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Congenital anomalies of the kidney and urinary tract (CAKUT) are a family of often-concurrent diseases with various anatomical spectra. Null-mutant Gen1 mice frequently develop multiple urinary phenotypes, most commonly duplex kidneys, and are ideal subjects for research on ectopic budding in CAKUT development. The upper and lower kidney poles of the Gen1

Intrauterine low-protein diet can affect kidney development and hence final nephron number. In this study, we reported that intrauterine low-protein diet can cause congenital anomalies of the kidney and urinary tract (CAKUT) phenotypes, which was dominated by the duplicated collecting system phenotype. At the same time, ectopic ureteric buds were increased under intrauterine low-protein diet and the number of UB branches was reduced in the serum-free culture. Intrauterine low-protein diet can change metanephric gene expression. Slit2/Robo2 and Spry1 expression levels were decreased, Ret expression was increased, and downstream p-Akt activity enhanced with apoptosis abnormal in ureteric bud tissue, which may be the mechanisms that intrauterine low-protein diet causes increased incidence of CAKUT in offspring. Thus, we showed correlation between intrauterine low-protein diet and CAKUT in offspring.

Willed-movement (WM) training has been implicated in the promotion of motor function in human stroke survivors and focal ischemic rats. However, the molecular basis of changes in synaptic transmission following WM training remains unclear. In addition, studies examining the influence of rehabilitative training, such as skilled motor learning, on long-term depression (LTD) of synapses in the primary motor cortex have produced conflicting results. To identify the possible effects of willed movement on motor recovery, on expression of the protein interacting with C kinase 1 protein (PICK1), and on PICK1 related LTD, littermate rats were randomly divided into four groups: normal control, middle cerebral artery occlusion (MCAO), WM and environmental modification. Neurological and neurobehavioral assessments were performed for the rats with occlusion of the right middle cerebral artery. Double-labeling immunofluorescence staining was performed to detected expression of PICK1 and NeuN. Extracellular recordings were used to detect the basal extracellular field excitatory postsynaptic potentials and LTD with or without PICK1 inhibitor FSC231. The results showed that willed-movement training facilitated motor recovery after MCAO in rats, increased the PICK1 protein levels, and enhanced LTD in the ischemia hemisphere. The enhanced LTD for the rats after willed-movement training was attenuated by FSC231. Our results indicated that willed-movement training can enhance activity-dependent LTD through PICK1-dependent mechanisms in the ischemic hemisphere of rats.