Wall Lake, South Dakota : A Case Study in Geographic Planning

Wall Lake is a hypereutrophic (overenriched with nutrients) glacial lake similar in character to many other glacial lakes in South Dakota. As is the case with most glacial lakes, Wall Lake is naturally eutrophic (nutrient enriched) because of the nutrient rich loess which usually occurs in close proximity to glacial kettles and is mixed with nutrient rich glacial till. A hypereutrophic state occurs when additional nutrients are added to the lake by such sources as agricultural runoff, mixing of water with enriched sediments, and by wastewater systems. The result is the accelerated natural progression from lake, to wetland, to dry land. Overenrichment and contamination of the lake cause the overabundant growth of algae, fish kill due to oxygen depletion, unsafe bacterial conditions for water immersion recreation, and the aesthetically displeasing odor of hydrogen sulfide which smells like rotten eggs. Wall Lake is experiencing hypereutrophication which limits the recreational use by residents of Minnehaha County. Agricultural practices and wastewater systems influx has accelerated the natural processes of the lake so that it is feared that it may become a swamp prematurely. The purpose of this study is to determine the feasibility of restoring the lake for Minnehaha County residents. Initially, current, consistent data analysis of runoff from the watershed area of Wall Lake was to be included. Drought prevented watershed runoff from being sampled for the majority of the testing period. Water samples disclosed that bacterial contamination and high nutrient levels continued to occur. This paper suggests that the most probable source of bacterial contamination during this period of testing was wastewater systems

Left Ventricular Endocardial Pacing Improves Resynchronization Therapy in Canine Left Bundle-Branch Hearts

Background— We investigated the benefits of the more physiological activation achieved by left ventricular (LV) endocardial pacing (ENDO) as compared with conventional epicardial (EPI) LV pacing in cardiac resynchronization therapy. Methods and Results— In 8 anesthetized dogs with experimental left bundle-branch block, pacing leads were positioned in the right atrium, right ventricle, and at 8 paired (EPI and ENDO) LV sites. Systolic LV pump function was assessed as LVdP/dtmax and stroke work and diastolic function as LVdP/dtmin. Electrical activation and dispersion of repolarization were determined from 122 epicardial and endocardial electrodes and from analysis of the surface ECG. Overall, ENDO-biventricular (BiV) pacing more than doubled the degree of electrical resynchronization and increased the benefit on LVdP/dtmax and stroke work by 90% and 50%, respectively, as compared with EPI-BiV pacing. During single-site LV pacing, the range of AV intervals with a >10% increase in LV resynchronization (79�31 versus 32�24 ms, P <0.05) and LVdP/dtmax (92�29 versus 63�39 ms) was significantly longer for ENDO than for EPI pacing. EPI-BiV but not ENDO-BiV pacing created a significant (40�21 ms) transmural dispersion of repolarization. Conclusions— Data from this acute animal study indicate that the use of an endocardial LV pacing electrode may increase the efficacy of resynchronization therapy as compared with conventional epicardial resynchronization therapy

Physical and Pharmacological Restraints in Hospital Care:Protocol for a Systematic Review

Background: Physical and pharmacological restraints, defined as all measures limiting a person in his or her freedom, are extensively used to handle unsafe or problematic behavior in hospital care. There are increasing concerns as to the extent with which these restraints are being used in hospitals, and whether their benefits outweigh their potential harm. There is currently no comprehensive literature overview on the beneficial and/or adverse effects of the use of physical and pharmacological restraints in the hospital setting. Methods: A systematic review of the existing literature will be performed on the beneficial and/or adverse effects of physical and pharmacological restraints in the hospital setting. Relevant databases will be systematically searched. A dedicated search strategy was composed. A visualization of similarities (VOS) analysis was used to further specify the search. Observational studies, and if available, randomized controlled trials reporting on beneficial and/or adverse effects of physical and/or pharmacological restraints in the general hospital setting will be included. Data from included articles will be extracted and analyzed. If the data is suitable for quantitative analysis, meta-analysis will be applied. Discussion: This review will provide data on the beneficial and/or adverse effects of the use of physical and pharmacological restraints in hospital care. With this review we aim to guide health professionals by providing a critique of the available evidence regarding their choice to either apply or withhold from using restraints. A limitation of the current review will be that we will not specifically address ethical aspects of restraint use. Nevertheless, the outcomes of our systematic review can be used in the composition of a multidisciplinary guideline. Furthermore, our systematic review might determine knowledge gaps in the evidence, and recommendations on how to target these gaps with future research. Systematic Review Registration: PROSPERO registration number: CRD42019116186

Coagulation Factor Xa Induces Proinflammatory Responses in Cardiac Fibroblasts via Activation of Protease-Activated Receptor-1

Coagulation factor (F) Xa induces proinflammatory responses through activation of protease-activated receptors (PARs). However, the effect of FXa on cardiac fibroblasts (CFs) and the contribution of PARs in FXa-induced cellular signalling in CF has not been fully characterised. To answer these questions, human and rat CFs were incubated with FXa (or TRAP-14, PAR-1 agonist). Gene expression of pro-fibrotic and proinflammatory markers was determined by qRT-PCR after 4 and 24 h. Gene silencing of F2R (PAR-1) and F2RL1 (PAR-2) was achieved using siRNA. MCP-1 protein levels were measured by ELISA of FXa-conditioned media at 24 h. Cell proliferation was assessed after 24 h of incubation with FXa ± SCH79797 (PAR-1 antagonist). In rat CFs, FXa induced upregulation of Ccl2 (MCP-1; >30-fold at 4 h in atrial and ventricular CF) and Il6 (IL-6; ±7-fold at 4 h in ventricular CF). Increased MCP-1 protein levels were detected in FXa-conditioned media at 24 h. In human CF, FXa upregulated the gene expression of CCL2 (>3-fold) and IL6 (>4-fold) at 4 h. Silencing of F2R (PAR-1 gene), but not F2RL1 (PAR-2 gene), downregulated this effect. Selective activation of PAR-1 by TRAP-14 increased CCL2 and IL6 gene expression; this was prevented by F2R (PAR-1 gene) knockdown. Moreover, SCH79797 decreased FXa-induced proliferation after 24 h. In conclusion, our study shows that FXa induces overexpression of proinflammatory genes in human CFs via PAR-1, which was found to be the most abundant PARs isoform in this cell type