Periarticular osteophyte formation protects against total knee arthroplasty in rheumatoid arthritis patients with advanced joint damage

Clinical Rheumatology - Periarticular osteophyte formation is observed during the repair of damaged joints in rheumatoid arthritis (RA); however, little is known about its clinical and functional...     

Sitosterolemia Exhibiting Severe Hypercholesterolemia with Tendon Xanthomas Due to Compound Heterozygous ABCG5 Gene Mutations Treated with Ezetimibe and Alirocumab

We herein report a rare case presenting with severe hypercholesterolemia, massive Achilles tendon xanthomas, and multi-vessel coronary artery disease. Initially, the patient was misdiagnosed with familial hypercholesterolemia. However, a genetic analysis using our custom sequencing panel covering genes associated with Mendelian lipid disorders revealed him to have a genetic basis of sitosterolemia with compound heterozygous mutations in the adenosine triphosphate binding cassette subfamily G5 (ABCG5) gene. A comprehensive genetic analysis can be particularly useful for diagnosing cases with severe phenotypes, leading to appropriate and medical therapies. Our patient was refractory to statins, whereas ezetimibe and PCSK9 inhibitor with a low-plant-sterol diet successfully reduced his serum levels of low-density lipoprotein cholesterol.     

Prostaglandin E2 and its receptor EP2 trigger signaling that contributes to YAP‐mediated cell competition

Cell competition is a biological process by which unfit cells are eliminated from “cell society.” We previously showed that cultured mammalian epithelial Madin‐Darby canine kidney (MDCK) cells expressing constitutively active YAP were eliminated by apical extrusion when surrounded by “normal” MDCK cells. However, the molecular mechanism underlying the elimination of active YAP‐expressing cells was unknown. Here, we used high‐throughput chemical compound screening to identify cyclooxygenase‐2 (COX‐2) as a key molecule triggering cell competition. Our work shows that COX‐2‐mediated PGE₂ secretion engages its receptor EP2 on abnormal and nearby normal cells. This engagement of EP2 triggers downstream signaling via an adenylyl cyclase‐cyclic AMP‐PKA pathway that, in the presence of active YAP, induces E‐cadherin internalization leading to apical extrusion. Thus, COX‐2‐induced PGE₂ appears a warning signal to both abnormal and surrounding normal cells to drive cell competition.     

Histopathology of tenosynovium in trigger fingers

Stenosing flexor tenosynovitis, trigger finger, is a common clinical disorder causing painful locking or contracture of the involved digits, and most instances are idiopathic. This problem is generally caused by a size mismatch between the swollen flexor tendon and the thickened first annular pulley. Although hypertrophic pulleys have been histologically and ultrasonographically detected, little is known about the histopathology of the tenosynovium covering the tendons of trigger fingers. We identified chondrocytoid cells that produced hyaluronic acid in 23 (61%) fingers and hypocellular collagen matrix in 32 (84%) fingers around the tenosynovium among 38 specimens of tenosynovium from patients with trigger fingers. These chondrocytoid cells expressed the synovial B cell marker CD44, but not the chondrocyte marker S‐100 protein. The incidence of these findings was much higher than that of conventional findings of synovitis, such as inflammatory infiltrate (37%), increased vascularity (37%), hyperplasia of synovial lining cells (21%), or fibrin exudation (5%). We discovered the following distinctive histopathological features of trigger finger: hyaluronic acid‐producing chondrocytoid cells originated from fibroblastic synovial B cells, and a hypocellular collagen matrix surrounding the tenosynovium. Thus, an edematous extracellular matrix with active hyaluronic acid synthesis might increase pressure under the pulley and contribute to the progression of stenosis.     

A mother's complaints of overeating by her 25-month-old daughter: A proposal of anorexia nervosa by proxy

The following is a report on a case of a 25-month-old girl brought in by her mother with complaints of overeating. The patient was referred to the Psychiatric Clinic of Nagoya University Hospital from the Department of Pediatric Surgery. The mother indicated the patient to have begun overeating before the age of 1 year. However, the patient was of low height and low body weight, and appeared, rather, to have been underfed. The issue was the mother placing severe restrictions on the child's diet, pathologically afraid of the child overeating. The mother seemed to have been suffering from a disorder similar to anorexia nervosa, although not typical. Her fear that her child might eat too much was believed to be a projection of the mentality characteristic of anorexia nervosa on to her child, which would justify labeling the child's condition anorexia nervosa by proxy. © 1996 by John Wiley & Sons, Inc.     

Synthesis and free radical polymerization of p-methylseleno- and p-phenylselenostyrenes

p-Methylselenostyrene ( 1 ) and p-phenylselenostyrene ( 2 ) as selenium-containing vinyl monomers were prepared. Both monomers are readily polymerized free radically to afford the corresponding polymers having molecular weight of about 20 000 ∼ 150 000. These homopolymers are stable below 300°C. From the copolymerization with styrene, Q values of 1 and 2 were calculated to be 1,18 and 1,03, respectively. On the other hand, e values of these monomers are −0,24 and −0,04, respectively, indicating the electron withdrawing character of the seleno groups.