ABSTRACT Introduction: With the extensive and in-depth development of Taekwondo in China, more and more people participate in Taekwondo training. Due to the lack of experience of some coaches and the misunderstanding of scientific sports training by young athletes, injuries occur from time to time. This has a bad effect on Taekwond itself, and it can also damage the health of athletes. Objective: This article discusses joint injuries in Taekwondo and analyzes the characteristics of Taekwondo sports injuries and preventive methods. Methods: This article uses a questionnaire applied to young athletes to gain an understanding of the sports injuries situation. Results: The most common injury sites were feet and joints. The nature of the injuries is mostly soft tissue injury, ligament laceration, and muscle strain. The most serious injuries are kidney and perineal damage. Conclusion: Improving the level of training, strengthening medical supervision, and paying attention to the timely treatment of acute injuries are important ways to reduce the occurrence of trauma. Level of evidence II; Therapeutic studies - investigation of treatment results.
<sec> <title>Objective:</title> The purpose of this research is to explore the influences of thymosin β4 (Tβ4) in deepsecond-degree scald wound healing of rat skin and its relationship with Wnt/β-catenin pathway. </sec>
<sec> <title>Methods:</title> Deep second-degree scalded model rats were prepared and divided into normal saline (NS) treatment group, Tβ4 treatment group and FH535 inhibitor group. Then, the concentrations of inflammatory factors in the rats were monitored
via adopting the correlated TNF-α and IL-1β ELISA kits. In the meantime, the wound healing rate was analyzed via photography. Subsequently, the qRTPCR procedure was wielded to determine Wnt1 and β-catenin expression in wound tissues, and the degree of wound
tissue injury was examined via hematoxylin and eosin (HE) staining. Finally, Western blotting (WB) was adopted to assess Wnt/β-catenin pathway-associated protein levels. </sec> <sec> <title>Results:</title> Releasing amount of TNF-α
and IL-1β were conspicuously up-regulated after scalding (p <0.01), and Wnt1 and β-catenin expression at molecular transcription level was also significantly raised (p < 0.01). Besides, treatment with 18 μg of Tβ4 significantly
increased the wound healing rate of scalded rats (p < 0.01). In addition, Tβ4 treatment significantly promoted wound healing (p < 0.01) and increased the Wnt1 and β-catenin expression levels (p < 0.01). Moreover, FH535 significantly restrained
the Wnt/β-catenin pathway-correlated protein levels (p < 0.01) and wound healing. </sec> <sec> <title>Conclusion:</title> Tβ4 can promote scald wound healing in rats and may play a role via evoking Wnt/β-catenin
pathway activation. </sec>
Mesenchymal stem cells (MSCs) are indicated to severe pancreatitis (SAP), whilst level of Shh/GLi axis varies in severe acute pancreatitis (SAP). However, little is known the interaction between MSCs and Shh in SAP. In this study, we established animal model of SAP in 10 rats and transplanted
MSCs into 10 rats, with another 10 sham-operated rats as control group. The pathological changes of rat pancreatic tissue were observed. ELISA was conducted to determine the MPO level of pancreatic inflammation, and Western blot to detect the expression level of Shh, Gli1 and Gli2 in tissues.
Administration of MSCs remarkably alleviated the pancreatic tissue necrosis and inflammation and decreased blood loss in SAP rats. Up-regulated expression of Shh, Gli1 and Gli2 was observed in SAP tissues when compared to tissues in control group, but their expressions declined in the presence
of MSCs, and 24 hour later returned to normal levels. Collectively, MSCs regulates the balance of Shh/GLi axis by decreasing Shh and Gli1, thereby attenuating progression and symptoms of SAP.
High mobility group box 1 (HMGB1) protein is a damage-associated molecular pattern (DAMP) molecule that plays an important role in the repair and regeneration of tissue injury. It also acts as a pro-inflammatory cytokine through the activation of toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), to elicit the neuroinflammatory response. HMGB1 may aggravate several cellular responses which may lead to pathological inflammation and cellular death. Thus, there have been a considerable amount of research into the pathological role of HMGB1 in diseases. However, whether the mechanism of action of HMGB1 is similar in all neurodegenerative disease pathology remains to be determined.
Therefore, this systematic review aimed to critically evaluate and elucidate the role of HMGB1 in the pathology of neurodegeneration based on the available literature.
A comprehensive literature search was performed on four databases; EMBASE, PubMed, Scopus, and CINAHL Plus.
A total of 85 articles were selected for critical appraisal, after subjecting to the inclusion and exclusion criteria in this study. The selected articles revealed that HMGB1 levels were found elevated in most neurodegeneration except in Huntington’s disease and Spinocerebellar ataxia, where the levels were found decreased. This review also showcased that HMGB1 may act on distinctive pathways to elicit its pathological response leading to the various neurodegeneration processes/diseases.
While there have been promising findings in HMGB1 intervention research, further studies may still be required before any HMGB1 intervention may be recommended as a therapeutic target for neurodegenerative diseases.
Inflammation and fibrosis are two inter‐related disease pathologies with several overlapping components. Three specific cell types, macrophages, T helper cells and myofibroblasts, each play important roles in regulating both processes. Following tissue injury, an inflammatory stimulus is often necessary to initiate tissue repair, where cytokines released from infiltrating and resident immune and inflammatory cells stimulate the proliferation and activation of extracellular matrix-producing myofibroblasts. However, persistent tissue injury drives an inappropriate pro‐fibrotic response. Additionally, activated myofibroblasts can take on the role of traditional antigen-presenting cells, secrete pro‐inflammatory cytokines, and recruit inflammatory cells to fibrotic foci, amplifying the fibrotic response in a vicious cycle. Moreover, inflammatory cells have been shown to play contradictory roles in the initiation, amplification and resolution of fibrotic disease processes. The central role of the inflammasome molecular platform in contributing to fibrosis is only beginning to be fully appreciated. In this review, we discuss the immune mechanisms that can lead to fibrosis, the inflammasomes that have been implicated in the fibrotic process in the context of the immune response to injury, and also discuss current and emerging therapies that target inflammasome-induced collagen deposition to treat organ fibrosis.
BackgroundHepatic ischemia and reperfusion (I/R) injury is commonly associated with surgical liver resection or transplantation, and represents a major cause of liver damage and graft failure. Currently, there are no effective therapies to prevent hepatic I/R injury other than ischemic preconditioning and some preventative strategies. Previously, we have revealed the anti-inflammatory activity of a sweat gland-derived peptide, dermcidin (DCD), in macrophage/monocyte cultures. Here, we sought to explore its therapeutic potential and protective mechanisms in a murine model of hepatic I/R.MethodsMale C57BL/6 mice were subjected to hepatic ischemia by clamping the hepatic artery and portal vein for 60 min, which was then removed to initiate reperfusion. At the beginning of reperfusion, 0.2 ml saline control or solution of DCD (0.5 mg/kg BW) or DCD-C34S analog (0.25 or 0.5 mg/kg BW) containing a Cys (C)→Ser (S) substitution at residue 34 was injected via the internal jugular vein. For survival experiments, mice were subjected to additional resection to remove non-ischemic liver lobes, and animal survival was monitored for 10 days. For mechanistic studies, blood and tissue samples were collected at 24 h after the onset of reperfusion, and subjected to measurements of various markers of inflammation and tissue injury by real-time RT-PCR, immunoassays, and histological analysis.ResultsRecombinant DCD or DCD-C34S analog conferred a significant protection against lethal hepatic I/R when given intravenously at the beginning of reperfusion. This protection was associated with a significant reduction in hepatic injury, neutrophilic CXC chemokine (Mip-2) expression, neutrophil infiltration, and associated inflammation. Furthermore, the administration of DCD also resulted in a significant attenuation of remote lung inflammatory injury. Mechanistically, DCD interacted with epidermal growth factor receptor (EGFR), a key regulator of liver inflammation, and significantly inhibited hepatic I/R-induced phosphorylation of EGFR as well as a downstream signaling molecule, protein kinase B (AKT). The suppression of EGFR expression by transducing Egfr-specific shRNA plasmid into macrophages abrogated the DCD-mediated inhibition of nitric oxide (NO) production induced by a damage-associated molecular pattern (DAMP), cold-inducible RNA-binding protein, CIRP.ConclusionsThe present study suggests that human DCD and its analog may be developed as novel therapeutics to attenuate hepatic I/R-induced inflammatory injury possibly by impairing EGFR signaling.
Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.
While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a comprehensive understanding of the nociceptive mechanism leading to tissue injury-associated persistent pain. Epigenetic events leading the altered transcription in the nervous system are pivotal in the maintenance of pain in tissue injury. However, the mechanisms through which those events contribute to the persistence of pain are not fully understood. This review provides a summary and critical evaluation of two epigenetic mechanisms, DNA methylation and non-coding RNA expression, on transcriptional modulation in nociceptive pathways during the development of tissue injury-associated pain. We assess the pre-clinical data and their translational implication and evaluate the potential of controlling DNA methylation and non-coding RNA expression as novel analgesic approaches and/or biomarkers of persistent pain.
<b>Objective: </b>Type 2
diabetes (T2D) is a leading cause of end stage kidney disease
(ESKD) worldwide. Recent studies suggest a more aggressive clinical course of
diabetic kidney disease (DKD) in youth-onset than adult-onset T2D. We compared kidney
structural lesions in youth- and adult-onset T2D to determine if youth-onset
was associated with greater early tissue injury.<b></b>
<p><b>Methods: </b>Quantitative microscopy
was performed on kidney tissue obtained from research kidney biopsies in 161
Pima Indians (117 women, 44 men) with T2D. Onset of T2D was established by
serial oral glucose tolerance testing and participants were stratified as
youth-onset (<25 years) or adult-onset (≥25 years). Associations between clinical
and morphometric parameters and age of onset were tested using linear models.<b></b></p>
<p><b>Results: </b>At biopsy, the 52 participants
with youth-onset T2D were younger than the 109 with adult-onset T2D (39.1±9.9 <i>vs.</i>
51.4±10.2 years, <i>p</i><0.0001), but their diabetes duration was similar
(19.3±8.1 <i>vs.</i> 17.0±7.8 years, <i>p</i>=0.09). Median urine
albumin-to-creatinine ratio was higher in the youth-onset group (58 [25<sup>th</sup>-75<sup>th</sup>
<i>vs.</i> 27 [13-73] mg/g, <i>p</i>=0.02). Youth-onset participants
had greater glomerular basement membrane (GBM) width (552±128 nm <i>vs.</i> 490±114nm,
<i>p</i>=0.002) and mesangial fractional volume (0.31±0.10 <i>vs</i>. 0.27±0.08,
<i>p</i>=0.001) than adult-onset participants. Percentage glomerular sclerosis,
glomerular volume, mesangial fractional volume, and GBM width were also inversely
associated with age of diabetes onset as a continuous variable.<b></b></p>
<p><b>Conclusion: </b>Younger age
of T2D onset strongly associates with more severe kidney structural
lesions. Studies are underway to elucidate
the pathways underlying these associations.</p>