Carlssonmikkelsen7172

Millions of tons of oil are spilled in aquatic environments every decade, and this oil has the potential to greatly impact fish populations. Here, we review available information on the physiological effects of oil and polycyclic aromatic hydrocarbons on fish. Oil toxicity affects multiple biological systems, including cardiac function, cholesterol biosynthesis, peripheral and central nervous system function, the stress response, and osmoregulatory and acid-base balance processes. We propose that cholesterol depletion may be a significant contributor to impacts on cardiac, neuronal, and synaptic function as well as reduced cortisol production and release. Furthermore, it is possible that intracellular calcium homeostasis-a part of cardiotoxic and neuronal function that is affected by oil exposure-may be related to cholesterol depletion. A detailed understanding of oil impacts and affected physiological processes is emerging, but knowledge of their combined effects on fish in natural habitats is largely lacking. read more We identify key areas deserving attention in future research.

Numerous bacterial behaviors are regulated by a cell-density dependent mechanism known as Quorum Sensing (QS). QS relies on communication between bacterial cells using diffusible signaling molecules known as autoinducers. QS regulates physiological processes such as metabolism, virulence, and biofilm formation. Quorum Quenching (QQ) is the inhibition of QS using chemical or enzymatic means to counteract behaviors regulated by QS.

We examine the main, diverse QS mechanisms present in bacterial species, with a special emphasis on AHL-mediated QS. We also discuss key

and

systems in which interference in QS was investigated. Additionally, we highlight promising developments, such as the substrate preference of the used enzymatic quencher, in the application of interference in QS to counter bacterial virulence.

Enabled

the recent isolation of highly stable quorum quenching enzymes and/or molecular engineering efforts, the effects of the interference in QS were recently evaluated outside of the traditional model of single species culture. Signal disruption in complex microbial communities was shown to result in the disruption of complex microbial behaviors, and changes in population structures. These new findings, and future studies, may result in significant changes in the traditional views about QS.

Enabled via the recent isolation of highly stable quorum quenching enzymes and/or molecular engineering efforts, the effects of the interference in QS were recently evaluated outside of the traditional model of single species culture. Signal disruption in complex microbial communities was shown to result in the disruption of complex microbial behaviors, and changes in population structures. These new findings, and future studies, may result in significant changes in the traditional views about QS.The use of seclusion is controversial and has been deemed an encroachment on human rights and dignity which can cause psychological trauma and physical injury to patients in the psychiatric setting. This quality improvement project used a quasi-experimental design to implement the TeamSTEPPS educational program, an evidenced-based program to inform nurses about verbal de-escalation to reduce patient aggressive behavior that can lead to patient seclusion. The targeted patient population included all patients admitted 2 months prior to initiation of Team STEPPS (n = 388) and 2 months following completion of the education modules (n = 342). After the implementation of the educational program there was a statistically significant difference in the rate of charting aggressive behavior (p = 0.024). The pre rate was 17.3%, and the post rate was 11.4%. While there was not a statistically significant difference in the rate of seclusion events, (p = 0.349) there was a clinically significant reduction. The pre rate was 5.9%, and the post rate was 4.4%. The results of this study support the importance of educating psychiatric nurses on verbal-de-escalation to reduce patients placed in seclusion and decrease patients' aggressive behavior in the psychiatric settings.Aquamin is a calcium-rich multi-mineral supplement derived from the red marine algae, Lithothamnion species. Calcium supplementation has been shown to exert a prebiotic-like effect on the gut microbiota and has been associated with distinct changes in lactate and short chain fatty acid (SCFA) production. Irritable bowel syndrome (IBS) subtype is associated with changes in SCFA levels compared with healthy controls. Using an ex vivo simulation model, and a fecal inoculum from a patient diagnosed with IBS, we evaluated the effects of Aquamin (at 6 and 30 mg/mL) on SCFAs and lactate production, pH and gas production, and human microbiota composition. Our results demonstrate that Aquamin increased SCFA production (acetate and propionate by 8% and 24%, respectively, at 30 mg/mL dose), significantly decreased lactate production (30 mg/mL), and increased colonic fluid pH without inducing changes in colonic gas production or gastrointestinal (GI) microbiota composition. These results indicate that Aquamin may play a role in optimizing GI microbial function in an ex vivo setting.Regulation of proteoglycan and glycosaminoglycan synthesis is critical throughout development, and to maintain normal adult functions in wound healing and the immune system, among others. It has become increasingly clear that these processes are also under tight metabolic control and that availability of carbohydrate and amino acid metabolite precursors has a role in the control of proteoglycan and glycosaminoglycan turnover. The enzyme uridine diphosphate (UDP)-glucose dehydrogenase (UGDH) produces UDP-glucuronate, an essential precursor for new glycosaminoglycan synthesis that is tightly controlled at multiple levels. Here, we review the cellular mechanisms that regulate UGDH expression, discuss the structural features of the enzyme, and use the structures to provide a context for recent studies that link post-translational modifications and allosteric modulators of UGDH to its function in downstream pathways.