• Title/Summary/Keyword: CNS involvement

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Mumps meningoencephalitis without parotitis, after secondary vaccination of Measles-Mumps-Rubella (MMR) : A Case Report (MMR 2차 예방접종을 받은 후 이하선염 없이 발생한 볼거리 뇌염 1례)

  • Choi, Pahn Kyu;Kang, Hyun Goo
    • Journal of the Korea Academia-Industrial cooperation Society
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    • v.18 no.9
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    • pp.123-126
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    • 2017
  • Mumps, which are also known as epidemic parotitis,lead to viral infectious diseases that can cause complication such as pancreatitis, orchitis, hearing impairments, oophoritis, parotitis and meningitis. Central nervous system involvement has been reported in up to 65% of mumps patients, with most of these including meningitis. Meningoencephalitis is a rare central nervous system (CNS) complication of the mumps. Measles-Mumps-Rubella (MMR) vaccination has been reported protective effect against clinical complications and hospitalization. Here, we describe acute mumps meningoencephalitis in a 24-year-old female without parotitis who had received the MMR vaccination by age related schedule. She initially visited our hospital with aggravated cognition and confusion. After conservative viral treatment, she recovered cognitive function rapidly and complication was not remained. We report here a case of a patient with good recovery of mumps meningoencephalitis without parotitis after secondary vaccination for MMR.

The Surveillance of Adverse Drug Reaction(ADR) Reported (3차 병원에서 보고된 의약품 부작용 현황 조사와 약물 부작용 관리를 위한 약사의 인식도 조사)

  • Choi, Yun Hee;Sohn, Uy Dong
    • Korean Journal of Clinical Pharmacy
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    • v.13 no.2
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    • pp.72-81
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    • 2003
  • Adverse drug reaction (ADR) may increase hospital admission, morbidity and mortality and adding extra cost to healthcare expenditures. AIMS: This study was performed to identify the types of ADR being reported in a tertiary hospital, and to find out the ways to improve current ADR monitoring system. To investigate the attitudes of hospital pharmacists towards, and their understanding of ADR reporting. METHODS: Of 117 reports submitted to the pharmacy department during 3 months survey period, A questionnaire survey of 75 randomly selected hospital pharmacists was conducted. RESULT: Of the report was from patients aged between 60 and 70. The medical department with the high frequency in ADR reporting was Internal Medicines $(60\%)$. The most common ADR manifestations were gastrointestinal complaints $(47.8\%)\;and\;80\%$ of the reported cases were mild in their severity. The most common drugs suspected of causing ADR were CNS drugs which accounted for $38.4\%.\;55.5\%$ of respondent were aware of the need to education and information about ADR monitoring. The important reasons for unreporting ADR were unknown of how to report ADRs $(94.6\%)$. CONCLUSIONS: An ADR reporting system based on reporting by staff pharmacists has been effective increasing the number of reported reactions and pharmacist involvement in monitoring patients for ADRs. Pharmacists have the knowledge and responsibility to contribute to ADR reporting program. A great opportunity exists for pharmacists to contribute in this area of patient care.

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3,4,5-Trihydroxycinnamic Acid Inhibits Lipopolysaccharide-Induced Inflammatory Response through the Activation of Nrf2 Pathway in BV2 Microglial Cells

  • Lee, Jae-Won;Choi, Yong-Jun;Park, Jun-Ho;Sim, Jae-Young;Kwon, Yong-Soo;Lee, Hee Jae;Kim, Sung-Soo;Chun, Wanjoo
    • Biomolecules & Therapeutics
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    • v.21 no.1
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    • pp.60-65
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    • 2013
  • 3,4,5-Trihydroxycinnamic acid (THC) is a derivative of hydroxycinnamic acids, which have been reported to possess a variety of biological properties such as anti-inflammatory, anti-tumor, and neuroprotective activities. However, biological activity of THC has not been extensively examined. Recently, we reported that THC possesses anti-inflammatory activity in LPS-stimulated BV2 microglial cells. However, its precise mechanism by which THC exerts anti-inflammatory action has not been clearly identified. Therefore, the present study was carried out to understand the anti-inflammatory mechanism of THC in BV2 microglial cells. THC effectively suppressed the LPS-induced induction of pro-inflammatory mediators such as NO, TNF-${\alpha}$, and IL-$1{\beta}$. THC also suppressed expression of MCP-1, which plays a key role in the migration of activated microglia. To understand the underlying mechanism by which THC exerts these anti-inflammatory properties, involvement of Nrf2, which is a cytoprotective transcription factor, was examined. THC resulted in increased phosphorylation of Nrf2 with consequent expression of HO-1 in a concentration-dependent manner. THC-induced phosphorylation of Nrf2 was blocked with SB203580, a p38 MAPK inhibitor, indicating that p38 MAPK is the responsible kinase for the phosphorylation of Nrf2. Taken together, the present study for the first time demonstrates that THC exerts anti-inflammatory properties through the activation of Nrf2 in BV2 microglial cells, suggesting that THC might be a valuable therapeutic adjuvant for the treatment of inflammation-related disorders in the CNS.

The Surveillance of Adverse Drug Reactions (ADR) Reported in Samsung Medical Center (삼성서울병원에서 보고된 의약품 부작용의 현황 조사)

  • Cho, Jeong Ah;Lee, Hu Kyung;Sohn, Kie Ho;Choi, Kyung Eub
    • Korean Journal of Clinical Pharmacy
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    • v.10 no.1
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    • pp.30-37
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    • 2000
  • Adverse drug reactions (ADR) may result in increased hospital admissions, morbidity and mortality, adding extra cost to healthcare expenditures. Thus, it is critical to activate ADR monitoring and reporting program in tertiary hospitals in developing countries such as Korea. This study was performed to identify the types of ADR being reported in a tertiary hospital, Samsung Medical Center, and to find out the ways to improve current ADR monitoring system. Of 464 ADR reports submitted to the pharmacy department during the 6-month survey period, $97.8\%$ of the reports were from out patient and $48.5\%$ were from patients aged between 50 and 60. The medical department with the highest frequency in ADR reporting was Internal Medicines $(35.6\%)$. The most common ADR manifestations were gastrointestinal complaints $(43.4\%)\;and\;75\%$ of the reported cases were mild in their severity. The most common drugs suspected of causing ADR were CNS drugs which accounted for $32.8\%$. In terms of causality assessment, $85.1\%$ of the reports were probable cases by WHO causality assessment criteria. In regards to sources of report, $75.6\%$ of ADR were reported by physicians and $24.4\%$ by nurses. There were no ADR reported by pharmacists. In conclusion, there is an urgent need to improve ADR monitoring system for inpatient and to motivate pharmacist involvement in ADR monitoring and reporting in Korea.

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Exploring amygdala structural changes and signaling pathways in postmortem brains: consequences of long-term methamphetamine addiction

  • Zahra Azimzadeh;Samareh Omidvari;Somayeh Niknazar;Saeed Vafaei-Nezhad;Navid Ahmady Roozbahany;Mohammad-Amin Abdollahifar;Foozhan Tahmasebinia;Gholam-Reza Mahmoudiasl;Hojjat Allah Abbaszadeh;Shahram Darabi
    • Anatomy and Cell Biology
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    • v.57 no.1
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    • pp.70-84
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    • 2024
  • Methamphetamine (METH) can potentially disrupt neurotransmitters activities in the central nervous system (CNS) and cause neurotoxicity through various pathways. These pathways include increased production of reactive nitrogen and oxygen species, hypothermia, and induction of mitochondrial apoptosis. In this study, we investigated the long-term effects of METH addiction on the structural changes in the amygdala of postmortem human brains and the involvement of the brain- cAMP response element-binding protein/brain-derived neurotrophic factor (CREB/BDNF) and Akt-1/GSK3 signaling pathways. We examined ten male postmortem brains, comparing control subjects with chronic METH users, using immunohistochemistry, real-time polymerase chain reaction (to measure levels of CREB, BDNF, Akt-1, GSK3, and tumor necrosis factor-α [TNF-α]), Tunnel assay, stereology, and assays for reactive oxygen species (ROS), glutathione disulfide (GSSG), and glutathione peroxidase (GPX). The findings revealed that METH significantly reduced the expression of BDNF, CREB, Akt-1, and GPX while increasing the levels of GSSG, ROS, RIPK3, GSK3, and TNF-α. Furthermore, METH-induced inflammation and neurodegeneration in the amygdala, with ROS production mediated by the CREB/BDNF and Akt-1/GSK3 signaling pathways.

Cognitive Impairment in the Patients with Mildly Active Systemic Lupus Erythematosus (경증 전신성 홍반성 루프스 환자의 인지기능장애)

  • Kim, Jin-Hee;Lee, Chul;Lee, Chang-Uk;Paik, In-Ho
    • Korean Journal of Psychosomatic Medicine
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    • v.5 no.1
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    • pp.89-96
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    • 1997
  • This study was designed to determine whether cognitive impairment was evident in patients with SLE. Also, it aimed to examine the association of cognitive impairment with other clinical variables. The subjects consisted of 20 patients with mildly active SLE and 20 healthy controls. Methods : A total of 20 SLE patients and 20 normal controls completed a computerized neuropsychological test battery using Vienna Test System. These included Cognitrone test, Continuous attention test, Corsi block tapping test, Standard progressive matrices. Also, neuro-behavioral cognitive status examination was done. The symptom severity of depression was measured with Beck Depression Inventory, Hamilton Depression Rating Scale, and current medications were documented. Disease activity was rated using the SLE diasease activity index (SLEDAI). Results : SLE patients had poorer performance than normal controls on the tests of Cognitrone, attention, nonverbal IQ and memory, independent of age, education, disease activity, steroid use and depression status. Conclusion : Cognitive dysfunction was not uncommon in ambulatory SLE patients as measured by standardized neuropsychological tests. It seemed to occur independently of various clinical variables. These findings would suggest that cognitive dysfunction in SLE may be explained by reflecting subclinical central nervous system(CNS) involvement, rather than coexisting psychological distress due to chronic illness or side effect of medication.

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Studies About the Effect of Excitatory Amino Acid Receptor Antagonist on Traumatic Spinal Cord Injury (척수신경손상에 대한 흥분성 아미노산 수용체 길항제의 효과에 대한연구)

  • Kim Jong-Keun
    • The Korean Journal of Pharmacology
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    • v.31 no.1 s.57
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    • pp.1-9
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    • 1995
  • The slow development of histopathological changes and long period required for stabilization of lesions have suggested that secondary injury processes exacerbate the effect of initial mechanical insult after traumatic spinal cord injury (SCI). The importance of glutamate receptors in the normal functions of spinal cord, in concert with the large body of evidence that points to their involvement in neurotoxicity due to both ischemic and traumatic insults to the CNS, suggested a probable role of glutamate receptors in secondary injury process after traumatic SCI. In order to investigate the involvement of excitatory amino acid in the secondary injury process after SCI, this study examined the effect of dextrorphan, a noncompetitive NMDA receptor antagonist, on the recovery of hindlimb function and the residual tissue at injury site following SCI. Locomotor function was assessed using open field test (21 point scale). At 8 weeks spinal cord tissue was examined using quantitative histopathologic technique. Prior to surgery female Long-Evans rats were adapted to the test environment. Rats received laminectomies (T9/T10), and spinal cord contusions (NYU impactor) were produced by a 10 gm weight dropped 25 mm. DXT (15 or 30 mg/kg, i.p.) or saline was injected 15 min before contusion. Behavioral testing resumed 2 days post-injury and continued twice a week for 8 weeks. No differences between DXT and saline groups were found for hindlimb function and sparing tissue at the lesion site. These results suggest that NMDA receptor might not be involved in secondary injury processes after traumatic SCI.

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Effects of Oxygen-Derived Free Radicals on Brain Microsomal $Na^+-K^+-ATPase$ Activity (산소유리라디칼이 뇌조직 미크로좀분획의 $Na^+-K^+-ATPase$ 활성도에 미치는 영향)

  • Oh, Sae-Moon;Son, Young-Sook;Choi, Kil-Soo;Lim, Jung-Kyoo;Chung, Myung-Hee
    • The Korean Journal of Pharmacology
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    • v.18 no.2
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    • pp.1-14
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    • 1982
  • The effects of xanthine-xanthine oxidase reaction on brain microsomal $Na^+-K^+-ATPase$ activity were studied to see possible involvement of oxygen free radicals in pathologic change occurring in ischemic state of CNS accompanied by cerebral vascular occlusion or impact injury. When microsomal fraction was incubated with xanthine ana xanthine oxidase, $Na^+-K^+-ATPase$ activity of the fraction was markedly inactivated (80% inactivation) whereas btssl $Mg^{++}-ATPase$ was much less sensitive (less than 10% inactivation) compared to that of $Na^+-K^+-ATPase$. The inactivation was observed only in the presence of both xanthine and xanthine oxidase, not either of them alone, and the extent of inactivation was dependent on the concentration of xanthine. In an attempt to determine which of the oxygen species was responsible for the inactivation, the ability of various scavengers to overcome the inactivation was tested. Superoxide dismutase, catalase and 1,4-diazabicyclo(2,2,2)octane were shown to reverse the inactivation of the ATPase in dose-dependent manner. In contrast, mannitol as well as other $OH{\cdot}$quenchers were ineffective in limiting oxygen radical-induced inactivation. Thus $O_{\bar{2}}{\cdot},\;H_2O_2$ and $^1O_2$ were implicated to be mediators involved in the inactivation. Since oxygen radicals are suspected as being a cause of the peroxidative damaging process in train ischemia, the ATPase inactivation by oxygen radicals may be a possible contributing factor which gives rise to functional derangement of nerve cells observed in the pathologic process.

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