The CGT provided many benefits to functional mobility, motor impairment, bradykinesia, balance, and quality of life. However, these effect magnitudes were not influenced by stimulation, but tDCS seems to prolong the effects of cueing therapy on functional mobility.

The cerebellum plays an important role in the planning, initiation and stability of movements, as well as in postural control and balance. Modulation of neural regions underlying balance control may be a potential alternative to treat balance impairments in cerebellar patients. Transcranial direct current stimulation (tDCS) is a noninvasive and safe tool capable to modulate cerebellar activity. We aim to investigate the effects of cerebellar tDCS (ctDCS) on postural balance in healthy individuals. Fifteen healthy and right-handed subjects were submitted to three sessions of ctDCS (anodal, cathodal and sham), separated by at least 48 h. In each session, tests of static (right and left Athlete Single Leg tests) and dynamic balance (Limits of Stability test) were performed using the Biodex Balance System before and immediately after the ctDCS. The results revealed that cathodal ctDCS impaired static balance of healthy individuals, reflected in higher scores on overall stability index when compared to baseline for right (p = 0.034) and left (p = 0.01) Athlete Single Leg test. In addition, we found significant impairment for left Athlete Single Leg test in comparison to sham stimulation (p = 0.04). As far as we know, this is the first study that points changes on balance control after ctDCS in healthy individuals. This finding raises insights to further investigation about cerebellar modulation for neurological patients.

Background Ammonia is produced and excreted by the kidney, contributing to systemic acid‐base homeostasis through the production of bicarbonate. Disorders of acid‐base balance can lead to many clinical problems and measuring ammonia excretion helps in determining if the kidneys are responding to acid‐base challenges appropriately. Reference intervals are integral to clinical decision‐making, and there is no current RI for the urine ammonia‐to‐creatinine ratio (UACR) in dogs. Objective This study aimed to generate an RI for the UACR in healthy adult dogs. Methods The study used adult, client‐owned dogs that were presented to the University of Florida Primary Care and Dentistry service (n = 60). Physical examinations were performed and serum chemistry and urinalysis samples were obtained. Urine ammonia and creatinine concentrations were determined. Dogs were excluded if there were significant abnormalities in either their urinalysis or serum chemistry results. The RI for the UACR was calculated according to the recommendation of the American Society for Veterinary Clinical Pathology. Data were evaluated for correlation with serum bicarbonate, weight, age, and sex. Results The RIs for the UACR were 0.16‐23.69 with 90% confidence intervals for the lower and upper limits of (0.13‐1.17) and (20.50‐23.75), respectively. No significant impact of age, sex, or weight was found. There was no discernable relationship between serum bicarbonate and UACR. Conclusions Establishing an RI for UACR in healthy adult dogs will allow for further studies to determine if alterations are observed during specific disease states.

Background: There are sex differences in renal ammonia metabolism and structure, many of which are mediated by testosterone. This study's goal was to determine the role of renal expression of testosterone's canonical receptor, androgen receptor (AR), in these sexual dimorphisms. Methods: We studied mice with kidney-specific AR deletion (KS-AR-KO) generated using Cre/loxP techniques; control mice were Cre-negative littermates (WT). Results: In male, but not female, mice, KS-AR-KO increased ammonia excretion, which eliminated sex differences. Although renal structural size typically parallel ammonia excretion, KS-AR-KO decreased kidney size, cortical proximal tubule volume density and cortical proximal tubule cell height in males; neither were altered in females and collecting duct volume density was unaltered in both sexes. Analysis of key protein involved in ammonia handling showed in male mice that KS-AR-KO increased both PEPCK and NKCC2 expression, and decreased NHE3 and NBCe1-A expression. In female mice, KS-AR-KO did not alter these parameters. These effects occurred even though KS-AR-KO did not alter plasma testosterone, food intake or serum Na+, K+, or HCO3- significantly in either sex. Conclusions: AR-dependent signaling pathways in male, but not female, kidney regulate PEPCK and NKCC2 expression and lead to the sexual differences in ammonia excretion. Opposing effects on NHE-3 and NBCe1-A expression likely limit the magnitude of ammonia excretion changes. Since AR is not present in the TAL, the effect of KS-AR-KO on NKCC2 expression is indirect. Finally, AR mediates the greater kidney size and PT volume density in male than in female mice.