Design of wireless smart chair system for people with cognitive deficiency

2019 ◽  
Author(s):  
Vasily G. Moshnyaga ◽  
Koji Hashimoto ◽  
Tomohiro Nogami ◽  
Kazuki Nojima
Keyword(s):  
Cognitive Deficiency

COGNITIVE DEFICIENCY AT ISCHEMIC OM STROKE

2020 ◽  
Vol 1 (1) ◽  
pp. 55-57
Author(s):  
Dildora Khaydarova ◽  
◽  
Hilola Davronova ◽  
Asliddin Akbarov ◽  
Keyword(s):  
Social Problems ◽  
Cerebrovascular Diseases ◽  
Cerebral Stroke ◽  
Number Of Patients ◽  
High Prevalence ◽  
The World ◽  
Cognitive Deficiency ◽  
Complications And Mortality

Cerebrovascular diseases remain one of the most pressing medical and social problems in many countries of the world, due to their high prevalence, severity of complications and mortality. In Uzbekistan, the number of patients with cerebral stroke is quite large -about 40-45 thousandcases of cerebral stroke are registered annually

Autism

2018 ◽  
Author(s):  
Joseph N. Straus
Keyword(s):  
Twelve Tone ◽  
Serial Music ◽  
Cognitive Deficiency

Autism and twelve-tone serial music are related, mutually reinforcing forms of cultural modernism. Both have been understood as excessively isolated or alone, with each entity self-contained and self-enclosed; as uncommunicative, or communicating in atypical ways, with an excess of private meanings and self-references; as demonstrating an unproductive preference for routines and rituals; as incongruously hypertrophied in certain respects (often hyperrational) and atrophied in others (often emotionally or expressively defective). They have also been understood as inaccessible fortresses; as incomprehensible aliens; as cold, unfeeling machines (especially computational machines); and as idiot savants (with isolated islands of excellence in a sea of cognitive deficiency).

scholarly journals Congenital hypothyroidism impairs spine growth of dentate granule cells by downregulation of CaMKIV

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Qingying Tang ◽  
Shuxia Chen ◽  
Hui Wu ◽  
Honghua Song ◽  
Yongjun Wang ◽  
...  
Keyword(s):  
Congenital Hypothyroidism ◽  
Granule Cells ◽  
Spine Density ◽  
Drug Induced ◽  
Distinct Cell Type ◽  
Cognitive Behaviors ◽  
Dentate Granule Cells ◽  
Rat Pups ◽  
Cognitive Deficiency ◽  
Underlying Mechanisms

AbstractCongenital hypothyroidism (CH), a common neonatal endocrine disorder, can result in cognitive deficits if delay in diagnose and treatment. Dentate gyrus (DG) is the severely affected subregion of the hippocampus by the CH, where the dentate granule cells (DGCs) reside in. However, how CH impairs the cognitive function via affecting DGCs and the underlying mechanisms are not fully elucidated. In the present study, the CH model of rat pups was successfully established, and the aberrant dendrite growth of the DGCs and the impaired cognitive behaviors were observed in the offspring. Transcriptome analysis of hippocampal tissues following rat CH successfully identified that calcium/calmodulin-dependent protein kinase IV (CaMKIV) was the prominent regulator involved in mediating deficient growth of DGC dendrites. CaMKIV was shown to be dynamically regulated in the DG subregion of the rats following drug-induced CH. Interference of CaMKIV expression in the primary DGCs significantly reduced the spine density of dendrites, while addition of T3 to the primary DGCs isolated from CH pups could facilitate the spine growth of dendrites. Insights into relevant mechanisms revealed that CH-mediated CaMKIV deficiency resulted in the significant decrease of phosphorylated CREB in DGCs, in association with the abnormality of dendrites. Our results have provided a distinct cell type in hippocampus that is affected by CH, which would be beneficial for the treatment of CH-induced cognitive deficiency.

The Core of Negative Symptoms in Schizophrenia: Affect or Cognitive Deficiency?

1995 ◽  
Vol 28 (1) ◽  
pp. 46-54 ◽  
Author(s):  
Ch. Mundt ◽  
W. Barnett ◽  
G. Witt
Keyword(s):  
Negative Symptoms ◽  
The Core ◽  
Cognitive Deficiency

Sleep Deprivation Impairs Ca2+ Expression in the Hippocampus: Ionic Imaging Analysis for Cognitive Deficiency with TOF-SIMS

2012 ◽  
Vol 18 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hung-Ming Chang ◽  
Wen-Chieh Liao ◽  
Ji-Nan Sheu ◽  
Chun-Chao Chang ◽  
Chyn-Tair Lan ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Neuronal Plasticity ◽  
Molecular Mechanisms ◽  
Secondary Ion Mass Spectrometry ◽  
Maze Learning ◽  
Behavioral Testing ◽  
Adult Rats ◽  
Cognitive Deficiency ◽  
Learning Test ◽  
Oxide Synthase

AbstractSleep deprivation causes cognitive dysfunction in which impaired neuronal plasticity in hippocampus may underlie the molecular mechanisms of this deficiency. Considering calcium-mediated NMDA receptor subunit 1 (NMDAR1) and neuronal nitric oxide synthase (nNOS) activation plays an important role in the regulation of neuronal plasticity, the present study is aimed to determine whether total sleep deprivation (TSD) would impair calcium expression, together with injury of the neuronal plasticity in hippocampus. Adult rats subjected to TSD were processed for time-of-flight secondary ion mass spectrometry, NMDAR1 immunohistochemistry, nNOS biochemical assay, cytochrome oxidase histochemistry, and the Morris water maze learning test to detect ionic, neurochemical, bioenergetic as well as behavioral changes of neuronal plasticity, respectively. Results indicated that in normal rats, strong calcium signaling along with intense NMDAR1/nNOS expression were observed in hippocampal regions. Enhanced calcium imaging and neurochemical expressions corresponded well with strong bioenergetic activity and good performance of behavioral testing. However, following TSD, both calcium intensity and NMDAR1/nNOS expressions were significantly decreased. Behavioral testing also showed poor responses after TSD. As proper calcium expression is essential for maintaining hippocampal neuronal plasticity, impaired calcium expression would depress downstream NMDAR1-mediated nNOS activation, which might contribute to the initiation or development of TSD-related cognitive deficiency.

Ropren® is a polyprenol preparation from coniferous plants that ameliorates cognitive deficiency in a rat model of beta-amyloid peptide-(25–35)-induced amnesia

Phytomedicine ◽  
2012 ◽  
Vol 19 (5) ◽  
pp. 451-456 ◽  
Author(s):  
Julia Fedotova ◽  
Vagif Soultanov ◽  
Tamara Nikitina ◽  
Victor Roschin ◽  
Natalia Ordayn
Keyword(s):  
Rat Model ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Beta Amyloid Peptide ◽  
Cognitive Deficiency
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