Dietary factors related to physical fitness among navy shipboard men

Abstract This study examines the relationship between habitual dietary practices and performance on the physical readiness test required of active duty Navy personnel. Participants were 1,013 men (mean age = 26.2 years) stationed aboard nine Navy ships. The men completed a self-report survey of lifestyle and dietary habits and were evaluated on four tests of physical fitness: 1.5-mile Run, Sit-ups, Sit-reach, and Percent Body Fat. A standardized Overall Fitness score was also computed for each person. Results indicated that the participants tended to skip breakfast, ingest moderate amounts of caffeine, and favor a high-fat, low-fiber diet. Fitness scores were associated with a number of dietary variables, including caffeine intake, between-meal snacking, and overeating (all negatively related to fitness, p <.01), and having a general "nutrition orientation" (positively related to fitness, p <.001). The relationships were confounded by the influence of age, exercise, and smoking, but even after controlling for these, diet was a significant predictor of fitness (p <.001).     

Separate and variably shaped chromosome arm domains are disclosed by chromosome arm painting in human cell nuclei

Fluorescence in situ hybridization (FISH) with microdissection probes from human chromosomes 3 and 6 was applied to visualize arm and subregional band domains in human amniotic fluid cell nuclei. Confocal laser scanning microscopy and quantitative three-dimensional image analysis showed a pronounced variability of p- and q-arm domain arrangements and shapes. Apparent intermingling of neighbouring arm domains was limited to the domain surface. Three-dimensional distance measurements with pter and qter probes supported a high variability of chromosome territory folding.     

Possible involvement of unstable sites on chromosomes 7 and 14 in human cancer

Specific sites on human chromosomes appear to have a tendency to rearrange in so-called "sporadic translocations," which are found in approximately 1 of 1000 metaphases from peripheral blood lymphocyte cultures. We now present data that implicates four sites in the human genome as displaying this distinct type of chromosomal instability (7p13, 7q34, 14q11, and 14q32). Chromosome 14q11 was found to be involved in sporadic translocations most often, followed by 7p13 greater than 7q34 greater than 14q32. The 14q11 locus also shows the highest frequency of spontaneous sister chromatid exchange. It is proposed that these sporadic translocations involving chromosomes #7 and #14 arise following recombinational errors occurring at sites of T- and B-cell genes known to be located at these four sites. Evidence is presented that in some cases "fixation" of a sporadic translocation might be involved in malignancy of lymphoid origin.     

Filipino beta zero thalassaemia: a high Hb A2 beta zero thalassaemia resulting from a large deletion of the 5'' beta globin gene region.

A large novel deletional beta zero thalassaemia mutation associated with unusually high levels of haemoglobin (Hb) A2 in heterozygotes is described in two unrelated subjects of Filipino background. The deletion was characterised by DNA mapping including pulsed field gel electrophoresis. Filipino beta zero thalassaemia extends for approximately 45 kb beginning approximately 1.5 kb 3' to the delta globin gene. It is the largest deletion to date which gives rise to the beta zero thalassaemia phenotype. This mutation, similar to previously described deletional beta zero thalassaemias associated with high Hb A2, removes sequences 5' to the beta globin gene promoter and emphasises the functional importance of the 5' beta globin region in eliciting the unusually high level of Hb A2. This example also suggests that it is the 3' sequences which are transposed rather than the actual deletion size which are significant in the raised fetal haemoglobin (Hb F) found with some of the thalassaemias.     

Dorsal raphé stimulation modifies striatal-evoked antidromic invasion of nigral dopaminergic neurons in vivo

Summary Extracellular single unit recordings were obtained from antidromically identified nigrostriatal dopaminergic neurons in anesthetized rats to determine the effects of dorsal raphé stimulation on the somatodendritic excitability of substantia nigra dopaminergic neurons. Stimulation of the dorsal raphé with a brief train of pulses delivered 7–2 ms prior to the neostriatal-evoked antidromic response significantly reduced the proportion of neostriatal-evoked antidromic responses that consisted of both initial segment and somatodendritic components without significantly altering the neostriatal-evoked post-stimulus inhibitory period. Raphé stimulation alone facilitated post-stimulus neuronal firing in almost half of the cells examined. The raphé-induced decrease in somatodendritic excitability was blocked by the serotonin antagonist, metergoline (0.5–2.0 mg/kg, i.v.), without significantly affecting the rate or pattern of spontaneous activity. The tryptophan hydroxylase inhibitor, parachlorophenylalanine (400 mg/kg, i.p. for three consecutive days), abolished the decrease in somatodendritic excitability following raphé stimulation which could be re-instated by intravenous administration of 5-HTP. The dopamine antagonists haloperidol (25–100 g/kg, i.v.) and sulpiride (10–30 mg/kg, i.v.) also blocked the effects of dorsal raphé stimulation on somatodendritic invasion. These data suggest that in vivo, serotonin liberated from raphé-nigral terminals facilitates the release of dopamine from nigrostriatal dendrites resulting in a local, autoreceptor-mediated reduction in somatodendritic excitability without affecting the spontaneous firing rate and excitability of the neuron as a whole.     

Denaturing high performance liquid chromatography: high throughput mutation screening in familial hypertrophic cardiomyopathy and SNP genotyping in motor neurone disease

AIMS: To evaluate the usefulness of denaturing high performance liquid chromatography (DHPLC) as a high throughput tool in: (1) DNA mutation detection in familial hypertrophic cardiomyopathy (FHC), and (2) single nucleotide polymorphism (SNP) discovery and validation in sporadic motor neurone disease (MND). METHODS: The coding sequence and intron-exon boundaries of the cardiac beta myosin heavy chain gene (MYH7) were screened by DHPLC for mutation identification in 150 unrelated patients diagnosed with FHC. One hundred and forty patients with sporadic MND were genotyped for the A67T SNP in the poliovirus receptor gene. All DHPLC positive signals were confirmed by conventional methods. RESULTS: Mutation screening of MYH7 covered 10 kb with a total of 5700 amplicons, and more than 6750 DHPLC injections were completed within 35 days. The causative mutation was identified in 14% of FHC cases, including seven novel missense mutations (L227V, E328G, K351E, V411I, M435T, E894G, and E927K). Genotyping of the A67T SNP was performed at two different temperatures both in MND cases and 280 controls. This coding SNP was found more frequently in MND cases (13.6%) than in controls (6.8%). Furthermore, 19 and two SNPs were identified in MYH7 and the poliovirus receptor gene, respectively, during DHPLC screening. CONCLUSIONS: DHPLC is a high throughput, sensitive, specific, and robust platform for the detection of DNA variants, such as disease causing mutations or SNPs. It enables rapid and accurate screening of large genomic regions.     

Molecular determinants of human uveal melanoma invasion and metastasis

The molecular analysis of cancer has benefited tremendously from the sequencing of the human genome integrated with the science of bioinformatics. Microarray analysis technology has the potential to classify tumors based on the differential expression of genes. In the current study, a collaborative, multidisciplinary approach was utilized to study the molecular determinants of human uveal melanoma invasion and metastasis. Uveal melanoma is considered the most common primary intraocular cancer in adults, resulting in the death of approximately 50% of patients affected. Unfortunately, at the time of diagnosis, many patients already harbor microscopic metastases, thus underscoring a critical need to identify prognostic markers indicative of metastatic potential. The investigative strategy consisted of isolating highly invasive vs. poorly invasive uveal melanoma cells from a heterogeneous tumor derived from cells that had metastasized from the eye to the liver. The heterogeneous tissue explant MUM-2 led to the derivation of two clonal cell lines: MUM-2B and MUM-2C. Further morphological and functional analyses revealed that the MUM-2B cells were epithelioid, interconverted (expressing mesenchymal and epithelial phenotypes) highly invasive, and demonstrated vasculogenic mimicry. The MUM-2C cells were spindle-like, expressed only a vimentin mesenchymal phenotype, poorly invasive, and were incapable of vasculogenic mimicry. The molecular analysis of the MUM-2B vs. the MUM-2C clones resulted in the differential expression of 210 known genes. Overall, the molecular signature of the MUM-2B cells resembled that of multiple phenotypes – similar to a pluripotent, embryonic-like genotype. Validation of select genes that were upregulated and down-regulated was conducted by semiquantitative RT-PCR measurement. This study provides a molecular profile that will hopefully lead to the development of new molecular targets for therapeutic intervention and possible diagnostic markers to predict the clinical outcome of patients with uveal melanoma. This revised version was published online in July 2006 with corrections to the Cover Date.