Acute Upper-Body and Lower-Body Neuromuscular Fatigue Effect on Baseball Pitchers' Velocity: A Pilot Study.

ABSTRACT: Tremblay, M, Anderson Sirois, S, Verville, W, Auger, M, Abboud, J, and Descarreaux, M. Acute upper-body and lower-body neuromuscular fatigue effect on baseball pitchers' velocity: A pilot study. J Strength Cond Res 38(8): 1447-1452, 2024-The purpose of this pilot study was to explore the acute effect of upper-body and lower-body neuromuscular fatigue protocols on baseball pitchers' velocity. Sixteen baseball pitchers were recruited, and a crossover design was used to meet the study purpose. Pitchers were tested twice, 7 days apart, with their upper-body and lower-body explosiveness, pitching velocity, and muscle soreness perception of their throwing arm (forearm flexors, biceps, anterior deltoid, and upper trapezius muscles) assessed before and after an upper-body and lower-body neuromuscular fatigue protocol. Two-way analysis of variances and paired t tests ( p < 0.05) were used to identify and compare prescores and postscores. Following both fatigue protocols, results revealed a significant decrease in time for pitching velocity ( p = 0.005, ηp 2 = 0.462), and increases in muscle soreness perception of the forearm flexors ( p = 0.005, ηp 2 = 0.470), anterior deltoid ( p = 0.045, ηp 2 = 0.274), and upper trapezius ( p = 0.023, ηp 2 = 0.339) muscles. Paired t test results showed a significant decrease in preneuromuscular and postneuromuscular fatigue protocol in the upper-body ( p < 0.01) and lower-body ( p < 0.01) explosiveness scores. These pilot study results show the impact of different exercise protocols on pitchers' explosiveness, velocity, and muscle soreness perception emphasizing the need for further investigation into the acute effect of exercise targeting the upper or lower-body on pitching performance, specifically at the pitcher's position.

GATA transcription factors in development and disease.

The GATA family of transcription factors is of crucial importance during embryonic development, playing complex and widespread roles in cell fate decisions and tissue morphogenesis. GATA proteins are essential for the development of tissues derived from all three germ layers, including the skin, brain, gonads, liver, hematopoietic, cardiovascular and urogenital systems. The crucial activity of GATA factors is underscored by the fact that inactivating mutations in most GATA members lead to embryonic lethality in mouse models and are often associated with developmental diseases in humans. In this Primer, we discuss the unique and redundant functions of GATA proteins in tissue morphogenesis, with an emphasis on their regulation of lineage specification and early organogenesis.

A Bi-Spectral Microbolometer Sensor for Wildfire Measurement.

This study describes the development of a prototype bi-spectral microbolometer sensor system designed explicitly for radiometric measurement and characterization of wildfire mid- and long-wave infrared radiances. The system is tested experimentally over moderate-scale experimental burns coincident with FLIR reference imagery. Statistical comparison of the fire radiative power (FRP; W) retrievals suggest that this novel system is highly reliable for use in collecting radiometric measurements of biomass burning. As such, this study provides clear experimental evidence that mid-wave infrared microbolometers are capable of collecting FRP measurements. Furthermore, given the low resource nature of this detector type, it presents a suitable option for monitoring wildfire behaviour from low resource platforms such as unmanned aerial vehicles (UAVs) or nanosats.

Bmp signaling maintains a mesoderm progenitor cell state in the mouse tailbud.

Caudal somites are generated from a pool of progenitor cells located in the tailbud region. These progenitor cells form the presomitic mesoderm that gradually differentiates into somites under the action of the segmentation clock. The signals responsible for tailbud mesoderm progenitor pool maintenance during axial elongation are still elusive. Here, we show that Bmp signaling is sufficient to activate the entire mesoderm progenitor gene signature in primary cultures of caudal mesoderm cells. Bmp signaling acts through the key regulatory genes brachyury (T) and Nkx1-2 and contributes to the activation of several other regulators of the mesoderm progenitor gene network. In the absence of Bmp signaling, tailbud mesoderm progenitor cells acquire aberrant gene expression signatures of the heart, blood, muscle and skeletal embryonic lineages. Treatment of embryos with the Bmp inhibitor noggin confirmed the requirement for Bmp signaling for normal T expression and the prevention of abnormal lineage marker activation. Together, these results identify Bmp signaling as a non-cell-autonomous signal necessary for mesoderm progenitor cell homeostasis.

Contactless Capacitive Electrocardiography Using Hybrid Flexible Printed Electrodes.

Traditional capacitive electrocardiogram (cECG) electrodes suffer from limited patient comfort, difficulty of disinfection and low signal-to-noise ratio in addition to the challenge of integrating them in wearables. A novel hybrid flexible cECG electrode was developed that offers high versatility in the integration method, is well suited for large-scale manufacturing, is easy to disinfect in clinical settings and exhibits better performance over a comparable rigid contactless electrode. The novel flexible electrode meets the frequency requirement for clinically important QRS complex detection (0.67-5 Hz) and its performance is improved over rigid contactless electrode across all measured metrics as it maintains lower cut-off frequency, higher source capacitance and higher pass-band gain when characterized over a wide spectrum of patient morphologies. The results presented in this article suggest that the novel flexible electrode could be used in a medical device for cECG acquisition and medical diagnosis. The novel design proves also to be less sensitive to motion than a reference rigid electrode. We therefore anticipate it can represent an important step towards improving the repeatability of cECG methods while requiring less post-processing. This would help making cECG a viable method for remote cardiac health monitoring.

A Point Mutation in p190A RhoGAP Affects Ciliogenesis and Leads to Glomerulocystic Kidney Defects.

Rho family GTPases act as molecular switches regulating actin cytoskeleton dynamics. Attenuation of their signaling capacity is provided by GTPase-activating proteins (GAPs), including p190A, that promote the intrinsic GTPase activity of Rho proteins. In the current study we have performed a small-scale ENU mutagenesis screen and identified a novel loss of function allele of the p190A gene Arhgap35, which introduces a Leu1396 to Gln substitution in the GAP domain. This results in decreased GAP activity for the prototypical Rho-family members, RhoA and Rac1, likely due to disrupted ordering of the Rho binding surface. Consequently, Arhgap35-deficient animals exhibit hypoplastic and glomerulocystic kidneys. Investigation into the cystic phenotype shows that p190A is required for appropriate primary cilium formation in renal nephrons. P190A specifically localizes to the base of the cilia to permit axoneme elongation, which requires a functional GAP domain. Pharmacological manipulations further reveal that inhibition of either Rho kinase (ROCK) or F-actin polymerization is able to rescue the ciliogenesis defects observed upon loss of p190A activity. We propose a model in which p190A acts as a modulator of Rho GTPases in a localized area around the cilia to permit the dynamic actin rearrangement required for cilia elongation. Together, our results establish an unexpected link between Rho GTPase regulation, ciliogenesis and glomerulocystic kidney disease.

Modeling T-cell acute lymphoblastic leukemia induced by the SCL and LMO1 oncogenes.

Deciphering molecular events required for full transformation of normal cells into cancer cells remains a challenge. In T-cell acute lymphoblastic leukemia (T-ALL), the genes encoding the TAL1/SCL and LMO1/2 transcription factors are recurring targets of chromosomal translocations, whereas NOTCH1 is activated in >50% of samples. Here we show that the SCL and LMO1 oncogenes collaborate to expand primitive thymocyte progenitors and inhibit later stages of differentiation. Together with pre-T-cell antigen receptor (pre-TCR) signaling, these oncogenes provide a favorable context for the acquisition of activating Notch1 mutations and the emergence of self-renewing leukemia-initiating cells in T-ALL. All tumor cells harness identical and specific Notch1 mutations and Tcrbeta clonal signature, indicative of clonal dominance and concurring with the observation that Notch1 gain of function confers a selective advantage to SCL-LMO1 transgenic thymocytes. Accordingly, a hyperactive Notch1 allele accelerates leukemia onset induced by SCL-LMO1 and bypasses the requirement for pre-TCR signaling. Finally, the time to leukemia induced by the three transgenes corresponds to the time required for clonal expansion from a single leukemic stem cell, suggesting that SCL, LMO1, and Notch1 gain of function, together with an active pre-TCR, might represent the minimum set of complementing events for the transformation of susceptible thymocytes.

SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.

The molecular determinants that render specific populations of normal cells susceptible to oncogenic reprogramming into self-renewing cancer stem cells are poorly understood. Here, we exploit T-cell acute lymphoblastic leukemia (T-ALL) as a model to define the critical initiating events in this disease. First, thymocytes that are reprogrammed by the SCL and LMO1 oncogenic transcription factors into self-renewing pre-leukemic stem cells (pre-LSCs) remain non-malignant, as evidenced by their capacities to generate functional T cells. Second, we provide strong genetic evidence that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1. Moreover, LYL1 can substitute for SCL to reprogram thymocytes in concert with LMO1. In contrast, inhibition of E2A was not sufficient to substitute for SCL, indicating that thymocyte reprogramming requires transcription activation by SCL-LMO1. Third, only a specific subset of normal thymic cells, known as DN3 thymocytes, is susceptible to reprogramming. This is because physiological NOTCH1 signals are highest in DN3 cells compared to other thymocyte subsets. Consistent with this, overexpression of a ligand-independent hyperactive NOTCH1 allele in all immature thymocytes is sufficient to sensitize them to SCL-LMO1, thereby increasing the pool of self-renewing cells. Surprisingly, hyperactive NOTCH1 cannot reprogram thymocytes on its own, despite the fact that NOTCH1 is activated by gain of function mutations in more than 55% of T-ALL cases. Rather, elevating NOTCH1 triggers a parallel pathway involving Hes1 and Myc that dramatically enhances the activity of SCL-LMO1 We conclude that the acquisition of self-renewal and the genesis of pre-LSCs from thymocytes with a finite lifespan represent a critical first event in T-ALL. Finally, LYL1 and LMO1 or LMO2 are co-expressed in most human T-ALL samples, except the cortical T subtype. We therefore anticipate that the self-renewal network described here may be relevant to a majority of human T-ALL.

RARα-PLZF oncogene inhibits C/EBPα function in myeloid cells.

In acute promyelocytic leukemia, granulocytic differentiation is arrested at the promyelocyte stage. The variant t(11;17) translocation produces two fusion proteins, promyelocytic leukemia zinc finger-retinoic acid receptor α (PLZF-RARα) and RARα-PLZF, both of which participate in leukemia development. Here we provide evidence that the activity of CCAAT/enhancer binding protein α (C/EBPα), a master regulator of granulocytic differentiation, is severely impaired in leukemic promyelocytes with the t(11;17) translocation compared with those associated with the t(15;17) translocation. We show that RARα-PLZF inhibits myeloid cell differentiation through interactions with C/EBPα tethered to DNA, using ChIP and DNA capture assays. Furthermore, RARα-PLZF recruits HDAC1 and causes histone H3 deacetylation at C/EBPα target loci, thereby decreasing the expression of C/EBPα target genes. In line with these results, HDAC inhibitors restore in part C/EBPα target gene expression. These findings provide molecular evidence for a mechanism through which RARα-PLZF acts as a modifier oncogene that subverts differentiation in the granulocytic lineage by associating with C/EBPα and inhibiting its activity.

Gata3 antagonizes cancer progression in Pten-deficient prostates.

Loss of the tumor suppressor PTEN is a common occurrence in prostate cancer. This aberration leads to the ectopic activation of the PI3K-Akt pathway, which promotes tumor growth. Here, we show that the transcription factor Gata3 is progressively lost in Pten-deficient mouse prostate tumors as a result of both transcriptional down-regulation and increased proteasomal degradation. To determine the significance of this loss, we used conditional loss- and gain-of-function approaches to manipulate Gata3 expression levels in prostate tumors. Our results show that Gata3 inactivation in Pten-deficient prostates accelerates tumor invasion. Conversely, enforced expression of GATA3 in Pten-deficient tissues markedly delays tumor progression. In Pten-deficient prostatic ducts, enforced GATA3 prevented Akt activation, which correlated with the down-regulation of Pik3cg and Pik3c2a mRNAs, encoding respectively class I and II PI3K subunits. Remarkably, the majority of human prostate tumors similarly show loss of active GATA3 as they progress to the aggressive castrate-resistant stage. In addition, GATA3 expression levels in hormone-sensitive tumors holds predictive value for tumor recurrence. Together, these data establish Gata3 as an important regulator of prostate cancer progression.

Genetic interaction between Kit and Scl.

SCL/TAL1, a tissue-specific transcription factor of the basic helix-loop-helix family, and c-Kit, a tyrosine kinase receptor, control hematopoietic stem cell survival and quiescence. Here we report that SCL levels are limiting for the clonal expansion of Kit⁺ multipotent and erythroid progenitors. In addition, increased SCL expression specifically enhances the sensitivity of these progenitors to steel factor (KIT ligand) without affecting interleukin-3 response, whereas a DNA-binding mutant antagonizes KIT function and induces apoptosis in progenitors. Furthermore, a twofold increase in SCL levels in mice bearing a hypomorphic Kit allele (W41/41) corrects their hematocrits and deficiencies in erythroid progenitor numbers. At the molecular level, we found that SCL and c-Kit signaling control a common gene expression signature, of which 19 genes are associated with apoptosis. Half of those were decreased in purified megakaryocyte/erythroid progenitors (MEPs) from W41/41 mice and rescued by the SCL transgene. We conclude that Scl operates downstream of Kit to support the survival of MEPs. Finally, higher SCL expression upregulates Kit in normal bone marrow cells and increases chimerism after bone marrow transplantation, indicating that Scl is also upstream of Kit. We conclude that Scl and Kit establish a positive feedback loop in multipotent and MEPs.

A core transcriptional network composed of Pax2/8, Gata3 and Lim1 regulates key players of pro/mesonephros morphogenesis.

Translating the developmental program encoded in the genome into cellular and morphogenetic functions requires the deployment of elaborate gene regulatory networks (GRNs). GRNs are especially crucial at the onset of organ development where a few regulatory signals establish the different programs required for tissue organization. In the renal system primordium (the pro/mesonephros), important regulators have been identified but their hierarchical and regulatory organization is still elusive. Here, we have performed a detailed analysis of the GRN underlying mouse pro/mesonephros development. We find that a core regulatory subcircuit composed of Pax2/8, Gata3 and Lim1 turns on a deeper layer of transcriptional regulators while activating effector genes responsible for cell signaling and tissue organization. Among the genes directly affected by the core components are the key developmental molecules Nephronectin (Npnt) and Plac8. Hence, the pro/mesonephros GRN links together several essential genes regulating tissue morphogenesis. This renal GRN sheds new light on the disease group Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) in that gene mutations are expected to generate different phenotypic outcomes as a consequence of regulatory network deficiencies rather than threshold effects from single genes.

Kinesiophobia among health professionals' interventions: a scoping review.

Health professionals are regularly confronted with patients suffering from a fear of movement-related pain (unknown as kinesiophobia). The fear-avoidance attitudes and beliefs of healthcare professionals are likely to play a key role in their patients' therapeutic approach. However, kinesiophobia among health professionals is a relatively young topic. This scoping review aims to explore and catalogue the extent of scientific research that identifies the causes and consequences of kinesiophobia among health professionals while they perform their interventions. The review was based on the Joanna Briggs Institute manual and the PRISMA method for a scoping review. The research was conducted in May 2024 using CINHAL, Medline and Sportdiscus databases with the search terms "fear-avoidance", "kinesiophobia", "pain-related" and "physical therapist". Out of 2,162 potential studies, thirteen articles were included. No study directly mentioned kinesiophobia among health professionals, but it was studied through fear-avoidance beliefs. Two-thirds of the articles indicate that professionals with fear-avoidance beliefs tend to refer their patients to other specialists less frequently and limit their patients' activity, despite treatment guidelines. Most of the studies found were physiotherapists' interventions for chronic back pain patients. The current review emphasizes the need for additional studies involving more healthcare professionals and diverse health conditions.

What are the functional and clinical characteristics shared by fibromyalgia and low back pain? A scoping review.

BACKGROUND: Fibromyalgia and chronic primary low back pain are two chronic pain conditions with a significant biopsychosocial burden. Recently, the International Association for the Study of Pain has grouped them under the term chronic primary pain. To further explore similarities and differences between these two conditions, the objective of this scoping review is to explore the pain-related, physiological and psychological outcomes in individuals with fibromyalgia and low back pain. METHODS: The following databases were used to find relevant studies, using the PRISMA guidelines: Medline, Psycinfo, and CINAHL. Studies were included if they encompassed both participants with fibromyalgia or low back pain, with the objective to compare pain-related, physiological and/or psychological outcomes. RESULTS: Nineteen studies were selected for extraction. Among the 2801 participants, 968 had fibromyalgia (mean age 48.56 ± 7.97 years, with 94% being female) and 896 had low back pain (mean age 47.48 ± 8.15 years, with 80% being female). Pain sensitivity, physical dysfunction, illness perception, psychological distress, alexithymia, depression, and anxiety were generally more severe in participants with fibromyalgia. Most studies found similar levels of pain intensity, kinesiophobia, quality of pain, quality of life, impact of pain, suicidal risk, anger, and social support comparing individuals with fibromyalgia and individuals with low back pain. DISCUSSION: This scoping review highlights that although both conditions show similar pain intensity and impact on quality of life, fibromyalgia is associated with greater overall severity than low back pain, especially in sensitivity to pain and depression/anxiety.

Effect of physical activity education on shoulder girdle pain and muscle strength in participants with fibromyalgia: a pilot experimental study.

Background: In patients with fibromyalgia, exercise and education are recommended to decrease pain level and improve pain management. The latest scientific evidence recommends to focus interventions on the upper limb. The aim of this pilot study was to compare the immediate effect of physical activity education vs. a control group on pain and muscle capacity in fibromyalgia patients. Method: Fifty-six participants with fibromyalgia were randomized into an experimental group and a control group. The intervention consisted in watching a five-minute video that provided information about fibromyalgia, pain, kinesiophobia and physical activity. The control group watched a neutral five-minute video about beavers in Quebec. Following the video, participants performed a muscular fatigue task consisting of a repeated unilateral shoulder abduction task. At baseline and following the muscular fatigue task, maximal voluntary contraction (MVC) in shoulder abduction was assessed as well as pain level and pressure pain threshold (PPT) in the upper limb. Electromyographic activity was also assessed for upper trapezius and middle deltoid muscles. Two-way repeated measures analysis of variance was used to compare the MVC, PPT, and pain level before and after the muscular fatigue task between groups. Results: The experimental group showed a significantly lower increase in pain than the control group in the middle deltoid muscle (p = 0.002) when assessed by verbal pain rating scale. No significant interaction or main effect of Group and Time were observed for the pain level at the upper trapezius and elbow extensor muscles nor for any of the PPT measures. According to electromyographic data, the median frequency values indicate that neither group experienced muscle fatigue during the repeated contraction task. Conclusions: The preliminary results suggest that a short physical activity education video positively influenced middle deltoid pain following repeated abduction in participants with fibromyalgia. Electromyographic analysis showed no evidence of objective muscle fatigue, suggesting that there might be a partial disconnection between the perception of muscle fatigue and the physiological biomarkers associated with muscle fatigue.

Occupational health and safety portrait of lobster fishers from a St. Lawrence Gulf community.

Lobstering industry workers are known to have poor overall health and low safety records, but there is still a gap in information concerning Canadian lobster fishers. This study aimed to report occupational health and safety characteristics of an Atlantic Canada community of lobster fishers and to assess differences between captains and deckhands. Twenty-eight participants (10 captains, 18 deckhands) were questioned and self-reported on lifestyle, general health status, work-related musculoskeletal disorders and traumatic injuries. The data collected reveal both groups' high prevalence of cardiometabolic and musculoskeletal health issues. Captains reported more occupational exposition and health issues, and showed poorer lifestyle habits than deckhands. Fishers reported potential solutions to reduce occupational risks, presented as three types: lifestyle, working behaviours and leadership. This study evaluated a community of Canadian lobster fishers regarding their occupational health and safety. Potential avenues for mitigating occupational risk specific to this community will nurture future implementation.

Classification of myo-connective tissue injuries for severity grading and return to play prediction: A scoping review.

OBJECTIVES: To conduct a systematic literature search to identify currently used classifications of acute non-contact muscle injuries in sporting adults. DESIGNS: Scoping review. METHODS: A systematic literature search from January 1, 2010 to April 19, 2022 of Medline and SPORTDiscus yielded 13,426 articles that were screened for eligibility. Findings from included studies were qualitatively synthesized. Classifications and their grading, as well as outcomes and definitions were extracted. RESULTS: Twenty-four classifications were identified from the 37 included studies, most of which had low evidence study designs. Majority (57 %) of classifications were published after 2009 and were mostly developed for hamstring or other lower limb injuries. The six most cited classifications accounted for 70 % of the reports (BAMIC, modified Peetrons, Munich, Cohen, Chan and MLG-R). Outcome reporting was sparse, making it difficult to draw conclusions. Still, significant relationships between grading and time to return to play were reported for the BAMIC, modified Peetrons, Munich and Cohen classifications. Other classifications either had a very low number of reported associations, reported no associations, reported inconclusive associations, or did not report an assessment of the association. Other outcomes were poorly investigated. CONCLUSIONS: There is no agreed-upon use of muscle classification, and no consensus on definitions and terminology. As a result, reported outcomes and their relationship to severity grading are inconsistent across studies. There is a need to improve the generalizability and applicability of existing classifications and to refine their prognostic value. High-level evidence studies are needed to resolve these inconsistencies.

Removal of Motion Artifacts in Capacitive Electrocardiogram Acquisition: A Review.

Capacitive electrocardiogram (cECG) systems are increasingly used for the monitoring of cardiac activity. They can operate within the presence of a small layer of air, hair or cloth and do not require a qualified technician. They can be integrated into wearables, clothing or objects of daily life, such as beds or chairs. While they offer many advantages over conventional electrocardiogram systems (ECG) that rely on wet electrodes, they are more prone to be affected by motion artifacts (MAs). These effects, which are due to the relative movement of the electrode in relation to the skin, are several orders of magnitude higher than ECG signal amplitudes, they occur in frequencies that might overlap with the ECG signal, and they may saturate the electronics in the most severe cases. In this paper, we provide a detailed description of MA mechanisms that translate into capacitance variations due to electrode-skin geometric changes or into triboelectric effects due to electrostatic charge redistribution. A state-of-the-art overview of the different approaches based on materials and construction, analog circuits and digital signal processing is provided as well as the trade-offs to be made using these techniques, to mitigate MAs efficiently.

Active training and driving-specific feedback improve older drivers' visual search prior to lane changes.

BACKGROUND: Driving retraining classes may offer an opportunity to attenuate some effects of aging that may alter driving skills. Unfortunately, there is evidence that classroom programs (driving refresher courses) do not improve the driving performance of older drivers. The aim of the current study was to evaluate if simulator training sessions with video-based feedback can modify visual search behaviors of older drivers while changing lanes in urban driving. METHODS: In order to evaluate the effectiveness of the video-based feedback training, 10 older drivers who received a driving refresher course and feedback about their driving performance were tested with an on-road standardized evaluation before and after participating to a simulator training program (Feedback group). Their results were compared to a Control group (12 older drivers) who received the same refresher course and in-simulator active practice as the Feedback group without receiving driving-specific feedback. RESULTS: After attending the training program, the Control group showed no increase in the frequency of the visual inspection of three regions of interests (rear view and left side mirrors, and blind spot). In contrast, for the Feedback group, combining active training and driving-specific feedbacks increased the frequency of blind spot inspection by 100% (32.3 to 64.9% of verification before changing lanes). CONCLUSIONS: These results suggest that simulator training combined with driving-specific feedbacks helped older drivers to improve their visual inspection strategies, and that in-simulator training transferred positively to on-road driving. In order to be effective, it is claimed that driving programs should include active practice sessions with driving-specific feedbacks. Simulators offer a unique environment for developing such programs adapted to older drivers' needs.

Different sit:stand time ratios within a 30-minute cycle change perceptions related to musculoskeletal disorders.

Regular standing interruptions to sedentary work are recommended, but their dosage is understudied. To measure perception variations associated with different sit:stand ratios, 16 people used six ratios (30:0, 27:3, 24:6, 21:9, 18:12 and 15:15) within 30-min cycles in their normal office environment. At start and end of each workday, study participants recorded their perception of 11 factors on a 10-point scale. Musculoskeletal discomfort in 10 body regions was measured before and after exposure to sit-stand ratios. Overall preferred ratios were recorded. Sit:stand ratio affected all perceived factors, with impact varying. Standing at least 6 min improved results most overall; however, individual perceived factors were least impacted by any of 30:0, 27:3, 24:6 or 21:9. Preferred sit:stand ratios were 15:15, 18:12 and 21:9. Typically, least liked ratios involved briefest standing (30:0, 27:3, 24:6) although two participants least liked 15:15. Understanding these variations contributes to appropriate standing dosage recommendations.