Rheology of the gel formed in the California Mastitis Test

The California Mastitis Test has previously been adapted for use in an inline, cow-side sensor and relies on the fact that the viscosity of the gel formed during the test is proportional to the somatic cell concentration. In this paper, the use of capillary and rotational viscometry was compared in light of the expected rheology of the gel formed during the test. It was found that the gel is non-Newtonian, but the initial phase of viscosity increase was not due to shear dependence, but rather due to the gelation reaction. The maximum apparent viscosity of the gel was shear dependent while the time it took to reach the maximum was not truly shear dependent, but was rather dependent on the degree of mixing during gelation. This was confirmed by introducing a delay time prior to viscosity measurement, in both capillary and rotational viscometry. It was found that by mixing the reagent and infected milk, then delaying viscosity measurement for 30 s, shortened the time it took to reach maximum viscosity by more than 60 s. The maximum apparent viscosity, however, was unaffected. It was found that capillary viscometry worked well to correlate relative viscosity with somatic cell count, but that it was sensitive to the reagent concentration. It can therefore be deduced that the rheology of the gel is complicated not only by it being non-Newtonian, but also by the strong dependence on test conditions. These make designing a successful sensor much more challenging

Unmet Needs in Dystonia:Genetics and Molecular Biology-How Many Dystonias?

Genetic findings of the past years have provided ample evidence for a substantial etiologic heterogeneity of dystonic syndromes. While an increasing number of genes are being identified for Mendelian forms of isolated and combined dystonias using classical genetic mapping and whole-exome sequencing techniques, their precise role in the molecular pathogenesis is still largely unknown. Also, the role of genetic risk factors in the etiology of sporadic dystonias is still enigmatic. Only the systematic ascertainment and precise clinical characterization of very large cohorts with dystonia, combined with systematic genetic studies, will be able to unravel the complex network of factors that determine disease risk and phenotypic expression

Huge decreases in the risk of breast cancer relapse over the last three decades

Introduction The aim of this study was to evaluate local and systemic breast cancer control by comparing the risk of relapse in breast cancer patients in 2003–2004 with that in 1972–1979 and in 1980–1986. Methods About 8,570 women diagnosed with invasive breast cancer in 2003–2004 were selected from the population-based Netherlands Cancer Registry and compared with 133 patients treated in 1972–1979 and 174 in 1980–1986. Five-year risk of relapse was calculated by the Kaplan–Meier method. Cox-proportional hazard models were applied to adjust for tumour size, nodal status and age at diagnosis. Results Patients diagnosed in 2003–2004 had smaller tumours and a less advanced nodal stage than patients diagnosed in 1972–1986. In 1972–1979, 1980–1986 and 2003–2004, treatment included mastectomy in 94%, 72% and 47%; postmastectomy radiotherapy in 75%, 70% and 30%; chemotherapy in 9%, 14% and 37% and hormonal therapy in 3%, 3% and 42% of patients, respectively. Five-year risk of locoregional and distant recurrence decreased from 37% and 34% to 15%, respectively. The 5-year risk of second primary breast cancer did not differ and was 1%, 4% and 2%, respectively. The improved relapse-free survival in patients diagnosed in 2003–2004 as compared with 1972–1979 hardly changed after adjustment (HR = 0.38, 95% CI = 0.28–0.52). Conclusion Over the last decades, local breast cancer therapies have become less rigorous, whereas systemic therapy use has increased. Simultaneously, the risk of breast cancer relapse has tremendously decreased. Future novel therapies may lead to such small additional decreases in relapse rates, while the long-term side effects in breast cancer survivors will increas

Randomized controlled trials are needed to close the evidence gap in the prevention of preterm birth

Pregnant women have been advised to avoid heavy lifting during pregnancy due to concerns of adverse pregnancy outcomes including premature delivery. To date there is no evidence on the effectiveness of advice in preventing preterm birth as found in a recent systematic search and appraisal of published literature. This letter employs the findings of the review to inform future studies

Specificity Enhancement in microRNA Target Prediction through Knowledge Discovery

Computer Systems, Imagery and Medi

On Negotiation as Concurrency Primitive

We introduce negotiations, a model of concurrency close to Petri nets, with multiparty negotiation as primitive. We study the problems of soundness of negotiations and of, given a negotiation with possibly many steps, computing a summary, i.e., an equivalent one-step negotiation. We provide a complete set of reduction rules for sound, acyclic, weakly deterministic negotiations and show that, for deterministic negotiations, the rules compute the summary in polynomial time

Pathogenetic Insights into Developmental Coordination Disorder Reveal Substantial Overlap with Movement Disorders

Developmental Coordination Disorder (DCD) is a neurodevelopmental condition characterized by non-progressive central motor impairments. Mild movement disorder features have been observed in DCD. Until now, the etiology of DCD has been unclear. Recent studies suggested a genetic substrate in some patients with DCD, but comprehensive knowledge about associated genes and underlying pathogenetic mechanisms is still lacking. In this study, we first identified genes described in the literature in patients with a diagnosis of DCD according to the official diagnostic criteria. Second, we exposed the underlying pathogenetic mechanisms of DCD, by investigating tissue- and temporal gene expression patterns and brain-specific biological mechanisms. Third, we explored putative shared pathogenetic mechanisms between DCD and frequent movement disorders with a known genetic component, including ataxia, chorea, dystonia, and myoclonus. We identified 12 genes associated with DCD in the literature, which are ubiquitously expressed in the central nervous system throughout brain development. These genes are involved in cellular processes, neural signaling, and nervous system development. There was a remarkable overlap (62%) in pathogenetic mechanisms between DCD-associated genes and genes linked with movement disorders. Our findings suggest that some patients might have a genetic etiology of DCD, which could be considered part of a pathogenetic movement disorder spectrum.</p

The pathogenetic basis for a disease continuum in early- and late-onset ataxia-dystonia supports a unified genetic diagnostic approach

INTRODUCTION: Genetically inherited ataxic disorders are classified by their age of disease presentation into early- and late-onset ataxia (EOA and LOA, presenting before or after the 25th year-of-life). In both disease groups, comorbid dystonia co-occurs frequently. Despite overlapping genes and pathogenetic features, EOA, LOA and dystonia are considered as different genetic entities with a separate diagnostic approach. This often leads to diagnostic delay. So far, the possibility of a disease continuum between EOA, LOA and mixed ataxia-dystonia has not been explored in silico. In the present study, we analyzed the pathogenetic mechanisms underlying EOA, LOA and mixed ataxia-dystonia.METHODS: We analyzed the association of 267 ataxia genes with comorbid dystonia and anatomical MRI lesions in literature. We compared anatomical damage, biological pathways, and temporal cerebellar gene expression between EOA, LOA and mixed ataxia-dystonia.RESULTS: The majority (≈65%) of ataxia genes were associated with comorbid dystonia in literature. Both EOA and LOA gene groups with comorbid dystonia were significantly associated with lesions in the cortico-basal-ganglia-pontocerebellar network. EOA, LOA and mixed ataxia-dystonia gene groups were enriched for biological pathways related to nervous system development, neural signaling and cellular processes. All genes revealed similar cerebellar gene expression levels before and after 25 years of age and during cerebellar development.CONCLUSION: In EOA, LOA and mixed ataxia-dystonia gene groups, our findings show similar anatomical damage, underlying biological pathways and temporal cerebellar gene expression patterns. These findings may suggest the existence of a disease continuum, supporting the diagnostic use of a unified genetic approach.</p