Does financial compensation for living kidney donation change willingness to donate?

The potential use of financial compensation to increase living kidney donation rates remains controversial in potentially introducing undue inducement of vulnerable populations to donate. This cross-sectional study assessed amounts of financial compensation that would generate motivation and an undue inducement to donate to family/friends or strangers. Individuals leaving six Departments of Motor Vehicles were surveyed. Of the 210 participants who provided verbal consent (94% participation rate), respondents' willingness to donate would not change (70%), or would increase (29%) with compensation. Median lowest amounts of financial compensation for which participants would begin to consider donating a kidney were $5000 for family/friends, and $10,000 for strangers; respondents reporting $0 for family/friends (52%) or strangers (26%) were excluded from analysis. Median lowest amounts of financial compensation for which participants could no longer decline (perceive an undue inducement) were $50,000 for family/friends, and $100,000 for strangers; respondents reporting $0 for family/friends (44%) or strangers (23%) were excluded from analysis. The two most preferred forms of compensation included: direct payment of money (61%) and paid leave (21%). The two most preferred uses of compensation included: paying off debt (38%) and paying nonmedical expenses associated with the transplant (29%). Findings suggest tolerance for, but little practical impact of, financial compensation. Certain compensation amounts could motivate the public to donate without being perceived as an undue inducement.

Lithium alters the morphology of neurites regenerating from cultured adult spiral ganglion neurons.

The small-molecule drug lithium (as a monovalent ion) promotes neurite regeneration and functional recovery, is easy to administer, and is approved for human use to treat bipolar disorder. Lithium exerts its neuritogenic effect mainly by inhibiting glycogen synthase kinase 3, a constitutively-active serine/threonine kinase that is regulated by neurotrophin and "wingless-related MMTV integration site" (Wnt) signaling. In spiral ganglion neurons of the cochlea, the effects of lithium and the function of glycogen synthase kinase 3 have not been investigated. We, therefore, set out to test whether lithium modulates neuritogenesis from adult spiral ganglion neurons. Primary cultures of dissociated spiral ganglion neurons from adult mice were exposed to lithium at concentrations between 0 and 12.5 mM. The resulting neurite morphology and growth-cone appearance were measured in detail by using immunofluorescence microscopy and image analysis. We found that lithium altered the morphology of regenerating neurites and their growth cones in a differential, concentration-dependent fashion. Low concentrations of 0.5-2.5 mM (around the half-maximal inhibitory concentration for glycogen synthase kinase 3 and the recommended therapeutic serum concentration for bipolar disorder) enhanced neurite sprouting and branching. A high concentration of 12.5 mM, in contrast, slowed elongation. As the lithium concentration rose from low to high, the microtubules became increasingly disarranged and the growth cones more arborized. Our results demonstrate that lithium selectively stimulates phases of neuritogenesis that are driven by microtubule reorganization. In contrast, most other drugs that have previously been tested on spiral ganglion neurons are reported to inhibit neurite outgrowth or affect only elongation. Lithium sensitivity is a necessary, but not sufficient condition for the involvement of glycogen synthase kinase 3. Our results are, therefore, consistent with, but do not prove lithium inhibiting glycogen synthase kinase 3 activity in spiral ganglion neurons. Experiments with additional drugs and molecular-genetic tools will be necessary to test whether glycogen synthase kinase 3 regulates neurite regeneration from spiral ganglion neurons, possibly by integrating neurotrophin and Wnt signals at the growth cone.

Biofeedback-aided relaxation and meditation in the management of hypertension.

Based on clinical, epidemiological, and experimental work, a possible pathogenesis of essential hypertension is outlined. In the light of this possible pathogenesis, a behavioral treatment program is suggested which centers on the regular use of systematic training. Several controlled studies are described in which experimental patients given such training show clinically significant and lasting reductions in systolic and diastolic pressure. Following training, experimental patients also show quicker recovery of blood pressures to baseline levels after exposure to standardized laboratory stressors. Probable long-term benefits of relaxation training are suggested. Such benefits, however, can only be maintained if the patient regularly practices relaxation and integrates this into his everyday activities. How to motivated symptomless hypertensives to accept this requirement is discussed in the light of the writer's personal experience.