Dural MALT lymphoma with disseminated disease

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

The exceptionally high rate of spontaneous mutations in the polymerase delta proofreading exonuclease-deficient Saccharomyces cerevisiae strain starved for adenine

BACKGROUND: Mutagenesis induced in the yeast Saccharomyces cerevisiae by starvation for nutrilites is a well-documented phenomenon of an unknown mechanism. We have previously shown that the polymerase delta proofreading activity controls spontaneous mutagenesis in cells starved for histidine. To obtain further information, we compared the effect of adenine starvation on mutagenesis in wild-type cells and, in cells lacking the proofreading activity of polymerase delta (phenotype Exo(-), mutation pol3-01). RESULTS: Ade(+ )revertants accumulated at a very high rate on adenine-free plates so that their frequency on day 16 after plating was 1.5 × 10(-4 )for wild-type and 1.0 × 10(-2 )for the Exo(- )strain. In the Exo(- )strain, all revertants arising under adenine starvation are suppressors of the original mutation, most possessed additional nutritional requirements, and 50% of them were temperature sensitive. CONCLUSIONS: Adenine starvation is highly mutagenic in yeast. The deficiency in the polymerase delta proofreading activity in strains with the pol3-01 mutation leads to a further 66-fold increase of the rate of mutations. Our data suggest that adenine starvation induces genome-wide hyper-mutagenesis in the Exo(- )strain

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

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

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

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