Antiphospholipid antibodies (aPL) are a heterogeneous group of autoantibodies, detected in the sera of patients with both autoimmune and various non-autoimmune diseases. They are also detected in subjects with no overt underlying disease - the primary antiphosphilipid syndrome (PAPS). High titers of APL are associated with arterial and venous thrombosis, recurrent fetal loss and thrombocytopenia. There have been many suggestions explaining the potential mechanisms of the procoagulant effect of aPL. These include endothelial cell (EC) activation; increased adhesion molecule expression; inhibition of EC prostacyclin release, increased leucocyte adhesion to EC, downregulation of thrombomodulin expression. APL induce the procoagulant activity of monocytes via increased tissue factor expression and directly stimulate platelet hyperactivity with resultant production of enhanced amounts of the proaggregatory molecule of TXA(2). In vitro studies show that prepro-endothelin-1 mRNA is induced by human monoclonal anticardiolipin antibodies and this might contribute to vasospasm, and, ultimately, to arterial occlusion. The hypercoagulable state in APS patients is associated with alterations in the protein C/S pathway. It is suggested that aPL may impair the protein C anticoagulant system. Acquired protein C and protein S deficiency is described in patients with APS. Beta2- glycoprotein I, (Beta2-GPI) a natural anticoagulant, is involved in the regulation of protein S anticoagulant activity by preventing the binding of protein S to C4b-binding protein. APL were shown to inhibit this effect of Beta2- GP I. As the group of aPL is very heterogeneous, it is unlikely that a single mechanism is responsible for the thrombogenic activity of all aPLs associated with thrombosis.

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Aim: The objective of the present study was to make a complex evaluation of behaviour, lipid metabolism, inflammation, and bone turnover in an ovariectomized rat model used to simulate postmenopausal clinical findings.Materials and methods: Female Wistar rats were divided into 2 groups of 16 animals each: sham operated (SO) animals and ovariectomized (OVX) animals. Three months after the operation, a battery of behavioural tests was performed including an open field test (OFT), elevated pus-maze test (EPM), the social interaction test (SIT), the forced swim test (FST), and a hot plate test (HPT). At termination of experiment, weight gain and fat deposits (total and retroperitoneal) were measured. Serum concentrations of blood lipids were determined. Tumor necrosis factor alpha (TNF-alpha) and alkaline phosphatase (ALP) serum concentrations were used for evaluation of the inflammation and bone turnover, respectively. Femur bone mineral density (BMD) was evaluated using dual energy X-ray absorptiometry.Results: OVX rats did not demonstrate any significant behavioural changes in OFT and EPM tests but showed a decreased interaction time in SIT and an increased immobility time in FST test which indicated anxiety and depression. The OVX rats had a significantly lower pain sensitivity threshold. They had greater weight gain, increased total and retroperitoneal fat deposits, as well as elevated total fat/body weight and retroperitoneal fat/body weight ratios. Blood cholesterol, ALP and TNF-alpha of the OVX group were also significantly higher. Femur BMD of OVX rats was slightly but not significantly reduced.Conclusions: Estrogen deficiency in OVX rats caused depression, anxiety, hyperalgesia, obesity, dyslipidemia, and inflammationbefore the reduction in bone mineral density was prominent.

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The epidemiology of subacute sclerosing panencephalitis (SSPE) has changed substantially since the introduction of measles vaccine. We studied the incidence of SSPE in Bulgaria based on cases admitted to the Child Neurology Clinic, University Hospital of Neurology and Psychiatry, Sofia, for a 25-year period (1978–2002). The SSPE incidence prior to and during the period of routine measles immunization was analyzed. SSPE was diagnosed in 40 children (29 males and 11 females, mean age 8.5 years), 28 from 1978 to 1984 (average 4 patients/year), and 12 from 1995 to 2002 (average 1.7 patients/year). Thirty-eight cases (95%) were non-immunized and had early measles infection. Age at onset of SSPE ranged from 8 to 11 years (52.5%) with a mean latent period of 7 years following measles infection. The increase in SSPE incidence (1995–2002) following a 10-year disease-free period (1985–1994) appears to be related to early measles infection (mean age 11 months) during the measles epidemic of 1991–1992. During the period 1995–2002, children had earlier measles infection (average 11 months) and earlier onset of SSPE (mean age 8.4 years) than in the period 1978–1984 (mean age at measles infection 18 months, and of SSPE onset 11.2 years). The SSPE incidence in Bulgaria during the 25-year period from 1978 to 2002 confirms the importance of early measles infection as a risk factor for SSPE, and the role of routine measles immunization in SSPE prevention.

Carrageenan-induced paw oedema is a widely used model of acute inflammation. The objective of this study was to assess the effect of the flavonoid fustin on carrageenan-induced acute paw inflammation in rats. Thirty male Wistar rats were distributed equally between three groups – control, F10, and F20. In the course of 1 week, animals were treated once daily by intragastric gavage as follows: control group – with distilled water (10 mL kg−1) containing 50 μL Tween 80; groups F10 and F20 – with 10 mL kg−1 suspensions containing fustin in two doses (10 mg kg−1 and 20 mg kg−1, respectively) and 50 μL Tween 80. After the treatment period, carrageenan was injected in the left hind paw and paw oedema was evaluated 0, 30, 60, 120, 180, 240, and 300 min after the injection using a plethysmometer. In the control group, paw oedema increased gradually and peaked at the 180th minute. Fustin treatment reduced the oedema in all time intervals and the effect was significant on the 30th and 60th minute after the injection. The present study indicated that fustin could suppress acute inflammation.