252 results match your criteria: "Wellcome Centre for Molecular Parasitology[Affiliation]"

Class 1 myosins (Myo1s) were the first unconventional myosins identified and humans have eight known Myo1 isoforms. The Myo1 family is involved in the regulation of gene expression, cytoskeletal rearrangements, delivery of proteins to the cell surface, cell migration and spreading. Thus, the important role of Myo1s in different biological processes is evident.

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Background: Human African Trypanosomiasis (HAT) is a neglected tropical disease caused by infections due to Trypanosoma brucei subspecies. In addition to the well-established environmental and behavioural risks of becoming infected, there is evidence for a genetic component to the response to trypanosome infection. We undertook a candidate gene case-control study to investigate genetic associations further.

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Insect β-1,3-glucanases belong to Glycoside Hydrolase Family 16 (GHF16) and are involved in digestion of detritus and plant hemicellulose. In this work, we investigated the role of GHF16 genes in larvae, due to their detritivore diet. genome has six genes belonging to GHF16 (Aae GH16.

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This work reports the biological evaluation of a copper complex of the type [Cu(O-O)(N-N)ClO], in which O-O = 4,4,4-trifluoro-1-phenyl-1,3-butanedione (Hbta) and N-N = 1,10-phenanthroline (phen), whose generic name is CBP-01. The cytotoxic effect of CBP-01 was evaluated by resazurin assay and cell proliferation was determined by MTT assay. DNA fragmentation was analyzed by gel electrophoresis.

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Parasite specific 7SL-derived small RNA is an effective target for diagnosis of active trypanosomiasis infection.

PLoS Negl Trop Dis

February 2019

The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, United Kingdom.

Human and animal African trypanosomiasis (HAT & AAT, respectively) remain a significant health and economic issue across much of sub-Saharan Africa. Effective control of AAT and potential eradication of HAT requires affordable, sensitive and specific diagnostic tests that can be used in the field. Small RNAs in the blood or serum are attractive disease biomarkers due to their stability, accessibility and available technologies for detection.

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A Macrophage-Pericyte Axis Directs Tissue Restoration via Amphiregulin-Induced Transforming Growth Factor Beta Activation.

Immunity

March 2019

Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK. Electronic address:

The epidermal growth factor receptor ligand Amphiregulin has a well-documented role in the restoration of tissue homeostasis after injury; however, the mechanism by which Amphiregulin contributes to wound repair remains unknown. Here we show that Amphiregulin functioned by releasing bioactive transforming growth factor beta (TGF-β) from latent complexes via integrin-α activation. Using acute injury models in two different tissues, we found that by inducing TGF-β activation on mesenchymal stromal cells (pericytes), Amphiregulin induced their differentiation into myofibroblasts, thereby selectively contributing to the restoration of vascular barrier function within injured tissue.

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Article Synopsis
  • * Researchers studied sand flies infected with a genetically modified parasite that expresses green fluorescent protein (GFP), allowing for the visualization of infection without harming the flies, using specialized microscopy techniques.
  • * The experiments revealed that while infected flies showed localized fluorescence indicating higher parasite populations in certain areas, non-infected flies had better survival rates, demonstrating a potential model for future research into sand fly infections and parasite transmission.
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Animal models have for long been pivotal for parasitology research. Over the last few years, techniques such as intravital, optoacoustic and magnetic resonance imaging, optical projection tomography, and selective plane illumination microscopy developed promising potential for gaining insights into host-pathogen interactions by allowing different visualization forms in vivo and ex vivo. Advances including increased resolution, penetration depth, and acquisition speed, together with more complex image analysis methods, facilitate tackling biological problems previously impossible to study and/or quantify.

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Genomic instability at the locus of sterol C24-methyltransferase promotes amphotericin B resistance in Leishmania parasites.

PLoS Negl Trop Dis

February 2019

Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity & Inflammation, University of Glasgow, Glasgow, United Kingdom.

Amphotericin B is an increasingly important tool in efforts to reduce the global disease burden posed by Leishmania parasites. With few other chemotherapeutic options available for the treatment of leishmaniasis, the potential for emergent resistance to this drug is a considerable threat. Here we characterised four novel amphotericin B-resistant Leishmania mexicana lines.

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Ever since the first known written report of schistosomiasis in the mid-19th century, researchers have aimed to increase knowledge of the parasites, their hosts, and the mechanisms contributing to infection and disease. This knowledge generation has been paramount for the development of improved intervention strategies. Yet, despite a broad knowledge base of direct risk factors for schistosomiasis, there remains a paucity of information related to more complex, interconnected, and often hidden drivers of transmission that hamper intervention successes and sustainability.

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Single-celled protists use elaborate cytoskeletal structures, including arrays of microtubules at the cell periphery, to maintain polarity and rigidity. The obligate intracellular parasite Toxoplasma gondii has unusually stable cortical microtubules beneath the alveoli, a network of flattened membrane vesicles that subtends the plasmalemma. However, anchoring of microtubules along alveolar membranes is not understood.

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Resolving the apparent transmission paradox of African sleeping sickness.

PLoS Biol

January 2019

Wellcome Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, United Kingdom.

Article Synopsis
  • Human African trypanosomiasis (HAT), or African sleeping sickness, is a deadly disease primarily found in sub-Saharan Africa, showing signs of potential elimination but historically at risk of reemergence.
  • Research indicates that asymptomatic infections may act as a hidden source for transmission due to skin-dwelling parasites, challenging previous assumptions about disease spread.
  • The study calls for a reevaluation of current treatment policies, suggesting that asymptomatic cases are significant enough to sustain transmission and should not be ignored.
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Hypoxia by Altitude and Welfare of Captive Beaded Lizards () in Mexico: Hematological Approaches.

J Appl Anim Welf Sci

June 2020

Facultad de Medicina Veterinaria y Zootecnia, Universidad Autónoma del Estado de México, Toluca, México.

 is one of the few known venomous lizards in the world. Their populations are in decline due to habitat destruction and capture for the pet trade. In México, many zoos have decided to take care of this species, most of them at altitudes greater than the natural altitudinal distribution.

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Sequestration of -infected erythrocytes (IE) within the brain microvasculature is a hallmark of cerebral malaria (CM). Using a microchannel flow adhesion assay with TNF-activated primary human microvascular endothelial cells, we demonstrate that IE isolated from Malawian paediatric CM cases showed increased binding to brain microvascular endothelial cells compared to IE from uncomplicated malaria (UM) cases. Further, UM isolates showed significantly greater adhesion to dermal than to brain microvascular endothelial cells.

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Gluconeogenesis using glycerol as a substrate in bloodstream-form Trypanosoma brucei.

PLoS Pathog

December 2018

The Wellcome Centre for Anti-Infectives Research, School of Life Sciences, University of Dundee, Dow Street, Dundee, United Kingdom.

Bloodstream form African trypanosomes are thought to rely exclusively upon glycolysis, using glucose as a substrate, for ATP production. Indeed, the pathway has long been considered a potential therapeutic target to tackle the devastating and neglected tropical diseases caused by these parasites. However, plasma membrane glucose and glycerol transporters are both expressed by trypanosomes and these parasites can infiltrate tissues that contain glycerol.

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A Major Step towards Defining the Elusive Stumpy Inducing Factor in Trypanosoma brucei.

Trends Parasitol

January 2019

Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK; Department of Immunology and Infectious Disease, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address:

Trypanosoma brucei stumpy forms are the only stage that can transmit from human to tsetse fly. Stumpy formation is regulated by a quorum sensing mechanism that depends on parasite density and an unknown stumpy induction factor (SIF). Recently, an elegant study by Matthews and colleagues (Cell 176, 1-12) has identified several crucial components of this pathway, including the putative SIF and its receptor.

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Ribonuclease H1-targeted R-loops in surface antigen gene expression sites can direct trypanosome immune evasion.

PLoS Genet

December 2018

The Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.

Article Synopsis
  • Switching the Variant Surface Glycoprotein (VSG) is a key strategy used by Trypanosoma brucei to evade the host's immune response, facilitated by transcription and recombination processes within specialized expression sites.
  • The study identifies that RNA-DNA hybrids, known as R-loops, form in the actively expressed VSG site and can also spread to inactive sites when the enzyme RNase H1, which typically degrades these hybrids, is absent.
  • The absence of RNase H1 not only increases VSG switching but also causes genome damage, suggesting that the structure of VSG expression sites plays a crucial role in both immune evasion and the formation of R-loops.
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Effects of host-derived chemokines on the motility and viability of Trypanosoma brucei.

Parasite Immunol

February 2019

The Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, UK.

African trypanosomes (Trypanosoma brucei spp.) are extracellular, hemoflagellate, protozoan parasites. Mammalian infection begins when the tsetse fly vector injects trypanosomes into the skin during blood feeding.

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Background: The sand fly Lutzomyia longipalpis is the main vector of American visceral leishmaniasis, a disease caused by parasites of the genus Leishmania. Adults of this insect feed on blood (females only) or sugar from plant sources, but their digestion of carbohydrates is poorly studied. Beta-glycosides as esculin and amygdalin are plant compounds and release toxic compounds as esculetin and mandelonitrile when hydrolyzed.

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The DNA damage response is developmentally regulated in the African trypanosome.

DNA Repair (Amst)

January 2019

The Wellcome Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, University of Glasgow, Sir Graeme Davies Building, 120 University Place, Glasgow, G12 8TA, UK. Electronic address:

Genomes are affected by a wide range of damage, which has resulted in the evolution of a number of widely conserved DNA repair pathways. Most of these repair reactions have been described in the African trypanosome Trypanosoma brucei, which is a genetically tractable eukaryotic microbe and important human and animal parasite, but little work has considered how the DNA damage response operates throughout the T. brucei life cycle.

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Helminths are extraordinarily successful parasites due to their ability to modulate the host immune response. They have evolved a spectrum of immunomodulatory molecules that are now beginning to be defined, heralding a molecular revolution in parasite immunology. These discoveries have the potential both to transform our understanding of parasite adaptation to the host and to develop possible therapies for immune-mediated disease.

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Evaluation of mechanisms that may generate DNA lesions triggering antigenic variation in African trypanosomes.

PLoS Pathog

November 2018

The Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.

Article Synopsis
  • Antigenic variation through VSG coat switching is a complex immune evasion technique used by African trypanosomes to escape host defenses, primarily mediated by changes in transcription of VSG genes.
  • The process of VSG switching mainly involves DNA recombination at the bloodstream VSG expression site, which is influenced by mechanisms like homologous recombination triggered by DNA breaks.
  • Research is ongoing to identify the sources of these DNA breaks, including factors like nucleases, repetitive DNA, and transcriptional activity, indicating that understanding these mechanisms could lead to new treatments against trypanosomiasis.
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Leishmania species are protozoan parasites whose remarkably plastic genome limits the establishment of effective genetic manipulation and leishmaniasis treatment. The strategies used by Leishmania to maintain its genome while allowing variability are not fully understood. Here, we used DiCre-mediated conditional gene deletion to show that HUS1, a component of the 9-1-1 (RAD9-RAD1-HUS1) complex, is essential and is required for a G2/M checkpoint.

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Probing sexual commitment at the single-cell level.

Wellcome Open Res

October 2018

Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity & Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.

Malaria parasites go through major transitions during their complex life cycle, yet the underlying differentiation pathways remain obscure. Here we apply single cell transcriptomics to unravel the program inducing sexual differentiation in . Parasites have to make this essential life-cycle decision in preparation for human-to-mosquito transmission.

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