Publication data was extracted from the Web of Science Core Collection database. A bibliometric analysis, carried out with CiteSpace and VOSviewer, explored the co-occurrence and collaborative relationships of countries/regions, institutions, and authors, revealing research hotspots within the field.
The database search process unearthed 3531 English articles that spanned the years 2012 to 2021. We noted a significant burgeoning of publications commencing in the year 2012. reactive oxygen intermediates China and the United States led the pack in article output, with each having over 1000 articles. The Chinese Academy of Sciences' publication volume reached 153, representing the most contributions (n = 153).
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Publications (14 and 13) in tumor ablation and immunity might suggest a keen interest. The top ten co-cited authors include,
A remarkable 284 citations earned first place, with the subsequent entry coming in second…
A considerable body of 270 citations exists.
Citations numbering 246, each sentence uniquely rendered. Photothermal therapy and immune checkpoint blockade emerged as key research areas, according to co-occurrence and cluster analysis.
For the last ten years, there has been a substantial increase in focus on the neighborhood of tumor ablation domain immunity. In this field, the leading research initiatives presently emphasize the investigation of immunological mechanisms in photothermal therapy for enhanced efficacy, along with the integration of ablation therapy with treatments utilizing immune checkpoint inhibitors.
Researchers have devoted more and more attention to the field of tumor ablation domain immunity in the past ten years. The forefront of research in this field now involves scrutinizing the immunological aspects of photothermal therapy to achieve better results, along with the integration of ablation therapy and immune checkpoint inhibitor treatments.
The occurrence of rare inherited syndromes, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) and poikiloderma with tendon contractures, myopathy, and pulmonary fibrosis (POIKTMP), is linked to biallelic pathogenic variants.
heterozygous pathogenic variants, and those in
The JSON schema, respectively, lists sentences. To clinically diagnose APECED and POIKTMP, the development of two or more defining disease characteristics is imperative for establishing the respective syndrome. In this patient case, we compare and contrast the shared and distinct clinical, radiographic, and histological features of APECED and POIKTMP, and describe the impact of azathioprine therapy on the POIKTMP-related hepatitis, myositis, and pneumonitis.
With IRB-approved protocols (NCT01386437, NCT03206099) and informed consent, the patient underwent a complete clinical evaluation at the NIH Clinical Center. This evaluation included exome sequencing, copy number variation analysis, comprehensive autoantibody studies, peripheral blood immunophenotyping, and salivary cytokine assays.
The NIH Clinical Center received a referral for a 9-year-old boy with a clinical picture akin to APECED, marked by the classical APECED dyad: chronic mucocutaneous candidiasis and hypoparathyroidism. The presentation and evaluation are detailed. The subject was diagnosed with POIKTMP, fulfilling the clinical diagnostic criteria involving poikiloderma, tendon contractures, myopathy, and pneumonitis; exome sequencing was employed to delve deeper into the underlying genetic makeup.
A pathogenic variant, c.1292T>C, heterozygous, was found in the provided sample.
Although a thorough investigation was conducted, no damaging single nucleotide variants or copy number variations emerged.
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The genetic, clinical, autoantibody, immunological, and treatment-response information regarding POIKTMP is explored in this report.
This report explores the genetic, clinical, autoantibody, immunological, and treatment response characteristics of POIKTMP, providing more thorough insight than previously presented data.
Hiking or visiting altitudes surpassing approximately 2500 meters leads to altitude sickness in sea-level residents, which is directly caused by the hypobaric hypoxia (HH) conditions prevalent in those high-altitude areas. HH-driven cardiac inflammation in both ventricles is linked to maladaptive metabolic reprogramming in macrophages. This maladaptive programming in turn evokes amplified pro-inflammatory responses, resulting in myocarditis, fibrotic remodeling, arrhythmias, heart failure, and sudden cardiac death. Studies have repeatedly shown the cardioprotective impact of using salidroside or altitude preconditioning (AP) before experiencing higher altitudes. Although these therapeutic interventions are effective, geographical limitations render them unavailable or inaccessible to the majority of the population. Hypoxia-induced cardiomyocyte damage is effectively prevented by occlusion preconditioning (OP), which instigates endogenous cardioprotective cascades to diminish myocardial injury. Considering OP's potential applicability, we examined its efficacy as a treatment for preventing HH-induced myocarditis, remodeling, and arrhythmias.
Following a 7-day intervention program, comprising 6 cycles of 5-minute hindlimb occlusions (200 mmHg) followed by 5-minute reperfusion at 0 mmHg on alternate hindlimbs daily, the influence of this procedure on cardiac electrical activity, immune system response, myocardial remodeling, metabolic equilibrium, oxidative stress response, and behavioral performance was studied in mice both prior to and after high-height exposure. Cardiopulmonary exercise testing (CPET) was performed on all subjects before and after 6 days of OP intervention, consisting of 6 cycles each day, with 5 minutes of occlusion at 130% systolic pressure alternating with 5 minutes of reperfusion at 0 mmHg, applied to the alternate upper limb.
The impact of OP and AP interventions was assessed, revealing a trend. Comparable to AP, OP preserved cardiac electric function, mitigated maladaptive myocardial restructuring, initiated adaptive immunomodulation, maintained metabolic homeostasis within the heart, augmented antioxidant defenses, and lessened the susceptibility to HH-induced anxiety-related behaviors. Ultimately, OP augmented respiratory and oxygen-transporting capability, metabolic balance, and endurance in humans.
The study's findings indicate that OP acts as a potent alternative intervention in the prevention of hypoxia-induced myocarditis, cardiac remodeling, arrhythmias, and cardiometabolic disorders, and may have the capacity to ameliorate other inflammatory, metabolic, and oxidative stress-related conditions.
OP's efficacy in preventing hypoxia-induced myocarditis, cardiac remodeling, arrhythmias, and cardiometabolic disorders suggests a potent alternative therapeutic approach, capable of potentially mitigating the progression of other inflammatory, metabolic, and oxidative stress-related diseases.
The potent anti-inflammatory and regenerative actions of mesenchymal stromal cells (MSCs) and their extracellular vesicles (EVs) in situations of inflammation and tissue damage make them a highly attractive therapeutic tool for cellular interventions. This research explored how MSCs and their EVs exhibit inducible immunoregulation when exposed to varied combinations of cytokines. Following IFN-, TNF-, and IL-1 priming, MSCs exhibited an augmented expression of PD-1 ligands, underpinning their immunomodulatory mechanism. The immunosuppressive effects on activated T cells, and the induction of regulatory T cells, were more pronounced in the case of primed MSCs and MSC-EVs, as opposed to unstimulated counterparts, with this enhancement occurring in a PD-1-dependent manner. Critically, EVs produced by primed mesenchymal stem cells (MSCs) showed a decrease in clinical scoring and an improvement in survival duration for mice experiencing graft-versus-host disease. The in vitro and in vivo reversal of these effects was achieved by the addition of neutralizing antibodies directed against PD-L1 and PD-L2 to both the MSCs and their EVs. In closing, the data presented support a priming method that strengthens the immunoregulatory effect of mesenchymal stem cells and their extracellular vesicles. Nimodipine MSC therapies, whether cellular or exosome-based, can also gain from this concept's contribution to their clinical applicability and streamlined execution.
Human urinary proteins, a treasure trove of natural proteins, streamline their transformation into therapeutic biologics. This goldmine, in conjunction with the ligand-affinity-chromatography (LAC) purification method, was instrumental in achieving successful isolation. In the quest for predictable and unpredictable proteins, LAC's specificity, efficiency, simplicity, and inherent indispensability are superior to any other protein separation technique. The unrestricted availability of recombinant cytokines and monoclonal antibodies (mAbs) hastened the culmination of the triumph. Anti-retroviral medication Thirty-five years of global research into the Type I IFN receptor (IFNAR2) reached its apex with my approach, leading to significant advancements in our comprehension of this interferon's signal transduction. The use of TNF, IFN, and IL-6 as bait proteins enabled the isolation of their soluble receptor counterparts. Subsequently, analyzing the N-terminal amino acid sequences of these isolated proteins led to the cloning of their corresponding cell surface proteins. The bait proteins IL-18, IL-32, and heparanase, unexpectedly, yielded the following proteins: IL-18 Binding Protein (IL-18BP), Proteinase 3 (PR3), and the hormone Resistin. In the realm of Multiple Sclerosis treatment, IFN demonstrated substantial benefits, with Rebif standing as a prime example. Remicade's TNF mAb formulation played a pivotal role in the translation and application of treatment for Crohn's disease. Enbrel, utilizing TBPII, is a treatment option for individuals with Rheumatoid Arthritis. Both are cinematic blockbusters, a surefire sign of popularity. Phase III clinical trials are underway for Tadekinig alfa, a recombinant IL-18 binding protein, targeting inflammatory and autoimmune diseases. The life-saving impact of Tadekinig alfa, administered compassionately for seven years to children with NLRC4 or XIAP mutations, exemplifies the power of tailored medicine.