Group items tagged

New findings in rodents and human brain shed light on the mechanisms of major depressive disorder (MDD), uncovering over-expression of MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1)...and identifying a new therapeutic target. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival This study identifies MKP-1 as a key factor in MDD pathophysiology, and as a new target for therapeutic interventions.f Here we use whole-genome expression profiling of postmortem tissue and show significantly increased expression of mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1, encoded by DUSP1, but hereafter called MKP-1) in the hippocampal subfields of subjects with MDD compared to matched controls. MKP-1, also known as dual-specificity phosphatase-1 (DUSP1), is a member of a family of proteins that dephosphorylate both threonine and tyrosine residues and thereby serves as a key negative regulator of the MAPK cascade4, a major signaling pathway involved in neuronal plasticity, function and survival. We tested the role of altered MKP-1 expression in rat and mouse models of depression and found that increased hippocampal MKP-1 expression, as a result of stress or viral-mediated gene transfer, causes depressive behaviors. Conversely, chronic antidepressant treatment normalizes stress-induced MKP-1 expression and behavior, and mice lacking MKP-1 are resilient to stress. These postmortem and preclinical studies identify MKP-1 as a key factor in MDD pathophysiology and as a new target for therapeutic interventions.

Few tips for women that will help you deal with your partner's impotence and support him during this phase.You can advise him to try the ED trial pack, which has all three medication in equal quantities.

Unlike simple starvation, where body fat is lost preferentially, cancer cachexia is associated with depletion of both fat and skeletal muscle mass. Although anorexia is frequently associated with cachexia a reduction of nutrient intake alone could not explain the progressive wasting. Instead the process appears to be mediated by circulatory tumor-produced catabolic factors acting either alone or in concert with certain cytokines. A knowledge of the mechanisms involved should lead to the development of effective pharmacological intervention. Effective therapy should not only improve the quality of life of the cancer patient, but should lead to an increase in survival. Since cachexia is so common in cancer host products may be required for tumor homeostasis. Thus further knowledge in this area may lead to the development of new agents for the treatment of cancer.

Skinner JS, Staiger DO, Fisher ES. Is technological change in medicine always worth it? The case of acute myocardial infarction. Health Aff (Millwood) 2006;25:w34-w47.