Hydromechanics of low-Reynolds-number flow. Part 1. Rotation of axisymmetric prolate bodies

The present series of studies is concerned with low-Reynolds-number flow in general; the main objective is to develop an effective method of solution for arbitrary body shapes. In this first part, consideration is given to the viscous flow generated by pure rotation of an axisymmetric body having an arbitrary prolate form, the inertia forces being assumed to have a negligible effect on the flow. The method of solution explored here is based on a spatial distribution of singular torques, called rotlets, by which the rotational motion of a given body can be represented. Exact solutions are determined in closed form for a number of body shapes, including the dumbbell profile, elongated rods and some prolate forms. In the special case of prolate spheroids, the present exact solution agrees with that of Jeffery (1922), this being one of very few cases where previous exact solutions are available for comparison. The velocity field and the total torque are derived, and their salient features discussed for several representative and limiting cases. The moment coefficient C[sub]M = M/(8[pi][mu][omega sub 0]ab^2) (M being the torque of an axisymmetric body of length 2a and maximum radius b rotating at angular velocity [omega], about its axis in a fluid of viscosity [mu]) of various body shapes so far investigated is found to lie between 2/3 and 1, usually very near unity for not extremely slender bodies. For slender bodies, an asymptotic relationship is found between the nose curvature and the rotlet strength near the end of its axial distribution. It is also found that the theory, when applied to slender bodies, remains valid at higher Reynolds numbers than was originally intended, so long as they are small compared with the (large) aspect ratio of the body, before the inertia effects become significant

Kinematics of the swimming of Spiroplasma

\emph{Spiroplasma} swimming is studied with a simple model based on resistive-force theory. Specifically, we consider a bacterium shaped in the form of a helix that propagates traveling-wave distortions which flip the handedness of the helical cell body. We treat cell length, pitch angle, kink velocity, and distance between kinks as parameters and calculate the swimming velocity that arises due to the distortions. We find that, for a fixed pitch angle, scaling collapses the swimming velocity (and the swimming efficiency) to a universal curve that depends only on the ratio of the distance between kinks to the cell length. Simultaneously optimizing the swimming efficiency with respect to inter-kink length and pitch angle, we find that the optimal pitch angle is 35.5$^\circ$ and the optimal inter-kink length ratio is 0.338, values in good agreement with experimental observations.Comment: 4 pages, 5 figure

Floppy swimming: Viscous locomotion of actuated elastica

Actuating periodically an elastic filament in a viscous liquid generally breaks the constraints of Purcell's scallop theorem, resulting in the generation of a net propulsive force. This observation suggests a method to design simple swimming devices - which we call "elastic swimmers" - where the actuation mechanism is embedded in a solid body and the resulting swimmer is free to move. In this paper, we study theoretically the kinematics of elastic swimming. After discussing the basic physical picture of the phenomenon and the expected scaling relationships, we derive analytically the elastic swimming velocities in the limit of small actuation amplitude. The emphasis is on the coupling between the two unknowns of the problems - namely the shape of the elastic filament and the swimming kinematics - which have to be solved simultaneously. We then compute the performance of the resulting swimming device, and its dependance on geometry. The optimal actuation frequency and body shapes are derived and a discussion of filament shapes and internal torques is presented. Swimming using multiple elastic filaments is discussed, and simple strategies are presented which result in straight swimming trajectories. Finally, we compare the performance of elastic swimming with that of swimming microorganisms.Comment: 23 pages, 6 figure

Genetic Modulation of Rpd3 Expression Impairs Long-Term Courtship Memory in Drosophila

There is increasing evidence that regulation of local chromatin structure is a critical mechanism underlying the consolidation of long-term memory (LTM), however considerably less is understood about the specific mechanisms by which these epigenetic effects are mediated. Furthermore, the importance of histone acetylation in Drosophila memory has not been reported. The histone deacetylase (HDAC) Rpd3 is abundant in the adult fly brain, suggesting a post-mitotic function. Here, we investigated the role of Rpd3 in long-term courtship memory in Drosophila. We found that while modulation of Rpd3 levels predominantly in the adult mushroom body had no observed impact on immediate recall or one-hour memory, 24-hour LTM was severely impaired. Surprisingly, both overexpression as well as RNAi-mediated knockdown of Rpd3 resulted in impairment of long-term courtship memory, suggesting that the dose of Rpd3 is critical for normal LTM

Identification of Combinatorial Patterns of Post-Translational Modifications on Individual Histones in the Mouse Brain

Post-translational modifications (PTMs) of proteins are biochemical processes required for cellular functions and signalling that occur in every sub-cellular compartment. Multiple protein PTMs exist, and are established by specific enzymes that can act in basal conditions and upon cellular activity. In the nucleus, histone proteins are subjected to numerous PTMs that together form a histone code that contributes to regulate transcriptional activity and gene expression. Despite their importance however, histone PTMs have remained poorly characterised in most tissues, in particular the brain where they are thought to be required for complex functions such as learning and memory formation. Here, we report the comprehensive identification of histone PTMs, of their combinatorial patterns, and of the rules that govern these patterns in the adult mouse brain. Based on liquid chromatography, electron transfer, and collision-induced dissociation mass spectrometry, we generated a dataset containing a total of 10,646 peptides from H1, H2A, H2B, H3, H4, and variants in the adult brain. 1475 of these peptides carried one or more PTMs, including 141 unique sites and a total of 58 novel sites not described before. We observed that these PTMs are not only classical modifications such as serine/threonine (Ser/Thr) phosphorylation, lysine (Lys) acetylation, and Lys/arginine (Arg) methylation, but also include several atypical modifications such as Ser/Thr acetylation, and Lys butyrylation, crotonylation, and propionylation. Using synthetic peptides, we validated the presence of these atypical novel PTMs in the mouse brain. The application of data-mining algorithms further revealed that histone PTMs occur in specific combinations with different ratios. Overall, the present data newly identify a specific histone code in the mouse brain and reveal its level of complexity, suggesting its potential relevance for higher-order brain functions

Longitudinal Evaluation of an N-Ethyl-N-Nitrosourea-Created Murine Model with Normal Pressure Hydrocephalus

Normal-pressure hydrocephalus (NPH) is a neurodegenerative disorder that usually occurs late in adult life. Clinically, the cardinal features include gait disturbances, urinary incontinence, and cognitive decline.Herein we report the characterization of a novel mouse model of NPH (designated p23-ST1), created by N-ethyl-N-nitrosourea (ENU)-induced mutagenesis. The ventricular size in the brain was measured by 3-dimensional micro-magnetic resonance imaging (3D-MRI) and was found to be enlarged. Intracranial pressure was measured and was found to fall within a normal range. A histological assessment and tracer flow study revealed that the cerebral spinal fluid (CSF) pathway of p23-ST1 mice was normal without obstruction. Motor functions were assessed using a rotarod apparatus and a CatWalk gait automatic analyzer. Mutant mice showed poor rotarod performance and gait disturbances. Cognitive function was evaluated using auditory fear-conditioned responses with the mutant displaying both short- and long-term memory deficits. With an increase in urination frequency and volume, the mutant showed features of incontinence. Nissl substance staining and cell-type-specific markers were used to examine the brain pathology. These studies revealed concurrent glial activation and neuronal loss in the periventricular regions of mutant animals. In particular, chronically activated microglia were found in septal areas at a relatively young age, implying that microglial activation might contribute to the pathogenesis of NPH. These defects were transmitted in an autosomal dominant mode with reduced penetrance. Using a whole-genome scan employing 287 single-nucleotide polymorphic (SNP) markers and further refinement using six additional SNP markers and four microsatellite markers, the causative mutation was mapped to a 5.3-cM region on chromosome 4.Our results collectively demonstrate that the p23-ST1 mouse is a novel mouse model of human NPH. Clinical observations suggest that dysfunctions and alterations in the brains of patients with NPH might occur much earlier than the appearance of clinical signs. p23-ST1 mice provide a unique opportunity to characterize molecular changes and the pathogenic mechanism of NPH