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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
Severity: Warning
Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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Function: str_replace
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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In the present study, the effect of 6-((4-fluorophenyl) selanyl)-9H-purine (FSP) was tested against memory impairment and sensitivity to nociception induced by intracerebroventricular injection of amyloid-beta peptide (Aβ) (25-35 fragment), 3 nmol/3 μl/per site in mice. Memory impairment was determined by the object recognition task (ORT) and nociception by the Von-Frey test (VFT). Aβ caused neuroinflammation with upregulation of glial fibrillary acidic protein (GFAP) (in hippocampus), nuclear factor-κB (NF-κB), and the proinflammatory cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in cerebral cortex and hippocampus. Additionally, Aβ increased oxidant levels and lipid peroxidation in cerebral cortex and hippocampus, but decreased heme oxygenase-1 (HO-1) and peroxiredoxin-1 (Prdx1) expression in the hippocampus. Anti-neuroinflammatory effects of FSP were demonstrated by a decrease in the expression of GFAP and NF-κB in the hippocampus, as well as a decrease in proinflammatory cytokines in both the hippocampus and cerebral cortex FSP protected against oxidative stress by decreasing oxidant levels and lipid peroxidation and by increasing HO-1 and Prdx1 expressions in the hippocampus of mice. Moreover, FSP prevented the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2) in the hippocampus of mice induced by Aβ. In conclusion, treatment with FSP attenuated memory impairment, nociception sensitivity by decreasing oxidative stress, and neuroinflammation in a mouse model of Alzheimer's disease.
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http://dx.doi.org/10.1007/s12035-022-03110-z | DOI Listing |
Vopr Kurortol Fizioter Lech Fiz Kult
December 2024
S.I. Spasokukotsky Moscow Centre for Research and Practice in Medical Rehabilitation, Restorative and Sports Medicine, Moscow, Russia.
Unlabelled: Post-stroke cognitive impairments are widespread and significantly reduce the quality of life and rehabilitation prognosis of patients. Clinical observations show a serious variability of cognitive impairments in patients after acute cerebrovascular accident. Thus, the classification of above mentioned disorders, based on which it would be possible to determine the order of individualization of a cognitive rehabilitation program, is currently not available in literature.
View Article and Find Full Text PDFDrug Saf
December 2024
Division of Neurology, Department of Clinical Sciences Lund, Lund University, Box 117, 22100, Lund, Sweden.
Drug-induced cognitive impairment (DICI) is a well-established, yet under-recognised, complication of many types of pharmacological treatment. While there is a large body of scientific literature on DICI, most papers are about drug-induced dementia in the elderly and one specific drug class. However, DICI also comprises subclinical symptoms, domain-specific forms of cognitive impairment as well as mild cognitive impairment (MCI), and delirium.
View Article and Find Full Text PDFCrit Care Med
December 2024
Department of Neurology, Northwestern University, Chicago, IL.
Objectives: To determine whether cognitive impairments of important severity escape detection by guideline-recommended delirium and encephalopathy screening instruments in critically ill patients.
Design: Cross-sectional study with random patient sampling.
Setting: ICUs of a large referral hospital with protocols implementing the Society of Critical Care Medicine's ICU Liberation Bundle.
NEJM Evid
January 2025
TIMI Study Group, Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston.
Background: Concerns persist regarding the cognitive safety of achieving very low levels of low-density lipoprotein (LDL) cholesterol. Although short-term studies are reassuring, the long-term cognitive effects of sustained exposure to very low LDL cholesterol levels through combined proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibition and statin therapy remain unknown.
Methods: This prospective study enrolled a subset of adults with atherosclerotic cardiovascular disease who had completed a neurocognitive substudy (EBBINGHAUS) of a placebo-controlled randomized trial of evolocumab (FOURIER) and were eligible for a long-term open-label extension.
Brain Behav Immun Health
February 2025
Institute of Cognitive Neuroscience, University College London, London, United Kingdom.
Background: Cognitive impairment, colloquially termed "brain fog", is one of the most prevalent manifestations of post-Covid syndrome and a major contributor to impaired daily function and reduced quality of life. However, despite the high numbers of affected individuals presenting to clinical services with cognitive impairment, little work has been undertaken to date on the suitability of current memory clinic tests for identifying the cognitive deficits in this new acquired cognitive disorder.The aim of this study was therefore to determine the performance of people with post-Covid syndrome presenting with cognitive impairment on the Addenbrooke's Cognitive Examination-III (ACE-III), a cognitive test used widely in memory clinics.
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