Myeloperoxidase (MOP) is present in monocyte and neutrophil lysosomes, catalyzing hydrogen peroxide and chloride ion conversion to hypochlorous acid. MOP seems to destroy pathogens during phagocytosis by neutrophils and is considered an important defense against innumerous bacteria. We present a patient who had MOP deficiency, who presented with a subacute form of paracoccidioidomycosis and later with peritoneal tuberculosis. MOP deficiency leads to the diminished destruction of phagocytized pathogens. This case gives important evidence of an association between MOP deficiency and increased susceptibility to infection by Paracoccidioides brasiliensis and Mycobacterium tuberculosis.
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http://dx.doi.org/10.1590/0037-8682-0462-2016 | DOI Listing |
BMC Oral Health
November 2024
Department of Orthodontics, Faculty of Dentistry, Mansoura University, Mansoura, Egypt.
Trial Design: Parallel.
Objectives: To assess the effect of mini-screw assisted rapid palatal expansion (MARPE) with/without micro-osteoperforation (MOP) on the airway and pain intensity in non-growing patients with maxillary transverse deficiency.
Method: Two equal groups of twenty-four individuals aged ≥ 19 years old with maxillary transverse deficit were randomly assigned.
Sci Rep
July 2024
Douglas Hospital Research Centre, Douglas Mental Health University Institute, 6875 LaSalle Boulevard, Montreal, QC, H4H 1R3, Canada.
Dysbindin-1, a protein encoded by the schizophrenia susceptibility gene DTNBP1, is reduced in the hippocampus of schizophrenia patients. It is expressed in various cellular populations of the brain and implicated in dopaminergic and glutamatergic transmission. To investigate the impact of reduced dysbindin-1 in excitatory cells on hippocampal-associated behaviors and synaptic transmission, we developed a conditional knockout mouse model with deletion of dysbindin-1 gene in CaMKIIα expressing cells.
View Article and Find Full Text PDFActa Neuropathol
June 2024
Centre for Research in Neuroscience, The BRAiN Program, The Research Institute of the McGill University Health Centre, Livingston Hall, Room L7-210, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada.
We show that redox active iron can induce a regulated form of non-apoptotic cell death and tissue damage called ferroptosis that can contribute to secondary damage and functional loss in the acute and chronic periods after spinal cord injury (SCI) in young, adult, female mice. Phagocytosis of red blood cells at sites of hemorrhage is the main source of iron derived from hemoglobin after SCI. Expression of hemeoxygenase-1 that induces release of iron from heme, is increased in spinal cord macrophages 7 days after injury.
View Article and Find Full Text PDFNat Med
June 2024
Diabetes Unit, Endocrine Division, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
Reduced insulin sensitivity (insulin resistance) is a hallmark of normal physiology in late pregnancy and also underlies gestational diabetes mellitus (GDM). We conducted transcriptomic profiling of 434 human placentas and identified a positive association between insulin-like growth factor binding protein 1 gene (IGFBP1) expression in the placenta and insulin sensitivity at ~26 weeks gestation. Circulating IGFBP1 protein levels rose over the course of pregnancy and declined postpartum, which, together with high gene expression levels in our placenta samples, suggests a placental or decidual source.
View Article and Find Full Text PDFMol Brain
April 2024
Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Synaptopodin (SP), an actin-associated protein found in telencephalic neurons, affects activity-dependant synaptic plasticity and dynamic changes of dendritic spines. While being required for long-term depression (LTD) mediated by metabotropic glutamate receptor (mGluR-LTD), little is known about its role in other forms of LTD induced by low frequency stimulation (LFS-LTD) or spike-timing dependent plasticity (STDP). Using electrophysiology in ex vivo hippocampal slices from SP-deficient mice (SPKO), we show that absence of SP is associated with a deficit of LTD at Sc-CA1 synapses induced by LFS-LTD and STDP.
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