The C-terminal portion of the prion protein (PrP), corresponding to a protease-resistant core fragment of the abnormal isoform of the prion protein (PrP Sc), is essential for prion propagation. Antibodies to the C-terminal portion of PrP are known to inhibit PrP Sc accumulation in cells persistently infected with prions. Here it was shown that, in addition to monoclonal antibodies (mAbs) to the C-terminal portion of PrP, a mAb recognizing the octapeptide repeat region in the N-terminal part of PrP that is dispensable for PrP Sc formation reduced PrP Sc accumulation in cells persistently infected with prions. The 50 % effective dose was as low as~1 nM, and, regardless of their epitope specificity, the inhibitory mAbs shared the ability to bind cellular prion protein (PrP C) expressed on the cell surface. Flow cytometric analysis revealed that mAbs that bound to the cell surface during cell culture were not internalized even after their withdrawal from the growth medium. Retention of the mAb-PrP C complex on the cell surface was also confirmed by the fact that internalization was enhanced by treatment of cells with dextran sulfate. These results suggested that anti-PrP mAb antagonizes PrP Sc formation by interfering with the regular PrP C degradation pathway.

Cardiac diseases are well known among patients on maintenance hemodialysis (HD), and carnitine deficiency may be an important factor in cardiac morbidity. We studied the effects of low-dose L-carnitine treatment (500 mg/day) on chest symptoms (dyspnea on exertion, chest pain, palpitation), cardiac function, and left ventricular (LV) mass in 9 HD patients with reduced ejection fraction (EF). After 6 months of L-carnitine treatment, most patients had at least some improvement in chest symptoms, while LVEF was increased and LV mass was decreased. Carnitine fractions increased and reached plateaus at 2–3 times the baseline levels. These results suggest that prolonged low-dose L-carnitine treatment can improve the cardiac morbidity by restoring decreased carnitine tissue levels and impaired oxidation of FFA.

The LLLT could accelerate healing of sutured wounds of the teat in dairy cattle.

No abstract

Low-density lipoprotein apheresis (LDLA) leads to an improvement of microcirculation during the very early stages of treatment, and continued treatment may produce antiatherogenic effects in patients with peripheral arterial disease (PAD). Suppression of oxidative stress, improvement of endothelial functions and alteration in the action of vasoactive compounds may occur with the improvement of the rheological property of blood as a result of aggressive removal of atherogenic factors including LDL, possibly resulting in the suppression of development of atherosclerosis. As these effects of LDLA may ameliorate not only PAD but also ischemia in other organs, it is suggested that repeated LDLA prevents the progression of atherosclerotic diseases and probably improves the long-term prognosis of patients with PAD.