Most of the literature on the taxonomy of Afrotropical species are in the need for revision. Anthracyclines are the drugs most closely related to acute and late cardiac toxicity. It has been known since the 1970s that anthracycline treatment is associated with an increased risk of heart failure, and that this is dependent on cumulative dose and schedule. One of the Saikosaponin-B2 mechanisms responsible for doxorubicin cardiotoxicity is the formation of reactive oxygen species, which can harm membrane lipids and other cellular components, leading to cardiomyocyte apoptosis and death. In addition, oxidative stress is considered to be an important factor of controlling heart aging. Senescence marker protein 30, a 34-kDa protein, was originally identified as a novel aging marker protein in rat liver, whose expression decreases androgen-independently with age. SMP30 transcripts are detected in almost all organs, and the SMP30 gene is highly conserved among numerous animal species including humans. It has been demonstrated that SMP30 plays multifunctional roles as Ca2+ regulator, anti-oxidants, and gluconolactonase which is a key enzyme in the ascorbic acid biosynthesis. SMP30 knockout mice were generated and 
showed a shorter life span than that of wild-type mice on a vitamin C-deficient diet. Using SMP30 KO mice, recent reports have demonstrated that SMP30 functions to protect cells from apoptosis in the liver and that SMP30 has protectiveeffects againstage-associated oxidative stressin the brain and lungs. Furthermore, SMP30 KO mice have shown accelerated senescence in the kidney and the worsening of glucose tolerance. Taken together, SMP30 is assumed to behave as an anti-aging factor. Recently, we have demonstrated that deficiency of SMP30 exacerbates angiotensin II-induced cardiac hypertrophy, dysfunction and remodeling in mice. For patients with stable coronary artery disease, the presence and extent of myocardial ischemia is the most important prognostic factor for myocardial infarction and death. On the other hand, patients who have coronary artery stenoses which do not significantly obstruct blood flow and consequently do not cause ischemia have a good prognosis, annual event rates being lower than 1%. The biological mechanisms that mediate the increased risk in patients with inducible myocardial ischemia are not clear. Increased platelet reactivity is associated with increased risk of myocardial infarction in patients with stable coronary artery disease and antithrombotic therapy has been shown to be effective in reducing the risk of future MI. Furthermore, variation in response to antithrombotic therapy is associated with increased occurrence of atherothrombotic events in patients treated with percutaneous intervention. Increased levels of platelet-monocyte complexes and increased platelet reactivity have been found in peripheral blood of patients with stable coronary artery disease compared to healthy control subjects acute coronary syndromes and ischemic stroke. Platelets are functionally affected by conditions of high shear stress and platelets form larger aggregates in response to increasing microshear gradients, independent of soluble agonists. Previous reports have shown that lesion severity and calculated shear stress correlate with increased platelet-monocyte complexes distal to a Isoacteoside stenosis and further in the coronary sinus, as compared with samples from the proximal coronary artery. Also, experimental evidence suggests myocardial ischemia itself as a factor in platelet behavior, by secretion of proaggregratory substances. Apart from thrombosis, it has become increasingly clear that platelets are actively involved in all stages of atherosclerosis.