Exclusive Lambda_b -> Lambda l^+ l^- decay in two Higgs doublet model

Rare Lambda_b -> Lambda l^+ l^- decay is investigated in framework of general two Higgs doublet model, in which a new source of CP violation exists (model III). The polarization parameter, CP asymmetry and decay width are calculated. It is shown that CP asymmetry is a very sensitive tool for establishing model III.Comment: 16 pages, 3 figures, LaTeX formatte

Global alterations to the choroid plexus blood-CSF barrier in amyotrophic lateral sclerosis

© 2020 The Author(s). The choroid plexus (CP) is a highly vascularized structure located in the ventricles that forms the blood-CSF barrier (BCSFB) and separates the blood from the cerebrospinal fluid (CSF). In addition to its role as a physical barrier, the CP functions in CSF secretion, transport of nutrients into the central nervous system (CNS) and a gated point of entry of circulating immune cells into the CNS. Aging and neurodegeneration have been reported to affect CP morphology and function and increase protein leakage from blood to the CSF. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease associated with both upper and lower motor neuron loss, as well as altered proteomic and metabolomic signatures in the CSF. The role of the BCSFB and the CP in ALS is unknown. Here we describe a transcriptomic and ultrastructural analysis of BCSFB and CP alterations in human postmortem tissues from ALS and non-neurologic disease controls. ALS-CP exhibited widespread disruptions in tight junctional components of the CP epithelial layer and vascular integrity. In addition, we detected loss of pericytes around ALS blood vessels, accompanied by activation of platelet aggregation markers vWF and Fibrinogen, reminiscent of vascular injury. To investigate the immune component of ALS-CP, we conducted a comprehensive analysis of cytokines and chemokine panels in CP lysates and found a significant down-regulation of M-CSF and V-CAM1 in ALS, as well as up-regulation of VEGF-A protein. This phenotype was accompanied by an infiltration of MERTK positive macrophages into the parenchyma of the ALS-CP when compared to controls. Taken together, we demonstrate widespread structural and functional disruptions of the BCSFB in human ALS increasing our understanding of the disease pathology and identifying potential new targets for ALS therapeutic development

Medicines adherence: Involving patients in decisions about prescribed medicines and supporting adherence

It is thought that between a third and a half of all medicines1 There are many causes of non-adherence but they fall into two overlapping categories: intentional and unintentional. Unintentional non-adherence occurs when the patient wants to follow the agreed treatment but is prevented from doing so by barriers that are beyond their control. Examples include poor recall or difficulties in understanding the instructions, problems with using the treatment, inability to pay for the treatment, or simply forgetting to take it. prescribed for long-term conditions are not taken as recommended. If the prescription is appropriate, then this may represent a loss to patients, the healthcare system and society. The costs are both personal and economic. Adherence presumes an agreement between prescriber and patient about the prescriber’s recommendations. Adherence to medicines is defined as the extent to which the patient’s action matches the agreed recommendations. Non-adherence may limit the benefits of medicines, resulting in lack of improvement, or deterioration, in health. The economic costs are not limited to wasted medicines but also include the knock-on costs arising from increased demands for healthcare if health deteriorates. Non-adherence should not be seen as the patient’s problem. It represents a fundamental limitation in the delivery of healthcare, often because of a failure to fully agree the prescription in the first place or to identify and provide the support that patients need later on. Addressing non-adherence is not about getting patients to take more medicines per se. Rather, it starts with an exploration of patients’ perspectives of medicines and the reasons why they may not want or are unable to use them. Healthcare professionals have a duty to help patients make informed decisions about treatment and use appropriately prescribed medicines to best effec

Higgs-photon associated production at eeˉe\bar{e} colliders

We present complete analytical expressions for the amplitudes of the process $e\bar{e}\rightarrow H\gamma$. The calculation is performed using nonlinear gauges, which significantly simplifies both the actual analytical calculation and the check of its gauge invariance. After comparing our results with a previous numerical calculation, we extend the range of Higgs masses and center of mass energies to those appropriate to LEP 200 and a future linear collider.Comment: To appear in PRD. 18 pages latex, uses REVTEX; 5 postscript figure

Outcome of carotid stent-assisted angioplasty versus open surgical repair of recurrent carotid stenosis

AbstractPurposeWe compared outcome and durability of carotid stent-assisted angioplasty (CAS) with open surgical repair (ie, repeat carotid endarterectomy [CEA]) to treat recurrent carotid stenosis (RCS).MethodsA retrospective review of anatomic and neurologic outcomes was carried out after 27 repeat CEA procedures (1993-2002) and 52 CAS procedures (1997-2002) performed to treat high-grade internal carotid artery (ICA) RCS after CEA. The incidence of intervention because of symptomatic RCS was similar (repeat CEA, 63%; CAS, 60%), but the interval from primary CEA to repeat intervention was greater (P < .05) in the repeat CEA group (83 ± 15 months) compared with the CAS group (50 ± 8 months). In the CAS group, 17 of 52 arteries (33%) were judged not to be surgical candidates because of surgically inaccessible high lesions (n = 8), medical comorbid conditions (n = 4), neck irradiation (n = 3), or previous surgery with cranial nerve deficit or stroke (n = 2). Three patients who underwent repeat CEA had lesions not appropriate for treatment with CAS.ResultsOverall 30-day morbidity was similar after CAS (12%; death due to ipsilateral intracranial hemorrhage, 1; nondisabling stroke, 1; reversible neurologic deficits or transient ischemic attack, 2; access site complication, 2) and repeat CEA (11%; no death; nondisabling stroke, 1; reversible cranial nerve injury, 1; cervical hematoma, 1). Combined stroke and death rate was 3.7% for repeat CEA and 5.7% for CAS (P > .1). All duplex ultrasound scans obtained within 3 months after CEA and CAS demonstrated patent ICA and velocity spectra of less than 50% stenosis. During follow-up, no repeat CEA (mean, 39 months) or CAS (mean, 26 months) repair demonstrated ICA occlusion, but two patients (8%) who underwent repeat CEA and 4 patients (8%) who underwent CAS required balloon or stent angioplasty because of 80% RCS. At last follow-up, no patient had ipsilateral stroke and all ICA remain patent. At duplex scanning, stenosis-free (<50% diameter reduction) ICA patency at 36 months was 75% after repeat CEA and 57% after CAS (P = .26, log-rank test).ConclusionsCarotid angioplasty for treatment of high-grade stenotic ICA after CEA resulted in similar anatomic and neurologic outcomes compared with open surgical repair. Most lesions are amenable to endovascular therapy, and CAS enabled treatment in patients judged not to be suitable surgical candidates. Duplex scanning surveillance after repeat CEA or CAS is recommended, because stenosis can recur after either secondary procedure

The Neutron Electric Dipole Moment and CP-violating Couplings in the Supersymmetric Standard Model without R-parity

We analyze the neutron electric dipole moment (EDM) in the Minimal Supersymmetric Model with explicit R-parity violating terms. The leading contribution to the EDM occurs at the 2-loop level and is dominated by the chromoelectric dipole moments of quarks, assuming there is no tree-level mixings between sleptons and Higgs bosons or between leptons and gauginos. Based on the experimental constraint on the neutron EDM, we set limits on the imaginary parts of complex couplings ${\lambda'}_{ijk}$ and ${\lambda}_{ijk}$ due to the virtual b-loop or tau-loop.Comment: final manuscript to appear in Phys. Rev. D, 15 pages, latex, 4 figures include

The CP asymmetry for B--> K^* l^+ l^- decay in the general two Higgs doublet model

We study CP asymmetry for the exclusive decay B --> K^* l^+ l^- in the two Higgs doublet model with three level flavor changing neutral currents (model III). We analyse the dependency of this quantity to the new phase coming from the complex Yukawa couplings in the theory and we find that there exist a considerable CP violation for the relevant process. Further, we see that the sign of the Wilson coefficient C_7^{eff} can be determined by fixing dilepton mass. Therefore, the future measurements of CP asymmetry for B --> K^* l^+ l^- decay will give a powerful information about the sign of Wilson coefficient C_{7}^{eff} and the new physics beyond the SM.Comment: 22 pages, 8 figure

Enhancing the top signal at Tevatron using Neural Nets

We show that Neural Nets can be useful for top analysis at Tevatron. The main features of $t\bar t$ and background events on a mixed sample are projected in a single output, which controls the efficiency and purity of the $t\bar t$ signal.Comment: 11 pages, 6 figures (not included and available from the authors), Latex, UB-ECM-PF 94/1

Mechanisms, models and biomarkers in amyotrophic lateral sclerosis

The last 30 years have seen a major advance in the understanding of the clinical and pathological heterogeneity of amyotrophic lateral sclerosis (ALS), and its overlap with frontotemporal dementia. Multiple, seemingly disparate biochemical pathways converge on a common clinical syndrome characterized by progressive loss of upper and lower motor neurons. Pathogenic themes in ALS include excitotoxicity, oxidative stress, mitochondrial dysfunction, neuroinflammation, altered energy metabolism, and most recently RNA mis-processing. The transgenic rodent, overexpressing mutant superoxide dismutase-1, is now only one of several models of ALS pathogenesis. The nematode, fruit fly and zebrafish all offer fresh insight, and the development of induced pluripotent stem cell-derived motor neurons holds promise for the screening of candidate therapeutics. The lack of useful biomarkers in ALS contributes to diagnostic delay, and the inability to stratify patients by prognosis may be an important factor in the failure of therapeutic trials. Biomarkers sensitive to disease activity might lessen reliance on clinical measures and survival as trial endpoints and reduce study length. Emerging proteomic markers of neuronal loss and glial activity in cerebrospinal fluid, a cortical signature derived from advanced structural and functional MRI, and the development of more sensitive measurements of lower motor neuron physiology are leading a new phase of biomarker-driven therapeutic discovery