Terrorism: A History

Rarely is a book written to fulfill the author’s own need for a scholarly work on a topic that he teaches at university. So when Associate Professor Randall Law determined that he must write a book on the history of terrorism, he sought to satisfy a need not only for himself but for other professors and researchers who deal with the subject. According to Law, “When I started teaching a course on the subject shortly after September 11, 2001, I could not find a book for my students that told this story in a clear chronological fashion, that provided sufficient analytical framework, that made use of the most recent scholarly work, and that was comprehensive but succinct.” Law’s book does exactly what he intended

Going for the Trunk

Although angiogenesis (new blood vessel formation) is an absolute requirement for tumor growth, therapies designed to treat cancer by targeting specific angiogenic factors have had limited success. One theory is that there are many different angiogenic factors that can compensate for the loss of a single factor. Therefore, a more effective strategy may be to move upstream, identify a factor that regulates the expression of many different downstream angiogenic mediators, and then measure the effect of blocking this single common factor on angiogenesis-mediated tumor growth

Feasibility, Safety and Acceptability of Soy-Based Diet for Pregnant Women: Preliminary Results from a Pilot Randomized Controlled Trial

Background: Previous evidence suggests that soy containing foods may have beneficial effects on lipid and glycemic metabolism. Pregnancy is associated with a progressive deterioration in glucose and lipid metabolism, partially attributable to elevated estrogen concentrations. Little is known about the effects of soy intake on cardiometabolic risk factors in pregnant women. Methods: A pilot RCT was conducted in 30 pregnant women who were randomized to receive counseling to consume a high-soy or low-soy foods containing diet. Assessments (physical measurements, food frequency questionnaires, fasting blood samples) were conducted at 14 and 28 weeks of pregnancy, and 6 weeks’ postpartum. Monthly follow-up calls were conducted to assess safety and encourage adherence. Results: Both the high-soy and low-soy groups demonstrated high adherence (80-90%), defined as consuming soy foods ≥ 15 days in the past four weeks for high-soy group and ≤ 5 days for low-soy group. Five adverse events possibly associated with soy intake were reported (nausea, vomiting, diarrhea, itchy mouth); all were transient and resolved without sequelae. The high-soy group lost body fat between baseline and postpartum while the low-soy group gained body fat, as reflected by change in triceps skinfold thickness (-4.8 mm vs +3.6 mm, p=0.04). There was a trend towards an improvement in BMI in the high-soy group, both at 28 weeks (+1.4 vs. +3.6 kg/m2, p=0.15) and postpartum (-1.2 vs. +0.6 kg/m2, p=0.14). There were no differences between groups in fasting glucose, HDL-C, LDL-C, TG, or VLDL levels. Conclusion: Initial results from this pilot RCT support the acceptability and safety of consuming soy-based whole foods during pregnancy. A larger-scale RCT is needed to further elucidate the effects of soy diet on cardiometabolic risk among pregnant women

Labor-associated gene expression in the human uterine fundus, lower segment, and cervix

Background Preterm labor, failure to progress, and postpartum hemorrhage are the common causes of maternal and neonatal mortality or morbidity. All result from defects in the complex mechanisms controlling labor, which coordinate changes in the uterine fundus, lower segment, and cervix. We aimed to assess labor-associated gene expression profiles in these functionally distinct areas of the human uterus by using microarrays. Methods and Findings Samples of uterine fundus, lower segment, and cervix were obtained from patients at term (mean +/- 6 SD = 39.1 +/- 0.5 wk) prior to the onset of labor (n = 6), or in active phase of labor with spontaneous onset (n = 7). Expression of 12,626 genes was evaluated using microarrays ( Human Genome U95A; Affymetrix) and compared between labor and non-labor samples. Genes with the largest labor-associated change and the lowest variability in expression are likely to be fundamental for parturition, so gene expression was ranked accordingly. From 500 genes with the highest rank we identified genes with similar expression profiles using two independent clustering techniques. Sets of genes with a probability of chance grouping by both techniques less than 0.01 represented 71.2%, 81.8%, and 79.8% of the 500 genes in the fundus, lower segment, and cervix, respectively. We identified 14, 14, and 12 those sets of genes in the fundus, lower segment, and cervix, respectively. This enabled networks of coregulated and co-expressed genes to be discovered. Many genes within the same cluster shared similar functions or had functions pertinent to the process of labor. Conclusions Our results provide support for many of the established processes of parturition and also describe novel-to-labor genes not previously associated with this process. The elucidation of these mechanisms likely to be fundamental for controlling labor is an important prerequisite to the development of effective treatments for major obstetric problems - including prematurity, with its long-term consequences to the health of mother and offspring

The Mechanisms by Which the Ketone Body D-β-Hydroxybutyrate May Improve the Multiple Cellular Pathologies of Parkinson's Disease

Parkinson's disease, a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, is strongly associated with the death of dopaminergic neurons in the brain's substantia nigra. Although dopamine replacement therapy temporarily helps patients manage their motor symptoms, this current standard of care fails to address the underlying network of pathologies that contribute to the persistent death of dopaminergic neurons. Thus, new treatment approaches are needed that address the underlying pathologies and, thereby, slow or halt the progression of the actual disease. D-β-hydroxybutyrate – a ketone body produced by the liver to support brain function during periods of starvation – may provide an option. Lifestyle interventions that induce endogenous D-β-hydroxybutyrate production, such as caloric restriction and ketogenic diets, are known to increase healthspan and lifespan in animal models and are used to treat neurological disorders. The efficacy of these ketosis-inducing interventions, along with the recent development of commercially available D-β-hydroxybutyrate-based nutritional supplements, should inspire interest in the possibility that D-β-hydroxybutyrate itself exerts neuroprotective effects. This review provides a molecular model to justify the further exploration of such a possibility. Herein, we explore the cellular mechanisms by which the ketone body, D-β-hydroxybutyrate, acting both as a metabolite and as a signaling molecule, could help to prevent the development, or slow the progression of, Parkinson's disease. Specifically, the metabolism of D-β-hydroxybutyrate may help neurons replenish their depleted ATP stores and protect neurons against oxidative damage. As a G-protein-coupled receptor ligand and histone deacetylase inhibitor, D-β-hydroxybutyrate may further protect neurons against energy deficit and oxidative stress, while also decreasing damaging neuroinflammation and death by apoptosis. Restricted to the available evidence, our model relies largely upon the interpretation of data from the separate literatures on the cellular effects of D-β-hydroxybutyrate and on the pathogenesis of Parkinson's disease. Future studies are needed to reveal whether D-β-hydroxybutyrate actually has the potential to serve as an adjunctive nutritional therapy for Parkinson's disease

Thyroid markers and body composition predict LDL-cholesterol change in lean healthy women on a ketogenic diet: experimental support for the lipid energy model

Introduction: There is a large heterogeneity in LDL-cholesterol change among individuals adopting ketogenic diets. Interestingly, lean metabolically healthy individuals seem to be particularly susceptible, with an inverse association between body mass index and LDL-cholesterol change. The lipid energy model proposes that, in lean healthy individuals, carbohydrate restriction upregulates systemic lipid trafficking to meet energy demands. To test if anthropometric and energy metabolism markers predict LDL-cholesterol change during carbohydrate restriction. Methods: Ten lean, healthy, premenopausal women who habitually consumed a ketogenic diet for ≥6 months were engaged in a three-phase crossover study consisting of continued nutritional ketosis, suppression of ketosis with carbohydrate reintroduction, and return to nutritional ketosis. Each phase lasted 21 days. The predictive performance of all available relevant variables was evaluated with the linear mixed-effects models. Results: All body composition metrics, free T3 and total T4, were significantly associated with LDL-cholesterol change. In an interaction model with BMI and free T3, both markers were significant independent and interacting predictors of LDL-cholesterol change. Neither saturated fat, HOMA-IR, leptin, adiponectin, TSH, nor rT3 was associated with LDL-cholesterol changes. Discussion: Among lean, healthy women undergoing carbohydrate restriction, body composition and energy metabolism markers are major drivers of LDL-cholesterol change, not saturated fat, consistent with the lipid energy model