Sonocrystallisation of Lactose in an Aqueous System

Although research on sonocrystallisation of lactose has been reported in the literature (yield and crystal size), the effect of ultrasound variables on nucleation and growth rate of lactose have not been studied. In this study, lactose crystallisation with ultrasound was compared with mechanical agitation using the induction time method at 22 °C. Ultrasound had a significant effect in reducing induction times and narrowing the metastable zone width but had no effect on individual crystal growth rate or morphology. A rapid decrease in induction time was observed up to 0.46 Wg-1 power density. Sonication up to 3 min decreased the induction time, but no further reduction was observed beyond 3 min. It was not possible to generate the nucleation rates achieved by sonication using agitation alone. 1 min sonication at 0.46 Wg1 power density followed by continuous stirring was found to be the optimum under the experimental conditions tested

A novel form of recessive limb girdle muscular dystrophy with mental retardation and abnormal expression of alpha-dystroglycan

Cataloged from PDF version of article.The limb girdle muscular dystrophies are a heterogeneous group of conditions characterized by proximal muscle weakness and disease onset ranging from infancy to adulthood. We report here eight patients from seven unrelated families affected by a novel and relatively mild form of autosomal recessive limb girdle muscular dystrophy (LGMD2) with onset in the first decade of life and characterized by severe mental retardation but normal brain imaging. Immunocytochemical studies revealed a significant selective reduction of α-dystroglycan expression in the muscle biopsies. Linkage analysis excluded known loci for both limb girdle muscular dystrophy and congenital muscular dystrophies in the consanguineous families. We consider that this represents a novel form of muscular dystrophy with associated brain involvement. The biochemical studies suggest that it may belong to the growing number of muscular dystrophies with abnormal expression of α-dystroglycan. © 2003 Published by Elsevier B.V

Structure-based design and synthesis of antiparasitic pyrrolopyrimidines targeting pteridine reductase 1

The treatment of Human African Trypanosomiasis remains a major unmet health need in sub-Saharan Africa. Approaches involving new molecular targets are important and pteridine reductase 1 (PTR1), an enzyme that reduces dihydrobiopterin in Trypanosoma spp. has been identified as a candidate target and it has been shown previously that substituted pyrrolo[2,3-d]pyrimidines are inhibitors of PTR1 from T. brucei (J. Med. Chem. 2010, 53, 221-229). In this study, 61 new pyrrolo[2,3-d]pyrimidines have been prepared, designed with input from new crystal structures of 23 of these compounds complexed with PTR1, and evaluated in screens for enzyme inhibitory activity against PTR1 and in vitro antitrypanosomal activity. 8 compounds were sufficiently active in both screens to take forward to in vivo evaluation. Thus although evidence for trypanocidal activity in a stage I disease model in mice was obtained, the compounds were too toxic to mice for further development

Analysis of Various Polarization Asymmetries In The Inclusive b→sℓ+ℓ−b\to s \ell^+ \ell^- Decay In The Fourth-Generation Standard Model

In this study a systematical analysis of various polarization asymmetries in inclusive b \rar s \ell^+ \ell^- decay in the standard model (SM) with four generation of quarks is carried out. We found that the various asymmetries are sensitive to the new mixing and quark masses for both of the $\mu$ and $\tau$ channels. Sizeable deviations from the SM values are obtained. Hence, b \rar s \ell^+ \ell^- decay is a valuable tool for searching physics beyond the SM, especially in the indirect searches for the fourth-generation of quarks ($t', b')$.Comment: 19 Pages, 10 Figures, 3 Table

Lepton polarization asymmetry in radiative dileptonic B-meson decays in MSSM

In this paper we study the polarization asymmetries of the final state lepton in the radiative dileptonic decay of B meson (\bsllg) in the framework of Minimal Supersymmetric Standard Model (MSSM) and various other unified models within the framework of MSSM e.g. mSUGRA, SUGRA (where condition of universality of scalar masses is relaxed) etc. Lepton polarization, in addition of having a longitudinal component (\pl), can have two other components, \pt and \pn, lying in and perpendicular to the decay plane, which are proportional to \ml and hence are significant for final state being $\mu^+ ~ \mu^-$ or $\tau^+ \~\tau^-$. We analyse the dependence of these polarization asymmetries on the parameters of the various models.Comment: typos corrected to match with published versio

New Physics in b -> s mu+ mu-: CP-Conserving Observables

We perform a comprehensive study of the impact of new-physics operators with different Lorentz structures on decays involving the b -> s mu+ mu- transition. We examine the effects of new vector-axial vector (VA), scalar-pseudoscalar (SP) and tensor (T) interactions on the differential branching ratios and forward-backward asymmetries (A_{FB}'s) of Bsbar -> mu+ mu-, Bdbar -> Xs mu+ mu-, Bsbar -> mu+ mu- gamma, Bdbar -> Kbar mu+ mu-, and Bdbar -> K* mu+ mu-, taking the new-physics couplings to be real. In Bdbar -> K* mu+ mu-, we further explore the polarization fraction f_L, the angular asymmetry A_T^{(2)}, and the longitudinal-transverse asymmetry A_{LT}. We identify the Lorentz structures that would significantly impact these observables, providing analytical arguments in terms of the contributions from the individual operators and their interference terms. In particular, we show that while the new VA operators can significantly enhance most of the asymmetries beyond the Standard Model predictions, the SP and T operators can do this only for A_{FB} in Bdbar -> Kbar mu+ mu-.Comment: 54 pages, JHEP format, 45 figures (included). 5/6/2013: typos in K* mu mu angular coefficients corrected, typos in Eq. (D.12) corrected, added a missing term in I3LT in Eq. (D.16). Numerical analysis unchange

The integration of social concerns into electricity power planning : a combined delphi and AHP approach

The increasing acceptance of the principle of sustainable development has been a major driving force towards new approaches to energy planning. This is a complex process involving multiple and conflicting objectives, in which many agents were able to influence decisions. The integration of environmental, social and economic issues in decision making, although fundamental, is not an easy task, and tradeoffsmust be made. The increasing importance of social aspects adds additional complexity to the traditional models that must now deal with variables recognizably difficult to measure in a quantitative scale. This study explores the issue of the social impact, as a fundamental aspect of the electricity planning process, aiming to give a measurable interpretation of the expected social impact of future electricity scenarios. A structured methodology, based on a combination of the Analytic Hierarchy Process and Delphi process, is proposed. The methodology is applied for the social evaluation of future electricity scenarios in Portugal, resulting in the elicitation and assignment of average social impact values for these scenarios. The proposed tool offers guidance to decision makers and presents a clear path to explicitl

Comparing cortical signatures of atrophy between late-onset and autosomal dominant Alzheimer disease

Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. Since late-onset Alzheimer disease (LOAD) participants tend to have age-related comorbidities, the younger-onset age in autosomal dominant AD (ADAD) may provide a more idealized model of cortical thinning in AD. To test this, the goals of this study were to compare the degree of overlap between the ADAD and LOAD cortical thinning maps and to evaluate the ability of the ADAD cortical signature regions to predict early pathological changes in cognitively normal individuals. We defined and analyzed the LOAD cortical maps of cortical thickness in 588 participants from the Knight Alzheimer Disease Research Center (Knight ADRC) and the ADAD cortical maps in 269 participants from the Dominantly Inherited Alzheimer Network (DIAN) observational study. Both cohorts were divided into three groups: cognitively normal controls (nADRC = 381; nDIAN = 145), preclinical (nADRC = 153; nDIAN = 76), and cognitively impaired (nADRC = 54; nDIAN = 48). Both cohorts underwent clinical assessments, 3T MRI, and amyloid PET imaging with either 11C-Pittsburgh compound B or 18F-florbetapir. To generate cortical signature maps of cortical thickness, we performed a vertex-wise analysis between the cognitively normal controls and impaired groups within each cohort using six increasingly conservative statistical thresholds to determine significance. The optimal cortical map among the six statistical thresholds was determined from a receiver operating characteristic analysis testing the performance of each map in discriminating between the cognitively normal controls and preclinical groups. We then performed within-cohort and cross-cohort (e.g. ADAD maps evaluated in the Knight ADRC cohort) analyses to examine the sensitivity of the optimal cortical signature maps to the amyloid levels using only the cognitively normal individuals (cognitively normal controls and preclinical groups) in comparison to hippocampal volume. We found the optimal cortical signature maps were sensitive to early increases in amyloid for the asymptomatic individuals within their respective cohorts and were significant beyond the inclusion of hippocampus volume, but the cortical signature maps performed poorly when analyzing across cohorts. These results suggest the cortical signature maps are a useful MRI biomarker of early AD-related neurodegeneration in preclinical individuals and the pattern of decline differs between LOAD and ADAD.Fil: Dincer, Aylin. Washington University in St. Louis; Estados UnidosFil: Gordon, Brian A.. Washington University in St. Louis; Estados UnidosFil: Hari-Raj, Amrita. Ohio State University; Estados UnidosFil: Keefe, Sarah J.. Washington University in St. Louis; Estados UnidosFil: Flores, Shaney. Washington University in St. Louis; Estados UnidosFil: McKay, Nicole S.. Washington University in St. Louis; Estados UnidosFil: Paulick, Angela M.. Washington University in St. Louis; Estados UnidosFil: Shady Lewis, Kristine E.. University of Kentucky; Estados UnidosFil: Feldman, Rebecca L.. Washington University in St. Louis; Estados UnidosFil: Hornbeck, Russ C.. Washington University in St. Louis; Estados UnidosFil: Allegri, Ricardo Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia; ArgentinaFil: Ances, Beau M.. Washington University in St. Louis; Estados UnidosFil: Berman, Sarah B.. University of Pittsburgh; Estados UnidosFil: Brickman, Adam M.. Columbia University; Estados UnidosFil: Brooks, William S.. Neuroscience Research Australia; Australia. University of New South Wales; AustraliaFil: Cash, David M.. UCL Queen Square Institute of Neurology; Reino UnidoFil: Chhatwal, Jasmeer P.. Harvard Medical School; Estados UnidosFil: Farlow, Martin R.. Indiana University; Estados UnidosFil: Fougère, Christian la. German Center for Neurodegenerative Diseases; Alemania. University Hospital of Tübingen; AlemaniaFil: Fox, Nick C.. UCL Queen Square Institute of Neurology; Reino UnidoFil: Fulham, Michael J.. Royal Prince Alfred Hospital; Australia. University of Sydney; AustraliaFil: Jack, Clifford R.. Mayo Clinic; Estados UnidosFil: Joseph-Mathurin, Nelly. Washington University in St. Louis; Estados UnidosFil: Karch, Celeste M.. Washington University in St. Louis; Estados UnidosFil: Lee, Athene. University Brown; Estados UnidosFil: Levin, Johannes. German Center for Neurodegenerative Diseases; Alemania. Ludwig Maximilians Universitat; Alemania. Munich Cluster for Systems Neurology; AlemaniaFil: Masters, Colin L.. University of Melbourne; AustraliaFil: McDade, Eric M.. Washington University in St. Louis; Estados UnidosFil: Oh, Hwamee. University Brown; Estados UnidosFil: Perrin, Richard J.. Washington University in St. Louis; Estados Unido