These were calculated in order to compare our results to previous

These were calculated in order to compare our results to previous studies that have investigated the relationship between percent strength ratios and injury occurrences. Percent strength ratios were ranked for both the barefoot and

shod conditions from largest percentage to smallest. The largest percentage was ranked as a 1 with the smallest percentage ranked as an 8. During the basketball season, injuries were recorded (Table 1). An injury was defined as a lower extremity impairment that caused Regorafenib a functional limitation of play or caused the athlete to miss practice(s) or game(s). The University athletic trainers provided diagnosis and reporting of injuries. The university athletic trainers completed ranking of the athletes based on the severity of injuries that were sustained during the season. To maximize objectivity, injuries were first divided into ankle/foot complex injuries and all other lower extremity injuries. Ankle/foot complex injuries were ranked first and severity was based on the number of practices and games missed. After the ranking of all ankle/foot complex injuries all other lower extremity injuries

were ranked. Severity Trichostatin A research buy of lower extremity injuries was based on the total number of practices and games missed, as with the ankle/foot complex. An injury ranking of 1 would indicate the most severe injury and a ranking

of 8 would indicate no injuries. Peak torque, time to peak torque, and percent strength ratio were checked for normality using Shapiro–Wilk’s almost W test. Thus, mean difference between conditions was investigated by employing dependent t tests. The ranked difference between barefoot and shod conditions for inversion and eversion, time to peak torque as well as the ranked percent strength ratio for both conditions was correlated with injury ranking using a Spearman rho correlation (ρ). Based on the hypothesis, a positive relationship would be present. An individual with an injury ranking of 1 would have a large difference in torque or large percent strength ratio; whereas, an individual with an injury ranking of 8 would have a difference in torque near zero or a small percent strength ratio. Strengths of correlations were defined as follows: ±1.00 to 0.80 = very strong; ±0.79 to 0.60 = strong; ±0.59 to 0.40 = moderate; ±0.39 to 0.20 = weak; ±0.19 to 0 = no relationship. 22 All statistical analysis was done using SPSS 16.0 (IBM Corporation, Armonk, NY, USA). The α level was set at 0.05. There were no significant differences in peak torque between barefoot and shod conditions for either inversion or eversion (Table 2). There was no significant difference in time to peak torque or eversion-to-inversion percent strength ratio between barefoot and shod conditions.

After NMDAR activation, BAPTA blocked changes in rectification, i

After NMDAR activation, BAPTA blocked changes in rectification, implicating the involvement of elevated Ca2+ and supporting a role for NMDARs in this process (n = 8; RI, 0.54 ± 0.06 to 0.57 ± 0.07; p = 0.39). Our hypothesis is that the NMDAR-induced changes in rectification we observe are due to a loss of CI-AMPARs with a possible replacement by CP-AMPARs. There are several different mechanisms by which the loss of CI-AMPARs could occur. One is mTOR inhibitor through lateral diffusion of AMPARs from the synaptic to the extrasynaptic membrane (Borgdorff and Choquet, 2002). However, the best-characterized mechanism

of AMPAR removal is dynamin-dependent endocytosis, triggered by an NMDAR-induced rise in postsynaptic Ca2+ (Carroll et al., 2001). We tested whether the CI-AMPARs are internalized due to dynamin activity by dialyzing RGCs with 10 mM PCI-32765 mouse dynamin-inhibitory peptide (DIP), which blocks endocytosis of AMPARs by interfering with the binding of amphiphysin with dynamin (Lüscher et al., 1999). In RGCs, DIP causes a run up of the extrasynaptic, not synaptic,

AMPAR-mediated response due to unbalanced insertion of AMPARs undergoing rapid cycling (Xia et al., 2007). To ensure that this separate effect of DIP would not confound our results, we first recorded a 10 min baseline of light responses during DIP dialysis before recording the control I-V. The light responses of all ten cells remained stable during this period (3.2% ± 1.3% change over Sodium butyrate 10 min; data not shown), indicating that synaptic AMPARs under our recording condition are stable and that DIP does not affect the initial AMPAR ratio. While the mean baseline RI was higher in DIP-loaded cells than that of the control cells (Figure 4F; RI = 0.74), this effect was not significant (p = 0.15, t test) and probably reflects the variability of RIs as seen in Figure 1D. We find that inclusion of DIP in the pipette solution consistently

blocked the induction of synaptic plasticity with NMDA. The average rectification was 0.74 ± 0.04 before and 0.73 ± 0.07 after application of NMDA (Figure 4; n = 10, p = 0.64). Although, on average, there was no change in RI, in three out of ten cells, there was an increase in response amplitude at −60mV and no change in amplitude at +40mV. This result suggests that new CP-AMPARs were inserted into the membrane, presumably through persistent exocytosis or membrane diffusion, and supports the hypothesis that NMDAR activation induces an exchange of CI-AMPARs for CP-AMPARs. Our findings suggest that direct pharmacological activation of NMDARs on ON and ON-OFF RGCs drives AMPAR plasticity, but they do not establish whether endogenous transmitter release from presynaptic ON bipolar cells can similarly drive NMDAR-dependent plasticity.

To locate the S435 (β4) and D397 (α5) residues within the recepto

To locate the S435 (β4) and D397 (α5) residues within the receptor pentamer, we performed homology modeling with the Torpedo nAChR using one possible α3β4α5 subunit arrangement. This

model predicted the formation of a very similar disposition of α helices in the α3β4α5 and mapped both residues to the intracellular vestibule ( Figure 2B). Electrostatic mapping of the vestibule showed a particular disposition of charges with S435 and D397 located at the more distal and positively charged part of the vestibule ( Figure 2C). These data indicate first that the critical residue in β4 that mediates the β4 effect is located in the receptor structure near the most common SNP of α5 to be associated with heavy smoking; and second, that this is a highly charged domain of the receptor where single residue changes may have a particularly strong effect on receptor activity. To test the hypothesis Protease Inhibitor Library manufacturer that β4 is rate limiting for nAChR Akt inhibitor assembly and function in vivo and that overexpression of β4 can strongly influence nicotine-evoked currents and behavioral responses to nicotine, we characterized a bacterial artificial chromosome (BAC) transgenic line spanning the Chrnb4-Chrna3-Chrna5

gene cluster ( Gong et al., 2003). The BAC transgene included the intact coding sequences of the Chrnb4 gene, modified sequences of Chrna3, and incomplete sequences of Chrna5. Chrna3 was modified by insertion of an eGFP cassette followed by polyadenylation signals at the ATG translation initiator codon of Chrna3 ( Figure 3A). The upstream sequences of Chrna5, encoding exon 1 splice variants ( Flora et al., 2000), are missing in the BAC transgene ( Figure 3A). To promote correct expression of Chrnb4, the BAC included the intergenic and 5′ flanking regions encompassing the cis-regulatory elements that coordinate cotranscriptional control of the genes in the cluster ( Bigger et al., 1997, Medel and Gardner,

2007 and Xu et al., 2006). As a result of these modifications in the BAC transgene, these Tabac mice express high levels of β4, but not α5 ( Figure 3B), and expression of α3 is replaced by expression of an eGFP reporter cassette to monitor the sites expressing the transgene ( Figures 3C–3H). As shown in Figure 3, neurons science expressing eGFP were evident in autonomic ganglia ( Figure 3C), and in very restricted brain structures ( Figures 3D–3H) known to express these genes ( Zoli et al., 1995). Immunostaining with cholinergic (ChAT) and dopaminergic (TH) markers indicated high expression of Chrna3/eGFP in ChAT neurons of the Hb-IPN system ( Figures 3G and 3H). Intense Chrna3/eGFP expression was also detected in other brain areas ( Figures 3D and 3E) involved in nicotine addiction, such as the ventral tegmental area (VTA), the caudal linear nucleus (Cli), the supramammilary nucleus (SuM) ( Ikemoto et al., 2006), and the laterodorsal tegmental nucleus ( Figure 3F), which provides modulatory input to the VTA ( Maskos, 2008).

A monitoring process modulates the strength of the input (λ) to e

A monitoring process modulates the strength of the input (λ) to each group of neurons simulating different trial history conditions: λ increases its value as the number of Stop trials preceding a Go trial increases and decreases its value as the number of Go trials preceding a Go trial increases (Figure 4B). We observe that the model reproduces the same relationship between the probability of failure and SSDs as observed

during the countermanding task, i.e., the probability of failing in the Stop trials increases as the SSD increases (Mirabella et al., 2006) (Figure S3A). To compute decision times in the simulations, we considered that the decision process was terminated when the difference in activity between Go and Stop pools was above a fixed threshold (Roxin and Ledberg, this website 2008). The RT was calculated by adding 150 ms to the decision time, consistent

with the peak in FR Selleckchem Epacadostat observed 150 ms before movement onset in the physiological data (Figure 2A). The mean and SD of RT obtained from the simulations (Figures 4C and S3B) exhibit the same trend as observed in the physiology of PMd (Figures 2C and S2C): the mean and SD of RT in a Go trial are longer/shorter as the number of preceding Stop/Go trials increase. Consistent with our analysis of the physiological data, the different simulated trial history conditions have a similar impact on the variability of the Go pool response (Figure 4D). those This impact of the monitoring signal λ on RT and VarCE can be intuitively understood in terms of the competition between the two neuronal pools Stop and Go through mutual inhibition (Figure 4A). The model is tuned such that the firing rate of the Go pool is not affected by this neuronal competition (Figure S3C), as observed in the response of the neurons we have analyzed (Figure S2E). We observe that, given these assumptions that reflect the physiological properties of PMd, the addition of the monitoring signal leads to the modulation of the effect that

the Stop pool has on the dynamics of the overall network, leading to a change in the mean RT. In addition, when the influence of the Stop pool on the dynamics is increased, the intrinsic noise of the system starts to have a larger impact on the performance and dynamics of the network, resulting in an increase in VarCE and RT variability. Indeed, it has been demonstrated that the neural response variability changes with the strength of the input to this model, due to a shift in the distance from the working point of the system to the bifurcation point (Deco and Hugues, 2012; Roxin and Ledberg, 2008). Here we exploit this effect through the monitoring signal. Hence, perceptual input defines the mean rate, while the history-dependent monitoring signal defines a modulation around this rate expressed in VarCE.

L K ), a predoctoral fellowship from the Nakajima Foundation (to

L.K.), a predoctoral fellowship from the Nakajima Foundation (to R.L.M.), NRSA F31NS056558-01A1 (to O.C.), the Veterans Administration (to I.S.S. and N.S.P.), the Foundation Fighting Blindness (to N.S.P.), R01 NS065048 (to Y.Y.), the Foundation pour la Rechereche Médicale (Programme équipe FRM) (to A.C.), and R01 NS047333 (to R.J.G.). A.L.K. and J.N. are investigators of the Howard Hughes Medical Institute. trans-isomer manufacturer
“The accumulation of synaptic vesicles at the nerve terminal enables the sustained release of neurotransmitter

in response to persistent stimulation. However, not all synaptic vesicles contribute equally to evoked release. At most synapses, only a fraction of the synaptic vesicles present take up external tracers with stimulation, and this fraction Capmatinib ic50 has been termed the recycling pool (Harata et al., 2001 and Rizzoli and Betz, 2005). Even after prolonged stimulation, a large proportion of synaptic vesicles at most boutons do not undergo exocytosis (Fernandez-Alfonso and Ryan, 2008), and the properties of this resting pool have remained elusive. What accounts for the inability to release a large fraction of the synaptic vesicles at a presynaptic bouton? Resting pool vesicles may simply reside too far from the active zone, although previous

work has shown that they intermingle with the recycling pool (Rizzoli and Betz, 2004). Differences in tethering to the cytoskeleton may influence vesicle mobilization by activity, and a number of proteins associated with the cytoskeleton, such as the synapsins, have been shown to influence release (Chi et al., 2001, Fenster et al., 2003, Leal-Ortiz et al., 2008 and Takao-Rikitsu

et al., 2004). Recent work has also suggested a role for regulation of the recycling pool by cyclin-dependent kinase 5 (cdk5) (Kim and Ryan, 2010). Consistent mafosfamide with a role for extrinsic factors in pool identity, synaptic vesicles within a single bouton generally appear homogeneous, and multiple synaptic vesicle proteins localize in similar proportions to recycling and resting pools (Fernandez-Alfonso and Ryan, 2008). Alternatively, intrinsic differences in molecular composition may account for the distinct behavior of recycling and resting pool vesicles. Previous work has indeed shown that synaptic vesicles recycle by multiple mechanisms (Glyvuk et al., 2010, Newell-Litwa et al., 2007, Takei et al., 1996 and Zhang et al., 2009), raising the possibility that these pathways produce vesicles with different proteins. Synaptic vesicles can recycle through an endosomal intermediate (Heuser and Reese, 1973 and Hoopmann et al., 2010) as well as directly from the plasma membrane, through clathrin-dependent endocytosis (Takei et al., 1996). Synaptic vesicle formation from endosomes depends on the endosomal heterotetrameric adaptor proteins AP-3 and possibly AP-1 (Blumstein et al., 2001, Faúndez et al., 1998 and Glyvuk et al.

, 2011) In this study, we directly investigate Ca2+’s role in re

, 2011). In this study, we directly investigate Ca2+’s role in regulating adaptation in mammalian auditory hair cells. In voltage-clamped Neratinib price hair cells, adaptation manifests itself in two

ways, as a time-dependent decrease in current amplitude during mechanical stimulation and as a shift in the peak current-displacement (I–X) plot. We developed piezo-coupled devices that allow stimulation rates up to 30 kHz producing rise times as fast as 11 μs, resulting in very fast adaptation time constants. Clamp speeds averaging 28 μs and output filtering up to 100 kHz also allow for better resolution of adaptation kinetics than previously possible. Here, we used 50 ms step stimulations from −170 nm to 600 nm to measure both fast and slow adaptation processes in rat MG-132 in vivo cochlear outer hair cells (OHCs; Figure 1A). Current-displacement plots for the peak and steady state responses illustrate the adaptation shift (Figure 1B). Double exponential fits to each MET current response produced time constants ranging between 0.1 and 5 ms for bundle deflections eliciting up to ∼75% of the maximal current (Figures 1C and 1E). Larger stimulations required three time constants (Figures 1C and 1D) with the third time constant ranging between 8 and 50 ms (Figure 1E). The two faster time

constants likely underlie fast adaptation, as the sensitivity, operating range, and kinetics are most consistent with previous reports (Kennedy et al., 2003, Ricci et al., 2005 and Waguespack et al., 2007). The two time constants likely reflect the faster stimulus rise time rather than the existence of multiple mechanisms, given that the absolute values of these time constants do not change, but rather, the proportion of each varies with stimulus intensity. The slowest time constant may

represent saturation of fast adaptation or recruitment of a distinct slower process. This mechanism contributes at most 30% of the total adaptation observed at maximal stimulations, with no contribution at stimulation levels eliciting less than 75% of the maximal current (Figure 1F), in agreement with other reports in mammals (Kennedy et al., 2003, Ricci et al., 2005 and Waguespack et al., why 2007). In contrast, low-frequency cells show near 100% motor adaptation contribution for maximal stimulations and 50% motor adaptation with 50% maximum stimulations (Wu et al., 1999). Thus, mammalian data are consistent with the hypothesis that fast adaptation is the predominant mode of adaptation in mammalian auditory hair cells. Depolarization reverses the MET current and eliminates Ca2+ entry into stereocilia, and thus, provides a means to assess whether Ca2+ is driving adaptation (Assad et al., 1989 and Crawford et al., 1989).

, 2008 and Quirk et al , 2003) Although considerable evidence in

, 2008 and Quirk et al., 2003). Although considerable evidence indicates that an IL-ITC circuit maintains extinguished fear, there are both behavioral and neural data that are not readily explained by this model. First, an IL-mediated inhibition of CE (which presumably operates to suppress fear output nonspecifically) by an extinguished CS should block fear to another unextinguished CS when the two stimuli are presented together, but evidence for this is scant (Leung and Westbrook, 2008). Moreover, an IL-mediated suppression of fear by inhibitory ITC cells

overlooks the observation that neurons upstream in the basal and lateral amygdala themselves show decrements in activity after extinction (Herry et al., 2008 and Repa et al., 2001) that readily renew outside of the extinction context (Hobin et al., 2003). These observations suggest that local inhibition within the BA may selectively Selleckchem MEK inhibitor (and reversibly) silence neurons in the BA after extinction to suppress fear. In an article in the current issue of Neuron, Trouche et al. (2013) examined this possibility by

labeling neurons in the BA involved in contextual fear conditioning and then examining whether those neurons are reactivated during memory retrieval after extinction. To this end, Tariquidar research buy they used a TetTag reporter mouse that expresses GFP under the control of a c-fos promoter when doxycycline is removed from the diet ( Reijmers et al., 2007). After labeling neurons during fear Edoxaban conditioning, Trouche et al. (2013) then assessed ex vivo GFP and Zif expression after a retrieval test to determine whether neurons active during fear conditioning remained active after extinction. Interestingly, they found that roughly 15% of the BA neurons tagged during fear conditioning were reactivated in nonextinguished

mice. However, only half that number of neurons was reactivated in animals that underwent an extinction procedure. In other words, extinction training silenced a large proportion of BA neurons that had been active during fear conditioning. They did not observe extinction-induced silencing in either hippocampal area CA1 or IL, suggesting that the silencing was rather specific to the BA. Hence, these results imply that the extinction of fear drives local inhibitory interneurons to establish synaptic contacts with a subset of excitatory BA neurons recruited during fear conditioning. To further explore this possibility, Trouche et al. (2013) examined the colocalization of proteins unique to inhibitory interneurons in active and silenced BA neurons. Interestingly, they found that silenced neurons exhibited significantly greater perisomatic GAD67 labeling, suggesting a proliferation of inhibitory GABAergic synapses on these neurons. In line with this idea, they found that the density of perisomatic parvalbumin (PV) staining was greater in silenced neurons and these changes were only observed in animals undergoing extinction.

5°C or 49°C), then quantified latency to flick the tail At both

5°C or 49°C), then quantified latency to flick the tail. At both temperatures, check details there was a significant (∼2-fold) increase in the latency to

flick in DTX-treated males and females (Table 1). Next, we placed the mice on a hot plate heated to 52°C and measured the latency to flick, lick, or shake a hindpaw. DTX-treated mice of both sexes exhibited over a 2-fold increase in withdrawal latency (Table 1). Finally, we pharmacologically activated the thermosensor TRPV1 by injecting 0.1 μg/μl capsaicin into the left hindpaw. We found that the DTX-treated male and female mice showed a 2-fold reduction in the time spent licking the capsaicin-injected hindpaw. Collectively, these experiments revealed that CGRPα DRG neurons were required to sense and behaviorally respond to noxious heat and capsaicin. Heat and mechanical hypersensitivity are two common symptoms of inflammatory pain and neuropathic pain (Basbaum et al., 2009). To determine whether CGRPα DRG neuron ablation impaired heat and mechanical hypersensitivity, we studied saline- and DTX-treated CGRPα-DTR+/− mice in the complete Freund’s adjuvant (CFA) model of inflammatory pain (Figures 4A–4F) and in the spared nerve injury (SNI) model

of neuropathic pain (Figures 4G and 4H). We monitored heat and mechanical sensitivity before, during, and after saline/DTX treatment. We also monitored plasma extravasation in the noninflamed (contralateral) and buy Small molecule library CFA-inflamed hindpaw with Evans Blue dye. We found that plasma extravasation was increased in both groups of mice after inflammation of the hindpaw; however, plasma extravasation was significantly lower in the inflamed hindpaw of DTX-treated male and female mice (when compared to the inflamed paw of saline-treated mice; Figures 4A and 4B). This reduction supports a role for peptidergic, because CGRP+ afferents in neurogenic inflammation (Basbaum et al., 2009). In both chronic pain models, heat withdrawal latencies increased to the cutoff time (20 s) after the second DTX injection and remained at this level for at least 2 weeks (Figures 4C, 4D, and 4G). Moreover, DTX-treated animals showed

no sign of heat hyperalgesia after inflammation (CFA) or nerve injury (SNI). In contrast, mechanical sensitivity and hypersensitivity were not impaired in DTX-treated animals in either chronic pain model (Figures 4E, 4F, and 4H). Likewise, noxious (tail clip) and innocuous (cotton swab) mechanical sensitivity was not impaired in DTX-treated animals (Table 1). Taken together, these behavioral experiments provide direct evidence that CGRPα DRG neurons are required for noxious thermosensation but are not required for noxious or innocuous mechanosensation in vivo. Capsaicin-responsive DRG neurons respond to the pruritogens histamine and chloroquine (Imamachi et al., 2009; Liu et al., 2009; Schmelz et al., 2003; Sikand et al., 2011).

Furthermore, we find that the axonal boutons

of these int

Furthermore, we find that the axonal boutons

of these interneurons also show a baseline RG7420 concentration level of turnover. Following removal of sensory input by focal retinal lesions, we observed a rapid loss of both dendritic spines and axonal boutons of inhibitory neurons. This effect is not spatially limited to the silenced cortical region, but gradually decreases with increasing distance from the border of the LPZ, and appears to be driven to a large degree, by reduced cortical activity levels. Because the changes in inhibitory structures precede increases in excitatory spine turnover (Keck et al., 2008), these data suggest that inhibitory structural plasticity may be the first step in cortical reorganization after sensory

deprivation. Most studies of synaptic structural plasticity in vivo thus far have focused on excitatory synapses, particularly postsynaptic dendritic spines. Here, we report that a subset of inhibitory neurons (mostly NPY positive cells) in adult mouse visual cortex bears dendritic spines. We have observed these spines under very different experimental conditions: in fixed tissue sections, in vivo and in acute cortical brain slices. Many, if not all, Paclitaxel mw of these spines carry functional excitatory synapses, as revealed by immunohistochemistry and their response to glutamate uncaging. As has been observed for excitatory cells (Hofer et al., 2009, Holtmaat et al., 2006, Keck et al., 2008, Majewska et al., 2006, Trachtenberg et al., 2002 and Zuo et al., 2005), inhibitory cell spines demonstrate a baseline level of turnover in naive adult animals over a period of days. Following sensory deprivation, changes to excitatory cell spines occur on the time scale of days (Hofer et al., 2009, Holtmaat et al., 2006, Keck et al., 2008, Trachtenberg et al., 2002 and Zuo et al., 2005), typically in the form of increased dynamics, lasting for weeks to months. Here, we observe that spines on inhibitory neurons

change much more rapidly—in the first 6 hr after deprivation—mainly via increased Bay 11-7085 spine loss resulting in a decrease in spine density. This increase in dynamics occurs through the first 72 hr after deprivation, but not afterward, suggesting that inhibitory cell spine plasticity ends well before changes in excitatory spines subside. Axonal boutons in the naive cortex have been reported to demonstrate a baseline turnover in excitatory cells, the rate of which depends largely on cell type (De Paola et al., 2006 and Stettler et al., 2006). Previous studies using chronic two-photon imaging of PV positive inhibitory neurons (Kuhlman and Huang, 2008), GABA positive inhibitory neurons (Chen et al., 2011) or GAD65 positive inhibitory neurons (Marik et al., 2010) demonstrated a baseline turnover of axonal boutons in adult cortex.

The two randomized clinical trials reported non-significant diffe

The two randomized clinical trials reported non-significant differences between groups on all study variables,36 and 37 while the quasi-experimental, cross-over and cross-sectional studies reported that those in Tai Ji Quan had improved aerobic endurance/exercise capacity, balance, strength, flexibility, mood, social support, exercise self-efficacy, lipid profile and glucose metabolism, and lowered blood pressure, body weight and Vorinostat stress (p < 0.05, includes within and between group differences). 32, 33, 34, 35, 38 and 39 Numerous studies conducted during

the past 5 decades have clearly established the benefits of regular exercise for adult men and women with CVD and CVD risk factors.3, 4, 5, 6 and 7 Despite the popularity of Tai Ji Quan as an exercise modality among older adults, little research has been conducted in the past decade on the potential benefits of Tai Ji Quan exercise to prevent and manage CVD.16, 40 and 41 Since the phenotype and treatment goals for coronary artery disease, chronic heart

failure, stroke, and CVD risk factors are different, the extant Tai Ji Quan research literature involves a variety of study variables, making comparisons across studies difficult. The effect of Tai Ji Quan on aerobic PD-1/PD-L1 inhibitor 2 endurance/exercise capacity or QoL was most frequently examined (40% of studies). Overall, participants enrolled in Tai Ji Quan had better outcomes, though mixed results were reported. Only

55% of the studies in this review were randomized clinical trials (RCTs). However, all of the studies (n = 9) conducted among persons with chronic heart failure and stroke survivors were RCTs, while the other two randomized clinical trials because reviewed focused on those with CVD risk factors. Although coronary artery disease is more prevalent than chronic heart failure or stroke, no randomized clinical trials involving Tai Ji Quan in this population were found. 2 In addition, the majority of studies in this review were likely underpowered to detect statistically significant and/or clinically meaningful differences over time between groups as only 20% of these studies enrolled ≥100 participants. Finally, the Tai Ji Quan exercise dose (i.e., frequency, intensity, time, and type) varied greatly among these studies, and likely affected the reported study outcomes, further limiting generalizability of the reported results. Collectively, these studies indicate that Tai Ji Quan is a safe form of exercise to prevent and manage CVD. No serious adverse findings were reported, even among these higher risk participants with CVD. It is readily apparent that further research examining the effects of Tai Ji Quan as an exercise modality to prevent and manage CVD is needed.