Search

Atherosclerotic disease, such as myocardial infarction and stroke, is the number one killer worldwide. Atherosclerosis is considered to be caused by multiple factors, including genetic and environmental factors. In humans, it takes several decades until the clinical complications develop. There are many known risk factors for atherosclerosis, including hypercholesterolemia, hypertension, diabetes and smoking, which are involved in the pathogenesis of atherosclerosis; however, it is generally believed that atherosclerosis is vascular chronic inflammation initiated by interactions of these risk factors and arterial wall cells. In the past 30 years, the molecular mechanisms underlying the pathogenesis of atherosclerosis have been investigated extensively using genetically modified animals, and lipid-reducing drugs, such as statins, have been demonstrated as the most effective for the prevention and treatment of atherosclerosis. However, despite this progress, questions regarding the pathogenesis of atherosclerosis remain and there is a need to develop new animal models and novel therapeutics to treat patients who cannot be effectively treated by statins. In this review, we will focus on two topics of atherosclerosis, "pathology" and "pathogenesis," and discuss unanswered questions.

Atherosclerosis and its complications, such as myocardial infarction and stroke, are the major causes of morbidity and mortality, and development of effective therapies for both prevention and treatment of this disease is critically important. Currently, there are many drugs available for atherosclerotic disease, but the lipid-lowering drugs statins are still the first-choice for treatment of hypercholesterolemia, a major risk factor for atherosclerosis. On the other hand, traditional Chinese medicines, mainly Chinese herbal medicines (CHM), have been widely used in China and in other Asian countries for the treatment of atherosclerotic diseases. Although many CHMs have been reported to be effective for treating atherosclerotic diseases for more than two thousand years, there are still many difficulties for their use, such as lack of scientific evidence assessed by rigorous clinical trials, complicated components and unclear pharmacological mechanisms, which often hamper the widespread use of CHMs in Western countries. Due to these concerns, CHMs are usually considered as complimentary or alternative treatment for atherosclerotic diseases. In this review, we provide an overview of the pathophysiology of atherosclerosis viewed by Western and traditional Chinese medicine, summarize pros and cons on the efficacy of CHMs for atherosclerosis and discuss what is necessary for CHM use to spread to Western societies.

Natural levels of solar UVR were shown to break and alter the spiral structure of Arthrospira (Spirulina) platensis (Nordst.) Gomont during winter. However, this phenomenon was not observed during summer at temperatures of ∼30°C. Since little has been documented on the interactive effects of solar UV radiation (UVR; 280-400 nm) and temperature on cyanobacteria, the morphology, photosynthesis, and DNA damage of A. platensis were examined using two radiation treatments (PAR [400-700 nm] and PAB [PAR + UV-A + UV-B: 280-700]), three temperatures (15, 22, and 30°C), and three biomass concentrations (100, 160, and 240 mg dwt [dry weight] · L(-1) ). UVR caused a breakage of the spiral structure at 15°C and 22°C, but not at 30°C. High PAR levels also induced a significant breakage at 15°C and 22°C, but only at low biomass densities, and to lesser extent when compared with the PAB treatment. A. platensis was able to alter its spiral structure by increasing helix tightness at the highest temperature tested. The photochemical efficiency was depressed to undetectable levels at 15°C but was relatively high at 30°C even under the treatment with UVR in 8 h. At 30°C, UVR led to 93%-97% less DNA damage when compared with 15°C after 8 h of exposure. UV-absorbing compounds were determined as negligible at all light and temperature combinations. The possible mechanisms for the temperature-dependent effects of UVR on this organism are discussed in this paper.