Search tips
Search criteria

Results 1-8 (8)

Clipboard (0)

Select a Filter Below

Year of Publication
Document Types
1.  Correlates of posttraumatic epilepsy 35 years following combat brain injury(CME) 
Neurology  2010;75(3):224-229.
The Vietnam Head Injury Study (VHIS) is a prospective, longitudinal follow-up of 1,221 Vietnam War veterans with mostly penetrating head injuries (PHIs). The high prevalence (45%–53%) of posttraumatic epilepsy (PTE) in this unique cohort makes it valuable for study.
A standardized multidisciplinary neurologic, cognitive, behavioral, and brain imaging evaluation was conducted on 199 VHIS veterans plus uninjured controls, some 30 to 35 years after injury, as part of phase 3 of this study.
The prevalence of seizures (87 patients, 43.7%) was similar to that found during phase 2 evaluations 20 years earlier, but 11 of 87 (12.6%) reported very late onset of PTE after phase 2 (more than 14 years after injury). Those patients were not different from patients with earlier-onset PTE in any of the measures studied. Within the phase 3 cohort, the most common seizure type last experienced was complex partial seizures (31.0%), with increasing frequency after injury. Of subjects with PTE, 88% were receiving anticonvulsants. Left parietal lobe lesions and retained ferric metal fragments were associated with PTE in a logistic regression model. Total brain volume loss predicted seizure frequency.
Patients with PHI carry a high risk of PTE decades after their injury, and so require long-term medical follow-up. Lesion location, lesion size, and lesion type were predictors of PTE.
= Analysis of Brain Lesions;
= Armed Forces Qualification Test;
= Automated Image Registration;
= closed head injury;
= glutamic acid decarboxylase;
= phase 1;
= phase 2;
= phase 3;
= penetrating head injury;
= posttraumatic epilepsy;
= traumatic brain injury;
= Vietnam Head Injury Study;
= Wechsler Adult Intelligence Scale.
PMCID: PMC2906177  PMID: 20644150
2.  The Met66 allele of the functional Val66Met polymorphism in the brain‐derived neurotrophic factor gene confers protection against neurocognitive dysfunction in systemic lupus erythematosus 
Annals of the Rheumatic Diseases  2006;65(10):1330-1335.
A common functional polymorphism of the brain‐derived neurotrophic factor gene (BDNF Val66Met) was previously associated with diminished episodic memory performance in healthy people. As cognitive function is commonly impaired in patients with systemic lupus erythematosus (SLE), the association of the BDNF Val66Met with neurocognitive function was studied.
To study the association of the BDNF Val66Met with neurocognitive function in a cohort of patients with SLE.
Cognitive function was assessed in 59 patients with SLE with no previous or current central nervous system involvement. Cognitive tests were grouped into five domains (memory, attention/executive function, visuospatial skills, motor function and psychomotor speed) and used to obtain domain Z scores, reflecting the difference between averaged scores of performance on individual tests and published norms in each domain. Genotyping was carried out using a 5′‐nuclease assay with 99.9% accuracy. Unpaired t test was used to assess the relationship between genotypes and cognitive function, whereas the effect of possible confounders was assessed in a multivariate analysis.
Patients carrying the Met66 allele scored significantly higher on psychomotor, attention/executive and motor function tests, resulting in significantly higher domain Z scores for the psychomotor (p = 0.005) and motor (p = 0.002) domains.
The BDNF Met66 allele was associated with better cognitive functioning in the psychomotor and motor domains, even after controlling for differences in ethnicity, sex, depression status and prednisone treatment. These data suggest that the BDNF Met66 allele confers protection against the decline of motor and psychomotor cognitive functions in patients with longstanding SLE.
PMCID: PMC1798324  PMID: 16606648
3.  Nucleotide sequence variation within the human tyrosine kinase B neurotrophin receptor gene (NTRK2): association with antisocial alcohol dependence 
The pharmacogenomics journal  2007;7(6):368-379.
To identify sequence variants in genes that may have roles in neuronal responses to alcohol, we resequenced the 5′ region of NTRK2 and determined linkage disequilibrium (LD) values, haplotype structure, and performed association analyses using 43 single nucleotide polymorphisms (SNPs) covering the entire NTRK2 region in a Finnish Caucasian sample of 229 alcohol dependent subjects with antisocial personality disorder and 287 healthy controls. Individually, three SNPs were associated with alcohol dependence and alcohol abuse (AD)(P-value from 0.0019 to 0.0059, significance level was set at P ≤ 0.01 corrected for multiple testing), while a common eighteen-locus haplotype within the largest LD block of NTRK2, a 119 kb region containing the 5′ flanking region and exons 1 through 15, was marginally overrepresented in control subjects compared to AD individuals (global P = 0.057). Taken together, these results support a role for the NTRK2 gene in addiction in a Caucasian population with AD and a subtype of antisocial personality disorder.
PMCID: PMC2099305  PMID: 17200667
alcoholism; gene; tyrosine kinase B receptor; TrkB; NTRK2 gene; single nucleotide polymorphism; SNP; association
4.  Defective specialized SP beta transducing bacteriophages of Bacillus subtilis that carry the sup-3 or sup-44 gene. 
Journal of Bacteriology  1981;148(3):1012-1015.
We isolated defective specialized transducing phages of SP beta that carry one of the extracistronic suppressors, sup-3 or sup-44. Lysates containing these phages can be used in a simple spot test to determine whether an auxotrophic mutation can be suppressed. The sup-3 and sup-44 mutations are distinct, in that their suppression patterns differ for the markers hisA1, metC3, and thr-5; and they are not alleles.
PMCID: PMC216309  PMID: 6796561

Results 1-8 (8)