Heart failure with Sarcopenia: A Bibliometric review from 1995 to 2022.

This study aimed to dynamically track the priorities and potential research hotspots in the field of heart failure with sarcopenia. Using CiteSpace, we analyzed the literature on heart failure with sarcopenia from the Web of Science database from 1995 to 2022. The analysis encompassed 507 records, revealing an overall upward trend in annual publication volume. Europe and the United States emerged as the primary regions for publishing, particularly driven by contributions from developed countries such as the United States, Germany, and Italy. Productive institutions included the Charite Universitatsmedizin Berlin, University Medical Center Gottingen, the German Center for Cardiovascular Research (DZHK), Universita Cattolica del Sacro Cuore, and the National Institute on Aging (NIA). Noteworthy academic groups have formed around these institutions; von Haehling S, Anker Stefan D, Springer J, and Doehner W frequently collaborated. The core journals that frequently published articles in this area included Circulation, European Heart Journal, and The Journals of Gerontology Series A-Biological Sciences and Medical Sciences. Based on the keyword analysis, we identified three key research areas. First, the diagnosis and definition of sarcopenia emerged as significant themes. Second, researchers have focused on exploring the mechanisms underlying heart failure with sarcopenia, including inflammation, insulin resistance, and oxidative stress. Finally, treatment strategies, such as physical activity and nutritional support, constitute another critical research theme. Furthermore, potential research hotspots within this field include clinical randomized controlled trials, investigations into inflammatory mechanisms, cardiac rehabilitation, studies on physical activity, androgen receptor modulators, and investigations into clinical outcomes such as cognitive impairment.

Drug resistance in ovarian cancer: from mechanism to clinical trial.

Ovarian cancer is the leading cause of gynecological cancer-related death. Drug resistance is the bottleneck in ovarian cancer treatment. The increasing use of novel drugs in clinical practice poses challenges for the treatment of drug-resistant ovarian cancer. Continuing to classify drug resistance according to drug type without understanding the underlying mechanisms is unsuitable for current clinical practice. We reviewed the literature regarding various drug resistance mechanisms in ovarian cancer and found that the main resistance mechanisms are as follows: abnormalities in transmembrane transport, alterations in DNA damage repair, dysregulation of cancer-associated signaling pathways, and epigenetic modifications. DNA methylation, histone modifications and noncoding RNA activity, three key classes of epigenetic modifications, constitute pivotal mechanisms of drug resistance. One drug can have multiple resistance mechanisms. Moreover, common chemotherapies and targeted drugs may have cross (overlapping) resistance mechanisms. MicroRNAs (miRNAs) can interfere with and thus regulate the abovementioned pathways. A subclass of miRNAs, "epi-miRNAs", can modulate epigenetic regulators to impact therapeutic responses. Thus, we also reviewed the regulatory influence of miRNAs on resistance mechanisms. Moreover, we summarized recent phase I/II clinical trials of novel drugs for ovarian cancer based on the abovementioned resistance mechanisms. A multitude of new therapies are under evaluation, and the preliminary results are encouraging. This review provides new insight into the classification of drug resistance mechanisms in ovarian cancer and may facilitate in the successful treatment of resistant ovarian cancer.

Meiotic protein SYCP2 confers resistance to DNA-damaging agents through R-loop-mediated DNA repair.

Drugs targeting the DNA damage response (DDR) are widely used in cancer therapy, but resistance to these drugs remains a major clinical challenge. Here, we show that SYCP2, a meiotic protein in the synaptonemal complex, is aberrantly and commonly expressed in breast and ovarian cancers and associated with broad resistance to DDR drugs. Mechanistically, SYCP2 enhances the repair of DNA double-strand breaks (DSBs) through transcription-coupled homologous recombination (TC-HR). SYCP2 promotes R-loop formation at DSBs and facilitates RAD51 recruitment independently of BRCA1. SYCP2 loss impairs RAD51 localization, reduces TC-HR, and renders tumors sensitive to PARP and topoisomerase I (TOP1) inhibitors. Furthermore, our studies of two clinical cohorts find that SYCP2 overexpression correlates with breast cancer resistance to antibody-conjugated TOP1 inhibitor and ovarian cancer resistance to platinum treatment. Collectively, our data suggest that SYCP2 confers cancer cell resistance to DNA-damaging agents by stimulating R-loop-mediated DSB repair, offering opportunities to improve DDR therapy.

Neonatal lupus erythematosus as a rare trigger of gastrointestinal involvement in neonates.

Cutaneous and cardiac involvement in neonatal lupus erythematosus (NLE) has been extensively studied; however, gastrointestinal system involvement (GSI) remains unexplored. This study aimed to investigate the clinical features of GSI in patients with NLE with a particular focus on feeding intolerance (FI) and diarrhea. We conducted a retrospective analysis of the clinical data of patients diagnosed with NLE at the Children's Hospital of Soochow University between 2011 and 2022. In this study, of 39 patients diagnosed with NLE, 27 presented with GSI. 9 patients who presented with FI or diarrhea as the primary manifestation were positive for anti-SSA antibody, and 5 were dual positive for anti-SSA and anti-SSB antibodies. Among the mothers of the NLE patients with GSI, 18 had systemic lupus erythematosus, 3 had Sjogren's syndrome, 2 had mixed connective tissue disease, and one each had autoantibody abnormalities and photosensitivity symptoms; 4 mothers denied having any autoimmune disease. In this study, 69.23% of patients with NLE exhibited GSI, which was linked to hypocomplementemia and anti-SSA antibodies. Thus, clinicians should remain vigilant for NLE in neonates, particularly when accompanied with rash and other organ dysfunction and when the high-risk factors of FI and diarrhea have been excluded.

Bibliometric analysis of atrial fibrillation and ion channels.

Atrial fibrillation (AF) is a common clinical malignant arrhythmia with an increasing global incidence. Ion channel dysfunction is an important mechanism in the development of AF. In this study, we used bibliometrics to analyze the studies of ion channels and AF, aiming to provide inspiration and reference for researchers. A total of 3179 literature citations were obtained from Web of Science core databases. Analysis software included Excel 2019, VOSviewer 1.6.16, and CiteSpace 5.7.R2. This field of research has been growing since 1985. The most active country is the United States. The University of Montreal is the most important research institution. The journal Cardiovascular Research has published the largest number of articles in this field. Stanley Nattel and Dobromir Dobrev are the most frequently cited authors. The most cited literature was published in Nature and Science. Cardiac electrophysiology, gene expression, pathogenesis of AF, and AF prevention and treatment are the hot topics for this field research. Cardiac fibrillation and catheter ablation may be future research hotspots in this field.

Necrotizing enterocolitis: current understanding of the prevention and management.

Necrotizing enterocolitis (NEC) is one of the diseases in neonates, with a high morbidity and mortality rate, especially in preterm infants. This review aimed to briefly introduce the latest epidemiology, susceptibility factors, and clinical diagnosis and presentation of NEC. We also organized new prevention strategies by risk factors according to different pathogeneses and then discussed new treatment methods based on Bell's staging and complications, and the classification of mild to high severity based on clinical and imaging manifestations. Such a generalization will help clinicians and researchers to gain a deeper understanding of the disease and to conduct more targeted classification, grading prevention, and exploration. We focused on prevention and treatment of the early and suspected stages of NEC, including the discovery of novel biomarkers and drugs to control disease progression. At the same time, we discussed its clinical application, future development, and shortcomings.

Knowledge domain and emerging trends of autophagy in cardiovascular research: A bibliometric analysis.

BACKGROUND: Autophagy is essential for the homeostasis and function of the cardiovascular system. Citespace is a visual analysis software developed in the context of scientometrics and data visualization. The purpose of this study is to use Citespace software to conduct bibliometric and visual analysis of the research on autophagy in cardiovascular diseases, identify the current status, hot spots and trends in this field, help researchers clarify the future research focus and direction of autophagy in cardiovascular diseases, and provide more positive and broader ideas for the treatment and drug development of cardiovascular diseases. METHODS: In the Web of Science Core Collection database to download the data from 2004 to 2022 regarding autophagy in cardiovascular research. CitespaceV was used to collect the research status, hotspots and development trends for visual analysis. RESULTS: The 3568 articles were published by 547 authors from 397 institutions in 75 countries. From 2004 to 2021, the annual publications increased over time. The top 3 productive nations were China, the United States, and Germany. The leading institution was China's Fudan University. The most cited paper is Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). The research hotpots include monitoring methods for autophagy activity, changes in autophagy levels in different types of cardiovascular diseases, autophagy signal transduction mechanism in cardiovascular diseases, etc. CONCLUSION: Bibliometric analysis provided valuable information for autophagy research in cardiovascular disease, which is full of opportunities and challenges. The research of autophagy in the field of cardiovascular diseases is still worthy of in-depth exploration. A challenge with autophagy-targeted therapies is their dichotomy in which the goal is to target maladaptive autophagy while maintaining a baseline level of cell survival to optimize a beneficial outcome. It is necessary for scientists to develop new methods to evaluate the level of autophagy from basic application to human body and reveal the signaling mechanism of autophagy in different types of cardiovascular diseases.

Active polypeptide MDANP protect against necrotizing enterocolitis (NEC) by regulating the PERK-eIF2ɑ-QRICH1 axis.

The effect of MDANP effects on ER stress signalling not well known or elucidated. Endoplasmic reticulum (ER) stress plays a critical role in necrotizing enterocolitis (NEC) pathogenesis through the PERK-eIF2ɑ-QRICH1 axis. The present study aimed to explore the protective effects of MDANP in NEC development. Firstly, a function screening was designed to identify the candidate peptides in human milk, and then the identified peptides were validated in NEC patients. In vivo, NEC was induced in mice pups and divided into four groups: (1) control group, (2) NEC group, (3) MDANP + NEC group, and (4) NS + NEC group. In vitro, lentivirus-mediated QRICH1 silencing, was used to transfect NCM460 cell lines, then stimulated with LPS. After LPS stimulation, cells were treated with chemically synthesized MDANP, and the essential proteins in the QRICH1 signalling pathway in cells were tested and compared. After the small-scale screening, a peptide (SKSKKFRRPDIQYPDATDED) named MDANP was determined as the principal peptide. Its protective effect against NEC through inhibiting the expression of ERS key proteins and impeding the intestinal cells' apoptosis was observed in the animal models. Furthermore, the inhibitive effect of MDANP on apoptosis of intestinal epithelial cells through modulating the PERK-eIF2ɑ-QRICH1 ERS pathway was also confirmed in vitro. Taken together, our data suggest that MDANP effectively ameliorates apoptosis in NEC through attenuating PERK-eIF2ɑ-QRICH1.

Knowledge mapping of B cell and atherosclerosis over the past 20 years: A bibliometric analysis.

Atherosclerosis (AS) is the main underlying cause of cardiovascular disease, and B cells are considered a key immune cell type to regulate AS. So far, there is no bibliometric study on B cell and AS. This study aims to comprehensively analyze the scientific output about B cell and AS, summarize the literature characteristics, explore research hotspots, and point out emerging trends. We searched the literature from 2003 to 2022 from the Web of Science Core Collection (WoSCC) database. CiteSpace, VOSviewer, and the R package "Bibliometrix" were used for literature analysis and visualization. A total of 1,062 articles and reviews were identified. The number of annual publications generally showed an upward trend. The United States and China were the most productive countries. Medical University of Vienna was the most productive research institution, and Binder Christoph J. was the most productive author, who was also from Medical University of Vienna. "Arteriosclerosis Thrombosis and Vascular Biology" was the most published journal and the most frequently cited journal. The most cited reference was written by Caligiuri G (2002) in "Journal of Clinical Investigation." The most frequent keywords were "inflammation," "macrophages," "cardiovascular disease," "T cells," "apoptosis," "immunity," "cytokines," "lymphocytes," etc. The trend topics were mainly focused on "immune infiltration," "immunoglobulins," and "biomarkers." The complex role of B cell subtypes and a variety of B cell mediators is the main research direction at present. In-depth analysis of B cell-specific targets can provide new ideas and methods for the prevention and treatment of AS.

Cutting Edge: CCR8 Signaling Regulates IL-25- and IL-33-Responsive Skin Group 2 Innate Lymphoid Cell Migration and Function.

Group 2 innate lymphoid cells (ILC2s) are sentinels of barrier immunity, and their activation by the epithelial alarmins IL-25 and IL-33 is a defining trait. In this study, we identified a role for the chemokine receptor CCR8 in modulating skin ILC2 abundance and activation. CCR8 signaling facilitated IL-25-induced increases in skin and lung ILC2s, ILC2 activation and systemic IL-13 production, and ligand-directed ILC2 entry into skin and lung. CCR8 controlled ILC2 tissue entry in IL-25-treated naive mice, but only transferred bone marrow ILC2 progenitors were equipped to enter the skin, whereas multiple tissue-sourced ILC2s entered the lung. CCR8 selectively regulated IL-33-induced increases in skin ILC2s, their proliferation, and production of IL-13/IL-5, as well as IL-33-responsive transferred ILC2 trafficking only to the skin. Collectively, we illuminate (to our knowledge) novel aspects of CCR8 signaling-regulated ILC2 motility and function, especially in the skin, in response to two hallmark ILC2-activating alarmins.

The RNA m5C modification in R-loops as an off switch of Alt-NHEJ.

The roles of R-loops and RNA modifications in homologous recombination (HR) and other DNA double-stranded break (DSB) repair pathways remain poorly understood. Here, we find that DNA damage-induced RNA methyl-5-cytosine (m5C) modification in R-loops plays a crucial role to regulate PARP1-mediated poly ADP-ribosylation (PARylation) and the choice of DSB repair pathways at sites of R-loops. Through bisulfite sequencing, we discover that the methyltransferase TRDMT1 preferentially generates m5C after DNA damage in R-loops across the genome. In the absence of m5C, R-loops activate PARP1-mediated PARylation both in vitro and in cells. Concurrently, m5C promotes transcription-coupled HR (TC-HR) while suppressing PARP1-dependent alternative non-homologous end joining (Alt-NHEJ), favoring TC-HR over Alt-NHEJ in transcribed regions as the preferred repair pathway. Importantly, simultaneous disruption of both TC-HR and Alt-NHEJ with TRDMT1 and PARP or Polymerase θ inhibitors prevents alternative DSB repair and exhibits synergistic cytotoxic effects on cancer cells, suggesting an effective strategy to exploit genomic instability in cancer therapy.

Science mapping analysis of computed tomography-derived fractional flow reverse: a bibliometric review from 2012 to 2022.

Background: Computed tomography-derived fractional flow reserve (CT-FFR) is a non-invasive imagological examination used for diagnosing suspected coronary atherosclerotic heart disease, providing the morphological and functional value on a three-dimensional (3D) coronary artery model. This article aimed to collate the existing knowledge and predict this novel technology's future research hotspots. Methods: To collect data, 1,712 articles were retrieved from the Web of Science Core Collection (WoSCC) database from 2012-2022. CiteSpace5.8.R3 was used to visually analyze the research status and predict future research hotspots. Results: Firstly, the United States, China, and the Netherlands were identified as the countries having published the most articles about CT-FFR. Jonathan Leipsic's group ranked first for the highest number of published articles. Secondly, the visualized analysis indicated that the exploration of CT-FFR is multi-disciplinary and involves cardiology, radiology, engineering, and computer science. Thirdly, the hotspots in this field, which were inferred from the keyword distribution and clustering, included the following: "diagnostic performance", "accuracy", and the "prognostic value" of CT-FFR, and comparison of CT-FFR and other imaging methods sharing similarities. The research frontiers included technologies utilized to obtain more accurate CT-FFR values, such as artificial intelligence (AI) and deep learning. Conclusions: As the first visualized bibliometric analysis on CT-FFR, this study captured the current accumulated information in this field and offer more insight and guidance for future research.

Human breast milk: A promising treatment for necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disorder occurring in newborns, with a mortality rate ranging from 20 % to 30 %. The existing therapeutic approaches for NEC are limited in their effectiveness. Various factors contribute to the development of NEC, including disruption of barrier function, dysregulation of the intestinal immune system, and abnormal colonization of the intestinal microbiota. Researchers have shown considerable interest in exploring the therapeutic potential of the constituents present in human breast milk (HBM) for treating NEC. HBM contains numerous bioactive components, such as exosomes, growth factors, and oligosaccharides. However, the precise mechanisms by which HBM exerts its protective effects against NEC remain incompletely understood. In this study, our objective was to comprehensively review the bioactive substances present in HBM, aiming to facilitate the development of novel therapeutic strategies for NEC.

Neurological and endocrinological involvement in neonatal lupus erythematosus: a retrospective study at a tertiary hospital in Eastern China.

INTRODUCTION: Neonatal lupus erythematosus (NLE) is a rare autoimmune disease that causes transient impairment of multi-organ functions and is mainly caused by maternally transmitted antibodies. OBJECTIVE: This study aims to investigate the clinical features of infants with NLE, focusing on the presence of neurological and endocrinological involvement. METHODS: The clinical data of infants diagnosed with NLE at the Children's Hospital of Soochow University from 2011 to 2022 were collected and retrospectively analyzed. RESULT: In all, 39 patients with NLE were included, and the most common symptom was rash, followed by hematological, hepatic, cardiac, gastrointestinal, neurological, and endocrine symptoms. Among the 10 patients with neurological impairment, intracranial hemorrhage was the most common, followed by convulsions, hydrocephalus, extracerebral space enlargement, and aseptic meningitis. All patients with neurological impairment were positive for anti-SSA/Ro antibodies. Five of these patients were double positive for anti-SSA/Ro and anti-SSB/La antibodies. All 10 patients had multi-organ system involvement, with hematological involvement being the most common, and three patients had varying degrees of developmental delay at the post-discharge follow-up. Nine patients with endocrine impairment were positive for anti-SSA/Ro antibodies, with pancreatic impairment being the most common. There were four cases of hyperinsulinemia and hypoglycemia, one case of diabetes mellitus with ketoacidosis, two cases of hypothyroidism, one case of hypoadrenocorticism, and one case of lysinuric protein intolerance, all of which were normalized before discharge. All patients with endocrine impairment showed hematological involvement, and some showed feeding intolerance as their first symptom. One patient had abnormal liver function at post-discharge follow-up, and two patients had a rash caused by a severe allergy to milk protein. CONCLUSIONS: At our hospital, no significant gender differences were observed in the occurrence of NLE, and a predominance of skin, blood, liver, and heart involvement was observed. Patients with multiple central nervous system injuries and organ involvement are more likely to have growth retardation. Endocrine disorders are transient in NLE patients, and some showed feeding intolerance as the first manifestation. Key Points •A retrospective investigation of the clinical characteristics and prognosis of 39 NLE patients was performed, focusing on the clinical features of patients with neurological and endocrine system involvement to improve clinicians' understanding of this disease.

[Chloroplast genomic characterization and phylogenetic analysis of Castanopsis hystrix].

The structure and size of the chloroplast genome of Castanopsis hystrix was determined by Illumina HiSeq 2500 sequencing platform to understand the difference between C. hystrix and the chloroplast genome of the same genus, and the evolutionary position of C. hystrix in the genus, so as to facilitate species identification, genetic diversity analysis and resource conservation of the genus. Bioinformatics analysis was used to perform sequence assembly, annotation and characteristic analysis. R, Python, MISA, CodonW and MEGA 6 bioinformatics software were used to analyze the genome structure and number, codon bias, sequence repeats, simple sequence repeat (SSR) loci and phylogeny. The genome size of C. hystrix chloroplast was 153 754 bp, showing tetrad structure. A total of 130 genes were identified, including 85 coding genes, 37 tRNA genes and 8 rRNA genes. According to codon bias analysis, the average number of effective codons was 55.5, indicating that the codons were highly random and low in bias. Forty-five repeats and 111 SSR loci were detected by SSR and long repeat fragment analysis. Compared with the related species, chloroplast genome sequences were highly conserved, especially the protein coding sequences. Phylogenetic analysis showed that C. hystrix is closely related to the Hainanese cone. In summary, we obtained the basic information and phylogenetic position of the chloroplast genome of red cone, which will provide a preliminary basis for species identification, genetic diversity of natural populations and functional genomics research of C. hystrix.

Comparison and Investigation of Exosomes from Human Amniotic Fluid Stem Cells and Human Breast Milk in Alleviating Neonatal Necrotizing Enterocolitis.

In view of the devastating impact of neonatal necrotizing enterocolitis (NEC) on newborns, the research on its intervention is particularly important. Although exosomes from human amniotic fluid stem cells (AFSC) and human breast milk (HBM) can protect against NEC, their mechanisms remain unclear. Here, we intend to compare the intervention effects of two types of exosomes on NEC mouse model and reveal their respective regulatory mechanisms. In general, both AFSC-derived exosomes (AFSC-exos) and HBM-derived exosomes (HBM- exos) can alleviate NEC- associated intestinal injury, significantly reduce NEC score, and reduce systemic and ileal inflammation and NEC related brain injury during experimental NEC. However, the mode and mechanism of action of the two sources of exosomes were not identical. In vivo, the number of ileal crypts was more significantly restored after HBM-exos intervention than AFSC-exos, and in vitro, HBM-exos preferentially inhibited the inflammatory response of intestinal epithelial cells (IECs), whereas AFSC-exos preferentially regulated the migration of IECs. Mechanistically, GO and KEGG analyses revealed the different therapeutic mechanisms of AFSC-exos and HBM-exos in NEC. Taken together, our results illustrate that AFSC-exos and HBM-exos reduce the severity of experimental NEC and intestinal damage through different mechanisms, supporting the potential of cell-free or breast milk free exosome therapy for NEC.

The Role of VEGF Family in Lipid Metabolism.

The vascular endothelial growth factor (VEGF) family plays a major role in tumors and ophthalmic diseases. However, increasingly more data reported its potential in regulating lipids. With its biological functions mainly expressed in lymphatic vessels, some factors in the families, like VEGF-A and VEGF-C, have been proved to regulate intestinal absorption of lipids by affecting chylous ducts. Other effects, including regulating lipoprotein lipase (LPL), endothelial lipase (EL), and recombinant syndecan 1 (SDC1), have also been confirmed. However, given the scant-related studies, further research should be conducted to examine the concrete mechanisms and provide pragmatic ways to apply them in the clinic. The VEGF family may treat dyslipidemia in specific ways that are different from common methods and concurrently contribute to the treatment of other metabolic diseases, like diabetes and obesity.

Erratum: [Corrigendum] Stormorken syndrome caused by STIM1 mutation: A case report and literature review.

[This corrects the article DOI: 10.3892/mi.2022.54.].

Acute necrotizing encephalopathy associated with lymphoma-associated hemophagocytic lymphohistiocytosis: A case report and literature review.

Damage associated with lymphoma-associated hemophagocytic lymphohistiocytosis (LA-HLH) to the central nervous system (CNS) is not uncommon. However, the combination with brain damage resembling acute necrotizing encephalopathy (ANE) is rarely reported. Herein, we introduce the diagnosis and treatment of a case of ANE associated with LA-HLH in our hospital and review the relevant literature. After treatment, the child was discharged with only dysarthria and decreased sucking ability. The child is now discharged from the hospital for 6 months with regular follow-up. There were no disease recurrence signs. LA-HLH and ANE were related to cytokine storm. Therefore, early steroid application is essential for treating these diseases.