MOVEMENT OF EELWORMS

Experiments on vertical migration through saturated soil fractions, horizontal migration through soil fractions at different pressure deficiencies and migration in single layers of particles showed that the beet eelworm, Heterodera schachtii Schmidt, attained maximum speed when the pore diameters were between 30–60 μ. Speed of the eelworms increased as lateral displacement of the body was restricted by external resistances acting perpendicularly to the body axis; at the maximum speed there was no lateral movement, each part of the body following the part immediately in front of it. The speed of beet eelworm larvae in water films of various thickness was measured; maximum speed occurred in a film 2–5 μ thick. Four arbitrarily classified types of progression were observed in the pore spaces. It is suggested that the 'moisture characteristic' supplies most of the information required about the physical properties of the soil in relation to eelworm movement. By examining such a curve the pore size distribution can be ascertained and the probable behaviour of beet eelworm larvae in the medium predicted.     

Two New Subspecies of Herpetomonas muscarum (Leidy, 1856) Kent, 1880

SYNOPSIS. Herpetomonas muscarum muscarum n. subsp. was isolated from Musca domestica L. In culture at 20 C it assumed the opisthomastigote (up to 15%), double-flagellate and flagellate promastigote forms. At 30 C or with 4% urea added to cultures at 20 C, the proportion of opisthomastigotes was greater (up to 40%). In experimentally infected flies only transient infections, which included both opisthomastigotes and promastigotes, occurred. The promastigotes were 15–30 μ long and the kinetoplast was small and subspherical or transversely elongate. H. muscarum ingenoplastis n. subsp. was isolated from Phormia regina (Meigen). In culture at 20 C almost all individuals were double-flagellate promastigotes 20–40 μ long and less than 1% were opisthomastigotes. At 30 C or with added urea there was no increase in the proportion of opisthomastigotes and the cultures were not vigorous. In experimentally infected flies opisthomastigotes were 5–39% of the population depending on the part of the gut sampled. In all stages the kinetoplast was large (1.5–2.5 μ long) and tear-drop-shaped with the point directed posteriorly.
In artificially mixed cultures of H. m. muscarum and H. m. ingenoplastis the former predominated after a short time and eventually survived alone. A mixed culture that was about 98% H. m. muscarum was fed to Phormia regina and produced heavy pure infections of H. m. ingenoplastis , which lasted for 22 days with no indication of decline. No evidence of cyst formation was found in either subspecies.     

Cholesterol accumulation caused by low density lipoprotein receptor deficiency or a cholesterol-rich diet results in ectopic bone formation during experimental osteoarthritis

Introduction

Osteoarthritis (OA) is associated with the metabolic syndrome, however the underlying mechanisms remain unclear. We investigated whether low density lipoprotein (LDL) accumulation leads to increased LDL uptake by synovial macrophages and affects synovial activation, cartilage destruction and enthesophyte/osteophyte formation during experimental OA in mice.

Methods

LDL receptor deficient (LDLr^−/−) mice and wild type (WT) controls received a cholesterol-rich or control diet for 120 days. Experimental OA was induced by intra-articular injection of collagenase twelve weeks after start of the diet. OA knee joints and synovial wash-outs were analyzed for OA-related changes. Murine bone marrow derived macrophages were stimulated with oxidized LDL (oxLDL), whereupon growth factor presence and gene expression were analyzed.

Results

A cholesterol-rich diet increased apolipoprotein B (ApoB) accumulation in synovial macrophages. Although increased LDL levels did not enhance thickening of the synovial lining, S100A8 expression within macrophages was increased in WT mice after receiving a cholesterol-rich diet, reflecting an elevated activation status. Both a cholesterol-rich diet and LDLr deficiency had no effect on cartilage damage; in contrast, ectopic bone formation was increased within joint ligaments (fold increase 6.7 and 6.1, respectively). Moreover, increased osteophyte size was found at the margins of the tibial plateau (4.4 fold increase after a cholesterol-rich diet and 5.3 fold increase in LDLr^−/− mice). Synovial wash-outs of LDLr^−/− mice and supernatants of macrophages stimulated with oxLDL led to increased transforming growth factor-beta (TGF-β) signaling compared to controls.

Conclusions

LDL accumulation within synovial lining cells leads to increased activation of synovium and osteophyte formation in experimental OA. OxLDL uptake by macrophages activates growth factors of the TGF-superfamily.