Risk Factors for Adjacent Fractures After Cement-Augmented Thoracolumbar Pedicle Screw Instrumentation.

Background: The aim of our study was to identify factors that influence the occurrence of adjacent fractures in patients with cement-augmented pedicle screw instrumentation.

Methods: Data were retrospectively collected from medical charts and operative reports for every surgery in which cement-augmented instrumentation was used in our hospital of 4 consecutive years. A total of 93 operations were included and examined for gender, age, T-score, number of fused segments, number of implanted screws, broken screws, loosening of screws, leakage and distribution pattern of cement, pre- and postoperative kyphosis angle, revision surgery and adjacent fractures in follow-up.

Long-term consequences of soman poisoning in mice Part 1. Neuropathology and neuronal regeneration in the amygdala.

To date, studies on soman-induced neuropathology mainly focused on the hippocampus, since this brain region is a well-delimited area with easily detectable pyramidal neurons. Moreover, the hippocampus is severely damaged after soman exposure leading to a substantial alteration of behavioral mnemonic processes. The neuropathology described in the hippocampus, however, and its behavioral consequences cannot be extrapolated to all other limbic damaged brain areas such as the amygdala.

Soman poisoning induces delayed astrogliotic scar and angiogenesis in damaged mouse brain areas.

Gliotic scar formation and angiogenesis are two biological events involved in the tissue reparative process generally occurring in the brain after mechanically induced injury, ischemia or cerebral tumor development. For the first time, in this study, neo-vascularization and glial scar formation were investigated in the brain of soman-poisoned mice over a 3-month period after nerve agent exposure (1.2 LD50 of soman).

Effects of aspirin and mefenamic acid on soman poisoning-induced neuropathology in mice.

The efficacy of aspirin and mefenamic acid to counteract soman-induced brain damage was investigated in mice. Neuronal damage was evaluated in the hippocampus and amygdala by performing omega3 receptor density measurements and hemalun-phloxin staining. The effect of both drugs on the proliferation of neural progenitors after soman exposure was also assessed.

Early reduction of NeuN antigenicity induced by soman poisoning in mice can be used to predict delayed neuronal degeneration in the hippocampus.

The neuronal nuclei (NeuN) antigen is increasingly being used as a specific marker to identify neuronal cell loss under various pathological conditions. However, recent studies pointed out that a decrease in NeuN labeling could also be due to the reduction of protein expression level or loss of antigenicity and this was not necessarily related to neuronal cell disappearance. We also investigated the presence of damaged neurons, the loss of NeuN immunoreactivity and the level of NeuN protein in the brain hippocampus of mice subjected to soman poisoning (1.

Neuronal regeneration partially compensates the delayed neuronal cell death observed in the hippocampal CA1 field of soman-poisoned mice.

Soman poisoning induces long-term neuropathology characterized by the presence of damaged neurons up to 2 months after exposure in various central brain areas, especially the hippocampal CA1 layer. Rapid depletion of this layer could therefore be expected. Surprisingly, the CA1 layer remained consistently visible, suggesting delayed death of these damaged neurons, potentially accompanied by neuronal regeneration.

Efficacy of the ketamine-atropine combination in the delayed treatment of soman-induced status epilepticus.

Nerve agent poisoning is known to induce full-blown seizures, seizure-related brain damage (SRBD), and lethality. Effective and quick management of these seizures is critical. In conditions of delayed treatment, presently available measures are inadequate calling for optimization of therapeutic approaches.

Effect of cytokine treatment on the neurogenesis process in the brain of soman-poisoned mice.

We previously described that enhanced proliferation of neural progenitors occurred in the subgranular zone (SGZ) of the dentate gyrus and in the subventricular zone (SVZ) of the mouse brain following soman poisoning. Then, a discrete number of these cells seemed to migrate and engraft into the main damaged brain regions (hippocampus; septum and amygdala) and subsequently differentiate into neurons. In the present study, the effect of a cytokine treatment on the neurogenesis process was evaluated.

Soman poisoning increases neural progenitor proliferation and induces long-term glial activation in mouse brain.

To date, only short-term glial reaction has been extensively studied following soman or other warfare neurotoxicant poisoning. In a context of cell therapy by neural progenitor engraftment to repair brain damage, the long-term effect of soman on glial reaction and neural progenitor division was analyzed in the present study. The effect of soman poisoning was estimated in mouse brains at various times ranging from 1 to 90 days post-poisoning.

Uptake of locally applied deoxyglucose, glucose and lactate by axons and Schwann cells of rat vagus nerve.

We asked whether, in a steady state, neurons and glial cells both take up glucose sufficient for their energy requirements, or whether glial cells take up a disproportionate amount and transfer metabolic substrate to neurons. A desheathed rat vagus nerve was held crossways in a laminar flow perfusion chamber and stimulated at 2 Hz. (14)C-labelled substrate was applied from a micropipette for 5 min over a < 0.

Compared efficacy of diazepam or avizafone to prevent soman-induced electroencephalographic disturbances and neuropathology in primates: relationship to plasmatic benzodiazepine pharmacokinetics.

We performed an experiment to characterize the toxicity of soman in cynomolgus monkeys in which organophosphorus intoxication was followed by treatment with either the current three-drug therapy atropine/pralidoxime/diazepam or a combination of atropine/pralidoxime/avizafone, avizafone being the water soluble prodrug of diazepam. Clinical, electrophysiological, and histological approaches were combined. When benzodiazepines were injected at the similar molar dose of 0.

Memory impairment after soman intoxication in rat: correlation with central neuropathology. Improvement with anticholinergic and antiglutamatergic therapeutics.

The effects of soman, a potent irreversible inhibitor of acetylcholinesterase, on central neuropathology in rats were studied in relation with subsequent spatial memory impairments. In a first step, it was found that, without treatment, neuropathology and learning impairment were observed only in rats which experienced convulsions. Then, treatment consisting of atropine sulfate, and/or TCP and/or NBQX was administered to intoxicated animals at infraanticonvulsant doses to obtain a graded subsequent neuropathology and to appreciate an eventual relation between neuropathology and spatial memory impairment.

Acute soman poisoning in primates neither pretreated nor receiving immediate therapy: value of gacyclidine (GK-11) in delayed medical support.

Organophosphorus (OP) nerve agents are still used as warfare and terrorism compounds. Classical delayed treatment of victims of organophosphate poisoning includes combined i.v.

Heat stress, even extreme, does not induce penetration of pyridostigmine into the brain of guinea pigs.

Stress due to forced swimming was recently shown to allow penetration of pyridostigmine (PYR) into the brain of mice. Accordingly, it was suggested that in troops exposed to emotional stress under conditions of war, as during the Gulf War, the BBB may have unexpectedly become permeable to PYR thus leading to an increased frequency of CNS symptoms. In this study, the entry of PYR into the brain was investigated in guinea pigs subjected to different heat stress levels.

Nerve agent poisoning in primates: antilethal, anti-epileptic and neuroprotective effects of GK-11.

Organophosphorus nerve agents are still in use today in warfare and as terrorism compounds. Classical emergency treatment of organophosphate poisoning includes the combined administration of a cholinesterase reactivator (an oxime), a muscarinic cholinergic receptor antagonist (atropine) and a benzodiazepine anticonvulsant (diazepam). However, recent experiments with primates have demonstrated that such treatment, even when administered immediately after organophosphate exposure, does not rapidly restore normal electroencephalographic (EEG) activity and fails to totally prevent neuronal brain damage.

Absorption kinetics of a 14C-labelled Escherichia coli extract after oral administration in mice.

The fate of orally administered total 14C-labelled Escherichia coli extract (TEC, OM-89) was compared to that of its major 14C-labeled high molecular weight fractions (HEC, > 30 kD) in mice. High molecular weight substances (> 30 kD) were observed in blood 1 h after oral administration of the products, TEC and HEC. This suggests absorption from the digestive tract of the total E.

Efficacy of huperzine in preventing soman-induced seizures, neuropathological changes and lethality.

Huperzine A (HUP) is a potent reversible inhibitor of acetylcholinesterase (AChE) that crosses the blood-brain barrier. Its ability to prevent seizures and subsequent hippocampal neuropathological changes induced by the organophosphate soman was studied in guinea pigs. Results were compared to guinea pigs treated with pyridostigmine (PYR, 0.

GK 11: promising additional neuroprotective therapy for organophosphate poisoning.

Recent experiments with primates have demonstrated that treatment with atropine/pralidoxime/diazepam, even if administered immediately after organophosphate exposure, does not totally prevent neuronal brain damage. Using primates, we have studied, for the first time, the ability of GK-11 (gacyclidine), an antiglutamatergic drug in the process of agreement for human use, given as an additional therapy, to counteract the neuropathology due to organophosphate exposure that persists after classical treatment with oxime/atropine/benzodiazepine. We have also examined the recovery of the organophosphate-intoxicated primates.

Time course and regional expression of C-FOS and HSP70 in hippocampus and piriform cortex following soman-induced seizures.

The time course of induction of the proto-oncogene c-fos and the inducible heat shock hsp70 gene was studied from 5 minutes to 24 hours at both transcriptional (c-fos and hsp70 mRNA) and translational levels (C-FOS and HSP72 proteins) in the rat hippocampus and piriform cortex (Pir) after soman-induced seizures. Induction of c-fos was noticed as early as 5 minutes after seizures onset in all fields of hippocampal formation (CA1, CA3, CA4, and dentate gyrus) and in piriform cortex. The most intense induction was observed in piriform cortex.

Early regional changes of GFAP mRNA in rat hippocampus and dentate gyrus during soman-induced seizures.

We investigated the time course of GFAP levels in the hippocampal formation during the first 24 h following soman intoxication in rats. GFAP mRNA expression was detected by in situ hybridization. Intense GFAP mRNA expression was present in the molecular layer of the dentate gyrus as early as 6 h after intoxication.

Use of digoxigenin-labeled RNA probe to test hepatitis A virus antiviral drugs.

A nucleic acid hybridization assay was used to evaluate inhibitory activity of antiviral compounds against hepatitis A virus (HAV) in cell culture and compared to radioimmunoassay by analysis of variance procedure. The 5' genomic end of the HM-175 strain was used as digoxigenin-labeled RNA probe. Dot-blot examination showed a reduction of detectable HAV RNA in infected cells when treated with amphotericin B.

Modulation of soman-induced neuropathology with an anticonvulsant regimen.

Rat hippocampus and piriform cortex were examined for pathological changes 48 hours after exposure to a convulsant dose of soman. Animals were treated with a low dose of atropine just after soman and were then injected, after 10 or 40 minutes of seizures, with both the anticonvulsant drugs NBQX and TCP. Atropine given alone counteracted the extensive neuronal loss due to soman in both areas without prevention of neuronal suffering.

Effects of neutron-gamma irradiation on striatal D1 and D2 receptor distribution.

The early effects of neutron irradiation on the striatal D1 and D2 dopaminergic receptor distribution were investigated by quantitative receptor autoradiography. One hour after exposure at the dose of 8.4 Gy, an increase of D1 (+21%) and D2 (+25%) receptor density was observed in the striatum, located at the most anterior levels, containing the richest plexus of dopaminergic fibers afferent from the substantia nigra.

[Detection of hepatitis A virus by riboprobe labeled with digoxigenin: comparison of methods].

A riboprobe (RNA probe), corresponding to the 5' end of the HM175 hepatitis A virus (HAV) genome, was synthetized in vitro and was digoxigenin-labeled. Then the riboprobe was used to detect the CF53 HAV strain. Conditions of virus denaturation (with or without SDS and proteinase K, timing of assay) to release viral RNA were tested by dot-blot hybridization on a ten fold dilution of HAV suspension.

Influence of a bacterial extract on antigen presentation and protection against experimental infections.

Although substances known as immunodulators are usually used to stimulate nonspecific immunity, their mode of action is not well understood. In an effort to clarify this mechanism, we investigated the effect of a lyophilized bacterial extract (Broncho-Vaxom) on experimental infections, on normal or irradiated mice, and on antigen processing.