Initiation and runout characteristics of partially saturated debris flows in Ohya landslide scar, Japan

A partially saturated flow, which has an unsaturated layer in its upper part, has been monitored in the steep initiation zones of debris flows. Understanding the initiation and runout characteristics of partially saturated flows is essential for predicting the timing and magnitude of downstream debris flows. Monitoring performed using time-lapse cameras and water pressure sensors in the Ohya landslide scar in central Japan allowed us to obtain data on a series of partially saturated debris flow surges from initiation to termination on July 6, 2020, and July 13, 2021. Debris flow surges were mainly induced by repetitive mass movement of sediment deposit caused by the overland flow erosion of channel deposits, channel deposit slides, and water and sediment supply from channel banks and tributaries. The excess pore water pressure in a partially saturated flow on July 6, 2020, was clearly higher than that on July 13, 2021. Rainfall patterns, which control the water content in channel deposits, and the flow height likely affect the magnitude of the excess pore water pressure in partially saturated flows

Experimental study on the effects of local sediment accumulation on a debris flow surge in a steep channel

Debris flow surges can terminate in a steep channel of > 15°. However, the termination process and mechanisms remain unknown. This study conducted small-scale flume experiments to investigate the effects of local sediment accumulation on debris-flow surges in a steep channel. The experiments demonstrated that local accumulation of bed sediment terminates a debris flow surge owing to abrupt changes in bed gradients and infiltration of debris flow interstitial water. Subsequently, the mass of the terminated debris-flow surge and bed sediment began to move, triggering a larger debris-flow surge. This result suggests that predicting the scale of a debris flow arriving downstream requires measuring the distribution of bed sediment in the debris flow initiation zone

Urocortin1-induced anorexia is regulated by activation of the serotonin 2C receptor in the brain

AbstractThis study was conducted to determine the mechanisms by which serotonin (5-hydroxytryptamine, 5-HT) receptors are involved in the suppression of food intake in a rat stress model and to observe the degree of activation in the areas of the brain involved in feeding. In the stress model, male Sprague–Dawley rats (8 weeks old) were given intracerebroventricular injections of urocortin (UCN) 1. To determine the role of the 5-HT2c receptor (5-HT2cR) in the decreased food intake in UCN1-treated rats, specific 5-HT2cR or 5-HT2b receptor (5-HT2bR) antagonists were administered. Food intake was markedly reduced in UCN1-injected rats compared with phosphate buffered saline treated control rats. Intraperitoneal administration of a 5-HT2cR antagonist, but not a 5-HT2bR antagonist, significantly inhibited the decreased food intake. To assess the involvement of neural activation, we tracked the expression of c-fos mRNA as a neuronal activation marker. Expression of the c-fos mRNA in the arcuate nucleus, ventromedial hypothalamic nucleus (VMH) and rostral ventrolateral medulla (RVLM) in UNC1-injected rats showed significantly higher expression than in the PBS-injected rats. Increased c-fos mRNA was also observed in the paraventricular nucleus (PVN), the nucleus of the solitary tract (NTS), and the amygdala (AMG) after injection of UCN1. Increased 5-HT2cR protein expression was also observed in several areas. However, increased coexpression of 5-HT2cR and c-fos was observed in the PVN, VMH, NTS, RVLM and AMG. Whereas, pro-opiomelanocortin mRNA expression was not changed. In an UNC1-induced stress model, 5-HT2cR expression and activation was found in brain areas involved in feeding control

Peripheral α2-β1 adrenergic interactions mediate the ghrelin response to brain urocortin 1 in rats

SummaryThe autonomic nervous system (ANS) conveys neuronal input from the brain to the stomach. We investigated mechanisms through which urocortin 1 (UCN1) injected intracerebroventricularly (ICV, 300pmol/rat) inhibits circulating ghrelin in rats. This was achieved by assessing (1) the induction of c-fos gene expression as a marker of neuronal activation in specific hypothalamic and caudal brainstem regulating ANS; (2) the influence of vagotomy and pharmacological blockade of central and peripheral α- and β-adrenergic receptor (AR) on ICV UCN1-induced reduction of plasma ghrelin levels (determined by ELISA); and (3) the relevance of this pathway in the feeding response to a fast in rats. UCN1 increased c-fos mRNA expression in key brain sites influencing sympathetic activity namely the hypothalamic paraventricular and ventromedial nuclei, locus coeruleus, nucleus of the solitary tract, and rostral ventrolateral medulla, by 16-, 29-, 6-, 37-, and 13-fold, respectively. In contrast, the dorsal motor nucleus of the vagus had little c-fos mRNA expression and ICV UCN1 induced a similar reduction in acylated ghrelin in the sham-operated (31%) and vagotomized (41%) rats. An intraperitoneal (IP) injection of either a non-selective α- or selective α2-AR antagonist reduced, while a selective α2-AR agonist enhanced ICV UCN1-induced suppression of plasma acylated ghrelin levels. In addition, IP injection of a non-selective β- or selective β1-AR agonist blocked, and selective β1-AR antagonist augmented, the ghrelin response to ICV UCN1. The IP injections of a selective α1- or non-selective β or β2-AR antagonists, or any of the pretreatments given ICV had no effect. ICV UCN1 reduced the 2-h food intake in response to a fast by 80%, and this effect was partially prevented by a selective α2-AR antagonist. These data suggest that ICV UCN1 reduces plasma ghrelin mainly through the brain sympathetic component of the ANS and peripheral AR specifically α2-AR activation and inactivation of β1-AR. The α2-AR pathway contributes to the associated reduction in food intake

Experimental study on the effects of local sediment accumulation on a debris flow surge in a steep channel

Debris flow surges can terminate in a steep channel of > 15°. However, the termination process and mechanisms remain unknown. This study conducted small-scale flume experiments to investigate the effects of local sediment accumulation on debris-flow surges in a steep channel. The experiments demonstrated that local accumulation of bed sediment terminates a debris flow surge owing to abrupt changes in bed gradients and infiltration of debris flow interstitial water. Subsequently, the mass of the terminated debris-flow surge and bed sediment began to move, triggering a larger debris-flow surge. This result suggests that predicting the scale of a debris flow arriving downstream requires measuring the distribution of bed sediment in the debris flow initiation zone

Initiation and runout characteristics of partially saturated debris flows in Ohya landslide scar, Japan

A partially saturated flow, which has an unsaturated layer in its upper part, has been monitored in the steep initiation zones of debris flows. Understanding the initiation and runout characteristics of partially saturated flows is essential for predicting the timing and magnitude of downstream debris flows. Monitoring performed using time-lapse cameras and water pressure sensors in the Ohya landslide scar in central Japan allowed us to obtain data on a series of partially saturated debris flow surges from initiation to termination on July 6, 2020, and July 13, 2021. Debris flow surges were mainly induced by repetitive mass movement of sediment deposit caused by the overland flow erosion of channel deposits, channel deposit slides, and water and sediment supply from channel banks and tributaries. The excess pore water pressure in a partially saturated flow on July 6, 2020, was clearly higher than that on July 13, 2021. Rainfall patterns, which control the water content in channel deposits, and the flow height likely affect the magnitude of the excess pore water pressure in partially saturated flows

Peripheral α2-β1 adrenergic interactions mediate the ghrelin response to brain urocortin 1 in rats.

The autonomic nervous system (ANS) conveys neuronal input from the brain to the stomach. We investigated mechanisms through which urocortin 1 (UCN1) injected intracerebroventricularly (ICV, 300 pmol/rat) inhibits circulating ghrelin in rats. This was achieved by assessing (1) the induction of c-fos gene expression as a marker of neuronal activation in specific hypothalamic and caudal brainstem regulating ANS; (2) the influence of vagotomy and pharmacological blockade of central and peripheral α- and β-adrenergic receptor (AR) on ICV UCN1-induced reduction of plasma ghrelin levels (determined by ELISA); and (3) the relevance of this pathway in the feeding response to a fast in rats. UCN1 increased c-fos mRNA expression in key brain sites influencing sympathetic activity namely the hypothalamic paraventricular and ventromedial nuclei, locus coeruleus, nucleus of the solitary tract, and rostral ventrolateral medulla, by 16-, 29-, 6-, 37-, and 13-fold, respectively. In contrast, the dorsal motor nucleus of the vagus had little c-fos mRNA expression and ICV UCN1 induced a similar reduction in acylated ghrelin in the sham-operated (31%) and vagotomized (41%) rats. An intraperitoneal (IP) injection of either a non-selective α- or selective α2-AR antagonist reduced, while a selective α2-AR agonist enhanced ICV UCN1-induced suppression of plasma acylated ghrelin levels. In addition, IP injection of a non-selective β- or selective β1-AR agonist blocked, and selective β1-AR antagonist augmented, the ghrelin response to ICV UCN1. The IP injections of a selective α1- or non-selective β or β2-AR antagonists, or any of the pretreatments given ICV had no effect. ICV UCN1 reduced the 2-h food intake in response to a fast by 80%, and this effect was partially prevented by a selective α2-AR antagonist. These data suggest that ICV UCN1 reduces plasma ghrelin mainly through the brain sympathetic component of the ANS and peripheral AR specifically α2-AR activation and inactivation of β1-AR. The α2-AR pathway contributes to the associated reduction in food intake