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Background/Objectives: Many maternal traits are associated with a neonate’s gestational duration, birth weight, and birth length. These birth outcomes are subsequently associated with late-onset health conditions. The causal mechanisms and the relative contributions of maternal and fetal genetic effects behind these observed associations are unresolved. Methods and findings: Based on 10,734 mother–infant duos of European ancestry from the UK, Northern Europe, Australia, and North America, we constructed haplotype genetic scores using single-nucleotide polymorphisms (SNPs) known to be associated with adult height, body mass index (BMI), blood pressure (BP), fasting plasma glucose (FPG), and type 2 diabetes (T2D). Using these scores as genetic instruments, we estimated the maternal and fetal genetic effects underlying the observed associations between maternal phenotypes and pregnancy outcomes. We also used infant-specific birth weight genetic scores as instrument and examined the effects of fetal growth on pregnancy outcomes, maternal BP, and glucose levels during pregnancy. The maternal nontransmitted haplotype score for height was significantly associated with gestational duration (p = 2.2 × 10⁻⁴). Both maternal and paternal transmitted height haplotype scores were highly significantly associated with birth weight and length (p < 1 × 10⁻¹⁷). The maternal transmitted BMI scores were associated with birth weight with a significant maternal effect (p = 1.6 × 10⁻⁴). Both maternal and paternal transmitted BP scores were negatively associated with birth weight with a significant fetal effect (p = 9.4 × 10⁻³), whereas BP alleles were significantly associated with gestational duration and preterm birth through maternal effects (p = 3.3 × 10⁻² and p = 4.5 × 10⁻³, respectively). The nontransmitted haplotype score for FPG was strongly associated with birth weight (p = 4.7 × 10⁻⁶); however, the glucose-increasing alleles in the fetus were associated with reduced bi

[Background] MSR1 repeats are a 36–38 bp minisatellite element that have recently been implicated in the regulation of gene expression, through copy number variation (CNV)., [Patients and methods] Bioinformatic and experimental methods were used to assess the distribution of MSR1 across the genome, evaluate the regulatory potential of such elements and explore the role of MSR1 elements in cancer, particularly non-familial breast cancer and prostate cancer., [Results] MSR1s are predominately located at chromosome 19 and are functionally enriched in regulatory regions of the genome, particularly regions implicated in short-range regulatory activities (H3K27ac, H3K4me1 and H3K4me3). MSR1-regulated genes were found to have specific molecular roles, such as serine-protease activity (P = 4.80 × 10−7) and ion channel activity (P = 2.7 × 10−4). The kallikrein locus was found to contain a large number of MSR1 clusters, and at least six of these showed CNV. An MSR1 cluster was identified within KLK14, with 9 and 11 copies being normal variants. A significant association with the 9-copy allele and non-familial breast cancer was found in two independent populations (P = 0.004; P = 0.03). In the white British population, the minor allele conferred an increased risk of 1.21–3.51 times for all non-familial disease, or 1.7–5.3 times in early-onset disease. The 9-copy allele was also found to be associated with increased risk of prostate cancer in an independent population (odds ratio = 1.27–1.56; P =0.009)., [Conclusions] MSR1 repeats act as molecular switches that modulate gene expression. It is likely that CNV of MSR1 will affect risk of development of various forms of cancer, including that of breast and prostate. The MSR1 cluster at KLK14 represents the strongest risk factor identified to date in non-familial breast cancer and a significant risk factor for prostate cancer. Analysis of MSR1 genotype will allow development of precise stratification of disease risk and provide a novel target for therapeutic agents.

"Speed and time create tempo. Tempo is the rate of military action and has significance only in relation to that of the enemy... It is not enough to move faster than the enemy only now and then. When the friendly force is not moving faster, the advantage and initiative passes to the enemy..." Tempo is a powerful advantage that can make one unit sub come to the will of another unit. However, the Marine Corps is passing the advantage and initiative to the enemy by mandating the amount of gear Marines are required to wear in Iraq and Afghanistan. Personal protective equipment (PPE) and mission critical gear must be reduced in weight because they degrade the unit's capabilities to maneuver and defeat the enemy, which ultimately degrades the Corps' abilities to accomplish the mission. In Vietnam, a Marine's typical load weighed 75 pounds. The difference in weight of a combat-loaded Marine in Vietnam to a marine in Operation Iraqi Freedom (OIF) or Operation Enduring Freedom (OEF) is an increase of 62 pounds. In 2009, a typical Marine's combat load is an average of "137 pounds worth of body armor and gear." Marines pride themselves on their expeditionary nature and ability to adapt to a changing environment. As an organization, the Marine Corps does not need to hinder this mentality, but rather encourage it. Higher level commanders need to make tough decisions and realize that risks must be taken in war. They must give subordinate commanders the autonomy to make the right decisions for their unit. When an estimate of a situation is conducted by a battalion commander and it determines that only a certain level of PPE is required for an operation, allow the commander to make the decision. If general level officers refuse to allow subordinate commanders to make these decisions, the Marine Corps will continue to give the initiative to the enemy.

Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. H. pylori infects approximately 50% of the world's population. and infections can persist throughout the lifetime of the host. Motility and chemotaxis have been shown to be important in the infection process of H. pylori. We sought to address the specific roles of chemotaxis in infection of a mouse model system. We found that mutants lacking cheW, cheA, or cheY are all nonchemotactic and infect FVB/N mice with an attenuated phenotype after 2 weeks of infection. If infections proceeded for 6 months, however, this attenuation disappeared. Histological and culture analysis revealed that nonchemotactic mutants were found only in the corpus of the stomach, while the wild type occupied both the corpus and the antrum. Further analysis showed that nonchemotactic H. pylori isolates had an increased 50% infectious dose and were greatly outcompeted when coinfected with the wild type. If nonchemotactic mutants were allowed to establish an infection, subsequent infection with the wild type partially displaced the nonchemotactic mutants. indicating a role for chernotaxis in maintenance of infection. he data presented here support four roles for chemotaxis in H. pylori mouse infections: (i) establishing infection. (ii) achieving high-level infection, (iii) maintaining an infection when there are competing H. pylori present. and (iv) colonizing all regions of the stomach.

Objective: To determine the minimum effective dose of folic acid required to appreciably increase serum folate and to produce a significant reduction in plasma total homocysteine (tHcy). Design: Double-blind, randomised placebo-controlled intervention trial. Setting: Community-based project in a New Zealand city. Subjects: Seventy free living men and women with tHcy10 µmol/l. Mean age (range) was 58 (29-90) y. Interventions: Daily consumption over 4 weeks of 20 g breakfast cereal either unfortified (placebo) or fortified with 100, 200 or 300 µg folic acid. Dietary intake was determined by weighed diet records and consumption of commercially fortified products was avoided. Main outcome measures: Plasma tHcy and serum folate concentrations. Results: Average serum folate concentrations (95% CI) increased significantly in the treatment groups relative to the control group by 28(9-51)%, 60(37-87)% and 79(51-114)% for supplementation with 100, 200 and 300 µg folic acid, respectively. A reduction in tHcy was observed, being 16(8-22)%, 12(4-18)% and 17(9-24)% in the three treatment groups, respectively. Conclusions: A regular intake of as little as 100 µg folic acid per day was sufficient to lower tHcy in persons at the upper end of the normal range for tHcy. Low-level fortification may also be appropriate for lowering the risk of neural tube defects given that, when aggregated from all sources, the total intake of folic acid may be sufficiently high to adequately improve the folate status of young women.