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BACKGROUNDThe comprehensive data on psoriasis research are numerous and complex, making it difficult to retrieve and classify manually. The ability to quickly mine literature based on various fine topics using deep learning natural language processing technology to assess research topics and trends in the field of psoriasis disease will have a significant impact on doctors’ research and patients’ health educationMETHODA neural topic model is used to identify fine topics of psoriasis literature published in the PubMed database from 2000 to 2021. Dermatologists evaluate the algorithm-modeled topics, summarize the categories into the most effective topics, and perform linear trend model analysis. The accurate classified topics are presented on an interactive web page to identify research hotspots and trends.RESULTSAt the categorical level, after review by clinicians, 158 out of 160 generated topics were found effective and categorized into 8 groups: Therapeutic methods (34.34%), pathological mechanisms (23.46%), comorbidity (20.04%), Clinical manifestations and differential diagnosis (12.77%), experimental modalities and methods (3.22%), diagnostic tools (2.99%), epidemiology (1.75%), and meetings/guidelines (1.43%). A linear regression model had good accuracy (MSE=0.252602, SSE=42.1845) and strong correlation (R-Squared=0.898009). ANOVA results showed that categories significantly impacted the model (phttps://psknlr.github.io) facilitates quick retrieval of titles, journals, and abstracts in different categories, as well as browsing literature information under specific topics and accessing corresponding article pages for professional knowledge on psoriasis.CONCLUSIONSThe neural topic model and interactive web tool can effectively identify the research hotspots and trends in psoriasis literature, assisting clinicians and patients in retrieving and comparing pertinent topics and research accomplishments of various years.

Aims Calcitonin gene‐related peptide (CGRP) as a regulator of astrocyte activation may facilitate spinal nociceptive processing. Histone H3 lysine 9 acetylation (H3K9ac) is considered an important regulator of cytokine and chemokine gene expression after peripheral nerve injury. In this study, we explored the relationship between CGRP and H3K9ac in the activation of astrocytes, and elucidated the underlying mechanisms in the pathogenesis of chronic neuropathic pain. Methods Astroglial cells (C6) were treated with CGRP and differentially enrichments of H3K9ac on gene promoters were examined using ChIP‐seq. A chronic constriction injury (CCI) rat model was used to evaluate the role of CGRP on astrocyte activation and H3K9ac signaling in CCI‐induced neuropathic pain. Specific inhibitors were employed to delineate the involved signaling. Results Intrathecal injection of CGRP and CCI increased the number of astrocytes displaying H3K9ac in the spinal dorsal horn of rats. Treatment of CGRP was able to up‐regulate H3K9ac and glial fibrillary acidic protein (GFAP) expression in astroglial cells. ChIP‐seq data indicated that CGRP significantly altered H3K9ac enrichments on gene promoters in astroglial cells following CGRP treatment, including 151 gaining H3K9ac and 111 losing this mark, which mostly enriched in proliferation, autophagy, and macrophage chemotaxis processes. qRT‐PCR verified expressions of representative candidate genes (ATG12, ATG4C, CX3CR1, MMP28, MTMR14, HMOX1, RET) and RTCA verified astrocyte proliferation. Additionally, CGRP treatment increased the expression of H3K9ac, CX3CR1, and IL‐1β in the spinal dorsal horn. CGRP antagonist and HAT inhibitor attenuated mechanical and thermal hyperalgesia in CCI rats. Such analgesic effects were concurrently associated with the reduced levels of H3K9ac, CX3CR1, and IL‐1β in the spinal dorsal horn of CCI rats. Conclusion Our findings highly indicate that CGRP is associated with the development of neuropathic pain through astrocytes‐mediated neuroinflammatory responses via H3K9ac in spinal dorsa horn following nerve injury. This study found that CGRP act on their astrocytic receptors and lead to H3K9 acetylation (H3K9ac), which are mainly associated with proliferation‐, autophagy‐, and inflammation‐related gene expression. The number of astrocytes with H3K9ac expression is increased after nerve injury. Inhibition of CGRP attenuates the development of neuropathic pain, which was accompanied by the suppression of H3K9ac, CX3CR1, and IL‐1β expression in CCI rats., This study find that CGRP act on their astrocytic receptors and lead to H3K9 acetylation (H3K9ac), which are mainly associated with proliferation‐, autophagy‐ and inflammation‐related gene expression. The number of astrocytes with H3K9ac expression is increased after nerve injury. Inhibition of CGRP attenuates the development of neuropathic pain, which was accompanied by the suppression of H3K9ac, CX3CR1, IL‐1β expression in CCI rats.

The human gut harbors a dense and highly diverse microbiota of approximately 1,000 bacterial species. The interaction between the host and gut bacteria strongly influences human health. Numerous evidence suggest that intestinal flora imbalance is closely associated with the development and treatment of liver diseases, including acute liver injury and chronic liver diseases (cirrhosis, autoimmune liver disease, and fatty liver). Therefore, regulating the gut microbiota is expected to be a new method for the adjuvant treatment of liver diseases. Fecal microbiota transplantation (FMT) is defined as the transplantation of gut microbiota from healthy donors to sick patients via the upper or lower gastrointestinal route to restore the normal intestinal balance. In this study, we briefly review the current research on the gut microbiota and its link to liver diseases and then summarize the evidence to elucidate the clinical application and development of FMT in liver disease treatment.

Non-small-cell lung cancer (NSCLC) is one of the most common malignancies, and specific molecular targets are still lacking. Angiogenesis plays a central regulatory role in the growth and metastasis of malignant tumor. Angiogenic factors (AFs) are involved. Although there are many studies comparing AFs and cancer, a prognostic risk model for AFs and cancer in humans has not been reported in the literature. This study aimed to identify the key AFs closely related to the process of NSCLC development, and four genes have been found, C1QTNF6, SLC2A1, PTX3, FSTL3. Then we constructed a novel prognostic risk model based on these four genes in non-small-cell lung cancer (NSCLC) and fully analyzed the relationship with clinical features, immune infiltration, genomes and predictors. This model had good discrimination and calibration and will perform well for predicting the prognosis of treatment in clinical practice.

Additional file 1: Supplementary Table S1. Gene specific primer sequences used in the study.