Modified Broström repair with suture tape augmentation for lateral ankle instability: A systematic review

BackgroundThere is increasing interest in augmentation of modified Broström repairs for lateral ankle instability with a prosthetic reconstruction using suture tape internal bracing. The aim of this study was to investigate if suture tape augmentation resulted in improved clinical and radiological outcomes compared to a standard modified Broström repair alone.MethodsA systematic review following PRISMA guidelines was undertaken. All clinical studies published in Medline, Embase, Pubmed and the Cochrane Library Database from inception until January 2020 reporting on the use of suture tape augmentation to a modified Broström repair for lateral ankle instability.Results78 studies were identified of which 10 (assessing 333 patients) met the criteria for inclusion. Mean follow up was 24.8 months (range 6–52 months). All studies showed a statistically significant improvement across multiple clinical outcome measures post-surgery in both suture tape augmentation and modified Broström groups, however there were no statistically significant inter-group differences.Pooled results suggested there may be a reduction in recurrence of instability with suture tape augmentation when compared to modified Broström repair alone (p < 0.05). Overall quality of evidence was moderate to poor with limited data to support use of suture tape augmentation.ConclusionClinical and radiographic outcomes using a suture tape internal bracing for lateral ankle instability are excellent, and are equivalent to standard treatment across multiple clinical and radiographic assessment measures. There is minimal evidence to suggest functional outcomes are better, or recurrence rates are lower than modified Broström repair alone.PROSPERO REGISTRYCRD42020169876.Level of evidenceII.     

Pulsion severity showed a good correlation with cognitive function in Parkinson’s disease

Abstract

Objectives:

To examine the correlation between cognitive impairment and postural instability in Parkinson’s disease (PD) patients by using posturography.

Methods:

We investigated 88 PD patients comparing clinical scorings of cognitive functions and pulsion severity, and quantitative measurement of postural instability by posturography with the length of the center of gravity (LNG) and envelope area (ENV).

Results:

The number of patients with severe pulsion increased in PD with disease progression assessed by Hoehn and Yahr (H & Y) scale regardless of age, and a significant correlation was observed between the pulsion severity and both LNG (R = 0·4242) and ENV (R = 0·4335). Both LNG and ENV showed a good correlation with all cognitive assessments such as mini-mental state examination (MMSE), Montreal cognitive assessment (MoCA), and frontal assessment battery (FAB), suggesting that cognitive impairment became worse with the longer LNG and the larger ENV. Among the cognitive assessments, MoCA showed the highest correlation (R = 0·56–0·62) with both LNG and ENV, reflecting that MoCA is the most sensitive and reliable screening for dementia in PD.

Discussion:

The present study showed that posturography is useful to quantify the pulsion severity in PD patients, that pulsion severity and cognitive function showed a good correlation especially assessed by MoCA, and that posturography thus provides a more detailed quantitative correlation of postural instability to cognitive impairment.     

The role of dynamin-related protein 1 in cancer growth: a promising therapeutic target?

Mitochondrial functions are altered in many human diseases including cancer. Development of mitochondria-targeted therapies, either through restoring normal mitochondrial function or promoting mitochondrial-induced cell death, is one of the attractive strategies to improve the outcome of cancer treatment. Recent advances have revealed the important functional involvement of mitochondrial dynamics in cancer biology. Dynamin-related protein 1 (Drp1), a member of the dynamin family of GTPases required for mitochondrial fission, has been found upregulated in certain types of cancers, such as lung and breast cancers. In addition, the roles of Drp1 in cell cycle progression, genome instability, cell migration and apoptosis in cancer cells have also been recently uncovered. These findings raise the possibility of targeting Drp1-mediated mitochondrial fission as an effective therapy for treating cancer. This article explores the function of Drp1 in cancer cells and discusses the theoretical basis for the development of potential targeted therapy.     

Deregulated expression of DNA polymerase β is involved in the progression of genomic instability

Deregulated expression of DNA polymerase beta (pol β) has been implicated in genomic instability that leads to tumorigenesis, yet the mechanisms underlying the pol β‐mediated genetic instability remain elusive. In this study, we investigated the roles of deregulated expression of pol β in spontaneous and xenobiotic‐induced genetic instability using mouse embryonic fibroblasts (MEFs) that express distinct pol β levels (wild‐type, null, and overexpression) as a model system. Three genetic instability endpoints, DNA strand breaks, chromosome breakage, and gene mutation, were examined under various expression levels of pol β by comet assay, micronuclei test, and hprt mutation assay. Our results demonstrate that neither pol β deficiency nor pol β overexpression is sufficient for accumulation of spontaneous DNA damage that promotes a hyperproliferation phenotype. However, pol β null cells exhibit increased sensitivity to exogenous DNA damaging agents with increased genomic instability compared with pol β wild‐type and overexpression cells. This finding suggests that a pol β deficiency may underlie genomic instability induced by exogenous DNA damaging agents. Interestingly, pol β overexpression cells exhibit less chromosomal or DNA damage, but display a higher hprt mutation frequency upon methyl methanesulfonate exposure compared with the other two cell types. Our results therefore indicate that an excessive amount of pol β may promote genomic instability, presumably through an error‐prone repair response, although it enhances overall BER capacity for induced DNA damage. Environ. Mol. Mutagen. 2012. © 2012Wiley Periodicals, Inc.