Genetic Assessment of Living Kidney Transplant Donors: A Survey of Canadian Practices.

Background: Kidney failure is a prevalent condition with tendency for familial clustering in up to 27% of the affected individuals. Living kidney donor (LKD) transplantation is the optimal treatment option; however, in Canada, more than 45% of LKDs are biologically related to their recipients which subjects recipients to worse graft survival and donors to higher future risk of kidney failure. Although not fully understood, this observation could be partially explained by genetic predisposition to kidney diseases.

Not all eplet mismatches are created equal - A cohort study illustrating implications to long-term graft outcomes.

We assessed implications of various eplet-compatibility strategies to death-censored graft failure (DCGF), defined as return to dialysis or re-transplantation, in a base-case scenario from the Scientific Registry of Transplant Recipients. To inform personalized care, we evaluated how recipient, donor, and transplant characteristics affect DCGF by ascending categories of eplet mismatches (EMM), and derived adjusted hazard ratios (HR). The base-case analysis demonstrated 15-year estimated survival probabilities of 77.

Structure and proteolytic susceptibility of the inhibitory C-terminal tail of cardiac troponin I.

Background: Cardiac troponin I (cTnI) has two flexible tails that control the cardiac cycle. The C-terminal tail, cTnI, binds actin to shut off cardiac muscle contraction, whereas the competing calcium-dependent binding of the switch region, cTnI, by cardiac troponin C (cTnC) triggers contraction. The N-terminal tail, cTnI, regulates the calcium affinity of cTnC.

Proteolytic Digestion of Serum Cardiac Troponin I as Marker of Ischemic Severity.

Background: The serum troponin assay is the biochemical gold standard for detecting myocardial infarction (MI). A major diagnostic issue is that some believe troponin levels can rise with reversible injury, in the absence of radiologically detectable infarct.

Hypothesis: Because cell death activates intracellular proteases, troponin released by irreversible infarct will be more proteolyzed than that released by milder processes.

Combining a PagP fusion protein system with nickel ion-catalyzed cleavage to produce intrinsically disordered proteins in E. coli.

Many proteins contain intrinsically disordered regions that are highly solvent-exposed and susceptible to post-translational modifications. Studying these protein segments is critical to understanding their physiologic regulation, but proteolytic degradation can make them difficult to express and purify. We have designed a new protein expression vector that fuses the target protein to the N-terminus of the integral membrane protein, PagP.