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Summary In 2006, the Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS) Farm Program was implemented in sentinel grower-finisher swine herds in Quebec, Ontario, Manitoba, Saskatchewan and Alberta. Herds were visited 1–3 times annually. Faecal samples were collected from pens of close-to-market (CTM) weight (>80 kg) pigs and antimicrobial use (AMU) data were collected via questionnaires. Samples were cultured for generic Escherichia coli and Salmonella and tested for antimicrobial susceptibility. This paper describes the findings of this program between 2006 and 2008. Eighty-nine, 115 and 96 herds participated in this program in 2006, 2007 and 2008 respectively. Over the 3 years, antimicrobial resistance (AMR) levels remained consistent. During this period, resistance to one or more antimicrobials was detected in 56–63% of the Salmonella spp. isolates and 84–86% of E. coli isolates. Resistance to five or more antimicrobials was detected in 13–23% of Salmonella and 12–13% of E. coli. Resistance to drugs classified as very important to human health (Category I) by the Veterinary Drug Directorate (VDD), Health Canada, was less than or equal to 1% in both organisms. AMU data were provided by 100 herds in 2007 and 95 herds in 2008. Nine herds in 2007 and five herds in 2008 reported no AMU. The most common route of antimicrobial administration (75–79% of herds) was via feed, predominantly macrolides/lincosamides (66–68% of herds). In both 2007 and 2008, the primary reasons given for macrolide/lincosamide use were disease prevention, growth promotion and treatment of enteric disease. The Category I antimicrobials, ceftiofur and virginiamycin were not used in feed or water in any herds in 2008, but virginiamycin was used in feed in two herds in 2007. Parenteral ceftiofur was used in 29 herds (29%) in 2007 and 20 herds (21%) in 2008. The reasons for ceftiofur use included treatment of lameness, respiratory disease and enteric disease.

In 2006, the Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS) Farm Program was implemented in sentinel grower-finisher swine herds in Québec, Ontario, Manitoba, Saskatchewan and Alberta. Herds were visited 1-3 times annually. Faecal samples were collected from pens of close-to-market (CTM) weight (80 kg) pigs and antimicrobial use (AMU) data were collected via questionnaires. Samples were cultured for generic Escherichia coli and Salmonella and tested for antimicrobial susceptibility. This paper describes the findings of this program between 2006 and 2008. Eighty-nine, 115 and 96 herds participated in this program in 2006, 2007 and 2008 respectively. Over the 3 years, antimicrobial resistance (AMR) levels remained consistent. During this period, resistance to one or more antimicrobials was detected in 56-63% of the Salmonella spp. isolates and 84-86% of E. coli isolates. Resistance to five or more antimicrobials was detected in 13-23% of Salmonella and 12-13% of E. coli. Resistance to drugs classified as very important to human health (Category I) by the Veterinary Drug Directorate (VDD), Health Canada, was less than or equal to 1% in both organisms. AMU data were provided by 100 herds in 2007 and 95 herds in 2008. Nine herds in 2007 and five herds in 2008 reported no AMU. The most common route of antimicrobial administration (75-79% of herds) was via feed, predominantly macrolides/lincosamides (66-68% of herds). In both 2007 and 2008, the primary reasons given for macrolide/lincosamide use were disease prevention, growth promotion and treatment of enteric disease. The Category I antimicrobials, ceftiofur and virginiamycin were not used in feed or water in any herds in 2008, but virginiamycin was used in feed in two herds in 2007. Parenteral ceftiofur was used in 29 herds (29%) in 2007 and 20 herds (21%) in 2008. The reasons for ceftiofur use included treatment of lameness, respiratory disease and enteric disease.

Traumatic brain injury (TBI) is one of the most common causes of death and dismal outcome among children and young adults. The morbidity and mortality differ but more aggressive monitoring and more designated neuro intensive care units have improved the results. Studies have demonstrated a connection between apolipoprotein E (APOE) genotype and outcome after TBI, but few are prospective and none is from northern Europe. APOE has three alleles: epsilon2, epsilon3 and epsilon4.A total of 96 patients with Glasgow coma score (GCS)or =8 were prospectively and consecutively included. APOE genotypes were all analyzed at the same laboratory from blood samples by polymerase chain reaction-restriction fragment length polymorphism.All patients were assessed at 1 year with Glasgow outcome scale extended (GOSE), National Institute of Health Stroke Scale (NIHSS) and the Barthel daily living index. The genotype was available in all patients. Twenty-six patients expressed APOE epsilon4 while 70 patients did not. Outcome demonstrated that patients with APOE epsilon4 had worse outcome vs. those lacking this allele. When subdividing patients into gender, males with APOE epsilon4 did worse, a difference not detected among female patients.APOE epsilon4 correlated to worse outcome in TBI patients. We also found that males with APOE epsilon4 had poor outcome while females did not. Thus, the results indicate that genetic polymorphism may influence outcome after TBI.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative syndrome with familial and sporadic forms. Most ALS-associated mutations are found in the superoxide dismutase 1 (SOD1) gene. We conducted a study including 60 sporadic and 19 familial ALS patients, 206 reference patients with other neurological disorders and 40 age- and sex-matched healthy controls to test the hypothesis that cerebrospinal fluid (CSF) levels of neurofilament light (NF-L) protein, a marker of axonal degeneration, might provide diagnostic and prognostic information on the disease. All ALS patients were screened for SOD1 mutations. Ten of the familial and five of the sporadic cases carried SOD1 mutations. NF-L concentration [median (range)] was strongly elevated in ALS [2110 (255-10 800) ng/l] compared with reference patients and healthy controls [277 (125-15 506) and 175 (125-710) ng/l, respectively, P0.001] and correlated inversely with disease duration (Spearman R = -0.518, P = 0.001). NF-L levels were lower in SOD1 mutation-associated ALS compared with SOD1 wild-type (wt) ALS (P = 0.03). In conclusion, CSF NF-L levels may provide both diagnostic and prognostic information, particularly in SOD1 wt ALS.

A technique for controlling the tip–sample distance in near-field optical microscopes is presented. It consists of mechanically exciting a fiber tip inserted without any adhesive between the two prongs of a high Q-piezoelectric tuning fork. The detection of the shear forces is classically achieved by measuring the decrease of the dithering amplitude when the tip approaches the surface. This simple setup greatly simplifies tip replacement and its resonance frequency tuning.

In a previous study we found that nine of 47 siblings to multiple sclerosis (MS) patients with a normal neurological examination carry an intrathecal oligoclonal immunopathy with limited specificity, a condition we termed MS immunopathic trait. The purpose of this study is to further characterize the MS immunopathic trait phenotype. We found that the neurofilament light protein (NFL) and glial fibrillary acidic protein (GFAp) concentrations were increased in the group of patients with clinically definite MS (n = 47) in latent or slowly progressive phases. There was no increase in GFAp and NFL in cerebrospinal fluid in the healthy siblings of MS patients (n = 47), nor in the subgroup of these siblings with MS immunopathic trait (n = 9) compared with a group of healthy control subjects (n = 50). Thus, there was no indication of presymptomatic CNS parenchymal involvement in MS immunopathic trait.

Changes in expression of the proto-oncogene Bcl-2 are well known in the developing brain, with a high expression level in young post-mitotic neurons that are beginning the outgrowth of processes. The physiological significance of the Bcl-2 up-regulation in these neurons is not fully understood. We used a differentiation model for human CNS neurons to study the expression and function of Bcl-2. NT2/D1 human neuronal precursor cells differentiated into a neuronal phenotype in the presence of 10 microM retinoic acid for 3-5 weeks. This concentration of retinoic acid was not toxic to undifferentiated NT2/D1 cells but was sufficient to up-regulate the BCL-2 protein in 6 days. The BCL-2 levels increased further after 3 weeks, i.e. when the cells started to show neuronal morphology. Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. The loss of neuron-like cells from differentiating cultures indicated that the dead cells were those committed to neuronal differentiation. Death was related to the presence of retinoic acid since withdrawal of retinoic acid after 16 days of treatment dramatically increased cell surviving. The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Furthermore, down-regulation of BCL-2 levels by an antisense oligonucleotide in neuronally differentiated NT2/D1 cells increased their susceptibility to retinoic acid-induced apoptosis. These results indicate that one function of the up-regulation of endogenous BCL-2 during neuronal differentiation is to regulate the sensitivity of young post-mitotic neurons to retinoic acid-mediated apoptosis.

The clinical application of a newly developed highly sensitive ELISA method (20) to assay glial fibrillary acidic protein (GFAP) in the cerebrospinal fluid (CSF) was investigated in children and adolescents with neurological disorders. GFAP analysis was explored as a tool to differentiate disorders with ongoing astrocytosis. A consecutive series of 34 subjects, 17 boys and 17 girls, with nonprogressive and progressive neurological encephalopathies was compared to 10 healthy controls. The mean CSF GFAP concentration of the controls was 60.6 ± 54 ng/l (SD). The group of 24 subjects (12 boys and 12 girls) with progressive neurologic disorders had higher mean CSF GFAP levels than the group of 10 subjects (5 boys and 5 girls) with non-progressive disorders, 222.6 ± 186 and 127.5 ± 86 ng/l, respectively. The progressive encephalopathies differed significantly from controls (p < 0.01) while the non-progressive did not. The mean GFAP concentration of the epilepsy cases (n = 18) and non-epilepsy cases (n = 16) was 212.9 ± 196 and 174.0 ± 132 ng/l, respectively. The epilepsy cases differed significantly from controls which could be explained by the dominance of progressive cases (15 out of 18). Six subjects with known gliotic progressive disorders (glutaric aciduria Type 1, Unverricht-Lundborg disease, Hallervorden-Spatz disease, Jansky-Bielschowsky disease and juvenile Huntington disease) differed significantly, as expected, from controls with a mean CSF GFAP concentration of 326.2 ± 132.5 ng/l, p < 0.001. The group with Lennox-Gastaut syndrome (3 boys and 3 girls) also differed significantly from controls (205.0 ± 107.6, p

Young adult rats were fed an isocaloric diet for 28 days. The diet consisted of either 22% casein, or protein-restricted food consisting of a 5% mixture of soy and whey protein, or a synthetic amino acid mixed diet devoid of the essential amino acids tryptophan, valine, lysine, and threonine. The level of the nervous tissue-specific S-100 protein was quantified immunoelectrophoretically in 9 different brain areas. A marked decrease of S-100 was observed in hippocampus and posterior part of the cerebellar vermis per g wet weight in protein-restricted rats. An additional lowering was noticed in sensory motor cortex per mg soluble protein. This effect was potentiated with the amino acid-deficient diet. The in vitro incorporation of 3H-leucine into cerebellar proteins was slightly decreased in the low-protein-fed rats, and more markedly decreased in those receiving an amino acid-restricted diet.