An Analytical Model for Rotator Cuff Repairs

Background: Currently, natural and synthetic scaffolds are being explored as augmentation devices for rotator cuff repair. When used in this manner, these devices are believed to offer some degree of load sharing; however, no studies have quantified this effect. Furthermore, the manner in which loads on an augmented rotator cuff repair are distributed among the various components of the repair is not known, nor is the relative biomechanical importance of each component. The objectives of this study are to (1) develop quasi-static analytical models of simplified rotator cuff repairs, (2) validate the models, and (3) predict the degree of load sharing provided by an augmentation scaffold. Methods: The individual components of the repair constructs were modeled as non-linear springs, and the model equations were formulated based on the physics of springs in series and parallel. The model was validated and used to predict the degree of load sharing provided by a scaffold. Parametric sensitivity analysis was used to identify which of the component(s)/parameter(s) most influenced the mechanical behavior of the augmented repair models. Findings: The validated models predict that load will be distributed ~70-80% to the tendon repair and ~20-30% to the augmentation component. The sensitivity analysis suggests that the greatest improvements in the force carrying capacity of a tendon repair may be achieved by improving the properties of the bone-suture-tendon interface. Future studies will perform parametric simulation to illustrate the manner in which changes to the individual components of the repair, representing different surgical techniques and scaffold devices, may influence the biomechanics of the repair construct

APOE gene polymorphism as a risk factor for cerebral amyloid angiopathy-related hemorrhage

Cerebral amyloid angiopathy (CAA) due to the accumulation of amyloid beta-protein (Abeta) occurs in up to half of elderly individuals and in most cases of Alzheimer's disease (AD). Following identification of the apolipoprotein E (APOE) epsilon4 allele as a risk factor for AD, APOE epsilon4 was also found to be associated with asymptomatic CAA. The major clinical manifestation of CAA is stroke due to a lobar hemorrhage. A complex relationship between APOE epsilon4, APOE epsilon2 and hemorrhage associated with CAA (CAAH) is emerging. Pathological studies have demonstrated that APOE epsilon2 is over-represented among patients with CAAH. This remains the case for patients with co-existing Alzheimer's disease, who otherwise have a very low epsilon2 allele frequency. Other forms of intracranial hemorrhage do not share the same association, indicating that APOE epsilon2 has a specific association with CAAH. Patients with the epsilon2 allele and CAAH are more likely to have taken anticoagulant or antiplatelet medication, had hypertension or had minor head trauma than non-epsilon2 carriers. In addition, the epsilon2 allele is specifically associated with CAA-associated microangiopathic changes such as fibrinoid necrosis and concentric splitting of the vessel wall

Association between interleukin-1A polymorphism and cerebral amyloid angiopathy-related hemorrhage

Background and Purpose— It has been suggested that the interleukin-1A (IL-1A) allele 2 is a risk factor for Alzheimer’s disease (AD). Because cerebral amyloid angiopathy–related hemorrhage (CAAH) often coexists with AD, we examined the IL-1A polymorphism in CAAH. Methods— In a case-control study, patients with pathologically verified CAAH, AD patients without intracerebral hemorrhage, and neuropathologically normal control subjects were studied. DNA was extracted from brain tissue, and IL-1A was genotyped. Logistic regression was used to examine the IL-1A polymorphism in CAAH patients with and without AD compared with AD and non-AD control subjects. Results— There were 42 patients with CAAH, 232 AD patients, and 167 non-AD control subjects. In age-adjusted analyses, there was no association between possession of IL-1A allele 2 and risk of CAAH compared with AD control subjects (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.45 to 1.97; P=0.87) or non-AD control subjects (OR, 0.94; 95% CI, 0.47 to 1.87; P=0.86). Stratifying for the presence of apolipoprotein E 2 or 4 demonstrated the known increased risk of CAAH from these lipoprotein E alleles. Subgroup analyses demonstrated a nonsignificant excess of the IL-1A 2,2 genotype in patients with CAAH and AD compared with those CAAH patients who did not have histological evidence indicating AD (OR, 2.17; 95% CI, 0.15 to 122.3; P=0.64). Comparisons between CAAH patients with AD and AD control subjects and between CAAH patients without AD and non-AD control subjects did not demonstrate an association between CAAH and possession of either the IL-1A allele 2 or the 2,2 genotype. Conclusions— The IL-1A allele 2 or 2,2 genotype does not appear to be a major risk factor for CAAH

Apolipoprotein E genotype, coagulation, and survival following acute stroke

The authors hypothesized that divergent influences of the APOE ?4 allele on ischemic and hemorrhagic stroke survival might result from differences in coagulation profiles. In 49 hemorrhagic stroke patients, ?4 carriers had higher partial thromboplastin time ratios (p < 0.01) than non-?4 carriers. Among 529 ischemic stroke patients, increasing ?4 allele dose was associated with improved survival (p = 0.03) after adjusting for baseline NIH stroke scale (p = 0.00001) and partial thromboplastin time ratio (p = 0.01). Relative anticoagulation does not fully explain the survival advantage in ?4-carrying ischemic stroke patients