Earthworm Populations in a Wheat-Soybean Double-Crop System under Seven Years of Established Residue Management Practices

Earthworms improve soil structure, distribute litter and microbes, stimulate microbial activity, facilitate decomposition, and increase nitrogen (N) availability for plant growth. Earthworm density is often reduced in low organic matter soils that are intensively managed to grow row crops. This study was designed to relate earthworm density and community composition to residue management after seven years of established management practices in a wheat (Triticum aestivum L.)-soybean (Glycine max (L.) Merr.) double-crop system maintained in Marianna, AR. Residue management practices included conventional tillage (CT) and no-tillage (NT), N fertilization to produce high and low wheat residue amounts left in the field, and burning and non-burning of residue after wheat harvest. Total earthworm densities ranged from 271 to 508 m-2 across treatments. Both exotic Aporrectodea trapezoides (Duges) and native Diplocardia sylvicola (Gates) adult earthworms were present with very little difference in diversity among sampled communities; however, more than 50 % of adults were D. sylvicola in all treatments. Residue level and burning influenced total, juvenile, and native earthworm densities differently in CT and NT. Native, total, or juvenile earthworm densities in different treatment combinations were related to soil properties, including pH, electrical conductivity, and Mehlich-III- K, Mn, Mg, Cu, S and Ca concentrations. Native earthworms predominated with a common exotic species in a wheat-soybean double-crop system in Arkansas with residue management practices interacting to impact the density of earthworms

Earthworm populations in a wheat-soybean double-crop system under seven years of established residue management practices

Earthworms improve soil structure, distribute litter and microbes, stimulate microbial activity, facilitate decomposition, and increase nitrogen (N) availability for plant growth. Earthworm density is often reduced in low organic matter soils that are intensively managed to grow row crops. This study was designed to relate earthworm density and community composition to residue management after seven years of established management practices in a wheat (Triticum aestivum L.)-soybean (Glycine max (L.) Merr.) double-crop system maintained in Marianna, Ark. Residue management practices included conventional tillage (CT) and no-tillage (NT), N fertilization to produce high and low wheat residue amounts left in the field, and burning and non-burning of residue after wheat harvest. Total earthworm densities ranged from 271 to 508 m-2 across treatments. Both exotic Aporrectodea trapezoides (Duges) and native Diplocardia sylvicola (Gates) adult earthworms were present with very little difference in diversity among sampled communities; however, more than 50 % of adults were D. sylvicola in all treatments. Residue level and burning influenced total, juvenile, and native earthworm densities differently in CT and NT. Adult native earthworms predominated over a common exotic species in a wheat-soybean double-crop system in Arkansas with residue management practices interacting to impact the density of earthworms

Quiet Time for Mechanically Ventilated Patients in The Medical Intensive Care Unit

Objective: Sleep disruption occurs frequently in critically ill patients. The primary aim of this study was to examine the effect of quiet time (QT) on patient sedation frequency, sedation and delirium scores; and to determine if consecutive QTs influenced physiologic measures (heart rate, mean arterial blood pressure and respiratory rate). Method: A prospective study of a quiet time protocol was conducted with 72 adult patients on mechanical ventilation. Setting: A Medical Intensive Care Unit (MICU) in the Midwest region of the United States. Results: Sedation was given less frequently after QT (p = 0.045). Those who were agitated prior to QT were more likely to be at goal sedation after QT (p \u3c 0.001). Although not statistically significant, the majority of patients who were negative on the Confusion Assessment Method (CAM-ICU) prior to QT remained delirium free after QT. Repeated measures analysis of variance (ANOVA) for three consecutive QTs showed a significant difference for respiratory rate (p = 0.035). Conclusion: QT may influence sedation administration and promote patient rest. Future studies are required to further understand the influence of QT on mechanically ventilated patients in the intensive care unit

Integration of IRF6 and Jagged2 signalling is essential for controlling palatal adhesion and fusion competence

In mammals, adhesion and fusion of the palatal shelves are essential mechanisms during the development of the secondary palate; failure of these processes leads to the congenital anomaly, cleft palate. The mechanisms that prevent pathological adhesion between the oral and palatal epithelia while permitting adhesion and subsequent fusion of the palatal shelves via their medial edge epithelia remain obscure. In humans, mutations in the transcription factor interferon regulatory factor 6 (IRF6) underlie Van der Woude syndrome and popliteal pterygium syndrome. Recently, we have demonstrated that mice homozygous for a mutation in Irf6 exhibit abnormalities of epithelial differentiation that results in cleft palate as a consequence of adhesion between the palatal shelves and the tongue. In the current paper, we demonstrate that Irf6 is essential for oral epithelial differentiation and that IRF6 and the Notch ligand Jagged2 function in convergent molecular pathways during this process. We further demonstrate that IRF6 plays a key role in the formation and maintenance of the oral periderm, spatio-temporal regulation of which is essential for ensuring appropriate palatal adhesion

Mutant p63 causes defective expansion of ectodermal progenitor cells and impaired FGF signalling in AEC syndrome

Peer reviewe

Facial clefting in Tp63 deficient mice results from altered Bmp4, Fgf8 and Shh signaling

AbstractDuring embryogenesis, the transcription factor Tp63 is expressed in the basal cells of multiple epithelial tissues. In humans, mutations in TP63 have been identified in five distinct human developmental disorders that are characterized by limb abnormalities, ectodermal dysplasia, and facial anomalies. To dissect the molecular pathogenesis of the bilateral cleft lip and cleft palate that results from mutation of Tp63, we analysed Tp63 mutant mice. At E10.5, Tp63-deficient mice exhibited abnormal morphogenesis of the medial nasal, lateral nasal and maxillary processes. Analysis of key signaling molecules revealed that these defects result from increased Bmp4 signaling in the epithelia of the facial processes. Acting antagonistically on Fgf8 and Shh, this aberrant signaling led to a reduction in mesenchymal cell proliferation and increased cell death in specific regions of the facial processes. In addition, a proliferative defect in the mesenchyme of the maxillary processes at E11.5 resulted in absence of the anterior region of the palatal shelves and, subsequently, cleft palate. Our results are consistent with a role for Tp63 in the regulation of Bmp signaling controlling the growth, modelling and fusion events underlying facial development and shed new light on the complex abnormality of facial clefting

Cooperation between the transcription factors p63 and IRF6 is essential to prevent cleft palate in mice

Cleft palate is a common congenital disorder that affects up to 1 in 2,500 live human births and results in considerable morbidity to affected individuals and their families. The etiology of cleft palate is complex, with both genetic and environmental factors implicated. Mutations in the transcription factor–encoding genes p63 and interferon regulatory factor 6 (IRF6) have individually been identified as causes of cleft palate; however, a relationship between the key transcription factors p63 and IRF6 has not been determined. Here, we used both mouse models and human primary keratinocytes from patients with cleft palate to demonstrate that IRF6 and p63 interact epistatically during development of the secondary palate. Mice simultaneously carrying a heterozygous deletion of p63 and the Irf6 knockin mutation R84C, which causes cleft palate in humans, displayed ectodermal abnormalities that led to cleft palate. Furthermore, we showed that p63 transactivated IRF6 by binding to an upstream enhancer element; genetic variation within this enhancer element is associated with increased susceptibility to cleft lip. Our findings therefore identify p63 as a key regulatory molecule during palate development and provide a mechanism for the cooperative role of p63 and IRF6 in orofacial development in mice and humans