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Antiphospholipid syndrome (APS) is a systemic syndrome whose etiology involves both environmental and genetic factors. Infections may play an important part in the etiology by using different mechanisms, predominantly molecular mimicry, to induce antiphospholipid antibodies (aPL). aPL are often associated with false-positive serological tests for toxoplasmosis, rubella, cytomegalovirus, herpes, human immunodeficiency virus, Lyme disease, and syphilis. A higher prevalence of aPL has been seen in the serum of patients of similar descent, and in mouse models. The hypercoagulable state in APS involves all three major components governing hemostasis: platelets, fibrinolysis, and the coagulation cascade. aPL inhibit both protein C activation and the function of activated protein C, thereby preventing the inactivation of activated factor V and VIII. Potentiation of the procoagulant activity of human umbilical vein endothelial cells by aPL is strongly decreased after depleting IgG from the serum.

Eclampsia has been studied extensively over the last decades. Several pathophysiological mechanisms and animal models have been proposed for the disease. However, to date, none of t hem can fully explain the neuronal pathophysiology of eclamptic convulsions and the associated deleterious complications. Magnesium is the drug of choice for the prophylaxis and treatment of eclampsia in addition to prompt delivery. There is evidence to su ggest that the beneficial effect of magnesium is exerted via modulation of the N - Methyl - D - Aspartate Receptor (NMDAR). The aim of this review is to explore the molecular mechanism by which magnesium exerts its neuroprotective effect and prevents eclamptic c onvulsions through the NMDAR activation pathway. Future investigations and alternative treatments are discussed.

Vaccine adjuvants and vaccines may induce autoimmune and inflammatory manifestations in susceptible individuals. To date most human vaccine trials utilize aluminum (Al) adjuvants as placebos despite much evidence showing that Al in vaccine-relevant exposures can be toxic to humans and animals. We sought to evaluate the effects of Al adjuvant and the HPV vaccine Gardasil versus the true placebo on behavioral and inflammatory parameters in female mice. Six-week-old C57BL/6 female mice were injected with either, Gardasil, Gardasil + pertussis toxin (Pt), Al hydroxide, or, vehicle control in amounts equivalent to human exposure. At 7.5 months of age, Gardasil and Al-injected mice spent significantly more time floating in the forced swimming test (FST) in comparison with vehicle-injected mice (Al, p = 0.009; Gardasil, p = 0.025; Gardasil + Pt, p = 0.005). The increase in floating time was already highly significant at 4.5 months of age for the Gardasil and Gardasil + Pt group (p ? 0.0001). No significant differences were observed in the number of stairs climbed in the staircase test which measures locomotor activity. These results indicate that differences observed in the FST were unlikely due to locomotor dysfunction, but rather due to depression. Moreover, anti-HPV antibodies from the sera of Gardasil and Gardasil + Pt-injected mice showed cross-reactivity with the mouse brain protein extract. Immunohistochemistry analysis revealed microglial activation in the CA1 area of the hippocampus of Gardasil-injected mice. It appears that Gardasil via its Al adjuvant and HPV antigens has the ability to trigger neuroinflammation and autoimmune reactions, further leading to behavioral changes. © 2016, Springer Science+Business Media New York.