Fault Models for Quantum Mechanical Switching Networks

The difference between faults and errors is that, unlike faults, errors can be corrected using control codes. In classical test and verification one develops a test set separating a correct circuit from a circuit containing any considered fault. Classical faults are modelled at the logical level by fault models that act on classical states. The stuck fault model, thought of as a lead connected to a power rail or to a ground, is most typically considered. A classical test set complete for the stuck fault model propagates both binary basis states, 0 and 1, through all nodes in a network and is known to detect many physical faults. A classical test set complete for the stuck fault model allows all circuit nodes to be completely tested and verifies the function of many gates. It is natural to ask if one may adapt any of the known classical methods to test quantum circuits. Of course, classical fault models do not capture all the logical failures found in quantum circuits. The first obstacle faced when using methods from classical test is developing a set of realistic quantum-logical fault models. Developing fault models to abstract the test problem away from the device level motivated our study. Several results are established. First, we describe typical modes of failure present in the physical design of quantum circuits. From this we develop fault models for quantum binary circuits that enable testing at the logical level. The application of these fault models is shown by adapting the classical test set generation technique known as constructing a fault table to generate quantum test sets. A test set developed using this method is shown to detect each of the considered faults.Comment: (almost) Forgotten rewrite from 200

Molecular motion in cell membranes: analytic study of fence-hindered random walks

A theoretical calculation is presented to describe the confined motion of transmembrane molecules in cell membranes. The study is analytic, based on Master equations for the probability of the molecules moving as random walkers, and leads to explicit usable solutions including expressions for the molecular mean square displacement and effective diffusion constants. One outcome is a detailed understanding of the dependence of the time variation of the mean square displacement on the initial placement of the molecule within the confined region. How to use the calculations is illustrated by extracting (confinement) compartment sizes from experimentally reported published observations from single particle tracking experiments on the diffusion of gold-tagged G-protein coupled mu-opioid receptors in the normal rat kidney cell membrane, and by further comparing the analytical results to observations on the diffusion of phospholipids, also in normal rat kidney cells.Comment: 10 pages, 5 figure

A Pipeline Program to Address the South African Crisis in Human Resources for Health

Background: The WHO Africa Region faces a shortage of health workers due to inadequate production of health workers and emigration of physicians and nurses to wealthier countries. South Africa and the United States share a history of discriminatory policies and practices resulting in groups that are under-represented amongst health professionals. One US response is the Area Health Education Centers Program (AHEC), a pipeline program to recruit members of under-represented groups into the health professions. Objectives: (1) Compare and contrast the United States’ AHEC model with that developed in South Africa by Stellenbosch University Faculty of Medicine and Health Sciences SA AHEC in partnership with Morehouse School of Medicine in the United States. (2) Describe a formative evaluation of the Stellenbosch AHEC Program. Methods: Four hundred students (grades 7–12) and 150 teachers participated in SA AHEC with the goal of preparing the students to better compete for university admission. Students received after-school tutoring, holiday schools, and counselling on study skills, health careers, and university entry. Educators received continuing professional education, classroom observation, and feedback. The program was evaluated through a series of interviews and focus groups involving AHEC staff, educators, and parents and caregivers. Results: Program strengths included educator training, collaboration, and increased student maturity, motivation, and academic success. Challenges included limited time with students, the location of some sites, and the educators’ need for more engagement with AHEC staff and schools. Quarterly workshops were conducted to address challenges. Over 50% of program alumni are currently enrolled in institutions of higher education. Students will be tracked to determine whether they are able to complete their health professions studies and return to the communities where they grew up, or to similar communities. Conclusions: With appropriate adaptation and attention to context, it might be possible to implement similar programmes in other African countries. The comparison of the United States and South African models suggested that more parent and teacher participation in an advisory capacity might help to avoid some challenges

KERUSAKAN TANAMAN PALA AKIBAT SERANGAN PENYAKIT BUSUK BUAH KERING DAN HAMA PENGGEREK BATANG PALA DI KECAMATAN LEIHITU KABUPATEN MALUKU TENGAH

Fungus Stigmina myristicae causes rot dried fruit disease and pest Batocera herculesstem borer on nutmeg plants are found in Central Maluku, Province Maluku as the cause of plant damage nutmeg. Surveys in the District Laitutu Maluku Central was conducted in August 2014 with the aim to determine the intensity of the large and spacious dried fruit rot disease and stem borer, and the greater the intensity of dried fruit rot disease on various strata in the nutmeg crop. The results showed that the intensity of dried fruit rot disease is more prevalent in the nutmeg in the middle and lower strata of plants reached 1.42% and 2.09%, and in general to be 1.24%, while the area of the attack reached 23.90%. The intensity of the attacks stem borer reaches 1.76% and spacious attacks reached 0.56%. These results indicate that the nutmeg crop damage by Stigmina myristicae and Batocera hercules classified low category.Keywork:Stigmina myristicae, Batocera hercules,Nutmeg, Stem borer, Dried fruit rot

Quantifying single nucleotide variant detection sensitivity in exome sequencing

BACKGROUND: The targeted capture and sequencing of genomic regions has rapidly demonstrated its utility in genetic studies. Inherent in this technology is considerable heterogeneity of target coverage and this is expected to systematically impact our sensitivity to detect genuine polymorphisms. To fully interpret the polymorphisms identified in a genetic study it is often essential to both detect polymorphisms and to understand where and with what probability real polymorphisms may have been missed. RESULTS: Using down-sampling of 30 deeply sequenced exomes and a set of gold-standard single nucleotide variant (SNV) genotype calls for each sample, we developed an empirical model relating the read depth at a polymorphic site to the probability of calling the correct genotype at that site. We find that measured sensitivity in SNV detection is substantially worse than that predicted from the naive expectation of sampling from a binomial. This calibrated model allows us to produce single nucleotide resolution SNV sensitivity estimates which can be merged to give summary sensitivity measures for any arbitrary partition of the target sequences (nucleotide, exon, gene, pathway, exome). These metrics are directly comparable between platforms and can be combined between samples to give “power estimates” for an entire study. We estimate a local read depth of 13X is required to detect the alleles and genotype of a heterozygous SNV 95% of the time, but only 3X for a homozygous SNV. At a mean on-target read depth of 20X, commonly used for rare disease exome sequencing studies, we predict 5–15% of heterozygous and 1–4% of homozygous SNVs in the targeted regions will be missed. CONCLUSIONS: Non-reference alleles in the heterozygote state have a high chance of being missed when commonly applied read coverage thresholds are used despite the widely held assumption that there is good polymorphism detection at these coverage levels. Such alleles are likely to be of functional importance in population based studies of rare diseases, somatic mutations in cancer and explaining the “missing heritability” of quantitative traits

The nonlinear time-dependent response of isotactic polypropylene

Tensile creep tests, tensile relaxation tests and a tensile test with a constant rate of strain are performed on injection-molded isotactic polypropylene at room temperature in the vicinity of the yield point. A constitutive model is derived for the time-dependent behavior of semi-crystalline polymers. A polymer is treated as an equivalent network of chains bridged by permanent junctions. The network is modelled as an ensemble of passive meso-regions (with affine nodes) and active meso-domains (where junctions slip with respect to their positions in the bulk medium with various rates). The distribution of activation energies for sliding in active meso-regions is described by a random energy model. Adjustable parameters in the stress--strain relations are found by fitting experimental data. It is demonstrated that the concentration of active meso-domains monotonically grows with strain, whereas the average potential energy for sliding of junctions and the standard deviation of activation energies suffer substantial drops at the yield point. With reference to the concept of dual population of crystalline lamellae, these changes in material parameters are attributed to transition from breakage of subsidiary (thin) lamellae in the sub-yield region to fragmentation of primary (thick) lamellae in the post-yield region of deformation.Comment: 29 pages, 12 figure

Role of estrogen related receptor beta (ESRRB) in DFN35B hearing impairment and dental decay

BACKGROUND: Congenital forms of hearing impairment can be caused by mutations in the estrogen related receptor beta (ESRRB) gene. Our initial linkage studies suggested the ESRRB locus is linked to high caries experience in humans. METHODS: We tested for association between the ESRRB locus and dental caries in 1,731 subjects, if ESRRB was expressed in whole saliva, if ESRRB was associated with the microhardness of the dental enamel, and if ESRRB was expressed during enamel development of mice. RESULTS: Two families with recessive ESRRB mutations and DFNB35 hearing impairment showed more extensive dental destruction by caries. Expression levels of ESRRB in whole saliva samples showed differences depending on sex and dental caries experience. CONCLUSIONS: The common etiology of dental caries and hearing impairment provides a venue to assist in the identification of individuals at risk to either condition and provides options for the development of new caries prevention strategies, if the associated ESRRB genetic variants are correlated with efficacy.Fil: Weber, Megan L.. University of Pittsburgh; Estados UnidosFil: Hsin, Hong Yuan. University of Pittsburgh; Estados UnidosFil: Kalay, Ersan. Karadeniz Technical University; TurquíaFil: Brožková, Dana Š. Charles University; República Checa. University Hospital Motol; República ChecaFil: Shimizu, Takehiko. Nihon University. School of Dentistry; JapónFil: Bayram, Merve. Medipol Istanbul University; TurquíaFil: Deeley, Kathleen. University of Pittsburgh; Estados UnidosFil: Küchler, Erika C.. University of Pittsburgh; Estados UnidosFil: Forella, Jessalyn. University of Pittsburgh; Estados UnidosFil: Ruff, Timothy D.. University of Pittsburgh; Estados UnidosFil: Trombetta, Vanessa M.. University of Pittsburgh; Estados UnidosFil: Sencak, Regina C.. University of Pittsburgh; Estados UnidosFil: Hummel, Michael. University of Pittsburgh; Estados UnidosFil: Briseño Ruiz, Jessica. University of Pittsburgh; Estados UnidosFil: Revu, Shankar K.. University of Pittsburgh; Estados UnidosFil: Granjeiro, José M.. Universidade Federal Fluminense; BrasilFil: Antunes, Leonardo S.. Universidade Federal Fluminense; BrasilFil: Antunes, Livia A.. Universidade Federal Fluminense; BrasilFil: Abreu, Fernanda V.. Universidade Federal Fluminense; BrasilFil: Costabel, Marcelo C.. Universidade Federal do Rio de Janeiro; BrasilFil: Tannure, Patricia N.. Veiga de Almeida University; Brasil. Salgado de Oliveira University; BrasilFil: Koruyucu, Mine. Istanbul University; TurquíaFil: Patir, Asli. Medipol Istanbul University; TurquíaFil: Poletta, Fernando Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mereb, Juan C.. Estudio Colaborativo Latino Americano de Malformaciones Congénitas; ArgentinaFil: Castilla, Eduardo Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Orioli, Iêda M.. Universidade Federal do Rio de Janeiro; BrasilFil: Marazita, Mary L.. University of Pittsburgh; Estados UnidosFil: Ouyang, Hongjiao. University of Pittsburgh; Estados UnidosFil: Jayaraman, Thottala. University of Pittsburgh; Estados UnidosFil: Seymen, Figen. Istanbul University; TurquíaFil: Vieira, Alexandre R.. University of Pittsburgh; Estados Unido

Identification of the first ATRIP-deficient patient and novel mutations in ATR define a clinical spectrum for ATR-ATRIP Seckel Syndrome

A homozygous mutational change in the Ataxia-Telangiectasia and RAD3 related (ATR) gene was previously reported in two related families displaying Seckel Syndrome (SS). Here, we provide the first identification of a Seckel Syndrome patient with mutations in ATRIP, the gene encoding ATR-Interacting Protein (ATRIP), the partner protein of ATR required for ATR stability and recruitment to the site of DNA damage. The patient has compound heterozygous mutations in ATRIP resulting in reduced ATRIP and ATR expression. A nonsense mutational change in one ATRIP allele results in a C-terminal truncated protein, which impairs ATR-ATRIP interaction; the other allele is abnormally spliced. We additionally describe two further unrelated patients native to the UK with the same novel, heterozygous mutations in ATR, which cause dramatically reduced ATR expression. All patient-derived cells showed defective DNA damage responses that can be attributed to impaired ATR-ATRIP function. Seckel Syndrome is characterised by microcephaly and growth delay, features also displayed by several related disorders including Majewski (microcephalic) osteodysplastic primordial dwarfism (MOPD) type II and Meier-Gorlin Syndrome (MGS). The identification of an ATRIP-deficient patient provides a novel genetic defect for Seckel Syndrome. Coupled with the identification of further ATR-deficient patients, our findings allow a spectrum of clinical features that can be ascribed to the ATR-ATRIP deficient sub-class of Seckel Syndrome. ATR-ATRIP patients are characterised by extremely severe microcephaly and growth delay, microtia (small ears), micrognathia (small and receding chin), and dental crowding. While aberrant bone development was mild in the original ATR-SS patient, some of the patients described here display skeletal abnormalities including, in one patient, small patellae, a feature characteristically observed in Meier-Gorlin Syndrome. Collectively, our analysis exposes an overlapping clinical manifestation between the disorders but allows an expanded spectrum of clinical features for ATR-ATRIP Seckel Syndrome to be define