Vastus medialis necrosis secondary to the combination of the subvastus and median parapatellar approaches for implantation of a total knee replacement

We describe a case where a subvastus approach was used for implantation of a primary total knee replacement, which subsequently became infected. Medial parapatellar approaches were then used for the revision surgery at weeks four and twelve after the primary procedure. Vastus medialis necrosis and lateral subluxation of the patella then followed. The patella was centralised electively by performing an open lateral release and semitendinosus tenodesis. This report therefore indicates that combining these two approaches over a short time interval set against a background of haematoma and infection can lead to ischaemic necrosis of the vastus medialis muscle and lateral subluxation of the patella.     

Alpha indirect conversion radioisotope power source.

Advantages of radioisotope-powered electric generators include long service life, wide temperature range operation and high-energy density. We report development of a long-life generator based on indirect conversion of alpha decay energy. Prototyping used 300 mCi Pu-238 alpha emitter and AlGaAs photovoltaic cells designed for low light intensity conditions. The alpha emitter, phosphor screens, and voltaic arrays were assembled into a power source with the following characteristics: Isc=14 microA; Uoc=2.3 V; power output -21 microW. Using this prototype we have powered an eight-digit electronic calculator and wrist watch.     

Diabetic Peripheral Neuropathy: Epidemiology,Diagnosis, and Pharmacotherapy

Purpose

Diabetic peripheral neuropathy (DPN) is the commonest cause of neuropathy worldwide, and its prevalence increases with the duration of diabetes. It affects approximately half of patients with diabetes. DPN is symmetric and predominantly sensory, starting distally and gradually spreading proximally in a glove-and-stocking distribution. It causes substantial morbidity and is associated with increased mortality. The unrelenting nature of pain in this condition can negatively affect a patient's sleep, mood, and functionality and result in a poor quality of life. The purpose of this review was to critically review the current literature on the diagnosis and treatment of DPN, with a focus on the treatment of neuropathic pain in DPN.

SNAIL1 combines competitive displacement of ASCL2 and?epigenetic mechanisms to rapidly silence the EPHB3 tumor suppressor in colorectal cancer

EPHB3 is a critical cellular guidance factor in the intestinal epithelium and an important tumor suppressor in colorectal cancer (CRC) whose expression is frequently lost at the adenoma‐carcinoma transition when tumor cells become invasive. The molecular mechanisms underlying EPHB3 silencing are incompletely understood. Here we show that EPHB3 expression is anti‐correlated with inducers of epithelial‐mesenchymal transition (EMT) in primary tumors and CRC cells. In vitro, SNAIL1 and SNAIL2, but not ZEB1, repress EPHB3 reporter constructs and compete with the stem cell factor ASCL2 for binding to an E‐box motif. At the endogenous EPHB3 locus, SNAIL1 triggers the displacement of ASCL2, p300 and the Wnt pathway effector TCF7L2 and engages corepressor complexes containing HDACs and the histone demethylase LSD1 to collapse active chromatin structure, resulting in rapid downregulation of EPHB3. Beyond its impact on EPHB3, SNAIL1 deregulates markers of intestinal identity and stemness and in vitro forces CRC cells to undergo EMT with altered morphology, increased motility and invasiveness. In xenotransplants, SNAIL1 expression abrogated tumor cell palisading and led to focal loss of tumor encapsulation and the appearance of areas with tumor cells displaying a migratory phenotype. These changes were accompanied by loss of EPHB3 and CDH1 expression. Intriguingly, SNAIL1‐induced phenotypic changes of CRC cells are significantly impaired by sustained EPHB3 expression both in vitro and in vivo. Altogether, our results identify EPHB3 as a novel target of SNAIL1 and suggest that disabling EPHB3 signaling is an important aspect to eliminate a roadblock at the onset of EMT processes.