[Mild cognitive impairment: a prevalence and sociodemographic factors study in the city of Córdoba, Argentina]. / Deterioro cognitivo leve: estudio de prevalencia y factores sociodemográficos en la ciudad de Córdoba, Argentina.

INTRODUCTION: The increase in life expectancy and the significant growth in the population of the elderly have generated an interest in secondary prevention of different diseases, especially from the age of 50. In Argentina, those over 65 represent 10% of the total population, what makes important to research into their mental health. A trans-sectional descriptive study has been carried out in four neuropsychology services in the city of Cordoba, within the framework of a campaign assessing memory for people over 50. SUBJECTS AND METHODS: In three months, 418 volunteers took part, with an average age of 64.24 years and 12.76 years of instruction, mostly belonging to a urban environment (80%). They were administered Folstein's Minimental State, neuropsychological tests and behavioral measures in two work sessions. RESULTS: The majority was found to have normal performances (75.6%, n = 316) at both behavioral and neuropsychological levels. A lower percentage was found at the borders of normality (8.6%, n = 36). 9.1% (n = 38) of those studied were found to have an amnesiac type of mild cognitive impairment, and 4.5% (n = 19) a multidomain type of deterioration. In sum, about 13.6% of people have a greater chance of developing dementia in coming years. CONCLUSION: The socio-demographic variables that most influence cognitive state appear to be the female gender, age higher than 65 years, lower levels of instruction, fewer children and fewer siblings.

The value of pharmacist involvement in a point-of-care service, walk-in lipid screening program.

The leading cause of death in the United States is heart disease. Because an elevated serum cholesterol level is an independent risk factor for development of coronary heart disease (CHD), individuals older than 20 years of age are advised to have their cholesterol level checked every 5 years. Walk-in screening programs are becoming popular as a method of health care delivery. The program at the University of California-Irvine Medical Center administers point-of-care, low-cost lipid profile testing, directly involves patients in their own care, and provides individualized education to patients regarding cardiovascular risk reduction. A total of 301 patients participated in the program between August 1998 and September 2000. Fifty percent of them (150 patients) required intervention; 34% of these (52 patients) were previously undiagnosed. Their mean age was 57 +/- 13 years; 35% were women, 53% had two or more cardiac risk factors, and 5% had CHD. Based on the National Cholesterol Education Program guidelines, 29% had low-density lipoprotein levels above target, 23% had triglyceride levels higher than recommended, and 21% had high-density lipoprotein levels below target. It is our hope that our successful experience with the program will encourage pharmacists to develop similar programs.

Identification of two new Pmp22 mouse mutants using large-scale mutagenesis and a novel rapid mapping strategy.

Mouse mutants have a key role in discerning mammalian gene function and modelling human disease; however, at present mutants exist for only 1-2% of all mouse genes. In order to address this phenotype gap, we have embarked on a genome-wide, phenotype-driven, large-scale N-ethyl-N--nitrosourea (ENU) mutagenesis screen for dominant mutations of clinical and pharmacological interest in the mouse. Here we describe the identification of two similar neurological phenotypes and determination of the underlying mutations using a novel rapid mapping strategy incorporating speed back-crosses and high throughput genotyping. Two mutant mice were identified with marked resting tremor and further characterized using the SHIRPA behavioural and functional assessment protocol. Back-cross animals were generated using in vitro fertilization and genome scans performed utilizing DNA pools derived from multiple mutant mice. Both mutants were mapped to a region on chromosome 11 containing the peripheral myelin protein 22 gene (Pmp22). Sequence analysis revealed novel point mutations in Pmp22 in both lines. The first mutation, H12R, alters the same amino acid as in the severe human peripheral neuropathy Dejerine Sottas syndrome and Y153TER in the other mutant truncates the Pmp22 protein by seven amino acids. Histological analysis of both lines revealed hypo-myelination of peripheral nerves. This is the first report of the generation of a clinically relevant neurological mutant and its rapid genetic characterization from a large-scale mutagenesis screen for dominant phenotypes in the mouse, and validates the use of large-scale screens to generate desired clinical phenotypes in mice.

Biochemical studies on the mutagen, 6-N-hydroxylaminopurine. Synthesis of the deoxynucleoside triphosphate and its incorporation into DNA in vitro.

The nucleotide analogue, 6-N-hydroxylaminopurine deoxynucleoside triphosphate (dHAPTP) has been synthesized from 6-chloropurine by a procedure involving both enzymatic and chemical reagents. In a series of experiments involving several different DNA polymerases including 3 procaryotic and 2 eucaryotic enzymes, it was shown that dHAPTP is ambiguous in its base-pairing characteristics, since it can replace both dATP and dGTP in DNA synthesis. It was also shown that different enzymes have different capacities to distinguish dHAPTP from the canonical deoxynucleoside triphosphates. These results are consistent with (but do not prove) the hypothesis that the mechanism of 6-N-hydroxylaminopurine mutagenesis seen in both eucaryotic and procaryotic organisms is due to its conversion, in vivo, to a deoxynucleoside triphosphate which is incorporated ambiguously for dATP and dGTP during DNA replication.