1 Given that antidepressants act on neurotransmitter mechanisms also involved in circadian rhythm generation and entrainment, only untreated patients may reveal an “endogenous”

rhythm disturbance, if present. The second question regards conceptual clarity. What do we mean by a clock disturbance in depression? What one sees clinically may have its origins at a variety of different levels―not necessarily the hypothalamic biological clock itself, but epiphenomena related to altered rhythmic behavior, disturbed sleep, or abnormal environmental input. The third question is whether the studies purporting to document circadian rhythm disturbances in Inhibitors,research,lifescience,medical depression have been adequately carried

out. Alas, methodological issues characterize most investigations―not in terms of scientific caliber or intent, but because it was previously not sufficiently recognized how strongly “masking” (behavioral or environmental factors that modify the variable measured) obscures the underlying endogenous rhythms. This Inhibitors,research,lifescience,medical is a particular problem with measuring the core body temperature rhythm, since temperature is easily Inhibitors,research,lifescience,medical and rapidly masked by motor activity, postural change, meals, etc. Cortisol increases with stress, Selleckchem MS275 particularly at the evening nadir; thus, this circadian marker is also often masked by psychophysiological response. Melatonin, the pineal hormone considered to provide the best estimate of circadian rhythm phase, is suppressed by light, particularly in the evening: it is sensitive to masking by light as Inhibitors,research,lifescience,medical low as ca 100 lux.10 Thus, even indoor room light may delay the apparent

onset of nocturnal secretion. Only in the last decade have controlled protocols using state-oft-he-art chronobiological techniques provided unequivocal circadian markers. The fourth question concerns which models Inhibitors,research,lifescience,medical are useful. Concepts of an underlying genetic and stress-related vulnerability for depression can be discussed in terms of both neurotransmitter and circadian rhythm dysregulation. Here, I will draw on the two-process model of sleep-wake regulation11 as a way because of understanding some aspects of depressive symptomatology. Trie final question is whether we can find out about putative circadian mechanisms underlying affective disorder through understanding clinically successful chronobiological treatments. Circadian rhythm or sleep manipulations do improve depression and provide some fascinating clues. Clinical observations Periodicity in affective disorders (from seasonal recurrence to 48-h rapid cycling) is the clinical observation; diurnal variation of mood, early morning awakening, and sleep disturbances are the classical symptoms that have linked depression with circadian rhythm function.

The mean fluorescence intensity of the cells isolated from the peritoneal cavity 20 or 60hrs after the administration was 4.78 or 47.61 per 10000 cells, respectively. The calculated concentration of Hoechst 33342 was 40.1ng/mL after 20hrs or 491.0ng/mL after 60hrs. Figure 8 (a) Fluorescence intensity of U-937 cells was analyzed after

staining with serial concentrations of Hoechst 33342 using FACS Aria II. The segments P1, P2, P3, or P4 correspond to the range of fluorescence intensity at 0, 10, 100, or 1000ng/mL … In the present study we have used Hoechst 33342-incorporated PLGA to identify, isolate, and characterize cells exposed to this Inhibitors,research,lifescience,medical fluorescent dye. The nuclear staining of Hoechst 33342 in vivo is a powerful marker for the isolation of cells from blood, ascites, pleural effusions, and even tissues when the tissue dissociation

and cell isolation protocol is established. In addition, we can also collect cells that are negative for fluorescence. Once the various cells have Inhibitors,research,lifescience,medical been isolated, they can be analyzed for cell type and expression of specific molecules such as surface markers that may be important in cell targeting. One major limitation of the present approach is that Hoechst 33342 used as an imitating drug will be different from the actual drug in terms of molecular weight, structure, electrical charge, and/or presence/absence of specificity Inhibitors,research,lifescience,medical for a target molecule. Nonetheless, the present approach is useful for investigating the likely distribution of released Inhibitors,research,lifescience,medical materials from individual PLGA particles in the microenvironment of target tissues. 4. Conclusion The present study successfully demonstrated that Hoechst 33342-incorporated PLGA particles can be used to simulate the drug exposure of cells in Inhibitors,research,lifescience,medical situ. We isolated cells exposed to this fluorescent dye as well as those that were not. These two classes of cells can then be further characterized, especially with regard to the expression of specific molecules that may be important in the targeting this website mechanism. The present approach may provide

essential information concerning cell targeting in any type of PLGA DDS. Conflict of Interests The authors certify that there is no conflict of interest’s with any financial organization regarding the material discussed in the paper. Acknowledgments The study (-)-p-Bromotetramisole Oxalate was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan and a grant from the Intractable Diseases, the Health and Labor, and Labor Sciences Research Grants from the Ministry of Health, Labor and Welfare of Japan. Some of the results were generated by using the facilities of Biomedical Research Core of Tohoku University Graduate School of Medicine. The authors also acknowledge the support of Tohoku University Global COE Program “Global Nano-Biomedical Engineering Education and Research Network Centre.

(2009). A secondary analysis of these two randomized trials revealed a postoperative decrease in the incidence

of acute kidney injury in nondiabetic preconditioned patients after CABG compared with controls (Venugopal et al. 2010). Thielmann et al. (2010) used the same preconditioning protocol in a single-blind, randomized clinical trial of 53 nondiabetic patients Inhibitors,research,lifescience,medical with triple-vessel disease who underwent CABG with crystalloid cardioplegic arrest. They found both a significant decrease in mean troponin T release (44.5%) and peak serum creatinine concentration postoperatively in the preconditioned group when compared with controls (Thielmann et al. 2010). Hong et al. (2010) found a 26% total reduction in postoperative troponin T in 65 patients preconditioned with four cycles of 5-min upper limb ischemia followed by reperfusion that underwent off-pump CABG, when compared with controls. Inhibitors,research,lifescience,medical However, this decrease did not reach statistical significance (Hong et al. 2010). In a single-blind, randomized clinical trial of 120 patients undergoing elective cardiac surgery (CABG, Inhibitors,research,lifescience,medical valve surgery, combined, or other), Zimmerman et

al. (2011) found that preconditioning (three cycles of 5-min limb ischemia followed by 5-min reperfusion) decreased the incidence of acute kidney injury within 48 h after surgery by 27%; even though a history of previous heart surgery – a known risk factor for acute kidney injury – was significantly more common in control patients compared with the preconditioned group. Using the aforementioned Inhibitors,research,lifescience,medical preconditioning stimulus in a larger, randomized clinical trial of 162 patients undergoing coronary artery bypass surgery, Rahman et al. (2010) found no correlation of RIPC with troponin release, blood hemodynamics, renal dysfunction, lung injury, or total hospital/ICU stay. However, it should be taken into consideration that patients with angina or with Inhibitors,research,lifescience,medical an acute coronary syndrome within 30 days of surgery were not excluded in this study protocol by Rahman et al. (2010). RIPC in clinical trials of patients undergoing percutaneous coronary intervention for acute myocardial infarction Table ​Table33

summarizes the design and results of five randomized clinical trials evaluating the safety and efficacy of RIPC in patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction. In a randomized clinical trial of others 41 consecutive patients with stable angina and single-vessel disease undergoing PCI and stent implantation, Iliodromitis et al. (2006) found that preconditioned patients with three cycles of 5-min upper limb ischemia followed by 5-min reperfusion had significantly higher troponin T and CK-MB Dactolisib chemical structure levels 24 h after the intervention, when compared with controls. Interestingly, a milder rise of cardiac enzymes was observed in the subgroup of preconditioned patients who were on statin treatment, suggesting that statins may ameliorate the inflammatory response after preconditioning (Iliodromitis et al. 2006).

14,15 From a legal

perspective, each country or state has its legal regulations for death. On the basis of these regulations, each hospital establishes criteria for the determination of brain death. Subsequently, a large variability in the determination of brain death between and within individual hospitals has been reported in American and European hospitals.14,15 ETHICAL RULES FOR LIVING DONORS Living Inhibitors,research,lifescience,medical donor donations are widely used worldwide, and the numbers are constantly increasing. According to recent publications, 27,000 living donor kidney and 2,000 living donor liver transplants are performed worldwide annually.16,17 The shortage of deceased donor organs led to a steady increase in live donors over the last years. The ethical rules for live donation are different than those for deceased donors, but what is common to both is the Inhibitors,research,lifescience,medical extensive

attention to the act of organ donation by ethicists, religions, and the medical communities. The majority of live organ donations are kidney Inhibitors,research,lifescience,medical transplants, followed by partial liver and partial lung transplants. The main ethical principle in live donations is to cause little or no harm to the donor. Organ donations between family members are well accepted and valued by society. It is also accepted that altruistic donations, those with a pure and non-financial motivation to help a patient suffering, are a noble thing. However, any donation which is associated with financial payment for Inhibitors,research,lifescience,medical the organ is generally unacceptable. While arguments are voiced that patients may have the rights over their bodies and they can “sell” organs as they wish, it is widely accepted that such practice is Lapatinib unethical and should be banned. Organ trafficking has been and continues to be a major problem in the world. Modern societies worldwide are now strictly against organ trafficking, and international

actions are taken to prevent such cases. In 2008, the Declaration of Inhibitors,research,lifescience,medical Istanbul on Organ Trafficking and Transplant Tourism, the European Parliament, and the Asian heptaminol Taskforce on Organ Trafficking each issued formal statements urging member states to define conditions in which reimbursement can be granted.18 A clear distinction is made between the acceptable practice of reimbursement of legitimate expenses incurred due to the transplant process and payment resulting in illegal financial gain. In Israel, according to a recent law on organ transplantation that is in effect since 2008, direct payments to donors from another source or from insurance are now illegal.19 At the same time the law allows for compensation of the direct expenses of organ donation incurred by the donor and also adjustment of his medical insurance benefit to his new more liable condition.

It is widely agreed that a shortage of organs in a certain country cannot be corrected

through transplantation programs elsewhere in the world. It is the responsibility of the health care system within each country, together with its social ethicists and religious leaders, to assure that an efficient organ transplantation program is implemented and that the public is educated towards donating organs and saving lives. In Israel, a very organized and well defined program is present at the national level; however, the apparent shortage of organs is in part due #learn more keyword# to the public’s relatively low acceptance of organ donations. Intensive programs to enhance the public awareness towards organ transplantation and to increase the consent rate to organ donations are now being carried out in Israel. It includes national public awareness programs that involve all communication media, discussions with religious Inhibitors,research,lifescience,medical and community leaders, and comprehensive Inhibitors,research,lifescience,medical research and surveys to understand the multiple parameters that affect public opinion with respect to organ donation. THE FUTURE OF TRANSPLANTATION MEDICINE The surgical expertise, logistics, biology, and pharmacology of organ transplantation are constantly progressing and continue to impact this field. Organ preservation is becoming more efficient and

is associated with less injury to the transplanted organs. We are now able to transplant

organs which are less optimal and to older and sicker patients. With the excellent medical and surgical expertise and progress in immunology and pharmacology, Inhibitors,research,lifescience,medical the main limitation is public awareness and the general consent of society to organ donations. It is a complex problem that involves intense ethical and religious discussions, but it is up to the societies across the world to be Inhibitors,research,lifescience,medical convinced that this is the only way today to save lives and increase the quality of lives in these devastated groups of patients who need vital organ donations. As to very futuristic ideas of being able to engineer organs and use transplants from animals32 this is still years and maybe decades away from any possible solution. As an alternative to heart transplantation, ventricular assist devices and artificial hearts Isotretinoin are being used today as a definite therapeutic mode and have been shown to prolong lives as compared to medical therapy alone. However, no artificial organ, kidney, or heart can be comparable, in providing the span or the quality of life, to a successfully transplanted organ. SUMMARY The world of transplantation has gone through major changes and progress over many years, with superb methods to enhance our organ preservation and surgical and immunologicpharmacologic therapeutic abilities.

The reality is that physicians are

often unaware of the indicated disorders for many medicines. In one large US study of primary care physicians and psychiatrists, less than 50% could identify the FDA approved diagnoses for selected medicines [Chen et al. 2009]. Similar rates are seen in the UK. General practitioners (GPs) are unaware of the extent of off- label prescribing [Ekins Daukes et al. 2005], although many are aware of the explicit problems with dosing in children [Ekins Daukes et al. 2005]. Perhaps Inhibitors,research,lifescience,medical most importantly clinicians often have only a limited understanding of the issues around off-label prescribing, the frequency of side effects and lack of efficacy data. There can also be problems concerning informed consent [Ekins Daukes et al. Inhibitors,research,lifescience,medical 2005], as while prescribers of psychotropics may be aware that the prescription is off-label, it is clear that it is only rarely known by the patient [Haw and Stubbs,

2005]. Overall there are few established systems to support and manage off-licence medicine prescribing [Ansani et al. 2006]. Psychiatrists continue to express unease about the extent of prescribing off-licence in the mental health field and the legal, as well as clinical risk that they expose themselves to [Lowe-Ponsford and Baldwin, 2000]. Furthermore, while it is not considered a Inhibitors,research,lifescience,medical breach of care to prescribe off-licence, if and when that decision is supported by clinical evidence and a broad body of clinical opinion, it is possible to face sanction if a off-label treatment is withheld [Henry, 1999]. In reality, only a small minority are ever involved Inhibitors,research,lifescience,medical in such a grievance [Lowe-Ponsford and Baldwin, 2000]. Safeguards can be implemented to ensure drug accessibility is controlled, and that prescribing remains the prerogative of appropriately

trained clinical practitioners. Medicines prescriber information sheets list patient safety data, while black-box warnings continue to update clinicians when extra vigilance is needed [Stafford, 2008]. In the UK at least there appears to be a confusing range of opinion on what can Inhibitors,research,lifescience,medical be prescribed and for whom, from national medicines information services, expert opinion such as the Maudsley Prescribing Guidelines [Taylor et al. 2012], the MHRA and NICE, to guidance from individual hospitals, NHS trusts and insurance companies [Bücheler et al. 2002]. A framework to protect unlicensed Cabozantinib chemical structure groups Blinded randomised controlled trials remain the highest quality individual study design. They crotamiton provide the most reliable and objective data to support effectiveness, efficacy and safety of innovative treatments, and need to be conducted before regulators award full licensed approval for a medicine. However, change in the current regulatory process is required, to generate greater incentive to conduct new drug research for mental disorders and, to guarantee long-term added efficacy and safety [Segman and Weizman, 2008].

Due to the presence of multiple endogenous transporters, BBB allows a selective entry of nutrients and minerals across it and limits the entry of foreign substances like drugs as well as neuropharmaceutical agents. This makes the CNS treatment ineffective. The conventional drug delivery systems which release the drug into general circulation fail to deliver drugs effectively to brain and are, therefore, not very useful in treating certain diseases that affect CNS including Alzheimer’s disease, dementia, Parkinson’s disease, mood disorders,

AIDS, and viral and bacterial meningitis. Therefore, #check details keyword# there is a need to develop and design approaches which specifically target to brain in a better and effective way [24] (Figure Inhibitors,research,lifescience,medical 2). Figure 2 The antibodies of the immunoliposomes recognise the specific receptor of the BBB releasing the drug of the immunoliposomes only close to the targeting cells. Drug delivery to the brain is hindered by the presence of the CNS barriers. Although the BBB and B-CSFB restrict the passage of many substances, both

are actually selectively permeable to nutrients necessary for healthy brain function. In the last decades, despite the advances in drug discovery, there has been little improvement on the prognosis of patients with brain diseases, like cancer, neurodegenerative diseases, Inhibitors,research,lifescience,medical or neurological disorders. Often, in clinical trials it has been found that promising agents in vitro have little impact on the disease. These disappointing results can be, at least in part, explained by the inability to deliver therapeutic agents to the

brain across CNS barriers avoiding Inhibitors,research,lifescience,medical various resistance mechanisms to reach the desired targets [25]. 3. Liposomes Liposomes have received widespread attention as a carrier system for therapeutically active compounds, due to their unique characteristics such as capability to incorporate hydrophilic and hydrophobic drugs, good compatibility, low toxicity, lack of immune system activation, and targeted delivery of Inhibitors,research,lifescience,medical bioactive compounds to the site of actions [26]. Liposomes are spherical vesicles that resemble cells in that they contain an inner hydrophilic core and a relatively impermeable outer lipophilic phospholipid bilayer [22, Suplatast tosilate 27]. The lipid components of liposomes are predominantly phosphatidylcholine derived from egg or soybean lecithin [28]. Liposomes have been shown to provide stable encapsulation for various drugs and offer distinct advantages over unencapsulated agents; thus, liposomes have been proposed for use in a variety of applications in research, industry, and medicine, particularly for the use as carriers of diagnostic and therapeutic compounds (Figure 1). Liposomes are synthetic lipid spheres composed by fatty acid on polymers with a bilayered membrane structure surrounding an aqueous core that can be used to encapsulate small molecules.

The attenuated HPA axis negative feedback (consequent on attenuated check details cortisol synthesis) after repeated metyrapone administration results in increased levels of ACTH, DHEA and 11-deoxycortisol levels, though with near normal plasma levels of cortisol [Jahn et al. 2004; Otte et al. 2007]. Metyrapone also inhibits 11β-HSD1

and the subsequent unopposed inactivation of cortisol by 11β-HSD2 results in an increase in the plasma cortisone:cortisol plasma ratio. Metyrapone also inhibits the production of aldosterone. Figure 1. Steroid synthesis pathway. Metyrapone acts by blocking the conversion Inhibitors,research,lifescience,medical of 11-deoxycortisol to cortisol by P450c11 (11β hydroxylase). In humans, metyrapone is rapidly absorbed following oral administration. Blood levels peak 1 h after ingestion [eMC, 2010]. It has a half life of 20–26 min. Metyrapone’s main active metabolite –metyrapol – has a half life twice that of the parent compound. Metyrapone is excreted Inhibitors,research,lifescience,medical in the urine as metyrapone or as metyrapol [eMC, 2010]. Metyrapone is used in clinical practise as an aid for the differential diagnosis of ACTH-dependent

Cushing’s syndrome and in the medical management of Cushing’s syndrome and aldosterone-induced oedema. Metyrapone is administered in doses varying from 250 mg to 6 g per day depending on the indication [Joint Formulary Inhibitors,research,lifescience,medical Committee, 2011]. Metyrapone is well tolerated. In a blinded study on patients with TRD, in which metyrapone was used alongside serotonergic antidepressants, only headaches and nausea were reported more frequently by participants in the metyrapone group compared with the placebo group [Jahn Inhibitors,research,lifescience,medical et al. 2004]. Other undesirable effects of metyrapone use include occasional vomiting, dizziness, sedation, hypotension and rarely hypoadrenalism, hirsuitism, allergic skin reactions and abdominal pain [eMC, 2010]. Metyrapone and treatment of treatment-resistant depression There is limited evidence for the use of metyrapone in the treatment of depressive illness. Most of the evidence comes from three sources:

preclinical Inhibitors,research,lifescience,medical studies, where the effect of metyrapone on animal models of depression is examined; studies on patients with Cushing’s syndrome and secondary depressive illness; and clinical studies of the effect of metyrapone in patients with depression. The data from preclinical studies are based on studies of the effect of metyrapone treatment medroxyprogesterone on the behaviour of rat models of depression or on the neurochemistry of the brain of rats. Healy and colleagues compared the effect of metyrapone with that of desipramine and placebo treatment in two rodent models of depression: the olfactory bulbectomized (OB) rat and the forced swim test (FST) [Healy et al. 1999]. In the OB rats, 14-day treatment with metyrapone (50 mg/kg) or desipramine attenuated OB-related hyperactivity.

2010b). Increased activation of CREB in the nucleus accumbens is associated with increased neuronal survival (Mantamadiotis et al. 2002) and has also been associated with reduced anxiety (Barrot et al. 2005). Inhibition of phosphodiesterase E2 (PDE2), which in turn inhibits activity of NADPH oxidase, reduces anxiety

behavior associated with http://www.selleckchem.com/products/Vorinostat-saha.html induced oxidative stress (Masood et al. 2009). Increased hippocampal NADPH oxidase 1 activity appeared to increase anxiety behavior in rats with adjuvant arthritis (Skurlova et al. 2011). Subchronic oxidative stress may mediate anxiety responses through effects on NTs and enzymatic activity. Inhibitors,research,lifescience,medical Subchronic oxidative stress appears to induce downregulation of brain-derived neurotrophic factor (BDNF), glyoxalase 1 (GLO1), and GSR1 (Salim et al. 2011). BDNF is a critical brain NT and also acts as a potential antioxidant mediator (Lee and Son 2009; Chan et al. 2010). Local increases in GLO1 and GSR1 enzyme expression, whose functions include protection against dicarbonylglycation

Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical and production of glycation end products (Hambsch 2011), have previously been associated with increased anxiety-like behaviors (Hovatta et al. 2005). However, Salim et al. (2011) demonstrated that subchronic oxidative stress downregulates GLO1 and GSR1 via induction of calpain expression in the hippocampus, predisposing to increased protein glycation and subsequent further oxidative stress. This increased oxidative stress, in concert with calpain activation (Shumway et al. 1999), is proposed to induce NFĸB transcription, leading to enhanced production of proinflammatory cytokines (IL-1, CRP, TNF-α) and inflammatory-mediated Inhibitors,research,lifescience,medical cellular damage (Salim et al. 2011). The induction of calpain mediated decreased

expression of BDNF (see section Neurotrophins Inhibitors,research,lifescience,medical below) (Salim et al. 2011). Cigarette smoke, a significant source of exogenous free radicals (Stedman 1968), contains thousands of chemicals that increase O&NS, and smokers or those exposed to passive smoke appear to have significantly reduced circulating antioxidants (Sobczak et al. 2004; Swan and Lessov-Schlaggar 2007). Many studies have demonstrated changes consistent with increased O&NS in the brains of animals exposed to cigarette either smoke. Such changes include increased levels of ROS (Luchese et al. 2009) and RNS including superoxide, TBARS, carbonylated proteins (Tuon et al. 2010), measures of lipid peroxidation (Anbarasi et al. 2005a; Stangherlin et al. 2009; Thome et al. 2011), and reduction of antioxidant enzymes (Stangherlin et al. 2009) including SOD (Luchese et al. 2009), catalase (Luchese et al. 2009), glutathione peroxidase, GSR, glutathione, and vitamins (A, C, E) (Anbarasi et al. 2006a). It should be noted that there are some exceptions to this trend (Delibas et al. 2003; Fuller et al. 2010).

15,17 Given the strong representation of synaptic activity in the EEG, the question arises as to whether fMRI signals are related to similar or different aspects of neuronal activity, such as neuronal spiking. In fact, in many experimental situations, synaptic activity is highly correlated with the firing rate of the neuron to which the synapses

under consideration belong. Accordingly, it is not surprising that in many cases the fMRI signal correlates equally well with LFPs and spiking activity. However, in a few studies, there has been successful differentiation Inhibitors,research,lifescience,medical between synaptic activity and spiking activity with regard to the related hemodynamic changes.18 These studies have provided evidence for a much closer relationship between the blood oxygenation level-dependent (BOLD) contrast mechanism Inhibitors,research,lifescience,medical and presynaptic and postsynaptic processing of incoming afferents to a region and only to a lesser degree the activity of its output efferents.19-22 In summary, although obviously very different in terms of the signal that is Inhibitors,research,lifescience,medical actually measured, both EEG and fMRI have a considerable overlap concerning the neuronal activity that they represent, which is mainly synaptic activity. Technique: safety and quality issues From the very early days of simultaneous EEG-fMRI, safety issues have been an important aspect. Radiofrequency-related heating of electrodes or brain tissue has to be

considered, and there are several factors that are relevant such as the scanning sequence, the number of EEG electrodes, or the field strength of the MRI scanner.23 Taking all aspects into account, simultaneous EEG-fMRI recordings have been Inhibitors,research,lifescience,medical safely performed at many different MRI centers, and simultaneous EEG-fMRI is considered as a standard imaging technique. Since simultaneous EEG-fMRI recordings today are typically Inhibitors,research,lifescience,medical performed with commercially Vandetanib manufacturer available MR-compatible EEG equipment, specific safety instructions are provided by the companies. Another issue in simultaneous EEG-fMRI is the quality of the EEG recorded in found the scanner. Here, two main artefacts have to be considered: the cardiac pulse-related

artefact and the image acquisition artefact. For both types of artefacts, today there are post-processing artefact removal strategies available with sufficient efficacy. The pulse-related artefact, which is often also referred to as a ballistocardiogram, or BCG artefact, is complex in its origin with a role of pulsatile movements of scalp vessels on adjacent electrodes and head rotation. Post-processing strategies are based either on waveform removal approaches such as the average artefact subtraction algorithm24 or on pattern removal approaches such as independent component analysis.25 In addition to a priori avoiding of BCG artefacts,26 new strategies include the application of optical motion tracking systems.