As ligaments, lateral compartment and patellofemoral anatomy are preserved with UKA; the unloaded knee closely resembles native kinematics. The slight kinematic changes that were found under load are probably due to loss of the conforming medial meniscus and to the mismatch in geometry and stiffness introduced by UKA. These patterns resemble those found in knees with significant loss of function of the medial meniscus.

No abstract

Lowest stresses and micromotion were found for long cemented stems. Cementless stems showed more micromotion and increased stress levels especially at the level of the stem tip, which may explain the clinical phenomenon of stem-end pain following revision knee arthroplasty. These findings will help the surgeon with optimal individual implant choice.

Orexin-A (OXA) regulates food intake and energy homeostasis. It increases insulin secretion in vivo and in vitro, although controversial effects of OXA on plasma glucagon are reported. We characterized the effects of OXA on glucagon secretion and identify intracellular target molecules in glucagon-producing cells. Glucagon secretion from in situ perfused rat pancreas, isolated rat pancreatic islets, and clonal pancreatic A-cells (InR1-G9) were measured by RIA. The expression of orexin receptor 1 (OXR1) was detected by Western blot and immunofluorescence. The effects of OXA on cAMP, adenylate-cyclase-kinase (AKT), phosphoinositide-dependent kinase (PDK)-1, forkhead box O-1 (Foxo1), and cAMP response element-binding protein were measured by ELISA and Western blot. Intracellular calcium (Ca(2+)(i)) concentration was detected by fura-2and glucagon expression by real-time PCR. Foxo1 was silenced in InR1-G9 cells by transfecting cells with short interfering RNA. OXR1 was expressed on pancreatic A and InR1-G9 cells. OXA reduced glucagon secretion from perfused rat pancreas, isolated rat pancreatic islets, and InR1-G9 cells. OXA inhibited proglucagon gene expression via the phosphatidylinositol 3-kinase-dependent pathway. OXA decreased cAMP and Ca(2+)(i) concentration and increased AKT, PDK-1, and Foxo1 phosphorylation. Silencing of Foxo1 caused a reversal of the inhibitory effect of OXA on proglucagon gene expression. Our study provides the first in vitro evidence for the interaction of OXA with pancreatic A cells. OXA inhibits glucagon secretion and reduces intracellular cAMP and Ca(2+)(i) concentration. OXA increases AKT/PDK-1 phosphorylation and inhibits proglucagon expression via phosphatidylinositol 3-kinase- and Foxo-1-dependent pathways. As a physiological inhibitor of glucagon secretion, OXA may have a therapeutic potential to reduce hyperglucagonemia in type 2 diabetes.

IntroductionSynthol is a site enhancement oil used by bodybuilders to boost the cosmetic appearance of muscles. Here, we describe the case of a patient with severe side effects following repeated intramuscular injections of synthol in his right biceps muscle.Case presentationA 29-year-old Middle Eastern male bodybuilder, following intramuscular injections of synthol five years ago, presented with painful pressure in his right upper arm. On presentation to our clinic, his muscle appeared disfigured. Magnetic resonance imaging revealed scattered cystic fatty lesions in the muscle. The affected part was surgically removed and histopathology showed inflammatory changes with fibrosis and a so-called Swiss cheese pattern.ConclusionSynthol injections that are used for the short-term enhancement of muscle appearance by bodybuilders bear the danger of long-term painful muscle fibrosis and disfigurement.