Global research hotspots and trends of acute rejection after liver transplantation from 1988 to 2022: a bibliometric analysis.

Background: Acute rejection (AR) is the predominant form of rejection observed in liver transplantation and plays a crucial role in transplant immunology. This study aims to utilize bibliometric analysis to understand the status quo, hotspots, and future trends of research on AR after liver transplantation. Methods: We searched the Web of Science Core Collection (WoSCC) for studies on AR after liver transplantation published from 1988 to 2022. The Bibliometric Online Analysis Platform, VOSviewer, and CiteSpace were used for analysis of all extracted publications. Results: This study included 2,398 articles published in 456 journals by 12,568 authors from 1,965 institutions in 55 countries/regions. The United States and its affiliated institution, the University of Pittsburgh, were the most productive contributors. Transplantation (n = 12,435) was the most frequently cited journal. Neuhaus P (n = 38) was the highest output author, and Demetris AJ (n = 670) was the most co-cited author. The research hotspots of AR after liver transplantation include pathogenesis, immunosuppressive therapy, and prognosis. Emerging research directions include regulatory T cells, immunosuppression minimization, intra-patient variability (IPV) of tacrolimus, and novel non-invasive diagnostic markers. Conclusion: Our study utilized bibliometric methods to analyze the study of AR after liver transplantation over the past 35 years. With the prolonged survival of liver transplant recipients, the most active areas currently focus on individualized treatment and improving patient prognosis. Minimizing adverse reactions to immunosuppressive therapy while simultaneously avoiding an increase in the risk of AR remains a future research focus.

A bibliometric analysis of macrophages associated with non-alcoholic fatty liver disease research from 2005 to 2023.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition associated with the risk of progressing to decompensated cirrhosis and hepatocellular carcinoma. While macrophages play a crucial role in the development of NAFLD, their heterogeneity and plasticity allow them to undertake diverse roles in immune response, tissue repair, and maintaining tissue homeostasis. Thus, the exact involvement of macrophages in the onset and progression of NAFLD remains to be further explored. This study aims to employ bibliometric analysis to elucidate the role of macrophages in the pathogenesis of NAFLD, analyze research focal points in this domain, and speculate on future research trends. The literature search, conducted using the Web of Science Core Collection, encompassed articles and reviews related to macrophages and NAFLD published between 2005 and 2023. A bibliometric analysis of 1264 extracted publications was performed using VOSviewer 1.6.17 and Citespace 6.1. R2, evaluating parameters such as spatial and temporal distribution, authors, thematic categories, topic distribution, references, and keywords. The findings revealed a steady global increase in publications in this field, with the United States contributing the most followed by China. The University of California System produced the highest volume of publications, while the Journal of Hepatology had the highest impact factors among the top 10 publishing journals. Tacke Frank emerged as both the most prolific author and the most cited. Co-occurrence and burst analysis of keywords and references highlighted the hotspots in this research area, emphasizing the mechanisms of NAFLD pathogenesis, metabolic regulation, immune modulation, and oxidative stress. Maintaining hepatic homeostasis by liver macrophages and macrophage polarization were identified as trending research directions in this field. Based on the bibliometric analysis, continued attention toward NAFLD therapeutic research involving hepatic macrophages is anticipated. As the mechanisms underlying NAFLD pathogenesis are further elucidated, the development of more treatment approaches related to macrophage immunology and metabolic regulation may expand therapeutic options. This study offers valuable insights into the current state and future trends in the field, providing beneficial guidance to researchers aiming to make significant contributions.

Global research status analysis of the association between aortic aneurysm and inflammation: a bibliometric analysis from 1999 to 2023.

Background: Aortic aneurysm is a chronic arterial disease that can lead to aortic rupture, causing severe complications and life-threatening risks for patients, and it is one of the common causes of death among the elderly. Increasing evidence suggests that inflammation plays an important role in the progression of aortic aneurysm. However, there is a lack of literature-based quantitative analysis in this field. Methods: Up to March 30, 2023, we collected 3,993 articles related to aortic aneurysm and inflammation from the Web of Science Core Collection (WoSCC) database for bibliometric analysis. The collected literature data were subjected to visual analysis of regional distribution, institutions, authors, keywords, and other information using tools such as CiteSpace, VOSviewer, the R package "bibliometric," and online platforms. Results: The number of publications in this research field has been steadily increasing each year, with the United States and China being the main contributing countries. Harvard University in the United States emerged as the most active and influential research institution in this field. Jonathan Golledge and Peter Libby were identified as the authors with the highest publication output and academic impact, respectively. Researchers in this field tend to publish their findings in influential journals such as the Journal of Vascular Surgery and Arteriosclerosis Thrombosis and Vascular Biology. "Abdominal aortic aneurysm," "giant cell arteritis," "arterial stiffness," and "smooth muscle cells" were identified as the hottest topics in the field of aortic aneurysm and inflammation. In terms of keyword co-occurrence analysis, "Clinical relevant studies of AA" (red), "Inflammatory activation" (green), "Inflammatory mechanisms related to pathogenesis" (dark blue), "Cytokines" (yellow), "Risk factors" (purple), and "Pathological changes in vascular wall" (cyan) formed the major research framework in this field. "Inflammation-related pathogenesis" and "inflammation activation" have emerged as recent hot research directions, with "monocytes," "progression," and "proliferation" being the prominent topics. Conclusion: This study provides a comprehensive analysis of the knowledge network framework and research hotspots in the field of aortic aneurysm and inflammation through a literature-based quantitative approach. It offers valuable insights to guide scholars in identifying meaningful research directions in this field.

Global trends in research of acute type a aortic dissection: A bibliometric analysis from 2002 to 2022.

Background: Acute type A aortic dissection (ATAAD) is life-threatening and needs urgent and highly invasive surgery. So far, there is no comprehensive review of the status quo of ATAAD studies. Therefore, this study aimed to quantify and identify the global trends of ATAAD research over the past two decades through bibliometric analysis and to provide reference for clinical practice, research funding allocation, and decision-making. Methods: The original research articles and reviews related to ATAAD research were downloaded from the Web of Science Core Collection on March 19, 2023. CiteSpace (6.2.1) and VOSviewer (1.6.18) were used for bibliometric analysis of the number of publications by each country, institution, and authors and the establishment of knowledge maps. The raw data collected were examined using the Online Analysis Platform of Bibliometric to assess the collaboration of countries in the field. Results: The number of documents on ATAAD research increased continuously. A total of 1,943 publications published from 2002 to 2022 from 66 countries/regions were identified: 637 (32.78%) were conducted in China and 360 (18.53%) in the United States; 152 (cited frequency 941) were conducted by Capital Medical University and 107 (cited frequency 370) by Fujian Medical University. The Journal of Cardiac Surgery was the most frequently published journal (143 publications, cited frequency 695). The highest citation and co-cited journal was the Annals of Thoracic Surgery (cited frequency 3,888, co-cited frequency 6,224). We identified 8,050 authors among which Lizhong Sun (61 publications, cited frequency 721) had the largest number of publications, and Nienaber Christoph A (cited frequency 1,536, co-cited frequency 392) was co-cited most often. Meanwhile, the most common keywords were acute type A aortic dissection (occurrences, 1,211), surgery (occurrences, 657), repair (occurrences, 404), and management (occurrences, 386). The earliest and latest used keywords were "axillary artery" (average publication year: 2011.23) and "inflammation" (average publication year: 2019.09), respectively. The keyword "surgical treatment" (strength 12.31) and the co-cited reference "Evangelista A, 2018, Circulation" (strength 28.55) had the highest citation bursts. The keywords "impact" and "acute kidney injury" remained high citation bursts. The co-cited references with the largest and smallest size clusters were "cerebral protection" (#0, size = 126) and "pregnancy" (#12, size = 11). The reference "Hagan PG, 2000, JAMA" (cited frequency, 350) had the highest co-citations. Conclusions: The bibliometric and visualized analysis generated objective evidence for a comprehensive understanding and evaluation of ATAAD research.

Association between depressive symptoms in the postpartum period and COVID-19: A meta-analysis.

BACKGROUND: With the pandemic of COVID, the public are faced with tremendous threatens both physically and mentally. Postpartum depression (PPD) is one of the most serious complications of childbearing, bringing severe impact on a woman's mental state and mood after birth. Research has shown that maternal mental state is closely correlated with PPD, those undergo the emergency or significant life changes during the postpartum period are more likely to suffer from PPD. In this study, we conducted the meta-analysis to estimate the association between PPD and COVID-19 pandemic. METHODS: PubMed, Web of Science, PsycINFO, ScienceDirect, CNKI, China Science and Technology Journal Database, and WANFANG Database were searched for potentially relevant articles published before April 2022. Review Manager 5.2 was used to perform a meta-analysis and subgroup analysis to compute the pooled odds ratio. RESULTS: A total of 26 studies were included in this review. The overall pooled prevalence of PPD in the review was 24 % (95 % CI: 0.19-0.29), with China's at 22 % (95 % CI 0.16-0.28) and other countries at 25 % (95 % CI 0.18-0.32) during the COVID-19 pandemic. Moreover, compared to those who did not experience COVID-19, those who experienced it had an increased risk of PPD[OR:1.83(95 % CI 1.70-1.97)]. CONCLUSIONS: According to this analysis, there was a significantly higher prevalence and odds of PPD in those who suffered from the COVID-19 pandemic. Additionally, we also found that China had a lower prevalence of postpartum depression than other countries during the COVID-19 pandemic. Our study may provide the instruction for the care of new mother under the situation of COVID-19 prevalence.

Preclinical evidence of reno-protective effect of quercetin on acute kidney injury: a meta-analysis of animal studies.

Objective: This study evaluated the reno-protective effects of quercetin in animal models of acute kidney injury (AKI). Methods: We conducted a systematic search of literature published before April 2023 in PubMed, Web of Science, and EMBASE databases. Methodological quality was assessed by SYRCLE's RoB tool. Funnel plot, Egger's test, and Begg's test were used to determine publication bias. Results: A total of 19 studies with 288 animals were included in this meta-analysis. The methodology quality scores of the included studies ranged from 4 to 7. The results indicated that quercetin reduced blood urea nitrogen (SMD = -4.78; 95% CI: 6.45, -3.12; p < 0.01; I2 = 84%) and serum creatinine (SMD: 2.73, 95% CI: 3.66, -1.80; p < 0.01; I2 = 80%) in AKI models. The result of sensitivity analysis was stable, while the results of funnel plot indicated asymmetric. In addition, we further analyzed inflammatory cytokines, oxidative stress levels, and kidney injury scores, and found that quercetin treatment had antioxidant and anti-inflammatory effects and improved kidney injury scores in animal models of AKI. Conclusion: Quercetin exhibited a promising reno-protective effect in AKI animal models. Systematic Review Registration: PROSPERO (CRD42023433333).

MKI67 as a potential diagnostic biomarker in pulmonary hypertension.

Background: Right heart failure results from advanced pulmonary hypertension (PH) and has a poor prognosis. There are few available treatments for right heart failure. Pulmonary artery remodeling, including changes in pulmonary artery endothelial cells to endothelial-mesenchymal cells, and aberrant fibroblast and pulmonary artery smooth muscle cell (PASMC) proliferation, are characteristics of the pathophysiological process of PH. As a result, the clinical situation requires novel PH diagnostic and treatment targets. Methods: Monocrotaline was used to create an animal model of PH, and lung tissue was removed for transcriptome sequencing. The targets with the highest differences were chosen for transfection after possible targets were identified using bioinformatic techniques and confirmed by qPCR to examine their function in hypoxic PASMCs. Results: After sequencing 781 differentially expressed mRNAs, we compared them with the GEO dataset and found 43 differentially expressed genes. We chose the top three scores for further study and verification and discovered that MKI67, a crucial element of the cell cycle that regulates PASMC proliferation, had the greatest effect. After suppressing MKI67 in PASMCs, both cell proliferation and migration decreased. Conclusion: Several potential targets were chosen for this study, and MKI67 was found to play a regulatory role in cell migration and proliferation. This implies that PH can be diagnosed and treated using MKI67.

Sulfiredoxin-1 attenuates injury and inflammation in acute pancreatitis through the ROS/ER stress/Cathepsin B axis.

Acinar cell injury and the inflammatory response are critical bioprocesses of acute pancreatitis (AP). We investigated the role and underlying mechanism of sulfiredoxin-1 (Srxn1) in AP. Mild AP was induced by intraperitoneal injection of cerulein and severe AP was induced by partial duct ligation with cerulein stimulation or intraperitoneal injection of L-arginine in mice. Acinar cells, neutrophils, and macrophages were isolated. The pancreas was analyzed by histology, immunochemistry staining, and TUNEL assays, and the expression of certain proteins and RNAs, cytokine levels, trypsin activity, and reactive oxygen species (ROS) levels were determined. Srxn1 was inhibited by J14 or silenced by siRNA, and overexpression was introduced by a lentiviral vector. Transcriptomic analysis was used to explore the mechanism of Srxn1-mediated effects. We also evaluated the effect of adeno-associated virus (AAV)-mediated overexpression of Srxn1 by intraductal administration and the protection of AP. We found that Srxn1 expression was upregulated in mild AP but decreased in severe AP. Inhibition of Srxn1 increased ROS, histological score, the release of trypsin, and inflammatory responses in mice. Inhibition of Srxn1 expression promoted the production of ROS and induced apoptosis, while overexpression of Srxn1 led to the opposite results in acinar cells. Furthermore, inhibition of Srxn1 expression promoted the inflammatory response by accumulating and activating M1 phenotype macrophages and neutrophils in AP. Mechanistically, ROS-induced ER stress and activation of Cathepsin B, which converts trypsinogen to trypsin, were responsible for the Srxn1 inhibition-mediated effects on AP. Importantly, we demonstrated that AAV-mediated overexpression of Srxn1 attenuated AP in mice. Taken together, these results showed that Srxn1 is a protective target for AP by attenuating acinar injury and inflammation through the ROS/ER stress/Cathepsin B axis.

SR18292 exerts potent antitumor effects in multiple myeloma via inhibition of oxidative phosphorylation.

AIMS: Multiple myeloma (MM) was recently reported to rely on increased oxidative phosphorylation (OXPHOS) for survival, providing a potential opportunity for MM therapy. Herein, we aimed to propose a novel targeted drug for MM treatment, followed by the exploration of reason for OXPHOS enhancement in MM cells. MATERIALS AND METHODS: The expression of OXPHOS genes and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) was analyzed using bioinformatics analyses, followed by verification in MM cell lines. The effects of SR18292 on OXPHOS were measured by qRT-PCR, Western blot, transmission electron microscopy, oxygen consumption rate and so on. The proliferation and apoptosis were evaluated by CCK-8, flow cytometry and Western blot. The efficiency and safety of SR18292 were assessed in a mouse model of MM. KEY FINDINGS: The OXPHOS genes were generally overexpressed in MM cells, which was associated with poorer prognosis of MM patients. PGC-1α, a transcriptional coactivator, was upregulated in MM cells, and MM patients with higher PGC-1α expression exhibited increased enrichment of the OXPHOS gene set. Treatment with SR18292 (an inhibitor of PGC-1α) significantly impaired the proliferation and survival of MM cells due to OXPHOS metabolism dysfunction, which leads to energy exhaustion and oxidative damage. Besides, SR18292 potently inhibited tumor growth at a well-tolerated dose in MM model mice. SIGNIFICANCE: The overexpression of OXPHOS gene set mediated by upregulated PGC-1α provides a structural basis for enhanced OXPHOS in MM cells, and SR18292 (a PGC-1α inhibitor) exerts potent antimyeloma effects, offering a potential tangible avenue for MM therapy.

Electrochemical immunoassay for the tumor marker CD25 by coupling magnetic sphere-based enrichment and DNA based signal amplification.

Interleukin-2 receptor alpha chain (also called CD25) is a tumor biomarker that is frequently expressed on the surface of hematological tumor cells. The authors describe an electrochemical immunoassay for CD25 that involves (a) enrichment of CD25 from samples by using magnetic nanospheres, and (b) utilization of DNA modulated current as the detection signal. Primary anti-CD25 antibody was immobilized onto F3O4 magnetic nanospheres to capture CD25 from samples. A polycytosine DNA sequence (dC20) was conjugated to the secondary antibody through glutaric dialdehyde via the amino groups on both antibody and the end of the DNA sequence. This leads to the formation of a sandwich structure on the magnetic spheres. dC20 is then reacted with molybdate to form redox molybdophosphate and generate electrochemical current (best measured at 0.2 V vs. Ag/AgCl) that is proportional to the concentration of CD25. The method is sensitive, selective, and has a wide linear response that extends from 1 pg.mL-1 to 1 ng.mL-1. The immunoassay was applied in a recovery test for CD25 in spiked serum samples. Graphical abstract Electrochemical immunoassay for CD25 is reported by initial enrichment of CD25 from samples with magnetic nanospheres and then utilizing DNA generated electrochemical current as detection signal.

Co-administration of 20(S)-protopanaxatriol (g-PPT) and EGFR-TKI overcomes EGFR-TKI resistance by decreasing SCD1 induced lipid accumulation in non-small cell lung cancer.

BACKGROUND: Non-small cell lung cancer (NSCLC) patients with sensitive epidermal growth factor receptor (EGFR) mutations are successfully treated with EGFR tyrosine kinase inhibitors (EGFR-TKIs); however, resistance to treatment inevitably occurs. Given lipid metabolic reprogramming is widely known as a hallmark of cancer and intimately linked with EGFR-stimulated cancer growth. Activation of EGFR signal pathway increased monounsaturated fatty acids (MUFA) and lipid metabolism key enzyme Stearoyl-CoA Desaturase 1 (SCD1) expression. However the correlation between EGFR-TKI resistance and lipid metabolism remains to be determined. METHODS: In this study the differences in lipid synthesis between paired TKI-sensitive and TKI-resistant patient tissues and NSCLC cell lines were explored. Oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) was used to simulate a high lipid metabolic environment and detected the affection on the cytotoxic effect of TKIs (Gefitinib and osimertinib) in cell lines with EGFR-activating mutations. (20S)-Protopanaxatriol (g-PPT), an aglycone of ginsenosides, has been reported to be an effective lipid metabolism inhibitor, was used to inhibit lipid metabolism. Additionally, synergism in cytotoxic effects and signal pathway activation were evaluated using CCK-8 assays, Western blotting, flow cytometry, Edu assays, plate clone formation assays and immunofluorescence. Furthermore, two xenograft mouse models were used to verify the in vitro results. RESULTS: Gefitinib-resistant cells have higher lipid droplet content and SCD1 expression than Gefitinib-sensitive cells in both NSCLC cell lines and patient tissues. Additionally oleic acid (OA, a kind of MUFA, the SCD1 enzymatic product) abrogates the cytotoxic effect of both Gefitinib and osimertinib in cell lines with EGFR-activating mutations. As a reported effective lipid metabolism inhibitor, g-PPT significantly inhibited the expression of SCD1 in lung adenocarcinoma cells, and then down-regulated the content of intracellular lipid droplets. Combined treatment with Gefitinib and g-PPT reverses the resistance to Gefitinib and inhibits the activation of p-EGFR and the downstream signaling pathways. CONCLUSIONS: Our findings uncover a link between lipid metabolic reprogramming and EGFR-TKI resistance, confirmed that combination target both EGFR and abnormal lipid metabolism maybe a promising therapy for EGFR-TKI resistance and highlighting the possibility of monitoring lipid accumulation in tumors for predicting drug resistance.

Pterostilbene inhibits nutrient metabolism and induces apoptosis through AMPK activation in multiple myeloma cells.

Multiple myeloma (MM) cells are characterized by an abnormal nutrient metabolism that is distinct from normal plasma cells. Pterostilbene (PTE), a bioactive component of blueberries, has been demonstrated to induce apoptosis in multiple types of cancer cell. The present study evaluated whether PTE treatment affected the survival of MM cells from a metabolic perspective, and the potential mechanisms of this. It was observed that the administration of PTE induced apoptosis, which was mediated by the increased activation of AMP­activated protein kinase (AMPK). Once activated, AMPK decreased the expression and/or activity of key lipogenic enzymes, including fatty acid synthase and acetyl­CoA carboxylase. In addition, the activation of AMPK suppressed the downstream substrate, mechanistic target of rapamycin, which dephosphorylated eukaryotic initiation factor 4E­binding protein 1, leading to a general decrease in mRNA translation. Pre­treatment with the AMPK inhibitor compound C prior to PTE treatment compromised the anti­myeloma apoptosis effect, suggesting the critical role of AMPK in mediating PTE­induced cell toxicity. Consistent results were obtained in vivo. Finally, autophagy was adaptively upregulated subsequent to PTE treatment; the pro­apoptotic efficacy of PTE was potentiated once autophagic flux was inhibited by 3­methyladenine. Taken together, these data demonstrated that PTE exerts anti­tumor effects on MM cells via AMPK­induced nutrient suppression.

Coupling antibody based recognition with DNA based signal amplification using an electrochemical probe modified with MnO2 nanosheets and gold nanoclusters: Application to the sensitive voltammetric determination of the cancer biomarker alpha fetoprotein.

The authors describe a sensitive electrochemical immunoassay for the cancer biomarker α-fetoprotein (AFP). It is based on a combination of an immunoassay with DNA-based signal amplification. Two-dimensional MnO2 nanosheets modified with gold nanoclusters (AuNC-MnO2) were synthesized through one-pot process and utilized as an electrochemical probe. Bovine serum albumin served as templating agent to guide the formation and assembly of the modified sheets. The detection antibody against AFP and a polycytosine DNA sequence (dC20) were immobilized onto the modified nanosheets. The electrochemical assay follows the usual sandwich protocol. The antibodies on the nanosheets then bind to AFP, while dC20 causes signal amplification. The reaction of the phosphate backbone of dC20 with molybdate leads to the formation of redox-active molybdophosphate which generates an electrochemical current, typically measured at 0.20 V (vs. Ag/AgCl). The method allows AFP to be determined in the 0.01 to 10 ng·mL-1 concentration range, and the detection limit is as low as 5 pg·mL-1. This strategy overcomes the drawbacks of conventional immunoassays whose sensitivity is often limited because many immunoassays are rather difficult to amplify. The method has a wide scope in that various other DNA signal amplification methods such as rolling circle amplification and hybridization chain reactions may also be applied. Graphical abstract Schematic of an electrochemical immunosensor for the detection of alpha fetoprotein (AFP) by combining an antibody based immunoassay with DNA based signal amplification utilizing gold clusters anchored 2D MnO2 (Au NCs-MnO2) nanosheets as electrochemical probe.

[Raman spectra of cell from breast cancer patients].

Raman spectra of normal and cancer cell from breast cancer patients a represented. It is reported that all of the Ramanlines become weak. The intensities of Raman lines 782 and 1 084 cm(-1) of DNA phosphate group and 1 155 and 1 262 cm(-1) of deoxyribosephosphate decrease. The spectral lines 812 cm(-1) of A-type DNA and 979 and 668 cm(-1) disappear, and the 905 cm(-1) peak is shifted to lower frequency by 6 cm(-1). This means that the phosphate backbone of DNA is destroyed to a certain extent and the fissiparity of cancer cell can't be controlled effectively. In addition, the authors found a kind of Raman line 960 cm(-1) concerning calcificationand sclerosis of cancer cell. The results indicate that Raman spectra may offer the experiment basis for the cancer diagnosis and treatment.

[Resonance Raman spectra of single red-cell from human blood].

Resonance Raman spectra of single red-cell from human blood are presented by different laser sources. It is reported that there is 1002 cm(-1) line of insensitive conformation of phenylalanine aromatic ring stretching and 1620 cm(-1) line of C-N breathing stretching band of pyrrole ring, which cause strong and sharp resonance lines when excited by 782 nm laser source. They are weaker and the intensity of other lines of high wave number is large and clear when excited by 514 nm laser source. But the intensity of lines of low wave number is strong and clear when excited by 782 nm laser source. At the same time, the authors got Raman spectra lines at different times after taking blood under the same laser source. When using 782 nm laser source, there is no difference except for 1601 cm(-1). There are a lot of weakened lines and lines shifting about 4-10 cm(-1) toward low wave number. The results indicate that Raman spectra may offer the experimental basis for studying structure, function and variability of single red-cell.