Publications by authors named "Wolfs E"

Pathologic lesions of the orbitozygomaticomaxillary complex (OZMC) and caudal oral cavity can be a challenge in veterinary oromaxillofacial surgery. Neoplastic lesions that are in close proximity to or invading the orbit may result in significant loss of structural integrity after curative intent surgery. This in turn may alter the topography of the bulbous oculi (globe) with resultant enophthalmos, diplopia, and entropion.

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Objective: To describe an ultrasound-guided suprazygomatic approach to the trigeminal nerve block in cat cadavers.

Study Design: Prospective descriptive study.

Animals: Ten feline cadaver heads.

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Digital pathology has become increasingly popular for research and clinical applications. Using high-quality microscopes to produce Whole Slide Images of tumor tissue enables the discovery of insights into biological aspects invisible to the human eye. These are acquired through downstream analyses using spatial statistics and artificial intelligence.

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Wolfram syndrome (WS) is a rare childhood disease characterized by diabetes mellitus, diabetes insipidus, blindness, deafness, neurodegeneration and eventually early death, due to autosomal recessive mutations in the WFS1 (and WFS2) gene. While it is categorized as a neurodegenerative disease, it is increasingly becoming clear that other cell types besides neurons may be affected and contribute to the pathogenesis. MRI studies in patients and phenotyping studies in WS rodent models indicate white matter/myelin loss, implicating a role for oligodendroglia in WS-associated neurodegeneration.

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Inherited peripheral neuropathies (IPNs) are a group of diseases associated with mutations in various genes with fundamental roles in the development and function of peripheral nerves. Over the past 10 years, significant advances in identifying molecular disease mechanisms underlying axonal and myelin degeneration, acquired from cellular biology studies and transgenic fly and rodent models, have facilitated the development of promising treatment strategies. However, no clinical treatment has emerged to date.

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Article Synopsis
  • Charcot-Marie-Tooth disease type 1A (CMT1A) is caused by a duplication of the PMP22 gene on chromosome 17, leading to disrupted myelination in peripheral nerves.
  • Through studies on CMT1A mouse models and patient-derived stem cells, researchers found significant downregulation of cholesterol and lipid metabolism, as well as disturbances in plasma membrane components and cell signaling pathways.
  • Interventions that stimulate autophagy and lipolysis showed potential for rescuing the negative effects of PMP22 duplication, suggesting that targeting lipid metabolism could be a therapeutic strategy for CMT1A.
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Background: Dysregulation of the endo-lysosomal-autophagy pathway has been identified as a critical factor in the pathology of various demyelinating neurodegenerative diseases, including peripheral neuropathies. This pathway plays a crucial role in transporting newly synthesized myelin proteins to the plasma membrane in myelinating Schwann cells, making these cells susceptible to lysosome-related dysfunctions. Nevertheless, the specific impact of lysosomal dysfunction in Schwann cells and its contribution to neurodegeneration remain poorly understood.

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Objective: This study aims to report the surgical and medical management of generalized chronic maxillofacial infection with multiple intra- and extraoral draining tracts in a dog.

Case Summary: A 6 years-old, male neutered pit bull terrier dog underwent a staged procedure. First, a diagnostic work-up including hematologic and biochemical analysis, conventional computed tomography (CT) with contrast of the skull, and a rhinoscopic evaluation of the draining tracts was performed.

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Doxorubicin (DOX) is commonly used in cancer treatment but associated with cardiotoxicity. Pyridoxamine (PM), a vitamin B6 derivative, could be a cardioprotectant. This study investigated the effect of PM on DOX cardiotoxicity and DOX antitumor effectiveness.

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The use of doxorubicin (DOX) chemotherapy is restricted due to dose-dependent cardiotoxicity. Pyridoxamine (PM) is a vitamin B6 derivative with favorable effects on diverse cardiovascular diseases, suggesting a cardioprotective effect on DOX-induced cardiotoxicity. The cardioprotective nature of PM was investigated in a rat model of DOX-induced cardiotoxicity.

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Article Synopsis
  • Sphingosine-1-phosphate receptor (S1PR) modulators are used to treat multiple sclerosis (MS) by preventing lymphocyte movement from lymph nodes, reducing neuroinflammation, and showing potential in promoting remyelination.* -
  • The study focused on ponesimod, which selectively targets the S1P1 receptor in oligodendrocyte precursor cells (OPCs), hypothesizing that it enhances OPC differentiation to aid remyelination.* -
  • Results from a mouse model indicated that ponesimod improved visual response times, reversed memory deficits, and increased myelination and OPC differentiation, suggesting its efficacy in promoting remyelination in demyelination conditions.*
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Macrophages play major roles in the pathophysiology of various neurological disorders, being involved in seemingly opposing processes such as lesion progression and resolution. Yet, the molecular mechanisms that drive their harmful and benign effector functions remain poorly understood. Here, we demonstrate that extracellular vesicles (EVs) secreted by repair-associated macrophages (RAMs) enhance remyelination ex vivo and in vivo by promoting the differentiation of oligodendrocyte precursor cells (OPCs).

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Purpose: The accuracy of heart rate (HR) measured with a wrist-worn photoplethysmography (PPG) monitor is altered during rest-exercise and exercise-rest transitions, which questions the validity of postexercise HR-recovery (HRR) parameters estimated from this device.

Methods: Thirty participants (50% female) randomly performed two 13-minute sequences (3' rest, 5' submaximal-intensity exercise, and 5' passive recovery) on treadmill and bicycle ergometers. HR was measured concomitantly with a 10-lead electrocardiogram (ECG) and a wrist-worn PPG monitor (Polar Unite).

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Multiple sclerosis (MS) pathology features autoimmune-driven neuroinflammation, demyelination, and failed remyelination. Carnosine is a histidine-containing dipeptide (HCD) with pluripotent homeostatic properties that is able to improve outcomes in an animal MS model (EAE) when supplied exogenously. To uncover if endogenous carnosine is involved in, and protects against, MS-related neuroinflammation, demyelination or remyelination failure, we here studied the HCD-synthesizing enzyme carnosine synthase (CARNS1) in human MS lesions and two preclinical mouse MS models (EAE, cuprizone).

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Leukocyte- and Platelet-Rich Fibrin (L-PRF) is a second-generation platelet concentrate that is prepared directly from the patient's own blood. It is widely used in the field of regenerative medicine, and to better understand its clinical applicability we aimed to further explore the biological properties and effects of L-PRF on cells from the central and peripheral nervous system. To this end, L-PRF was prepared from healthy human donors, and confocal, transmission, and scanning electron microscopy as well as secretome analysis were performed on these clots.

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Type 1 Charcot-Marie-Tooth disease (CMT1) is the most common demyelinating peripheral neuropathy. Patients suffer from progressive muscle weakness and sensory problems. The underlying disease mechanisms of CMT1 are still unclear and no therapy is currently available, hence patients completely rely on supportive care.

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Purpose: The accuracy of heart rate measured with a wrist photoplethysmography monitor can be influenced by the tightening of the wristband, movement of arms, or kinetics of the signal (eg, steady-state exercise vs on- and off-transients). To test these hypotheses, photoplethysmographic and electrocardiographic (ECG) signals were compared.

Methods: Thirty participants (50% female) randomly performed two 13' sequences (3' rest, 5' submaximal-intensity exercise, and 5' passive recovery) on a motorized treadmill and a bicycle ergometer.

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A significant number of veterans experience irritability and aggression symptoms as a result of being exposed to extremely stressful and life-threatening situations. In addition to the well-established involvement of the brain's cortico-subcortical circuit in aggression-related behaviours, a role of the deep cerebellar nuclei (DCN) in reactive aggression has been suggested. In the present study, seed-based resting-state functional connectivity between the DCN and cortico-subcortical areas was explored in veterans with and without reactive aggression symptoms.

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Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by focal inflammatory lesions and prominent demyelination. Even though the currently available therapies are effective in treating the initial stages of disease, they are unable to halt or reverse disease progression into the chronic progressive stage. Thus far, no repair-inducing treatments are available for progressive MS patients.

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Failure of remyelination underlies the progressive nature of demyelinating diseases such as multiple sclerosis. Why endogenous repair mechanisms frequently fail in these disorders is poorly understood. However, there is now evidence indicating that this is related to an overly inflammatory microenvironment combined with the intrinsic inability of oligodendrocyte precursor cells (OPCs) to differentiate into mature myelinating cells.

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Treatment of craniomaxillofacial (CMF) trauma in dogs often requires a multidisciplinary approach and a thorough understanding of the CMF anatomical structures involved. This retrospective study aimed to utilize computed tomography (CT) studies of immature dogs evaluated for CMF trauma and to describe common fracture locations, treatment modalities, and complications, as well as the fracture healing outcomes. The medical records and CT studies of 94 dogs under 1 year of age over a 13-year period were evaluated.

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Foamy macrophages containing abundant intracellular myelin remnants are an important pathological hallmark of multiple sclerosis. Reducing the intracellular lipid burden in foamy macrophages is considered a promising therapeutic strategy to induce a phagocyte phenotype that promotes central nervous system repair. Recent research from our group showed that sustained intracellular accumulation of myelin-derived lipids skews these phagocytes toward a disease-promoting and more inflammatory phenotype.

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Several lines of evidence point towards the involvement of the cerebellum in reactive aggression. In addition to the posterior cerebellar hemisphere, the vermis has been suggested to play a prominent role in impulse regulation. In the present study, we set out to further examine the relationships between cerebellar grey matter volumes, aggression, and impulsivity in 201 healthy volunteers.

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Neuralgic amyotrophy is a common peripheral nerve disorder caused by autoimmune inflammation of the brachial plexus, clinically characterized by acute pain and weakness of the shoulder muscles, followed by motor impairment. Despite recovery of the peripheral nerves, patients often have residual motor dysfunction of the upper extremity, leading to persistent pain related to altered biomechanics of the shoulder region. Building on clinical signs that suggest a role for cerebral mechanisms in these residual complaints, here we show and characterize cerebral alterations following neuralgic amyotrophy.

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