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text of working memory training. Methodological considerations are discussed, and our findings are embedded to the cognitive aging literature, considering, for example, the cognitive reserve framework and the compensation vs. magnification account. The need for personalized cognitive prevention and intervention methods to counteract cognitive decline in the aging population is high and the potential enormous. Registration PROSPERO, ID CRD42019142750.Neurodegenerative diseases of the central nervous system (CNS) are characterized by progressive neuronal death and neurological dysfunction, leading to increased disability and a loss of cognitive or motor functions. Compound 9 chemical structure Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis have neurodegeneration as a primary feature. However, in other CNS diseases such as multiple sclerosis, stroke, traumatic brain injury, and spinal cord injury, neurodegeneration follows another insult, such as demyelination or ischaemia. Although there are different primary causes to these diseases, they all share a hallmark of neuroinflammation. Neuroinflammation can occur through the activation of resident immune cells such as microglia, cells of the innate and adaptive peripheral immune system, meningeal inflammation and autoantibodies directed toward components of the CNS. Despite chronic inflammation being pathogenic in these diseases, local inflammation after insult can also promote endogenous regenerative processes in the CNS, which are key to slowing disease progression. The normal aging process in the healthy brain is associated with a decline in physiological function, a steady increase in levels of neuroinflammation, brain shrinkage, and memory deficits. Likewise, aging is also a key contributor to the progression and exacerbation of neurodegenerative diseases. As there are associated co-morbidities within an aging population, pinpointing the precise relationship between aging and neurodegenerative disease progression can be a challenge. The CNS has historically been considered an isolated, "immune privileged" site, however, there is mounting evidence that adaptive immune cells are present in the CNS of both healthy individuals and diseased patients. Adaptive immune cells have also been implicated in both the degeneration and regeneration of the CNS. In this review, we will discuss the key role of the adaptive immune system in CNS degeneration and regeneration, with a focus on how aging influences this crosstalk.Bilateral macular hole is a rare secondary effect of tamoxifen, a condition which is probably underdiagnosed. We describe the case of a 63-year-old woman who had received low-dose treatment with tamoxifen for 10 years. She presented with a best-corrected visual acuity of 20/40 in both eyes and bilateral macular hole with posterior hyaloid attachment. No reflective deposits were observed. A 23-gauge pars plana vitrectomy with internal limiting membrane peeling and gas tamponade was performed in the right eye with no anatomical or functional improvement. The most accepted mechanism of macular hole related to tamoxifen is Müller cell toxicity with retinal tissue loss. Therefore, it seems that the standard procedure used in idiopathic macular hole is not the optimal choice, due to a different pathogenic mechanism.A 58-year-old Caucasian female presented to the retina service with a 2-week history of bilateral decrease in vision. She had stage 4 renal cell carcinoma with osseous metastasis and choroidal metastasis for which she has been treated with Nivolumab immunotherapy. Her exudative retinal detachments resolved after cessation of Nivolumab in association with subtenon steroids (STK) and intravitreal bevacizumab injections. To the best of our knowledge, this is the first report in the literature describing the resolution of Nivolumab-related exudative retinal detachment after early local therapy using STK injections (10 mg), bevacizumab intravitreal injections, and cessation of Nivolumab. We hope by sharing this report to provide new insight into the management of similar patients.We describe a case of Behçet's disease (BD) in a young child that presented with recurrent neuroretinitis and developed retinal lesions during follow-up. A 4.5-year-old girl presented with fever of 39.5°C, erythema nodosum in her legs, bilateral knee arthritis, and perineum aphthae. On ocular examination, visual acuity was 20/25 in both eyes. Right eye examination was normal and the left eye (LE) showed mild anterior and intermediate uveitis, normal optic disc, and a macular star appearance. Laboratory workup demonstrated elevated C-reactive protein levels, a normal abdominal ultrasound, and a normal colonoscopy. The patient was diagnosed with BD. One month post initial presentation, the patient presented with visual acuity of finger counting in the LE with significant anterior uveitis, mild intermediate uveitis, and recurrent neuroretinitis. Under treatment of IV methylprednisolone, oral betamethasone, infliximab, and colchicine, a complete systemic remission was noticed, and uveitis became quiescent. On last examination, 4.5 years post first presentation, visual acuity was 20/25 in both eyes and the LE demonstrated a remnant of a juxtafoveal retinal scar. To the best of our knowledge, this is the first case of neuroretinitis presenting as a manifestation of pediatric BD. Ophthalmologists should be aware of these unique manifestations of ocular BD.Our aim is to describe clinical and optical coherence tomographic features of acute paraneoplastic focal outer retinitis associated with optic neuropathy in a patient diagnosed with small cell lung carcinoma. Bilateral focal outer retinitis, bilateral optic disc oedema and vitritis were identified in a patient with progressive bilateral visual loss and ataxia. Spectral domain optical coherence tomography (SD-OCT) revealed various extents of granular hyperreflectivity and atrophy of the macular outer retinal layers. Serum and cerebrospinal fluid positivity for anti-CRMP5, anti-HU and anti-amphiphysin antibodies intensified the search for an underlying malignancy, and a small cell lung carcinoma (SCLC) was finally diagnosed. Local and oral steroids along with systemic chemotherapy and radiotherapy achieved cancer remission and partial recovery from the ophthalmic manifestations. Focal outer retinitis associated with optic disc oedema and antibody positivity facilitated the diagnosis of SCLC in a localized stage.

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