Exploring the landscape of stem cell extracellular vesicle research for angiogenesis: A bibliometric analysis from 2003 to 2023.

BACKGROUND: Exosomes and other secretory membrane vesicles are collectively referred to as extracellular vesicles (EVs). Relevant data indicate that stem cell-derived extracellular vesicles (SC-EVs) play a critical role in angiogenesis by transmitting crucial information such as proteins, second messengers, and genetic material between cells. Therefore, this study aimed to map current trends on SC-EVs for angiogenesis and provide directions for future research to advance this important field. METHODS: We conducted a thorough search for relevant studies on SC-EVs for angiogenesis from 2003 to 2023 using the Web of Science database. Subsequently, we used VOSviewer and CiteSpace to analyze the collected data. RESULTS: A total of 2359 relevant publications, which included original articles and reviews, related to the role of SC-EVs in angiogenesis were screened in this study based on the search strategy. China and the United States were leading in this field, with China having a higher output in terms of publications and citations (1172, 43681). Also, the top five universities were located in China, with Shanghai Jiao Tong University having the highest output. Stem Cell Research & Therapy and International Journal of Molecular Sciences, are prominent platforms for researchers in this field to share their findings and advancements, and they had most of published studies on SC-EVs for angiogenesis. The results derived from the cluster analysis suggested that future investigations should predominantly prioritize studying the involvement of SC-EVs in angiogenesis across various diseases, with a specific emphasis on skin wound healing. CONCLUSION: In this comprehensive review, global trends in SC-EVs for angiogenesis were analyzed. The analysis of journals, institutions, references, and keywords could assist researchers in deciding on the direction of research. The role of SC-EVs in promoting angiogenesis during wound healing and repair represents an emerging research focus.

The tooth-specific basic helix-loop-helix factor AmeloD promotes differentiation of ameloblasts.

Tissue-specific basic helix-loop-helix (bHLH) transcription factors play an important role in cellular differentiation. We recently identified AmeloD as a tooth-specific bHLH transcription factor. However, the role of AmeloD in cellular differentiation has not been investigated. The aim of this study was to elucidate the role of AmeloD in dental epithelial cell differentiation. We found that AmeloD-knockout (AmeloD-KO) mice developed an abnormal structure and altered ion composition of enamel in molars, suggesting that AmeloD-KO mice developed enamel hypoplasia. In molars of AmeloD-KO mice, the transcription factor Sox21 encoding SRY-Box transcription factor 21 and ameloblast differentiation marker genes were significantly downregulated. Furthermore, overexpression of AmeloD in the dental epithelial cell line M3H1 upregulated Sox21 and ameloblast differentiation marker genes, indicating that AmeloD is critical for ameloblast differentiation. Our study demonstrated that AmeloD is an important transcription factor in amelogenesis for promoting ameloblast differentiation. This study provides new insights into the mechanisms of amelogenesis.

A Comprehensive Review of Microneedling as a Potential Treatment Option for Androgenetic Alopecia.

BACKGROUND: Microneedling refers to a minimally invasive technique that uses multiple fine needles targeted skin epidermis for mechanical stimulation to obtain therapeutic or cosmetic effects. It is suitable for the treatment of a variety of dermatological conditions, including androgenetic alopecia (AGA). OBJECTIVE: This article aims to make a comprehensive review of the relevant studies on microneedling for the management of AGA. METHODS: Extensive literature search was performed using PubMed, Web of Science, and EBSCO databases. 4 in vivo studies and 25 clinical trials were included according to the inclusion and exclusion criteria. RESULTS: The effects of microneedling on AGA was investigated in animal experiments. Several clinical trials, including randomized controlled trials, strengthen the validity of the findings. Microneedling therapy showed some encouraging results with minor complications when used alone or in combination with topical products. CONCLUSIONS: Microneedling appears to be a safe and effective therapeutic option for AGA. Larger and more randomized controlled trials regarding the role of microneedling in AGA are strongly recommended to provide more definitive evidence. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

Prostaglandin E3 attenuates macrophage-associated inflammation and prostate tumour growth by modulating polarization.

Alternative polarization of macrophages regulates multiple biological processes. While M1-polarized macrophages generally mediate rapid immune responses, M2-polarized macrophages induce chronic and mild immune responses. In either case, polyunsaturated fatty acid (PUFA)-derived lipid mediators act as both products and regulators of macrophages. Prostaglandin E3 (PGE3 ) is an eicosanoid derived from eicosapentaenoic acid, which is converted by cyclooxygenase, followed by prostaglandin E synthase successively. We found that PGE3 played an anti-inflammatory role by inhibiting LPS and interferon-γ-induced M1 polarization and promoting interleukin-4-mediated M2 polarization (M2a). Further, we found that although PGE3 had no direct effect on the growth of prostate cancer cells in vitro, PGE3 could inhibit prostate cancer in vivo in a nude mouse model of neoplasia. Notably, we found that PGE3 significantly inhibited prostate cancer cell growth in a cancer cell-macrophage co-culture system. Experimental results showed that PGE3 inhibited the polarization of tumour-associated M2 macrophages (TAM), consequently producing indirect anti-tumour activity. Mechanistically, we identified that PGE3 regulated the expression and activation of protein kinase A, which is critical for macrophage polarization. In summary, this study indicates that PGE3 can selectively promote M2a polarization, while inhibiting M1 and TAM polarization, thus exerting an anti-inflammatory effect and anti-tumour effect in prostate cancer.

Transcriptional regulation of the basic helix-loop-helix factor AmeloD during tooth development.

The epithelial-mesenchymal interactions are essential for the initiation and regulation of the development of teeth. Following the initiation of tooth development, numerous growth factors are secreted by the dental epithelium and mesenchyme that play critical roles in cellular differentiation. During tooth morphogenesis, the dental epithelial stem cells differentiate into several cell types, including inner enamel epithelial cells, which then differentiate into enamel matrix-secreting ameloblasts. Recently, we reported that the novel basic-helix-loop-helix transcription factor, AmeloD, is actively engaged in the development of teeth as a regulator of dental epithelial cell motility. However, the gene regulation mechanism of AmeloD is still unknown. In this study, we aimed to uncover the mechanisms regulating AmeloD expression during tooth development. By screening growth factors that are important in the early stages of tooth formation, we found that TGF-ß1 induced AmeloD expression and ameloblast differentiation in the dental epithelial cell line, SF2. TGF-ß1 phosphorylated ERK1/2 and Smad2/3 to induce AmeloD expression, whereas treatment with the MEK inhibitor, U0126, inhibited AmeloD induction. Promoter analysis of AmeloD revealed that the proximal promoter of AmeloD showed high activity in dental epithelial cell lines, which was enhanced following TGF-ß1 stimulation. These results suggested that TGF-ß1 activates AmeloD transcription via ERK1/2 phosphorylation. Our findings provide new insights into the mechanisms that govern tooth development.

Early-life fingolimod treatment improves intestinal homeostasis and pancreatic immune tolerance in non-obese diabetic mice.

Fingolimod has beneficial effects on multiple diseases, including type 1 diabetes (T1D) and numerous preclinical models of colitis. Intestinal dysbiosis and intestinal immune dysfunction contribute to disease pathogenesis of T1D. Thus, the beneficial effect of fingolimod on T1D may occur via the maintenance of intestinal homeostasis to some extent. Herein, we investigated the role of fingolimod in intestinal dysfunction in non-obese diabetic (NOD) mice and possible mechanisms. NOD mice were treated with fingolimod (1 mg · kg-1 per day, i.g.) from weaning (3-week-old) to 31 weeks of age. We found that fingolimod administration significantly enhanced the gut barrier (evidenced by enhanced expression of tight junction proteins and reduced intestinal permeability), attenuated intestinal microbial dysbiosis (evidenced by the reduction of enteric pathogenic Proteobacteria clusters), as well as intestinal immune dysfunction (evidenced by inhibition of CD4+ cells activation, reduction of T helper type 1 cells and macrophages, and the expansion of regulatory T cells). We further revealed that fingolimod administration suppressed the activation of CD4+ cells and the differentiation of T helper type 1 cells, promoted the expansion of regulatory T cells in the pancreas, which might contribute to the maintenance of pancreatic immune tolerance and the reduction of T1D incidence. The protection might be due to fingolimod inhibiting the toll-like receptor 2/4/nuclear factor-κB/NOD-like receptor protein 3 inflammasome pathway in the colon. Collectively, early-life fingolimod treatment attenuates intestinal microbial dysbiosis and intestinal immune dysfunction in the T1D setting, which might contribute to its anti-diabetic effect.

Chondrogenic Characteristics of Auricular Chondrocytes Cocultured With Adipose-Derived Stem Cells are Superior to Stromal Vascular Fraction of Adipose Tissue.

ABSTRACT: Reconstruction of craniofacial cartilage defects is among the most challenging operations in facial plastic surgery. The co-culture system of partial replacement of chondrocytes by stem cells has been confirmed effective in the repair of cartilaginous defects. The aim of this study is to compare chondrogenic properties of expanded adipose-derived stem cells (ADSCs) and stromal vascular fraction (SVF), including ADSCs/SVF monoculture and coculture with rabbit auricular chondrocytes (ACs). Analysis of morphology, histology, real-time polymerase chain reaction and glycosaminoglycans (GAG) quantification were performed to characterize the chondrogenesis of pellets. The triple differentiation potential of ADSCs had been confirmed. Further, using flow cytometry, the authors demonstrated that ADSCs and SVF have different characteristics in cell surface markers, and ADSCs are more enriched in cells from the mesenchymal lineage than SVF. GAG production of ADSCs is significantly higher than that of SVF in pellet monoculture, and pellet coculture of ADSCs and ACs are better in depositing cartilage matrix than the mixture of SVF and ACs. Our study suggests that ADSCs may be more suitable seed cells for craniofacial cartilage defect or deformity repair.

Cloning, expression and purification of d-tagatose 3-epimerase gene from Escherichia coli JM109.

An unknown d-tagatose 3-epimerase (DTE) containing a IoIE domain was identified and cloned from Escherichia coli. This gene was subcloned into the prokaryotic expression vector pET-15b, and induced by IPTG in E. coli BL21 expression system. Through His-select gel column purification and fast-protein liquid chromatography, highly purified and stable DTE protein was produced. The molecular weight of the DTE protein was estimated to be 29.8kDa. The latest 83 DTE sequences from public database were selected and analyzed by molecular clustering, multi-sequence alignment. DTEs were roughly divided into five categories.

Comparison of daclatasvir resistance barriers on NS5A from hepatitis C virus genotypes 1 to 6: implications for cross-genotype activity.

A comparison of the daclatasvir (DCV [BMS-790052]) resistance barrier on authentic or hybrid replicons containing NS5A from hepatitis C virus (HCV) genotypes 1 to 6 (GT-1 to -6) was completed using a replicon elimination assay. The data indicated that genotype 1b (GT-1b) has the highest relative resistance barrier and genotype 2a (GT-2a M31) has the lowest. The rank order of resistance barriers to DCV was 1b>4a≥5a>6a≅1a>2a JFH>3a>2a M31. Importantly, DCV in combination with a protease inhibitor (PI) eliminated GT-2a M31 replicon RNA at a clinically relevant concentration. Previously, we reported the antiviral activity and resistance profiles of DCV on HCV genotypes 1 to 4 evaluated in the replicon system. Here, we report the antiviral activity and resistance profiles of DCV against hybrid replicons with NS5A sequences derived from HCV GT-5a and GT-6a clinical isolates. DCV was effective against both GT-5a and -6a hybrid replicon cell lines (50% effective concentrations [EC50s] ranging from 3 to 7 pM for GT-5a, and 74 pM for GT-6a). Resistance selection identified amino acid substitutions in the N-terminal domain of NS5A. For GT-5a, L31F and L31V, alone or in combination with K56R, were the major resistance variants (EC50s ranging from 2 to 40 nM). In GT-6a, Q24H, L31M, P32L/S, and T58A/S were identified as resistance variants (EC50s ranging from 2 to 250 nM). The in vitro data suggest that DCV has the potential to be an effective agent for HCV genotypes 1 to 6 when used in combination therapy.

Aggravation of clozapine-induced hepatotoxicity by glycyrrhetinic acid in rats.

Clozapine (CLZ) was reported to be associated with hepatotoxicity. Glycyrrhetinic acid (GA) has a liver protective effect. Our preliminary experiments showed that GA aggravated rather than attenuated CLZ-induced hepatotoxicity in primary cultured rat hepatocytes. The study aimed to describe the enhancing effect of GA on CLZ-induced hepatotoxicity in vivo and in vitro. Data from primary cultured rat hepatocytes showed the decreased formation of metabolites demethylclozapine (nor-CLZ) and clozapine N-oxide (CLZ N-oxide). The results in vivo showed that 7-day CLZ treatment led to marked accumulation of triglyceride (TG) and increase in γ-glutamyl transpeptidase (γ-GT) activity, liver weight, and serum AST in rats. Co-administration of GA enhanced the increases in hepatic TG, γ-GT, liver weight, and serum total cholesterol induced by CLZ. GA decreased plasma concentrations of nor-CLZ and CLZ N-oxide. Compared with control rats, hepatic microsomes of GA rats exhibited the decreased formations of nor-CLZ and CLZ N-oxide, accompanied by decreases in activities of CYP2C11 and CYP2C19 and increased activity of CYP1A2. QT-PCR analysis demonstrated that GA enhanced expression of CYP1A2, but suppressed expression of CYP2C11 and CYP2C13. All these results support the conclusion that GA aggravated CLZ-induced hepatotoxicity, which was partly via inhibiting CYP2C11 and CYP2C13 or inducing CYP1A2.

Co-administration of paroxetine and pravastatin causes deregulation of glucose homeostasis in diabetic rats via enhanced paroxetine exposure.

AIM: Clinical evidence shows that co-administration of pravastatin and paroxetine deregulates glucose homeostasis in diabetic patients. The aim of this study was to verify this phenomenon in diabetic rats and to elucidate the underlying mechanisms. METHODS: Diabetes mellitus was induced in male SD rats by a high-fat diet combined with a low-dose streptozotocin injection. The rats were orally administered paroxetine (10 mg/kg) and pravastatin (10 mg/d) or both the drugs daily for 28 d. The pharmacokinetics of paroxetine and pravastatin were examined on d 1 and d 28. Biochemical parameters including serum insulin, glucose and lipids were monitored during the treatments. An insulin-secreting cell line (INS-1) was used for measuring insulin secretion. RESULTS: In diabetic rats, co-administration of paroxetine and pravastatin markedly increased the concentrations of both the drugs compared with administration of each drug alone. Furthermore, co-administration severely impaired glucose homeostasis in diabetic rats, as demonstrated by significantly increased serum glucose level, decreased serum and pancreatic insulin levels, and decreased pancreatic Insulin-2 mRNA and tryptophan hydroxylase-1 (Tph-1) mRNA levels. Treatment of INS-1 cells with paroxetine (5 and 10 µmol/L) significantly inhibited insulin secretion, decreased the intracellular insulin, 5-HT, Insulin-2 mRNA and Tph-1 mRNA levels. Treatment of the cells with pravastatin (10 µmol/L) significantly stimulated insulin secretion, which was weakened by co-treatment with paroxetine. CONCLUSION: Paroxetine inhibits insulin secretion at least via decreasing intracellular 5-HT and insulin biosynthesis. The deregulation of glucose homeostasis by co-administration of paroxetine and pravastatin in diabetic rats can be attributed to enhanced paroxetine exposure.

Decreased exposure of simvastatin and simvastatin acid in a rat model of type 2 diabetes.

AIM: Simvastatin is frequently administered to diabetic patients with hypercholesterolemia. The aim of the study was to investigate the pharmacokinetics of simvastatin and its hydrolysate simvastatin acid in a rat model of type 2 diabetes. METHODS: Diabetes was induced in 4-week-old rats by a treatment of high-fat diet combined with streptozotocin. After the rats received a single dose of simvastatin (20 mg/kg, po, or 2 mg/kg, iv), the plasma concentrations of simvastatin and simvastatin acid were determined. Simvastatin metabolism and cytochrome P4503A (Cyp3a) activity were assessed in hepatic microsomes, and its uptake was studied in freshly isolated hepatocytes. The expression of Cyp3a1, organic anion transporting polypeptide 2 (Oatp2), multidrug resistance-associated protein 2 (Mrp2) and breast cancer resistance protein (Bcrp) in livers was measured using qRT-PCR. RESULTS: After oral or intravenous administration, the plasma concentrations and areas under concentrations of simvastatin and simvastatin acid were markedly decreased in diabetic rats. Both simvastatin metabolism and Cyp3a activity were markedly increased in hepatocytes of diabetic rats, accompanied by increased expression of hepatic Cyp3a1 mRNA. Furthermore, the uptake of simvastatin by hepatocytes of diabetic rats was markedly increased, which was associated with increased expression of the influx transporter Oatp2, and decreased expression of the efflux transporters Mrp2 and Bcrp. CONCLUSION: Diabetes enhances the metabolism of simvastatin and simvastatin acid in rats via up-regulating hepatic Cyp3a activity and expression and increasing hepatic uptake.

Bioinspired engineering ADSC nanovesicles thermosensitive hydrogel enhance autophagy of dermal papilla cells for androgenetic alopecia treatment.

Androgenic alopecia (AGA) is a highly prevalent form of non-scarring alopecia but lacks effective treatments. Stem cell exosomes have similar repair effects to stem cells, suffer from the drawbacks of high cost and low yield yet. Cell-derived nanovesicles acquired through mechanical extrusion exhibit favorable biomimetic properties similar to exosomes, enabling them to efficiently encapsulate substantial quantities of therapeutic proteins. In this study, we observed that JAM-A, an adhesion protein, resulted in a significantly increased the adhesion and resilience of dermal papilla cells to form snap structures against damage caused by dihydrotestosterone and macrophages, thereby facilitating the process of hair regrowth in cases of AGA. Consequently, adipose-derived stem cells were modified to overexpress JAM-A to produce engineered JAM-A overexpressing nanovesicles (JAM-AOE@NV). The incorporation of JAM-AOE@NV into a thermosensitive hydrogel matrix (JAM-AOE@NV Gel) to effectively addresses the limitations associated with the short half-life of JAM-AOE@NV, and resulted in the achievement of a sustained-release profile for JAM-AOE@NV. The physicochemical characteristics of the JAM-AOE@NV Gel were analyzed and assessed for its efficacy in promoting hair regrowth in vivo and vitro. The JAM-AOE@NV Gel, thus, presents a novel therapeutic approach and theoretical framework for promoting the treatment of low cell adhesion diseases similar to AGA.

In vitro activity of daclatasvir on hepatitis C virus genotype 3 NS5A.

The NS5A replication complex inhibitor daclatasvir (DCV; BMS-790052) inhibits hybrid replicons containing hepatitis C virus (HCV) genotype 3a (HCV3a) NS5A genes with 50% effective concentrations (EC(50)s) ranging from 120 to 870 pM. Selection studies with a hybrid HCV3a replicon identified NS5A residues 31 and 93 as sites for DCV-selected resistance. Our results support the potential use of DCV as a component in combination therapies for HCV3a chronic infection.

Loss of function of FATTY ACID DESATURASE7 in tomato enhances basal aphid resistance in a salicylate-dependent manner.

We report here that disruption of function of the ω-3 FATTY ACID DESATURASE7 (FAD7) enhances plant defenses against aphids. The suppressor of prosystemin-mediated responses2 (spr2) mutation in tomato (Solanum lycopersicum), which eliminates the function of FAD7, reduces the settling behavior, survival, and fecundity of the potato aphid (Macrosiphum euphorbiae). Likewise, the antisense suppression of LeFAD7 expression in wild-type tomato plants reduces aphid infestations. Aphid resistance in the spr2 mutant is associated with enhanced levels of salicylic acid (SA) and mRNA encoding the pathogenesis-related protein P4. Introduction of the Naphthalene/salicylate hydroxylase transgene, which suppresses SA accumulation, restores wild-type levels of aphid susceptibility to spr2. Resistance in spr2 is also lost when we utilize virus-induced gene silencing to suppress the expression of NONEXPRESSOR OF PATHOGENESIS-RELATED PROTEINS1 (NPR1), a positive regulator of many SA-dependent defenses. These results indicate that FAD7 suppresses defenses against aphids that are mediated through SA and NPR1. Although loss of function of FAD7 also inhibits the synthesis of jasmonate (JA), the effects of this desaturase on aphid resistance are not dependent on JA; other mutants impaired in JA synthesis (acx1) or perception (jai1-1) show wild-type levels of aphid susceptibility, and spr2 retains aphid resistance when treated with methyl jasmonate. Thus, FAD7 may influence JA-dependent defenses against chewing insects and SA-dependent defenses against aphids through independent effects on JA synthesis and SA signaling. The Arabidopsis (Arabidopsis thaliana) mutants Atfad7-2 and Atfad7-1fad8 also show enhanced resistance to the green peach aphid (Myzus persicae) compared with wild-type controls, indicating that FAD7 influences plant-aphid interactions in at least two plant families.

A bibliometric and visualized research on global trends of scar, 2011-2021.

OBJECTIVE: Pathological scars are the results of abnormal wound healing, which not only affect the appearance, but may also be accompanied by significant psychosocial burdens. In this study, we aimed to conduct a bibliometric and visualized analysis on pathological scars and provide directions for future research. METHODS: The articles on scar research from 2011 to 2021 in the Web of Science Core Collection database were collected. The bibliometrics records were retrieved and analyzed with Excel, CiteSpace V and VOSviewer. RESULTS: A total of 944 scar research records published between 2011 and 2021 were collected. Publication output has shown an upward trend as a whole. China ranked first in terms of country contributions (418 publications, 5176 citations), while Germany, with only 22 studies published, had the highest average citation rate (57.18). Shanghai Jiaotong University was the institution with the largest number of related articles published, followed by the fourth military medical university, the University of Alberta and the Second military medical university. Wound repair and regeneration, Burns, Journal of Burn Care & Research, Journal of Cosmetic Dermatology published the most research in this field. Dahai Hu was the most prolific author, while Rei Ogawa was the most cited. The cluster analysis of the reference contributions and keywords indicated that current research hotspots mainly include pathogenesis, treatment strategies, and the safety evaluation of new scar treatment options. CONCLUSION: This study provides a comprehensive summary and analysis of the current status and research trends of pathological scars. International research interest in pathological scars is on the rise, and high-quality studies related to the field have also increased in the last decade. The pathogenesis of pathological scars, treatment strategies, such as fractional ablative CO2 laser and molecular targeted therapy, and the safety evaluation of new treatment options will be the focus of future research.

A bibliometric and visualized study on global trends of breast augmentation complications, 2011-2021.

Background: Women undergo breast augmentation surgery for a variety of reasons, but surgical complications can seriously affect patient outcomes and quality of life, making it a hot research topic. Although a large body of literature exists in this field, a lack of systemic generalization hinders the ability to guide clinical practice. We aimed to identify the current research hotspots and common surgical approaches of breast augmentation and to predict future research hotspots by analyzing the literature of the past 10 years. Methods: All relevant literature on breast augmentation complications were screened in the Web of Science (WoS) platform from 2011 to 2021. We analyzed the research within this field using the software programs VOSviewer and CiteSpace. Results: In total, 2,798 publications were selected. The United States ranked first in the world (1,173 articles), followed by Italy (243 articles), and the United Kingdom (208 articles). Memorial Sloan Kettering Cancer Center was the institution with the most publications, but the academic achievements of Harvard were the most recognized. Plastic and Reconstructive Surgery was the most prominent of all journals in terms of both the number and quality of the articles published. Albornoz was the hub author in the co-citation network. Keyword cluster analysis showed that capsular contracture, breast cancer, and postoperative nausea, among others, were the hotspots and trends of research in recent years. Conclusions: This study comprehensively summarized and analyzed the research trends of breast augmentation complications worldwide. Capsular contracture and postoperative nausea are current research hotspots. Periareolar incision and the breast crease incision are the most common incision approaches. Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a future research hotspot.

Dietary docosahexaenoic acid plays an opposed role in ferroptotic and non-ferroptotic acute kidney injury.

Ferroptosis due to polyunsaturated fatty acid (PUFA) peroxidation has been implicated in the pathogenesis of acute kidney injury (AKI), suggesting the risk of dietary intake of PUFA for people susceptible to AKI. Clinically, however, in addition to ferroptosis, other mechanisms also contribute to different types of AKI such as inflammation associated necroptosis and pyroptosis. Therefore, the role of PUFA, especially ω3 PUFA which is a common food supplement, in various AKIs deserves further evaluation. In this study, rhabdomyolysis- and folic acid-induced AKI (Rha-AKI and FA-AKI) were established in mice fed with different fatty acids Histology of kidney, blood urea nitrogen and creatinine, lipid peroxidation, and inflammatory factors were examined. Results showed that these two types of AKIs had diametrically different pathogenesis indicated by that ferrostatin-1 (Fer-1), a lipid antioxidant, can attenuate FA-AKI rather than Rha-AKI. Further, dietary DHA (provided by fish oil) reduced tubular injury and renal lesion by inhibiting peroxidation and inflammation in mice with Rha-AKI while increasing cell death, tissue damage, peroxidation and inflammation in mice with FA-AKI. In human renal tubular epithelial cell line HK-2, MTT assay and DHE staining showed that both myoglobin and ferroptosis inducers can cause cell death and oxidative stress. Ferroptosis inducer-induced cell death was promoted by DHA, while such result was not observed in myoglobin-induced cell death when adding DHA. This study illustrates that the mechanisms of AKI might be either ferroptosis dependent or -independent and the deterioration effect of dietary DHA depends on whether ferroptosis is involved.

A bibliometric and visualized research on global trends of immune checkpoint inhibitors related complications in melanoma, 2011-2021.

Background: Melanoma is a malignant tumor that originates from the canceration of melanocytes with a high rate of invasiveness and lethality. Immune escape has been regarded as an important mechanism for tumor development, while the treatment of immune checkpoint inhibitors (ICIs) is beneficial in restoring and enhancing the body's anti-tumor immune response to kill tumor cells. To date, ICIs therapy has achieved remarkable efficacy in treating melanoma patients. Despite the significant clinical benefits of ICIs, multiple complications such as rashes, thyroiditis, and colitis occur in melanoma patients. In this study, we aim to explore the development process and trends in the field of ICIs-related complications in melanoma, analyze current hot topics, and predict future research directions. Methods: We screened the most relevant literatures on ICIs-related complications in melanoma from 2011 to 2021 in the Web of Science Core Collection (WoSCC). Using VOSviewer, CiteSpace and R language packages, we analyzed the research trends in this field. Results: A total of 1,087 articles were screened, and the USA had the highest number of publications (publications = 454, citations = 60,483), followed by Germany (publications = 155, citations = 27,743) and Italy (publications = 139, citations = 27,837). The Memorial Sloan Kettering Cancer Center had the most publications, but the Angeles Clinic and Research Institute had the highest average citation rate. Lancet oncology (IF, 2021 = 54.43) was the most prominent of all journals in terms of average citation rate. Reference and keyword cluster analysis revealed that anti-tumor efficacy, adjuvant treatment, clinical response, clinical outcome, etc. were the hotspots and trends of research in recent years. Conclusions: This study offers a comprehensive summary and analysis of global research trends on ICIs-related complications in melanoma. Over the past decade, there has been a significant increase in the number of publications on this topic. However, the safety and benefits of retreatment after the recovery of ICIs-related complications remain unknown. Therefore,the establishment of related prediction models, as well as the immunotherapy of melanoma with ICIs in combination with other adjuvant therapies, are future research hotspots.

Long-Term Retrogradation Properties and In Vitro Digestibility of Waxy Rice Starch Modified with Pectin.

In recent years, the blending of hydrocolloids and natural starch to improve the properties of natural starch has become a research hotspot. In this study, the effects of pectin (PEC) on the retrogradation properties and in vitro digestibility of waxy rice starch (WRS) were investigated. The results showed that PEC could significantly (p < 0.05) reduce the retrogradation enthalpy and reduce the hardness of WRS gel. X-ray diffraction results indicated that PEC could reduce the relative crystallinity of the composite system, and the higher the PEC content, the lower the relative crystallinity. When the PEC content was 10%, the relative crystallinity of the composite system was only 10.6% after 21 d of cold storage. Fourier transform infrared spectroscopy results proved that the interaction between PEC and WRS was mainly a hydrogen bond interaction. Furthermore, after 21 d of cold storage, the T23 free water signal appeared in the natural WRS paste, while only a small free water signal appeared in the compound system with 2% PEC addition. Moreover, addition of PEC could reduce the starch digestion rate and digestibility. When the content of PEC increased from 0% to 10%, the digestibility decreased from 82.31% to 71.84%. This study provides a theoretical basis for the further application of hydrocolloids in starch-based foods.