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Electrical properties of implant encapsulation tissue

The purpose of this study was to determine the electrical properties of the encapsulation tissue that surrounds electrodes chronically implanted in the body. Two four-electrode arrays, fabricated from either epoxy or silicone rubber, were implanted in each of six adult cats for 82 to 156 days.In vivo measurements of tissue resistivity using the four-electrode technique indicated that formation of the encapsulation tissue resulted in a significant increase in the resistivity of the tissue around the arrays.In vitro measurements of tissue impedance using a four-electrode cell indicated that the resistivity of the encapsulation tissue was a function of the tissue morphology. The tight layers of fibroblasts and collagen that formed around the silicone rubber arrays had a resistivity of 627±108 Ω-cm (mean ± SD; n=6), which was independent of frequency from 10 Hz to 100 kHz, and was significantly larger than the resistivity of the epoxy encapsulation tissue at all frequencies between 20 Hz and 100 kHz. The combination of macrophages, foreign body giant cells, loose collagen, and fibroblasts that formed around the epoxy arrays had a frequency-dependent resistivity that decreased from 454±123 Ω-cm (n=5) to 193±98 Ω-cm between 10 Hz and 1 kHz, and was independent of frequency between 1 kHz and 100 kHz, with a mean value of 195 ±88 Ω-cm. The results indicate that the resistivity of the encapsulation tissue is sufficient to alter the shape and magnitude of the electric field generated by chronically implanted electrodes.     

Molecular pathology of well-differentiated thyroid carcinomas

The newly discovered molecular features of well-differentiated thyroid carcinomas derived from follicular cells are reviewed, within the frame of the 2004 WHO classification of thyroid tumours, under the following headings: “Follicular carcinoma”, “Papillary carcinoma”, “Follicular variant of papillary carcinoma” and “Hürthle cell tumours”. A particular emphasis is put on the meaning of PAX8–PPARγ rearrangements, RAS and BRAF mutations, and deletions and mutations of mitochondrial genes and of nuclear genes encoding for mitochondrial enzymes, for thyroid tumorigenesis.     

Cellular effects of deep brain stimulation: model-based analysis of activation and inhibition

Deep brain stimulation (DBS) is an effective therapy for medically refractory movement disorders. However, fundamental questions remain about the effects of DBS on neurons surrounding the electrode. Experimental studies have produced apparently contradictory results showing suppression of activity in the stimulated nucleus, but increased inputs to projection nuclei. We hypothesized that cell body firing does not accurately reflect the efferent output of neurons stimulated with high-frequency extracellular pulses, and that this decoupling of somatic and axonal activity explains the paradoxical experimental results. We studied stimulation using the combination of a finite-element model of the clinical DBS electrode and a multicompartment cable model of a thalamocortical (TC) relay neuron. Both the electric potentials generated by the electrode and a distribution of excitatory and inhibitory trans-synaptic inputs induced by stimulation of presynaptic terminals were applied to the TC relay neuron. The response of the neuron to DBS was primarily dependent on the position and orientation of the axon with respect to the electrode and the stimulation parameters. Stimulation subthreshold for direct activation of TC relay neurons caused suppression of intrinsic firing (tonic or burst) activity during the stimulus train mediated by activation of presynaptic terminals. Suprathreshold stimulation caused suppression of intrinsic firing in the soma, but generated efferent output at the stimulus frequency in the axon. This independence of firing in the cell body and axon resolves the apparently contradictory experimental results on the effects of DBS. In turn, the results of this study support the hypothesis of stimulation-induced modulation of pathological network activity as a therapeutic mechanism of DBS.     

Morphological observations and morphometric analysis in three human fetuses with bilateral cervical cystic hygroma

Three human fetuses (crown-rump length, CRL, ranging from 71 to 77 mm), presenting bilateral cervical cystic hygroma were examined. The specimens were cleared and double-stained with alcian blue and alizarin red S for detecting the ossification growth patterns in the vertebral column, ribs, ischium, limbs, and face. Longitudinal measurements of some long bones in the upper (humerus, ulna, radius) and lower (femur, tibia, fibula) limb were taken. The values of both the total length (TL) and the ossified part (OL) of each long bone, as well as the OL/TL per cent ratio were considered. Reference points were located on the mandible, i.e. condylar process (Pcl), coronoid process (Pco), gnathion (GN), gonion (GO), inferior interdental point (IDI) for measuring linear dimensions. All values obtained were related with those relative to a group of fetuses, without any detectable malformation and chromosomal abnormalities, with CRL mean value 75 mm, in order to assess the presence of further anomalies, besides the cystic hygroma, in the three fetuses considered.     

Immunocytochemical expression of protein kinase C isoenzymes alpha, delta, epsilon and zeta in differentiating chick chondrocytes in vitro

In our previous work we have investigated the expression of the serine-threonine kinase protein kinase C (PKC) in the vertebral column of mouse foetuses. In the present work we would verify the expression of four PKC-isoenzymes (alpha, delta, epsilon, zeta) in two distinct phases of the chondrogenesis and the endochondral osteogenesis in vitro. We performed primary cultures of chondrocytes collected from tibiae of 6-day old chick embryos. This cells were cultured for 20 days and than collected on coverslips (stage 1 culture). Other cells of the stage 1 were undergone further differentiation towards the phenotype of osteoblast-like cells (stage 2 culture), in accord to the protocol of Descalzi Cancedda et al. (1992). In stage 1 culture, PKC-epsilon was the most expressed isoform, whereas PKC-alpha exhibited the least intense positivity. In stage 2 culture, PKC-alpha was the most expressed isoform, whereas a marked decrease of PKC-epsilon expression was detected compared to stage 1. No relevant differences were evidenced as regards,the expression of PKC-zeta between the two considered cell culture stages. On these bases, it could be reasonable that these PKC-isoenzymes may be involved at different levels in chondrocytes differentiation as well as in the endochondral ossification process.     

Immunohistochemical localization of parathyroid hormone-related protein in parathyroid adenoma and hyperplasia

Parathyroid hormone-related protein (PTHrP) is invoked as the cause of humoral hypercalcaemia of malignancy (HHM); it is contained in the keratinocyte layer of normal skin; and there is evidence that is is produced by fetal parathyroids. Antibodies against synthetic PTHrP peptides have been raised in rabbits and sheep. This immunohistochemical study has found that primary parathyroid adenomata and hyperplastic glands from patients with chronic renal failure stain positively with antisera against PTHrP(1-34) and PTHrP(50-69). Primary hyperplastic glands are negative. No staining with anti-PTHrP(106-141) antiserum could be detected immunohistochemically in any of the parathyroid adenomata or hyperplasia.     

Catastrophic antiphospholipid syndromes in systemic lupus erythematosus

The objective of this study was to look for the occurrence of catastrophic antiphospholipid syndromes (APS) and to try to detect discriminating factors for predicting a worse prognosis, related to Lupus anticoagulant (LA) and antiphospholipid antibodies (aPL), in systemic lupus erythematosus (SLE) with main renal involvement. Regression, recursive partition and logistic regression analyses were applied to our 80 SLE patients prospectively followed up since 1980. Immunologic and other laboratory parameters including beta 2-glycoprotein 1 dependence, resistance to activated protein C caused by a substitution on the coagulation factor V gene, induction of monocyte procoagulant activity. Regression studies demonstrated an overall worse prognosis in term of both thrombosis and death for the group of LA/aPL positive patients (33/80). However, recursive partition analysis was able to isolate a small high risk-subgroup (8/33) characterized by persistent LA/aPL antibodies positive result, widespread signs of noninflammatory vasculopathy (skin, brain, kidney) and renal pathology mimicking that of thrombotic microangiopathy or arteriolosclerosis, also in the absence of classic SLE-nephritis. Only in this subset, three catastrophic APS were recorded, while, in traditional SLE nephritis, even persistent LA/aPL positive results (sometimes after one previous thrombosis) did not seem to imply a particularly severe prognosis. All serologic criteria employed are unable to identify high-risk patients. We conclude that catastrophic APS is a rare event in renal SLE. Before more predictive serologic markers become available, a simple algorithm, dealing with clinical data and renal histologic patterns, may help physicians to identify putatively high risk-LA/aPL antibodies in SLE patients with main renal involvement. This ominous subset does not belong to the group of classic SLE-nephritis.     

Elimination of basal lamina and the collagen "scar" after spinal cord injury fails to augment corticospinal tract regeneration

The production of specific extracellular matrix molecules is upregulated following injury to the adult CNS, and some of these molecules have been postulated to inhibit axonal regeneration. In particular, the deposition of collagen in conjunction with basal lamina formation has been correlated with the failure of CNS axons to extend beyond sites of injury. In the present experiment, the spatial and temporal distribution of fibrillar collagen type III and the main constituents of basal lamina (collagen type IV and laminin) were characterized after defined lesions of the adult spinal cord at cervical and thoracic levels. The deposition of collagen was then blocked in animals undergoing defined mid-thoracic spinal cord lesions by administration of the iron chelator 2,2'-bipyridine, and subsequent effects on corticospinal axonal growth were examined. At time points from 1 to 6 weeks postinjury, collagen and laminin were deposited at spinal cord lesion sites as a dense matrix at the host-lesion interface that extended for short distances into the surrounding spinal cord parenchyma. The failure of corticospinal axons to grow beyond the lesioned region correlated spatially and temporally with collagen III formation and basal lamina production. However, successful blockade of collagen and basal lamina formation with 2,2'-bipyridine injections failed to enhance corticospinal axon regeneration or sprouting. These results suggest either that collagen and basal lamina formation after CNS injury do not contribute to corticospinal axonal growth failure or, more likely, that molecules in addition to collagen and basal lamina contribute to axonal growth failure and must be collectively blocked to promote corticospinal regeneration.