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Visar resultat 1 - 5 av 103 avhandlingar som matchar ovanstående sökkriterier.
1. Unraveling Mechanisms of Insulin Resistance in Type 2 Diabetes in Human Adipocytes : Role of extracellular signal regulated kinase 1/2 (ERK1/2) and forkhead box protein 01 (FOX01)
Sammanfattning : Type 2 Diabetes is characterized by hyperglycemia primarily caused due to insulin resistance in insulin responsive tissues and insufficient production of insulin by the β-cells. Insulin resistance appears to develop first in the expanding adipose tissue during caloric surplus and affects other tissues like liver and muscle by ectopic fat accumulation. LÄS MER
2. Striatal adaptations in experimental parkinsonism and L-DOPA-induced dyskinesia
Sammanfattning : Parkinson’s disease (PD) is a neurodegenerative disorder, characterized by the loss of dopamine (DA) producing neurons in the substantia nigra pars compacta (SNc), resulting in typical motor symptoms. DA replacement with L-DOPA is the standard therapy for PD. LÄS MER
3. Regulation and Function of MAP Kinases in PDGF Signaling
Sammanfattning : Platelet-derived growth factor (PDGF) is a family of signaling molecules that stimulates cell growth, survival and migration. PDGF is recognized by specific transmembrane proteins, the PDGF receptors, which relay the signals to the cell activating the Mitogen-activated protein (MAP) kinases and other signaling pathways. LÄS MER
4. Mechanisms of stretch-induced growth and contractile differentiation in vascular smooth muscle
Sammanfattning : Vascular smooth muscle can adapt to increased intraluminal pressure by remodelling and hypertrophy, as seen in hypertension. The molecular mechanisms responsible for this are still incompletely characterized. LÄS MER
5. The Role of Protein Kinase C in the Extracellular Ca2+-regulated Secretion of Parathyroid Hormone
Sammanfattning : Parathyroid hormone (PTH) is the major physiological regulator of the extracellular Ca2+ concentration ([Ca2+]o) in the body. The secretion of this hormone is suppressed at high [Ca2+]o. LÄS MER