• Title/Summary/Keyword: Impairment Loss

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Hypothermia alleviates hypoxic ischemia-induced dopamine dysfunction and memory impairment in rats

  • Ko, Il-Gyu;Cho, Han-Jin;Kim, Sung-Eun;Kim, Ji-Eun;Sung, Yun-Hee;Kim, Bo-Kyun;Shin, Mal-Soon;Cho, Seh-Yung;KimPak, Young-Mi;Kim, Chang-Ju
    • Animal cells and systems
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    • v.15 no.4
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    • pp.279-286
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    • 2011
  • Hypoxic ischemia injury is a common cause of functional brain damage, resulting from a decrease in cerebral blood flow and oxygen supply to the brain. The main problems associated with hypoxic ischemia to the brain are memory impairment and dopamine dysfunction. Hypothermia has been suggested to ameliorate the neurological impairment induced by various brain insults. In this study, we investigated the effects of hypothermia on memory function and dopamine synthesis following hypoxic ischemia to the brain in rats. For this purpose, a step-down avoidance task, a radial eight-arm maze task, and immunohistochemistry for tyrosine hydroxylase (TH) and 5-bromo-2'-deoxyuridine (BrdU) were performed. The present results indicated that the hypoxic ischemia-induced disturbance of the animal's performances and spatial working memory was associated with a decrement in TH expression in the substantia nigra and striatum, and an increase in cell proliferation in the hippocampal dentate gyrus. Hypothermia treatment improved the animals' performance and spatial working memory by suppressing the decrement in TH expression in the substantia nigra and striatum and the increase in cell proliferation in the dentate gyrus. We suggest that hypothermia can be an efficient therapeutic modality to facilitate recovery following hypoxic ischemia injury to the brain, presumably by modulating the dopaminergic cell loss.

Safety and efficacy of transcutaneous bone conduction implant surgery for hearing improvement in microtia patients with bilateral hearing impairment

  • Cheon, Jeong Hyun;Lee, Hyung Chul;Im, Gi Jung;Park, Jung Youl;Park, Chul
    • Archives of Plastic Surgery
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    • v.46 no.6
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    • pp.525-534
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    • 2019
  • Background In microtia patients with bilateral hearing impairment, hearing improvement is crucial for language development and performance. External auditory canal reconstruction (EACR) has been performed to improve hearing, but often results in complications. We performed transcutaneous bone conduction implant (TBCI) surgery in these patients. This study aimed to evaluate the safety and efficacy of TBCI surgery. Methods A retrospective review was performed of five patients who underwent auricular reconstruction and TBCI surgery and 12 patients who underwent EACR between March 2007 and August 2018. Hearing improvement was measured based on the air-bone gap values using pure-tone audiometry over a 6-week postoperative period. We reviewed other studies on hearing improvement using EACR and compared the findings with our results. The surgical techniques for TBCI were reviewed through case analyses. Results Postoperative hearing outcomes showed a significant improvement, with a mean gain of 34.1 dB in the TBCI cohort and 14.1 dB in the EACR cohort. Both gains were statistically significant; however, the TBCI cohort showed much larger gains. Only three of the 12 patients who underwent EACR achieved hearing gains of more than 20 dB, which is consistent with previous studies. All patients who underwent TBCI surgery demonstrated hearing gains of more than 20 dB and experienced no device-related complications. Conclusions TBCI is a safe and effective method of promoting hearing gains in microtia patients with bilateral hearing impairment. TBCI surgery provided better hearing outcomes than EACR and could be performed along with various auricular reconstruction techniques using virgin mastoid skin.

A Review Study on Movement System Impairment Syndromes (동태손상(動態損傷) 증후군(症候群)에 관한 연구 현황 고찰)

  • Kim, Jeong-Kyun;Kim, Hyun-Ho;Seo, Jae-Ho;Kim, Dong-Won;Park, Young-Jae;Park, Young-Bae
    • The Journal of Korean Medicine
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    • v.33 no.1
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    • pp.79-89
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    • 2012
  • Objectives: Sahrmann, an American physical therapist, has developed a set of movement-related diagnoses on musculoskeletal pain syndromes (MPS). We reviewed articles for studies of objectification and quantification of Oriental medicine diagnosis system about MPS. Methods: The authors reviewed a total of 12 studies found on PubMed to obtain movement system impairment (MSI)-based classification categories. Results: The MSI system has been developed for objectification and quantification of physical therapists' MPS diagnoses. The MSI system of classification is based on the basic premise that loss of precise movement is the result of specific repetitive movements and positions in everyday life. The MSI system defines 8 categories in the shoulder region, 5 in the lumbar region, and 7 in the knee region. Treatment involves (1) educating the person about the specific directions of alignment and movement that appear to be contributing to the musculoskeletal problem, (2) modifying the direction - specific alignment and movement patterns during daily activities, and (3) exercises to address the impairments. Conclusions: The authors propose that MSI studies could help to advance an Oriental medical diagnosis system on musculoskeletal pain syndromes, because MSI shares similarity with Oriental medicine in terms of holism, views of constant motion, and mi-byung (subhealth) treatment.

Effect of Steamed Codonopsis lanceolata on Spatial Learning and Memory in Mice (증숙 더덕 추출물의 인지능력 개선 효과)

  • Weon, Jin Bae;Yun, Bo-Ra;Lee, Jiwoo;Eom, Min Rye;Ko, Hyun-Jeong;Lee, Hyeon Yong;Park, Dong-Sik;Chung, Hee-Chul;Chung, Jae Youn;Ma, Choong Je
    • Korean Journal of Pharmacognosy
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    • v.45 no.1
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    • pp.48-54
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    • 2014
  • Alzheimer's disease is progressive neurodegenerative disorder by the loss of memory and learning abilities. Codonopsis lanceolata (C. lanceolata) is traditional medicinal plant used for the treatment of inflammatory diseases. The aim of study was to evaluate the effect of steamed C. lanceolata on scopolamine-induced memory impairment in the Morris water maze test and passive avoidance test. In addition, this study investigated the neuroprotective effects of steamed C. lanceolata on glutamate-induced cell death in HT22 cells using MTT assay. The results showed that steamed C. lanceolata (500 mg/kg body weight, p.o.) reversed spatial memory impairment by scopolamine in Morris water maze test and passive avoidance test. Steamed C. lanceolata attenuated memory impairment by scopolamine compared with common C. lanceolata. In addition, administration of steamed C. lanceolata significantly also reduced cell death. We suggest that steaming process more improve cognitive enhancing and neuroprotective effect of C. lanceolata than common C. lanceolata.

Effects of Cupping Therapy on Memory Impairment after Hemorrhage in Rats (뇌출혈 동물 모델에서 부항이 뇌 인지기능 회복에 미치는 효과)

  • Lee, Ji Hye;Joh, Day;Choi, Young Ho;Chung, Chan Kyung;Choi, Yoon Suk;Cha, Mi Gyoung;Jung, Ji Wook
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.27 no.6
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    • pp.789-794
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    • 2013
  • Hemorrhage is a devastating type of stroke, accounts for 15-20% of all strokes. This disease can cause cognitive dysfunction with a very high mortality rate. Cupping therapy of Traditional Korean medicine has frequently been used to relieve a variety of diseases or clinical conditions, although not in the memory loss after hemorrhage. This study was designed to evaluate the effects of cupping therapy on learning and memory with Y-maze test, as well as its effects on different molecular changes in hippocampus following the induction of hemorrhage in rats. Cupping, using vacuum cupping machine, was applied at target area for 5 min daily for 7 consecutive days, commencing 1 day after brain impairment. As a result, induction of hemorrhage enhanced memory deficit, suppressed brain-derived neurotrophin factor (BDNF) in the hippocampus. Cupping treatment effectively reversed collagenase-induced cognitive impairment in SD rats which was represented by improvement of spontaneous alterations in Y-maze test. In addition, BDNF expression was enhanced after cupping therapy. The present results suggest that the therapeutic effects of cupping treatment after hemorrhage is involved in expression of BDNF.

Probiotics that Ameliorate Cognitive Impairment through Anti-Inflammation and Anti-Oxidation in Mice

  • Shinhui Lee;Sanung Eom;Jiwon Lee;Minsu Pyeon;Kieup Kim;Kyu Yeong Choi;Jung Hee Lee;Da Jeong Shin;Kun Ho Lee;Sejong Oh;Junho H Lee
    • Food Science of Animal Resources
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    • v.43 no.4
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    • pp.612-624
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    • 2023
  • The gut-brain axis encompasses a bidirectional communication pathway between the gastrointestinal microbiota and the central nervous system. There is some evidence to suggest that probiotics may have a positive effect on cognitive function, but more research is needed before any definitive conclusions can be drawn. Inflammation-induced by lipopolysaccharide (LPS) may affect cognitive function. To confirm the effect of probiotics on oxidative stress induced by LPS, the relative expression of antioxidant factors was confirmed, and it was revealed that the administration of probiotics had a positive effect on the expression of antioxidant-related factors. After oral administration of probiotics to mice, an intentional inflammatory response was induced through LPS i.p., and the effect on cognition was confirmed by the Morris water maze test, nitric oxide (NO) assay, and interleukin (IL)-1β enzyme-linked immunosorbent assay performed. Experimental results, levels of NO and IL-1β in the blood of LPS i.p. mice were significantly decreased, and cognitive evaluation using the Morris water maze test showed significant values in the latency and target quadrant percentages in the group that received probiotics. This proves that intake of these probiotics improves cognitive impairment and memory loss through anti-inflammatory and antioxidant mechanisms.

Apraxia of Phonation: a Case Report (발성실행증 사례연구)

  • Kwon, Mi-Seon;Na, Duk-L;Kim, Hyang-Hee;Jung, Jin-Sang
    • Speech Sciences
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    • v.12 no.2
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    • pp.101-108
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    • 2005
  • Apraxia of phonation (AOP) has often been described as a feature of apraxia of speech or of severe non-fluent type of aphasia. Pure AOP is rare and, to our knowledge, only two cases have been reported. Brain lesion sites of the reported cases were not those sites known to be responsible for apraxia of speech. This study presents a case of AOP which resulted from the secondary stroke in the left corona radiata immediately following the first stroke in the left temporoparietal lobe. A 61-year old right-handed man shwoed a global type of aphasia after the first cerebral infarction, but was able to generate spontaneously some short fragments of speech. On the day after the first infarction, he suffered from the secondary infarction, leaving him a complete loss of voluntary phonation. He did not showed any significant change in language functions. Several occurrences of involuntary phonation were observed upon laughing or crying. He was also able to cough unintentionally. A vidoe-stroboscopic examination failed to reveal any evidence of structural and functional impairment in larynx. Although this case is not of pure form of AOP, AOP appeared after the secondary stroke without significant changes of language impairment since the first stroke. Therefore, AOP may be a consequence of the brain lesion from the secondary stroke even though we cannot rule out the possibility of an additive effect of the secondary to the first stroke.

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Molecular and Cellular Basis of Neurodegeneration in Alzheimer's Disease

  • Jeong, Sangyun
    • Molecules and Cells
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    • v.40 no.9
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    • pp.613-620
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    • 2017
  • The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid ${\beta}-peptide$ ($A{\beta}$) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than $A{\beta}$ plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD. A growing amount of evidence suggests that soluble $A{\beta}$ oligomers in concert with hyperphosphorylated tau (pTau) serve as the major pathogenic drivers of neurodegeneration in AD. Increased $A{\beta}$ oligomers trigger neuronal dysfunction and network alternations in learning and memory circuitry prior to clinical onset of AD, leading to cognitive decline. Furthermore, accumulated damage to mitochondria in the course of aging, which is the best-known nongenetic risk factor for AD, may collaborate with soluble $A{\beta}$ and pTau to induce synapse loss and cognitive impairment in AD. In this review, I summarize and discuss the current knowledge of the molecular and cellular biology of AD and also the mechanisms that underlie $A{\beta}-mediated$ neurodegeneration.

Involvement of Cortical Damage in the Ischemia/Reperfusion-Induced Memory Impairment of Wistar Rats

  • Hong, Jin-Tae;Ryu, Seung-Rel;Kim, Hye-Jin;Lee, Sun-Hee;Lee, Byung-Moo;Kim, Pu-Young
    • Archives of Pharmacal Research
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    • v.23 no.4
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    • pp.413-417
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    • 2000
  • The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/repefusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.

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A Review on the Correlation between the Pathology of Alzheimer's Disease and microRNA

  • Kim, Soo-Jung;Cho, Hyun-Jeong
    • Biomedical Science Letters
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    • v.27 no.4
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    • pp.208-215
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    • 2021
  • The purpose of this study was to explain the pathology of Alzheimer's disease (AD) and to investigate the correlation between AD and microRNA. AD is the most common type of dementia, accounting for about 80% of all types of dementia, causing dysfunction in various daily activities such as memory loss, cognitive impairment, and behavioral impairment. The typical pathology of AD is explained by the accumulation of beta-amyloid peptide plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. On the other hand, microRNA is small non-coding RNA 22~23 nucleotides in length that binds to the 3' untranslated region of messenger RNA to inhibit gene expression. Many reports explain that microRNAs found in circulating biofluids are abundant in the central nervous system, are involved in the pathogenic mechanism of AD, and act as important factors for early diagnosis and therapeutic agents of AD. Therefore, this paper aims to clarify the correlation between AD and microRNA. In this review, the basic mechanism of miRNAs is described, and the regulation of miRNAs in the pathological processes of AD are highlighted. Furthermore, we suggest that miRNA-based system in development of therapeutic and diagnostic agents of AD can be a promising tool.