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Saw, S.

Publications and source records attributed to Saw, S..

2 recordsLinked to original sources

Standard touchscreen test procedures shift circadian rhythms in mice: a modified protocol to minimize circadian confounds

Touchscreen based cognitive testing for rodents offers considerable experimental benefits, including a semi automated battery approach and the use of appetitive rather than aversive reinforcement. However, food reward and touchscreen illumination introduce potential confounds, as both food and light can shift, entrain, or disrupt circadian rhythms, which in turn can affect learning and memory. The potential for the test apparatus to impact endogenous circadian rhythms is particularly problematic when probing relationships between sleep, circadian disruption, and cognitive performance. After observing phase shifting of circadian rhythms in nocturnal mice tested using standard touchscreen test procedures, which include testing during the active period (early lights off), we evaluated the relative contributions of the illuminated screen and the appetitive food reward. Our results indicate that light emitted by the touchscreen chambers is responsible for the circadian phase shifting effects, with standard screen conditions inducing a ~3.5 h phase delay in daily activity rhythms when training is conducted early in the dark period for 7 consecutive days. We then modified lighting in the test environment and the home cage to identify parameters that would minimize circadian shifting without impairing visual discrimination or performance on a widely used cognitive test (Trial Unique Nonmatching to Location, TUNL). From the 10 conditions tested, we offer specific recommendations for modifying touchscreen test protocols to minimize circadian confounds, without impacting task acquisition or performance.

animal behavior and cognition↗

The impact of genistein supplementation on tendon functional properties and gene expression in estrogen deficient rats

PurposeTendinopathy risk increases with menopause. The phytoestrogen genistein prevents collagen loss during estrogen deficiency [ovariectomy (OVX)]. The influence of genistein on tendon function and extracellular matrix (ECM) regulation are not well known. We determined the impact of genistein on tendon function and examined potential mechanisms by which genistein alters tendon ECM.\n\nMaterials and MethodsEight-week-old rats (n=42) were divided into three groups: intact, OVX, or OVX-genistein (6mg/kg/day) for 6-weeks. Tail fascicles were assessed with a Deben tensile stage. Achilles tendon mRNA expression was determined with digital droplet PCR. Tendon-derived fibroblasts were also treated with genistein in the presence of estrogen receptor (ER) antagonists.\n\nResultsCompared to intact, stress tended to be lower in untreated OVX rats (p=0.022). Further, modulus and energy density were greater in genistein-treated rats (p<0.05) compared to intact. Neither OVX nor genistein altered expression of Col1a1, Col3a1, Casp3, Casp8, Mmp1a, Mmp2, or Mmp9 (p>0.05). Compared to intact, Tnmd and Esr1 expression was greater and Pcna and Timp1 expression lower in OVX rats (p<0.05). Genistein treatment returned Tnmd, Pcna, and Timp1 to levels of Intact-Vehicle (p<0.05), but did not alter Scx or Esr1 (p>0.05). Several {beta}-catenin/Wnt signaling related molecules were not altered by OVX or genistein (p>0.05). In vitro, genistein blunted cell proliferation but not via ERs.\n\nConclusionsOur findings demonstrate that genistein improves tendon function. Genistein inhibits cell proliferation in vitro but not via ER. The effect of genistein in vivo was predominately on genes related to cell proliferation rather than collagen remodeling.

physiology↗