Functional results following surgical repair of post-traumatic hand tendon injuries

Introduction: The study aims to determine whether early physical therapy following hand tendon repair gives better results and to look at any possible limiting factors locally. Methods: Twenty adults were selected from those admitted to Mater Dei Hospital, with traumatic tendon injuries to the wrist and hand during the year 2014. Their medical records were reviewed and details on surgical repair and postoperative rehabilitation noted. Participants completed QuickDASH outcome measure questionnaires assessing their situation both on initial presentation to hand therapy and six months later. The range of motion in all joints of the injured digits, six months after commencement of therapy, was measured by manual hand goniometry and the Total Active Motion (TAM) score calculated. Results: A negative correlation was found between delay in starting hand therapy and both TAM score (r=-0.650, N=20, p<0.001) and QuickDASH score (r=-0.650, N=20, p<0.002). Comparison of the two outcome measures resulted in a strong negative correlation (r=-0.831, N=20, p<0.0005). Conclusion: These findings support current literature confirming that a shorter delay in starting hand therapy following tendon repair is associated with a better outcome for the patient. Better documentation and interdisciplinary handover is required, and a new operation report template is being put forward.peer-reviewe

The Libyan civil conflict : selected case series of orthopaedic trauma managed in Malta in 2014

Aim: The purpose of this series of cases was to analyse our management of orthopaedic trauma casualties in the Libyan civil war crisis in the European summer of 2014. We looked at both damage control orthopaedics and for case variety of war trauma at a civilian hospital. Due to our geographical proximity to Libya, Malta was the closest European tertiary referral centre. Having only one Level 1 trauma care hospital in our country, our Trauma and Orthopaedics department played a pivotal role in the management of Libyan battlefield injuries. Our aims were to assess acute outcomes and short term mortality of surgery within the perspective of a damage control orthopaedic strategy whereby aggressive wound management, early fixation using relative stability principles, antibiotic cover with adequate soft tissue cover are paramount. We also aim to describe the variety of war injuries we came across, with a goal for future improvement in regards to service providing.Methods: Prospective collection of six interesting cases with severe limb and spinal injuries sustained in Libya during the Libyan civil war between June and November 2014.Conclusions: We applied current trends in the treatment of war injuries, specifically in damage control orthopaedic strategy and converting to definitive treatment where permissible. The majority of our cases were classified as most severe (Type IIIB/C) according to the Gustilo-Anderson classification of open fractures. The injuries treated reflected the type of standard and improved weaponry available in modern warfare affecting both militants and civilians alike with increasing severity and extent of damage. Due to this fact, multidisciplinary team approach to patient centred care was utilised with an ultimate aim of swift recovery and early mobilisation. It also highlighted the difficulties and complex issues required on a hospital management level as a neighbouring country to war zone countries in transforming care of civil trauma to military trauma.peer-reviewe

Identification of 19 new risk loci and potential regulatory mechanisms influencing susceptibility to testicular germ cell tumor

Genome-wide association studies (GWAS) have transformed understanding of susceptibility to testicular germ cell tumors (TGCTs), but much of the heritability remains unexplained. Here we report a new GWAS, a meta-analysis with previous GWAS and a replication series, totaling 7,319 TGCT cases and 23,082 controls. We identify 19 new TGCT risk loci, roughly doubling the number of known TGCT risk loci to 44. By performing in situ Hi-C in TGCT cells, we provide evidence for a network of physical interactions among all 44 TGCT risk SNPs and candidate causal genes. Our findings implicate widespread disruption of developmental transcriptional regulators as a basis of TGCT susceptibility, consistent with failed primordial germ cell differentiation as an initiating step in oncogenesis. Defective microtubule assembly and dysregulation of KIT-MAPK signaling also feature as recurrently disrupted pathways. Our findings support a polygenic model of risk and provide insight into the biological basis of TGCT.We acknowledge National Health Service funding to the National Institute for Health Research Biomedical Research Centre. Genotyping of the OncoArray was funded by the US National Institutes of Health (NIH) (U19 CA 148537 for Elucidating Loci Involved in Prostate cancer Susceptibility (ELLIPSE) project and X01HG007492 to the Center for Inherited Disease Research (CIDR) under contract number HHSN268201200008I). Additional analytical support was provided by NIH NCI U01 CA188392. The PRACTICAL consortium was supported by Cancer Research UK Grants C5047/A7357, C1287/A10118, C1287/A16563, C5047/A3354, C5047/A10692 and C16913/A6135; the European Commission’s Seventh Framework Programme grant agreement 223175 (HEALTH-F2-2009-223175) (D.F.E., R.E. and Z.K.-J.); and the NIH Cancer Post-Cancer GWAS initiative grant 1 U19 CA 148537-01 (the GAME-ON initiative). We thank the following for funding support: the Institute of Cancer Research and the Everyman Campaign, the Prostate Cancer Research Foundation, Prostate Research Campaign UK (now Prostate Action), the Orchid Cancer Appeal, the National Cancer Research Network UK and the National Cancer Research Institute (NCRI) UK. We are grateful for NIHR funding to the Biomedical Research Centre at the Institute of Cancer Research and the Royal Marsden NHS Foundation Trust. We acknowledge funding from the Swedish Cancer Society (CAN2011/484 and CAN2012/823), the Norwegian Cancer Society (grants 418975-71081-PR-2006-0387 and PK01-2007- 0375) and the Nordic Cancer Union (grant S-12/07). This study was supported by the Movember Foundation and the Institute of Cancer Research. K.L. is supported by a PhD fellowship from Cancer Research UK. R.S.H. and P.B. are supported by Cancer Research UK (C1298/A8362 Bobby Moore Fund for Cancer Research UK)