“Purpose of review
Gout is increasing worldwide. An appreciation that hyperuricaemia and gout are associated with hypertension
and chronic kidney disease is well established, but the cause and effect relationships are controversial. Studies which address this conundrum have been reviewed.
Epidemiological surveys have confirmed the strong relationship of gout and hyperuricaemia with hypertension and diuretic treatment. There are multiple confounders such as obesity and alcohol consumption LY2606368 mw which despite adjustments make interpretation of the epidemiology difficult. There are data to suggest that hyperuricaemia itself causes hypertension and renovascular disease, and that lowering of serum urate may assist in control of hypertension. The mechanism for diuretic-induced hyperuricaemia may operate through volume depletion and reduced secretion of uric acid. The latter effect may be genetically influenced.
Recent population C59 Wnt nmr surveys have strongly supported the association of gout and hyperuricaemia with hypertension. The prevailing explanation that renal dysfunction causes both phenomena or that they are caused by shared factors is challenged by the evidence that hyperuricaemia drives hypertension. A confounder of epidemiology studies is the use of diuretics for treating hypertension. A closer understanding of the mechanisms
of diuretic-induced hyperuricaemia may lead to the creation of uricosuric diuretics. Losartan is exceptional amongst antihypertensive drugs in possessing mild uricosuric properties and therefore has a role in treating hypertensive patients with gout. Overcoming diuretic-induced hyperuricaemia is Dibutyryl-cAMP in vitro difficult and
there is need for a uricosuric diuretic.”
“Study Design. Finite element and in vitro study.
Objective. Finite element calculations to delineate a dynamic fixator and confirmation with an in vitro experiment.
Summary and Background Data. In the last few years, there was a paradigm shift from rigid to dynamic fixation of spinal segments. However, some so-called dynamic implants like the Dynesys performed still stiffer than anticipated. The aim of this study was to optimize a dynamic stabilization system.
Methods. The development steps of this implant design can be summarized in a development loop. First, a finite element model of an intact human L4-L5 segment was used to delineate implant stiffness parameters for the implant, in consideration of clinical concerns and safety aspects. These data were used in a second step, leading to the final implant design. This development process was completed with an appropriate in vitro experiment. The optimal axial and bending stiffness were computed to reduce the spinal motion by 30%. For the validation process, in vitro tests were performed on 6 human lumbar spinal segments L2-L3 with a median age of 52.