.. The pathological mechanisms leading from stable lesions to the formation of vulnerable plaques remain in doubt, and the associated clinical events are unpredictable.12 Several attempts have been made to use imaging techniques such as magnetic resonance imaging (MRI) to monitor the formation and progression of Compound C solubility dmso atherosclerotic plaques in rodents and rabbits.12-14 Skogsberg et al.15 reported that in atherosclerosis-prone

mice with human-like hypercholesterolemia, atherosclerotic lesions initially progressed slowly and then showed a rapid expansion. Subsequent to advanced lesions, a plateau trend existed Inhibitors,research,lifescience,medical in these atherosclerotic mice. Accumulation of lipid-poor macrophages was demonstrated to be associated with the rapid expansion Inhibitors,research,lifescience,medical phase. It is important to mention that the atherosclerotic lesion

is not pathologically homogeneous and atherosclerosis, far from being a linear model, is at times rapid and at others slow.16 The unpredictable and often episodic nature of atherosclerosis progression can be explained by the rapid increase of stenosis Inhibitors,research,lifescience,medical severity due to thrombosis.7 According to our proposed practical classification of atherosclerosis phases, atherosclerosis velocity includes the time-dependent development of the plaque from endothelial injury to acute arterial thrombosis. In terms of the phases of atherosclerosis, there is little information available on the evaluation of the factors that affect the duration of infrastructural and subsequent rupture-induced occlusion separately. If investigators

focus on the concept of “time” for atherosclerosis development, it may result in considerable prevention of cardiovascular events. As a consequence, atherosclerosis-related Inhibitors,research,lifescience,medical morbidity/mortality can be effectively prevented. Inhibitors,research,lifescience,medical Description of Atherosclerosis Velocity Our suggested description of atherosclerosis velocity (v) is described in this section. It is worthy of note that this formula/description is intended, for the time being, only to further clarify the concept of atherosclerosis velocity. Accordingly, it is completely hypothetical and its application should be tested in several animal and human studies. v=(V×I index)÷t V0 (%) is the true percentage of lumen stenosis/ or plaque volume at t0 time. V1 (%) is the true percentage of lumen stenosis/ or plaque volume at t1 time. V (%): V1-V0 t (months): t1-t0 v: atherosclerosis velocity (% or nm Edoxaban / months) The I index represents the instability of a plaque and either can be valued 1 for a plaque that does not experience any clinical acute event during time t or can be valued 2 for a plaque that experiences acute occlusion/ thrombosis. “I” is a parameter that may change during further investigations and new items or new scoring might be added to this parameter. If new imaging methods in the future (e.g.

65, 0.25, 0.6, 0.4, 0.49, 0.83, 0.77, 0.83, respectively, p < 0.05).

Peak TOR was negative correlation with mitral E wave deceleration time (DT), interventricular septum (IVS), LV mass index (LVMI) (-0.31, -0.34, -0.77, respectively, p < 0.05). There was no independent predictor for improvement before kidney transplantation. Fig. 1 Left ventricular rotation pre and post kidney transplantation. A: Left ventricular rotation at apex pre kidney transplantation. B: Left ventricular rotation at base pre kidney transplantation. C: Left ventricular rotation at apex post kidney transplantation. ... Reproducibility The inter observer variability was 0.94 and 0.92 for ROT-API Inhibitors,research,lifescience,medical and ROT-BAS respectively. The intra observer variability was 0.96 and 0.70 for ROT-API and ROT-BAS respectively. Discussion This Inhibitors,research,lifescience,medical study demonstrated that kidney transplantation resulted in improvement of left ventricular structure, function and torsion after 6 months transplantation. To our knowledge, this was the first study to focus on left ventricular torsion pre and post kidney transplantation. This Inhibitors,research,lifescience,medical study showed that conventional

echocardiographic indices of LV function, including LVEF and E/A were improved within 6 months after kidney transplantation. In our study, E/A ratio was significantly increased after kidney transplantation, but E/e’ was not changed significantly. And there was e’ < 0.08 m/s, which indicated left ventricular diastolic dysfunction. Our results were in accordance with prior studies, and indicated the left ventricular diastolic function was improved, but still abnormal. LV structure also showed improvement of interventricular septum thickness and left ventricular mass. In general, correction of the uremic state by Inhibitors,research,lifescience,medical renal transplantation Inhibitors,research,lifescience,medical leads to improvement of LV structure and function. Prior studies, not using VVI technology, demonstrated that there were structural and functional improvements in cardiac indices

post kidney transplantation.15),16) Wali et al.15) reported that kidney transplantation in end stage renal disease patients with very advanced systolic heart failure resulted in an increase in LVEF. Compared to pre kidney transplantation, ROT-BAS, ROT-API, TW and TOR were significantly higher post kidney transplantation, indicating an improvement in overall myocardial mechanical function, but there was no significant difference between absolute value of ROT-BAS and ROT-API. It has been selleck chemicals llc established that in healthy subjects rotation of the LV base is opposite to that of the apex but is significantly lower in its magnitude. In the normal heart, the counterdirectional rotation of the LV apex with respect to the base results in a wringing movement during ejection. The rotation angle increased with distance from base to apex, and subendocardial rotation was found to be higher than subepicardial rotation.

2× buffer 0.2 mM dNTPs, 7.5 mM of each primer, 0.01 mM Hot Start polymerase, and 1.0 mM Syto9 green fluorescent intercalating dye (Invitrogen, Eugene, OR). Amplification conditions were as follow: 95°C for 3 min, 45 cycles of 95°C for 10 sec, 64°C for 30 sec, and 72°C for 10 sec. Methylation status was identified by HRM set from 70°C to 95°C, with the temperature rising by 0.2°C per second. BDNF G196A polymorphism (rs6265) was genotyped by PCR followed by restriction enzyme Inhibitors,research,lifescience,medical digestion. A 133-bp segment was amplified by PCR on a 96-well plate thermal cycler (Biometra). The following primers were used:

F 5′-GAGGCTTGACATCATTGGCT-3′ type forward and 5′-CGTGTACAAGTCTGCGTCCT-3′ type reverse. Target sequences were amplified in a 25-μl reaction mix containing 100 ng of genomic DNA, 1U

Taq polymerase (Eurobio), 1.5 mM MgCl2, 200 nM dNTP, and 10 pmol Inhibitors,research,lifescience,medical of each primer. Amplification conditions were as follows: 95°C for 5 min, 30 cycles of 94°C for 30 sec, 54°C for 30 sec, and 72°C for 30 sec. PCR products were then digested overnight with 4 U of Eco72I (MBI Fermentas Inc., Glen Burne, MD). Then fragments were separated on a 10% polyacrylamide gel at 250 V and visualized with ethidium bromide. Inhibitors,research,lifescience,medical The A-allele undigested product size was 113 bp (A-allele) and the G-allele showed two fragments of 78 and 35 bp. Statistics SNPs with Hardy–Weinberg equilibrium below 0.001 in either cases or controls were excluded from analysis. Haplotype analyses were performed using logistic regression. All rare haplotypes with frequencies below 1% in both patients and controls were excluded from analyses. Interaction test Inhibitors,research,lifescience,medical and omnibus tests, which assessed global differences in haplotype distribution between SZ and controls, Inhibitors,research,lifescience,medical BD and controls, and SZ + BD and controls, were initially conducted. If significant (below P-value of 0.05), we then used a sliding window procedure to extract the core haplotype associated

with the diseases. Since we compared genotypic and allelic distributions of four polymorphic markers between controls and three case populations (BP, SZ, and the others sum of the two populations), a correction for multiple testing was required. Two approaches were applied to correct for multiple non-independent comparisons. First, we used the highly conservative Bonferroni correction taking into account the non-independence of tests. We effectively tested four independent polymorphisms, as linkage disequilibrium (LD) between polymorphisms within the same gene was not so BIBF 1120 ic50 strong. Two independent tests were considered for the different case populations as the sum of both of them would be closely related to the two case populations taken separately and because only significant results obtained in the whole population would be looked at in the two subpopulations.

Almost

90% of sponge’s species in the world are from Demospongiae class. Here in our sampling area we got 100% of Demospongian classes which divided into 5 orders of Haplosclereida (inhibitors specimen number 1, 4, 18), Dictyocertida (specimen number 2, 3), Handromerida (specimen number 15). The species of our haplosclereida referred to specimen 1 Xestospongia testudinaria, specimen 4 Callyspongia schulzei, specimen 6 Petrosia contignata, specimen 18 Xestopongi aexigua. Our specimen in group Dictyoceratida consisted of specimen 2 (Fascaplysinopsis reticulata). http://www.selleckchem.com/Proteasome.html On the Handromerida orders, only consist of specimen no 15, Aaptos aaptos ( Table 1). The result on our species diversity corresponded with the de Vogd & Clearly 2008 that Aaptos

suberitoides, 8Clathria (Thalysias) reinwardti, Petrosia (Petrosia) nigricans and Xestospongia testudinaria were the most common species in Jakarta bay Indonesia. 9 Antioxidant assay using DPPH method found that only Aaptos suberitoides that had been identified to show strong activity due to IC50 value of <30 μg/mL; meanwhile Fascaplysinopsis reticulata, Acanthella sp, Petrosia contignata and Xestospongia exigua showed moderate antioxidant activity with a IC50 < 100 μg/mL. Xestospongia sp, Callyspongia sp showed a value of IC50 > 100 μg/mL ( Table 2). However, the study was limited to testing coarse extracts; thus, there is a possibility that the pure compounds contained in the extracts have a stronger free-radical muffling activity compared to the extracts themselves. DPPH method was selected since Anticancer Compound Library chemical structure it is simple, fast, responsive, and requires fewer samples. The sponge extraction only recruited minimal 100 g weight yield. Therefore among 20 specimens, only

11 specimens fulfilled the minimal weight. Moreover, 11 crude extracts sponges were tested its toxicity with BST test which are the prescreening process for anticancer drug candidate. The probity analysis for LC50 value among sponge species ranged 61.28 ± 8.61–574.58 ± 29.36. Therefore all of those extracts had high toxicity ( Table 3). The A. salina bioassay developed is a useful tool for preliminary biological and pharmacological activity analysis. A. salina is an organism occurring in brackish and marine waters, adaptable to large ranges of salinity (5–250 g L−1) and temperature (6–35 °C).Moreover, this organism is vital to the pelagic ecology of a coastal ecosystem (estuaries, bays, harbors and other near-shore environments). Although it is still considered the basic screening test for cyanobacteria from coastal environments, other sensitive and more specific screening bioassays have been applied, specifically the ones using embryos of invertebrates, viruses and cell lines. As shown in Table 4 the extracts from species number 15, A. suberitoides has the highest toxicity compare to another species which valued level on tumor cell lines (HT-29, T47D and Casky).

62 Risk of Apoptosis Compound Library supplier complications and mortality Multiple large epidemiologic studies have examined whether comorbid depression in patients with CHD or diabetes increases risk of mortality. A recent meta-analysis found 22 papers that examined the association of depression with cardiovascular outcomes of patients experiencing a recent myocardial infarction (MI), defined as mortality or cardiovascular events occurring within 2 years of index MI.64 Comorbid depression was associated with an approximate 2.4-fold increase in allcause mortality, a 2.6-fold increase

in cardiovascularrelated mortality, and an almost 2.0-fold increase Inhibitors,research,lifescience,medical in new cardiovascular events.64 Depression has also been found across multiple studies to be a significant predictor of mortality and cardiac events in patients undergoing coronary artery bypass surgery,65-67 as well Inhibitors,research,lifescience,medical as those with congestive heart failure.68 Six prospective epidemiologic studies have shown that after controlling for sociodemographic factors and clinical severity of illness, comorbid depression in patients

Inhibitors,research,lifescience,medical with diabetes compared with those with diabetes alone was associated with a 33% to 52% increase in risk of allcause mortality.69-74 One recent study of over 4000 patients with diabetes examined specific causes of mortality associated with depression documented with both state mortality data and careful chart review. Comorbid depression Inhibitors,research,lifescience,medical was associated with an approximately 50% increase in risk of all-cause morbidity, and an over twofold risk of noncancer and nonatherosclerotic associated mortality.69 A large prospective study of an aging Hispanic population found that both depression and diabetes were independently associated with

an increased risk of all-cause mortality, and when combined they had a greater than additive effect on mortality.72 Thus, lifetime depression was associated with a 1.64 (95% CI 1.17-2.28) and diabetes a 1.51 (95% CI 1.23, Inhibitors,research,lifescience,medical 1.86) hazard ratio for allcause mortality respectively, compared with those without history of depression or diabetes.72 Patients with comorbid lifetime depression and diabetes had a hazard ratio of 4.59 (95% CI 2.12, 9.93) of all-cause mortality compared with controls without history of diabetes or depression.72 3-mercaptopyruvate sulfurtransferase In another study that followed over 10 000 participants for 8 years, compared with those without diabetes or depression, those with depression but no diabetes had a 1.20 (95% CI 1.03, 1.40) increase in all-cause mortality, those with diabetes but no depression had a 1.88 (95% CI 1.55, 2.27) increase, and those with both depression and diabetes a 2.50 (95% CI 2.04, 3.08) increase in all-cause mortality73 In patients with diabetes, recent prospective studies have examined the association of depression with subsequent development of macrovascular and microvascular complications.

Although much research into the etiology of PD has taken place, this has very largely focused on the role of mutant proteins in familial PD. Fourteen or more genetic loci have been identified and the pathophysiological action of mutant proteins encoded by genes in these loci are being elucidated. Nevertheless, the contribution of genetic mutation to the overall burden of PD is very small. The most optimistic estimates that are around 5–10% of all PD cases are due to such mutations. Of the remaining 90–95%, arguments have been made to show that environmental factors such as pesticide exposure are involved. This may be the case in a certain number of #selleck kinase inhibitor keyword# instances. Nonetheless, whether

a combination of a genetic susceptibility and toxin exposure accounts for the majority of cases of sporadic PD remains unclear. If these two factors are not the cause, it would be logical Inhibitors,research,lifescience,medical to look at the physiology of the brain itself. The hypothesis put forward by Surmeier and colleagues uses this as a basis (Guzman et al. 2009, 2010). They have pointed out that dopaminergic neurons of the substantia nigra have a relatively rare Inhibitors,research,lifescience,medical mechanism of autonomous pacemaking. During pacemaking in these neurons, calcium entry occurs via L-type Ca2+ channels with a Cav1.3 pore-forming subunit. They proposed

that the relatively open nature of these channels allows greater calcium entry, which in turn incurs a high metabolic cost in terms of ATP Inhibitors,research,lifescience,medical to maintain tight control of intracellular calcium by the endoplasmic reticulum and the mitochondria. The high ATP requirement, which has to be met by mitochondrial synthesis, results in greater Inhibitors,research,lifescience,medical ROS production that ultimately overwhelms neuronal antioxidant defenses and leads to cell death. Whether the complete

scenario envisaged by Surmeier et al. (2011) is correct awaits further substantiation. Nonetheless, there is long-established evidence for the role of calcium in the control of mitochondrial substrate oxidation (Hansford and Zorov 1998) and in neuronal cell death (Stout et al. 1998). This evidence has led to the possible involvement of UCPs, and UCP4 in particular. Chan et al. (2006), using PC-12 cell clones which either express UCP4 or not, have shown that UCP4 is a potent influence on store-operated calcium entry and secondly on mitochondrial sequestration of calcium (Chan et al. 2006). They proposed that prevention of calcium overload by UCP4 inhibition of store-operated calcium channels, with consequent reduction in oxidative stress, reduces the likelihood of calcium-primed cell death. Furthermore, in a DJ-1 knockout mouse model, the expression of both UCP4 and UCP5 was downregulated and DJ-1 modulated the magnitude of the response of these two UCPs to oxidative stress (Guzman et al. 2010).

However, tasks which aim at the examination of the selleck inhibitor resistance of a stress responsive physiological system under the influence of long-term or superimposed challenges, pharmacological treatment, or coexisting pathology, are by far more demanding. In such cases, careful evaluation of the condition and response capacity of the targeted system, alterations in its basal function resulting from Inhibitors,research,lifescience,medical each individual influence, and the time course of response must be added to the former requirements. End points for assessment

of the response to stress Stress induces mobilization of a broad array of reactions which involve virtually every physiological system, albeit with different time courses. Accordingly, numerous parameters can be used for response monitoring in models of stress, under the provision that their temporal profiles and the changes possibly occurring in the course of habituation/sensitization are sufficiently defined. Behavioral end points The original description of the response to stress as a “fight-or-flight” reaction and evidence Inhibitors,research,lifescience,medical that arousal activation is invariably associated with this response implies that observation of general behavior can reliably disclose symptoms of stress. Assessment of the explorative activity Inhibitors,research,lifescience,medical by means of well established quantifiable parameters is a frequently used behavioral descriptor of

the response to stress in laboratory rodents.6 As in most species exposure Inhibitors,research,lifescience,medical to novelty is a stressor perse, monitoring of stressinduced effects in this experimental condition should be preceded by careful baseline definition. Although outcome may vary depending on the characteristics and duration of the challenge, decreased exploratory activity is considered to be a reliable behavioral consequence of stress exposure. In its extreme expression, this response is described as “freezing,” a period of time during which Inhibitors,research,lifescience,medical locomotion and

exploration are completely abolished. The freezing response is reproducibly evoked in several stress paradigms, and protocols for its quantification have been developed.7 Behavioral deficits known as acquired immobility, behavioral despair, and learned helplessness can be viewed as alterations specifically associated with severe stress; however, a learning component has a leading role in the manifestation of these phenomena. Behavioral responses to stress are frequently Tryptophan synthase linked with anxiety, and there is a substantial overlap of neurochemical mechanisms activated by stressful challenges and those involved in the control of anxiety. Evaluation of anxiety belongs to the standard arsenal for the assessment of behavioral effects of stress, and offers a direct possibility to disclose stress-associated neuropathological consequences. Since habituation may rapidly occur in some experimental paradigms used for evaluation of anxiety,6 caution applies to their repeated use for the examination of long-term effects.

A predominant symptom is defined as the symptom with the highest ranking and all other symptoms are>=2 / 10 lower ranked. Complexity is defined as>=3 symptoms with>=6/10, with the exception of fatigue and anorexia (threshold>=9/10). To explore patients’ subjective adaptation to illness and burden of treatment two linear analogue self-assessment (LASA) indicators are included, assessing perceived adjustment to chronic illness (PACIS); [34] (‘no effort at all’ – ‘a great deal of effort) and overall treatment burden (‘not at all’ – ’severely’). The indicator for PACIS was confirmed to be responsive to cytotoxic side-effects, mental distress, and psychosocial dysfunction in patients with

Inhibitors,research,lifescience,medical early breast cancer [36]. It is suitable to describe patients’ adaptation over time. The IWR-1 purchase instruments are validated [37]. The indicator for overall treatment burden has been validated regarding side-effects of antiemetic and cytotoxic

therapy [38]. As indicator for decision-making preferences, the difference in number of mismatched decision-making preferences Inhibitors,research,lifescience,medical between week 3 and 6 will be compared between the two arms. Patients’ preferences for involvement in decision making will be assessed by a Inhibitors,research,lifescience,medical measure adapted from previous studies [39]. The patient chooses from among five categories ranging from ‘the doctor should make the decision using all that he/she knows about the treatment’ to ‘I should make the decision using all that I know and learn about the treatment’. In addition the physician Inhibitors,research,lifescience,medical is asked to choose from among the same five categories how he/she estimates the patients’ preferences. A mismatch is defined as follows: the patient ranks #1 or #2 and the physician #4 or #5 or vice versa. For neutral patients or physicians no mismatch is possible per definition. Sample size calculation Sample sizes are calculated for an inequality test for two means of change in QoL in a cluster randomized design using the software package

NCSS 2004 – PASS 2002, according to the formulation of Donner and Klar, assuming a two-sided Inhibitors,research,lifescience,medical significance level of 0.05, and a statistical power of 0.8 [40]. Further assumptions on design parameters are an overall variance (s2) of 400, an intracluster correlation coefficient (ICC, estimated by the ratio of between-cluster variation to overall variance) of 0.05 , an effect size (between-arm difference in G-QoL to be detected) of 10, and the cluster size (the number of evaluable patients per physician) [40]. For the cluster size several options are considered, but it is expected to stop these the trial at a cluster size of 8 with 12 physicians per arm, yielding a total sample size of 192 evaluable patients. Since the initial estimate of the ICC might not be appropriate, an interim analysis to adjust the sample size as suggested in Lake et al. is foreseen [41]. Once data for the first 100 patients are available, estimates of within-cluster variation and between-cluster variation are obtained. If the resulting ICC has to be at least 1.

56 The finding of increased platelet activation may partially contribute to increased CV risk in those already with pre-existing risk factors. Circulating activated platelets play an important role in thrombosis57 and most, but not all, acute coronary occlusions occur as the result of rupture of an unstable atherosclerotic plaque and superimposed thrombus formation58 Inhibitors,research,lifescience,medical As such, one approach to cardiovascular prevention

for those at increased risk in bereavement could be short-term use of Nutlin-3a mw antithrombotic medications, such as aspirin, in the early weeks of bereavement, as has been previously proposed for other transient periods of increased risk.49 The effect of bereavement interventions on physiological correlates Neuroendocrine Specific interventions designed to reduce cortisol response in bereavement have not been reported, although a randomized controlled clinical Inhibitors,research,lifescience,medical trial that examined the effect of support group sessions on immune response reported significantly lower plasma cortisol levels in the intervention group compared with the control group Inhibitors,research,lifescience,medical following 10 weekly 90-minute support group sessions.59

In this study, a reduction in physician visits was also reported in the intervention group,59 although it is unclear which aspect of the intervention contributed to these findings. Sleep To date two intervention approaches to improve sleep in CG have been reported; one a nonpharmacological approach and the other using a tricyclic antidepressant medication. Inhibitors,research,lifescience,medical Findings from one study suggest that a 16-week Complicated Grief Treatment (CGT) intervention has the potential to improve sleep, albeit modestly, in individuals suffering CG.60 In this study of 67

bereaved individuals with elevated scores greater than or equal to 30 on the Inventory of Complicated Grief,61 suggestive of intense grief reactions, Inhibitors,research,lifescience,medical subjects who were randomized to receive the CGT intervention reported lowered grief scores although scores remained elevated in participants after treatment, and they continued to experience clinically significant sleep problems.61 The potential CYTH4 effectiveness of cognitive behavioral therapy was highlighted in another study of 11 recently bereaved family members.62 In this study, the intervention consisted of cognitive behavioral therapy-insomnia (CBT-I) which included educational information about cognitive restructuring, stimulus control, sleep hygiene, relaxation techniques and goal setting, and monitoring. Self-reported sleep measures and depression scores decreased over the 5-week intervention period, although sleep actigraphy data (that provide limited measures of sleep patterns and circadian rhythms) showed no significant changes over the study period.

86 to 0.93) using goniometers. In contrast, Bovens et al (1990) reported poor reliability for measurements by physicians of physiological wrist extension using vision. Reliability for measuring physiological thumb abduction was reported to be higher using a pollexograph (ICC 0.59, 95% CI 0.42 to 0.89) than a goniometer (ICC 0.37, 95% CI –0.42 to 0.79). Finally, measuring accessory movements of carpal bones against the capitate bone using a 3-point scale yielded fair to moderate

reliability (weighted Kappa from 0.29 to 0.42) in healthy individuals and fair to almost perfect reliability (weighted Kappa from 0.33 to 0.87) in post-operative patients ( Staes et al 2009). This systematic review included 21 studies investigating inter-rater reliability selleck compound of measurements of passive movements of upper extremity joints, of which 11 demonstrated acceptable reliability (ICC > 0.75). Reliability varied considerably with the method of measurement and ICC ranged

from 0.26 (95% CI –0.01 to 0.69) for measuring the physiological range of shoulder internal rotation using vision to 0.99 (95% CI 0.98 to 1.0) for the physiological range of finger and thumb flexion/extension using a goniometer. In general, measurements of physiological range of motion using instruments were more reliable than measurements using vision. Furthermore, measurements of physiological range of motion were also more reliable than measurements of end-feel or of accessory range Bafilomycin A1 cost of motion. Overall, methodological quality of included studies was poor, although two high-quality studies reported almost perfect reliability (Glasgow et al 2003, Nomden et al 2009). In general, already reliability for measurements of passive movements of upper extremity joints were substantially higher than for measurements of passive

segmental intervertebral and sacroiliac joints which rarely exceed Kappa 0.40 (Van Trijffel et al 2005, Van der Wurff et al 2000). Seffinger et al (2004) attributed these differences in reliability to differences in size of joints. We think, however, that differences may be more linked to a joint’s potential physiological range of motion. For instance, measurement of large joints with limited range such as the sacroiliac joint is associated with poor reliability, whereas measurement of small joints with greater range, such as the atlantoaxial spinal Libraries segment and finger joints, has been shown to be reliable (Cleland et al 2006, Glasgow et al 2003, Ogince et al 2007, Van der Wurff et al 2000). We also found that measuring large physiological ranges of motion, like that in the shoulder and in the wrist, frequently yielded satisfactory levels of reliability and note that these levels were predominantly as a result of using goniometers or inclinometers.