Academic Factors Predicting NCLEX-RN Success.

This retrospective study examined the relationships among 10 academic predictors and first-time success on the NCLEX-RN in a sample of 92 bachelor of science in nursing minority and culturally diverse generic/traditional students at a large minority-serving, urban, public university. Predictors included the Test of Essential Academic Skills (overall, science, and reading), science grade point average (GPA), cumulative GPA, and scores on various standardized exams: Kaplan, HESI, and ATI. Discriminant analysis found science GPA of >3.

COVID-19 and Advanced Practice Registered Nurses: Frontline Update.

Coronavirus disease 2019 (COVID-19) emerged in 2019 and rapidly became a global pandemic, infecting millions and killing hundreds of thousands. The disease altered the practices of hospitals, clinics, and patients. These changes have implications for advanced practice registered nurses (APRNs).

Women's Choice Regarding Breastfeeding and Its Effect on Well-Being.

Because of the many known maternal and neonatal health benefits of breastfeeding, there have been significant efforts to encourage exclusive breastfeeding, and many hospitals follow the guidelines of the Baby-Friendly Hospital Initiative. However, even with the right support, many women are unable to exclusively breastfeed, which may make them feel anxious and/or depressed. Psychological pressure to exclusively breastfeed has the potential to contribute to postpartum depression symptoms in new mothers who are unable to achieve their breastfeeding intentions.

A Gluten-Free Diet, Not an Appropriate Choice without a Medical Diagnosis.

In the past, only people diagnosed with celiac disease, approximately 1% of the population, avoided gluten consumption through all their meals. However, popular media often now mistakenly present gluten-free foods as being a healthier choice, and more people have now concluded that gluten is a harmful part of the diet. A review of literature on gluten-free diets, gluten sensitivity, celiac disease, and attitudes toward gluten consumption was undertaken to examine the prevalence and consequences of adopting a gluten-free diet and to provide guidance to healthcare practitioners whose patients are now often adopting this diet without medical input.

Research in Academia: Creating and Maintaining High Performance Research Teams.

As universities strive to raise their academic rank through the quality and quantity of scholarship in order to maintain their competitive edge and funding sources, faculty face pressure to increase number of publications and externally funded research (or project proposals). There are many challenges that make it difficult for faculty to meet a university's research demand, such as increased work load in academia, teaching large-size classes of students, and other strict university deadlines related to book ordering, scheduling classes, posting grades, etc. Faculty work group conflicts, faculty incivility, and dwindling grant/research funding add to faculty stress.

Podocyte-specific GLUT4-deficient mice have fewer and larger podocytes and are protected from diabetic nephropathy.

Podocytes are a major component of the glomerular filtration barrier, and their ability to sense insulin is essential to prevent proteinuria. Here we identify the insulin downstream effector GLUT4 as a key modulator of podocyte function in diabetic nephropathy (DN). Mice with a podocyte-specific deletion of GLUT4 (G4 KO) did not develop albuminuria despite having larger and fewer podocytes than wild-type (WT) mice.

Regional distribution of SGLT activity in rat brain in vivo.

Na(+)-glucose cotransporter (SGLT) mRNAs have been detected in many organs of the body, but, apart from kidney and intestine, transporter expression, localization, and functional activity, as well as physiological significance, remain elusive. Using a SGLT-specific molecular imaging probe, α-methyl-4-deoxy-4-[(18)F]fluoro-D-glucopyranoside (Me-4-FDG) with ex vivo autoradiography and immunohistochemistry, we mapped in vivo the regional distribution of functional SGLTs in rat brain. Since Me-4-FDG is not a substrate for GLUT1 at the blood-brain barrier (BBB), in vivo delivery of the probe into the brain was achieved after opening of the BBB by an established procedure, osmotic shock.

Mouse SGLT3a generates proton-activated currents but does not transport sugar.

Sodium-glucose cotransporters (SGLTs) are secondary active transporters belonging to the SLC5 gene family. SGLT1, a well-characterized member of this family, electrogenically transports glucose and galactose. Human SGLT3 (hSGLT3), despite sharing a high amino acid identity with human SGLT1 (hSGLT1), does not transport sugar, although functions as a sugar sensor.

Podocytopathy in diabetes: a metabolic and endocrine disorder.

Diabetic nephropathy (DN) represents a major public health cost. Tight glycemic and blood pressure control can dramatically slow, but not stop, the progression of the disease, and a large number of patients progress toward end-stage renal disease despite currently available interventions. An early and key event in the development of DN is loss of podocyte function (or glomerular visceral epithelial cells) from the kidney glomerulus, where they contribute to the integrity of the glomerular filtration barrier.

Sugar binding residue affects apparent Na+ affinity and transport stoichiometry in mouse sodium/glucose cotransporter type 3B.

SGLT1 is a sodium/glucose cotransporter that moves two Na(+) ions with each glucose molecule per cycle. SGLT3 proteins belong to the same family and are described as glucose sensors rather than glucose transporters. Thus, human SGLT3 (hSGLT3) does not transport sugar, but extracellular glucose depolarizes the cell in which it is expressed.

Evidence for a third sodium-binding site in glutamate transporters suggests an ion/substrate coupling model.

Excitatory amino acid transporters (EAATs) remove glutamate from synapses. They maintain an efficient synaptic transmission and prevent glutamate from reaching neurotoxic levels. Glutamate transporters couple the uptake of one glutamate to the cotransport of three sodium ions and one proton and the countertransport of one potassium ion.

A single amino acid change converts the sugar sensor SGLT3 into a sugar transporter.

Background: Sodium-glucose cotransporter proteins (SGLT) belong to the SLC5A family, characterized by the cotransport of Na(+) with solute. SGLT1 is responsible for intestinal glucose absorption. Until recently the only role described for SGLT proteins was to transport sugar with Na(+).

Functional characterization of mouse sodium/glucose transporter type 3b.

Despite belonging to a family of sugar cotransporters, human sodium/glucose transporter type 3 (hSGLT3) does not transport sugar, but it depolarizes the cell in the presence of extracellular sugar, and thus it has been suggested to work as a sugar sensor. In the human genome there is one SGLT3 gene, yet in mouse there are two. In this study we cloned one of them, mouse SGLT3b (mSGLT3b) and characterized the protein.

Involvement of amino acid 36 in TM1 in voltage sensitivity in mouse Na+/glucose cotransporter SGLT1.

Human SGLT1 protein is an established sodium-glucose cotransporter. Despite widespread use of the mouse as a model organism, the mouse SGLT1 homologue has yet to be functionally characterized. Additionally, the crystal structure of a sugar transporter homologue, Vibrio SGLT, has recently been described, however, it offers limited information about the role of transmembrane segments outside of the core ligand binding domains.

Nonvesicular inhibitory neurotransmission via reversal of the GABA transporter GAT-1.

GABA transporters play an important but poorly understood role in neuronal inhibition. They can reverse, but this is widely thought to occur only under pathological conditions. Here we use a heterologous expression system to show that the reversal potential of GAT-1 under physiologically relevant conditions is near the normal resting potential of neurons and that reversal can occur rapidly enough to release GABA during simulated action potentials.

Sodium-dependent reorganization of the sugar-binding site of SGLT1.

The sodium-dependent glucose cotransporter SGLT1 undergoes a series of voltage- and ligand-induced conformational changes that underlie the cotransport mechanism. In this study we describe how the binding of external Na changes the conformation of the sugar-binding domain, exposing residues that are involved in sugar recognition to the external environment. We constructed 15 individual Cys mutants in the four transmembrane helices (TMHs) that form the sugar binding and translocation domain.

Imino sugars are potent agonists of the human glucose sensor SGLT3.

Imino sugars are used to treat type 2 diabetes mellitus [miglitol (Glyset)] and lysosomal storage disorders [miglustat (Zavesca)] based on the inhibition of alpha-glucosidases and glucosyltransferases. In this substrate specificity study, we examined the interactions of imino sugars with a novel human glucose sensor, sodium/glucose cotransporter type 3 (hSGLT3), using expression in Xenopus laevis oocytes and electrophysiology. The results for hSGLT3 are compared with those for alpha-glucosidases and human SGLT type 1 (hSGLT1), a well characterized sodium/glucose cotransporter of the SGLT family.

Mechanism of increased open probability by a mutation of the BK channel.

A missense mutation (D434G) has recently been identified in the alpha subunit of the human large-conductance calcium-activated potassium (BK) channel. Interestingly, although the mutation causes an increase in open probability, individuals that carry the mutation have epilepsy and/or paroxysmal dyskinesia, disorders of increased brain excitability. To define the mechanisms of the mutation, we have used recordings from single channels and measurement of macroscopic conductances to examine the gating of the alpha subunit, modulation by the regulatory beta4 subunit, and the effect of Mg2+ on channel properties.

Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder.

The large conductance calcium-sensitive potassium (BK) channel is widely expressed in many organs and tissues, but its in vivo physiological functions have not been fully defined. Here we report a genetic locus associated with a human syndrome of coexistent generalized epilepsy and paroxysmal dyskinesia on chromosome 10q22 and show that a mutation of the alpha subunit of the BK channel causes this syndrome. The mutant BK channel had a markedly greater macroscopic current.

Coupled sodium/glucose cotransport by SGLT1 requires a negative charge at position 454.

Na(+)/glucose cotransport by SGLT1 is a tightly coupled process that is driven by the Na(+) electrochemical gradient across the plasma membrane. We have previously proposed that SGLT1 contains separate Na(+)- and glucose-binding domains, that A166 (in the Na(+) domain) is close to D454 (in the sugar domain), and that interactions between these residues influence sugar specificity and transport. We have now expressed the mutant D454C in Xenopus laevis oocytes and examined the role of charge on residue 454 by replacing the Asp with Cys or His, and by chemical mutation of D454C with alkylating reagents of different charge (MTSES(-), MTSET(+), MMTS(0), MTSHE(0), and iodoacetate(-)).

A glucose sensor hiding in a family of transporters.

We have examined the expression and function of a previously undescribed human member (SGLT3/SLC5A4) of the sodium/glucose cotransporter gene family (SLC5) that was first identified by the chromosome 22 genome project. The cDNA was cloned and sequenced, confirming that the gene coded for a 659-residue protein with 70% amino acid identity to the human SGLT1. RT-PCR and Western blotting showed that the gene was transcribed and mRNA was translated in human skeletal muscle and small intestine.