For PA data, the time spent in sedentary activity, LPA and MVPA w

For PA data, the time spent in sedentary activity, LPA and MVPA were converted to percentage of monitored time to account for the variance in the participants’ average monitoring time. This approach at analysis has been done in other recent PA studies.33 and 34 Change scores (post-test – baseline) were also computed for the percentage of time spent in each activity category. 2 × 2 univariate analyses of variance (ANOVAs) were done on the change scores using Group (CP, TD) and Training (FMS, control) as fixed factors. Age was used as a covariate because FMS are

known to develop during the pre-pubescent years.12 Paired comparisons with Bonferroni adjustments were performed to follow up significant main effects. Paired samples Carfilzomib in vivo t tests were performed to follow up significant interactions, and to compare the weekday and weekend PA of participants. Pearson’s product moment correlation was computed to examine the association between change in FMS scores and change in activity category. Statistical significance was set at p < 0.05 for all tests. The minimal detectable change (MDC) for time spent in the three PA categories was also computed for the training groups (CP-FMS, TD-FMS) to verify that click here observed changes were not due to uncontrolled error. The MDC90 was computed based on the standard error of measurement (SEM) and the confidence interval (90%CI) of the mean changes in scores.35 The proportion of participants in the training groups who

achieved the MDC90 was then calculated. It was first verified that FMS proficiency had improved for participants in the training groups. Based on the analyses of change scores, participants in the FMS training groups appeared to have gained improvements in the quality of movement patterns and outcomes, as reported in detail below. A significant main

effect of Training was found on the change in scores of all five tested FMS: running (F(4, 49) = 8.407, p = 0.006, ç2 = 0.239), jumping (F(4, 49) = 20.357, p < 0.001, ç2 = 0.311), kicking (F(4, 49) = 16.207, p < 0.001, ç2 = 0.265), throwing (F(4, 49) = 10.798, p = 0.002, ç2 = 0.194), and catching (F(4, 49) = 8.407, p < 0.006, ç2 = 0.239). Pairwise comparisons showed that training groups had a significantly larger positive change in scores than the control groups (all p < 0.01). Age was also found to be a significant covariate of the change in three skills: jumping (F(4, Dichloromethane dehalogenase 49) = 12.291, p = 0.001, ç2 = 0.215), throwing (F(4, 49) = 15.86, p < 0.0001, ç2 = 0.261), and catching (F(4, 49) = 7.919, p = 0.007, ç2 = 0.150). No significant main effect of Group was found for any process-oriented FMS score. No significant Group × Training interactions were found either. Significant main effects of Training were found on the change in scores for all five tested skills: running duration (F(4, 49) = 7.86, p = 0.008, ç2 = 0.155), jumping distance (F(4, 49) = 14.03, p = 0.001, ç2 = 0.238), successful kick (F(4, 49) = 24.79, p < 0.001, ç2 = 0.

To show this, we put adult animals on a lawn of OP50 while exposi

To show this, we put adult animals on a lawn of OP50 while exposing them for 6 hr to the smell of a PA14 lawn, which was grown on the lid of the plate. In this experiment, trained animals were exposed to the smell of PA14, but were fed on OP50. These trained animals exhibited olfactory preference comparable to that of the control animals that fed on OP50 without exposure to the smell of PA14 ( Figure S1F). Previously, we used a two-choice assay that quantified the overall movements of populations of crawling worms to elucidate the role of serotonergic neurotransmission in aversive olfactory learning (Zhang et al.,

2005). Importantly, this website the automated microdroplet assay that we utilized in this study recapitulates the phenotypes that were obtained using the two-choice assay and supports the role of serotonin in aversive olfactory learning. The learn more cat-1 mutation, which disrupts both dopamine and serotonin neurotransmission ( Duerr et al., 1999), greatly reduced olfactory learning quantified using the microdroplet assay, whereas the cat-2 mutation, which specifically disrupts dopamine production ( Lints and Emmons, 1999), had no effect on learning ( Figure 1E). The tph-1(mg280) mutant, which is deficient in the

only C. elegans tryptophan hydroxylase required for biosynthesis of serotonin ( Sze et al., 2000), was completely defective in olfactory learning in the microdroplet assay Dipeptidyl peptidase ( Figure 1E). In addition,

the mod-1(ok103) mutant, which is defective in a serotonin-gated chloride channel ( Ranganathan et al., 2000), also showed greatly reduced learning in the microdroplet assay ( Figure 1F). Thus, the microdroplet assay for swimming animals assigns phenotypes that are consistent with the two-choice assay that we previously used. The important advantage of the microdroplet assay is that it allows us to quantify olfactory preference with small numbers of animals. To characterize the neuronal network that regulates the switch of olfactory preference, we began by identifying chemosensory neurons required for olfactory plasticity. We first tested an osm-6 mutant, which is defective in development and sensory function of all ciliated chemosensory neurons ( Collet et al., 1998). The osm-6 mutant showed significantly reduced learning to avoid the smell of PA14 ( Figure 2A). By comparing choice indexes before and after training, we found that the osm-6 mutant was unable to reduce its olfactory preference for the smell of PA14 after training ( Figure S2A). These results indicate a requirement for the function of chemosensory neurons in generating a learned preference. The residual learning ability of the osm-6 mutant likely results from its residual olfactory sensory ability in the microdroplet assay ( Figure S2B).

We show that CBP, via its intrinsic HAT activity, appears to acti

We show that CBP, via its intrinsic HAT activity, appears to activate the expression of the key ecdysone response gene sox14 and thereby govern ddaC dendrite pruning. In contrast, the dGcn5 HAT is dispensable for ddaC dendrite pruning despite its reported roles in activation

of various ecdsyone response genes and in progression of metamorphosis ( Carré et al., 2005). Thus, CBP, but not dGcn5, acts to regulate sox14 expression and dendrite pruning in sensory neurons during early metamorphosis. CBP induces histone H3K27 acetylation, a mark for transcriptionally active chromatin, at the sox14 locus find more in response to ecdysone. Our biochemical data indicate that EcR-B1 associates with CBP in an ecdysone-dependent manner, whereas Brm facilitates the formation of the EcR-B1/CBP complex. In accordance with its role in facilitating binding of CBP to EcR-B1, ecdysone strongly triggers CBP-dependent H3K27 acetylation on sox14 gene in an EcR-B1 and Brm-dependent manner, suggesting functional coordination among CBP, EcR-B1, and Brm in the activation of their common target gene sox14. Although HATs and ATP-dependent chromatin remodelers have been proposed to act in at least three different orders during gene activation ( Narlikar et al., 2002), our data support the model in which Brm-mediated MLN8237 nmr chromatin remodeling decompacts the chromatin structure of sox14 gene locus and facilitates the formation

of the ecdysone/EcR-B1/CBP complex, thereby triggering local histone acetylation and sox14 transcription in response to ecdysone ( Figure 8D). In mammals, the estrogen receptors, one of the mammalian homologs of the fly EcR-B1 and Usp receptors, can transduce extrinsic estrogen hormone signals to mediate neurite growth and differentiation (Toran-Allerand et al., 1999), as well as synapse plasticity associated

with learning and memory (McCarthy, 2008). Notably, the estrogen receptors cooperate with Brg-1, a mammalian Brm homolog, and CBP to activate estrogen hormone response genes in in vitro cell-based assays (DiRenzo et al., 2000). Our study shows the physiological significance of the coordination between systemic steroid hormone and intrinsic epigenetic very factors Brm/CBP during the remodeling of the Drosophila nervous system. Whether and how this mechanism controls the remodeling and maturation of the mammalian nervous systems awaits further studies. The most remarkable developmental changes in mammals are triggered by thyroid hormone, sex steroids, and their nuclear receptors during adolescence, a stage reminiscent of ecdysone-triggered metamorphosis in Drosophila ( King-Jones and Thummel, 2005). A dramatic decrease in synapse number and dendrite branches in primate brains, a process known as synaptic pruning, takes place during adolescence in response to robust changes in steroid hormone levels ( Paus et al., 2008).

Seven and fourteen days after treatment,

Seven and fourteen days after treatment, PLX3397 mouse the egg-mass weight was recorded. After six weeks, the percentage of larval hatching was registered by visual estimation of the amount of empty eggs in relation to the total egg-mass,

within a variation of 5%. Initially, a stock solution of 1% IVM was prepared in a mixture containing two parts trichloroethylene (Synth, Diadema, Brazil) and one part commercial olive oil (TCE-OO). This stock solution was used to prepare the following impregnation solutions in TCE-OO (in parts per million – ppm of IVM): 4000, 3000, 2500, 2000, 1800, 1500, 1200, 1000, 800, 500 and 300. A 750 mm × 850 mm filter paper (Whatman No. 1, Whatman Inc., Maldstone, England) was impregnated with 0.67 ml each of the solutions using an eight-channel micropipette. The material was left to selleck compound dry for 24 h at 25 °C to allow for TCE evaporation. After drying, the filter papers were folded in the middle and sealed on the sides with a metal clip to form the packets. Approximately 100 larvae were transferred to each packet using a paintbrush. The packets were sealed with a third clip and incubated at 27–28 °C and 80–90% relative humidity. The control group was exposed to the filter paper impregnated with acaricide-free TCE-OO. After 24 h, the larvae mortality was determined by counting the total dead and alive individuals. Larvae

that were paralysed or moving only their appendices without the capability to walk were considered dead. Twelve and three tests were performed in triplicate with the strains Mozo and ZOR, respectively. Initially, a solution of Triton X-100 2% (Sigma–Aldrich) was prepared in absolute ethanol (ETH-TX2%). The technical IVM was diluted to 1% in 10 ml the ETH-TX2% solution in order to prepare a stock solution, which

was stored at 4 °C for no more than a week. At the time of testing, 100 μl of the stock solution was added to 9.9 ml distilled water so that the following final concentrations were obtained 100 ppm IVM, 1% ethanol and 0.02% Triton X-100. This initial solution (100 ppm IVM) was serially diluted 17-DMAG (Alvespimycin) HCl 10 times at a 30% rate in a diluent composed of 1% ethanol and 0.02% Triton X-100 in order to obtain the final immersion solutions with the following concentrations (in ppm of IVM): 100, 70, 49, 34.3, 24, 16.8, 11.7, 8.2, 5.7, 4.0 and 2.8. As a control, diluent without acaricide was used. Five hundred microlitres of each immersion solution was distributed in three 1.5 ml microcentrifuge tubes. Using a paintbrush, approximately 100 larvae were transferred to each tube, which was then closed and shaken vigorously to ensure sinking of the larvae. After 10 min of immersion, the larvae were taken off the tube with a clean paintbrush, allowed to dry on a piece of paper towel, then transferred to a packet of filter paper folded in the middle and closed on the sides with metal clips.


with this conjecture, the main driving input t


with this conjecture, the main driving input to pulvinar arises from cortical layer 5 (Sherman, 2007). Contrastingly, the alpha that has been reported in a large number of electroencephalographic/magnetoencephalographic (EEG/MEG) studies to be reduced by functional activation might be related to supragranular alpha sources. Supragranular alpha sources might be more readily detected by EEG/MEG methods, because the synaptic inputs generated by those alpha sources probably impinge on the dendrites of large pyramidal cells, resulting in vertical currents for which EEG/MEG measures are sensitive. Alternatively or in addition, the increased alpha-band coherence during the delay period described by Saalmann et al. (2012) could reflect effects related to short-term memory load, which have been related Imatinib to increased alpha-band power in several studies (Jensen and Mazaheri, 2010). Saalmann et al. (2012) further extend their core findings related to pulvinar-driven alpha-band synchronization to establish a functional relationship between alpha- and gamma-band synchronization during attentional allocation. At the cortical level, previous studies have reported increases Galunisertib molecular weight in gamma coherence primarily in the context of selective visual attention (Fries, 2009), with the idea that it promotes a more efficient communication

between cortical areas (Fries, 2009). Important questions mafosfamide follow regarding the circuits needed to generate gamma oscillations and the attentional mechanisms modulating the phase synchrony across neurons. Regarding the former, current evidence indicates the importance of inhibitory mechanisms provided by local GABAergic input (Fries, 2009). Regarding the latter, several theories have suggested that nonspecific circuits that exhibit low-frequency oscillations could mediate gamma synchrony via cross-frequency coupling (VanRullen and Koch, 2003; Fries, 2009). The Saalmann et al. (2012) paper provides important new information in this respect, as the authors

show that, unlike cortical circuits, the pulvinar engages in local synchrony in the alpha and not in the gamma range. This is not surprising given the evidence for alpha generators in the thalamus and for an absence of gamma sources in deep cortical layers, where the cortico-thalamic projection neurons are located (Buffalo et al., 2011). Moreover, a supplementary figure provided by Saalmann et al. (2012) shows increased cross-frequency coupling between cortical alpha- and gamma-band activity with attention. Clarifying the mechanistic details and functional implications of this alpha-gamma coupling deserves further consideration in future research. An attractive speculation is that alpha rhythms generated during wakefulness by pulvinar neurons reflect periodic perceptual sampling (VanRullen and Koch, 2003; Fries, 2009; Landau and Fries, 2012).

, 2012) We can only speculate

, 2012). We can only speculate screening assay how big a role such dramatic variation will play in future pharmacogenomics findings—but it will probably be large. Genetics is not the whole answer but offers a solid starting point. Further knowledge of the basic disease processes at the cellular and molecular level will be required to discover ideal, curative treatments for most patients with neuropsychiatric disorders, but much could be achieved by personalizing the existing pharmacopeia. Personalized

medicine will bring new insights, more treatment options, and better outcomes to what psychiatrists have always strived for—caring for each patient as an individual. This work was supported by the NIMH Intramural Research Program. We thank Gonzalo Laje for helpful comments. “
“For decades, it has been recognized that axon regeneration is the only way to restore function after severe spinal cord injuries (SCI) that interrupt the long tracts that mediate motor and sensory function. Indeed, SCI and axon regeneration are so linked in the minds of scientists

and the lay public that enabling regeneration after SCI Fasudil nmr is iconic. Achieving axonal regeneration with recovery of function would truly be an extraordinary achievement. Despite progress, measured both as a gain in understanding of the molecular-, cellular-, and systems-level underpinnings of axonal growth, and in the number of investigators studying the topic, success has not yet been achieved. Indeed, progress in the field is nonlinear, with many instances of premature celebration of success, mistargeting, sidesteps, and occasional episodes of withdrawal. The during reasons for this are numerous, ranging from

lack of clarity in use of terminology related to axonal growth and limitations of experimental methods to a lack of rigor in interpretation. This primer aims to provide a framework for the study of axonal growth after spinal cord injury. We focus on SCI not only because it is iconic, but also because it exemplifies all of the issues that plague studies of axon regeneration in any CNS region with mixed white and gray matter. We begin by addressing the meaning of different terms used to describe growth after injury, especially the terms “regeneration” and “sprouting.” Inconsistent use of these terms in the scientific literature creates ambiguity or frank error in interpreting experimental findings. We then review several model systems for studying axonal growth after spinal cord injury, highlighting the advantages and limitations of several models. Finally, we will discuss the tools available to study axonal regeneration and how these might best be applied to reach new levels of insight that will point the way to strategies for improving outcomes after spinal cord injury.

We previously showed that different populations of cells in the m

We previously showed that different populations of cells in the monkey hippocampus monitored information about trial outcome including both success (correct up cells) and failure (error up cells) (Wirth et al., 2009). Here we confirm that this trial outcome signal is also present at the level of the LFP in monkeys and show for the first time that this signal is also seen at the level of BOLD fMRI signals in humans. We also show prominent trial outcome signals in the human striatum including the caudate, putamen, and nucleus accumbens. Previous studies in monkeys have shown associative learning signals in the anterior

caudate and putamen using tasks very similar to the one used here (Pasupathy and Miller, 2005 and Williams and Eskandar, 2006). How might the trial outcome and associative learning signals seen in both the medial temporal lobe (Wirth et al., 2003 and Wirth et al., 2009) and striatum (Pasupathy and Miller, 2005; present findings; Selleck Ribociclib ABT-263 purchase Williams and Eskandar, 2006) interact? Lisman and Grace (2005) hypothesized that activity in a hippocampal-VTA loop, connected via projections through the nucleus accumbens, may control the entry of new information into long-term

memory. Our findings suggest that a similar functional loop may also underlie the development of new conditional motor associations. Future studies recording both single-units and LFP activity simultaneously in the medial temporal lobe and striatum during new conditional motor learning in monkeys will be a powerful model system to test important unanswered questions about the nature, timing, and direction of the learning signals across these areas suggested by the Lisman and Grace (2005) model. Another striking feature of the trial outcome signal was that the polarity of the LFP signals seen in monkeys (error trials > correct trials) was opposite to the BOLD fMRI pattern observed in humans (correct trials > error trials). Phosphoprotein phosphatase Polarity differences were also seen in some of the areas and bandwidths for the new versus reference comparison (Figure 2B) and the novelty response (Figure 3B). There are

a number of possible explanations for these polarity differences. One possibility is that the underlying differential neural signals across species are equivalent and the polarity differences reflect the complex translation between LFP measures in monkeys and BOLD fMRI signals in humans. Alternatively, the polarity differences may reflect differences in behavioral strategy across species. For example, in the case of trial outcome, although both species use trial outcome data to solve the task, humans may focus on correct trials whereas monkeys may focus more on error trials. Further studies will be needed to differentiate between these possibilities. Our previous study in humans reported clear increases in BOLD fMRI signals across the medial temporal lobe as humans gradually learned new conditional motor associations (Law et al., 2005).

, 2011b, Lubin et al , 2008, Ma et al , 2009 and Miller and Sweat

, 2011b, Lubin et al., 2008, Ma et al., 2009 and Miller and Sweatt, 2007). The near-simultaneous discoveries of a hydroxylated Staurosporine solubility dmso form of

5mC (5hmC) (Kriaucionis and Heintz, 2009) and the Ten-eleven translocation (Tet) family of enzymes required for its conversion (Tahiliani et al., 2009) has now offered insight into how these changes in DNA methylation might occur. Specifically, all three Tets (TET1–TET3) have been shown to catalyze the conversion of 5mC to 5hmC as well as its further oxidation into 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC), respectively (He et al., 2011, Ito et al., 2010 and Ito et al., 2011). These modified bases may then function as DNA demethylation intermediates subject to deamination, glycosylase-dependent excision, and repair resulting in a reversion back to unmodified cytosine (Bhutani et al., 2011 and Branco et al., 2012). However, it has now become apparent that 5hmC is not merely a DNA demethylation intermediate but MK-1775 ic50 also functions as a stable epigenetic mark enriched within gene bodies, promoters, and transcription factor binding sites, where it may influence gene expression

(Hahn et al., 2013, Mellén et al., 2012 and Szulwach et al., 2011). In the adult brain, alterations in global DNA methylation patterns in response to neuronal activity (Guo et al., 2011a and Miller-Delaney et al., 2012) are at least partially mediated by TET1, which is both necessary and sufficient for demethylation of the fibroblast growth factor 1 (Fgf1) and the brain-derived neurotrophic factor (Bdnf) promoters in response to electroconvulsive shock ( Guo et al., 2011b). Complementary studies have shown that Bdnf is

critical for memory formation ( Bekinschtein et al., 2008 and Mizuno et al., 2000), and its promoter region undergoes rapid demethylation after associative learning in a fear conditioning paradigm in rodents ( Lubin et al., 2008), suggesting the possibility that Tet1 may contribute to memory formation. However, Dipeptidyl peptidase at present, the role of Tet-mediated regulation of 5hmC and subsequent active DNA demethylation in relation to the expression of neuronal plasticity genes and memory has not been extensively explored, although Zhang et al. recently reported that Tet1 deletion in a knockout mouse model resulted in altered neurogenesis and a deficit in spatial memory in the Morris water maze ( Zhang et al., 2013). In this study, we sought to investigate the role of TET1 enzymatic activity in memory formation, through its ability to promote demethylation and, therefore, gene expression. We found that endogenous TET1 is expressed in neurons throughout the hippocampus and that its transcript levels are regulated by neuronal activity.

Impaired phagocytic efficiency by beclin 1-deficient BV2 cells co

Impaired phagocytic efficiency by beclin 1-deficient BV2 cells could also be rescued by recovering beclin GSK2656157 clinical trial 1 levels (Figure 2B). To confirm these findings in primary cells, we next isolated microglia from beclin 1 heterozygous knockout mice (beclin 1+/−) ( Figure 2C), which show a 40%–50% reduction in beclin 1 levels ( Pickford et al., 2008 and Qu et al., 2003). In agreement with our lentiviral approach,

beclin 1+/− microglia also showed impairments in phagocytic efficiency when analyzed by flow cytometry ( Figure 2D). To determine if impaired phagocytic efficiency in beclin 1-deficient cells resulted from beads stalling at the cell surface or from a disruption in the kinetics of phagocytosis, we used microscopy and live-cell imaging. We observed that while beads were initially phagocytosed at a similar rate ( Figure S2A), beclin 1-deficient BV2 cells were less able to phagocytose subsequent beads ( Figure S2B and Figure 2E). Quantification of cell migration confirmed that beclin 1-deficient cells have a similar migratory capacity as control cells, indicating that impaired movement Erastin is not responsible for phagocytic deficits ( Figure 2F). Instead, our data suggest that beclin 1 deficiency impairs the ability of cells to phagocytose subsequent

beads beyond the initial phagocytic event (see Figure 2G for representative live-cell images), resulting in overall reduced phagocytic uptake ( Figure S2C). Phagocytosis is initiated by numerous receptors that recognize molecular structures on extracellular substrates. Upon binding and internalization of substrates, phagocytic receptors are recycled back to the cell surface to be used again. Accordingly, disruptions in Adenosine phagocytic receptor recycling have dramatic consequences on phagocytic efficiency (Chen et al., 2010). To determine if reduced phagocytic efficiency seen in beclin 1-deficient cells is due to

changes in phagocytic receptor dynamics, we used an established receptor recycling assay (Mitchell et al., 2004) (Figure 3B). Indeed, beclin 1-deficient BV2 cells showed a prominent reduction in recycling of the phagocytic receptor CD36 (Figures 3C and 3D), a class B scavenger receptor involved in phagocytosing a wide range of substrates, including Aβ (El Khoury et al., 2003) and latex beads (Figure 3A). Primary microglia obtained from beclin 1+/− mice also showed a similar deficit in CD36 recycling ( Figures 3E and 3F). Importantly, flow cytometric analysis demonstrated that beclin 1 shRNA did not affect baseline cell surface expression of CD36 in the absence of ligand ( Figure 3G). Additionally, because the phagocytic receptor Trem2 has been reported to recycle ( Prada et al., 2006) and is a risk factor for AD ( Guerreiro et al., 2013 and Jonsson et al.

The patient had extensive urology follow-up and was planned for <

The patient had extensive urology follow-up and was planned for suprapubic tube removal, when the patient was lost to follow-up. The patient returned to clinic 2 years later complaining of insidious onset severe dysuria and episodic retention of increasing frequency over multiple months. The patient states he has been voiding spontaneously from the neophallus

for almost 2 years with retention being only a recent issue. Suprapubic tube is nonfunctioning and on previously trying to self-extubate the suprapubic catheter, the patient discovered he could not remove it. The patient also complained of a firm midurethral mass in neophallus. Retention was partially EGFR inhibitor or fully resolved by manipulation of the mass, per patient. The patient underwent computed tomography, which showed 2 bladder stones of 4.4 × 3.6 and 1.8 × 1.0 cm and a 0.9 × 0.6 cm hyperdense mass in urethra (Fig. 1). The patient was scheduled for cystoscopy of neophallus and bladder and an open cystolithopaxy. A restrictive urethral diameter required the use of the ureteroscope to perform cystoscopy. At cystoscopy, a calculus was encountered in the penile urethra

of the neophallus corresponding to the density previously identified. The calculus was fractured with holmium laser, and the remainder of the urethra appeared clear of calculus, stricture, PCI-32765 in vivo or diverticuli. Within the bladder, a large calculus was observed forming around the suprapubic tube and a second stone free in the bladder. At this time cystoscopy was ended, and open litholapaxy was begun. Both stones were removed from the surgically incised bladder, and the bladder was closed without placement of a suprapubic tube. After surgery, a 16F Foley catheter was inhibitors placed through the urethra with mild resistance. Patient recovery was uncomplicated, and a retrograde cystourethrogram 2 weeks later would show an intact bladder and patent urethra. The patient currently urinates without issue. This case represents the long-term outcome of unmonitored complications in a patient with a neophallus from a hair-bearing donor site.

The patient had a previous history of multiple fistula formation and stricture formation in the time frame shortly after the operation, but it was the 2-year lost to follow-up that allowed other adverse events PD184352 (CI-1040) to develop so fully. The initial approach to surgery in this patient was to strongly consider a perineal urethrotomy to assure continued continence, as the urethral stone was not expected and stricturing (reported at 5.3%–6.7% rate) or fistula (at 10.5%–33.3%) was predicted.2 and 3 Initially, it was believed stricture would be the most likely reason for retention in this patient, but it appears a calculus secondary to a hairball nidus initiated the retention. As an additional nidus for calculus formation, the retained suprapubic tube became the center of a nearly 5 × 4 cm stone (Fig. 2), possibly larger if the second bladder stone is included.