Peripheral nerve injuries and diseases often lead to pain persisting beyond the resolution of damage, indicating an active disease-promoting process, which may result in chronic pain. This is regarded as a maladaptive mechanism resulting from neuroinflammation that originally serves to promote regeneration and healing. Knowledge on these physiological and pathophysiological processes has accumulated over the last few decades and has started to yield potential therapeutic targets. Key players are macrophages, T-lymphocytes, cytokines, and chemokines. In the spinal cord and brain, microglia and astrocytes are involved. Recently, data have been emerging on the regulation of these players. MicroRNAs and other noncoding RNAs have been discussed as potential master switches that may link nerve injury, pain, and inflammation. Clinical disorders most intensely studied in the context of neuroinflammation and pain are the complex regional pain syndrome, polyneuropathies, postherpetic neuralgia, and the fibromyalgia syndrome, in which recently a neuropathic component has been described. Research from several groups has shown an important role of both proinflammatory and anti-inflammatory cytokines in neuropathic and other chronic pain states in humans. There is ample evidence of an analgesic action of anti-inflammatory cytokines in animal models. The interplay of anti-inflammatory cytokines and the nociceptive system provides possibilities and challenges concerning treatment strategies based on this concept.

Inflammation in the pathophysiology of neuropathic pain.

New insights into the interplay between miRNAs and autophagy in the aging of intervertebral discs.

The aim of the present study was to investigate whether miRNA‑146a regulated the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis. miR‑146a expression was increased in human cervical cancer. Both overall survival (OS) and disease‑free survival (DFS) of low miR‑146a expression were higher than those of high miR‑146a expression. Additionally, IL‑17a expression was lower in patients with high miR‑146a expression compared to that of patients with lower miR‑146a expression. In a co‑culture of cervical cancer and CD4+ T cells, downregulation of miR‑146a inhibited cell growth and induced apoptosis of cervical cancer cells, while overexpression of miR‑146a promoted cell growth and reduced apoptosis of cervical cancer cells. Downregulation of miR‑146a induced TRAF6 and NF‑κB protein expression, increased IL‑6, IL‑17A and IL‑21 levels, and enhanced p‑STAT3 protein expression. The inhibition of TRAF6 attenuated the effects of anti‑miR‑146a on the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis. Collectively, miR‑146a regulated the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF‑κB signaling by targeting TRAF6. miR‑146a may function as an oncogene in cervical cancer via Th17 cell differentiation by targeting TRAF6.

/pdf/mir-146a-regulates-the-function-of-th17-cell-differentiation-4wivxu4x0l.pdf

miR‑146a regulates the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF‑κB signaling by targeting TRAF6

Autophagy is a homeostatic process designed to eliminate dysfunctional and aging organelles and misfolded proteins through a well-concerted pathway, starting with forming a double-membrane vesicle and culminating in the lysosomal degradation of the cargo enclosed inside the mature vesicle. As a vital sentry of cellular health, autophagy is regulated in every human disease condition and is an essential target for non-coding RNAs like microRNAs (miRNAs). miRNAs are short oligonucleotides that specifically bind to the 3'-untranslated region (UTR) of target mRNAs, thus leading to mRNA silencing, degradation, or translation blockage. This review summarizes the recent findings regarding the regulation of autophagy and autophagy-related genes by different miRNAs in various pathological conditions, including cancer, kidney and liver disorders, neurodegeneration, cardiovascular disorders, infectious diseases, aging-related conditions, and inflammation-related diseases. As miRNAs are being identified as prime regulators of autophagy in human disease, pharmacological molecules and traditional medicines targeting these miRNAs are also being tested in disease models, thus initiating a new series of therapeutic interventions targeting autophagy.

/pdf/regulation-of-autophagy-by-mirnas-in-human-diseases-wijiitjcvh.pdf

Regulation of autophagy by miRNAs in human diseases

Objectives The aim of our study was to ascertain the underlying role of microRNAs (miRNAs) in human intervertebral disc degeneration (IDD). Design Bioinformatic analysis from multiple databases. Methods Studies of the association of miRNAs and IDD were identified in multiple electronic databases. All potential studies were assessed by the same inclusion and exclusion criteria. We recorded whether miRNA expression was commonly increased or suppressed in the intervertebral disc tissues and cells of IDD subjects. We used String to identify biological process and cellular component pathways of differentially expressed genes. Results We included fifty-seven articles from 1,277 records in this study. This report identified 40 different dysregulated miRNAs in 53 studies, including studies examining cell apoptosis (26 studies, 49.06%), cell proliferation (15 studies, 28.3%), extracellular matrix (ECM) degradation (10 studies, 18.86%), and inflammation (five studies, 9.43%) in IDD patients. Three upregulated miRNAs (miR-19b, miR-32, miR-130b) and three downregulated miRNAs (miR-31, miR-124a, miR-127-5p) were considered common miRNAs in IDD tissues. The top three biological process pathways for upregulated miRNAs were positive regulation of biological process, nervous system development, and negative regulation of biological process, and the top three biological process pathways for downregulated miRNAs were negative regulation of gene expression, intracellular signal transduction, and negative regulation of biological process. Conclusions This study revealed that miRNAs could be novel targets for preventing IDD and treating patients with IDD by regulating their target genes. These results provide valuable information for medical professionals, IDD patients, and health care policy makers.

A Bioinformatic Analysis of MicroRNAs' Role in Human Intervertebral Disc Degeneration.

This study investigated the mechanism of microRNA-21 in regulating IL-6 inflammatory response and cell autophagy in intervertebral disc degeneration. A total of 10 patients with lumbar disc herniation accompanied by nerve root pain (observation group) and 10 patients with lumbar burst fractures (control group) were selected. The nucleus pulposus tissues of the lesion were obtained during operation for cell culture. Real-time quantitative polymerase chain reaction (PCR) was used to detect the expression of microRNA-21. The ELISA method was used to detect the levels of IL-6, and type II collagen (Col II). Aggrecan and western blotting was used to detect autophagy-related gene 7 (ATG7) and microtubule-associated protein 1 light chain 3 (LC3)-II/-I. As a result, the levels of microRNA-21 and IL-6 in the observation group were significantly higher than those in the control group, but the levels of Col II and aggrecan were significantly lower than those in the control group. The differences were statistically significant (P<0.05). The levels of ATG7 and LC3-II/-I in the observation group were significantly decreased (P<0.05). In conclusion, the expression of microRNA-21 is abnormally high in the nerve root pain of the lumbar intervertebral disc, which can increase the IL-6 inflammatory response and reduce the capacity of cell autophagy.

/pdf/mechanism-of-microrna-21-regulating-il-6-inflammatory-5g5czahmev.pdf

Mechanism of microRNA-21 regulating IL-6 inflammatory response and cell autophagy in intervertebral disc degeneration.

The aim of the study was to investigate the mechanism of microRNA (miR)-146a-mediated activation of interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3) in lumbar intervertebral disc degeneration. To obtain intervertebral tissue, we recruited 5 patients with lumbar intervertebral disc herniation (experimental group) and 5 patients with lumbar burst fracture (control group). Nucleus pulposus tissue was extracted by surgery and cultured. miR-146a empty vector, mimic, and inhibitor were transfected into the two groups of cells for 24 h and the levels of IL-6, type II collagen (Col II), aggrecan, STAT3, matrix metalloproteinase (MMP)-3, and a disintegrin and metalloproteinase with thrombospondin type I motifs (ADAMTS) were detected. We found no differences in the levels of IL-6, Col II, aggrecan, STAT3, MMP-3, and ADAMTS before and after treatment in the control group. However, the levels of miR-146a, IL-6, STAT3, MMP-3, and ADAMTS were significantly elevated, whereas Col II and aggrecan levels were lower in the experimental group before treatment. The levels of IL-6, STAT3, MMP-3, and ADAMTS were elevated after treatment with miR-146a mimic when compared with the miR-146a empty vector in the experimental group, and Col II and aggrecan levels were decreased. However, the cells treated with miR-146a inhibitor had the opposite result. Thus, the IL-6/STAT3 signaling pathway can be mediated by a high expression of miR-146a to regulate the occurrence of lumbar intervertebral disc degeneration.

/pdf/mechanism-of-microrna-146a-mediated-il-6-stat3-signaling-in-3uugrh71yh.pdf

Mechanism of microRNA-146a-mediated IL-6/STAT3 signaling in lumbar intervertebral disc degeneration.

We compared the biomechanics between improved percutaneous vertebroplasty (improved PVP) and traditional percutaneous kyphoplasty (PKP) in the treatment of vertebral peripheral wall damage-type osteoporotic vertebral compression fracture (OVCF) A total of 15 vertebral peripheral wall damage-type OVCF models of new calves (12-14 weeks) were treated with a decalcifying agent (Shandon TBD-1) with the vertebral compression fracture The vertebral volume and anterior height before modeling, and the vertebral BMD before and after modeling were measured The models were randomly divided into three groups: the improved PVP group (Group A), the traditional PKP group (Group B) and the control group (Group C) BMD of Groups A, B and C after decalcification was significantly lower than that before decalcification (P 005) There was no significant difference in the initial strength and stiffness among the three groups (P>005) The postoperative strength of Groups A and B was 1036±300 and 1045±200 N, respectively, which was significantly higher than the initial strength (P 005) In the comparison of postoperative strength and stiffness between Groups A and B, the postoperative strength in Group A was lower than that in Group B; differences were not statistically significant (P>005); there was no significant difference in the postoperative stiffness between Groups A and B (P>005) There were no significant differences of injection of bone cement between the two groups (P>005) Therefore, an improved PVP can basically realize the curative effects of traditional PKP in the treatment of vertebral peripheral wall damage-type OVCF, which can be used as clinical reference

/pdf/comparative-study-on-the-biomechanics-between-improved-pvp-2yzt8x1o5a.pdf

Comparative study on the biomechanics between improved PVP and traditional PKP in the treatment of vertebral peripheral wall damage-type OVCF

Background: The role of vascular endothelial growth factor (VEGF) rs3025039 polymorphism on osteosarcoma risk was not fully clear. Thus, we did a case-control study to evaluate the association between VEGF rs3025039 polymorphism and osteosarcoma risk.
Method: This study included 242 patients with osteosarcoma and 253 controls. The genotyping was conducted using the matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF MS).
Results: The VEGF rs3025039 TT genotype was significant higher in the osteosarcoma group than in the control group (OR=2.42, 95%CI 1.00-5.85, P=0.04). The TT genotype and CT genotype was also significantky associated with osteosarcoma risk (OR=1.43, 95%CI 1.00-2.05, P=0.04). Under the allelic model, T allele of rs3025039 was significantly associated with higher osteosarcoma risk (OR=1.41, 95%CI 1.05-1.90, P=0.02). In addition, VEGF rs3025039 TT genotype was not associated with tumor location (OR=1.02, 95%CI 0.59-1.77, P=0.94) and metastasis (OR=1.76, 95%CI 0.90-3.43, P=0.10).
Conclusion: In conclusion, this study confirmed that VEGF rs3025039 polymorphism was significantly associated with higher risk of osteosarcoma.

https://www.alliedacademies.org/articles/vascular-endothelial-growth-factor-vegf-rs3025039-polymorphism-is-associated-with-increased-risk-of-osteosarcoma.pdf

Vascular endothelial growth factor (VEGF) rs3025039 polymorphism is associated with increased risk of osteosarcoma

The utility model discloses a guide type bone cement propeller and a combination thereof, and belongs to the field of medical instruments. The guide type bone cement propeller comprises a sleeve and apush rod which are matched with each other, a guide inclined opening is formed in the inner end of the sleeve, and the included angle between the inclined section of the guide inclined opening and the axis of the sleeve ranges from 35 degrees to 65 degrees. A clamping handle is arranged at the outer end of the sleeve and extends outwards to form a clamping head; a push handle is arranged at the outer end of the push rod, and a clamping sleeve extending out of the push handle is matched with the clamping head. The end part of the sleeve of the bone cement propeller is provided with the inclined opening, so that the injection direction of bone cement can be controlled to a certain extent, and the bone cement propeller has a better use effect.

Guide type bone cement propeller and combination thereof

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Hao Lin

Author Tools

Chat about Author