The association between sport-related concussion and musculoskeletal injury in university rugby athletes

ObjectivesThe study aimed to analyse the association between Sports-Related Concussion (SRC) and Subsequent Musculoskeletal Injury (MSK) in United Kingdom university-aged rugby union players whilst considering the effects of sex, athlete playing position and injury location.DesignRetrospective cohort study. A period of 365 days with 0–90, 91–180 and 181–365 days sub-periods was analysed for the following variables; MSK injury incidence, occurrence, severity, injury location, playing position and sex.SettingInjury data was collected from the Sports Development Centre database at Loughborough University.ParticipantsA total of 408 injuries in 181 athletes (55 females and 126 males) were included.ResultsThe MSK injury incidence of SRC group was significantly higher than control and higher post-SRC than pre-SRC period over a 365-day period (p=0.012 and p=0.034, respectively). The odds ratios of MSK injury incidence between groups and between periods were 1.62 (95% CI, 1.10–2.25) and 1.57 (95% CI ,1.08–2.29). A SRC was not associated with a greater time loss from a subsequent MSK injury or a specific MSK injury location.ConclusionsAthletes with a second recorded injury were more likely to sustain a MSK injury if they had experienced SRC, however, there was no indication a SRC resulted in greater time loss from a MSK injury.     

Clinical Implications of HSC70 Expression in Clear Cell Renal Cell Carcinoma

Purpose: The role of heat shock protein 70 (HSC70) in the progression of clear cell renal cell carcinoma (ccRCC) is unclear. This study explored the effect of the HSC70 on the survival of ccRCC patients.Methods: Immunohistochemical analysis was performed to determine HSC70 expression in samples obtained from 121 ccRCC patients with at least 5 years of follow-up. We also analyzed the association between HSC70 expression and clinicopathological characteristics. Furthermore, the association of overall survival (OS) with HSC70 expression was analyzed using Kaplan-Meier curves. Finally, we used the Oncomine and CCLE databases to determine the effects of HSC70 mRNA expression on ccRCC.Results: HSC70 expression was associated with distant metastasis and death of ccRCC patients. HSC70 was expressed in the nucleus and/or cytoplasm of ccRCC cells. The incidence of distant organ metastasis and death was higher in patients with HSC70 expression than in those without it. Survival analysis revealed that patients with HSC70 expression had significantly shorter OS. Oncomine analyses also showed that the HSC70 mRNA was significantly upregulated in ccRCC tissues.Conclusions: HSC70 expression was related to adverse prognosis, and patients with HSC70 expression had a worse prognosis than those without HSC70 expression. HSC70 may thus serve as a potential therapeutic target for ccRCC.     

Fracture resistance and 2-body wear of 3-dimensional–printed occlusal devices

Statement of problem

Polymeric material for 3-dimensional printing can be used to fabricate occlusal devices. However, information about fracture resistance and wear is scarce.

Heat shock response in noise-induced hearing loss: effects of alanyl-glutamine dipeptide supplementation on heat shock proteins status

IntroductionThe 72 kDa heat shock protein, HSP72, located intracellularly provides cochlear cytoprotective and anti-inflammatory roles in the inner ear during stressful noise challenges. The expression of intracellular HSP72 (iHSP72) can be potentiated by alanyl-glutamine dipeptide supplementation. Conversely, these proteins act as pro-inflammatory signals in the extracellular milieu (eHSP72).ObjectiveWe explore whether noise-induced hearing loss promotes both intracellular and extracellular HSP72 heat shock response alterations, and if alanyl-glutamine dipeptide supplementation could modify heat shock response and prevent hearing loss.MethodsFemale 90 day-old Wistar rats (n = 32) were randomly divided into four groups: control, noise-induced hearing loss, treated with alanyl-glutamine dipeptide and noise-induced hearing loss plus alanyl-glutamine dipeptide. Auditory brainstem responses were evaluated before noise exposure (124 dB SPL for 2 h) and 14 days after. Cochlea, nuclear cochlear complex and plasma samples were collected for the measurement of intracellular HSP72 and extracellular HSP72 by a high-sensitivity ELISA kit.ResultsWe found an increase in both iHSP72 and eHSP72 levels in the noise-induced hearing loss group, which was alleviated by alanyl-glutamine dipeptide treatment. Furthermore, H-index of HSP72 (plasma/cochlea eHSP72/iHSP72 ratio) was increased in the noise-induced hearing loss group, but prevented by alanyl-glutamine dipeptide treatment, although alanyl-glutamine dipeptide had no effect on auditory threshold.ConclusionsOur data indicates that cochlear damage induced by noise exposure is accompanied by local and systemic heat shock response markers. Also, alanyl-glutamine reduced stress markers even though it had no effect on noise-induced hearing loss. Finally, plasma levels of 72 kDa heat shock proteins can be used as a biomarker of auditory stress after noise exposure.     

Immunohistochemical and molecular analysis of PI3K/AKT/mTOR pathway in esophageal carcinoma

Among the numerous signaling pathways involved in tumorigenesis, PI3K‐AKT‐mTOR is a key one that regulates diverse cellular functions. However, its prognostic value in esophageal carcinoma remains unclear. In our study, we examined the immunohistochemical expression of phosphorylated (p‐) AKT, mTOR, p70S6K and 4E‐BP1 along with the mutational status of PIK3CA and AKT1 genes by High Resolution Melting Analysis and Pyrosequencing in 44 esophageal carcinomas. The results were correlated with the clinicopathological characteristics of the patients in an effort to define their possible prognostic significance. Total p‐mTOR cytoplasmic expression, assessed in 10 random areas, was positively correlated with tumor stage (Kruskal–Wallis ANOVA, I/II vs III/IV, p = 0.0500). Μoreover, maximum p‐mTOR cytoplasmic immunoexpression, estimated in hot spot areas, was positively associated with tumor grade (Mann–Whitney U test, I/II vs III, p = 0.0565). Interestingly, p‐4E‐BP1 immunoreactivity was negatively correlated with tumor histological grade (Mann–Whitney U test, I/II vs III, p = 0.0427). No mutation was observed in exons 9 and 20 of PIK3CA gene and in exon 4 of AKT1 gene. In conclusion, our findings depict the presence of activated PI3K/AKT/mTOR pathway in esophageal cancer bringing forward p‐mTOR and p‐4E‐BP1 for their potential role in esophageal carcinogenesis. Additional studies are warranted to validate our findings.     

胶质瘤组织中miR-218的表达及其对血管生成的作用

目的 明确miR-218在胶质瘤组织中的表达，探讨其对胶质瘤血管生成的作用及机制。方法 采用荧光实时定量PCR法和免疫印迹法检测胶质瘤组织和细胞中miR-218、P70核糖体S6激酶1（p70s6k1）的表达情况，采用基质胶塞实验和小管形成实验分别在体内外检测miR-218对新血管生成的影响。结果 21例胶质瘤组织标本中miR-218表达较7例癌旁组织标本明显下调，且表达量与WHO分级有关。过表达miR-218能显著抑制血管生成。MiR-218直接靶向p70s6k1。过表达p70s6k1能部分逆转miR-218对血管新生的抑制作用。结论 MiR-218能通过靶向p70s6k1的表达调控胶质瘤血管生成，进而影响胶质瘤的进展。