Non-Invasive Assessment of Back Surface Topography: Technologies, Techniques and Clinical Utility.

(1) Background: Frequent exposure to ionising radiation is often used to determine the diagnosis of adolescent idiopathic scoliosis (AIS), a lateral curvature of the spine in those aged between 10 and 18 years, and a treatment plan according to Cobb angle. This narrative review outlines the clinical utility of surface topography (ST), a radiation-free imaging modality. (2) Methods: Publicly available databases were searched to yield literature related to ST. Identified articles were classified based on the equipment used and in order of how it was developed, i.e., historical, recent developments, and state-of-the-art developments. (3) Conclusions: ST is a reliable cost-effective non-invasive technique that provides an alternative to radiation-based imaging to aid with the diagnosis and potential screening of AIS. Several scanning methods are available, which allows ST to be used in several clinical environments. Limitations of inter-reliability and differences of apparatus resulting in variations of data have been noted through this narrative review.

"Local control": another core concept of physiology.

The maintenance of a more or less constant internal environment by homeostatic (negative feedback) mechanisms is well understood, and "homeostasis" is regarded as an important core concept for students to understand. However, there are critically important control mechanisms that operate at the local level and are more or less independent of homeostasis. Here we define a core concept of "local control," present examples of it in many different organ systems, and propose a conceptual framework for it. Local control, like all of the other core concepts, can provide students with a learning tool that can facilitate understanding physiology.NEW & NOTEWORTHY Local control of many physiological phenomena occurs to meet the needs of certain systems and to enable these systems to meet the episodic challenges that occur. The mechanisms by which local control is exerted include locally released chemical messengers, physical stimuli acting on the structures, and local neural networks. Examples of important local controls are present throughout the body.

Validity of sagittal thoracolumbar curvature measurement using a non-radiographic surface topography method.

PURPOSE: To estimate the criterion validity of sagittal thoracolumbar spine measurement using a surface topography method in a clinical population against the gold standard and to estimate concurrent validity against two non-radiographic clinical tools. METHODS: In this cross-sectional validity study, thoracolumbar curvature was measured in adults with spinal conditions recruited from a specialist orthopaedic hospital. A surface topography method using a Kinect sensor was compared to three other measurement methods: spinal radiograph (gold standard), flexicurve and digital inclinometer. Correlation coefficients and agreement between the measurement tools were analysed. RESULTS: Twenty-nine participants (79% female) were included in criterion validity analyses and 38 (76% female) in concurrent validity analyses. The surface topography method was moderately correlated with the radiograph (r = .70, p < .001) in the thoracic spine, yet there was no significant correlation with the radiograph in the lumbar spine (r = .32, p = .89). The surface topography method was highly correlated with the flexicurve (rs = .91, p < .001) and digital inclinometer (r = .82, p < .001) in the thoracic spine, and highly correlated with the flexicurve (r = .74, p < .001) and digital inclinometer (r = .74, p < .001) in the lumbar spine. CONCLUSIONS: The surface topography method showed moderate correlation and agreement in thoracic spine with the radiograph (criterion validity) and high correlation with the flexicurve and digital inclinometer (concurrent validity). Compared with other non-radiographic tools, this surface topography method displayed similar criterion validity for kyphosis curvature measurement.

Subcellular Propagation of Cardiomyocyte ß-Adrenergic Activation of Calcium Uptake Involves Internal ß-Receptors and AKAP7.

ß-adrenergic receptor (ß-AR) signaling in cardiac myocytes is central to cardiac function, but spatiotemporal activation within myocytes is unresolved. In rabbit ventricular myocytes, ß-AR agonists or high extracellular [Ca] were applied locally at one end, to measure ß-AR signal propagation as Ca-transient (CaT) amplitude and sarcoplasmic reticulum (SR) Ca uptake. High local [Ca]o, increased CaT amplitude under the pipette faster than did ISO, but was also more spatially restricted. Local isoproterenol (ISO) or norepinephrine (NE) increased CaT amplitude and SR Ca uptake, that spread along the myocyte to the unexposed end. Thus, local [Ca]i decline kinetics reflect spatio-temporal progression of ß-AR end-effects in myocytes. To test whether intracellular ß-ARs contribute to this response, we used ß-AR-blockers that are membrane permeant (propranolol) or not (sotalol). Propranolol completely blocked NE-dependent CaT effects. However, blocking surface ß-ARs only (sotalol) suppressed only ∼50% of the NE-induced increase in CaT peak and rate of [Ca]i decline, but these changes spread more gradually than NE alone. We also tested whether A-kinase anchoring protein 7γ (AKAP7γ; that interacts with phospholamban) is mobile, such that it might contribute to intracellular spatial propagation of ß-AR signaling. We found AKAP7γ to be highly mobile using fluorescence recovery after photobleach of GFP tagged AKAP7γ, and that PKA activation accelerated AKAP7γ-GFP wash-out upon myocyte saponin-permeabilization, suggesting increased AKAP7γ mobility. We conclude that local ß-AR activation can activate SR Ca uptake at remote myocyte sites, and that intracellular ß-AR and AKAP7γ mobility may play a role in this spread of activation.

A longitudinal study of the arterio-venous fistula maturation of a single patient over 15 weeks.

Arterio-venous fistula creation is the preferred vascular access for haemodialysis, but has a large failure rate in the maturation period. Previous research, considering the remodelling mechanisms for failure-to-mature patients, has been limited by obtaining the patient-specific boundary conditions at only a few points in the patient history. Here, a non-invasive imaging system was used to reconstruct the three-dimensional vasculature, and computational fluid dynamics was used to analyse the haemodynamics for one patient over 15 weeks. The analysis suggested evidence of a control mechanism, which adjusts the lumen diameter to keep the wall shear stress near constant in the proximal regions of the vein and artery. Additionally, the vein and artery were shown to remodel at different growth rates, and the blood flow rate also saw the largest increase within the first week. Wall shear stress at time of creation may be a useful indicator for successful AVF maturation.

Augmented flap reconstruction of complex pressure ulcers using synthetic hybrid-scale fiber matrix.

INTRODUCTION: Flap reconstruction of pressure ulcers offers an important clinical means of decreasing morbidity in hospitalized patients. A new, novel method of managing pressure ulcer wounds uses a synthetic hybrid-scale fiber matrix prior to tissue flap reconstruction. This synthetic hybrid-scale fiber matrix is comprised of micron-scale and nanoscale fiber structure similar to that of human extracellular matrix and supports cell ingrowth, retention, and granulation tissue formation. OBJECTIVE: The primary objective of the present study was to examine use of the synthetic hybrid-scale fiber matrix as a means of encouraging granulation tissue within complex wounds to promote successful and lasting wound closure following flap reconstruction. MATERIALS AND METHODS: Patients included in this retrospective study had pressure ulcers that were not successfully managed with other wound therapies; in addition, these patients presented with various risk factors for postoperative complications. Before treatment, sharp debridement of the wound margins and wound bed was performed. Wounds were subsequently treated by applying synthetic hybrid-scale fiber matrix prior to flap reconstruction, based on physician assessment of wound status. The primary objective to include the synthetic hybrid-scale fiber matrix in the treatment approach of pressure ulcers in this case series was to ensure (1) integration to the wound bed prior to flap closure to encourage granulation tissue formation at a later time and (2) lasting successful wound closure following flap reconstruction. RESULTS: Overall, the patient outcomes indicated that the synthetic hybrid-scale fiber matrix was used to manage pressure ulcers successfully, with a wound closure rate of 90.9% (10 cases of complete wound closure and 1 case of 97.2% wound area reduction). Additionally, no complication related to the application of each synthetic hybrid-scale fiber matrix was reported. CONCLUSIONS: Application of synthetic hybrid-scale fiber matrix to the wound bed prior to flap closure promotes cellular ingrowth and granulation tissue formation, which promotes successful and lasting wound closure following flap reconstruction.

Incidental finding of ileal gastrointestinal stromal tumour during prostate cancer staging with prostate-specific membrane antigen scan.

Prostate-specific membrane antigen (PSMA) positron emission tomography (PET)/computed tomography (CT) is used in managing and staging prostate cancer, but can identify other non-prostate pathology. We present the first reported case where small bowel gastrointestinal stromal tumour (GIST) has been incidentally identified on PSMA-PET scan and highlight the need for awareness of other pathology being identified on PSMA-PET/CT.

Phylogeny of the Eurasian Wren Nannus troglodytes (Aves: Passeriformes: Troglodytidae) reveals deep and complex diversification patterns of Ibero-Maghrebian and Cyrenaican populations.

The Mediterranean Basin represents a Global Biodiversity Hotspot where many organisms show high inter- and intraspecific differentiation. Extant phylogeographic patterns of terrestrial circum-Mediterranean faunas were mainly shaped through Pleistocene range shifts and range fragmentations due to retreat into different glacial refugia. Thus, several extant Mediterranean bird species have diversified by surviving glaciations in different hospitable refugia and subsequently expanded their distribution ranges during the Holocene. Such a scenario was also suggested for the Eurasian Wren (Nannus troglodytes) despite the lack of genetic data for most Mediterranean subspecies. Our phylogenetic multi-locus analysis comprised 18 out of 28 currently accepted subspecies of N. troglodytes, including all but one subspecies which are present in the Mediterranean Basin. The resulting phylogenetic reconstruction dated the onset of the entire Holarctic radiation of three Nannus species to the early Pleistocene. In the Eurasian Wren, two North African subspecies represented separate basal lineages from the Maghreb (N. t. kabylorum) and from the Libyan Cyrenaica (N. t. juniperi), being only distantly related to other Mediterranean populations. Although N. troglodytes appeared to be paraphyletic with respect to the Nearctic Winter Wren (N. hiemalis), respective nodes did not receive strong statistical support. In contrast, paraphyly of the Ibero-Maghrebian taxon N. t. kabylorum was strongly supported. Southern Iberian populations of N. t. kabylorum did not clade with Maghrebian populations of the same subspecies but formed a sister clade to a highly diverse European clade (including nominate N. t. troglodytes and eight further taxa). In accordance with a pattern also found in other birds, Eurasian populations were split into a western clade (Europe, Caucasus) and an eastern clade (Central Asia, Sino-Himalayas, East Asia). This complex phylogeographic pattern revealed cryptic diversification in N. troglodytes, especially in the Iberio-Maghrebian region.

The reliability and reproducibility of sagittal spinal curvature measurement using the Microsoft Kinect V2.

BACKGROUND: Abnormal sagittal spinal curvature is associated with pain, decreased mobility, respiratory problems and increased mortality. Time-of-flight technology of the Microsoft Kinect sensor can reconstruct a three-dimensional image of the back quickly and inexpensively. OBJECTIVE: To estimate the extent of the reproducibility of sagittal spine curvature measurement using the Microsoft Kinect sensor. METHODS: Simultaneous measurement of thoracic and lumbar spine using the Microsoft Kinect sensor in 37 participants. Two investigators gave standardised instructions and each captured 3 images. Thoracic kyphosis and lumbar lordosis angle indexes were calculated using maximum height divided by the length. RESULTS: Adult participants (mean age in years (SD) = 51.7 (20.6); 57% female; BMI in kg/m2 (SD) = 24.9 (3.3)) kyphosis and lordosis indexes showed high intra-rater and inter-rater ICC values (0.960-0.973). The means of the first images from both raters had significantly larger kyphosis indexes compared to the second and third images, yet no difference between means in lordosis data. CONCLUSIONS: The results indicate that the Microsoft Kinect sensor has a reproducible method with high intra-rater and inter-rater reliability. The difference between the means over repeated measures suggest the second image capture is more consistent. It is a reproducible and quick method in clinical and research settings.

ß-Adrenergic induced SR Ca2+ leak is mediated by an Epac-NOS pathway.

Cardiac ß-adrenergic receptors (ß-AR) and Ca2+-Calmodulin dependent protein kinase (CaMKII) regulate both physiological and pathophysiological Ca2+ signaling. Elevated diastolic Ca2+ leak from the sarcoplasmic reticulum (SR) contributes to contractile dysfunction in heart failure and to arrhythmogenesis. ß-AR activation is known to increase SR Ca2+ leak via CaMKII-dependent phosphorylation of the ryanodine receptor. Two independent and reportedly parallel pathways have been implicated in this ß-AR-CaMKII cascade, one involving exchange protein directly activated by cAMP (Epac2) and another involving nitric oxide synthase 1 (NOS1). Here we tested whether Epac and NOS function in a single series pathway to increase ß-AR induced and CaMKII-dependent SR Ca2+ leak. Leak was measured as both Ca2+ spark frequency and tetracaine-induced shifts in SR Ca2+, in mouse and rabbit ventricular myocytes. Direct Epac activation by 8-CPT (8-(4-chlorophenylthio)-2'-O-methyl-cAMP) mimicked ß-AR-induced SR Ca2+ leak, and both were blocked by NOS inhibition. The same was true for myocyte CaMKII activation (assessed via a FRET-based reporter) and ryanodine receptor phosphorylation. Inhibitor and phosphorylation studies also implicated phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt) downstream of Epac and above NOS activation in this pathway. We conclude that these two independently characterized parallel pathways function mainly via a single series arrangement (ß-AR-cAMP-Epac-PI3K-Akt-NOS1-CaMKII) to mediate increased SR Ca2+ leak. Thus, for ß-AR activation the cAMP-PKA branch effects inotropy and lusitropy (by effects on Ca2+ current and SR Ca2+-ATPase), this cAMP-Epac-NOS pathway increases pathological diastolic SR Ca2+leak. This pathway distinction may allow novel SR Ca2+ leak therapeutic targeting in treatment of arrhythmias in heart failure that spare the inotropic and lusitropic effects of the PKA branch.

Sarcoplasmic reticulum Ca2+, Mg2+, K+, and Cl- concentrations adjust quickly as heart rate changes.

During systole, Ca2+ is released from the sarcoplasmic reticulum (SR) through ryanodine receptors (RyRs) while, simultaneously, other ions (specifically K+, Mg2+, and Cl-) provide counter-ion flux. These ions move back into the SR during diastole through the SERCA pump and SR K+ and Cl- channels. In homeostasis, all ion concentrations in different cellular regions (e.g., junctional and non-junctional SR, dyadic cleft, and cytosol) are the same at the beginning and end of the cardiac cycle. Here, we used an equivalent circuit compartment model of the SR and the surrounding cytoplasm to understand the heart rate dependence of SR ion homeostasis. We found that the Ca2+, Mg2+, K+, and Cl- concentrations in the SR and the cytoplasm self-adjust within just a few heartbeats with only very small changes in Mg2+, K+, and Cl- concentrations and membrane voltages (just a few percent). However, those small changes were enough to compensate for the large heart-rate-dependent changes in SR and cytoplasmic Ca2+ concentrations in the new steady state. The modeling suggests that ion adaptation to increases in heart rate is inherent to the system and that physiological changes that increase contractility and cardiac output are accommodated by the same self-adjusting mechanism of producing small changes in ion driving forces. Our findings also support the long-held hypothesis that SR membrane potentials are small (~1-2mV).

Electrophysiological Determination of Submembrane Na(+) Concentration in Cardiac Myocytes.

In the heart, Na(+) is a key modulator of the action potential, Ca(2+) homeostasis, energetics, and contractility. Because Na(+) currents and cotransport fluxes depend on the Na(+) concentration in the submembrane region, it is necessary to accurately estimate the submembrane Na(+) concentration ([Na(+)]sm). Current methods using Na(+)-sensitive fluorescent indicators or Na(+) -sensitive electrodes cannot measure [Na(+)]sm. However, electrophysiology methods are ideal for measuring [Na(+)]sm. In this article, we develop patch-clamp protocols and experimental conditions to determine the upper bound of [Na(+)]sm at the peak of action potential and its lower bound at the resting state. During the cardiac cycle, the value of [Na(+)]sm is constrained within these bounds. We conducted experiments in rabbit ventricular myocytes at body temperature and found that 1) at a low pacing frequency of 0.5 Hz, the upper and lower bounds converge at 9 mM, constraining the [Na(+)]sm value to ∼9 mM; 2) at 2 Hz pacing frequency, [Na(+)]sm is bounded between 9 mM at resting state and 11.5 mM; and 3) the cells can maintain [Na(+)]sm to the above values, despite changes in the pipette Na(+) concentration, showing autoregulation of Na(+) in beating cardiomyocytes.

Prediction of bladder neck invasion and tumor extension to bladder neck margin by prostatic adenocarcinoma: a nomogram using biopsy data including transition zone tumor morphology.

Transition zone (TZ) prostatic adenocarcinoma can be identified on needle core biopsy based on tumor morphology, provided that the sample is preserved in a glutaraldehyde-based tissue fixative. TZ tumors have a propensity to grow larger than their peripheral counterparts without extraprostatic extension and finally to escape the gland by invading the bladder neck. We investigated the value of biopsy-determined parameters including TZ origin to predict the risk of isolated bladder neck invasion at radical prostatectomy. If reliable, this will enable urologists to expand their bladder neck dissection and avoid an isolated positive bladder neck margin. The study cohort consisted of 3942 patients with detailed pre operative biopsy information who underwent curative-intent radical prostatectomy between January 2010 and December 2015 in Western Australia. Multivariate logistic regression models were developed to predict isolated bladder neck invasion or isolated positive bladder neck margin. A predictive preoperative nomogram is presented. The predictive accuracy is shown in the calibration plot (the area under the curve: 0.777). The accuracy of the nomogram is dependent on the biopsy identification of transition zone cancer features, parameters only reliably interpretable after glutaraldehyde tissue fixation.

Sarcoplasmic Reticulum Structure and Functional Properties that Promote Long-Lasting Calcium Sparks.

Calcium (Ca) sparks are the fundamental sarcoplasmic reticulum (SR) Ca release events in cardiac myocytes, and they have a typical duration of 20-40 ms. However, when a fraction of ryanodine receptors (RyRs) are blocked by tetracaine or ruthenium red, Ca sparks lasting hundreds of milliseconds have been observed experimentally. The fundamental mechanism underlying these extremely prolonged Ca sparks is not understood. In this study, we use a physiologically detailed mathematical model of subcellular Ca cycling to examine how Ca spark duration is influenced by the number of functional RyRs in a junctional cluster (which is reduced by tetracaine or ruthenium red) and other SR Ca handling properties. One RyR cluster contains a few to several hundred RyRs, and we use a four-state Markov RyR gating model. Each RyR opens stochastically and is regulated by cytosolic and luminal Ca. We varied the number of functional RyRs in the single cluster, diffusion within the SR network, diffusion between network and junctional SR, cytosolic Ca diffusion, SERCA uptake activity, and RyR open probability. For long-lasting Ca release events, opening events within the cluster must occur continuously because the typical open time of the RyR is only a few milliseconds. We found the following: 1) if the number of RyRs is too small, it is difficult to maintain consecutive openings and stochastic attrition terminates the release; 2) if the number of RyRs is too large, the depletion of Ca from the junctional SR terminates the release; and 3) very long release events require relatively small-sized RyR clusters (reducing flux as seen experimentally with tetracaine) and sufficiently rapid intra-SR Ca diffusion, such that local junctional intra-SR [Ca] can be maintained by intra-SR diffusion and overall SR Ca reuptake.

Nitric oxide-dependent activation of CaMKII increases diastolic sarcoplasmic reticulum calcium release in cardiac myocytes in response to adrenergic stimulation.

Spontaneous calcium waves in cardiac myocytes are caused by diastolic sarcoplasmic reticulum release (SR Ca(2+) leak) through ryanodine receptors. Beta-adrenergic (ß-AR) tone is known to increase this leak through the activation of Ca-calmodulin-dependent protein kinase (CaMKII) and the subsequent phosphorylation of the ryanodine receptor. When ß-AR drive is chronic, as observed in heart failure, this CaMKII-dependent effect is exaggerated and becomes potentially arrhythmogenic. Recent evidence has indicated that CaMKII activation can be regulated by cellular oxidizing agents, such as reactive oxygen species. Here, we investigate how the cellular second messenger, nitric oxide, mediates CaMKII activity downstream of the adrenergic signaling cascade and promotes the generation of arrhythmogenic spontaneous Ca(2+) waves in intact cardiomyocytes. Both SCaWs and SR Ca(2+) leak were measured in intact rabbit and mouse ventricular myocytes loaded with the Ca-dependent fluorescent dye, fluo-4. CaMKII activity in vitro and immunoblotting for phosphorylated residues on CaMKII, nitric oxide synthase, and Akt were measured to confirm activity of these enzymes as part of the adrenergic cascade. We demonstrate that stimulation of the ß-AR pathway by isoproterenol increased the CaMKII-dependent SR Ca(2+) leak. This increased leak was prevented by inhibition of nitric oxide synthase 1 but not nitric oxide synthase 3. In ventricular myocytes isolated from wild-type mice, isoproterenol stimulation also increased the CaMKII-dependent leak. Critically, in myocytes isolated from nitric oxide synthase 1 knock-out mice this effect is ablated. We show that isoproterenol stimulation leads to an increase in nitric oxide production, and nitric oxide alone is sufficient to activate CaMKII and increase SR Ca(2+) leak. Mechanistically, our data links Akt to nitric oxide synthase 1 activation downstream of ß-AR stimulation. Collectively, this evidence supports the hypothesis that CaMKII is regulated by nitric oxide as part of the adrenergic cascade leading to arrhythmogenesis.

Sarcoplasmic reticulum K(+) (TRIC) channel does not carry essential countercurrent during Ca(2+) release.

The charge translocation associated with sarcoplasmic reticulum (SR) Ca(2+) efflux is compensated for by a simultaneous SR K(+) influx. This influx is essential because, with no countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium potential and SR Ca(2+) release would cease. The SR K(+) trimeric intracellular cation (TRIC) channel has been proposed to carry the essential countercurrent. However, the ryanodine receptor (RyR) itself also carries a substantial K(+) countercurrent during release. To better define the physiological role of the SR K(+) channel, we compared SR Ca(2+) transport in saponin-permeabilized cardiomyocytes before and after limiting SR K(+) channel function. Specifically, we reduced SR K(+) channel conduction 35 and 88% by replacing cytosolic K(+) for Na(+) or Cs(+) (respectively), changes that have little effect on RyR function. Calcium sparks, SR Ca(2+) reloading, and caffeine-evoked Ca(2+) release amplitude (and rate) were unaffected by these ionic changes. Our results show that countercurrent carried by SR K(+) (TRIC) channels is not required to support SR Ca(2+) release (or uptake). Because K(+) enters the SR through RyRs during release, the SR K(+) (TRIC) channel most likely is needed to restore trans-SR K(+) balance after RyRs close, assuring SR Vm stays near 0 mV.

Isoproterenol increases the fraction of spark-dependent RyR-mediated leak in ventricular myocytes.

Recent research suggests that the diastolic ryanodine-receptor-mediated release of Ca(2+) (J(leak)) from the sarcoplasmic reticulum of ventricular myocytes occurs in spark and nonspark forms. Further information about the role(s) of these release manifestations is scarce, however. This study addresses whether the fraction of spark-mediated J(leak) increases due to ß-adrenergic stimulation. Confocal microscopy was used to simultaneously image Ca(2+) sparks and quantify J(leak) in intact rabbit myocytes, either in the absence or in the presence of 125 nM isoproterenol. It was found that isoproterenol treatment shifts the spark-frequency-J(leak) relationship toward an increased sensitivity to a [Ca(2+)] trigger. In agreement, a small but significant increase in spark width was found for cells with matched baseline [Ca(2+)] and total SR [Ca(2+)]. The reconstruction of release fluxes, when applied to the average sparks from those selected cells, yielded a wider release source in the isoproterenol event, indicating the recruitment of peripheral ryanodine receptors. Overall, the results presented here indicate that ß-adrenergic stimulation increases the spark-dependent fraction of J(leak). Working together, the increased Ca(2+) sensitivity and the greater spark width found during isoproterenol treatment may increase the probability of Ca(2+) wave generation.

Calcium movements inside the sarcoplasmic reticulum of cardiac myocytes.

Sarcoplasmic reticulum (SR) Ca content ([Ca]SRT) is critical to both normal cardiac function and electrophysiology, and changes associated with pathology contribute to systolic and diastolic dysfunction and arrhythmias. The intra-SR free [Ca] ([Ca]SR) dictates the [Ca]SRT, the driving force for Ca release and regulates release channel gating. We discuss measurement of [Ca]SR and [Ca]SRT, how [Ca]SR regulates activation and termination of release, and how Ca diffuses within the SR and influences SR Ca release during excitation-contraction coupling, Ca sparks and Cac waves. The entire SR network is connected and its lumen is also continuous with the nuclear envelope. Rapid Ca diffusion within the SR could stabilize and balance local [Ca]SR within the myocyte, but restrictions to diffusion can create spatial inhomogeneities. Experimental measurements and mathematical models of [Ca]SR to date have greatly enriched our understanding of these [Ca]SR dynamics, but controversies exist and may stimulate new measurements and analysis.

Investigation of a low cost method to quantify cosmetic defect.

For many patients, the motivation in seeking treatment is the improvement of their appearance rather than to correct an underlying skeletal deformity, so cosmetic concerns and the psychosocial impacts of adolescent idiopathic scoliosis are important factors in the clinical decision-making process. In the current environment of evidence based medicine there is a growing need to quantify back surface shape and general body asymmetry with the objective of producing an agreed scoring to be used in developing treatment plans and assessing outcomes but to date many clinics continue to rely on qualitative or expensive methods to describe cosmetic deformity. In November 2010, Microsoft® Corporation launched the low cost Kinect™ camera with 18 million units sold (as at January 2012) throughout the world. The device incorporates proprietary light coding technology that reconstructs the three dimensional location of an estimated 50,000 projected points illuminating objects within its field of view in approximately 1/30th of a second. The aim of the research was to investigate the capabilities of a low cost, reliable and inherently safe apparatus based on Kinect depth sensing and video technology to simultaneously acquire back surface shape and the locations of bony landmarks with the goal of providing data to describe cosmetic defect. Work has been completed using both the apparatus and a commercially available optical motion capture system (Vicon Motion Systems, Oxford, U.K.) to acquire data from a test object representing an unaffected human torso. Results were obtained to compare tri-dimensional bony landmark reconstruction accuracy and combined with analyses of point cloud data to describe back shape. Early indications are that the proposed apparatus has potential to be a clinically useful tool.