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To report the electrophysiological and neuroimaging findings in a patient who developed visual loss after attempted suicide by hanging.
A 45-year-old male presented with bilateral visual loss and difficulty in walking following a suicide attempt by hanging six months ago. selleck compound He underwent a complete ophthalmologic examination, posterior segment optical coherence tomography (OCT), various electrophysiological tests and neuroimaging.
His bilateral best-corrected visual acuity was logMAR 1.08. Intraocular pressures and ocular examination were normal except for bilateral temporal disk pallor. Macular OCT showed bilateral ganglion cell layer-inner plexiform layer complex thinning. Electroretinogram showed reduced b/a wave amplitude ratio inall the dark- and light-adapted International Society for Clinical Electrophysiology of Vision protocols in both the eyes. Pattern-reversal visually evoked potential (VEP) showed delayed latency of the P100 component in both the eyes. Electrooculography showed a normal light peak-to-dark trough ratio in both the eyes. Magnetic resonance imaging (MRI) brain showed chronic infarct andgliosis in both the occipital lobes. MR angiography showed pruning of P4 segments of both the posterior cerebral artery. Perfusion imaging showed reduction of perfusion in both the parieto-occipital lobes.
Hanging survivors can develop visual loss after their recovery. The visual loss may be a result of simultaneous ischemic insult to the occipital lobe cortex, optic nerve and retina.
Hanging survivors can develop visual loss after their recovery. The visual loss may be a result of simultaneous ischemic insult to the occipital lobe cortex, optic nerve and retina.Paired associated stimulation (PAS) has been confirmed to play a role in motor recovery after stroke, but the underlying mechanism has not been fully elucidated. In this study, we employed a comprehensive battery of measurements, including behavioral test, electrophysiology and 1H-NMR approaches, to investigate the therapeutic effects of PAS in rat model of cerebral ischemia and its underlying mechanism. Rats were randomly divided into a transient middle cerebral artery occlusion group (tMCAO group), a tMCAO + PAS group (PAS group), and a sham group. PAS was applied over 7 consecutive days in PAS group. The behavioral function of rats was evaluated by modified Garcia Scores and Rota-rod test. Electrophysiological changes were measured by motor evoked potentials (MEP). Metabolic changes of ischemic penumbra were detected by 1H-NMR. After PAS intervention, the performances on Rota-rod test and Garcia test improved and the amplitude of MEP increased significantly. The gamma-aminobutyric acid (GABA) in penumbra cortex was decreased significantly, whereas the glutamate showed the opposite changes. The results suggested that post-stroke recovery promoted by PAS may be related to the metabolites alteration in ischemic penumbra and also regulate the excitability of motor cortex.Age-related declines in auditory temporal processing contribute to speech understanding difficulties of older adults. These temporal processing deficits have been established primarily among acoustic-hearing listeners, but the peripheral and central contributions are difficult to separate. This study recorded cortical auditory evoked potentials from younger to middle-aged ( less then 65 years) and older (≥ 65 years) cochlear-implant (CI) listeners to assess age-related changes in temporal processing, where cochlear processing is bypassed in this population. Aging effects were compared to age-matched normal-hearing (NH) listeners. Advancing age was associated with prolonged P2 latencies in both CI and NH listeners in response to a 1000-Hz tone or a syllable /da/, and with prolonged N1 latencies in CI listeners in response to the syllable. Advancing age was associated with larger N1 amplitudes in NH listeners. These age-related changes in latency and amplitude were independent of stimulus presentation rate. Further, CI listeners exhibited prolonged N1 and P2 latencies and smaller P2 amplitudes than NH listeners. Thus, aging appears to degrade some aspects of auditory temporal processing when peripheral-cochlear contributions are largely removed, suggesting that changes beyond the cochlea may contribute to age-related temporal processing deficits.The pros and cons of artificial intelligence in assisted reproductive technology are presented.
Lupus nephritis is one of the most common and severe systemic lupus erythematosus complications. However, the pathogenesis of lupus nephritis is still poorly understood. Increasing evidence has shown that microRNAs (miRNAs) are extensively involved in the pathophysiology of autoimmune diseases. NZBWF1 is the classical mouse model of lupus nephritis. The present study aimed to investigate the expression profiling of mRNA and miRNAs of NZBWF1 mice with lupus nephritis using microarray, and explored the potential molecular mechanism of miRNA.
miRNA and mRNA microarrays were performed to identify miRNA and mRNA expression changes between pre-diseased (8-week-old) NZBWF1 mice and diseased NZBWF1 mice with lupus nephritis (28-week-old). Quantitative polymerase chain reaction (qPCR) validated these results. The target of miRNA was confirmed through a dual-luciferase reporter and stimulated mesangial cells experiment.
The combined miRNA and mRNA analysis identified 43 differentially expressed miRNAs and 1796 differentially expressed mRNAs between pre-disease (8-week-old) (n = 4) and diseased (28-week-old) NZBWF1 mice. We found that miR-1968-5p was significantly decreased, and csf1 mRNA was significantly increased in lupus nephritis mouse and verified by RT-PCR. csf1 has been demonstrated to play important roles in SLE. Bioinformatics analysis predicted that the csf1 was a potential target gene of miR-1968-5p. A dual-luciferase reporter assay confirmed the target binding. In cell experiments, overexpression or knockdown of miR resulted in a decrease or increase of csf1 expression, respectively.
These resultssuggest that miR-1968-5p may be involved in the pathogenesis of lupus nephritis of NZBWF1 mice by targeting csf1.
These results suggest that miR-1968-5p may be involved in the pathogenesis of lupus nephritis of NZBWF1 mice by targeting csf1.
Homepage: https://www.selleckchem.com/products/baxdrostat.html
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