• The Korean Journal of Rehabilitation Nursing
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• v.8 no.2
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• pp.129-138
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• 2005

Purpose: Irritable bowel syndrome (IBS) is frequently yet little understood disease. Review was performed to promote understanding on the characteristics, pathophysiology, and risk factors of IBS. Content: IBS is characterized by abdominal discomfort associated with pain and altered bowel function; structural and biochemical abnormalities are absent. Generally IBS is more prevalent in women and people with higher educational and social background, but there are some controversies. IBS is diagnosed by the Rome II or Manning criteria after excluding organic gastrointestinal diseases. The pathophysioloy is explained by abnormal control mechanism of central and enteric nervous system. Mucosal immunity, secretions, and neurotransmitter are also associated with the hypersensitivity and motility change of bowel function. Stress is known as a major triggering factor and contributed to symptoms. Other risk factors are genetic elements, childhood experiences, inflammation, anxiety, depression, diet, and sleep disorders.

• Tuberculosis and Respiratory Diseases
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• v.52 no.2
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• pp.166-173
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• 2002

Transient peripheral eosinophilia occurs in several disorders, such as allergic diseases, cancer, and parasitic infections. However, in most cases, their presence is not accompanied by tissue destruction or organ dysfunction. In certain disease states, eosinophils can accumulate in any organ in the body and cause tissue destruction as a result of the eosinophil infiltration or the toxic effects of the degranulated proinflammatory products. Idiopathic hypereosinophilic syndrome is a rare disorder characterized by persistent eosinophilia of an unknown origin, usually associated with a dysfunction of organs such as the heart, lung, skin, and nervous system. Idiopathic hypereosinophilic syndrome usually has an indolent course over a period of several months. However, in some cases, they have grave symptoms if vital organs such as heart and lung are infiltrated. Here we report a case of idiopathic hypereosinophilic syndrome presenting acute pulmonary edema involving the heart, bone marrow, and lung with a review of the relevant literatures.

• Journal of the Korean neurological association
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• v.35 no.4
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• pp.211-214
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• 2017

Acute disseminated encephalomyelitis (ADEM) and Guillain-$Barr{\acute{e}}$ syndrome (GBS) are both rare post-infectious neurological disorders. The co-existence of these conditions has often been reported despite of low incidence. We describe a 20-year-old male, who presented with acute flaccid paralysis and encephalopathy. The patient showed reversible MRI lesions suggesting ADEM. This case showed anti-GT1a IgG and anti-GM1 IgM antibodies positivity. We suggest that certain immunogenicity within central and peripheral nervous system may share a common autoimmune process during the disease course.

• PNF and Movement
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• v.19 no.2
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• pp.195-203
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• 2021

Purpose: Neurodynamic tests are used to examine neural tissue in patients with neuro-musculoskeletal disorders, although this has not yet been established in the intensity of nerve tension application. This study aimed to investigate the acute effects of neural stretching intensity on nerve excitability using the latency and amplitude of nerve conduction velocity test (NCV) analysis. Methods: Thirty young, healthy male and female subjects (mean age = 21.30 years) voluntarily participated in this study. Nerve excitability was assessed using the median sensory NCV test. The latency and amplitude of the NCV test were measured under four different conditions: reference phase (supra-maximal stimulus, without neural stretching), baseline phase (2/3 of the supra-maximal stimulus, without neural stretching), weak stretch phase (2/3 of the supra-maximal stimulus, with weak neural stretching), and strong stretch phase (2/3 of the supra-maximal stimulus, with strong neural stretching). Results: The NCV latency was significantly delayed after one minute of neural stretching at the baseline, weak phase, and strong phase in comparison with the reference phase. The NCV latency was significantly delayed by increasing the strength of neural stretching. Furthermore, the NCV amplitude was significantly increased at the weak and strong phases, which were under neural stretching, in comparison with the baseline phase. The NCV amplitude was significantly increased by increasing the strength of the neural stretching. Conclusion: Transient neural stretching as a neurodynamic test can increase the sensitivity of the nerve without negatively affecting the nervous system. However, based on the results of this study, strong neural stretching in the neurodynamic test may delay the transmission of nerve impulses and hypersensitivity.

• Journal of Veterinary Science
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• v.21 no.3
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• pp.44.1-44.10
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• 2020

Background: Congenital portosystemic shunt (cPSS) is one of the most common congenital disorders diagnosed in dogs. Hepatic encephalopathy (HE) is a frequent complication in dogs with a cPSS and is a major cause of morbidity and mortality. Despite HE been a major cause of morbidity in dogs with a cPSS, little is known about the cellular changes that occur in the central nervous system of dogs with a cPSS. Objectives: The objective of this study was to characterise the histological changes in the cerebral cortex and cerebellum of dogs with cPSS with particular emphasis on astrocyte morphology. Methods: Eight dogs with a confirmed cPSS were included in the study. Results: Six dogs had substantial numbers of Alzheimer type II astrocytes and all cases had increased immunoreactivity for glial fibrillary acidic protein in the cerebral cortex, even if there were minimal other morphological changes. Conclusions: This study demonstrates that dogs with a cPSS have marked cellular changes in the cerebral cortex and cerebellum. The cellular changes that occur in the cerebral cortex and cerebellum of dogs with spontaneously arising HE are similar to changes which occur in humans with HE, further validating dogs with a cPSS as a good model for human HE.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.464-472
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• 2022

Background: Gut microbiota influence the central nervous system through gut-brain-axis. They also affect the neurological disorders. Gut microbiota differs in patients with Alzheimer's disease (AD), as a potential factor that leads to progression of AD. Oral intake of Korean Red Ginseng (KRG) improves the cognitive functions. Therefore, it can be proposed that KRG affect the microbiota on the gut-brain-axis to the brain. Methods: Tg2576 were used for the experimental model of AD. They were divided into four groups: wild type (n = 6), AD mice (n = 6), AD mice with 30 mg/kg/day (n = 6) or 100 mg/kg/day (n = 6) of KRG. Following two weeks, changes in gut microbiota were analyzed by Illumina HiSeq4000 platform 16S gene sequencing. Microglial activation were evaluated by quantitative Western blot analyses of Iba-1 protein. Claudin-5, occludin, laminin and CD13 assay were conducted for Blood-brain barrier (BBB) integrity. Amyloid beta (Aβ) accumulation demonstrated through Aβ 42/40 ratio was accessed by ELISA, and cognition were monitored by Novel object location test. Results: KRG improved the cognitive behavior of mice (30 mg/kg/day p < 0.05; 100 mg/kg/day p < 0.01), and decreased Aβ 42/40 ratio (p < 0.01) indicating reduced Aβ accumulation. Increased Iba-1 (p < 0.001) for reduced microglial activation, and upregulation of Claudin-5 (p < 0.05) for decreased BBB permeability were shown. In particular, diversity of gut microbiota was altered (30 mg/kg/day q-value<0.05), showing increased population of Lactobacillus species. (30 mg/kg/day 411%; 100 mg/kg/day 1040%). Conclusions: KRG administration showed the Lactobacillus dominance in the gut microbiota. Improvement of AD pathology by KRG can be medicated through gut-brain axis in mice model of AD.

• Biomolecules & Therapeutics
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• v.30 no.5
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• pp.455-464
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• 2022

Efonidipine, a calcium channel blocker, is widely used for the treatment of hypertension and cardiovascular diseases. In our preliminary study using structure-based virtual screening, efonidipine was identified as a potential inhibitor of c-Jun N-terminal kinase 3 (JNK3). Although its antihypertensive effect is widely known, the role of efonidipine in the central nervous system has remained elusive. The present study investigated the effects of efonidipine on the inflammation and cell migration induced by lipopolysaccharide (LPS) using murine BV2 and human HMC3 microglial cell lines and elucidated signaling molecules mediating its effects. We found that the phosphorylations of JNK and its downstream molecule c-Jun in LPS-treated BV2 cells were declined by efonidipine, confirming the finding from virtual screening. In addition, efonidipine inhibited the LPS-induced production of pro-inflammatory factors, including interleukin-1β (IL-1β) and nitric oxide. Similarly, the IL-1β production in LPS-treated HMC3 cells was also inhibited by efonidipine. Efonidipine markedly impeded cell migration stimulated by LPS in both cells. Furthermore, it inhibited the phosphorylation of inhibitor kappa B, thereby suppressing nuclear translocation of nuclear factor-κB (NF-κB) in LPS-treated BV2 cells. Taken together, efonidipine exerts anti-inflammatory and anti-migratory effects in LPS-treated microglial cells through inhibition of the JNK/NF-κB pathway. These findings imply that efonidipine may be a potential candidate for drug repositioning, with beneficial impacts on brain disorders associated with neuroinflammation.

• Journal of Preventive Medicine and Public Health
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• v.57 no.1
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• pp.55-64
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• 2024

Objectives: This study investigated the prevalence and characteristics of comorbid conditions in patients exposed to ionizing radiation and those who were involved in the Soviet-Afghan war. Methods: This study analyzed the frequency and spectrum of morbidity and comorbidity in patients over a long-term period (30-35 years) following exposure to ionizing radiation at the Semipalatinsk nuclear test site or the Chornobyl nuclear power plant, and among participants of the Soviet-Afghan war. A cohort study, both prospective and retrospective, was conducted on 675 patients who underwent comprehensive examinations. Results: Numerical data were analyzed using the Statistica 6 program. The results are presented as the mean±standard deviation, median, and interquartile range (25-75th percentiles). The statistical significance of between-group differences was assessed using the Student t-test and Pearson chi-square test. A p-value of less than 0.05 was considered statistically significant. We found a high prevalence of cardiovascular diseases, including hypertension (55.0%) and cardiac ischemia (32.9%); these rates exceeded the average for this age group in the general population. Conclusions: The cumulative impact of causal occupational, environmental, and ultra-high stress factors in the combat zone in participants of the Soviet-Afghan war, along with common conventional factors, contributed to the formation of a specific comorbidity structure. This necessitates a rational approach to identifying early predictors of cardiovascular events and central nervous system disorders, as well as pathognomonic clinical symptoms in this patient cohort. It also underscores the importance of selecting suitable methods and strategies for implementing treatment and prevention measures.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.2
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• pp.262-270
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• 2004

It is well known that long-term heavy ethanol intake causes alcoholic dementia, cerebellar degeneracy or Wernicke-Korsakoff syndrome and aggravates the conditions of many other neuro-psychotic disorders. Recently it is indicated that protein kinase C (PKC) plays an important role in the action of ethanol and in the neuro-adaptational mechanisms under chronic ethanol exposure. In order to investigate the effect of ethanol on PKC isoforms levels within the range of not showing any cytotoxicity, B103 neuroblastoma cell line trans-formed from murine central nervous system was employed and western blot analysis was carried out by using PKC isoform-specific antibodies. The changes of PKC-$\alpha$, ${\gamma}$, $\varepsilon$ and ζ level in the range of ethanol concentration 50∼200 mM were examined at the exposure time 1, 2, 8, 18 and 24 hrs in both cytosolic and membrane fraction. A typical ethanol concentration inducing the PKC isozymes was 100 mM, and the transforming time ranges of PKC isozymes could be considered as two different parts to each PKC isoform such as initial (0∼2 hrs) and prolonged (8∼24 hrs) stages. PKC-${\gamma}$ and PKC-$\varepsilon$ were clearly induced during the prolonged stages in cytosol at 18 hrs, and membrane fraction at 8 hrs and 18 hrs, respectively. On the other hand the PKC-$\alpha$ and PKC-ζ isozymes were largely induced in the prolonged stages at 18 hrs and 24 hrs, where the PKC-$\alpha$ isozyme was induced in both cytosol and membrane fractions at 200 mM ethanol concentration while the PKC-ζ isozyme was induced only in the membrane fractions at 100,200 mM. At 200 mM ethanol concentration of 24 hrs incubation in the prolonged stage, the PKC-$\alpha$ was maximally induced by 150% of the control values whereas the PKC-${\gamma}$ was significantly decreased to 47% of the control values. These results suggest that 100∼200 mM ethanol may modulate the signal transduction and neurotransmitter release in the central nervous system through the regulation of PKC isozymes, and the action of these isoforms may act differently each other in the cell.

• Tuberculosis and Respiratory Diseases
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• v.64 no.1
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• pp.39-43
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• 2008

A hiccup is caused by involuntary, intermittent, and spasmodic contractions of the diaphragm and intercostal muscles. It starts with a sudden inspiration and ends with an abrupt closure of the glottis. Even though a hiccup is thought to develop through the hiccup reflex arc, its exact pathophysiology is still unclear. The etiologies include gastrointestinal disorders, respiratory abnormalities, psychogenic factors, toxic-metabolic disorders, central nervous system dysfunctions and irritation of the vagus and phrenic nerves. Most benign hiccups can be controlled by traditional empirical therapy such as breath holding and swallowing water. However, though rare, a persistent hiccup longer than 48 hours can lead to significant adverse effects including malnutrition, dehydration, insomnia, electrolyte imbalance, and cardiac arrhythmia. An intractable hiccup can sometimes even cause death. We herein describe a patient with non-small cell lung cancer who was severely distressed by a persistent hiccup.