, a runner who demonstrates considerably less than 45?of knee flexion may

, a runner who demonstrates considerably less than 45?of knee MG-132 structure flexion may suggest reduced shock absorption, and intervention may be TF14016 molecular weight warranted. Some data exist suggesting that lower knee flexion (<40? may be associated with certain subgroups of patients with patellofemoral pain.22 Knee stiffness, a variable that includes both reduced knee flexion and/or increased knee flexion moment during stance phase, may be associated with tibial stress fractures.23 Hip Extension During Late Stance Reduced hip extension during late stance is a common observation in the recreational runner (Fig. 6). It is traditionally believed that lack of hip extension may be associated with reduced flexibility of the iliopsoas muscle. However, the optimal amount of hip extension during running remains elusive. It is possible that the required amount of hip extension is not the same for each runner, but related to other characteristics of their running form. For example, a fairly slow runner may have a very compact stride, demonstrate approximately 10?of peakAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptPhys Med Rehabil Clin N Am. Author manuscript; available in PMC 2016 February 01.SouzaPagehip extension and not require any intervention. However, a different runner, with a long stride and perhaps a faster pace, may also have approximately 10?of hip extension, but also concurrently demonstrate a significant overstride pattern (landing with the foot out in front of the center of mass) with higher impact loading and braking forces. The latter runner may require stride modification or improved hip extension during running to modify these forces that could contribute to injury. Commonly observed compensations for persons with reduced hip extension include (1) increased lumbar spine extension, (2) bounding, a strategy to increase float time to increase overall stride length in the absence of adequate hip extension, (3) increased overstriding, including excessive reaching during initial contact as a strategy to increase stride length, and (4) increased cadence to increase running speed in the presence of a limited hip extension. Trunk LeanAuthor Manuscript Author Manuscript Author ManuscriptOverstridingTrunk lean is a variable that has received little attention in the scientific literature. However, this is not the case in the popular running non eer-reviewed literature. Many running styles, including ChiRunning, pose running, and even barefoot running have included cues for novice runners to increase trunk lean. A focus on leaning “from the ankles,” rather than increasing hip flexion to achieve the trunk lean, seems to be a priority for some styles. Many running experts suggest that trunk lean is a key component to correct running posture. However, very little has been done on the research side of this issue. A recent article by Teng and Powers24 demonstrated that a small increase in trunk lean ( 7? resulted in a significant lowering of the stress across the patellofemoral joint without a significant increase in ankle demand, suggesting that this strategy may be important for runners with patellofemoral pain. The overall findings were that reduced trunk flexion (more upright posture) was associated with greater knee loads. In contrast, increased trunk flexion shifted demand away from the knee joint, and to the hip and ankle (although the latter was not statistically higher).25 However, the authors warn that this study was performed in healthy subj., a runner who demonstrates considerably less than 45?of knee flexion may suggest reduced shock absorption, and intervention may be warranted. Some data exist suggesting that lower knee flexion (<40? may be associated with certain subgroups of patients with patellofemoral pain.22 Knee stiffness, a variable that includes both reduced knee flexion and/or increased knee flexion moment during stance phase, may be associated with tibial stress fractures.23 Hip Extension During Late Stance Reduced hip extension during late stance is a common observation in the recreational runner (Fig. 6). It is traditionally believed that lack of hip extension may be associated with reduced flexibility of the iliopsoas muscle. However, the optimal amount of hip extension during running remains elusive. It is possible that the required amount of hip extension is not the same for each runner, but related to other characteristics of their running form. For example, a fairly slow runner may have a very compact stride, demonstrate approximately 10?of peakAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptPhys Med Rehabil Clin N Am. Author manuscript; available in PMC 2016 February 01.SouzaPagehip extension and not require any intervention. However, a different runner, with a long stride and perhaps a faster pace, may also have approximately 10?of hip extension, but also concurrently demonstrate a significant overstride pattern (landing with the foot out in front of the center of mass) with higher impact loading and braking forces. The latter runner may require stride modification or improved hip extension during running to modify these forces that could contribute to injury. Commonly observed compensations for persons with reduced hip extension include (1) increased lumbar spine extension, (2) bounding, a strategy to increase float time to increase overall stride length in the absence of adequate hip extension, (3) increased overstriding, including excessive reaching during initial contact as a strategy to increase stride length, and (4) increased cadence to increase running speed in the presence of a limited hip extension. Trunk LeanAuthor Manuscript Author Manuscript Author ManuscriptOverstridingTrunk lean is a variable that has received little attention in the scientific literature. However, this is not the case in the popular running non eer-reviewed literature. Many running styles, including ChiRunning, pose running, and even barefoot running have included cues for novice runners to increase trunk lean. A focus on leaning “from the ankles,” rather than increasing hip flexion to achieve the trunk lean, seems to be a priority for some styles. Many running experts suggest that trunk lean is a key component to correct running posture. However, very little has been done on the research side of this issue. A recent article by Teng and Powers24 demonstrated that a small increase in trunk lean ( 7? resulted in a significant lowering of the stress across the patellofemoral joint without a significant increase in ankle demand, suggesting that this strategy may be important for runners with patellofemoral pain. The overall findings were that reduced trunk flexion (more upright posture) was associated with greater knee loads. In contrast, increased trunk flexion shifted demand away from the knee joint, and to the hip and ankle (although the latter was not statistically higher).25 However, the authors warn that this study was performed in healthy subj.

Ampal CA1 subfield in individuals with MCI compared to NCI (Fig.

Ampal CA1 subfield in individuals with MCI compared to NCI (Fig. 4), which correlated with the subject’s Mini-Mental State Exam score (MMSE), but not with NFT Braak stage or apolipoprotein E (ApoE) status, a genetic risk factor for AD (Scheff et al., 2006). Unlike the outer molecular layer, CA1 receives input from the Schaffer collaterals arising from CA3 and not from the glutamatergic neurons of the entorhinal cortex, suggesting differential responses to synapse loss within the hippocampus based upon afferent innervation or chemical phenotype, some of which precipitate synaptic reorganization. A recent report characterized changes in the dendritic branching of the basilar tree of hippocampal CA1 pyramidal neurons. In this study, formalin-fixed tissue autopsy obtained from University of Kentucky Alzheimer’s Disease Center who died with a clinical diagnosis of NCI, MCI or AD was prepared for Golgi impregnation (Fig. 5). Camera lucida drawings of the basilar tree of randomly selected CA1 neurons were analyzed for alterations in dendritic arbor amount, distribution and complexity (Mervis et al., 2013). Quantitation showed a significant increase in dendritic length (18 ) and complexity (23 ) in CA1 neurons in MCI compared to NCI. Conversely, there was a significant reduction in branch length (-39 ) and arbor complexity (-25 ) during the progression from MCI to AD (Fig. 5). These findings suggest that the observed increase in CA1 dendritic parameters from NCI to MCI may be another example of a neuroplastic Avermectin B1aMedChemExpress Abamectin B1a compensatory response to a loss of afferent input early in the order Aviptadil course of the disease, which is not maintained as the disease progresses. The role that the reported reduction in total synapse number plays in CA1 neuroplasticity remains unknown. However, these examples of early CA1 neural reorganization may represent a viable window for potential therapeutic strategies aimed at restoring or maintaining hippocampal function during the transition from MCI to AD. Future studies should determine whether alterations in specific synapse subtypes (i.e., perforated vs. non-perforated) are differentially affected and their relation to cognitive decline and brain pathology during the onset of AD. Interestingly, the size of the synaptic contacts was found to be substantially larger in AD cortex compared to non-demented aged controls (Scheff et al., 1990), which was suggested to be part of a compensatory mechanism found in regions of the neocortex and hippocampus (see review Scheff and Price, 2006). These investigators found that as the number of synapses declined in a given region, the size of the residualAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptNeuroscience. Author manuscript; available in PMC 2016 September 12.Mufson et al.Pagesynapses increased. This synaptic compensatory response was also observed early in the course of the AD (DeKosky and Scheff, 1990). Neuronal structural alterations may not be the only factor(s) contributing to cognitive decline and hippocampal plasticity in MCI. For example, studies have reported significant reductions in synaptic vesicle trafficking-related genes in the AD brain, which interrupt the efficacy of normal synaptic transmission (Yao et al., 2003; Murphy et al., 2003; Kennedy et al., 2005). Counts et al. (2014) examined progressive changes in the expression classes of synaptic gene within single CA1 neurons in subjects who died with a clinical diagnosis of NCI, MCI or moderate AD obtain.Ampal CA1 subfield in individuals with MCI compared to NCI (Fig. 4), which correlated with the subject’s Mini-Mental State Exam score (MMSE), but not with NFT Braak stage or apolipoprotein E (ApoE) status, a genetic risk factor for AD (Scheff et al., 2006). Unlike the outer molecular layer, CA1 receives input from the Schaffer collaterals arising from CA3 and not from the glutamatergic neurons of the entorhinal cortex, suggesting differential responses to synapse loss within the hippocampus based upon afferent innervation or chemical phenotype, some of which precipitate synaptic reorganization. A recent report characterized changes in the dendritic branching of the basilar tree of hippocampal CA1 pyramidal neurons. In this study, formalin-fixed tissue autopsy obtained from University of Kentucky Alzheimer’s Disease Center who died with a clinical diagnosis of NCI, MCI or AD was prepared for Golgi impregnation (Fig. 5). Camera lucida drawings of the basilar tree of randomly selected CA1 neurons were analyzed for alterations in dendritic arbor amount, distribution and complexity (Mervis et al., 2013). Quantitation showed a significant increase in dendritic length (18 ) and complexity (23 ) in CA1 neurons in MCI compared to NCI. Conversely, there was a significant reduction in branch length (-39 ) and arbor complexity (-25 ) during the progression from MCI to AD (Fig. 5). These findings suggest that the observed increase in CA1 dendritic parameters from NCI to MCI may be another example of a neuroplastic compensatory response to a loss of afferent input early in the course of the disease, which is not maintained as the disease progresses. The role that the reported reduction in total synapse number plays in CA1 neuroplasticity remains unknown. However, these examples of early CA1 neural reorganization may represent a viable window for potential therapeutic strategies aimed at restoring or maintaining hippocampal function during the transition from MCI to AD. Future studies should determine whether alterations in specific synapse subtypes (i.e., perforated vs. non-perforated) are differentially affected and their relation to cognitive decline and brain pathology during the onset of AD. Interestingly, the size of the synaptic contacts was found to be substantially larger in AD cortex compared to non-demented aged controls (Scheff et al., 1990), which was suggested to be part of a compensatory mechanism found in regions of the neocortex and hippocampus (see review Scheff and Price, 2006). These investigators found that as the number of synapses declined in a given region, the size of the residualAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptNeuroscience. Author manuscript; available in PMC 2016 September 12.Mufson et al.Pagesynapses increased. This synaptic compensatory response was also observed early in the course of the AD (DeKosky and Scheff, 1990). Neuronal structural alterations may not be the only factor(s) contributing to cognitive decline and hippocampal plasticity in MCI. For example, studies have reported significant reductions in synaptic vesicle trafficking-related genes in the AD brain, which interrupt the efficacy of normal synaptic transmission (Yao et al., 2003; Murphy et al., 2003; Kennedy et al., 2005). Counts et al. (2014) examined progressive changes in the expression classes of synaptic gene within single CA1 neurons in subjects who died with a clinical diagnosis of NCI, MCI or moderate AD obtain.

, 18th and 19th of August, respectively) and affected nearly all HCWs

, 18th and 19th of August, respectively) and affected nearly all HCWs categories (buy N-hexanoic-Try-Ile-(6)-amino hexanoic amide figure 2),working areas (figure 3), and type of indication (data not shown).These evaluations coincided with the statutory lay-off proceeding that took place in our Center at that time. Statistical control related to “bimonthly AHRs consumption process” is shown in figure 4. From July 2008 until DecemberPLOS ONE | www.plosone.orgHospital Wide Hand Hygiene InterventionTable 3. Main epidemiological characteristics of the two Intervention phases.Variable Hand rub alcohol dispensers/beds (ratio) Direct observation sessions performed *(n) Opportunities for HH by session (median, IQR) Overall time observation (hours) Hand hygiene performance ( ) Alcohol Soap Alcohol Soap Not performed (not wearing gloves) Not performed (wearing gloves) HCWs observed by session (average, SD) Nurses Assistant Nurses Physicians Others Hand hygiene opportunities/hour Nurses Assistant Nurses Physicians Others HH adherence by HCW subcategories Nursing Nursing Staff N Compliance, (95 CI) Student nurses N Compliance, (95 CI) Nursing assistants Nursing assistants staff N Compliance, (95 CI) Student nursing assistants N Compliance, (95 CI) Physicians Clinicians N Compliance, (95 CI) Surgeons N Compliance, (95 CI) Medicine students N Compliance, (95 CI) Others Orderlies N Compliance, (95 CI)T1 (January 2010 ecember 2010) 0.57 (123/217) 277 14 (8?1) 138.T2 (January 2011 ecember 2011) 1.56 (340/217) 542 13 (9?9)70.8 8.3 0.5 14.2 6.76.2 7.8 0.6 11.6 3.1.94 (0.9) 1.73 (1.1) 1.02 (1.1) 0.61 (0.9)1.87 (0.9) 1.73 (0.9) 0.97 (1.1) 0.52 (0.8)13.9 10.1 4.77 2.13.9 9.8 4.14 1.1,803 83 (81.3?4.8)3,347 88 (87.5?9.6)127 96 (92.6?9.4)425 91.5 (88.9?4.2)1,062 89 (87.3?1.1)2,006 91(89.9?2.4)100 95 (90.7?9.3)188 92 (88.2?5.6)374 72 (67.9?6.9)625 69 (65.8?3.1)252 37 (30.9?2.9)343 46 (40.1?1.1)30 93 (84.4?9.9)141 84 (77.6?9.8)226 65 (58.8?1.3)317 72 (66.7?6.6)PLOS ONE | www.plosone.orgHospital Wide Hand Hygiene InterventionTable 3. Cont.Variable Laboratory technicians N Compliance, (95 CI) Radiology technicians N Compliance, (95 CI)T1 (January 2010 ecember 2010)T2 (January 2011 ecember 2011)50 74 (61.8?6.2)129 69 (61.1?6.9)65 21 (11.5?1.5)84 75 (65.7?4.3)*All wards were monitored the same day for a 30 minute session except for Intensive Care Unit and Emergency Department where two different observations by two different hand hygiene monitor team (HHMT) members were planned. doi:10.1371/journal.pone.0047200.t2011, a 172 increase in the expenditure was noted achieving levels above 22 L/1,000 patient-days during 2011. Negative and positive special causes were noted in the 2008?009 period and their probable aetiologies are shown. At the end of 2010 and 2011, numerous “positive special causes” were noted and a clear change of the process of “AHR consumption” was achieved. Time series analysis of “healthcare-acquired MRSA colonization/infections rates” process during the 2007?011 period is illustrated through a Poisson Exponential Weighted Moving Average (PEWMA) control chart (see figure 5). This chart shows a low PNB-0408 price incidence rate over time (median of 0.77 per 10,000 patientdays) achieving a small but significant decrease in healthcareacquired MRSA colonization/infections rates during the intervention period according to the rule that at least 10 out of 11 consecutive data points fall in zone C or beyond on the same side of the center line (referred as rule 4 in Figure 5). Dur., 18th and 19th of August, respectively) and affected nearly all HCWs categories (figure 2),working areas (figure 3), and type of indication (data not shown).These evaluations coincided with the statutory lay-off proceeding that took place in our Center at that time. Statistical control related to “bimonthly AHRs consumption process” is shown in figure 4. From July 2008 until DecemberPLOS ONE | www.plosone.orgHospital Wide Hand Hygiene InterventionTable 3. Main epidemiological characteristics of the two Intervention phases.Variable Hand rub alcohol dispensers/beds (ratio) Direct observation sessions performed *(n) Opportunities for HH by session (median, IQR) Overall time observation (hours) Hand hygiene performance ( ) Alcohol Soap Alcohol Soap Not performed (not wearing gloves) Not performed (wearing gloves) HCWs observed by session (average, SD) Nurses Assistant Nurses Physicians Others Hand hygiene opportunities/hour Nurses Assistant Nurses Physicians Others HH adherence by HCW subcategories Nursing Nursing Staff N Compliance, (95 CI) Student nurses N Compliance, (95 CI) Nursing assistants Nursing assistants staff N Compliance, (95 CI) Student nursing assistants N Compliance, (95 CI) Physicians Clinicians N Compliance, (95 CI) Surgeons N Compliance, (95 CI) Medicine students N Compliance, (95 CI) Others Orderlies N Compliance, (95 CI)T1 (January 2010 ecember 2010) 0.57 (123/217) 277 14 (8?1) 138.T2 (January 2011 ecember 2011) 1.56 (340/217) 542 13 (9?9)70.8 8.3 0.5 14.2 6.76.2 7.8 0.6 11.6 3.1.94 (0.9) 1.73 (1.1) 1.02 (1.1) 0.61 (0.9)1.87 (0.9) 1.73 (0.9) 0.97 (1.1) 0.52 (0.8)13.9 10.1 4.77 2.13.9 9.8 4.14 1.1,803 83 (81.3?4.8)3,347 88 (87.5?9.6)127 96 (92.6?9.4)425 91.5 (88.9?4.2)1,062 89 (87.3?1.1)2,006 91(89.9?2.4)100 95 (90.7?9.3)188 92 (88.2?5.6)374 72 (67.9?6.9)625 69 (65.8?3.1)252 37 (30.9?2.9)343 46 (40.1?1.1)30 93 (84.4?9.9)141 84 (77.6?9.8)226 65 (58.8?1.3)317 72 (66.7?6.6)PLOS ONE | www.plosone.orgHospital Wide Hand Hygiene InterventionTable 3. Cont.Variable Laboratory technicians N Compliance, (95 CI) Radiology technicians N Compliance, (95 CI)T1 (January 2010 ecember 2010)T2 (January 2011 ecember 2011)50 74 (61.8?6.2)129 69 (61.1?6.9)65 21 (11.5?1.5)84 75 (65.7?4.3)*All wards were monitored the same day for a 30 minute session except for Intensive Care Unit and Emergency Department where two different observations by two different hand hygiene monitor team (HHMT) members were planned. doi:10.1371/journal.pone.0047200.t2011, a 172 increase in the expenditure was noted achieving levels above 22 L/1,000 patient-days during 2011. Negative and positive special causes were noted in the 2008?009 period and their probable aetiologies are shown. At the end of 2010 and 2011, numerous “positive special causes” were noted and a clear change of the process of “AHR consumption” was achieved. Time series analysis of “healthcare-acquired MRSA colonization/infections rates” process during the 2007?011 period is illustrated through a Poisson Exponential Weighted Moving Average (PEWMA) control chart (see figure 5). This chart shows a low incidence rate over time (median of 0.77 per 10,000 patientdays) achieving a small but significant decrease in healthcareacquired MRSA colonization/infections rates during the intervention period according to the rule that at least 10 out of 11 consecutive data points fall in zone C or beyond on the same side of the center line (referred as rule 4 in Figure 5). Dur.

Ions in Barrett’s Esophagus [113,114] and ulcerative colitis [115], among a variety

Ions in Barrett’s Esophagus [113,114] and ulcerative colitis [115], among a variety of other cancer-predisposing diseases. Navin et al recently used the profile of CGH-identified copy number changes to study the clonal architecture of different regions of advanced breast cancers through phylogenetic inference [116]. Direct genomic sequencing provides the most detailed means possible of identifying clonal mutant markers. In contrast to conventional capillary-based techniques where individual PCR products or bacterial clones must be sequenced individually, a powerful new class of “Next Generation” sequencing technologies allows for simultaneous genotyping of tens of billions of base pairs [117]. The rapidly decreasing costs associated with these platforms have recently made it feasible to sequence the entire aggregate genome of a tissue sample without any regional targeting. From a clone detection perspective this means that multiple types of mutations of all functional varieties (both likely passengers and suspected drivers) can be simultaneously assessed. While it only takes a single clonal mutation to identify an expanded population, the redundancy conferred by screening the entire genome provides a huge amount of additional lineage data with the potential to be used for subanalyses such as approximation of a clone’s mitotic age or the phylogenetic relationship between different clones. The digital manner in which these novel sequencing technologies operate lend them a much greater dynamic range of sensitivity than conventional techniques, making it possible to resolve populations that are subclonal relative to a collected sample. Such an ability means that in situations where spatial coherence of an expanding clone is not maintained, for example in myelodysplasia preceding blood cancers, detection at an early stage can still be accomplished [118]. Similarly, a tolerance for clone mixing should allow for convenient, minimally invasive sampling techniques that disrupt cohesive growth patterns in epithelial tissues such as cell isolation from lavage, scrapings or body fluids rather than biopsy. The relatively high error rate of individual sequencing reads currently limits the average depth to which rare subclonal mutations can be accurately detected to about 2 orders of magnitude below pure clonality [26]. A variety of improvements at the level of chemistry, hardware and analysis are continuing to enhance this resolution for all current platforms [118,119]. An even newer generation of exotic “Fourth Generation” sequencing technologies on the horizon promises ultra-long read lengths with the ability to continuously re-sequence theChloroquine (diphosphate) solubility NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSemin Cancer Biol. Author manuscript; available in PMC 2011 October 15.Salk and HorwitzPagesame molecule for extremely accurate detection of rare molecular populations [120?22]. The pace of innovation in this area is staggering. Perhaps the only thing that can be stated with certainty about the technologies that will be available five years in the future is that they will look nothing like those from five years in the past.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Luteolin 7-glucoside cancer Manuscript9. The complex interpretation of clonality: false negatives, positives and assumptionsThe reasoning associated with clonality determination is complex and many potential confounders exist. In this section we highlight seven important ideas for consi.Ions in Barrett’s Esophagus [113,114] and ulcerative colitis [115], among a variety of other cancer-predisposing diseases. Navin et al recently used the profile of CGH-identified copy number changes to study the clonal architecture of different regions of advanced breast cancers through phylogenetic inference [116]. Direct genomic sequencing provides the most detailed means possible of identifying clonal mutant markers. In contrast to conventional capillary-based techniques where individual PCR products or bacterial clones must be sequenced individually, a powerful new class of “Next Generation” sequencing technologies allows for simultaneous genotyping of tens of billions of base pairs [117]. The rapidly decreasing costs associated with these platforms have recently made it feasible to sequence the entire aggregate genome of a tissue sample without any regional targeting. From a clone detection perspective this means that multiple types of mutations of all functional varieties (both likely passengers and suspected drivers) can be simultaneously assessed. While it only takes a single clonal mutation to identify an expanded population, the redundancy conferred by screening the entire genome provides a huge amount of additional lineage data with the potential to be used for subanalyses such as approximation of a clone’s mitotic age or the phylogenetic relationship between different clones. The digital manner in which these novel sequencing technologies operate lend them a much greater dynamic range of sensitivity than conventional techniques, making it possible to resolve populations that are subclonal relative to a collected sample. Such an ability means that in situations where spatial coherence of an expanding clone is not maintained, for example in myelodysplasia preceding blood cancers, detection at an early stage can still be accomplished [118]. Similarly, a tolerance for clone mixing should allow for convenient, minimally invasive sampling techniques that disrupt cohesive growth patterns in epithelial tissues such as cell isolation from lavage, scrapings or body fluids rather than biopsy. The relatively high error rate of individual sequencing reads currently limits the average depth to which rare subclonal mutations can be accurately detected to about 2 orders of magnitude below pure clonality [26]. A variety of improvements at the level of chemistry, hardware and analysis are continuing to enhance this resolution for all current platforms [118,119]. An even newer generation of exotic “Fourth Generation” sequencing technologies on the horizon promises ultra-long read lengths with the ability to continuously re-sequence theNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSemin Cancer Biol. Author manuscript; available in PMC 2011 October 15.Salk and HorwitzPagesame molecule for extremely accurate detection of rare molecular populations [120?22]. The pace of innovation in this area is staggering. Perhaps the only thing that can be stated with certainty about the technologies that will be available five years in the future is that they will look nothing like those from five years in the past.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript9. The complex interpretation of clonality: false negatives, positives and assumptionsThe reasoning associated with clonality determination is complex and many potential confounders exist. In this section we highlight seven important ideas for consi.

. This exploratory analysis can provide further information on functional similarities between

. This exploratory analysis can provide further information on functional similarities between regions, and, more specifically, on the extent to which NVP-QAW039 site activation profiles of category-selective regions are inherited from EVC. As for the replicability of within-category ranking (Fig. 5), we combined data across subjects either by Biotin-VAD-FMK supplier concatenating or averaging the activation profiles across subjects. The concatenation approach is sensitive to inter-region correlations of activation profiles even if the particular activation profiles differ across subjects. The averaging approach is sensitive to inter-region correlations of activation profiles that are consistent across subjects. We investigated the inter-region correlations for (1) the full activation profile, (2) the within-face activation profile, and (3) the withinplace activation profile. Statistical inference was performed by a standard one-sided test on Spearman’s r. p values were corrected8658 ?J. Neurosci., June 20, 2012 ?32(25):8649 ?Mur et al. ?Single-Image Activation of Category Regionsfor multiple testing using Bonferroni correction based on the total number of tests performed. Figure 7 shows the inter-region correlation results. The main pattern that emerges is that activation profiles are correlated between hemispheres for corresponding regions, and between hIT and EVC (red blocks on diagonals). We subsequently inspected the within-face correlation between FFA and EVC, and the within-place correlation between PPA and EVC. The within-face activation profile was correlated between left but not right FFA and EVC, and the within-place activation profile was not significantly correlated between PPA and EVC. Results were similar across ROI sizes. These results suggest that EVC is not a major contributor to the within-category activation profiles of PPA and right FFA. We then inspected the correlation between category-selective regions (FFA/PPA) and EVC for the full activation profile (top row). The full activation profile was correlated between EVC and both categoryselective regions, especially PPA. One interpretation of this finding would be that some degree of category selectivity is already present at the level of EVC, implying that low-level feature differences contribute to some extent to categoryselective responses. For places, this seems a plausible interpretation, consistent with our finding that single-image activation of EVC can discriminate places from nonplaces at an above-chance level (Fig. 2). For faces, this interpretation seems less likely: the correlation between EVC and FFA is not significant for the subjectaverage activation profile, suggesting that the correlation is driven by subjectspecific effects (e.g., idiosyncratic arousal effects) and not by face-selectivity of responses (shared across subjects in FFA). Categorical, yet graded Figure 8 summarizes our results. Singleimage activation profiles of categoryselective regions (1) show near-perfect discrimination of preferred from nonpreferred images and no preference inversions for particular object images, (2) show a step-like drop-off at the category boundary, and (3) are graded within and outside the preferred category. It can further be noted that single-image category selectivity is stronger in right than left FFA. In addition, gradedness seems to be more pronounced in FFA; the category step seems to be more pronounced in PPA. In sum, our findings indicate that the activation profiles of category-selec-Figure.. This exploratory analysis can provide further information on functional similarities between regions, and, more specifically, on the extent to which activation profiles of category-selective regions are inherited from EVC. As for the replicability of within-category ranking (Fig. 5), we combined data across subjects either by concatenating or averaging the activation profiles across subjects. The concatenation approach is sensitive to inter-region correlations of activation profiles even if the particular activation profiles differ across subjects. The averaging approach is sensitive to inter-region correlations of activation profiles that are consistent across subjects. We investigated the inter-region correlations for (1) the full activation profile, (2) the within-face activation profile, and (3) the withinplace activation profile. Statistical inference was performed by a standard one-sided test on Spearman’s r. p values were corrected8658 ?J. Neurosci., June 20, 2012 ?32(25):8649 ?Mur et al. ?Single-Image Activation of Category Regionsfor multiple testing using Bonferroni correction based on the total number of tests performed. Figure 7 shows the inter-region correlation results. The main pattern that emerges is that activation profiles are correlated between hemispheres for corresponding regions, and between hIT and EVC (red blocks on diagonals). We subsequently inspected the within-face correlation between FFA and EVC, and the within-place correlation between PPA and EVC. The within-face activation profile was correlated between left but not right FFA and EVC, and the within-place activation profile was not significantly correlated between PPA and EVC. Results were similar across ROI sizes. These results suggest that EVC is not a major contributor to the within-category activation profiles of PPA and right FFA. We then inspected the correlation between category-selective regions (FFA/PPA) and EVC for the full activation profile (top row). The full activation profile was correlated between EVC and both categoryselective regions, especially PPA. One interpretation of this finding would be that some degree of category selectivity is already present at the level of EVC, implying that low-level feature differences contribute to some extent to categoryselective responses. For places, this seems a plausible interpretation, consistent with our finding that single-image activation of EVC can discriminate places from nonplaces at an above-chance level (Fig. 2). For faces, this interpretation seems less likely: the correlation between EVC and FFA is not significant for the subjectaverage activation profile, suggesting that the correlation is driven by subjectspecific effects (e.g., idiosyncratic arousal effects) and not by face-selectivity of responses (shared across subjects in FFA). Categorical, yet graded Figure 8 summarizes our results. Singleimage activation profiles of categoryselective regions (1) show near-perfect discrimination of preferred from nonpreferred images and no preference inversions for particular object images, (2) show a step-like drop-off at the category boundary, and (3) are graded within and outside the preferred category. It can further be noted that single-image category selectivity is stronger in right than left FFA. In addition, gradedness seems to be more pronounced in FFA; the category step seems to be more pronounced in PPA. In sum, our findings indicate that the activation profiles of category-selec-Figure.

Ighlight the need to standardize protocols for the extraction and structural

Ighlight the need to standardize protocols for the extraction and structural identification of polar lipids molecular species. The same is valid for the deposit vouchers of screened taxa, in order to allow a reliable replication of results, as well as intraand interspecific comparisons.Acknowledgments: Thanks are due for the financial support to CESAM (UID/AMB/50017/2013) and QOPNA (UID/QUI/00062/2013) to FCT/MEC through national funds, and the co-funding by the FEDER, within the PT2020 Partnership Agreement and Compete 2020. E. Maciel benefits from a post-doc grant (SFRH/BPD/104165/2014) financed by FCT. We also acknowledge three anonymous reviewers for their insightful comments on a previous version of this work. Conflicts of Interest: The authors declare no conflict of interest.
Review ArticleThe Interstitial Cystitis Association of America: lessons learned over the past 30 yearsVicki RatnerFounder and President Emeritus, Interstitial Cystitis Association of America, USA Correspondence to: Vicki Ratner, MD. Founder and President Emeritus, Interstitial Cystitis Association of America, 1760 Old Meadow Road, suite 500, McLean, VA 22102, USA. Email: [email protected]: In 1984, interstitial cystitis (IC) was considered a rare psychosomatic disorder in post-menopausal women. In 2014, the Interstitial Cystitis Association of A-836339 site America (ICA) celebrated its 30th anniversary. We’ve come a long way since 1984 and great progress has been made. IC is now recognized as a condition that afflicts both men and women of all ages, including children and teenagers. It is not a psychiatric disorder. Though it was once thought to be an orphan disease (defined as affecting less than 200,000 people), we now know that there are millions of women and men who suffer from IC/BPS (bladder pain syndrome). In looking back over this period, there were seven key reasons why the ICA became so successful: an extremely dedicated ICA staff, Board of Directors and volunteers; a very strong Medical Advisory Board and participation of many other urologists from across the country and around the world; cooperation of the media; epidemiological studies; the ICA’s Pilot Research Program; our representation in Congress; and a strong working partnership with the National Institutes of Health (NIH). Our history may prove useful to other advocacy groups.Keywords: Interstitial cystitis/bladder pain syndrome (IC/BPS); bladder pain syndrome; Interstitial Cystitis Association of America (ICA); Interstitial Cystitis Association of America Advocacy Group; Interstitial Cystitis Association of America (ICA)-reasons for success Submitted Aug 01, 2015. A-836339 clinical trials Accepted for publication Aug 03, 2015. doi: 10.3978/j.issn.2223-4683.2015.09.02 View this article at: http://dx.doi.org/10.3978/j.issn.2223-4683.2015.09.The beginning In 1983, as a third year medical student, I came down with severe suprapubic pressure, urinary urgency, frequency and burning pain in my bladder. The pain felt like a lit match in my urethra. I was barely able to function, and found it almost impossible to concentrate. I assumed I had a UTI, but a complete work-up was negative and antibiotics failed to reduce the symptoms. In search of a diagnosis and relief from the severity of the symptoms, I sought help from one urologist after another. Many told me that the tests were negative, and that there was nothing they could do for me. Others suggested that I was not cut out to be a doctor and that I should drop out of medical sc.Ighlight the need to standardize protocols for the extraction and structural identification of polar lipids molecular species. The same is valid for the deposit vouchers of screened taxa, in order to allow a reliable replication of results, as well as intraand interspecific comparisons.Acknowledgments: Thanks are due for the financial support to CESAM (UID/AMB/50017/2013) and QOPNA (UID/QUI/00062/2013) to FCT/MEC through national funds, and the co-funding by the FEDER, within the PT2020 Partnership Agreement and Compete 2020. E. Maciel benefits from a post-doc grant (SFRH/BPD/104165/2014) financed by FCT. We also acknowledge three anonymous reviewers for their insightful comments on a previous version of this work. Conflicts of Interest: The authors declare no conflict of interest.
Review ArticleThe Interstitial Cystitis Association of America: lessons learned over the past 30 yearsVicki RatnerFounder and President Emeritus, Interstitial Cystitis Association of America, USA Correspondence to: Vicki Ratner, MD. Founder and President Emeritus, Interstitial Cystitis Association of America, 1760 Old Meadow Road, suite 500, McLean, VA 22102, USA. Email: [email protected]: In 1984, interstitial cystitis (IC) was considered a rare psychosomatic disorder in post-menopausal women. In 2014, the Interstitial Cystitis Association of America (ICA) celebrated its 30th anniversary. We’ve come a long way since 1984 and great progress has been made. IC is now recognized as a condition that afflicts both men and women of all ages, including children and teenagers. It is not a psychiatric disorder. Though it was once thought to be an orphan disease (defined as affecting less than 200,000 people), we now know that there are millions of women and men who suffer from IC/BPS (bladder pain syndrome). In looking back over this period, there were seven key reasons why the ICA became so successful: an extremely dedicated ICA staff, Board of Directors and volunteers; a very strong Medical Advisory Board and participation of many other urologists from across the country and around the world; cooperation of the media; epidemiological studies; the ICA’s Pilot Research Program; our representation in Congress; and a strong working partnership with the National Institutes of Health (NIH). Our history may prove useful to other advocacy groups.Keywords: Interstitial cystitis/bladder pain syndrome (IC/BPS); bladder pain syndrome; Interstitial Cystitis Association of America (ICA); Interstitial Cystitis Association of America Advocacy Group; Interstitial Cystitis Association of America (ICA)-reasons for success Submitted Aug 01, 2015. Accepted for publication Aug 03, 2015. doi: 10.3978/j.issn.2223-4683.2015.09.02 View this article at: http://dx.doi.org/10.3978/j.issn.2223-4683.2015.09.The beginning In 1983, as a third year medical student, I came down with severe suprapubic pressure, urinary urgency, frequency and burning pain in my bladder. The pain felt like a lit match in my urethra. I was barely able to function, and found it almost impossible to concentrate. I assumed I had a UTI, but a complete work-up was negative and antibiotics failed to reduce the symptoms. In search of a diagnosis and relief from the severity of the symptoms, I sought help from one urologist after another. Many told me that the tests were negative, and that there was nothing they could do for me. Others suggested that I was not cut out to be a doctor and that I should drop out of medical sc.

Rike patterns and running injuries, more work is necessary before broad

Rike patterns and running injuries, more work is necessary before broad conclusions on foot strike recommendations can be made to modify injury risk. Foot Inclination Angle at Initial Contact The angle created by the sole of the shoe and the treadmill belt is noted as the inclination angle of the foot (relative to a global coordinate system, not the tibia) at initial contact (Fig. 3). This variable is not applicable for midfoot strike and FFS runners. A recent study by Wille and colleagues21 found inclination angle to be particularly important in estimating ground reaction forces and joint kinetics during running. Specifically, increased foot inclination angle was found to be related to higher peak knee extensor moments, increased knee energy absorbed, higher peak vertical ground reaction force, and greater braking impulse during running. Each of these variables has been implicated in injury biomechanics, suggesting that a very high foot inclination angle at initial contact may not be desirable. This may be a source for intervention in runners whoPhys Med Rehabil Clin N Am. Author manuscript; available in PMC 2016 February 01.SouzaPageexperience injuries associated with high ground reaction forces or excessive joint kinetics. There are no cutoffs at which this angle is determined to be abnormal. Rather, it is likely on a sliding scale, where lower values are generally associated with lower ground reaction forces and joint kinetics, and higher values as associated with increased forces. However, it should be noted that a high foot inclination angle in isolation may be a benign finding and needs to be evaluated in the context of the entire running evaluations (see Overstriding). Tibia Angle at Loading Response The vertical alignment of the lower leg during loading response can be a valuable indicator of stride mechanics. Video of the runner should be evaluated using freeze-frames at the moment of loading response (as the shoe begins to deform just after initial contact). The alignment of the lower leg relative to a vertical line in the video field of view can be evaluated easily. An extended tibia is identified when the lateral knee joint marker is posterior to the lateral malleolus marker (Fig. 4A). Conversely, a flexed tibia is identified when the lateral knee marker is anterior to the lateral malleolus (Fig. 4C), and when these 2 markers are directly vertical to one another, this would be identified as a vertical tibia (Fig. 4B). For a runner that suffers from impact-related running injuries, an extended tibia is not ideal. A vertical or flexed tibia allows the runner to dissipate impact more readily though knee flexion. Similar to foot inclination angle, the tibia angle in itself may not be meaningful in isolation. It is a variable that can be grouped in a series of stride buy Aprotinin mechanics variables to better describe the characteristics of the runners stride and biomechanical risk profile. Knee order MG-132 flexion During Stance Peak knee flexion angle during stance may occur at slightly different phases in different runners. It is recommended to scroll through stance phase frames to identify maximum knee flexion. Key aspects of knee flexion during stance include the peak amount of knee flexion and the knee joint excursion during stance (difference in angle from initial contact to peak knee flexion). In general, normal peak knee flexion approaches approximately 45?at midstance (Fig. 5). Although explicit cutoffs have not been developed for this variable.Rike patterns and running injuries, more work is necessary before broad conclusions on foot strike recommendations can be made to modify injury risk. Foot Inclination Angle at Initial Contact The angle created by the sole of the shoe and the treadmill belt is noted as the inclination angle of the foot (relative to a global coordinate system, not the tibia) at initial contact (Fig. 3). This variable is not applicable for midfoot strike and FFS runners. A recent study by Wille and colleagues21 found inclination angle to be particularly important in estimating ground reaction forces and joint kinetics during running. Specifically, increased foot inclination angle was found to be related to higher peak knee extensor moments, increased knee energy absorbed, higher peak vertical ground reaction force, and greater braking impulse during running. Each of these variables has been implicated in injury biomechanics, suggesting that a very high foot inclination angle at initial contact may not be desirable. This may be a source for intervention in runners whoPhys Med Rehabil Clin N Am. Author manuscript; available in PMC 2016 February 01.SouzaPageexperience injuries associated with high ground reaction forces or excessive joint kinetics. There are no cutoffs at which this angle is determined to be abnormal. Rather, it is likely on a sliding scale, where lower values are generally associated with lower ground reaction forces and joint kinetics, and higher values as associated with increased forces. However, it should be noted that a high foot inclination angle in isolation may be a benign finding and needs to be evaluated in the context of the entire running evaluations (see Overstriding). Tibia Angle at Loading Response The vertical alignment of the lower leg during loading response can be a valuable indicator of stride mechanics. Video of the runner should be evaluated using freeze-frames at the moment of loading response (as the shoe begins to deform just after initial contact). The alignment of the lower leg relative to a vertical line in the video field of view can be evaluated easily. An extended tibia is identified when the lateral knee joint marker is posterior to the lateral malleolus marker (Fig. 4A). Conversely, a flexed tibia is identified when the lateral knee marker is anterior to the lateral malleolus (Fig. 4C), and when these 2 markers are directly vertical to one another, this would be identified as a vertical tibia (Fig. 4B). For a runner that suffers from impact-related running injuries, an extended tibia is not ideal. A vertical or flexed tibia allows the runner to dissipate impact more readily though knee flexion. Similar to foot inclination angle, the tibia angle in itself may not be meaningful in isolation. It is a variable that can be grouped in a series of stride mechanics variables to better describe the characteristics of the runners stride and biomechanical risk profile. Knee Flexion During Stance Peak knee flexion angle during stance may occur at slightly different phases in different runners. It is recommended to scroll through stance phase frames to identify maximum knee flexion. Key aspects of knee flexion during stance include the peak amount of knee flexion and the knee joint excursion during stance (difference in angle from initial contact to peak knee flexion). In general, normal peak knee flexion approaches approximately 45?at midstance (Fig. 5). Although explicit cutoffs have not been developed for this variable.

Ampal CA1 subfield in individuals with MCI compared to NCI (Fig.

Ampal CA1 subfield in individuals with MCI compared to NCI (Fig. 4), which correlated with the subject’s Mini-Mental State Exam score (MMSE), but not with NFT Braak stage or apolipoprotein E (ApoE) status, a genetic risk factor for AD (Scheff et al., 2006). Unlike the outer molecular layer, CA1 receives input from the Schaffer collaterals arising from CA3 and not from the glutamatergic neurons of the entorhinal cortex, suggesting differential responses to synapse loss within the hippocampus based upon afferent innervation or chemical phenotype, some of which precipitate synaptic reorganization. A recent report characterized changes in the dendritic branching of the basilar tree of hippocampal CA1 pyramidal neurons. In this study, formalin-fixed tissue autopsy obtained from University of Kentucky Alzheimer’s Disease Center who died with a clinical diagnosis of NCI, MCI or AD was Fruquintinib supplier prepared for Golgi impregnation (Fig. 5). Camera lucida drawings of the basilar tree of randomly selected CA1 neurons were analyzed for alterations in dendritic arbor amount, distribution and complexity (Mervis et al., 2013). Quantitation showed a significant increase in dendritic Sodium lasalocid web length (18 ) and complexity (23 ) in CA1 neurons in MCI compared to NCI. Conversely, there was a significant reduction in branch length (-39 ) and arbor complexity (-25 ) during the progression from MCI to AD (Fig. 5). These findings suggest that the observed increase in CA1 dendritic parameters from NCI to MCI may be another example of a neuroplastic compensatory response to a loss of afferent input early in the course of the disease, which is not maintained as the disease progresses. The role that the reported reduction in total synapse number plays in CA1 neuroplasticity remains unknown. However, these examples of early CA1 neural reorganization may represent a viable window for potential therapeutic strategies aimed at restoring or maintaining hippocampal function during the transition from MCI to AD. Future studies should determine whether alterations in specific synapse subtypes (i.e., perforated vs. non-perforated) are differentially affected and their relation to cognitive decline and brain pathology during the onset of AD. Interestingly, the size of the synaptic contacts was found to be substantially larger in AD cortex compared to non-demented aged controls (Scheff et al., 1990), which was suggested to be part of a compensatory mechanism found in regions of the neocortex and hippocampus (see review Scheff and Price, 2006). These investigators found that as the number of synapses declined in a given region, the size of the residualAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptNeuroscience. Author manuscript; available in PMC 2016 September 12.Mufson et al.Pagesynapses increased. This synaptic compensatory response was also observed early in the course of the AD (DeKosky and Scheff, 1990). Neuronal structural alterations may not be the only factor(s) contributing to cognitive decline and hippocampal plasticity in MCI. For example, studies have reported significant reductions in synaptic vesicle trafficking-related genes in the AD brain, which interrupt the efficacy of normal synaptic transmission (Yao et al., 2003; Murphy et al., 2003; Kennedy et al., 2005). Counts et al. (2014) examined progressive changes in the expression classes of synaptic gene within single CA1 neurons in subjects who died with a clinical diagnosis of NCI, MCI or moderate AD obtain.Ampal CA1 subfield in individuals with MCI compared to NCI (Fig. 4), which correlated with the subject’s Mini-Mental State Exam score (MMSE), but not with NFT Braak stage or apolipoprotein E (ApoE) status, a genetic risk factor for AD (Scheff et al., 2006). Unlike the outer molecular layer, CA1 receives input from the Schaffer collaterals arising from CA3 and not from the glutamatergic neurons of the entorhinal cortex, suggesting differential responses to synapse loss within the hippocampus based upon afferent innervation or chemical phenotype, some of which precipitate synaptic reorganization. A recent report characterized changes in the dendritic branching of the basilar tree of hippocampal CA1 pyramidal neurons. In this study, formalin-fixed tissue autopsy obtained from University of Kentucky Alzheimer’s Disease Center who died with a clinical diagnosis of NCI, MCI or AD was prepared for Golgi impregnation (Fig. 5). Camera lucida drawings of the basilar tree of randomly selected CA1 neurons were analyzed for alterations in dendritic arbor amount, distribution and complexity (Mervis et al., 2013). Quantitation showed a significant increase in dendritic length (18 ) and complexity (23 ) in CA1 neurons in MCI compared to NCI. Conversely, there was a significant reduction in branch length (-39 ) and arbor complexity (-25 ) during the progression from MCI to AD (Fig. 5). These findings suggest that the observed increase in CA1 dendritic parameters from NCI to MCI may be another example of a neuroplastic compensatory response to a loss of afferent input early in the course of the disease, which is not maintained as the disease progresses. The role that the reported reduction in total synapse number plays in CA1 neuroplasticity remains unknown. However, these examples of early CA1 neural reorganization may represent a viable window for potential therapeutic strategies aimed at restoring or maintaining hippocampal function during the transition from MCI to AD. Future studies should determine whether alterations in specific synapse subtypes (i.e., perforated vs. non-perforated) are differentially affected and their relation to cognitive decline and brain pathology during the onset of AD. Interestingly, the size of the synaptic contacts was found to be substantially larger in AD cortex compared to non-demented aged controls (Scheff et al., 1990), which was suggested to be part of a compensatory mechanism found in regions of the neocortex and hippocampus (see review Scheff and Price, 2006). These investigators found that as the number of synapses declined in a given region, the size of the residualAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptNeuroscience. Author manuscript; available in PMC 2016 September 12.Mufson et al.Pagesynapses increased. This synaptic compensatory response was also observed early in the course of the AD (DeKosky and Scheff, 1990). Neuronal structural alterations may not be the only factor(s) contributing to cognitive decline and hippocampal plasticity in MCI. For example, studies have reported significant reductions in synaptic vesicle trafficking-related genes in the AD brain, which interrupt the efficacy of normal synaptic transmission (Yao et al., 2003; Murphy et al., 2003; Kennedy et al., 2005). Counts et al. (2014) examined progressive changes in the expression classes of synaptic gene within single CA1 neurons in subjects who died with a clinical diagnosis of NCI, MCI or moderate AD obtain.

Monly used and widely available OTC medications and nutritional supplements were

Monly used and widely available OTC medications and nutritional supplements were safe and posed no short- or long-term threat to their health. Many used such products to improve their running performance, yet their risk normalized or neutralized by their presence at running expos, in running publications and at vitamin retail stores. Well aware that some substances–EPO, anabolic steroids, HGH–are banned and may be dangerous to health, these runners took for granted the surveillance and safety of products they could procure legally, under the belief that is something was not banned it would be safe. This belief makes runners vulnerable to tainted or dangerous products that are freely available and not considered harmful, even though non-elite athletes routinely feel they make correct decisions and engaging in adequate self-surveillance that is get Crotaline required in contemporary neoliberal citizenship (Rose 1999). As such, a product recommended as an effective and legal substance by another runner or by a retail sales clerk may contain substances that are either banned by agencies such as WADA and/or may pose a serious health risk. The recent controversy over the supplement ingredient DMAA illustrates availability cannot be substituted for safety.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSurveill Soc. Author manuscript; available in PMC 2014 November 04.HenningPageTogether, these perceptions and knowledge gaps result in a blind spot in the internalized buy ML390 anti-doping gaze. Runners do the work of self-surveillance believing they are acting as good citizens by conforming to anti-doping regulations and following expert advice on how to be healthy, as far as they understand these rules and recommendations. With regard to nutritional supplements, this self-surveillance blind spot can have major negative health repercussions. WADA and its affiliates claim athlete health is a top priority, yet its policies and methods confuse non-elite runners and lull them into a false sense of security. The nonelites in this research engaged in self-surveillance and did seek to conform to the clean ideal by avoiding what they understood to be prohibited or dangerous substances. However, their knowledge of anti-doping regulations was inadequate for avoiding all but the most commonly discussed prohibited enhancement products. Relying on their incomplete and often incorrect understandings of which substances are potentially harmful, these runners may wrongly presume they are avoiding harmful PEDs by focusing their attention on supplements that are commonly found in drug stores and nutritional supplement shops. This finding demonstrates how the quest to eradicate doping in sports using the surveillancebased system of regulations and banned substances seem to work against the underlying goals of anti-doping agencies in non-elite sports populations.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptAcknowledgmentsThe author was supported by NIDA grant (T32 DA007233); points of view are the author’s alone.
NIH Public AccessAuthor ManuscriptJ Res Adolesc. Author manuscript; available in PMC 2015 June 01.Published in final edited form as: J Res Adolesc. 2014 June 1; 24(2): 235?51. doi:10.1111/jora.12124.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSerious Delinquency and Gang Participation: Combining and Specializing in Drug Selling, Theft and ViolenceRachel A. Gordon, University of Illinois at Chi.Monly used and widely available OTC medications and nutritional supplements were safe and posed no short- or long-term threat to their health. Many used such products to improve their running performance, yet their risk normalized or neutralized by their presence at running expos, in running publications and at vitamin retail stores. Well aware that some substances–EPO, anabolic steroids, HGH–are banned and may be dangerous to health, these runners took for granted the surveillance and safety of products they could procure legally, under the belief that is something was not banned it would be safe. This belief makes runners vulnerable to tainted or dangerous products that are freely available and not considered harmful, even though non-elite athletes routinely feel they make correct decisions and engaging in adequate self-surveillance that is required in contemporary neoliberal citizenship (Rose 1999). As such, a product recommended as an effective and legal substance by another runner or by a retail sales clerk may contain substances that are either banned by agencies such as WADA and/or may pose a serious health risk. The recent controversy over the supplement ingredient DMAA illustrates availability cannot be substituted for safety.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSurveill Soc. Author manuscript; available in PMC 2014 November 04.HenningPageTogether, these perceptions and knowledge gaps result in a blind spot in the internalized anti-doping gaze. Runners do the work of self-surveillance believing they are acting as good citizens by conforming to anti-doping regulations and following expert advice on how to be healthy, as far as they understand these rules and recommendations. With regard to nutritional supplements, this self-surveillance blind spot can have major negative health repercussions. WADA and its affiliates claim athlete health is a top priority, yet its policies and methods confuse non-elite runners and lull them into a false sense of security. The nonelites in this research engaged in self-surveillance and did seek to conform to the clean ideal by avoiding what they understood to be prohibited or dangerous substances. However, their knowledge of anti-doping regulations was inadequate for avoiding all but the most commonly discussed prohibited enhancement products. Relying on their incomplete and often incorrect understandings of which substances are potentially harmful, these runners may wrongly presume they are avoiding harmful PEDs by focusing their attention on supplements that are commonly found in drug stores and nutritional supplement shops. This finding demonstrates how the quest to eradicate doping in sports using the surveillancebased system of regulations and banned substances seem to work against the underlying goals of anti-doping agencies in non-elite sports populations.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptAcknowledgmentsThe author was supported by NIDA grant (T32 DA007233); points of view are the author’s alone.
NIH Public AccessAuthor ManuscriptJ Res Adolesc. Author manuscript; available in PMC 2015 June 01.Published in final edited form as: J Res Adolesc. 2014 June 1; 24(2): 235?51. doi:10.1111/jora.12124.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptSerious Delinquency and Gang Participation: Combining and Specializing in Drug Selling, Theft and ViolenceRachel A. Gordon, University of Illinois at Chi.

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ……………………………………………… ….. ………….. 9 FI S Euthynuus affinis Fi red f. 3.20 Y 25 30 skinned single f. Johnston Brill [83] (kawakawa, Pacific ocean) ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 10 FI S Euthynuus affinis Fi white f. 3.20 Y 188 30 skinned single f. Johnston Brill [83] (kawakawa, Pacific ocean) ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 11 FI S Gadus morhua (North Sea Fi Isorhamnetin cost myotomal m. fast f., 2?2?84 Y 187 8 skinned single f. Johnston LM22A-4 cancer Altringham [84] cod,. temperate). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ………………………………………………. ……………… 12 FI S Gadus morhua (cod) Fi myotomal m. white f. (fast) 84 N 83 8 skinned single f. Altringham Johnston [85] ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 13. . . . . . . . . . . . . FI. . . . . . . . . . . .S. . . . . . . . . . .Gadus. morhua. .(cod). . . . . . . . . . . . . . . . . . . . . . .Fi. . . . . . . . . . . . . . . . . .myotomal. .m.. .red. .f.. .(slow). . . . . . . . . . . . . . . . . . . . . . . . . . .84. . . . . . . . . . . . . . . . . . . . . . . . . .N. . . . . . . . . . . 186. . . . . . . . . . . . . . . . . . . . .8. . . . . . . . . . . . . .skinned. . 2?. .f.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Altringham. . . . Johnston. .[85]. . . ….. .. . ……… ………… ……. .. …………… … …. . ……… .. . ….. . ……….. …… . …………….. . ………….. ….. (Continued.)rsos.royalsocietypublishing.org R. Soc. open sci. 3:…………………………………………Table 4. (Continued.) motor M (kg) I f (kPa) T ( ) comment referenceno.TyCspeciesgroup…………………… . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ……………………………………………… ….. ………….. 9 FI S Euthynuus affinis Fi red f. 3.20 Y 25 30 skinned single f. Johnston Brill [83] (kawakawa, Pacific ocean) ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 10 FI S Euthynuus affinis Fi white f. 3.20 Y 188 30 skinned single f. Johnston Brill [83] (kawakawa, Pacific ocean) ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 11 FI S Gadus morhua (North Sea Fi myotomal m. fast f., 2?2?84 Y 187 8 skinned single f. Johnston Altringham [84] cod,. temperate). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ………………………………………………. ……………… 12 FI S Gadus morhua (cod) Fi myotomal m. white f. (fast) 84 N 83 8 skinned single f. Altringham Johnston [85] ………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………………….. 13. . . . . . . . . . . . . FI. . . . . . . . . . . .S. . . . . . . . . . .Gadus. morhua. .(cod). . . . . . . . . . . . . . . . . . . . . . .Fi. . . . . . . . . . . . . . . . . .myotomal. .m.. .red. .f.. .(slow). . . . . . . . . . . . . . . . . . . . . . . . . . .84. . . . . . . . . . . . . . . . . . . . . . . . . .N. . . . . . . . . . . 186. . . . . . . . . . . . . . . . . . . . .8. . . . . . . . . . . . . .skinned. . 2?. .f.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Altringham. . . . Johnston. .[85]. . . ….. .. . ……… ………… ……. .. …………… … …. . ……… .. . ….. . ……….. …… . …………….. . ………….. ….. (Continued.)rsos.royalsocietypublishing.org R. Soc. open sci. 3:…………………………………………Table 4. (Continued.) motor M (kg) I f (kPa) T ( ) comment referenceno.TyCspeciesgroup…………………..