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Conrad Heide posted an update a month ago
On September 16, 2022, we retrieved articles and reviews from the Web of Science Core Collection, focusing on the intersection of necroptosis and cancer. The countries, institutions, authors, references, and keywords of this subject area were the focus of a visual analysis using CtieSpace 58.R3, VOSviewer 16.18, and the bibliometrix R package. In the period spanning 2006 to 2022, 2216 peer-reviewed original articles and reviews concerning necroptosis in tumors were published in 685 academic journals. This impressive body of research, originating from 13,009 authors connected to 789 institutions in 75 countries and territories, highlights the significant research activity in this area. A considerable upswing in publications examining necroptosis and its relation to cancer has taken place over the past 16 years, coinciding with a high point in citations around 2008-2011. The United States, despite not producing the largest volume of publications, nevertheless held a dominant position as a knowledge bridge in the field of necroptosis and cancer research, while China produced the majority of publications; in addition, Ghent University and the Chinese Academy of Sciences held significant publication records. Furthermore, a negligible portion of the articles were published across multiple countries. Though Alexei Degterev was commonly co-cited, Peter Vandenabeele’s publications were demonstrably more impactful. The exceptional h-index and g-index of Peter Vandenabeele are a testament to his significant contributions in this research field. Necroptosis and cancer research publications overwhelmingly favored Cell Death and Disease, a position substantiated by Bradford’s Law, which confirmed its status as the leading core source. Coincidentally, Cell was the most frequently cited journal alongside the focus areas of molecular biology, immunology, and their respective subfields. A substantial portion of high-frequency keywords were linked to molecular characteristics (MLKL, NF-kB, TNF, RIPK3, RIPK1), to disease-associated processes (necroptosis, apoptosis, cell-death, necrosis, autophagy), and also to mechanisms like activation, expression, and inhibition. This study, employing bibliometric and visual methods, provides a comprehensive overview of necroptosis and cancer research. Necroptosis-cancer research is demonstrating a considerable rise in activity. Further strengthening cooperation and communication between nations and institutions is essential. Scholars engaged in necroptosis and cancer research can utilize the valuable references found within our paper.
The aim of this research is to scrutinize the safety of immune checkpoint inhibitors in patients with primary liver cancer, and to determine the risk factors for immune-related adverse events (irAEs). This study involved the enrollment of 106 patients diagnosed with primary liver cancer, subdivided into 81 patients with hepatocellular carcinoma and 25 patients with intrahepatic cholangiocarcinoma. Our study investigated group disparities in the occurrence of irAE, including subgroups receiving targeted medications, those who did not receive such treatments, and those who received interventional therapy. Irrespective of other factors, thyroid, liver, and skin complications were the predominant irAEs observed in 39% of patients. The occurrence of irAE showed no relationship with the kind, advancement, or seriousness of liver cancer, Child-Pugh grade, or Barcelona Clinic Liver Cancer classification. Body mass index, when elevated, was a salient risk indicator for irAEs, which was associated with being overweight. The concurrent use of targeted pharmaceuticals and/or transcatheter arterial chemoembolization did not elevate the frequency of irAEs. The possibility of irAEs in primary liver cancer patients is influenced by their overweight status. Nonetheless, irAE occurrences exhibit no connection to liver cancer’s type, stage, severity, or any combination of targeted treatments or transarterial chemoembolization.
The presence of p53 mutations is a common characteristic of human cancers, affecting approximately half of those with esophageal cancer. Oncogenic functions of mutant p53 (mutp53) contribute to the progression of malignant tumors, as well as their invasion, metastasis, and resistance to drugs, culminating in a poor prognosis. Certain small molecules have been shown to lessen the oncogenic action of a mutated p53 protein by bringing back its characteristic wild-type activity. Though these molecules experienced evaluation in clinical trials, none ultimately demonstrated clinical success. In p53-mutant esophageal squamous cell carcinoma (ESCC), we examined the anti-tumor effects of phenethyl isothiocyanate (PEITC), scrutinizing its mechanism to discover novel therapeutic strategies. Our research revealed the p53R248Q mutation to be both a DNA binding and structural alteration, and PEITC was observed to reinstate the activity of p53R248Q both in laboratory and in living organisms. This further highlights the antitumor actions of PEITC across cancers exhibiting differing p53 mutations. PEITC effectively inhibits ESCC growth, induces apoptosis, and halts cell cycle progression, showing a marked preferential selectivity for ESCC cells with p53 mutations. Detailed mechanistic research showed that PEITC prompted apoptosis and arrested cells at the G2/M checkpoint in cells containing the mutated p53R248Q protein by reinstituting p53’s wild-type conformation and transactivation capability; these effects varied according to the concentration used. In addition, PEITC hindered the growth of subcutaneous xenografts implanted in living organisms and re-established the functional activity of the p53 mutant in these grafts. The antitumor effects of PEITC, as demonstrated in these findings, are intricately linked to its ability to reinstate the function of the p53R248Q protein, a critical molecular process.
Spaceflight, characterized by a microgravity environment, is known to have adverse effects on the learning and memory skills of astronauts. Currently, few viable strategies exist to counteract the impact of these effects. The potent neuroprotective effects of ginseng’s major steroidal components, Rg1 and Rb1, are coupled with a strong safety profile. In a hindlimb suspension (HLS) rat model, this study investigated the influence of Rg1 and Rb1 on learning and memory impairment caused by simulated microgravity and the associated underlying mechanisms. A significant improvement in spatial and associative learning and memory, compromised by 4-week HLS exposure, was achieved by administering Rg1 (30 and 60 mol/kg) and Rb1 (30 and 60 mol/kg) for two weeks, as indicated by results from the Morris water maze and Reward Operating Conditioning Reflex (ROCR) tests. Correspondingly, Rg1 and Rb1 administration improved the situation by decreasing reactive oxygen species and increasing antioxidant enzyme activities in the prefrontal cortex (PFC). Rb1 and Rg1 contributed to the recovery of mitochondrial complex I (NADH dehydrogenase) activity by increasing Mfn2 expression and diminishing the expression of the mitochondrial fission marker, dynamin-related protein (Drp)-1. screening libraries Treatment with Rg1 and Rb1 resulted in a noticeable rise in SYN and PSD95 protein expression, a decline in the Bax/Bcl-2 ratio, and a decrease in the expression levels of cleaved caspase-3 and cytochrome C. Subsequently, Rg1 and Rb1 treatment induced the activation of the BDNF-TrkB/PI3K-Akt pathway. HLS-induced cognitive impairments were counteracted, and mitochondrial dysfunction, oxidative stress, and apoptosis were lessened by the combined Rg1 and Rb1 treatments, alongside the enhancement of synaptic plasticity and the restoration of BDNF-TrkB/PI3K-Akt signaling pathways.
Baicalin and baicalein, flavonoids uniquely found within the root of Scutellaria baicalensis Georgi, are frequently incorporated into traditional Chinese medicine, herbal supplements, and healthcare products. Accumulated research has highlighted the therapeutic efficacy of baicalin in treating lung diseases, which is a consequence of its antioxidant, anti-inflammatory, immunomodulatory, antiapoptotic, anticancer, and antiviral mechanisms of action. PubMed and ClinicalTrials databases were consulted to locate articles published from September 1970 to March 2023, centered on the search string ‘baicalin and lung’ regarding baicalin and lung. We reviewed the therapeutic impact of baicalin on a variety of lung disorders, encompassing chronic obstructive pulmonary disease, asthma, pulmonary fibrosis, pulmonary hypertension, pulmonary infections, acute lung injury/acute respiratory distress syndrome, and lung cancer. Our conversation also included the root causes of baicalin’s effect on these lung diseases.
The unfortunate prognosis for tumor patients is frequently influenced by the presence of tumor metastasis. For this reason, the research into the metastasis mechanism is essential for overcoming this problem. Lipid peroxidation, a consequence of iron overload, characterizes ferroptosis, a novel cell death mechanism, causing membrane damage. Numerous studies demonstrate that an overabundance of ferroptosis can influence tumor metastasis, thereby hindering tumor development. The advancement of ferroptosis has been observed to be associated with circular RNA (circRNA), a type of non-coding RNA, thus impacting the growth of tumors. Nevertheless, the precise methods through which circular RNAs influence ferroptosis progression and their contributions to tumor metastasis remain unclear. This review methodically examines the part circRNAs play in governing tumor ferroptosis, their mode of operation via sponging miRNAs in different malignancies, and their resulting influence on metastasis. The study of ferroptosis-related circular RNAs in tumor metastasis is furthered by this review, aiming to furnish researchers with novel ideas and targeted therapeutic strategies for future research.
The clinical use of existing oxazolidinone antibiotics is considerably limited by their inherent adverse reactions, most notably thrombocytopenia. In the context of anti-infective therapies, when a patient presents with suspected drug-induced thrombocytopenia, immediate cessation of the implicated medication constitutes the initial intervention.