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While the prevalence is still being determined, more medical students are utilizing application consulting companies when applying to competitive residencies such as dermatology. We outline the structure of these companies, the scope of services provided, and the costs associated. We also discuss the ethical implications for the use in the residency application process of such firms and the impact of these practices on the candidate selection process. Finally, we offer possible solutions and measures that mitigate the impact of the use of consulting firms in residency applications. Application consulting services are meant to assist clients in maximizing their chances for a successful application cycle. Many companies cater to both prospective residency and pre-medical candidates, including "Med School Insiders," "BeMo Academic Consulting," and "Elite Medical Prep." The scope of application consulting services is vast. Clients can request services such as personalized school selection, application advising, document preparation review [e.g., curriculum vitae (CV), personal statements, and essays), electronic residency application service (ERAS)], and interview coaching. Another service offered is residency match advising, which details specific requirements programs desire. Prospective clients would gain a significant advantage, mainly when used at the outset of medical school training when planning a trajectory for competitive specialties. We review the ethical issues associated with using these consulting services.

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Naturally occurring manganese (Mn) oxide minerals often form by microbial Mn(II) oxidation, resulting in nanocrystalline Mn(III/IV) oxide phases with high reactivity that can influence the uptake and release of many metals (e.g., Ni, Cu, Co, and Zn). During formation, the structure and composition of biogenic Mn oxides can be altered in the presence of other metals, which in turn affects the minerals' ability to bind these metals. These processes are further influenced by the chemistry of the aqueous environment and the type and physiology of microorganisms involved. Conditions extending to environments that typify mining and industrial wastewaters (e.g., increased salt content, low nutrient, and high metal concentrations) have not been well investigated thus limiting the understanding of metal interactions with biogenic Mn oxides. By integrating geochemistry, microscopic, and spectroscopic techniques, we examined the capacity of Mn oxides produced by the Mn(II)-oxidizing Ascomycete fungus Periconia sp. SMF1 isolated from the Minnesota Soudan Mine to remove the metal co-contaminant Co(II) from synthetic waters that are representative of mining wastewaters currently undergoing remediation efforts. We compared two different applied remediation strategies under the same conditions: coprecipitation of Co with mycogenic Mn oxides versus adsorption of Co with pre-formed fungal Mn oxides. Co(II) was effectively removed from solution by fungal Mn oxides through two different mechanisms: incorporation into, and adsorption onto, Mn oxides. These mechanisms were similar for both remediation strategies, indicating the general effectiveness of Co(II) removal by these oxides. The mycogenic Mn oxides were primarily a nanoparticulate, poorly-crystalline birnessite-like phases with slight differences depending on the chemical conditions during formation. The relatively fast and complete removal of aqueous Co(II) during biomineralization as well as the subsequent structural incorporation of Co into the Mn oxide structure illustrated a sustainable cycle capable of continuously remediating Co(II) from metal-polluted environments.

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During biogeochemical iron cycling at redox interfaces, dissolved Fe(II) induces the recrystallization of Fe(III) oxides. Oxalate and other organic acids promote dissolution of these minerals and may also induce recrystallization. These processes may redistribute trace metals among the mineral bulk, mineral surface, and aqueous solution. However, the impact of interactions among organic acids, dissolved Fe(II), and iron oxide minerals on trace metal fate in such systems is unclear. The present study thus explores the effect of oxalate on Ni release from and incorporation into hematite and goethite in the absence and presence of Fe(II). When Ni is initially structurally incorporated into the iron oxides, both oxalate and dissolved Fe(II) promote the release of Ni to aqueous solution. When both species are present, their effects on Ni release are synergistic at pH 7 but inhibitory at pH 4, indicating that cooperative and competitive interactions vary with pH. In contrast, oxalate suppresses Ni incorporation into goethite and hematite during Fe(II)-induced recrystallization, decreasing the proportion of Ni substituting in a mineral structure by up to 36%. These observations suggest that at redox interfaces oxalate largely enhances trace metal mobility. In such settings, oxalate, and likely other organic acids, may thus enhance micronutrient availability and inhibit contaminant sequestration.

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Iron oxides are ubiquitous in soils and sediments and play a critical role in the geochemical distribution of trace elements and heavy metals via adsorption and coprecipitation. The presence of organic acids may potentially alter how metals associate with iron oxide minerals through a series of cooperative or competitive processes: solution complexation, ternary surface complexation, and surface site competition. The macroscopic and molecular-scale effects of these processes were investigated for Ni adsorption to hematite and goethite at pH 7 in the presence of oxalate. The addition of this organic acid suppresses Ni uptake on both minerals. Aqueous speciation suggests that this is dominantly the result of oxalate complexing and solubilizing Ni. Comparison of the Ni surface coverage to the concentration of free (uncomplexed) Ni2+ in solution suggests that the oxalate also alters Ni adsorption affinity. EXAFS and ATR-FTIR spectroscopies indicate that these changes in binding affinity are due to the formation of Ni-oxalate ternary surface complexes. These observations demonstrate that competition between dissolved oxalate and the mineral surface for Ni overwhelms the enhancement in adsorption associated with ternary complexation. Oxalate thus largely enhances Ni mobility, thereby increasing micronutrient bioavailability and inhibiting contaminant sequestration.

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To study the contribution of the Na(+)-Ca(2+) exchanger to Ca(2+) regulation and its interaction with the sarcoplasmic reticulum (SR), changes in cytoplasmic Ca(2+) concentration ([Ca(2+)](c)) were measured in single, voltage clamped, smooth muscle cells. Increases in [Ca(2+)](c) were evoked by either depolarisation (-70 mV to 0 mV) or by release from the SR by caffeine (10 mM) or flash photolysis of caged InsP(3) (InsP(3)). Depletion of the SR of Ca(2+) (verified by the absence of a response to caffeine and InsP(3)) by either ryanodine (50 microM), to open the ryanodine receptors (RyRs), or thapsigargin (500 nM) or cyclopiazonic acid (CPA, 10 microM), to inhibit the SR Ca(2+) pumps, reduced neither the magnitude of the Ca(2+) transient nor the relationship between the influx of and the rise in [Ca(2+)](c) evoked by depolarisation. This suggested that Ca(2+)-induced Ca(2+) release (CICR) from the SR did not contribute significantly to the depolarisation-evoked rise in [Ca(2+)](c). However, although Ca(2+) was not released from it, the SR accumulated the ion following depolarisation since ryanodine and thapsigargin each slowed the rate of decline of the depolarisation-evoked Ca(2+) transient. Indeed, the SR Ca(2+) content increased following depolarisation as assessed by the increased magnitude of the [Ca(2+)](c) levels evoked each by InsP(3) and caffeine, relative to controls. The increased SR Ca(2+) content following depolarisation returned to control values in approximately 12 min via Na(+)-Ca(2+) exchanger activity. Thus inhibition of the Na(+)-Ca(2+) exchanger by removal of external Na(+) (by either lithium or choline substitution) prevented the increased SR Ca(2+) content from returning to control levels. On the other hand, the Na(+)-Ca(2+) exchanger did not appear to regulate bulk average Ca(2+) directly since the rates of decline in [Ca(2+)](c), following either depolarisation or the release of Ca(2+) from the SR (by either InsP(3) or caffeine), were neither voltage nor Na(+) dependent. Thus, no evidence for short term (seconds) control of [Ca(2+)](c) by the Na(+)-Ca(2+) exchanger was found. Together, the results suggest that despite the lack of CICR, the SR removes Ca(2+) from the cytosol after its elevation by depolarisation. This Ca(2+) is then removed from the SR to outside the cell by the Na(+)-Ca(2+) exchanger. However, the exchanger does not contribute significantly to the decline in bulk average [Ca(2+)](c) following transient elevations in the ion produced either by depolarisation or by release from the store.

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