15 research outputs found

    Dural MALT lymphoma with disseminated disease

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    Central nervous system (CNS) lymphoma involving the dura mater is very rare and histologically is usually a subtype of non-Hodgkin's lymphoma (NHL) termed mucosa-associated lymphoid tissue (MALT) lymphoma. We present a case of a 46-year old woman with dural MALT lymphoma that was found to also involve a lacrimal gland, inguinal lymph nodes, and bone marrow. Magnetic resonance imaging of the brain showed an extra-axial enhancing mass approximately 6 cm in maximum diameter along the right frontotemporal convexity. Histopathology of the resected dural mass showed MALT lymphoma expressing CD20, CD52, CD19, and CD38. Molecular studies of the B-cell receptor heavy chain demonstrated monoclonality at the involved sites. The patient was treated with four cycles of fludarabine, mitoxantrone, and rituximab with complete remission. She had recurrence in the subcutaneous tissue of the back at 12 months but has remained free of intracranial disease for 31 months. A review of the literature reveals 57 cases of dural MALT lymphoma. Only 4 had extra-CNS involvement at presentation, and only 3 had local recurrence of the dural tumor. Because of the indolent behavior of this tumor, the intracranial portion can be treated conservatively after resection with or without chemotherapy. Deferral of brain radiation can be considered with close clinical and neuroimaging follow up

    A Stroke Transition of Care Intervention with Stroke Nurse Navigators and Early Stroke Clinic Follow-up Reduces Readmissions for Stroke at 12 Months

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    Background: One in four strokes occur in stroke victims, with hospital readmissions contributing to high-cost care. Transition of care programs have been successful in reducing hospital readmissions in other diseases, but the data on such programs for stroke are mixed. A transition of care program was implemented with the goal of reducing recurrent strokes and hospital readmissions. Methods: We implemented a transition of care program using nurse navigators and early outpatient follow-up with a vascular neurologist. Data were obtained on: Rate of recurrent stroke admissions within one-year, all-cause readmission within one-year, all-cause readmission within 30 days, initial follow-up scheduled within 7-10 days, compliance with follow up, and compliance rates with provision of two-day post-hospital discharge phone calls. Results: An improvement was seen in process measures reflecting adherence to the intervention across all 3 years. The rate of readmission for stroke at 12 months was 8.5%, 9.0%, 6.6%, and 4.2% for year 0, 1, 2, and 3, respectively, representing a 50% reduction from baseline year 0. All-cause readmission remained unchanged, at 38.9%, 42.6%, 36.6%, and 37.4% for year 0, 1, 2, and 3 respectively. Conclusions: Our nurse navigator led stroke transition intervention was associated with significant reduction in readmissions for stroke but did not impact all cause readmission at one year or 30 days. Our focus on Centers for Medicare/Medicaid intervention compliance has produced a sustainable program capable of now expanding to support other important patient needs

    A Stroke Transition Of Care Intervention With Stroke Nurse Navigator And Early Stroke Clinic Follow-up Reduces Readmissions For Stroke At 12 Months

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    Introduction: Stroke is a leading cause of disability in the United States, and one in four occur in people who have already had a stroke. Preventable hospital readmissions contribute to the high medical costs of stroke. Transition of care programs have been successful in reducing hospital readmissions in other diseases, but the data on such programs for stroke is mixed. A transition of care program was implemented at a large urban stroke center, utilizing interventions shown to be effective in the literature, with the goal of reducing recurrent strokes and hospital readmissions

    Survival of retinal ganglion cells after damage to the occipital lobe in humans is activity dependent

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    Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (four females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first two months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. There was a positive relation between ganglion cell complex (GCC) thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal GCC thinning six months later. These findings indicate that retinal ganglion cell survival after ischaemic damage to the geniculostriate pathway is activity dependent

    Survival of Retinal Ganglion Cells After Damage to the Occipital Lobe in Humans is Activity-Dependent

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    This dataset accompanies the following published paper: Schneider C., Prentiss E., Busza A., Matmati K., Matmati N., et. al. (2019). Survival of retinal ganglion cells after damage to the occipital lobe in humans is activity dependent. Proceedings of the Royal Society B: Biological Sciences, 286(1897) pp: 20182733. doi: 10.1098/rspb.2018.2733 Abstract:Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (4 females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first 2 months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. There was a positive relation between ganglion cell complex thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal ganglion cell complex thinning 6 months later. These findings indicate that retinal ganglion cell survival after ischemic damage to the geniculostriate pathway is activity-dependent.7/6/2020 - Sub-14_Ses-01 .events files updated with the correct information (they were empty before).</p

    The TLR and IL-1 signalling network at a glance

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    Toll-like receptors (TLRs) and the receptors for interleukin (IL)-1, IL-18 and IL-33 are required for defence against microbial pathogens but, if hyper-activated or not switched off efficiently, can cause tissue damage and inflammatory and autoimmune diseases. Understanding how the checks and balances in the system are integrated to fight infection without the network operating out of control will be crucial for the development of improved drugs to treat these diseases in the future. In this Cell Science at a Glance article and the accompanying poster, I provide a brief overview of how one of these intricate networks is controlled by the interplay of protein phosphorylation and protein ubiquitylation events, and the mechanisms in myeloid cells that restrict and terminate its activation to prevent inflammatory and autoimmune diseases. Finally, I suggest a few protein kinases that have been neglected as drug targets, but whose therapeutic potential should be explored in the light of recent advances in our understanding of their roles in the innate immune system
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