US physician perspective on the use of biomarker and ctDNA testing in patients with melanoma.

New treatments have increased survival of patients with melanoma, and methods to monitor patients throughout the disease process are needed. Circulating tumor DNA (ctDNA) is a predictive and prognostic biomarker that may allow routine, real-time monitoring of disease status. We surveyed 44 US physicians to understand their preferences and practice patterns for biomarker and ctDNA testing in their patients with melanoma.

Visualization of Latent Fingerprints on Aluminum.

For aluminum, a new visualization method is presented in which copper is deposited electrochemically. The fingerprint on the aluminum (trace carrier) serves as an insulator as it prevents direct contact between electrolyte and aluminum. The decisive factor is the choice of an ammoniacal copper sulfate solution, which acts as a corrosion inhibitor due to the ammonia molecules.

Impairment of Membrane Repolarization Accompanies Axon Transport Deficits in Glaucoma.

Glaucoma is a leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. In glaucoma, axon transport deficits appear to precede structural degeneration of RGC axons. The period of time between the onset of axon transport deficits and the structural degeneration of RGC axons may represent a therapeutic window for the prevention of irreversible vision loss.

Pressure-dependent modulation of inward-rectifying K channels: implications for cation homeostasis and K dynamics in glaucoma.

Glaucoma is the leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. Prior to structural degeneration, RGCs exhibit physiological deficits. Müller glia provide homeostatic regulation of ions that supports RGC physiology through a process called K siphoning.

Phenotypes of primary retinal macroglia: Implications for purification and culture conditions.

Many neurodegenerations, including those of the visual system, have complex etiologies that include roles for both neurons and glia. In the retina there is evidence that retinal astrocytes play an important role in neurodegeneration. There are several approaches for isolating and growing primary retinal astrocytes, however, they often lead to different results.

Impact of Graphene on the Efficacy of Neuron Culture Substrates.

How graphene influences the behavior of living cells or tissues remains a critical issue for its application in biomedical studies, despite the general acceptance that graphene is biocompatible. While direct contact between cells and graphene is not a requirement for all biomedical applications, it is often mandatory for biosensing. Therefore, it is important to clarify whether graphene impedes the ability of cells to interact with biological elements in their environment.

Probing electrical signals in the retina via graphene-integrated microfluidic platforms.

Graphene has attracted extensive attention in biological and biomedical fields due to its unique physical properties and excellent biocompatibility. We combine graphene field-effect transistors and scanning photocurrent microscopy with microfluidic platforms to investigate electrical signals in mouse retina. Remarkable photocurrent signals were detected from the graphene underneath the optic nerve head (ONH) of the retina, where the electrical activity from this region can modulate the carrier concentration of the graphene and induce local potential gradients.

Reversal of morphine-induced cell-type-specific synaptic plasticity in the nucleus accumbens shell blocks reinstatement.

Drug-evoked plasticity at excitatory synapses on medium spiny neurons (MSNs) of the nucleus accumbens (NAc) drives behavioral adaptations in addiction. MSNs expressing dopamine D1 (D1R-MSN) vs. D2 receptors (D2R-MSN) can exert antagonistic effects in drug-related behaviors, and display distinct alterations in glutamate signaling following repeated exposure to psychostimulants; however, little is known of cell-type-specific plasticity induced by opiates.

Sliding Scale Insulin vs Basal-Bolus Insulin Therapy in Long-Term Care: A 21-Day Randomized Controlled Trial Comparing Efficacy, Safety and Feasibility.

Introduction: Sliding scale insulin (SSI) therapy remains a common means of insulin therapy in long-term care (LTC) for the management of type 2 diabetes mellitus, despite current recommendations not supportive of the form of therapy today. Lack of randomized trial data on the efficacy and safety of basal-bolus insulin (B-BI) therapy in nursing home residents may have precluded this form of insulin administration in the LTC setting. Our study is a comparison of the efficacy of SSI (control) and B-BI (intervention) therapies during a 21-day intervention trial in older nursing home residents.

Cocaine and Amphetamine Induce Overlapping but Distinct Patterns of AMPAR Plasticity in Nucleus Accumbens Medium Spiny Neurons.

Repeated exposure to psychostimulant drugs such as cocaine or amphetamine can promote drug-seeking and -taking behavior. In rodent addiction models, persistent changes in excitatory glutamatergic neurotransmission in the nucleus accumbens (NAc) appear to drive this drug-induced behavioral plasticity. To study whether changes in glutamatergic signaling are shared between or exclusive to specific psychostimulant drugs, we examined synaptic transmission from mice following repeated amphetamine or cocaine administration.

Mechanisms underlying the activation of G-protein-gated inwardly rectifying K+ (GIRK) channels by the novel anxiolytic drug, ML297.

ML297 was recently identified as a potent and selective small molecule agonist of G-protein-gated inwardly rectifying K(+) (GIRK/Kir3) channels. Here, we show ML297 selectively activates recombinant neuronal GIRK channels containing the GIRK1 subunit in a manner that requires phosphatidylinositol-4,5-bisphosphate (PIP2), but is otherwise distinct from receptor-induced, G-protein-dependent channel activation. Two amino acids unique to the pore helix (F137) and second membrane-spanning (D173) domain of GIRK1 were identified as necessary and sufficient for the selective activation of GIRK channels by ML297.