Calcium in biology

Calcium has roles in cell signalling and skeletal structure. Dietary calcium intake and serum calcium are distinct quantities: physiological regulation means a change in one need not correspond to an equivalent change in the other.

A propagating spatial variation in cellular calcium concentration. Coupling local release and recovery to transport can produce pulses with rapid fronts and slower return to a resting state.

In a two-variable calcium-wave model, the fast front scale can reduce to the displayed dynamical system. Its equilibria are intersections of the kinetic nullcline $V=g(U)$ and a line of slope $-1/\gamma$. At a simple intersection with $f_V<0$, the Jacobian determinant is $f_V(1+\gamma g^{\prime })$; a negative determinant identifies a saddle point. Matching a rising front requires a heteroclinic orbit from one saddle to another, selected by a shooting method in the speed $s$. A falling connection must use the same speed. Between fronts the slow equation is $s(1+\gamma g^{\prime })U^{\prime }=\mu -U$. Recovery on the two outer rising branches requires the resting value $\mu$ to lie between the low landing value and the high takeoff value. The nullcline shape supplies this geometry but does not by itself prove existence of both connections.

Serum calcium is the concentration of calcium in blood serum. It can be an exposure in an observational study or Mendelian randomization, but genetically changing it need not reproduce the effect of changing dietary calcium intake.

Hypercalcaemia is an abnormally elevated serum calcium concentration. A diagnosis in medical records depends on testing and diagnostic practice, which can introduce selection bias into an observational study.

Calcium intake is the amount of calcium consumed, including food and supplements. It is an exposure that can be changed by an intervention, and should not be identified automatically with serum calcium in a causal inference analysis.