Prediction of haemorrhage in the early stage of acute myeloid leukaemia by flow cytometric analysis of platelet function

Haemorrhage is often responsible for the lethal course of acute myeloid leukaemia (AML). Previously, multiple platelet function defects were identified by flow cytometric analysis of platelet activation markers in AML. The role of flow cytometric analysis of platelet function in characterization of prognostic markers of haemorrhage in AML patients has not been well elucidated. The objective of this prospective study was to analyse platelet function in 50 AML patients at diagnosis and to compare results with clinical bleeding score, graded by common toxicity criteria. Platelet activation markers CD62P, CD42b, CD63 and PAC-1 were analysed following in vitro activation by thrombin receptor activating peptide. The following plasma haemostasis parameters were measured: soluble P-selectin, activated partial thromboplastin time, thrombin time, prothrombin time, D-dimer, fibrinogen, and von Willebrand factor antigen. In a multivariate analysis, P-selectin (CD62P) <36 molecules of equivalent soluble fluorochrome x 10(3) (P < 0.0015) and platelet count <40 x 10(9)/l (P = 0.01) were significant predictors of haemorrhage at diagnosis. Haemorrhage at diagnosis predicted grade 3-4 haemorrhage in the first 28 d following diagnosis (P = 0.018). The presented results indicate that low P-selectin is a prognostic marker of haemorrhage in AML.     

Adaptive response of human tendon to paralysis

To gain insight into the adaptive response of human tendon to paralysis, we compared the mechanical properties of the in vivo patellar tendon in six men who were spinal cord-injured (SCI) and eight age-matched, able-bodied men. Measurements were taken by combining dynamometry, electrical stimulation, and ultrasonography. Tendon stiffness and Young's modulus, calculated from force-elongation and stress-strain curves, respectively, were lower by 77% (P < 0.01) and 59% (P < 0.05) in the SCI than able-bodied subjects. The cross-sectional area (CSA) of the tendon was 17% smaller (P < 0.05) in the SCI subjects, but there was no difference in tendon length between the two groups. Our results indicate that paralysis causes substantial deterioration of the structural and material properties of tendon. This needs to be taken into consideration in the design of electrical stimulation protocols for rehabilitation and experimental purposes, and when interpreting changes in the contractile speed of paralyzed muscle.     

Morphology of the first metatarsal head and hallux rigidus: a cadaveric study

Purpose

Treatment options for hallux rigidus include several conservative and surgical measures. The aetiology leading to the disease has not sufficiently been examined so far.

Materials and methods

We analysed the anatomical configuration of the first metatarsal head of 120 metatarsal bones of different collectives aiming to find a possible correlation between the geometry of the first metatarsophalangeal joint and manifestation of hallux rigidus. Wet human cadaveric specimens and macerated dry specimens served as material. The relevant parameters used for analysis were an axis running through the metatarsal head, the anatomical longitudinal axis, and the radius of curvature of the first metatarsal bone.

Results

A significant difference was found in the radius of curvature of osteoarthritic and healthy subjects. Using the binary logistic regression, we were able to predict the probability of an occurence of hallux rigidus in dependence of the radius of curvature. Furthermore, we were enabled to calculate a correct prediction for the appearance of osteoarthritis in 85?% of the healthy subjects, and 73?% of the osteoarthritic subjects.

Conclusions

A consolidated view of the factors indicates that persons with a high risk for the appearance of hallux rigidus should be identified by measuring the radius of curvature in conventional radiographs and preventive measures to postpone the occurrence of clinically relevant hallux rigidus considered.     

Rab11 rescues synaptic dysfunction and behavioural deficits in a Drosophila model of Huntington's disease

Synapse abnormalities in Huntington's disease (HD) patients can precede clinical diagnosis and neuron loss by decades. The polyglutamine expansion in the huntingtin (htt) protein that underlies this disorder leads to perturbations in many cellular pathways, including the disruption of Rab11-dependent endosomal recycling. Impairment of the small GTPase Rab11 leads to the defective formation of vesicles in HD models and may thus contribute to the early stages of the synaptic dysfunction in this disorder. Here, we employ transgenic Drosophila melanogaster models of HD to investigate anomalies at the synapse and the role of Rab11 in this pathology. We find that the expression of mutant htt in the larval neuromuscular junction decreases the presynaptic vesicle size, reduces quantal amplitudes and evoked synaptic transmission and alters larval crawling behaviour. Furthermore, these indicators of early synaptic dysfunction are reversed by the overexpression of Rab11. This work highlights a potential novel HD therapeutic strategy for early intervention, prior to neuronal loss and clinical manifestation of disease.     

The new Epstein gleason score classification significantly reduces upgrading in prostate cancer patients

Purpose

To evaluate the differences between the old and the new Gleason score classification systems in upgrading and downgrading rates.

Motion compensation for interventional navigation on 3D static roadmaps based on an affine model and gating

Current cardiac interventions are performed under 2D fluoroscopy, which comes along with well-known burdens to patients and physicians, such as x-ray exposure and the use of contrast agent. Furthermore, the navigation on complex structures such as the coronaries is complicated by the use of 2D images in which the catheter position is only visible while the contrast agent is introduced. In this work, a new method is presented, which circumvents these drawbacks and enables the cardiac interventional navigation on motion-compensated 3D static roadmaps. For this, the catheter position is continuously reconstructed within a previously acquired 3D roadmap of the coronaries. The motion compensation makes use of an affine motion model for compensating the respiratory motion and compensates the motion due to cardiac contraction by gating the catheter position. In this process, only those positions which have been acquired during the rest phase of the heart are used for the reconstruction. The method necessitates the measurement of the catheter position, which is done by using a magnetic tracking system. Nevertheless, other techniques, such as image-based catheter tracking, can be applied. This motion compensation has been tested on a dynamic heart phantom. The evaluation shows that the algorithm can reconstruct the catheter position on the 3D static roadmap precisely with a residual motion of 1.0 mm and less.