Pain, what is it and why do we care?

In the first part a series of methodological remarks are presented mainly concerning the use and relevance of concepts such as pain and suffering, the ‘observer-oriented’ vs. the ‘ego-oriented’ approach, the principle of parsimony vs. the principle of caution, and the ethical vs. the factual approach. The general conclusion is that the concepts of pain and suffering have their proper value, conditional upon their use being restricted to their specific domain. In the second part some suggestions are made about the way in which a foundation for an ethics of pain and suffering may be laid

Evaluation of the First Commercial Hepcidin ELISA for the Differential Diagnosis of Anemia of Chronic Disease and Iron Deficiency Anemia in Hospitalized Geriatric Patients

Introduction. Anemia is a frequent problem in hospitalized geriatric patients, and the anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the 2 most prevalent causes. The aim of the study was to assess the possible role of serum hepcidin in the differential diagnosis between ACD and IDA. Methods. We investigated serum hepcidin, iron status, anemia, and C-reactive protein in 39 consecutive geriatric patients with ACD and IDA. Serum hepcidin levels were determined using a commercial ELISA kit (DRG Instruments, Marburg, Germany). We also measured hepcidin in 26 healthy controls. Results. The serum hepcidin levels were not significantly higher in the 28 patients with ACD as compared to the 11 patients with IDA. Conclusions. The serum hepcidin levels measured using the commercial ELISA kit (DRG) do not appear to increase in older patients with ACD. It should be noted that an assay-specific problem could explain our results

Ann Peralta v. Drew Anderson, Brad Anderson, Tammy Anderson, and Donna Hansen : Brief of Appellee

BRIEF OF APPELLEE APPELLEE\u27S RESPONSE BRIEF TO APPELLANT\u27S INTERLOCUTORY APPEAL FROM THE HONORABLE BEN H. HADFIELD\u27S, FIRST JUDICIAL DISTRICT COURT, CACHE COUNTY, MEMORANDUM DECISION GRANTING DONNA HANSEN\u27S MOTION FOR SUMMARY JUDGMENT (ORDER DOES NOT APPEAR IN FILE

APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin

The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but they also increase the risk of kidney disease. APOL1 and APOL3 are death-promoting proteins that are partially associated with the endoplasmic reticulum and Golgi membranes. We report that in podocytes, either APOL1 C-terminal helix truncation (APOL1Δ) or APOL3 deletion (APOL3KO) induces similar actomyosin reorganization linked to the inhibition of phosphatidylinositol-4-phosphate [PI(4)P] synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Both APOL1 and APOL3 can form K+ channels, but only APOL3 exhibits Ca2+-dependent binding of high affinity to neuronal calcium sensor-1 (NCS-1), promoting NCS-1-PI4KB interaction and stimulating PI4KB activity. Alteration of the APOL1 C-terminal helix triggers APOL1 unfolding and increased binding to APOL3, affecting APOL3-NCS-1 interaction. Since the podocytes of G1 and G2 patients exhibit an APOL1Δ or APOL3KO-like phenotype, APOL1 C-terminal variants may induce kidney disease by preventing APOL3 from activating PI4KB, with consecutive actomyosin reorganization of podocytes.info:eu-repo/semantics/publishe