93 research outputs found
Relationship of Some Semen Characteristics of the Boar to Fecundity of the Sow
As the price-cost squeeze be comes more critical to the pork producer, every fact or which affects net profit must be critically weighed. The profit making potential of a swine herd increases directly with an increase in the number of live offspring produced per sow. The production of large litters is dependent on high fertility in both the sow and the boar. The fertility of boars will vary from complete sterility to high fertility . An actual breeding test is the only highly reliable method of those used to measure fertility level in the boar, but boars of complete sterility can usually be detected by semen testing. Since an actual breeding test is a very expensive method of determining the fertility level of a boar, it would be highly desirable to develop a rapid inexpensive method for determining the fertility level o f boars so that boars of low to moderate fertility could be eliminated from the herd be fore use. The purpose of this study was to determine the relationship between certain measures of semen quality in the boar and fecundity in the sow and to measure the variation among boars with respect to these measures of semen quality
Exploitation of lettuce waste flour to increase bread functionality: effect on physical, nutritional, sensory properties and on consumer response
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The Dependence of the Superconducting Transition Temperature of Organic Molecular Crystals on Intrinsically Non-Magnetic Disorder: a Signature of either Unconventional Superconductivity or Novel Local Magnetic Moment Formation
We give a theoretical analysis of published experimental studies of the
effects of impurities and disorder on the superconducting transition
temperature, T_c, of the organic molecular crystals kappa-ET_2X and beta-ET_2X
(where ET is bis(ethylenedithio)tetrathiafulvalene and X is an anion eg I_3).
The Abrikosov-Gorkov (AG) formula describes the suppression of T_c both by
magnetic impurities in singlet superconductors, including s-wave
superconductors and by non-magnetic impurities in a non-s-wave superconductor.
We show that various sources of disorder lead to the suppression of T_c as
described by the AG formula. This is confirmed by the excellent fit to the
data, the fact that these materials are in the clean limit and the excellent
agreement between the value of the interlayer hopping integral, t_perp,
calculated from this fit and the value of t_perp found from angular-dependant
magnetoresistance and quantum oscillation experiments. If the disorder is, as
seems most likely, non-magnetic then the pairing state cannot be s-wave. We
show that the cooling rate dependence of the magnetisation is inconsistent with
paramagnetic impurities. Triplet pairing is ruled out by several experiments.
If the disorder is non-magnetic then this implies that l>=2, in which case
Occam's razor suggests that d-wave pairing is realised. Given the proximity of
these materials to an antiferromagnetic Mott transition, it is possible that
the disorder leads to the formation of local magnetic moments via some novel
mechanism. Thus we conclude that either kappa-ET_2X and beta-ET_2X are d-wave
superconductors or else they display a novel mechanism for the formation of
localised moments. We suggest systematic experiments to differentiate between
these scenarios.Comment: 18 pages, 5 figure
Novel genetic loci associated with hippocampal volume
The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness
Risk profiles and one-year outcomes of patients with newly diagnosed atrial fibrillation in India: Insights from the GARFIELD-AF Registry.
BACKGROUND: The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) is an ongoing prospective noninterventional registry, which is providing important information on the baseline characteristics, treatment patterns, and 1-year outcomes in patients with newly diagnosed non-valvular atrial fibrillation (NVAF). This report describes data from Indian patients recruited in this registry. METHODS AND RESULTS: A total of 52,014 patients with newly diagnosed AF were enrolled globally; of these, 1388 patients were recruited from 26 sites within India (2012-2016). In India, the mean age was 65.8 years at diagnosis of NVAF. Hypertension was the most prevalent risk factor for AF, present in 68.5% of patients from India and in 76.3% of patients globally (P < 0.001). Diabetes and coronary artery disease (CAD) were prevalent in 36.2% and 28.1% of patients as compared with global prevalence of 22.2% and 21.6%, respectively (P < 0.001 for both). Antiplatelet therapy was the most common antithrombotic treatment in India. With increasing stroke risk, however, patients were more likely to receive oral anticoagulant therapy [mainly vitamin K antagonist (VKA)], but average international normalized ratio (INR) was lower among Indian patients [median INR value 1.6 (interquartile range {IQR}: 1.3-2.3) versus 2.3 (IQR 1.8-2.8) (P < 0.001)]. Compared with other countries, patients from India had markedly higher rates of all-cause mortality [7.68 per 100 person-years (95% confidence interval 6.32-9.35) vs 4.34 (4.16-4.53), P < 0.0001], while rates of stroke/systemic embolism and major bleeding were lower after 1 year of follow-up. CONCLUSION: Compared to previously published registries from India, the GARFIELD-AF registry describes clinical profiles and outcomes in Indian patients with AF of a different etiology. The registry data show that compared to the rest of the world, Indian AF patients are younger in age and have more diabetes and CAD. Patients with a higher stroke risk are more likely to receive anticoagulation therapy with VKA but are underdosed compared with the global average in the GARFIELD-AF. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01090362
Exploration of shared genetic architecture between subcortical brain volumes and anorexia nervosa
In MRI scans of patientswith anorexia nervosa (AN), reductions in brain volume are often apparent. However, it is unknownwhether such brain abnormalities are influenced by genetic determinants that partially overlap with those underlyingAN. Here, we used a battery of methods (LD score regression, genetic risk scores, sign test, SNP effect concordance analysis, and Mendelian randomization) to investigate the genetic covariation between subcortical brain volumes and risk for AN based on summary measures retrieved from genome-wide association studies of regional brain volumes (ENIGMA consortium, n = 13,170) and genetic risk for AN (PGC-ED consortium, n = 14,477). Genetic correlationsrangedfrom-0.10to0.23(allp > 0.05). Thereweresomesigns ofaninverseconcordance between greater thalamus volume and risk for AN (permuted p = 0.009, 95% CI: [ 0.005, 0.017]). A genetic variant in the vicinity of ZW10, a gene involved in cell division, and neurotransmitter and immune systemrelevant genes, in particularDRD2, was significantly associated with AN only after conditioning on its association with caudate volume (pFDR = 0.025). Another genetic variant linked to LRRC4C, important in axonal and synaptic development, reached significance after conditioning on hippocampal volume (pFDR = 0.021). In this comprehensive set of analyses and based on the largest available sample sizes to date, there was weak evidence for associations between risk for AN and risk for abnormal subcortical brain volumes at a global level (that is, common variant genetic architecture), but suggestive evidence for effects of single genetic markers. Highly powered multimodal brain-and disorder-related genome-wide studies are needed to further dissect the shared genetic influences on brain structure and risk for AN.Stress-related psychiatric disorders across the life spa
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Self-regulation within outbreak populations of feral house mice: a test of alternative models
1. Outbreaks of feral house mice, Mus domesticus, in Australia represent a fundamental failure of the behavioural control mechanisms of population density, as proposed in the hypothesis of self-regulation. 2. Mice have the potential to keep numbers in check via a suite of spacing behaviours; however, the self-regulation hypothesis implies that some social change occurs that permits the population to erupt. It also suggests that at different phases of an outbreak, distinct patterns of social activity are evident. 3. We compare predictions from two models encapsulating the self-regulation hypothesis as applied to feral house mice in south-eastern Australia. Each model may be distinguished by the timing of aggressiveness between mice that leads to a closed social system. We compare individual turnover, residency and territoriality in each sex and age cohort during the increase, peak and low phases of a population outbreak that peaked in 2001. 4. The activity of 438 mice was monitored via intensive mark-recapture trapping and an automated event recording system that detected the activity of 300 marked individuals at burrow entrances. 5. Our findings support the second model, which suggests that mice switch from an almost asocial structure at low densities to a territorial system as abundance increases. Adult females appear more likely than males or juveniles to make the significant social shift. The trigger for this change remains unclear and several alternative mechanisms are proposed
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