The accumulation of perchlorate in vegetation is becoming a concern, with increasing numbers of sites reporting the presence of perchlorate in groundwater and surface water. This study investigated potential perchlorate uptake and distribution by a variety of forage and edible crops in both the laboratory and the field. Perchlorate concentrations in soybean leaves grown in the greenhouse were significantly higher than perchlorate concentrations in soybean seeds and pods. Perchlorate concentrations in alfalfa grown in sand were significantly lower than those in alfalfa grown in soil. The concentration of perchlorate in tomato was lower in the fruit than the leaves. Commercially grown wheat and alfalfa samples all contained perchlorate, 0.72-8.6 mg/kg of fresh weight (FW) in the wheat stems, 0.71-4.4 mg/kg of FW in the wheat heads, and 2.9 mg/kg of FW in alfalfa. All field garden samples tested (including cucumber, cantaloupe, and tomato) that were irrigated with perchlorate-tainted water contained perchlorate at various concentrations ranging from 0.040 to 1.65 mg/kg of FW. Bioconcentration factors (BCF), ratios of plant fresh weight concentrations to estimated or measured groundwater concentrations [(microg/kg of FW)/microg/L], were all in the same order of magnitude ranging from 215 +/- 126 for wheat stems to 233 +/- 264 for wheat heads and to 380 +/- 89 for alfalfa. BCF for garden fruit samples were much lower (0.5-20). Results from this study highlight the potential for perchlorate exposure by routes other than drinking water.

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Mechanisms modulating prostate cell fate determination remain unexplored. The leucine-rich repeat containing G-protein coupled receptors (LGRs) have been identified as important stem cell markers in various tissues. Here, we investigated the roles of Lgr4/Gpr48 in prostate stem cells and development. Lgr4 was ubiquitously expressed during early prostate development prior to lineage specification, with adult expression restricted to a few basal cells (principally Lin−Sca1+CD49f+). Lgr4−/− mice had compromised branching morphogenesis and delayed epithelial differentiation, leading to decreased prostate size and impaired luminal cell function. In vitro prostate sphere culture revealed that Lgr4−/− Lin−/Sca1+/CD49f+ (LSC) cells failed to generate p63low cells, indicating a differentiation deficiency. Furthermore, Lgr4 ablation arrested prostate stem cell (PSC) differentiation of in vivo kidney capsule prostate grafts, suggesting that Lgr4 modulates prostate stem cell properties independent of hormonal and mesenchymal effects. Analysis of neonatal prostates and prostate spheres revealed a decrease in Wnt, Sonic Hedgehog, and Notch1 expression in Lgr4−/− cells. Lgr4 loss blocked differentiation of prostate sphere p63hi cells to p63low. Treatment with exogenous Sonic Hedgehog partially restored the differentiation of p63hi cells in Lgr4−/− spheres. Taken together, our data revealed the roles of Lgr4 in early prostate development and in stem cell differentiation through regulation of the Wnt, Notch and Sonic Hedgehog signaling pathways.

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Abstract:The original intensity value recorded by terrestrial laser scanners is influenced by multiple variables, among which incidence angle and distance play a crucial and dominant role. Further studies on incidence angle and distance effects are required to improve the accuracy of currently available methods and to implement these methods in practical applications. In this study, the effects of incidence angle and distance on intensity data of the Faro Focus 3D 120 terrestrial laser scanner are investigated. A new method is proposed to eliminate the incidence angle and distance effects. The proposed method is based on the linear interpolation of the intensity values of reference targets previously scanned at various incidence angles and distances. Compared with existing methods, a significant advantage of the proposed method is that estimating the specific function forms of incidence angle versus intensity and distance versus intensity is no longer necessary; these are canceled out when the scanned and reference targets are measured at the same incidence angle and distance. Results imply that the proposed method has high accuracy and simplicity in eliminating incidence angle and distance effects and can significantly reduce the intensity variations caused by these effects on homogeneous surfaces.

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Activation of KISS1 receptor (KISS1R or GPR54) by its ligands (kisspeptins) regulates a diverse function both in normal physiology and pathophysiology. In cancer, KISS1-induced KISS1R signaling is known to inhibit tumor angiogenesis and metastasis. However, roles of KISS1 and KISS1R in earlier stages of tumor progression and metastasis in vivo are still unknown. In this study, we demonstrate a critical role for Kiss1r in early stages of tumor progression using mouse tumor models. PyMT/Kiss1r mice with different Kiss1r genotypes were obtained by crossing MMTV-PyMT transgenic mouse with Kiss1r heterozygous mouse (Kiss1r+/−). Kiss1r heterozygosity attenuated breast tumor initiation, growth, latency, multiplicity and metastasis in MMTV-PyMT/Kiss1r+/− mouse models. To confirm the effects of Kiss1r in tumor progression and limit any effect of endogenous hormones, we isolated primary tumor cells from PyMT/Kiss1r+/+ or PyMT/Kiss1r+/− mice and performed in vitro and in vivo tumorigenesis assays. Kiss1r heterozygosity inhibited PyMT-induced in vitro tumorigeneity and in vivo tumor growth in NOD.SCID/NCr mice. To understand the underlying mechanism, we showed that activation of KISS1R by kisspeptin-10 led to RhoA activation and RhoA-dependent gene expression through Gαq-p63RhoGEF signaling pathway. Furthermore, anchorage-independent growth was tightly linked to the dosage-dependent regulation of RhoA by KISS1R. When MCF10A cells overexpressing H-RasV12 were subjected to in vitro tumorigenesis assays, knockdown of KISS1R or inactivation of RhoA in MCF10A cells reduced Ras-induced anchorage-independent growth, similar to our data obtained from PyMT-Kiss1r+/− mouse models. Altogether, we conclude that Kiss1r haploinsufficiency delays breast tumor initiation, progression and metastasis through its downstream Gαq-p63RhoGEF-RhoA signaling pathway.

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