The diagnosis and treatment of primary dysmenorrhea

     Primary dysmenorrhea is defined as pain in the pelvic area that occurs for no specific reason during menstrual cycle. Dysmenorrhea occurs in 50% to 90% of adolescent girls and women of reproductive age which makes it one of the most common causes of pelvic pain in women. The mechanism of this condition is overproduction of prostaglandins by the endometrium, causing uterine hypercontractility, thereby leading to uterine muscle ischemia, hypoxia and pain. Dysmenorrhea significantly reduces the quality of women life, often making it impossible to perform daily activities and, in addition, it may cause a mental stress that makes both professional and school life difficult. Despite this, females often consider these symptoms as a normal part of their menstrual cycle, which makes this disease underrated and untreated. Dysmenorrhea can be treated in a various ways such as non-pharmacological, pharmacological and surgical. However, women with a typical history of primary dysmenorrhea can commence empirical therapy without any additional tests. Hormonal contraception and nonsteroidal antiinflammatory drugs have proved to be effective in this treatment. However, if conventional treatment is contraindicated, alternative treatments such as topical heat, lifestyle modification, transcutaneous electrical nerve stimulation, dietary supplements, acupuncture, and acupressure may be used. Surgical treatment is possible, but it is used rarely and only in severe cases of treatment-resistant dysmenorrhea. However, it should be emphasized how important it is to exclude secondary causes of dysmenorrhea

A minimum number of autoimmune T cells to induce autoimmunity?

While autoimmune T cells are present in most individuals, only a minority of the population suffers from an autoimmune disease. To better appreciate the limits of T cell tolerance, we carried out experiments to determine how many autoimmune T cells are required to initiate an experimental autoimmune disease. Variable numbers of autoimmune OT-I T cells were transferred into RIP-OVA mice, which were injected with antigen-loaded DCs in a single footpad; this restricted T cell priming to a few OT-I T cells that are present in the draining popliteal lymph node. Using selective plane illumination microscopy (SPIM) we counted the number of OT-I T cells present in the popliteal lymph node at the time of priming. Analysis of our data suggests that a single autoimmune T cell cannot induce an experimental autoimmune disease, but a "quorum" of 2-5 autoimmune T cells clearly has this capacity