Publications by authors named "Thomas Maack"

The success of total knee arthroplasty depends, in part, on the ability of the surgeon to properly manage the soft tissues surrounding the joint, but an objective definition as to what constitutes acceptable postoperative joint stability does not exist. Such a definition may not exist due to lack of suitable instrumentation, as joint stability is currently assessed by visual inspection while the surgeon manipulates the joint. Having the ability to accurately and precisely measure knee stability at the time of surgery represents a key requirement in the process of objectively defining acceptable joint stability.

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Mast cells are associated with inflammation and fibrosis. Whether they protect against or contribute to renal fibrosis is unclear. Based on our previous findings that mast cells can express and secrete active renin, and that angiotensin (ANG II) is profibrotic, we hypothesized that mast cells play a critical role in tubulointerstitial fibrosis.

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The small GTPase Rac and the second messenger cGMP (guanosine 3',5'-cyclic monophosphate) are critical regulators of diverse cell functions. When activated by extracellular signals via membrane signaling receptors, Rac executes its functions through engaging downstream effectors such as p21-activated kinase (PAK), a serine/threonine protein kinase. However, the molecular mechanism by which membrane signaling receptors regulate cGMP levels is not known.

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A brief non-inclusive review on natriuretic peptides (NP), their receptors, and their main functional properties is presented. The three main NP, atrial (ANP), brain (BNP) and C-type (CNP) are considered. Guanylyl cyclase receptors modulate all the known systemic effects of NP.

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Natriuretic peptides (NPs) are involved in many physiological processes, including the regulation of vascular tone, sodium excretion, pressure-volume homeostasis, inflammatory responses, and cellular growth. The two main receptors of NP, membrane-bound guanylyl cyclases A and B (GC-A and GC-B), mediate the effects of NPs via the generation of cGMP. NP-stimulated generation of cGMP can be modulated by intracellular processes, whose exact nature remains to be elucidated.

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