The clinical effect of glucose meter selection upon the detection of neonatal hypoglycemia.

Neonatal hypoglycemia is a common, transitional metabolic state that may lead to poor neurodevelopmental outcomes if unrecognized or managed inadequately. Given its frequency of presentation and immense clinical significance, a myriad of clinical practice guidelines have been published outlining appropriate screening, diagnosis, and treatment principles-many endorsing the use of glucose point-of-care testing (POCT). Unfortunately, the well-intended 'march' toward POCT, with bedside glucose meters as screening devices in the NICU, has resulted in unintended consequences with critical implications: a lack of international traceability to the 'gold' standard glucose method by POCT devices, under-recognition of POCT limitations, and a reliance upon a technology primarily driven to detect hyperglycemia in the adult population as opposed to neonatal hypoglycemia.

The Large-Conductance, Calcium-Activated Potassium Channel: A Big Key Regulator of Cell Physiology.

Large-conductance Ca-activated K channels facilitate the efflux of K ions from a variety of cells and tissues following channel activation. It is now recognized that BK channels undergo a wide range of pre- and post-translational modifications that can dramatically alter their properties and function. This has downstream consequences in affecting cell and tissue excitability, and therefore, function.

Fecal Calprotectin, CRP and Leucocytes in IBD Patients: Comparison of Biomarkers With Biopsy Results.

Background: This study aimed to compare fecal calprotectin (FC) levels with other commonly used parameters as part of patient care during evaluation for inflammatory bowel disease (IBD).

Methods: We recruited adult IBD patients with ulcerative colitis (UC) and Crohn's disease (CD) and compared the results of the patient's biopsy results (i.e.

Clinical false positives resulting from recent intravenous immunoglobulin therapy: case report.

Background: Many clinicians are aware that certain therapies administered to their patients can have downstream consequences in the form of clinical laboratory test interferences. This is particularly true of laboratory tests that depend on, or directly involve the use of, antibody-based methodology. Intravenously-administered immunoglobulin therapy is one such treatment that can in theory directly impact the results of particular tests in the area of viral serology.

COVID-19 Pandemic Planning: Simulation Models to Predict Biochemistry Test Capacity for Patient Surges.

Background: Patient surges beyond hospital capacity during the initial phase of the COVID-19 pandemic emphasized a need for clinical laboratories to prepare test processes to support future patient care. The objective of this study was to determine if current instrumentation in local hospital laboratories can accommodate the anticipated workload from COVID-19 infected patients in hospitals and a proposed field hospital in addition to testing for non-infected patients.

Methods: Simulation models predicted instrument throughput and turn-around-time for chemistry, ion-selective-electrode, and immunoassay tests using vendor-developed software with different workload scenarios.

KCa channel activation normalizes endothelial function in Type 2 Diabetic resistance arteries by improving intracellular Ca mobilization.

Background: Endothelial dysfunction is an early pathogenic event in the progression of cardiovascular disease in patients with Type 2 Diabetes (T2D). Endothelial KCa2.3 and KCa3.

Lrrc55 is a novel prosurvival factor in pancreatic islets.

Pancreatic islets adapt to the increase in insulin demand during pregnancy by upregulating β-cell number, insulin synthesis, and secretion. These changes require prolactin receptor (PrlR) signaling, as mice with PrlR deletion are glucose intolerant with a lower β-cell mass. Prolactin also prevents β-cell apoptosis.

The augmentation of BK channel activity by nitric oxide signaling in rat cerebral arteries involves co-localized regulatory elements.

Large conductance, Ca-activated K (BK) channels control cerebrovascular tone; however, the regulatory processes influencing these channels remain poorly understood. Here, we investigate the cellular mechanisms underlying the enhancement of BK current in rat cerebral arteries by nitric oxide (NO) signaling. In isolated cerebral myocytes, BK current magnitude was reversibly increased by sodium nitroprusside (SNP, 100 μM) and sensitive to the BK channel inhibitor, penitrem-A (100 nM).

Ion channels of the mammalian urethra.

The mammalian urethra is a muscular tube responsible for ensuring that urine remains in the urinary bladder until urination. In order to prevent involuntary urine leakage, the urethral musculature must be capable of constricting the urethral lumen to an extent that exceeds bladder intravesicular pressure during the urine-filling phase. The main challenge in anti-incontinence treatments involves selectively-controlling the excitability of the smooth muscles in the lower urinary tract.

The regulation of BK channel activity by pre- and post-translational modifications.

Large conductance, Ca(2+)-activated K(+) (BK) channels represent an important pathway for the outward flux of K(+) ions from the intracellular compartment in response to membrane depolarization, and/or an elevation in cytosolic free [Ca(2+)]. They are functionally expressed in a range of mammalian tissues (e.g.

Ca(V)3.2 channels and the induction of negative feedback in cerebral arteries.

Rationale: T-type (CaV3.1/CaV3.2) Ca(2+) channels are expressed in rat cerebral arterial smooth muscle.

The large conductance, calcium-activated K+ (BK) channel is regulated by cysteine string protein.

Large-conductance, calcium-activated-K(+) (BK) channels are widely distributed throughout the nervous system, where they regulate action potential duration and firing frequency, along with presynaptic neurotransmitter release. Our recent efforts to identify chaperones that target neuronal ion channels have revealed cysteine string protein (CSPα) as a key regulator of BK channel expression and current density. CSPα is a vesicle-associated protein and mutations in CSPα cause the hereditary neurodegenerative disorder, adult-onset autosomal dominant neuronal ceroid lipofuscinosis (ANCL).

Mechanisms underlying activation of transient BK current in rabbit urethral smooth muscle cells and its modulation by IP3-generating agonists.

We used the perforated patch-clamp technique at 37°C to investigate the mechanisms underlying the activation of a transient large-conductance K(+) (tBK) current in rabbit urethral smooth muscle cells. The tBK current required an elevation of intracellular Ca(2+), resulting from ryanodine receptor (RyR) activation via Ca(2+)-induced Ca(2+) release, triggered by Ca(2+) influx through L-type Ca(2+) (CaV) channels. Carbachol inhibited tBK current by reducing Ca(2+) influx and Ca(2+) release and altered the shape of spike complexes recorded under current-clamp conditions.

Specific phosphorylation sites underlie the stimulation of a large conductance, Ca(2+)-activated K(+) channel by cGMP-dependent protein kinase.

Smooth muscle contractility and neuronal excitability are regulated by large conductance, Ca(2+)-activated K(+) (BKCa) channels, the activity of which can be increased after modulation by type I cGMP-dependent protein kinase (cGKI) via nitric oxide (NO)/cGMP signaling. Our study focused on identifying key phosphorylation sites within the BKCa channel underlying functional enhancement of channel activity by cGKI. BKCa channel phosphorylation by cGKIα was characterized biochemically using radiolabeled ATP, and regulation of channel activity by NO/cGMP signaling was quantified in rat aortic A7r5 smooth muscle cells by cell-attached patch-clamp recording.

Cell culture alters Ca2+ entry pathways activated by store-depletion or hypoxia in canine pulmonary arterial smooth muscle cells.

Previous studies have shown that, in acutely dispersed canine pulmonary artery smooth muscle cells (PASMCs), depletion of both functionally independent inositol 1,4,5-trisphosphate (IP(3))- and ryanodine-sensitive Ca(2+) stores activates capacitative Ca(2+) entry (CCE). The present study aimed to determine if cell culture modifies intracellular Ca(2+) stores and alters Ca(2+) entry pathways caused by store depletion and hypoxia in canine PASMCs. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured in fura 2-loaded cells.