammatory diseases such as atherosclerosis and autoimmune disorders. Therefore, the maintenance and promotion of efferocytosis are considered crucial for preventing these diseases. In this study, we observed that resveratrol, a representative functional food ingredient, and its glycoside, piceid, promoted efferocytosis in both human THP-1 macrophages differentiated with phorbol 12-myristate 13-acetate and peritoneal macrophages from thioglycolate-elicited mice. Resveratrol and piceid significantly increased mRNA expression and protein secretion of MFG-E8 in THP-1 macrophages. Furthermore, the activation of efferocytosis and the increment in MFG-E8 protein secretion caused by resveratrol or piceid treatment were canceled by MFG-E8 knockdown in THP-1 macrophages. In conclusion, we have demonstrated for the first time that resveratrol and piceid promote efferocytosis through the upregulation of MFG-E8 excretion in human THP-1 macrophages. [ABSTRACT FROM AUTHOR]

As the aging population continues to increase, aging-related inflammation, oxidative stress, and neurodegenerative diseases have become serious global health threats. Resveratrol, a star molecule in natural polyphenols, has been widely reported to have physiological activities such as anti-aging, anti-inflammatory, antioxidant, and neuroprotection. However, its poor water solubility, rapid metabolism, low bioavailability and poor targeting ability, which limits its application. Accordingly, a brain-targeted resveratrol liposome (ANG-RES-LIP) was developed to solve these issues. Experimental results showed that ANG-RES-LIP has a uniform size distribution, good biocompatibility, and a drug encapsulation rate of over 90%. Furthermore, in vitro cell experiments showed that the modification of the targeting ligand ANG significantly increased the capability of RES to cross the BBB and neuronal uptake. Compared with free RES, ANG-RES-LIP demonstrated stronger antioxidant activity and the ability to rescue oxidatively damaged cells from apoptosis. Additionally, ANG-RES-LIP showed the ability to repair damaged neuronal mitochondrial membrane potential. In vivo experiments further demonstrated that ANG-RES-LIP improved cognitive function by reducing oxidative stress and inflammation levels in the brains of aging model mice, repairing damaged neurons and glial cells, and increasing brain-derived neurotrophic factor. In summary, this study not only provides a new method for further development and application of resveratrol but also a promising strategy for preventing and treating age-related neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Background: Growing incidences of chronic wounds recommend the development of optimal therapeutic wound dressings. Electrospun nanofibers have been considered to show potential wound healing properties when accompanied by other wound dressing materials. This study aimed to explore the potential role of Chitosan (CS) nanofibrous mats coated with resveratrol (RS) as an antioxidant and pro‐angiogenic agent in rat models of skin wound healing. Methods: Electrospun chitosan/polyethylene oxide (PEO) nanofibers were prepared using electrospinning technology and coated by 0.05 and 0.1 mg.ml resveratrol named as (CS/RS 0.05) and (CS/RS 0.1), respectively. The scaffolds were characterized physiochemically such as in vitro release study, TGA, FTIR spectroscopy analysis, biodegradability, and human dermal fibroblast seeding assay. The scaffold was subsequently used in vivo as a skin substitute on a rat skin wound model. Results: In vitro tests revealed that all scaffolds promoted cell adhesion and proliferation. However, more cell viability was observed in CS/RS 0.1 scaffold. The biocompatibility of the scaffolds was validated by MTT assay, and the results did not show any toxic effects on human dermal fibroblasts. It was observed that RS‐coated scaffolds had the ability to release RS in a controlled manner. In in vivo tests CS/RS 0.1 scaffold had the greatest impact on the healing process by improving the neodermis formation and modulated inflammation in wound granulation tissue. Histological analysis revealed enhanced vascular endothelial growth factor expression, epithelialization and increased depth of wound granulation tissue. Conclusions: The RS‐coated CS/PEO nanofibrous scaffold accelerates wound healing and may be useful as a dressing for cell transfer and clinical skin regeneration. [ABSTRACT FROM AUTHOR]

Melasma is a chronic, acquired disorder of focal hypermelanosis that carries significant psychosocial impact and is challenging for both the patient and the treating practitioner to manage in the medium to long term. Multiple treatments have been explored, often in combination given the many aetiological factors involved in its pathogenesis. Therapeutic discoveries to treat melasma are a focal topic in the literature and include a range of modalities, with recent developments including updates on visible light photoprotection, non-hydroquinone depigmenting agents, oral tranexamic acid, chemical peels, and laser and energy-based device therapy for melasma. It is increasingly important yet challenging to remain up-to-date on the arsenal of treatments available for melasma to find an efficacious and well-tolerated option for our patients. [ABSTRACT FROM AUTHOR]

Objective(s): Liver fibrosis is a wound healing response characterized by excessive accumulation of extracellular matrix proteins. This study aimed to investigate the effects of resveratrol treatment on the TGF-β/SMAD signaling pathway and related biochemical parameters, apoptosis, and liver regeneration phenobarbital-CCl4 induced hepatic fibrosis rat model. Materials and Methods: This model was created through phenobarbital and CCl4 (0.2–0.35 ml/kg). Resveratrol (1 mg/kg/day) was administered to the fibrosis and control groups. Immunohistochemical staining was performed to evaluate αSMA, TGF-β1, and PCNA in liver tissue. The TUNEL method and Masson’s Trichome staining were used to determine apoptosis and collagen accumulation. AST, ALP, ALT, total protein, and total bilirubin levels were measured to determine biochemical status. SMAD2, SMAD3, SMAD4, and SMAD7 expression levels were measured to determine TGF-β1 related hepatic fibrosis. Results: The SMAD2, SMAD3, and SMAD4 mRNA expression levels were increased and the SMAD7 mRNA expression level was decreased in the fibrosis control group. The SMAD7 mRNA expression level was higher in the phenobarbital-CCl4 induced resveratrol treated group. Increased biochemical parameters indicating hepatic damage, increased number of apoptotic cells, and collagen accumulation surrounding the central vein were observed in the fibrosis group compared with the other groups. It was concluded that administration of resveratrol ameliorates the adverse effects of hepatic fibrosis by regulating biochemical parameters, controlling TGF-β1/SMAD signaling, enhancing tissue regeneration, and reducing apoptosis in liver cells. Conclusion: Resveratrol can be a beneficial option for the prevention of liver damage in a phenobarbital-CCl4 induced hepatic fibrosis. [ABSTRACT FROM AUTHOR]

To investigate the effects of resveratrol (Res) on human fetal scleral fibroblasts (HFSFs) and its potential mechanism. HFSFs were randomly divided into the Res-treated group and the control group. Following, HFSFs were treated with or without a concentration of 10 μM Res for 48 h. To detect the expression of related genes, reverse transcription quantitative PCR (RT-qPCR) and western blotting were used. The apoptosis rate of different groups was determined using flow cytometry. The mRNA expression of matrix metalloproteinase 2 (MMP-2), Collagen, Type I, Alpha 1 (COL1A1), Janus Kinase 2 (JAK2), and Signal Transducer and Activator of Transcription 3 (STAT3)" was downregulated in the Res-treatment group compared to the control group, according to RT-qPCR. Western blotting revealed that Res therapy reduced the expression of MMP-2, JAK2, P-JAK2, STAT3, P-STAT3, and Bcl-2 associated protein X (Bax) while increasing the expression of COL1A1 and B-cell lymphoma-2 (Bcl-2). Flow cytometry showed that the cell apoptosis rate was significantly lower in HFSFs treated with Res. In conclusion, these findings suggest that Res increases COL1A1 expression while inhibiting MMP-2 and cell apoptosis in HFSFs, possibly through modulation of the JAK2/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Aim: This research endeavored to explore the impact and underlying mechanisms of resveratrol on the phenomenon of "metabolic memory" in cultured human retinal vascular endothelial cells (HRVECs) under high-glucose (HG) conditions. Materials and Methods: According to the glucose level and treatment, cultured HRVECs were divided into seven groups: normal glucose (NG), HG, high glucose followed by NG (HN), mannitol (Man), resveratrol, thioredoxin-interacting protein (TXNIP)-small interfering ribonucleic acid (siRNA), and N -acetylcysteine (NAC). The expression levels of TXNIP, nucleotide oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, intercellular adhesion molecule 1 (ICAM-1), caspase-1, interleukin-1β (IL-1β), B-cell lymphoma 2 (Bcl-2), caspase-3, and Bcl-2-associated X (BAX), as well as reactive oxygen species (ROS) production, were measured. Cell apoptosis was assessed through a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Results: In HRVECs from the HG group, expression levels of TXNIP, NLRP3, caspase-1, ICAM-1, and IL-1β were upregulated. However, in the HN group, the above upregulations were not reversed. After the administration of resveratrol, the expression levels of TXNIP, NLRP3, and other inflammatory cytokines were significantly reduced. Resveratrol mitigated the elevated ROS production induced by HG conditions. In the NAC group, the expression of TXNIP and inflammatory cytokines was downregulated. TXNIP-siRNA treatment showed similar effects. Resveratrol inhibited apoptosis as well as reversed the downregulation of BCL-2 and the upregulation of caspase-3 and BAX induced by HG conditions. Conclusion: Resveratrol mitigated the HG-induced phenomenon of "metabolic memory" by inhibiting inflammation and apoptosis via modulation of the ROS/TXNIP/NLRP3 signaling pathway in cultured HRVECs. Therefore, resveratrol may have therapeutic potential to treat diabetic retinopathy and related metabolic memory complications. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the impact of ethanol extracts from sea buckthorn and Cornelian cherry fruits and leaves on physiology of gastrointestinal tract cells. We used three cell lines relevant to the types of cells, which are exposed to bioactive compounds after oral administration, namely intestinal absorptive cells (Caco-2/HT-29 MTX model), hepatocytes (HepG2 cells) and immunocompetent cells (RAW 264.7 and P388D1 monocytes). The contents of antioxidant and bioactive polyphenols, such as cinnamic, caffeic and p-coumaric acids, rutin, myricetin, resveratrol, quercetin, apigenin and kaempferol, were assessed in the extracts using HPLC chromatography. The application of the extracts to Caco-2/HT-29-MTX cultures increased enterocyte differentiation markers (alkaline phosphatase and villin1 level) and goblet cell markers (mucins) over a fortnight. The extracts reduced lipid droplet size in hepatocytes challenged with hyperglycaemic glucose concentration, insulin and palmitate. Sea buckthorn leaf, fruit and Cornelian cherry leaf extracts blocked oxidative burst in the PMA-stimulated monocytes, while the sea buckthorn leaf and Cornelian cherry fruit extracts downregulated lipopolysaccharide-induced NO and IL-1β, respectively. The results indicate that the tested extracts modulate the behaviour of cells in the gastrointestinal tract in a beneficial way, especially regarding lipid accumulation and innate immunity actions. [ABSTRACT FROM AUTHOR]

In this study, we discovered the mechanisms underlying parecoxib and resveratrol combination's anti-cancer characteristics against human colorectal cancer DLD-1 cells. We studied its anti-proliferation and apoptosis-provoking effect by utilizing cell viability 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, fluorescence microscope, gene overexpression, Western blot, and flow cytometry analyses. Parecoxib enhanced the ability of resveratrol to inhibit cell viability and increase apoptosis. Parecoxib in combination with resveratrol strongly enhanced apoptosis by inhibiting the expression of thioredoxin domain containing 5 (TXNDC5) and Akt phosphorylation. Parecoxib enhanced resveratrol-provoked c-Jun N-terminal kinase (JNK) and p38 phosphorylation. Overexpression of TXNDC5 and repression of JNK and p38 pathways significantly reversed the inhibition of cell viability and stimulation of apoptosis by the parecoxib/resveratrol combination. This study presents evidence that parecoxib enhances the anti-cancer power of resveratrol in DLD-1 colorectal cancer cells via the inhibition of TXNDC5 and Akt signaling and enhancement of JNK/p38 MAPK pathways. Parecoxib may be provided as an efficient drug to sensitize colorectal cancer by resveratrol. [ABSTRACT FROM AUTHOR]

The medicinal properties of resveratrol have garnered increasing attention from researchers. Extensive data have been accumulated on its use in treating cardiovascular diseases, immune system disorders, cancer, neurological diseases, and behavioral disorders. The protective mechanisms of resveratrol, particularly in anxiety-related stress disorders, have been well documented. However, less attention has been given to the side effects of resveratrol. This review explores not only the mechanisms underlying the anxiolytic effects of resveratrol but also the mechanisms that may lead to increased anxiety following resveratrol treatment. Understanding these mechanisms is crucial for enhancing the efficacy of resveratrol in managing anxiety disorders associated with stress and PTSD. [ABSTRACT FROM AUTHOR]

Resveratrol (RES) is a lipophilic polyphenol susceptible to photo- and thermal-degradation. The strategies to enable its distribution in food matrices, prevent its degradation during storage and improve its bioaccessibility during digestion have obtained much attention and studies. In the present study, natural porous matrix in the form of freeze-dried yogurt cubes (FDYC) was investigated as an absorbent for loading RES. The sodium caseinate (NaCas)-coconut oil lotion was used as a carrier for delivering RES and was added to milk medium for L. helveticus MB2-1 fermentation to obtain freeze-dried Sayram ketteki yogurt cubes (SKYC) with fortified RES. The results showed that the loading capacity of RES in SKYC was 28.08 ± 0.31% in freshly prepared samples and was 26.34 ± 0.13% (93.80 ± 0.17% retention) after 90 d of ambient storage in amber vials. The photothermal stability of RES encapsulated in SKYC was significantly higher than that of the original RES due to the protective effect of SKYC (p < 0.05). During in vitro simulated gastrointestinal digestion, the RES release rate of the three treatments were in the following order: original RES < physical mixture of RES < encapsulated RES. Besides, the flavor of SKYC was enriched by the addition of NaCas-coconut oil lotion. Taken together, it can be demonstrated the SKYC has the potential to be loaded with lipophilic bioactive compounds for application in functional food. Highlights: The Sayram ketteki yogurt cubes fortified with RES were prepared. The RES changed into non-crystalline form after emulsification and encapsulation. The RES encapsulated in Sayram ketteki yogurt had significantly better stability. The 2H-pyrano-2 ketone enriched a rich coconut flavor to the fortified yogurt. [ABSTRACT FROM AUTHOR]

Diabetic peripheral neuropathy (DPN) is caused by several factors, including reactive free oxygen radicals (ROS)-induced excessive Ca2+ influx. Transient receptor potential (TRP) vanilloid 4 (TRPV4) is a member of the Ca2+-permeable TRP superfamily. Resveratrol (RESV) has been extensively utilized in TRP channel regulation due to its pharmacological properties, which include antioxidant and TRP inhibitory effects. The protective function of RESV and the contribution of TRPV4 to streptozotocin (STZ)-induced neuropathic pain in mice are still unclear. Here, we evaluated the effects of RESV through the modulation of TRPV4 on Ca2+ influx, ROS-mediated pain, apoptosis, and oxidative damage in the mouse dorsal root ganglion (DRGs). From the 32 mice, four groups were induced: control, RESV, STZ, and STZ + RESV. We found that the injection of RESV reduced the changes caused by the STZ-induced stimulation of TRPV4, which in turn increased mechanical/thermal neuropathic pain, cytosolic Ca2+ influx, TRPV4 current density, oxidants (lipid peroxidation, mitochondrial ROS, and cytosolic ROS), and apoptotic markers (caspase-3, -8, and -9). The RESV injection also increased the STZ-mediated reduction of viability of DRG and the amounts of glutathione, glutathione peroxidase, vitamin A, β-carotene, and vitamin E in the brain, erythrocytes, plasma, liver, and kidney. All of these findings suggest that TRPV4 stimulation generates oxidative neurotoxicity, neuropathic pain, and apoptosis in the STZ-induced diabetic mice. On the other hand, neurotoxicity and apoptosis were reduced due to the downregulation of TRPV4 carried out through the RESV injection. An overview of how resveratrol (RESV) inhibits TRPV4 in mice to modulate the effects of diabetes mellitus-induced diabetic peripheral neuropathy (DPN). Ruthenium red (RuR) inhibits TRPV4, while GSK1016790A (GSK) and reactive free oxygen radicals (ROS) activate it. In the mitochondria of DRGs, the glucose oxidation brought on by diabetes mellitus (STZ) causes an intracellular free Ca2+ and Zn2+ influx excess that is dependent on TRPV4. The administration of STZ leads to the DRG becoming more depolarized (ΔΨm), which in turn causes an increase in mitochondrial ROS, apoptosis, and caspases (caspase-3, caspase-8, and caspase-9) by downregulating enzymatic (glutathione peroxidase, GSH-Px) and non-enzymatic (glutathione (GSH), vitamin A, and vitamin E) antioxidants. The mice's molecular pathways were diminished by the RESV injections. (Increase (↑); diminish (↓)) [ABSTRACT FROM AUTHOR]

In the present study, fully bio-based photocurable trifunctional benzoxazines derived from resveratrol were designed and characterized for multi-dimensional applications. The molecular structure was confirmed using ATR-FTIR and 1H-NMR spectral techniques. The curing temperature and thermal stability were thoroughly studied using differential scanning calorimetry (DSC) and thermogravimetric analysis (TGA) respectively. Notably, in DSC analysis RE-dda exhibited the lowest curing temperature of 191 °C among the synthesised benzoxazines. All the synthesised polybenzoxazines exhibited good thermal stability and start degrading after 263°C. Under UV irradiation, intriguing photoisomerization phenomena was observed in the case of RE-ffa and RE-lee based benzoxazines. The photoluminescence behavior of the UV irradiated benzoxazines was studied using fluorescence spectroscopy and RE-oda displayed a Stokes shift value of 318. Further benzoxazines were reinforced with cashew nut shell cake ash (CNSA) with a view to attain a low value of dielectric constant and to enhance the thermal stability of the composites. An incorporation of 10 wt% CNSA contributes to a reduction in the value of dielectric constant to 1.66, accompanied with a minimal value of dielectric loss of 0.0017. Furthermore, the hydrophobic behavior of the polybenzoxazines, composites and poly(RE-ole) coated cotton fabric was evaluated using water contact angle measurement. Poly(RE-ole) exhibited an impressive water contact angle value of 146°. Moreover, poly(RE-ole) coated cotton fabric displayed enhanced value of water contact angle close to superhydrophobic value of 151°. Data obtained from different studies infer the developed benzoxazines can be considered for water repellent and microelectronics insulation applications. [ABSTRACT FROM AUTHOR]

Background: Resveratrol, a natural compound, may be an alternative to improving conventional breast cancer therapy. Thus, we assessed the capability of resveratrol at a low dose to enhance the in vitro effect of conventional theray in estrogen receptor (ER) and human epidermal growth factor receptor type 2 (HER2)-positive breast cancer cells. Methods: Cell viability of breast cancer cells was measured with neutral red uptake assay. Apoptosis, autophagy, cell cycle progression and cell proliferation were detected through hypotonic fluorescent solution assay, formation of acidic vesicular organelles, flow cytometry, and bromodeoxyuridine assay, respectively. Western blotting was performed to study the expression of pro-apoptotic, anti-apoptotic and autophagic proteins, and estrogen receptors. Results: Resveratrol combined with tamoxifen metabolites or trastuzumab reduced cell viability of ER- and HER2-positive breast cancer cells, respectively. This effect was mainly associated with induction of apoptosis due to a greater formation of hypodiploid nuclei, reduced protein expression of procaspase-7, Bcl-2, Bcl-xL, and PARP; and increased expression of cleaved PARP. Resveratrol decreased the expression of ERα and increased that of ERβ, contributing to the reduced viability on breast cancer cells. Combined treatments induced autophagy, evidenced by increased levels of acidic vesicular organelles and degradation of p62/SQSTM1 protein. Nevertheless, on inhibiting autophagy with 3-methyladenine, cell viability was further reduced and apoptosis was induced, suggesting a pro-survival role of autophagy, impairing apoptosis. Conclusions: Resveratrol increasead the in vitro cytotoxic effect of conventional therapy in breast cancer cells. However, it was necessary to block resveratrol-induced autophagy to improve the therapeutic response. [ABSTRACT FROM AUTHOR]

Resveratrol has been reported to promote immunity and decrease oxidative stress, but which demonstrates biphasic effects relied on the use concentration. In this study, the effects of diet supplement with a relative high concentration of resveratrol (0.32 mg/kg) on metabolism, antioxidation and apoptosis of liver were investigated in Siberian sturgeon. The results showed that resveratrol significantly increased the lipid synthesis and the apoptosis, but did not either activate the antioxidant NRF2/KEAP1 pathway or enhance the antioxidant enzyme activity. Transcriptome analysis revealed significant changes in regulatory pathways related to glycolipid, including PPAR signaling pathway, Insulin signaling pathway, Fatty acid biosynthesis, and Glycolysis/Gluconeogenesis. In addition, resveratrol significantly increased the lipid synthesis genes (accα and fas), fatty acid transport gene (fatp 6) and gluconeogenesis gene (gck), but decreased the survival-promoting genes (gadd45β and igf 1). These findings highlight a significant effect of resveratrol on glycolipid metabolism in Siberian sturgeon. Moreover, this study also demonstrated that 0.32 mg/kg resveratrol has physiological toxicity to the liver of Siberian sturgeon, indicating that this dose is too high for Siberian sturgeon. Thus, our study provides a valuable insight for future research and application of resveratrol in fish. [ABSTRACT FROM AUTHOR]

Neuroblastomas are the most common solid tumors outside of the brain that originate from immature neural crest cells, accounting for about 10% of all pediatric malignancies. The treatment for neuroblastomas involves a multimodal schedule, including surgery, radiation, chemotherapy, and immunotherapy. All these modalities are limited by side effects that might be severe, poor prognosis, and a high risk of recurrence. In the quest for additional therapeutic approaches, phytochemicals have attracted attention owing to their reported antitumor properties, safety, and multimechanistic mode of action. Several studies have used plant‐derived bioactive compounds such as phenolics and flavonoids, suggesting modulation of biomolecules and signal transduction pathways involved in neuroblastoma. We reviewed the findings of recent preclinical and clinical studies demonstrating the effects of phytochemicals on neuroblastoma, shedding light on their molecular mechanism of action and potential therapeutic applications. [ABSTRACT FROM AUTHOR]

Hypertrophic scarring is an aberrant wound-healing response to reestablish dermal integrity after an injury and can cause significant abnormalities in physical, aesthetic, functional, and psychological symptoms, impacting the patient's quality of life. There is currently no gold standard for preventing and treating hypertrophic scars. Therefore, many researchers have attempted to search for antihypertrophic scar agents with greater efficacy and fewer side effects. Natural therapeutics are becoming attractive as potential alternative anti-scarring agents because of their high efficacy, safety, biocompatibility, low cost, and easy accessibility. This review demonstrates various kinds of natural product-based therapeutics, including onion, vitamin E, Gotu kola, green tea, resveratrol, emodin, curcumin, and others, in terms of their mechanisms of action, evidence of efficacy and safety, advantages, and disadvantages when used as anti-scarring agents. We reviewed the literature based on data from in vitro, in vivo, and clinical trials. A total of 23 clinical trials were identified in this review; most clinical trials were ranked as having uncertain results (level of evidence 2b; n = 16). Although these natural products showed beneficial effects in both in vitro and in vivo studies of potential anti-scarring agents, there was limited clinical evidence to support their efficacy due to the limited quality of the studies, with individual flaws including small sample sizes, poor randomization, and blinding, and short follow-up durations. More robust and well-designed clinical trials with large-scale and prolonged follow-up durations are required to clarify the benefits and risks of these agents. [ABSTRACT FROM AUTHOR]

Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Herein, we demonstrate that triacetyl resveratrol (TRES) can be employed as an antioxidant additive to suppress the formation of oxidation-induced defects in air-fabricated perovskite films. When assembling into carbon-based CsPbIBr2 and CsPbI2Br cells, an enhanced efficiency of 10.38% and 14.98% has been achieved, with nearly unchanged efficiency after 1128 h of shelf storage in air and 86% of the initial efficiency after >1000 h aging at 85 °C. [ABSTRACT FROM AUTHOR]

The α-glucosidase from Schwanniomyces occidentalis (GAM1p) was expressed in Komagataella phaffii to about 70 mg/L, and its transferase activity studied in detail. Several isomaltooligosaccharides (IMOS) were formed using 200 g/L maltose. The major production of IMOS (81.3 g/L) was obtained when 98% maltose was hydrolysed, of which 34.8 g/L corresponded to isomaltose, 26.9 g/L to isomaltotriose, and 19.6 g/L to panose. The addition of glucose shifted the IMOS synthesis towards products containing exclusively α(1 → 6)-linkages, increasing the production of isomaltose and isomaltotriose about 2–4 fold, enabling the formation of isomaltotetraose, and inhibiting that of panose to about 12 times. In addition, the potential of this enzyme to glycosylate 12 possible hydroxylated acceptors, including eight sugars and four phenolic compounds, was evaluated. Among them, only sucrose, xylose, and piceid (a monoglucosylated derivative of resveratrol) were glucosylated, and the main synthesised products were purified and characterised by MS and NMR. Theanderose, α(1 → 4)-D-glucosyl-xylose, and a mixture of piceid mono- and diglucoside were obtained with sucrose, xylose, and piceid as acceptors, respectively. Maximum production of theanderose reached 81.7 g/L and that of the glucosyl-xylose 26.5 g/L, whereas 3.4 g/L and only 1 g/L were produced of the piceid mono- and diglucoside respectively. Key points: • Overexpression of a yeast α-glucosidase producing novel molecules. • Yeast enzyme producing the heterooligosaccharides theanderose and glucosyl-xylose. • Glycosylation of the polyphenol piceid by a yeast α-glucosidase. [ABSTRACT FROM AUTHOR]

Cancer is a complex disease that affects millions of people and remains a major public health problem worldwide. Conventional cancer treatments, including surgery, chemotherapy, immunotherapy, and radiotherapy, have limited achievements and multiple drawbacks, among which are healthy tissue damage and multidrug-resistant phenotype onset. Increasing evidence shows that many plants' natural products, as well as their bioactive compounds, have promising anticancer activity and exhibit minimal toxicity compared to conventional anticancer drugs. However, their widespread use in cancer therapy is severely restricted by limitations in terms of their water solubility, absorption, lack of stability, bioavailability, and selective targeting. The use of nanoformulations for plants' natural product transportation and delivery could be helpful in overcoming these limitations, thus enhancing their therapeutic efficacy and providing the basis for improved anticancer treatment strategies. The present review is aimed at providing an update on some phytocompounds (curcumin, resveratrol, quercetin, and cannabinoids, among others) and their main nanoformulations showing antitumor activities, both in vitro and in vivo, against such different human cancer types as breast and colorectal cancer, lymphomas, malignant melanoma, glioblastoma multiforme, and osteosarcoma. The intracellular pathways underlying phytocompound anticancer activity and the main advantages of nanoformulation employment are also examined. Finally, this review critically analyzes the research gaps and limitations causing the limited success of phytocompounds' and nanoformulations' clinical translation. [ABSTRACT FROM AUTHOR]

Nanotechnology has significantly impacted human life, particularly in overcoming the limitations associated with neurodegenerative diseases (NDs). Various nanostructures and vehicle systems, such as polymer nanoparticles, carbon nanotubes (CNTs), nanoliposomes, nano-micelles, lipid nanoparticles, lactoferrin, polybutylcyanoacrylate, and poly lactic-co-glycolic acid, have been shown to enhance drug efficacy, reduce side effects, and improve pharmacokinetics. NDs affect millions worldwide and are challenging to treat due to the blood-brain barrier (BBB), which hinders drug delivery to the central nervous system (CNS). Research suggests that natural ingredients can be formulated into nanoparticles, offering a promising approach for ND treatment. This review examines the advantages and disadvantages of herbal-based nanoformulations, highlighting their potential effectiveness when used alone or in combination with other medications. Herbal nanoparticles provide benefits over synthetic ones due to their biocompatibility, reduced toxicity, and potential for synergistic effects. The study's findings can be applied to develop more efficient drug delivery systems, improving the treatment of NDs by enhancing drug penetration across the BBB and targeting affected CNS areas more precisely. [ABSTRACT FROM AUTHOR]

Background: Resveratrol is a natural compound found in red wine. It has demonstrated anti-inflammatory properties in preclinical models. We compared the effect of oral resveratrol in a new patented formulation to oral placebo for individuals with painful knee osteoarthritis. Methods and findings: ARTHROL was a double-blind, randomized, placebo-controlled, Phase 3 trial conducted in 3 tertiary care centers in France. We recruited adults who fulfilled the 1986 American College of Rheumatology criteria for knee osteoarthritis and reported a pain intensity score of at least 40 on an 11-point numeric rating scale (NRS) in 10-point increments (0, no pain, to 100, maximal pain). Participants were randomly assigned (1:1) by using a computer-generated randomization list with permuted blocks of variable size (2, 4, or 6) to receive oral resveratrol (40 mg [2 caplets] twice a day for 1 week, then 20 mg [1 caplet] twice a day; resveratrol group) or matched oral placebo (placebo group) for 6 months. The primary outcome was the mean change from baseline in knee pain on a self-administered 11-point pain NRS at 3 months. The trial was registered at ClinicalTrials.gov: (NCT02905799). Between October 20, 2017 and November 8, 2021, we assessed 649 individuals for eligibility, and from November 9, 2017, we recruited 142 (22%) participants (mean age 61.4 years [standard deviation (SD) 9.6] and 101 [71%] women); 71 (50%) were randomly assigned to the resveratrol group and 71 (50%) to the placebo group. At baseline, the mean knee pain score was 56.2/100 (SD 13.5). At 3 months, the mean reduction in knee pain was −15.7 (95% confidence interval (CI), −21.1 to −10.3) in the resveratrol group and −15.2 (95% CI, −20.5 to −9.8) in the placebo group (absolute difference −0.6 [95% CI, −8.0 to 6.9]; p = 0.88). Serious adverse events (not related to the interventions) occurred in 3 (4%) in the resveratrol group and 2 (3%) in the placebo group. Our study has limitations in that it was underpowered and the effect size, estimated to be 0.55, was optimistically estimated. Conclusions: In this study, we observed that compared with placebo, oral resveratrol did not reduce knee pain in people with painful knee osteoarthritis. Trial registration: ClinicalTrials.gov ID: NCT02905799. In a phase 3 trial, Christelle Nguyen and team compared the effect of oral resveratrol in a new patented formulation to oral placebo for individuals with painful knee osteoarthritis. Author summary: Why was this study done?: Resveratrol has demonstrated anti-inflammatory properties in preclinical models and analgesic effects in painful conditions. For individuals with knee osteoarthritis, evidence before the study suggested a reduction in pain and an improvement in function at 3 months after resveratrol supplementation as an add-on therapy with meloxicam as compared with placebo. The optimal formulation of oral resveratrol was not addressed. What did the researchers do and find?: We conducted a double-blind, randomized, placebo-controlled, Phase 3 trial using oral resveratrol in a new patented formulation (Patent No. WO/2010/007252). We recruited adults with knee osteoarthritis who reported a pain intensity score of at least 40 on an 11-point numeric rating scale (NRS) in 10-point increments (0, no pain, to 100, maximal pain). Participants were randomly assigned (1:1) to receive oral resveratrol or matched oral placebo for 6 months. Oral resveratrol did not reduce knee pain at 3 months as compared with matched oral placebo in individuals with painful knee osteoarthritis. What do these findings mean?: These findings do not support the use of resveratrol supplementation for reducing knee pain in adults with painful knee osteoarthritis. The study has limitations in that it was underpowered and the effect size, estimated to be 0.55, was optimistically estimated. [ABSTRACT FROM AUTHOR]

Introduction Aim Methods Results Conclusions One of the markers of aging is oxidative stress, a condition characterized by an increase in free radicals concomitant with a reduction in antioxidant defenses. Within this, resveratrol is a compound that has been shown to act as a potent antioxidant. However, few studies highlight the cellular signaling pathways that are activated or inhibited during aging and that are responsible for this biological effect.To verify the antioxidant profile of resveratrol (5 μM) in leukocytes from donors in different age groups.The project was approved by the Ethics Committee. Individuals were divided into three groups: 20–39, 40–59, and 60–80 years old. After separating the leukocytes, assays were performed to evaluate the AMPK (AMP‐activated protein kinase) and Nrf2 (erythroid nuclear factor 2‐related factor 2) pathways. In addition, luciferase assay and enzyme‐linked immunosorbent assay were performed to evaluate transcription factor activation and Nrf2 expression, respectively. The analysis between age and treatment was performed using Pearson correlation (*P < 0.05).There was a reduction in the antioxidant effect of resveratrol during the aging process. In leukocytes from donors over 60 years of age, the AMPK pathway was silenced. Nrf2 was active at all ages. There was an increase in the activation of the transcription factor and phosphorylated protein in all age groups.Nrf2 is an important biochemical mechanism responsible for the antioxidant effect of resveratrol. This effect diminishes with aging but is still observed. Geriatr Gerontol Int 2024; ••: ••–••. [ABSTRACT FROM AUTHOR]

Inducing browning in white adipocytes has emerged as a promising therapeutic approach for addressing obesity. Bioactive that modulate the WAT microenvironment to induce trans browning in white adipocytes have been explored as a strategy to control unregulated lipid storage. However, relying on a single bioactive for modulating lipid metabolism has proven insufficient in obese individuals during human trials, because these compounds primarily activate a single biochemical pathway in promoting browning. Consequently, there is a growing emphasis on targeting multiple pathways to ensure a safe and effective browning process. The present study investigated the combinatorial effect of bioactives namely Apigenin and Resveratrol for activating multiple pathways for effective trans‐browning of white adipocytes. The combination was seen to promote the browning more effectively than the single bioactive, as the combination simultaneously activated multiple signaling pathways to induce angiogenesis‐mediated browning in primary white adipocytes isolated from obese mice. Activation of PI3K signaling via estrogen receptor‐α‐dependent pathway resulted in simultaneous activation of angiogenesis and trans browning in white adipocytes. The study provides valuable insights into the potential use of bioactives in combination with therapeutic intervention to improve the overall health of obese subjects by enhancing lipid metabolism by activating trans‐differentiation of white adipocytes. [ABSTRACT FROM AUTHOR]

This study was conducted for the main purpose of evaluating the effect of resveratrol and curcumin on changes in fatty acid composition in liver and kidney tissues of rats exposed to DMBA. Resveratrol groups: 40 mg/kg resveratrol was administered for only 3 days per week throughout the experiment. Curcumin groups: 40 mg/kg curcumin was administered for only 3 days per week throughout the experiment. DMBA groups: A single dose of 20 mg/kg DMBA was administered once throughout the duration of the experiment. Fatty acid composition, fat-soluble vitamins, cholesterol and phytosterol analyses analyses were performed in tissues. Antioxidant tests were also performed. It was found that the amounts of C16:0, C17:0, C17:1 and C22:5 n3 decreased significantly in the liver tissue of rats administered DMBA, but the amounts of C20:3 n6 ve C22:6 n3 increased significantly. It was found that C16:0 and C18:2 n6c levels increased significantly in kidney tissue, but C17:1 level decreased significantly. As a result of the administration of Curcumin, Resveratrol, DMBA + Curcumin and DMBA + Resveratrol in both liver and kidney tissue, it was determined that some fatty acid values decreased significantly and some fatty acid values increased significantly. Compared to the DMBA group, it was determined that all groups studied had significant changes in the amount of some fat-soluble vitamins, cholesterol, sitosterols in tissues. In conclusion the administration of DMBA, resveratrol and curcumin both single and in combination, it was found that there may be significant changes in the fatty acid composition, fat-soluble vitamins, cholesterol and phytosterols in tissue. [ABSTRACT FROM AUTHOR]

Purpose: There are no clinical treatments to prevent/revert age-related alterations associated with oocyte competence decline in the context of advanced maternal age. Those alterations have been attributed to oxidative stress and mitochondrial dysfunction. Our study aimed to test the hypothesis that in vitro maturation (IVM) medium supplementation with antioxidants (resveratrol or phloretin) may revert age-related oocyte competence decline. Methods: Bovine immature oocytes were matured in vitro for 23 h (young) and 30 h (aged). Postovulatory aged oocytes (control group) and embryos obtained after fertilization were examined and compared with oocytes supplemented with either 2 μM of resveratrol or 6 μM phloretin (treatment groups) during IVM. Results: Aged oocytes had a significantly lower mitochondrial mass and proportion of mitochondrial clustered pattern, lower ooplasmic volume, higher ROS, lower sirtuin-1 protein level, and a lower blastocyst rate in comparison to young oocytes, indicating that postovulatory oocytes have a lower quality and developmental competence, thus validating our experimental model. Supplementation of IVM medium with antioxidants prevented the generation of ROS and restored the active mitochondrial mass and pattern characteristic of younger oocytes. Moreover, sirtuin-1 protein levels were also restored but only following incubation with resveratrol. Despite these findings, the blastocyst rate of treatment groups was not significantly different from the control group, indicating that resveratrol and phloretin could not restore the oocyte competence of postovulatory aged oocytes. Conclusion: Resveratrol and phloretin can both revert the age-related oxidative stress and mitochondrial dysfunction during postovulatory aging but were insufficient to enhance embryo developmental rates under our experimental conditions. [ABSTRACT FROM AUTHOR]

Spinal cord ischemia has serious sequelae. The aim of this study is to investigate the effects of resveratrol and caffeic acid phenyl ester (CAPE), a propolis derivative, on spinal cord injury induced by ischemia-reperfusion (IR). In our research, 30 male Wistar albino rats, 200–250 gr, were used. Before the experiment, during a week of the process, the rats were fed with these two agents, and the experimental group rats were exposed to spinal cord IR injury. At the end of the experiment, spinal cord samples were taken from the sacrificed rats. Bax, p53, nNOS, and Beclin-1 immunoreactivity moreover TUNEL (+) cells were evaluated with immunohistochemically in the IR-induced damaged rats. It has been clearly determined that the TUNEL (+) apoptotic cell number and immunopositive cells of nNOS, Beclin-1, p53, Bax were raised in the IR group. However, these increments partially were restored in the resveratrol and CAPE-fed rats with IR-induced injury. In light of our data, resveratrol, and CAPE could be beneficial in spinal cord IR injury. Although both agents provide beneficial effects, it can be said that CAPE is partially more effective in spinal cord injury caused by IR. [ABSTRACT FROM AUTHOR]

Cyanidin has a protective effect on the nervous system and has been reported to treat tumor effectively. However, its impact on glioma stem cells (GSC) is unknown. Using seven GSC lines, the anti-tumor effect of cyanidin is tested. The effect of cyanidin on the cell viability in each cell line is evaluated. Wnt signaling pathway-related genes are checked after treatment of cyanidin. Cytoplasmic/nuclear β-catenin protein levels post cyanidin treatment is detected. Protein levels of c-Myc after cyanidin treatment are determined. Twist1 and Snail1 protein levels after cyanidin treatment are checked as well. Cyanidin significantly reduces the cell viability of all GSCs, and exhibited the most substantial effect in GBM2 but no apparent effect in 293T cells. It can regulate the Wnt signaling pathway of all GSC lines. In the GBM2, GBM7, G166, and G179 cell lines, there is upregulation of WNT1 and MYC genes, while in the G144 and GliNS2 cell line, these two genes are down-regulated after cyanidin treatment. Cytoplasmic and nuclear protein levels of β-catenin in all cell lines are down-regulated. Cyanidin treatment significantly decreases the protein level for c-Myc in the GBM2 cell line compared with untreated cells, not in G144 or GliNS2 cells. Furthermore, cyanidin strongly reduces the expression of Twist1 and Snail1 in GBM2, G179, and G144 cell lines, while the GliNS2 cells show an opposite change in the cytoplasm and no change in nuclear. Cyanidin exerts an anti-tumor effect in glioma stem cell lines, probably through the Wnt signaling pathway. [ABSTRACT FROM AUTHOR]

Monotherapy is often ineffective for treating colorectal cancer. In this study, we developed PEG-modified liposomes loaded with rapamycin (Rapa) and resveratrol (Res) (Rapa/Res liposomes, or RRL) to investigate their therapeutic potential in colorectal cancer. RRL were constructed using the reversed-phase evaporation method. We assessed the cytotoxicity, apoptosis, and ferroptotic effects of RRL on colorectal cancer HCT116 cells. The anti-tumor efficacy of RRL was evaluated in HCT116 xenograft mice. RRL had a particle size of 86.67 ± 1.10 nm and a zeta potential of -33.13 ± 0.49 mV. The coloaded formulation demonstrated satisfactory performance both in vitro and in vivo, resulting in increased cytotoxicity to HCT116 cells and significant suppression of HCT116 xenografts tumor growth. Mechanically, RRL significantly increased the apoptosis rate of HCT116 cells, induced ROS accumulation in tumor cells, and effectively downregulated the expression of the ferroptosis-associated proteins GPX4 and SLC7A11, demonstrating its superior efficacy compared to that of Rapa liposomes (Rapa/Lps) or Res liposomes (Res/Lps) alone. Coloading Rapa and Res into liposomes to promote apoptosis and ferroptosis in tumor cells represents a promising strategy for the treatment of colorectal cancer. [ABSTRACT FROM AUTHOR]

Resveratrol is a plant-derived polyphenolic compound with numerous biological activities and health-promoting properties. Rice wine is a popular traditional alcoholic beverage made from fermented rice grains, and widely consumed in Asia. To develop resveratrol-enriched rice wine, a heterologous resveratrol biosynthesis pathway was established by integrating the 4-coumaroyl-CoA ligase (Pc4CL) and the stilbene synthase (VvSTS) from Petroselinum crispum and Vitis vinifera at the δ locus sites of industrial rice wine strains Saccharomyces cerevisiae HJ. The resulting S. cerevisiae HJ01 produced a level of 0.6 ± 0.01 mg/L resveratrol. Next, the resveratrol production was increased 16.25-fold through employing the fused protein Pc4CL::VvSTS with a rigidly linked peptide (TPTP, EAAAK). Then, the strains were further modified by removing feedback inhibition of tyrosine through point mutation of ARO4 and ARO7, which integrated at the rDNA region of strain HJ03, and generated strain HJ06, HJ07, and HJ08. Subsequently, the highest resveratrol titer (34.22 ± 3.62 mg/L) was obtained by optimizing fermentation time and precursor addition amount. Finally, resveratrol content of rice wine fermented with strain HJ08 was 2.04 ± 0.08 mg/L and 1.45 ± 0.06 mg/L with or without the addition of 400 mg/L tyrosine after 7 days fermentation. [ABSTRACT FROM AUTHOR]

Oxyresveratrol is a stilbene compound with a simple chemical structure and various therapeutic potentials. This study summarized and analyzed the multiple pharmacological effects and mechanisms of oxyresveratrol, identifying its prominent performance in neuroprotection, hepatoprotection, and anti-inflammatory activities in the intestines. By integrating the pharmacological effects of oxyresveratrol with insights from the network pharmacology and molecular docking of its interactions with targets linked to gut–liver–brain axis disorders, it has been shown that oxyresveratrol may hold promise for the treatment of gut–liver–brain axis-related disorders. The synergistic effect between various mechanisms has inspired further research and the development of oxyresveratrol's application value. [ABSTRACT FROM AUTHOR]

Objective: Resveratrol, a natural product found in plants, is a polyphenolic compound with strong antioxidant activity. In order to enhance the antioxidant activity of resveratrol, we have used a natural product emodin, which has multiple hydroxyl group structure similar to resveratrol. Methods: In this study, we investigated the antioxidant activities of resveratrol and emodin in vitro respectively, including their abilities to scavenge 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals, hydroxyl radicals, and superoxide radicals. Results and Discussion: our results demonstrated that the combination of resveratrol and emodin significantly enhances antioxidant activity. And the process of their DPPH radical scavenging follows a first-order reaction kinetics equation. Finally, a possible mechanism for the scavenging of DPPH free radicals by resveratrol and emodin was proposed. Conclusions: We found that emodin combined with resveratrol can increase antioxidant activity. This study provides a new sight to enhance antioxidant activity. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a global health problem and it is stated that the use of resveratrol supplement contributes to the protection of kidney health. In this study, it was aimed to evaluate the effect of resveratrol supplementation on kidney function, inflammation and histopathological findings in rats with experimental adenine-induced kidney damage. Three different groups of 10 randomly selected rats were formed. The first group was the negative control group, the second group was the uremic control group (KDG), and the third group was the group in which uremia was created and resveratrol was applied (RG). Kidney damage was induced by administration of 200 mg/kg adenine. Resveratrol supplementation was administered at 20 mg/kg after kidney damage. Serum urea, creatinine, indoxyl sulfate (IS), p-cresol, glomerular filtration rate, C-reactive protein (CRP); interleukin (IL)-6 and tumor necrosis factor (TNF)-α gene expression levels and histopathological findings were evaluated. It was determined that resveratrol supplement applied after the formation of connective tissue in renal failure didn't have an improvement effect on the urine amount, kidney function and inflammatory parameters and histopathological changes (p > 0.05). Just, the increase in the CRP value of KDG (p < 0.05) was not observed in RG. The findings suggest that resveratrol administered after kidney damage with adenine has no effect on kidney disease. [ABSTRACT FROM AUTHOR]