31 research outputs found

    Posterior mini-incision total hip arthroplasty controls the extent of post-operative formation of heterotopic ossification.

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    Heterotopic ossification (HO) is the formation of bone at extra-skeletal sites. Reported rates of HO after hip arthroplasty range from 8 to 90 %; however, it is only severe cases that cause problems clinically, such as joint stiffness. The effects of surgical-related controllable intra-operative risk factors for the formation of HO were investigated. Data examined included gender, age of patient, fat depth, length of operation, incision length, prosthetic fixation method, the use of pulsed lavage and canal brush, and component size and material. All cases were performed by the same surgeon using the posterior approach. A total of 510 cases of hip arthroplasty were included, with an overall rate of HO of 10.2 %. Longer-lasting operations resulted in higher grades of HO (p = 0.047). Incisions >10 cm resulted in more widespread HO formation (p = 0.021). No further correlations were seen between HO formation and fat depth, blood loss, instrumentation, fixation methods or prosthesis material. The mini-incision approach is comparable to the standard approach in the aetiology of HO formation, and whilst the rate of HO may not be controllable, a posterior mini-incision approach can limit its extent

    A viscous switch for liquid-liquid dewetting

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    The spontaneous dewetting of a liquid film from a solid surface occurs in many important processes, such as printing and microscale patterning. Experience suggests that dewetting occurs faster on surfaces of higher film repellency. Here, we show how, unexpectedly, a surrounding viscous phase can switch the overall dewetting speed so that films retract slower with increasing surface repellency. We present experiments and a hydrodynamic theory covering five decades of the viscosity ratio between the film and the surrounding phase. The timescale of dewetting is controlled by the geometry of the liquid-liquid interface close to the contact line and the viscosity ratio. At small viscosity ratio, dewetting is slower on low film-repellency surfaces due to a high dissipation at the edge of the receding film. This situation is reversed at high viscosity ratios, leading to a slower dewetting on high film-repellency surfaces due to the increased dissipation of the advancing surrounding phase

    Electrostatic control of dewetting dynamics

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    The stability of liquid films on surfaces are critically important in microscale patterning and the semiconductor industry. If the film is sufficiently thin it may spontaneously dewet from the surface. The timescale and rate of dewetting depend on the film repellency of the surface and the properties of the liquid. Therefore, control over the repellency requires modifying surface chemistry and liquid properties to obtain the desired rate of film retraction. Here, we report how the dynamics of a receding thin liquid stripe to a spherical cap droplet can be controlled by programming surface repellency through a non-contact electrostatic method. We observe excellent agreement between the expected scaling of the dynamics for a wide range of voltage-selected final contact angles. Our results provide a method of controlling the dynamics of dewetting with high precision and locality relevant to printing and directed templating

    Bubble control, levitation and manipulation using dielectrophoresis

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    Bubbles attached to surfaces are ubiquitous in nature and in industry. However, bubbles are problematic in important technologies, including causing damage to the operation of microfluidic devices and being parasitic during heat transfer processes, so considerable efforts have been made to develop mechanical and electrical methods to remove bubbles from surfaces. In this work liquid dielectrophoresis is used to force a captive air bubble to detach away from an inverted solid surface and, crucially, the detached bubble is then held stationary in place below the surface at a distance controlled by the voltage. In this “levitated” state the bubble is separated from the surface by liquid layer with a voltage-selected thickness at which the dielectrophoresis force exactly counterbalances the gravitational buoyancy force. The techniques described here provide exceptional command over repeatable cycles of bubble detachment, levitation, and re-attachment. A theoretical analysis is presented that explains the observed detachment-reattachment hysteresis in which bubble levitation is maintained with voltages an order of magnitude lower than those used to create detachment. Our precision surface bubble removal and control concepts are relevant to situations such as nucleate boiling and micro-gravity environments, and offer an approach towards "wall-less" bubble microfluidic devices

    Evidence for HIV-1 cure after CCR5Δ32/Δ32 allogeneic haemopoietic stem-cell transplantation 30 months post analytical treatment interruption: a case report

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    BACKGROUND: The London patient (participant 36 in the IciStem cohort) underwent allogeneic stem-cell transplantation with cells that did not express CCR5 (CCR5Δ32/Δ32); remission was reported at 18 months after analytical treatment interruption (ATI). Here, we present longer term data for this patient (up to 30 months after ATI), including sampling from diverse HIV-1 reservoir sites. METHODS: We used ultrasensitive viral load assays of plasma, semen, and cerebrospinal fluid (CSF) samples to detect HIV-1 RNA. In gut biopsy samples and lymph-node tissue, cell-copy number and total HIV-1 DNA levels were quantified in multiple replicates, using droplet digital PCR (ddPCR) and quantitative real-time PCR. We also analysed the presence of intact proviral DNA using multiplex ddPCR targeting the packaging signal (ψ) and envelope (env). We did intracellular cytokine staining to measure HIV-1-specific T-cell responses. We used low-sensitive and low-avidity antibody assays to measure the humoral response to HIV-1. We predicted the probability of rebound using a mathematical model and inference approach. FINDINGS: HIV-1 viral load in plasma remained undetectable in the London patient up to 30 months (last tested on March 4, 2020), using an assay with a detection limit of 1 copy per mL. The patient's CD4 count was 430 cells per μL (23·5% of total T cells) at 28 months. A very low-level positive signal for HIV-1 DNA was recorded in peripheral CD4 memory cells at 28 months. The viral load in semen was undetectable in both plasma (lower limit of detection [LLD] <12 copies per mL) and cells (LLD 10 copies per 106 cells) at 21 months. CSF was within normal parameters at 25 months, with HIV-1 RNA below the detection limit (LLD 1 copy per mL). HIV-1 DNA by ddPCR was negative in rectum, caecum, and sigmoid colon and terminal ileum tissue samples at 22 months. Lymph-node tissue from axilla was positive for the long-terminal repeat (33 copies per 106 cells) and env (26·1 copies per 106 cells), negative for ψ and integrase, and negative by the intact proviral DNA assay, at 27 months. HIV-1-specific CD4 and CD8 T-cell responses have remained absent at 27 months. Low-avidity Env antibodies have continued to decline. Mathematical modelling suggests that the probability of remission for life (cure) is 98% in the context of 80% donor chimerism in total HIV target cells and greater than 99% probability of remission for life with 90% donor chimerism. INTERPRETATION: The London patient has been in HIV-1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal tissue, or lymphoid tissue. Donor chimerism has been maintained at 99% in peripheral T cells. We propose that these findings represent HIV-1 cure. FUNDING: Wellcome Trust and amfAR (American Foundation for AIDS Research)

    Active wetting of epithelial tissues

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    Development, regeneration and cancer involve drastic transitions in tissue morphology. In analogy with the behavior of inert fluids, some of these transitions have been interpreted as wetting transitions. The validity and scope of this analogy are unclear, however, because the active cellular forces that drive tissue wetting have been neither measured nor theoretically accounted for. Here we show that the transition between 2D epithelial monolayers and 3D spheroidal aggregates can be understood as an active wetting transition whose physics differs fundamentally from that of passive wetting phenomena. By combining an active polar fluid model with measurements of physical forces as a function of tissue size, contractility, cell-cell and cell-substrate adhesion, and substrate stiffness, we show that the wetting transition results from the competition between traction forces and contractile intercellular stresses. This competition defines a new intrinsic lengthscale that gives rise to a critical size for the wetting transition in tissues, a striking feature that has no counterpart in classical wetting. Finally, we show that active shape fluctuations are dynamically amplified during tissue dewetting. Overall, we conclude that tissue spreading constitutes a prominent example of active wetting --- a novel physical scenario that may explain morphological transitions during tissue morphogenesis and tumor progression
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