Bidet toilet use and incidence of hemorrhoids or urogenital infections: A one-year follow-up web survey.

Although bidet toilets are widely used in Japan, the relationship between habitual bidet toilet use and the incidence of hemorrhoids or urogenital infections has not been prospectively studied. We performed a web survey and followed bidet toilets users and non-users to assess the incidence of hemorrhoids or urogenital infections from 2013 to 2014. Study subjects were randomly selected from a research company's (Macromill, Inc.) web panel. The baseline survey inquired about toilet use and confounding parameters, and the follow-up survey examined outcome parameters. A total of 7637 subjects were analyzed using single or multiple logistic regression models. The prevalence odds ratios (ORs) between bidet toilet users and non-users for hemorrhoids, urological infections, and vulval pruritus were significantly > 1.0 but their incidence ORs were not significant. The adjusted incidence OR for bacterial vaginitis symptoms was significant (2.662, 95% confidence interval [CI] [1.315-5.520]). These findings suggest that positive relations between habitual bidet toilet use and hemorrhoids and urogenital symptoms, except bacterial vaginitis, were due to reverse causation. The incidence of bacterial vaginitis might be caused by bidet toilet use, but the incidence rates were too small to make a definite conclusion, and further studies are needed.

The interdependence and independence of amacrine cell dendrites: patch-clamp recordings and simulation studies on cultured GABAergic amacrine cells.

Previously we reported that cultured rat GABAergic amacrine cells can evoke subthreshold graded depolarization and action potentials. Both types of electrical signals are thought to contribute to neurotransmitter release from their dendrites, because Ca(2+) channels in amacrine cells can be activated at a subthreshold level (around -50 mV). The aim of the present study is to describe the spatiotemporal pattern of the spread of these electrical signals in an amacrine cell, using a computer simulation study. The simulation is based on physiological data, obtained by dual whole-cell patch-clamp recordings on the soma and the dendrites of cultured rat GABAergic amacrine cells. We determined passive and active properties of amacrine cells from the physiological recordings. Then, using the NEURON simulator, we conducted computer simulations on a reconstructed model of amacrine cells. We show that graded potentials and action potentials spread through amacrine cells with distinct patterns, and discuss the electrical interrelationship among the dendrites of an amacrine cell. Subthreshold graded potentials applied to a distal dendrite were sufficiently localized, so that each dendrite could behave independently (dendritic independence). However, at a suprathreshold level, once action potentials were triggered, they propagated into every dendrite, exciting the entire cell (dendritic interdependence). We also showed that GABAergic inhibitory inputs on the dendrites suppress the dendritic interdependence of amacrine cells. These results suggest that an inhibitory amacrine cell can mediate both local and wide-field lateral inhibition, regulated by the spatiotemporal pattern of excitatory and inhibitory synaptic inputs on its dendrites.

NMDA receptor-mediated depolarizing after-potentials in the basal dendrites of CA1 pyramidal neurons.

It was shown recently that the basal dendrites of cortical pyramidal neurons generate NMDA-spikes. In the present study, we made whole-cell recordings from hippocampal CA1 pyramidal neurons and examined whether NMDA receptor activation was involved in synaptic responses. At low input stimulus intensity, EPSPs with a fast decay time were induced. As the intensity of stimulation was increased in the presence of GABA receptor antagonists, a depolarizing after-potential (DAP) was generated in addition to a fast decaying potential. A DAP was never observed when the input was applied to the apical dendrites. The DAP was suppressed by hyperpolarization or by NMDA receptor antagonists, but not by Na+, K+, or Ca2+ channel blockers. One possible mechanism is that the morphology of the basal dendrites favors DAP generation. A compartmental model simulation showed that synaptic inputs to thinner shorter dendrites generated a potential that resembled a DAP. Our study shows that a synaptic input to the basal dendrites of a hippocampal pyramidal neuron can generate a NMDA receptor-mediated potential in the presence of GABA receptor blockade.