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OBJECTIVES: High energy long bone fractures with critical bone loss are at risk for nonunion without strategic intervention. We hypothesize that a synthetic membrane implanted at a single stage improves bone healing in a preclinical nonunion model. METHODS: Using standard laboratory techniques, microspheres encapsulating bone morphogenic protein-2 (BMP2) or platelet derived growth factor (PDGF) were designed and coupled to a type 1 collagen sheet. Critical femoral defects were created in rats and stabilized by locked retrograde intramedullary nailing. The negative control group had an empty defect. The induced membrane group (positive control) had a polymethylmethacrylate spacer inserted into the defect for four weeks and replaced with a bare polycaprolactone/beta-tricalcium phosphate (PCL/β-TCP) scaffold at a second stage. For the experimental groups, a bioactive synthetic membrane embedded with BMP2, PDGF or both enveloped a PCL/β-TCP scaffold was implanted in a single stage. Serial radiographs were taken at 1, 4, 8, and 12 weeks postoperatively from the definitive procedure and evaluated by two blinded observers using a previously described scoring system to judge union as primary outcome. RESULTS: All experimental groups demonstrated better union than the negative control (p=0.01). The groups with BMP2 incorporated into the membrane demonstrated higher average union Mehta scores than the other groups (p=0.01). The induced membrane group performed similarly to the PDGF group. Complete union was only demonstrated in groups with BMP2-eluting membranes. CONCLUSIONS: A synthetic membrane comprised of type 1 collagen embedded with controlled release BMP2 improved union of critical bone defects in a preclinical nonunion model.

This study evaluated if modifying electrocardiographic (ECG) precordial leads to a higher intercostal position improved the accuracy of outflow tract ventricular arrhythmia (OTVA) localization.Precordial ECG prediction algorithms that use a standard lead configuration localize OTVA with variable accuracy.Patients who underwent OTVA ablation were prospectively enrolled to have a standard and modified (high) precordial ECG. R- and S-wave amplitudes and intervals were measured to develop an algorithm that differentiated the right ventricular outflow tract (RVOT) and the left ventricular outflow tract (LVOT) with high accuracy-the modified lead R-wave deflection interval (RWDI). This interval was defined from the earliest QRS onset (using all modified leads) to the lead with longest R-wave deflection. The RWDI was compared with all other ECG algorithms.A total of 50 patients (38 women; mean age 51 ± 17 years) had successful catheter ablation for OTVA (RVOT 60%, LVOT 40%). The modified lead RWDI was significantly shorter in the RVOT group (18.5 ms, interquartile range 25th to 75th percentile [IQRThe modified lead RWDI is a simple, easily interpretable algorithm that can potentially differentiate a right- or left-sided origin of OTVA with high accuracy.

Background Clinical studies have reported that epicardial adipose tissue (EpAT) accumulation associates with the progression of atrial fibrillation (AF) pathology and adversely affects AF management. The role of local cardiac EpAT deposition in disease progression is unclear, and the electrophysiological, cellular, and molecular mechanisms involved remain poorly defined. Objectives The purpose of this study was to identify the underlying mechanisms by which EpAT influences the atrial substrate for AF. Methods Patients without AF undergoing coronary artery bypass surgery were recruited. Computed tomography and high-density epicardial electrophysiological mapping of the anterior right atrium were utilized to quantify EpAT volumes and to assess association with the electrophysiological substrate in situ. Excised right atrial appendages were analyzed histologically to characterize EpAT infiltration, fibrosis, and gap junction localization. Co-culture experiments were used to evaluate the paracrine effects of EpAT on cardiomyocyte electrophysiology. Proteomic analyses were applied to identify molecular mediators of cellular electrophysiological disturbance. Results Higher local EpAT volume clinically correlated with slowed conduction, greater electrogram fractionation, increased fibrosis, and lateralization of cardiomyocyte connexin-40. In addition, atrial conduction heterogeneity was increased with more extensive myocardial EpAT infiltration. Cardiomyocyte culture studies using multielectrode arrays showed that cardiac adipose tissue-secreted factors slowed conduction velocity and contained proteins with capacity to disrupt intermyocyte electromechanical integrity. Conclusions These findings indicate that atrial pathophysiology is critically dependent on local EpAT accumulation and infiltration. In addition to myocardial architecture disruption, this effect can be attributed to an EpAT-cardiomyocyte paracrine axis. The focal adhesion group proteins are identified as new disease candidates potentially contributing to arrhythmogenic atrial substrate.

This review presents bioprinting methods, biomaterials, and printing strategies that may be used for composite tissue constructs for musculoskeletal applications. The printing methods discussed include those that are suitable for acellular and cellular components, and the biomaterials include soft and rigid components that are suitable for soft and/or hard tissues. We also present strategies that focus on the integration of cell-laden soft and acellular rigid components under a single printing platform. Given the structural and functional complexity of native musculoskeletal tissue, we envision that hybrid bioprinting, referred to as hybprinting, could provide unprecedented potential by combining different materials and bioprinting techniques to engineer and assemble modular tissues.

In this report, we present a case of an adult patient with a mature teratoma of the conus medullaris. The patient was a 29-year-old postpartum female patient who developed unexplained urinary retention. Lumbar spine magnetic resonance imaging (MRI) examination revealed an intradural partly enhancing mixed cystic and solid lesion with intralesional intrinsic T1 hyperintense components that were suppressed on fat suppressed sequences, inseparable from the conus medullaris. Surgical resection was performed and histopathology findings were consistent with a mature teratoma. The patient made a complete recovery.

Cell-based therapy for augmentation of core decompression (CD) using mesenchymal stromal cells (MSCs) is a promising treatment for early stage osteonecrosis of the femoral head (ONFH). Recently, the therapeutic potential for immunomodulation of osteogenesis using preconditioned (with pro-inflammatory cytokines) MSCs (pMSCs), or by the timely resolution of inflammation using MSCs that over-express anti-inflammatory cytokines has been described. Here, pMSCs exposed to tumor necrosis factor-alpha and lipopolysaccharide for 3 days accelerated osteogenic differentiation in vitro. Furthermore, injection of pMSCs encapsulated with injectable hydrogels into the bone tunnel facilitated angiogenesis and osteogenesis in the femoral head in vivo, using rabbit bone marrow-derived MSCs and a model of corticosteroid-associated ONFH in rabbits. In contrast, in vitro and in vivo studies demonstrated that genetically-modified MSCs that over-express IL4 (IL4-MSCs), established by using a lentiviral vector carrying the rabbit IL4 gene under the cytomegalovirus promoter, accelerated proliferation of MSCs and decreased the percentage of empty lacunae in the femoral head. Therefore, adjunctive cell-based therapy of CD using pMSCs and IL4-MSCs may hold promise to heal osteonecrotic lesions in the early stage ONFH. These interventions must be applied in a temporally sensitive fashion, without interfering with the mandatory acute inflammatory phase of bone healing.

Intracranial dural arteriovenous fistulas (dAVF) are acquired lesions, with the most commonly reported findings on CT haemorrhage or focal oedema. We describe a case of progressive subcortical calcification on CT secondary to venous hypertension from a high grade dAVF.

The default mode network (DMN) is a major neuronal network that deactivates during goal-directed tasks. Recent advances in neuroimaging have shed light on its structure and function. Alterations in the DMN are increasingly recognized in a range of neurological and psychiatric conditions including epilepsy. This review first describes the current understanding of the DMN in health, normal aging, and disease as it is acquired via resting-state functional magnetic resonance imaging (MRI), before focusing on how it is affected in various types of focal and generalized epilepsy. These findings support the potential use of DMN parameters as future biomarkers in epilepsy research, diagnosis, and management.

Background: Much attention has been paid to radiation exposure with CT coronary angiography (CTCA) but less to the dose associatedwith invasive catheter angiography (CA). Methods: Radiation doses were reviewed from consecutive CTCA and diagnostic CA studies (100 CTCA, 400 CA) from January 2014. CT and CA studies for bypass graft or non-coronary indications were excluded. Effective radiation doses were estimated from the dose-length product and the dose-area product using the respective chest conversion coefficients (0.014 mSv/mGy x cm and 0.20 mSv/Gy x cm2). CTCA was performed on a 128 detector row dual source scanner. Doses were then compared with 2012 when a 1st generation dual source CT scanner was in use. Results: The median effective dose for CTCA was 2.0 mSv (IQR 1.3 to 3.6) vs 9.2 mSv (IQR 6.3 to 12.8) for CA, p < 0.001. The majority of CTCA patients (87/100) underwent calcium scoring with a median additional dose of 0.7 mSv. In patients weighing < 80kg, the median CTCA dose was 1.6 mSv vs 7.0 for CA (p < 0.001). Compared with 2012, CTCA radiation doses have reduced from 5.2mSv to 2.0 mSv (p < 0.001) while there has been no significant change in CA doses (9.1 vs 9.2 mSv, p = NS). Conclusion: At our institution, radiation exposure associated with CTCA is several-fold less than that with CA. With new hardware, CTCA doses have halved since 2012 while there has been no significant change in CA over the same period.

Table 1. Change in shock reduction programming after delivery of the first report. Programming parameter US/Canada Australia/New Zealand % on target pre-report % on target post-report % difference % on target pre-report % on target post-report % difference VF NID (PP) 18.7 33.4 14.7* 33.3 36.4 3.0 VF NID (SP) 91.2 97.0 5.9* 100.0 100.0 0.0 LTI (PP) 40.7 47.6 6.9* 40.0 45.5 5.5 LTI (SP) 27.6 30.8 3.2 30.0 27.3 −2.7 Wavelet 65.0 87.0 22.0* 53.9 82.6 28.8 PR logic 95.7 95.5 −0.1 88.5 71.9 −16.6 SVT limit 66.0 81.2 15.3* 70.0 69.1 −0.9 LIA 81.4 96.0 14.6* 85.0 96.4 11.4

B. Pang1,2,∗, S. Joshi 1,2, E. Lui 2,3, M. Tacey4, J. Alison5,6, S. Seneviratne5,6, J. Cameron5,6, H. Mond1,2 1 The Department of Cardiology, Royal Melbourne Hospital, Parkville, Australia 2 The Department of Medicine, University of Melbourne, Australia 3 The Department of Radiology, Royal Melbourne Hospital, University of Melbourne, Australia 4 Melbourne EpiCentre, University of Melbourne, Australia 5 Monash Cardiovascular Research Centre, MonashHEART, Australia 6 Southern Clinical School, Monash University, Melbourne, Australia