Dynamics of individual Brownian rods in a microchannel flow

We study the orientational dynamics of heavy silica microrods flowing through a microfluidic channel. Comparing experiments and Brownian dynamics simulations we identify different particle orbits, in particular in-plane tumbling behavior, which cannot be explained by classical Jeffery theory, and we relate this behavior to the rotational diffusion of the rods. By constructing the full, three-dimensional, orientation distribution, we describe the rod trajectories and quantify the persistence of Jeffery orbits using temporal correlation functions of the Jeffery constant. We find that our colloidal rods lose memory of their initial configuration in about a second, corresponding to half a Jeffery period.Comment: 5 pages, 4 figure

Search for the Radiative Capture d+d->^4He+\gamma Reaction from the dd\mu Muonic Molecule State

A search for the muon catalyzed fusion reaction dd --> ^4He +\gamma in the dd\mu muonic molecule was performed using the experimental \mu CF installation TRITON and NaI(Tl) detectors for \gamma-quanta. The high pressure target filled with deuterium at temperatures from 85 K to 800 K was exposed to the negative muon beam of the JINR phasotron to detect \gamma-quanta with energy 23.8 MeV. The first experimental estimation for the yield of the radiative deuteron capture from the dd\mu state J=1 was obtained at the level n_{\gamma}\leq 2\times 10^{-5} per one fusion.Comment: 9 pages, 3 Postscript figures, submitted to Phys. At. Nuc

Herpes Simplex Virus 1 and Chlamydophila (Chlamydia) pneumoniae promote Ab 1-42 amyloid processing in murine astrocytes linking an infectious process to Alzheimer\u27s disease

Background: Several studies have suggested an infectious etiology for Alzheimer\u27s disease (AD). Previously, our laboratory identified Chlamydia pneumoniae (Cpn) from autopsied sporadic AD brains, as well as developed a BALB/c mouse model that demonstrated infection-induced amyloid plaques similar to those found in AD. Hypothesis: We propose that an additional pathogen such as herpes simplex virus type 1 (HSV1), also may be a contributing factor in toin the pathology seen in AD. HSV1, in addition to Cpn, may be triggering the abnormal cleavage of the beta amyloid precursor protein (bAPP) into Ab1-42 , thereby contributing to amyloid plaque formation. Our current study examines amyloid processing following infection of primary and C8-DIA murine astrocytes with Cpn and HSV1. Materials and Methods: Immunocytochemistry and western analysis was used to analyze the outcome of infection by these two pathogens. Results: Cpn infection resulted in an increase in cytoplasmic labeling of Ab 1-42 relative to uninfected cells, while increased nuclear labeling of Ab 1-42 was observed following HSV1 infection. Co-infections with Cpn and HSV1 resulted in amyloid labeling resembling that of HSV1 infection alone, though Ab 1-42 labeling appeared decreased specifically in Cpn-infected cells of the co-infected monolayers. Conclusions: These data suggest that infection of astrocytic cells by HSV1 and (Cpn) alter the processing of bAPP, thereby producing Ab1-42. Therefore, these studies, inaddition to the previous research reported by our laboratory, support an emerging linkage of the infectious processs to the neuropathology characteristic of Alzheimer\u27s disease.https://digitalcommons.pcom.edu/posters/1008/thumbnail.jp

Analysis of Chlamydia pneumoniae and AD-like Pathology in the Brains of BALB/c Mice Following Direct Intra-cranial Infection

Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder and the most common form of dementia. The pathology in the central nervous system (CNS) impairs memory and cognition, hindering the capabilities and the quality of life of the individual. This project continues studying the role of infection and Alzheimer’s disease, as previous studies in this laboratory have done, and contributes to the overall understanding of the possible causes of this disease. In this study, BALB/c mice were infected, via direct intracranial injection, with a respiratory isolate (AR-39) of Chlamydia pneumoniae. Their brains were analyzed at 7 and 14 days post-infection, via immunohistochemistry, for the presence of C. pneumoniae, amyloid deposits and activated glial cells. The goal of this project was to measure the location and degree of C. pneumoniae burden, amyloid deposition and glial cell activation in the CNS following direct intracranial injection and to compare this data with results obtained from previous studies in this laboratory. We hypothesized that C. pneumoniae antigen and activated inflammatory cells will be observed in the infected mouse brains following direct intracranial injection and Aβ deposition will be observed in areas where inflammation occurs. C. pneumoniae, amyloid deposits and activated glial cells were detected in the brains following direct intracranial infection with C. pneumoniae. In infected mice there was an approximate 3.5-fold increase of C. pneumoniae antigen burden compared to uninfected mice at day 7 and there was an approximate 5.5-fold increase of C. pneumoniae antigen burden compared to uninfected mice at day 14. The burden of C. pneumoniae antigen, in the infected mice, increased 1.009-fold (no change) from day 7 to day 14 post-infection. The amyloid burden in infected mice increased approximately 3-fold compared to uninfected mice at day 7 and increased greater than10-fold compared to uninfected mice at day 14. The burden of amyloid, in the infected mice, increased 7-fold from day 7 to 14. From 7 to 14 days post-infection the C. pneumoniae and amyloid deposits located near the injection site spread distally from this location to other regions of the brain. Global activation of glia was observed in the CNS of infected mice at both 7 and 14 days post-infection. This data confirms that C. pneumoniae is capable of establishing an infection in the CNS. Although deposits were observed, the lack of a substantial amount of amyloid deposits suggested that the generation of deposits may require longer than 14 days following C. pneumoniae infection. As early as 7 days post-infection, inflammation is observed in response to the presence of C. pneumoniae and/or soluble amyloid in the CNS and the contribution of both infection with C. pneumoniae and the presence of soluble amyloid elicit the inflammatory response that presumably precedes and contributes to amyloid depositionhttps://digitalcommons.pcom.edu/posters/1003/thumbnail.jp

Effect of Age and Vaccination on Extent and Spread of Chlamydia pneumoniae Infection in C57BL/6 Mice

BACKGROUND: Chlamydia pneumoniae is an obligate intracellular respiratory pathogen for humans. Infection by C. pneumoniae may be linked etiologically to extra-respiratory diseases of aging, especially atherosclerosis. We have previously shown that age promotes C. pneumoniae respiratory infection and extra-respiratory spread in BALB/c mice. FINDINGS: Aged C57BL/6 mice had a greater propensity to develop chronic and/or progressive respiratory infections following experimental intranasal infection by Chlamydia pneumoniae when compared to young counterparts. A heptavalent CTL epitope minigene (CpnCTL7) vaccine conferred equal protection in the lungs of both aged and young mice. This vaccine was partially effective in protecting against C. pneumoniae spread to the cardiovascular system of young mice, but failed to provide cardiovascular protection in aged animals. CONCLUSIONS: Our findings suggest that vaccine strategies that target the generation of a C. pneumoniae-specific CTL response can protect the respiratory system of both young and aged animals, but may not be adequate to prevent dissemination of C. pneumoniae to the cardiovascular system or control replication in those tissues in aged animals

Comparison of Chlamydia antigen and AD-like pathology in the brains of BALB/c mice following intranasal infection with Chlamydia muridarum or Chlamydia pneumoniae

Previous research indicates BALB/c mice inoculated with Chlamydia pneumoniae (Cpn) demonstrated AD-like pathology which suggests that this mouse model is valid for studying the pathogenesis implicated in Alzheimer’s disease (AD). Studies have demonstrated that Chlamydia trachomatis (Ctr) can disseminate from its primary site of infection and plays a major role in the induction of reactive arthritis. The objectives of this lab are: (1) to identify and localize Chlamydia antigens in the brains of BALB/c mice infected with C. muridarum and (2) to determine if infection with C. muridarum induces AD-like pathology comparable to Cpn. Using mouse adapted respiratory isolates of C. muridarum, we investigated whether C. muridarum disseminated from the respiratory tract to the brain. Mice were intranasally infected with plaqued C small Weiss (CSW) or plaqued mouse pneumonitis Weiss (MoPn Weiss). Brain tissue was isolated at 2 months post-infection. Serial sections from brains infected mice were analyzed for amyloid or Chlamydia antigens. Preliminary analysis of brain tissue demonstrated no detectable difference in C. muridarum antigen between mice receiving 1 x105 IFU and mice receiving 1 x101 IFU, whereas a small but detectable difference was identified in amyloid-specific labeling between these two experimental groups. In contrast, prominent Chlamydia-specific labeling was identified in the brains of Cpn-infected mice as well as substantial amyloid deposition at 2 months p.i.. These data suggest that, relative to Cpn AR-39 infection, C. muridarum infection is a weaker stimulus for inflammation, resulting in decreased amyloid deposition in the brains of BALB/c mice

Microbes and Alzheimer\u27s Disease

We are researchers and clinicians working on Alzheimer\u27s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept

The Spectrum of Goldstini and Modulini

When supersymmetry is broken in multiple sectors via independent dynamics, the theory furnishes a corresponding multiplicity of "goldstini" degrees of freedom which may play a substantial role in collider phenomenology and cosmology. In this paper, we explore the tree-level mass spectrum of goldstini arising from a general admixture of F-term, D-term, and almost no-scale supersymmetry breaking, employing non-linear superfields and a novel gauge fixing for supergravity discussed in a companion paper. In theories of F-term and D-term breaking, goldstini acquire a mass which is precisely twice the gravitino mass, while the inclusion of no-scale breaking renders one of these modes, the modulino, massless. We argue that the vanishing modulino mass can be explained in terms of an accidental and spontaneously broken "global" supersymmetry.Comment: 10 pages, 2 figures; v2: typo corrected, references updated; v3: version to appear in JHE