Treatment varies by disorder and may involve counseling, dietary advice, reducing excessive exercise, and the reduction of efforts to eliminate food. Medications may be used to help with some of the associated symptoms. Hospitalization may be needed in more serious cases. About 70% of people with anorexia and 50% of people with bulimia recover within five years. Only 10% of people with eating disorders receive treatment, and of those, approximately 80% do not receive the proper care. Many are sent home weeks earlier than the recommended stay and are not provided with the necessary treatment. Recovery from binge eating disorder is less clear and estimated at 20% to 60%. Both anorexia and bulimia increase the risk of death. When people experience comorbidity with an eating disorder and OCD, certain aspects of treatment can be negatively impacted. OCD can make it harder to recover from obsession over weight and shape, body dissatisfaction, and body checking.This is impart because ED cognitions serve a similar purpose to OCD obsessions and compulsions (e.g., safety behaviors as temporary relief from anxiety). Research shows OCD does not have an impact on the BMI of patients during treatment.Estimates of the prevalence of eating disorders vary widely, reflecting differences in gender, age, and culture as well as methods used for diagnosis and measurement. In the developed world, anorexia affects about 0.4% and bulimia affects about 1.3% of young women in a given year. Binge eating disorder affects about 1.6% of women and 0.8% of men in a given year.
Tenecteplase, sold under the trade names TNKase, Metalyse and Elaxim, is an enzyme used as a thrombolytic drug. Tenecteplase is a tissue plasminogen activator (tPA) produced by recombinant DNA technology using an established mammalian cell line (Chinese hamster ovary cells). Tenecteplase is a 527 amino acid glycoprotein developed by introducing the following modifications to the complementary DNA (cDNA) for natural human tPA: a substitution of threonine 103 with asparagine, and a substitution of asparagine 117 with glutamine, both within the kringle 1 domain, and a tetra-alanine substitution at amino acids 296–299 in the protease domain. Tenecteplase is a recombinant fibrin-specific plasminogen activator that is derived from native t-PA by modifications at three sites of the protein structure. It binds to the fibrin component of the thrombus (blood clot) and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase has a higher fibrin specificity and greater resistance to inactivation by its endogenous inhibitor (PAI-1) compared to native  t-PA. The abbreviation TNK is common for referring to tenecteplase, but abbreviating drug names is not best practice in medicine, and in fact "TNK" is one of the examples given on the Institute for Safe Medication Practices (ISMP) do-not-use list. Research
Researchers at Newcastle University in Australia say they have had a significant breakthrough in treating stroke patients using the commonly used drug. The findings were published in the New England Medical Journal.