The Use of Palliative Performance Score in Patients with End-Stage Liver Disease

● Palliative Care services are often underutilized in patients with End-Stage Liver Disease (ESLD) and often only initiated at the end of life ● The Palliative Performance Score (PPS) is an important tool used in Palliative Care to assess functional status ● PPS has five functional dimensions: ambulation, activity level and evidence of disease, self-care, oral intake, and level of consciousness ● The aim of this study is to determine if there is a correlation between Model for End-Stage Liver Disease (MELD) score and PPS in ESLD patients ● MELD is used to predict mortality and to prioritize liver transplant allocation in ESLD patientshttps://jdc.jefferson.edu/medposters/1011/thumbnail.jp

The Anti-Epileptic Dilemma – A How to For Transitioning Patients on Seizure Medications to Hospice

Objective We propose an approach to antiepiletics in hospice that includes the evaluation of steroids, medication options, pharmacy consultation and seizure breakthrough plan so that we meet the goals of the patient on hospice

To Anticoagulate or Not: Decision Making Surrounding Anticoagulation in Patients in Hospice and Palliative Care Programs

Objectives Describe the current guidelines for CAT treatment. - Assess risk factors for bleeding and thrombosis in cancer patients and risk/benefits of anticoagulation. Recognize the need for individualized anticoagulation plans in order to make informed decisions that may differ from the guidelines. Propose anticoagulation in hospice if it will achieve the goals of the patient

Ion Channels Involvement in Neurodevelopmental Disorders

Inherited and sporadic mutations in genes encoding for brain ion channels, affecting membrane expression or biophysical properties, have been associated with neurodevelopmental disorders characterized by epilepsy, cognitive and behavioral deficits with significant phenotypic and genetic heterogeneity. Over the years, the screening of a growing number of patients and the functional characterization of newly identified mutations in ion channels genes allowed to recognize new phenotypes and to widen the clinical spectrum of known diseases. Furthermore, advancements in understanding disease pathogenesis at atomic level or using patient-derived iPSCs and animal models have been pivotal to orient therapeutic intervention and to put the basis for the development of novel pharmacological options for drug-resistant disorders. In this review we will discuss major improvements and critical issues concerning neurodevelopmental disorders caused by dysfunctions in brain sodium, potassium, calcium, chloride and ligand-gated ion channels

I-J loop involvement in the pharmacological profile of CLC-K channels expressed in Xenopus oocytes

CLC-K chloride channels and their subunit, barttin, are crucial for renal NaCl reabsorption and for inner ear endolymph production. Mutations in CLC-Kb and barttin cause Bartter syndrome. Here, we identified two adjacent residues, F256 and N257, that when mutated hugely alter in Xenopus oocytes CLC-Ka's biphasic response to niflumic acid, a drug belonging to the fenamate class, with F256A being potentiated 37-fold and N257A being potently blocked with a KD~1μM. These residues are localized in the same extracellular I-J loop which harbors a regulatory Ca(2+) binding site. This loop thus can represent an ideal and CLC-K specific target for extracellular ligands able to modulate channel activity. Furthermore, we demonstrated the involvement of the barttin subunit in the NFA potentiation. Indeed the F256A mutation confers onto CLC-K1 a transient potentiation induced by NFA which is found only when CLC-K1/F256A is co-expressed with barttin. Thus, in addition to the role of barttin in targeting and gating, the subunit participates in the pharmacological modulation of CLC-K channels and thus represents a further target for potential drugs

SFM study of the surface of halogen-bonded hybrid co-crystals containing long-chain perfluorocarbons

Different scanning force microscopy (SFM) techniques were employed to investigate the structure and composition of the fundamental crystal faces of prototype halogen-bonded co-crystals of long-chain perfluorocarbons. These crystals were found to show surfaces with well-defined ledges formed by intersecting crystal planes having different chemical compositions with the perfluorocarbons (PFCs) covering the largest area of the crystal as a reminiscence of the strong segregation observed in the bulk crystal structure

Fluvastatin and atorvastatin affect calcium homeostasis of rat skeletal muscle fibers in vivo and in vitro by impairing the sarcoplasmic reticulum/mitochondria Ca2+-release system

The mechanism by which the 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors (statins) induce skeletal muscle injury is still under debate. By using fura-2 cytofluorimetry on intact extensor digitorum longus muscle fibers, here we provided the first evidence that 2 months in vivo chronic treatment of rats with fluvastatin (5 and 20 mg kg-1) and atorvastatin (5 and 10 mg kg-1) caused an alteration of calcium homeostasis. All treated animals showed a significant increase of resting cytosolic calcium [Ca2+]i, up to 60% with the higher fluvastatin dose and up to 20% with the other treatments. The [Ca2+]i rise induced by statin administration was not due to an increase of sarcolemmal permeability to calcium. Furthermore, the treatments reduced caffeine responsiveness. In vitro application of fluvastatin caused changes of [Ca2+]i, resembling the effect obtained after the in vivo administration. Indeed, fluvastatin produced a shift of mechanical threshold for contraction toward negative potentials and an increase of resting [Ca2+]i. By using ruthenium red and cyclosporine A, we determined the sequence of the statin-induced Ca2+ release mechanism. Mitochondria appeared as the cellular structure responsible for the earlier event leading to a subsequent large sarcoplasmic reticulum Ca2+ release. In conclusion, we suggest that calcium homeostasis alteration may be a crucial event for myotoxicity induced by this widely used class of hypolipidemic drug

Investigating a Benzofurane Derivative Binding Site on Human CLC-5

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