An approach to identify the spatiotemporal patterns of nitrogen flows in food production and consumption systems within watersheds.

Human has greatly disturbed nitrogen (N) cycles through the food production and consumption (FPC) activities, which caused serious environmental consequences. A few studies address the pathways of N cycles to clarify the interrelationships between human activities and the altered N cycles, especially in terms of the spatial aspects of N flows, which are also influenced by natural factors. Here, we developed an integrated model to quantify the spatiotemporal patterns of N flows within the FPC and applied it to the Chaohu Watershed from 1949 to 2012. We found that total N inputs into the FPC increased by 6-fold during 1949-2012, while N inputs from chemical fertilizer had the largest increase, with an annual growth rate of 8.6%. N generation in manure doubled, but the recycling rate decreased by 50% in the study period. The total N losses increased from 17 to 130Gg-N/yr between 1949 and 2012. Annually, ~7% of total N losses was discharged into surface water annually, which peaked at 9.5Gg-N/yr during 1998-2003, two times as that in the early 1980s when algae blooms first occurred in Chaohu lake. Spatially, around one-fifth of the catchment area was responsible for all of N losses to surface water. These intensive areas located in the eastern and southern-central regions, which were identified as the critical areas for priority N mitigation. This study provided a method to depict spatiotemporal patterns of regional N flows for identifying the critical sources and areas of N pollution for precision watershed management.

Dysregulation of Wnt inhibitory factor 1 (Wif1) expression resulted in aberrant Wnt-ß-catenin signaling and cell death of the cloaca endoderm, and anorectal malformations.

In mammalian urorectal development, the urorectal septum (urs) descends from the ventral body wall to the cloaca membrane (cm) to partition the cloaca into urogenital sinus and rectum. Defective urs growth results in human congenital anorectal malformations (ARMs), and their pathogenic mechanisms are unclear. Recent studies only focused on the importance of urs mesenchyme proliferation, which is induced by endoderm-derived Sonic Hedgehog (Shh). Here, we showed that the programmed cell death of the apical urs and proximal cm endoderm is particularly crucial for the growth of urs during septation. The apoptotic endoderm was closely associated with the tempo-spatial expression of Wnt inhibitory factor 1 (Wif1), which is an inhibitor of Wnt-ß-catenin signaling. In Wif1(lacZ/lacZ) mutant mice and cultured urorectum with exogenous Wif1, cloaca septation was defective with undescended urs and hypospadias-like phenotypes, and such septation defects were also observed in Shh(-/-) mutants and in endodermal ß-catenin gain-of-function (GOF) mutants. In addition, Wif1 and Shh were expressed in a complementary manner in the cloaca endoderm, and Wif1 was ectopically expressed in the urs and cm associated with excessive endodermal apoptosis and septation defects in Shh(-/-) mutants. Furthermore, apoptotic cells were markedly reduced in the endodermal ß-catenin GOF mutant embryos, which counteracted the inhibitory effects of Wif1. Taken altogether, these data suggest that regulated expression of Wif1 is critical for the growth of the urs during cloaca septation. Hence, Wif1 governs cell apoptosis of urs endoderm by repressing ß-catenin signal, which may facilitate the protrusion of the underlying proliferating mesenchymal cells towards the cm for cloaca septation. Dysregulation of this endodermal Shh-Wif1-ß-catenin signaling axis contributes to ARM pathogenesis.

Deficient motor innervation of the sphincter mechanism in fetal rats with anorectal malformation: a quantitative study by fluorogold retrograde tracing.

BACKGROUND/PURPOSE: Deficiency of motoneuron innervation to the sphincter mechanism has been described in patients with anorectal malformation. Whether this event is primary or secondary remains unclear. METHODS: The authors quantified the motoneuron innervation of the sphincter mechanism by Fluorogold (FG) retrograde tracing experiment in fetal rats with anorectal malformation. Anorectal malformation was induced in rat fetuses by ethylenethiourea (ETU). Serial longitudinal sections encompassing the whole width of lumbosacral spinal cord were examined. The number of FG-labelled motoneurons were scored and compared between male fetuses with or without malformation in the ETU-fed group and normal controls. RESULTS: The number of FG-labelled motoneurons in the fetuses without defect, with imperforate anus (IA), with neural tube anomalies (NTA), with combined IA and NTA, and normal controls were determined to be (mean +/- SEM) 109.13 +/- 37.88, 55.05 +/- 25.85, 48.20 +/- 30.34, 54.43 +/- 28.55, and 135.22 +/- 28.78, respectively. FG-labelled motoneurons in the fetuses with IA, NTA, and combined IA and NTA are significantly fewer than that in fetuses without defects (P <.05) and in normal controls (P <.005). CONCLUSIONS: These findings suggest that defective motoneuron innervation to the sphincter mechanism is a primary anomaly that coexists with the alimentary tract anomaly in anorectal malformation during fetal development. The intrinsic neural deficiency is an important factor likely to contribute to poor postoperative anorectal function despite surgical correction of anorectal malformation.

[A study of left ventricular function of workers exposed to fluorine].

The left ventricular function of 26 workers exposed to fluorine was investigated. The results demonstrated that the LVET in the higher urine fluorine group (greater than 1.5 mg/L) was significantly shorter than the control group (P less than 0.01), the PEP was much longer than the control group (P less than 0.05), and the rate of PEP/LVET compared with the control group was increased. The difference was statistically significant (P less than 0.01). In the lower urine fluorine group (less than 1.5 mg/L) the time of LVET and PEP and the rate of PEP/LVET was not significantly different from the control group. The results showed that excessive fluorine ion in the body could cause decrease of myocardial contraction. The reason may be, that the fluorine ion inhibits the activities of certain enzymes in the body, thereby producing inhibition of ATP supply and utilization.