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Microorganisms Apr 2024Chronic HIV-1 infection can cause neurological illness, also known as HIV-associated neurocognitive disorders (HAND). The elevated level of pro-inflammatory cytokines... (Review)
Review
Chronic HIV-1 infection can cause neurological illness, also known as HIV-associated neurocognitive disorders (HAND). The elevated level of pro-inflammatory cytokines and chemokines, such as C-C Chemokine Ligand 5 (CCL5/RANTES), is one of the ways of causing HIV-1-mediated neuroinflammation. C-C Chemokine Receptor 5 (CCR5) is the main coreceptor for viral entry into host cells and for mediating induction of CCL5/RANTES. CCR5 and CCL5 are part of a correlated axis of immune pathways used for effective protection against the HIV-1 virus. The purpose of this paper was to review the literary knowledge about the immunopathological relationship between this immune complex and neuroAIDS. A systematic review of the literature was conducted based on the selection and search of articles, available in English, Spanish, or Portuguese in the time frame of 1990-2022, of primary and secondary types in the PUBMED, Science Direct, SciELO, and LILACS databases through descriptors (MeSH) together with "AND": "CCR5"; "CCL5"; "neurological manifestations"; or "HIV". The methodological quality of the articles was assessed using the JBI Checklists and the PRISMA 2020 writing guidelines were followed. A total of 36 articles were included in the final composition of the review. The main cells of the CNS affected by neuroAIDS are: neurons; microglia; astrocytes; and oligodendrocytes. Molecular devices and their associations with cellular injuries have been described from the entry of the virus into the host's CNS cell to the generation of mental disorders. Furthermore, divergent results were found about the levels of CCL5/RANTES secretion and the generation of immunopathogenesis, while all condensed research for CCR5 indicated that elevation of this receptor causes more neurodegenerative manifestations. Therefore, new therapeutic and interventional strategies can be conditioned on the immunological direction proposed in this review for the disease.
PubMed: 38674726
DOI: 10.3390/microorganisms12040782 -
Frontiers in Oncology 2023This study aims to depict the scientific advancements in immunotherapy for glioma by analyzing the top 100 most frequently cited articles over the past 20 years.
PURPOSE
This study aims to depict the scientific advancements in immunotherapy for glioma by analyzing the top 100 most frequently cited articles over the past 20 years.
METHODS
The top 100 most influential papers in immunotherapy for glioma were identified from the Web of Science Core Collection. Citations, countries/regions, institutions, journals, authorships, keywords, and references were extracted and analyzed by CiteSpace, VOSviewer, R software, and an online bibliometric platform.
RESULTS
The United States possessed a robust global presence, leading in terms of publications and maintaining strong collaborative ties with numerous countries. The institution that made the greatest contributions was Duke University, with 16 papers. Heimberger AB, Sampson JH, and Reardon DA secured the top three positions with 15, 12, and 11 papers, respectively. "Macrophage ontogeny," "microglia," "polarization," "mass cytometry," "tumor mutation burden," "sensitivity," "msh6," "pd-1 blockade," and "dna repair" were the recent hot keywords. "Microglia" and "polarization" as the emerging research directions should be given more consideration.
CONCLUSIONS
This is the first bibliometric analysis to identify the top 100 papers on immunotherapy for glioma. "Microglia" and "polarization" will be hot spots for future research. The clinical efficacy of glioma immunotherapy is not yet satisfactory, and there is an urgent need to search for more tumor specific antigens and targets that can assist in early diagnosis, precise treatment, prognosis, and recurrence prediction of glioma.
PubMed: 38293697
DOI: 10.3389/fonc.2023.1307924 -
International Journal of Molecular... May 2024Suicide is a major public health priority, and its molecular mechanisms appear to be related to glial abnormalities and specific transcriptional changes. This study... (Review)
Review
Suicide is a major public health priority, and its molecular mechanisms appear to be related to glial abnormalities and specific transcriptional changes. This study aimed to identify and synthesize evidence of the relationship between glial dysfunction and suicidal behavior to understand the neurobiology of suicide. As of 26 January 2024, 46 articles that met the inclusion criteria were identified by searching PubMed and ISI Web of Science. Most postmortem studies, including 30 brain regions, have determined no density or number of total Nissl-glial cell changes in suicidal patients with major psychiatric disorders. There were 17 astrocytic, 14 microglial, and 9 oligodendroglial studies using specific markers of each glial cell and further on their specific gene expression. Those studies suggest that astrocytic and oligodendroglial cells lost but activated microglia in suicides with affective disorder, bipolar disorders, major depression disorders, or schizophrenia in comparison with non-suicided patients and non-psychiatric controls. Although the data from previous studies remain complex and cannot fully explain the effects of glial cell dysfunction related to suicidal behaviors, they provide risk directions potentially leading to suicide prevention.
Topics: Humans; Neuroglia; Suicide; Brain; Biomarkers; Autopsy; Suicidal Ideation; Bipolar Disorder
PubMed: 38891940
DOI: 10.3390/ijms25115750 -
Frontiers in Immunology 2024Immunoregulation is a complex and critical process in the pathological process of spinal cord injury (SCI), which is regulated by various factors and plays an important...
OBJECTIVE
Immunoregulation is a complex and critical process in the pathological process of spinal cord injury (SCI), which is regulated by various factors and plays an important role in the functional repair of SCI. This study aimed to explore the research hotspots and trends of glial cell immunoregulation after SCI from a bibliometric perspective.
METHODS
Data on publications related to glial cell immunoregulation after SCI, published from 2004 to 2023, were obtained from the Web of Science Core Collection. Countries, institutions, authors, journals, and keywords in the topic were quantitatively analyzed using the R package "bibliometrix", VOSviewer, Citespace, and the Bibliometrics Online Analysis Platform.
RESULTS
A total of 613 papers were included, with an average annual growth rate of 9.39%. The papers came from 36 countries, with the United States having the highest output, initiating collaborations with 27 countries. Nantong University was the most influential institution. We identified 3,177 authors, of whom Schwartz, m, of the Weizmann Institute of Science, was ranked first regarding both field-specific H-index (18) and average number of citations per document (151.44). Glia ranked first among journals with 2,574 total citations. The keywords "microglia," "activation," "macrophages," "astrocytes," and "neuroinflammation" represented recent hot topics and are expected to remain a focus of future research.
CONCLUSION
These findings strongly suggest that the immunomodulatory effects of microglia, astrocytes, and glial cell interactions may be critical in promoting nerve regeneration and repair after SCI. Research on the immunoregulation of glial cells after SCI is emerging, and there should be greater cooperation and communication between countries and institutions to promote the development of this field and benefit more SCI patients.
Topics: Spinal Cord Injuries; Bibliometrics; Humans; Neuroglia; Animals; Astrocytes
PubMed: 38938572
DOI: 10.3389/fimmu.2024.1402349 -
Frontiers in Pharmacology 2024Intracerebral hemorrhage (ICH), a common subtype of hemorrhagic stroke, often causes severe disability or death. ICH induces adverse events that might lead to secondary...
Intracerebral hemorrhage (ICH), a common subtype of hemorrhagic stroke, often causes severe disability or death. ICH induces adverse events that might lead to secondary brain injury (SBI), and there is currently a lack of specific effective treatment strategies. To provide a new direction for SBI treatment post-ICH, the systematic review discussed how thrombin impacts secondary injury after ICH through several potentially deleterious or protective mechanisms. We included 39 studies and evaluated them using SYRCLE's ROB tool. Subsequently, we explored the potential molecular mechanisms of thrombin-mediated effects on SBI post-ICH in terms of inflammation, iron deposition, autophagy, and angiogenesis. Furthermore, we described the effects of thrombin in endothelial cells, astrocytes, pericytes, microglia, and neurons, as well as the harmful and beneficial effects of high and low thrombin concentrations on ICH. Finally, we concluded the current research status of thrombin therapy for ICH, which will provide a basis for the future clinical application of thrombin in the treatment of ICH.
PubMed: 38698822
DOI: 10.3389/fphar.2024.1293428