From microstructural design to surface engineering: A tailored approach for improving fatigue life of additively manufactured meta-biomaterials.

Recently, lattice titanium manufactured by additive manufacturing (AM) techniques has been utilized in various applications, including biomedical. The effects of topological design and processing parameters on the fatigue behaviour of such meta-biomaterials have been studied before. Most studies show that the fatigue life of additively manufactured lattice structures is limited. Post-processing techniques could play a major role in improving the fatigue of these promising biomaterials. This study aims to provide an in-depth investigation into the effects of heat treatments, hot isostatic pressing (HIP), sand blasting, and chemical etching on the microstructure, surface morphology, strength and fatigue resistance of selective laser melted titanium meta-biomaterials. It was found that the combination of microstructural design and surface engineering, induced by HIP and sand blasting respectively, allows to increase the endurance limit of these lattice meta-biomaterials by a factor of two. HIP treatment substantially decreased the internal porosity and transformed the microstructure to a more ductile mixture of α +â€¯ß phases. Sand blasting allowed to eliminate surface imperfections and induced favourable compressive stress in the surface layer of the struts. STATEMENT OF SIGNIFICANCE: Additively manufactured metallic meta-biomaterials are progressively being used as bone replacement orthopedic implants. While there is a great amount of research related to topological designs and their effect on mechanical (e.g. stiffness), physical (e.g. mass transport), and biological (e.g. osseointegration) properties, fatigue lifetime of such structures remains limited. This study provides fundamental investigation into the combined effect of microstructural design and surface engineering of titanium meta-biomaterial, enabled through various post treatment methods ranging from heat treatments to physical and chemical surface modifications. The findings show that fatigue life is significantly improved by applying developed herein novel method, which effortlessly can be used on other bone-mimicking metallic meta-biomaterials.

The role of proximal pulleys in preventing tendon bowstringing: pulley rupture and tendon bowstringing.

PURPOSE: The aim of this study was to investigate factors that contribute to tendon bowstringing at the proximal phalanx. We hypothesised that: (1) a partial rupture of the A2 pulley leads to significant bowstringing, (2) the location of the A2 rupture, starting proximally or distally, influences bowstringing, (3) an additional A3 pulley rupture causes a significant increase in bowstringing following a complete A2 pulley rupture and (4) the skin and tendon sheath may prevent bowstringing in A2 and A3 pulley ruptures. METHODS: Index, middle and ring fingers of eight freshly frozen cadaver arms were used. A loading device pulled with 100 N force was attached to the flexor digitorum profundus (FDP). The flexor digitorum superficialis (FDS) was preloaded with 5 N. Bowstringing was measured and quantified by the size of the area between the FDP tendon and the proximal phalanx over a distance of 5 mm with ultrasonography (US). RESULTS: US images showed that already a 30% excision of the A2 pulley resulted in significant bowstringing. In addition, a partial distal incision of the A2 pulley showed significantly more bowstringing compared to a partial proximal incision. Additional A3 pulley incision and excision of the proximal tendon sheath did not increase bowstringing. Subsequently, removing the skin did increase the bowstringing significantly. CONCLUSION: A partial A2 pulley rupture causes a significant bowstringing. A partial rupture of the A2 pulley at the distal rim of the A2 pulley resulted in more bowstringing than a partial rupture at the proximal rim.

Systematic review and meta-analysis of the association between diabetes mellitus and incidence and mortality in breast and colorectal cancer.

BACKGROUND: Increasing evidence suggests that diabetes mellitus (DM) is associated with increased cancer incidence and mortality. Several mechanisms involved in diabetes, such as promotion of cell proliferation and decreased apoptosis, may foster carcinogenesis. This study investigated the association between DM and cancer incidence and cancer-specific mortality in patients with breast and colorectal carcinoma. METHODS: A meta-analysis of controlled trials, prospective cohort studies and pooled cohort studies published after 2007 was conducted. Embase, PubMed and the Cochrane Library were searched. Summary hazard ratios (HRs) were calculated using a random-effects model. Sensitivity and subgroup analyses were performed to adjust for confounders, mode of DM assessment and follow-up time. RESULTS: Twenty studies were included to investigate the association between DM and breast and colorectal cancer incidence and cancer-specific mortality. The studies predominantly comprised patients with type II DM. The overall HR for breast cancer incidence was 1·23 (95 per cent confidence interval 1·12 to 1·34) and that for colorectal cancer was 1·26 (1·14 to 1·40) in patients with DM compared with those without diabetes. The overall HR was 1·38 (1·20 to 1·58) for breast cancer- and 1·30 (1·15 to 1·47) for colorectal cancer-specific mortality in patients with DM compared with those without diabetes. CONCLUSION: This meta-analysis indicated that DM is a risk factor for breast and colorectal cancer, and for cancer-specific mortality.

Gonadotropin and steroid receptors as prognostic factors in advanced ovarian cancer: a retrospective study

INTRODUCTION: Ovarian cancer is a chemosensitive tumour, but two thirds of women have a recurrence during the follow- up, even after an optimal surgical debulking followed by chemotherapy with a platinum and a taxane compound. Cytotoxic drugs are used in a second- or third-line setting but tumour progression is the rule. Also patients with the same histology achieve different outcomes in terms of survival. We decided to study gonadotropin and steroid receptors and to consider if these histological markers could select patients with different prognosis. MATERIALS AND METHODS: In our study we have measured by immunohistochemistry oestrogen, progestin and gonadotropin- releasing hormone receptors (Gn-RHRs) in paraffinembedded ovarian cancer tissue in a sample of 62 consecutive patients with advanced ovarian cancer treated with surgery and adjuvant chemotherapy. Descriptive methods, a survival analysis (Kaplan-Meier) and a Cox regression analysis were done. RESULTS: Oestrogen receptors (ERs) were positive in 65% of patients and the same positivity was obtained for progestin receptors (PRs), with 74% showing some positivity for Gn-RHR receptors. Maximal cytoreduction and ERs, but not gonadotropin receptors, were independently associated with overall survival, with better survival for oestrogennegative tumours. No association was established for progression- free survival. CONCLUSIONS: We can conclude that ER status in our series is an independent prognostic factor for ovarian cancer with better survival for oestrogen-negative receptor tumours. PRs could also have a prognostic role in association with ERs (AU)

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