Osteoblastom der Halswirbelsäule im Kindesalter

Expansively growing cervical spine osteoblastomas are rare but can cause severe neurological damage as a result of their anatomical relationship to nerve structures. Also, cerebral vessels, especially the vertebral artery in its transvertebral position, are often covered by tumor tissue. In complete resection of the tumor, it is sometimes possible to retain the affected vessel. In addition to conventional radiographic diagnostics, computed tomography, and magnetic resonance imaging, angiography and Doppler sonography of the intracranial arteries executed in parallel can provide evidence of the dimension of the neurological deficit to be expected during resection. This case report describes the staged diagnostic procedure and successful complete resection, retaining the affected vertebral artery, of an osteoblastoma of the 5th cervical body with massive intraspinal expansion in an 11-year-old child.     

Mutations in the molybdenum cofactor biosynthetic protein Cnx1G from Arabidopsis thaliana define functions for molybdopterin binding, molybdenum insertion, and molybdenum cofactor stabilization

The molybdenum cofactor (Moco), a highly conserved pterin compound coordinating molybdenum (Mo), is required for the enzymatic activities of molybdoenzymes. In all organisms studied so far Moco is synthesized by a unique and evolutionary old multistep pathway that requires the activities of at least six gene products. In eukaryotes, the last step of Moco synthesis, i.e., transfer and insertion of Mo into molybdopterin (MPT), is catalyzed by the two-domain proteins Cnx1 in plants and gephyrin in mammals. Both domains (E and G) of these proteins are able to bind MPT in vitro. Here, we show the identification and mutational dissection of functionally important regions within the Cnx1 G domain that are essential for MPT binding, the conversion of MPT to Moco, and Moco stabilization. By functional screening for mutants in the Cnx1 G domain that are no longer able to complement Escherichia coli mogA mutants, we found two classes of mutations in highly conserved amino acid residues. (i) The first class affects in vitro binding of MPT to the protein and the stabilization of Moco, the product of the G domain. (ii) The second class is represented by two independent mutations in the aspartate 515 position that is not affected in MPT binding and Moco stabilization; rather the conversion of MPT to Moco by using bound MPT and a yet unknown form of Mo is completely abolished. The results presented here provide biochemical evidence for a purified Cnx1 G domain catalyzing the insertion of Mo into MPT.     

Changes in the microbial flora of airline headset devices after their use

The bacterial flora of 20 headset devices were evaluated before and after they were worn for 1 hour. Bacteria were recovered from all headsets, and their number increased from a mean (± standard deviation) of 60 ± 5 organisms per device to 650 ± 51 organisms per device (P <.001). The predominant organisms recovered were Staphylococcus spp, Streptococcus spp, Propionibacterium spp, and Peptostreptococcus spp. This study demonstrates the presence of potential pathogens in headset devices, as well as the increase in the number of these pathogens after the headsets have been worn for 1 hour.     

Induction of conduction block by Campylobacter jejuni lipopolysaccharides and focal neural insult

A systemic exposure to gram negative LPS have caused transient conduction abnormalities in a certain strain of rats probably associated with the action of cytokines secreted by macrophages. Our previous studies demonstrated that anti-GM1 antibodies induced in rats by the cross-reactive Cj-LPS, caused no conduction abnormalities. We designed the present study to evaluate the effect of systemic exposure to Cj-LPS on nerve conduction after a focal minor neural trauma. Female Lewis rats were sensitized against KLH by repetitive subcutaneous injections. After 28 days rats were intraneurally injected with saline in the right sciatic nerve and concomitantly with intraperitoneal Cj-LPS. Sciatic nerve conduction studies were performed on days 0, 1, 2, 3, and 7 after injections. Nerve conduction blocks developed in all the rats (n=10) which received an intraneural injection of saline concomitantly with the systemic Cj-LPS exposure, before titers of anti-ganglioside antibodies were detected. We conclude that humoral factors (possibly cytokines), other than antibodies are secreted by lymphocytes and macrophages stimulated by gram negative LPS, and cause functional conduction abnormalities when the blood-nerve barrier is disrupted.     

Intensive care unit outcome of vehicle-related injury in elderly trauma patients

Vehicle-related trauma is a common mechanism of injury in elderly (age > or = 65 years) trauma patients. Several hospital-based studies have shown that patients with pedestrian injury have a higher mortality compared with those with motor vehicle collision (MVC) injury partially because of older patients found in the former group. In addition the injury patterns also differ significantly between these two mechanisms of vehicle-related trauma. The purpose of the present study is to compare the demographics, injury severity, injury patterns, and outcomes of elderly patients with pedestrian injury admitted to a surgical intensive care unit (SICU) of a Level I trauma center between January 1, 1994 and December 31, 2000 with those admitted with MVC injury. During the study period there were 187 elderly patients admitted to the surgical intensive care unit with vehicle-related injury. Fifty-one per cent of the patients had MVC injury. Patients were divided into two groups based on their mechanisms of injury (pedestrian vs MVC) for comparison. There was no difference in the mean age and gender between the two groups. Injury Severity Score, admission Simplified Acute Physiology Score, and mortality were significantly higher in the pedestrian group compared with the MVC group. Using logistic regression analysis three factors were found to be independently predictive of mortality: Simplified Acute Physiology Score, intracranial hemorrhage with mass effect on CT scan, and cardiac complications.     

Isolation of a glial-restricted tripotential cell line from embryonic spinal cord cultures

Neuroepithelial stem cells (NEPs), glial-restricted precursors (GRPs), and neuron-restricted precursors (NRPs) are present during early differentiation of the spinal cord and can be identified by cell surface markers. In this article, we describe the properties of GRP cells that have been immortalized using a regulatable v-myc retrovirus construct. Immortalized GRP cells can be maintained in an undifferentiated dividing state for long periods and can be induced to differentiate into two types of astrocytes and into oligodendrocytes in culture. A clonal cell line prepared from immortalized GRP cells, termed GRIP-1, was also shown to retain the properties of a glial-restricted tripotential precursor. Transplantation of green fluorescent protein (GFP)-labeled subclones of the immortalized cells into the adult CNS demonstrates that this cell line can also participate in the in vivo development of astrocytes and oligodendrocytes. Late passages of the immortalized cells undergo limited transdifferentiation into neurons as assessed by expression of multiple neuronal markers. The availability of a conditionally immortalized cell line obviates the difficulties of obtaining a large and homogeneous population of GRPs that can be used for studying the mechanism and signals for glial cell differentiation as well as their application in transplantation protocols.     

Phosphorylated MAP1B is induced in central sprouting of primary afferents in response to peripheral injury but not in response to rhizotomy

A peripheral nerve lesion induces sprouting of primary afferents from dorsal root ganglion (DRG) neurons into lamina II of the dorsal horn. Modifications of the environment in consequence to the axotomy provide an extrinsic stimulus. A potential neuron-intrinsic factor that may permit axonal sprouting is microtubule-associated protein 1B (MAP1B) in a specific phosphorylated form (MAP1B-P), restricted to growing or regenerating axons. We show here that both in rat and mouse, a sciatic nerve cut is rapidly followed by the appearance of MAP1B-P expression in lamina II, increasing to a maximum between 8 and 15 days, and diminishing after three months. Evidence is provided that sprouting and induction of MAP1B-P expression after peripheral injury are phenomena concerning essentially myelinated axons. This is in accordance with in situ hybridization data showing especially high MAP1B-mRNA levels in large size DRG neurons that give rise to myelinated fibers. We then employed a second lesion model, multiple rhizotomy with one spared root. In this case, unmyelinated CGRP expressing fibers do indeed sprout, but coexpression of MAP1B-P and CGRP is never observed in lamina II. Finally, because a characteristic of myelinated fibers is their high content in neurofilament protein heavy subunit (NF-H), we used NF-H-LacZ transgenic mice to verify that MAP1B-P induction and central sprouting were not affected by perturbing the axonal organization of neurofilaments. We conclude that MAP1B-P is well suited as a rapidly expressed, axon-intrinsic marker associated with plasticity of myelinated fibers.     

Stable expression of the alkaline phosphatase marker gene by neural cells in culture and after transplantation into the CNS using cells derived from a transgenic rat

Multipotent stem cells and more developmentally restricted precursors have previously been isolated from the developing nervous system and their properties analyzed by culture assays in vitro and by transplantation in vivo. However, the variety of labeling techniques that have been used to identify grafted cells in vivo have been unsatisfactory. In this article we describe the characteristics of cells isolated from a transgenic rat in which the marker gene human placental alkaline phosphatase (hPAP) is linked to the ubiquitously active R26 gene promoter. We show that hPAP is readily detected in embryonic neuroepithelial stem cells, neuronal-restricted precursor cells, and glial-restricted precursor cells. Transgene expression is robust and can be detected by both immunocytochemistry and histochemistry. Furthermore, the levels of hPAP on the cell surface are sufficient for live cell labeling and fluorescence-activated cell sorting. Expression of hPAP is stable in isolated cells in culture and in cells transplanted into the spinal cord for at least 1 month. We submit that cells isolated from this transgenic rat will be valuable for studies of neural development and regeneration.