Spinal lordosis optimizes the requirements for a stable erect posture

<p>Abstract</p> <p>Background</p> <p>Lordosis is the bending of the lumbar spine that gives the vertebral column of humans its characteristic ventrally convex curvature. Infants develop lordosis around the time when they acquire bipedal locomotion. Even macaques develop a lordosis when they are trained to walk bipedally. The aim of this study was to investigate why humans and some animals develop a lumbar lordosis while learning to walk bipedally.</p> <p>Results</p> <p>We developed a musculoskeletal model of the lumbar spine, that includes an asymmetric, dorsally shifted location of the spinal column in the body, realistic moment arms, and physiological cross-sectional areas (PCSA) of the muscles as well as realistic force-length and force-velocity relationships. The model was used to analyze the stability of an upright body posture. According to our results, lordosis reduces the local joint torques necessary for an equilibrium of the vertebral column during an erect posture. At the same time lordosis increases the demands on the global muscles to provide stability.</p> <p>Conclusions</p> <p>We conclude that the development of a spinal lordosis is a compromise between the stability requirements of an erect posture and the necessity of torque equilibria at each spinal segment.</p

Cardiac troponin I: a valuable biomarker indicating the cardiac involvement in fabry disease

Objectives: Assessment of the clinical severity of Fabry disease (FD), an X-linked, rare, progressive disorder based on a genetic defect in alpha-galactosidase is challenging, especially regarding cardiac involvement. The aim of the study was to evaluate the diagnostic value of cardiac troponin I (cTnI) in discriminating FD patients with cardiac involvement in a large FD patient cohort. Methods: cTnI levels were measured with a contemporary sensitive assay in plasma samples taken routinely from FD patients. The assay was calibrated to measure cTnI levels ≥0.01 ng/ml. Elevated cTnI values (cut-off ≥0.04 ng/ml) were correlated with clinical data. Results: cTnI was assessed in 62 FD patients (median age: 47 years, males: 36%). Elevated cTnI levels were detected in 23 (37%) patients. Patients with a cTnI elevation were older (median 55 years versus 36 years, p<0.001). Elevated cTnI levels were associated with the presence of a LVH (16/23 versus 1/39; OR 65.81, CI: 6.747–641.859; p<0.001). In almost all patients with a left ventricular hypertrophy (LVH) elevated cTnI levels were detected (16/17, 94%). Absolute cTnI levels in patients with LVH were higher than in those without (median 0.23 ng/ml versus 0.02 ng/ml; p<0.001). A cTnI level <0.04ng/ml had a high negative predictive value regarding the presence of a LVH (38/39, 97%). In a control group of non-FD patients (n = 17) with LVH (due to hypertension) none showed cTnI levels ≥0.01 ng/ml. Conclusions: Elevated cTnI levels are common in FD patients, reflecting cardiac involvement. FD patients might benefit from a continuous cTnI monitoring

Comparison of cardiac troponin I levels.

<p>Presented are patients with Fabry disease (FD) and left ventricular hypertrophy (LVH) (n = 17) versus FD patients without LVH (n = 18) and non-FD patients with LVH of other cause (n = 17). The cut-off level for cTnI in diagnosing myocardial infarction (≥0.04 ng/ml) is indicated in the figure.</p

Characteristics in 17 age- and sex-matched individuals with left ventricular hypertrophy due to hypertension.

<p>Characteristics in 17 age- and sex-matched individuals with left ventricular hypertrophy due to hypertension.</p

Patients with Fabry disease: comparison of patients with cTnI elevation ≥0.04 ng/ml versus without.

<p>Patients with Fabry disease: comparison of patients with cTnI elevation ≥0.04 ng/ml versus without.</p

Multiple logistic regression analysis for elevated cardiac troponin (cut-off ≥0.04 ng/ml) patients with Fabry disease (n = 62).

<p>Multiple logistic regression analysis for elevated cardiac troponin (cut-off ≥0.04 ng/ml) patients with Fabry disease (n = 62).</p