On the monodromy of the moduli space of Calabi-Yau threefolds coming from eight planes in P3\mathbb{P}^3

It is a fundamental problem in geometry to decide which moduli spaces of polarized algebraic varieties are embedded by their period maps as Zariski open subsets of locally Hermitian symmetric domains. In the present work we prove that the moduli space of Calabi-Yau threefolds coming from eight planes in $\mathbb{P}^3$ does {\em not} have this property. We show furthermore that the monodromy group of a good family is Zariski dense in the corresponding symplectic group. Moreover, we study a natural sublocus which we call hyperelliptic locus, over which the variation of Hodge structures is naturally isomorphic to wedge product of a variation of Hodge structures of weight one. It turns out the hyperelliptic locus does not extend to a Shimura subvariety of type III (Siegel space) within the moduli space. Besides general Hodge theory, representation theory and computational commutative algebra, one of the proofs depends on a new result on the tensor product decomposition of complex polarized variations of Hodge structures.Comment: 26 page

Cognitive decline heralds onset of symptomatic inherited prion disease

The clinical effectiveness of any disease-modifying treatment for prion disease, as for other neurodegenerative disorders, will depend on early treatment before damage to neural tissue is irrevocable. Thus, there is a need to identify markers that predict disease onset in healthy at-risk individuals. Whilst imaging and neurophysiological biomarkers have shown limited use in this regard, we recently reported progressive neurophysiological changes in individuals with the inherited prion disease mutation P102L. We have also previously demonstrated a signature pattern of fronto-parietal dysfunction in mild prion disease. Here we address whether these cognitive features anticipate the onset of symptoms in a unique sample of patients with inherited prion disease. In the cross-sectional analysis, we analysed the performance of patients at three time points in the course of disease onset: prior to symptoms (n = 27), onset of subjective symptoms without positive clinical findings (n = 8) and symptomatic with positive clinical findings (n = 24). In the longitudinal analysis, we analysed data from 24 patients who were presymptomatic at the time of recruitment and were followed up over a period of up to 17 years, of whom 16 remained healthy and eight converted to become symptomatic. In the cross-sectional analysis, the key finding was that, relative to a group of 25 healthy non-gene carrier controls, patients with subjective symptoms but without positive clinical findings were impaired on a smaller but similar set of tests (Trail Making Test part A, Stroop test, Performance IQ, gesture repetition, figure recall) to those previously found to be impaired in mild prion disease. In the longitudinal analysis, Trail Making Test parts A and B, Stroop test and Performance IQ scores significantly discriminated between patients who remained presymptomatic and those who converted, even before the converters reached criteria for formal diagnosis. Notably, performance on the Stroop test significantly discriminated between presymptomatic patients and converters before the onset of clinical symptoms [area under the curve = 0.83 (95% confidence interval, 0.62–1.00), P = 0.009]. Thus, we report here, for the first time, neuropsychological abnormalities in healthy patients prior to either symptom onset or clinical diagnosis of inherited prion disease. This constitutes an important component of an evolving profile of clinical and biomarker abnormalities in this crucial group for preventive medicine

Efficient computation of min and max sensor values in multihop networks

Consider a wireless sensor network (WSN) where a broadcast from a sensor node does not reach all sensor nodes in the network; such networks are often called multihop networks. Sensor nodes take sensor readings but individual sensor readings are not very important. It is important however to compute aggregated quantities of these sensor readings. The minimum and maximum of all sensor readings at an instant are often interesting because they indicate abnormal behavior, for example if the maximum temperature is very high then it may be that a fire has broken out. We propose an algorithm for computing the min or max of sensor readings in a multihop network. This algorithm has the particularly interesting property of having a time complexity that does not depend on the number of sensor nodes; only the network diameter and the range of the value domain of sensor readings matter

A randomized controlled trial of a physician-directed treatment program for low-income patients with high blood cholesterol: the Southeast Cholesterol Project

OBJECTIVE: To assess the effectiveness of a cholesterol-lowering intervention designed to facilitate the management of hypercholesterolemia by primary care clinicians. DESIGN: Randomized controlled trial, with randomization of clinician-patient groups. SETTING: Twenty-one community and rural health centers in North Carolina and Virginia. PARTICIPANTS: Primary care clinicians (n = 42, 71% physicians) and the patients they enrolled with high cholesterol (n = 372). Twenty-two clinicians were randomized to give the special intervention (184 patients) and 20 to give usual care (188 patients). Two thirds of participating patients were women, 40% were African American, and 11% were Native American. INTERVENTION: A 90-minute tutorial to train clinicians how to use a structured assessment and treatment program (Food for Heart Program) consisting of a brief dietary assessment and three 5- to 10-minute dietary counseling sessions given by the primary care clinician, referral to a local dietitian if the low-density lipoprotein cholesterol (LDL-C) remained elevated at 4-month follow-up, and a prompt for the clinician to consider lipid-lowering medication based on the LDL-C at 7-month follow-up. MAIN OUTCOME MEASURES: Changes in total and LDL cholesterol at 4-month follow-up and averaged over a 1-year follow-up period (4-, 7-, and 12-month follow-up). RESULTS: At 4-month follow-up, total cholesterol decreased 0.33 mmol/L (12.6 mg/dL) in the intervention group and 0.21 mmol/L (8.3 mg/dL) in the control group: the difference was 0.11 mmol/L (4.2 mg/dL) (90% confidence interval [CI], -0.02 to 0.24 mmol/L [-0.7 to 9.1 mg/dL]). The average reduction during the 1-year follow-up period was 0.09 mmol/L (3.6 mg/dL) greater in the intervention group (90% CI, -0.01 to 0.19 mmol/L [-0.3 to 7.5 mg/dL]). Eight percent of intervention patients were taking lipid-lowering medication at follow-up visits compared with 15% of control patients. In a subgroup analysis restricted to the 89% of returnees who were not taking lipid-lowering medication, the reduction in total cholesterol at 4-month follow-up was 0.14 mmol/L (5.5 mg/dL) greater in the intervention group (95% CI, 0.01 to 0.28 mmol/L [0.3 to 10.7 mg/dL]); averaged over 1 year, it was 0.14 mmol/L (5.3 mg/dL) greater (95% CI, 0.03 to 0.24 mmol/L [1.2 to 9.4 mg/dL]). Changes in LDL-C were similar. CONCLUSIONS: Total cholesterol and LDL-C decreased more in the intervention group than in the control group. Overall, the difference in lipid reduction between groups was modest and of borderline statistical significance; among participants who did not take lipid-lowering medication during follow-up, the difference in lipid reduction between groups was larger. We conclude that primary care clinicians can be trained to give a cholesterol-lowering intervention to low-income patients that results in modest, short-term reductions in total cholesterol and LDL-C