It has been shown elsewhere that the immunosuppressive drug cyclosporin A (CsA) exerts profound schistosomicidal activity when given to infected mice via a multiple administration regime. We show here that a single treatment regime also effects significant reductions in worm burden. Moreover, drug efficacy is maintained at CsA concentrations shown to be subimmunosuppressive in other systems. Subcutaneous treatment effected higher levels of schistosomicidal activity than intraperitoneal or oral treatment, irrespective of whether the drug was given prior to or during infection. Topical application of CsA to the skin site of cercarial penetration, prior to infection resulted in no reduction in worm burden. Systemic release of CsA from a slowly adsorbed, oil-based drug-vehicle combination effected greater levels of killing than when CsA was dissolved in an aqueous drug vehicle. All developmental stages of Schistosoma mansoni were susceptible to killing by a single dose of CsA but, in the case of liver-stage worms, an increased concentration of drug and a longer period between treatment and portal perfusion were needed for killing to be measurable as a reduction in worm numbers.

“Chemobrain” is the phenomenon of cognitive decline some patients may experience after chemotherapy. Current research indicates the cognitive domains that may be most impacted by chemotherapeutic agents are visual and verbal memory, attention, and psychomotor functioning. These cognitive deficits can have an effect on a patient's ability to make informed treatment decisions, pursue occupational or academic pursuits, and his or her overall quality of life. The potential mechanisms that cause this disruption remain largely unknown, although contributing factors could be vascular injury and oxidative damage, inflammation, direct injury to neurons, autoimmune responses, chemotherapy-induced anemia, and the presence of the apolipoprotein E ε4 (APOE ε 4) gene. Interventions to help alleviate the symptoms of chemobrain could include nonpharmacologic treatment such as antioxidants and cognitive-behavioral therapy. In addition, patients may benefit from pharmacologic treatment such as recombinant human erythropoietin and psychostimulant drugs such as methylphenidate. It is important to note that the proposed therapeutics treat the symptoms of chemobrain based on the hypothesized mechanisms. Therefore, a detailed understanding of the mechanisms that cause chemobrain, as well as a comprehension of what specific cognitive domains are impacted, is crucial in developing more specific treatments to improve patients' cognitive functioning and overall quality of life.