Objective: Oxidative stress (OS) is a pathological process arising from the excessive production of free radicals in the body. It has the potential to alter animal gene expression and cause damage to the jejunum. However, there have been few reports of changes in the expression of long noncoding RNAs (lncRNAs) in the jejunum in piglets under OS. The purpose of this research was to examine how lncRNAs in piglet jejunum change under OS. Methods: The abdominal cavities of piglets were injected with diquat (DQ) to produce OS. Raw reads were downloaded from the SRA database. RNA-seq was utilized to study the expression of lncRNAs in piglets under OS. Additionally, six randomly selected lncRNAs were verified using quantitative real-time polymerase chain reaction (qRT-PCR) to examine the mechanism of oxidative damage. Results: A total of 79 lncRNAs were differentially expressed (DE) in the treatment group compared to the negative control group. The target genes of DE lncRNAs were enriched in gene ontology (GO) terms and Kyoto encyclopedia of genes and genomes (KEGG) signaling pathways. Chemical carcinogenesis-reactive oxygen species, the Foxo signaling pathway, colorectal cancer, and the AMPK signaling pathway were all linked to OS. Conclusion: Our results demonstrated that DQ-induced OS causes differential expression of lncRNAs, laying the groundwork for future research into the processes involved in the jejunum's response to OS.
Son, Ji Young;Jung, Ji Ye;Ha, You Jung;Hong, Soo Jung;Jung, Min Kyu;Chung, Moon Jae;Seo, Yong Sung;Moon, Ji Ae;Byun, Min Kwang;Park, Byung Hoon;Moon, Jin Wook;Park, Moo Suk;Kim, Young Sam;Chang, Joon;Kim, Sang Kyum;Chung, Kyung Young;Kim, Se Kyu
Tuberculosis and Respiratory Diseases
/
v.65
no.4
/
pp.313-317
/
2008
Lipoma is a common neoplasm in soft tissues. However, an intrapulmonary lipoma is a rare benign tumor. Patients with a bronchial lipoma might have a malignant potential related to their smoking history due to the case reports of lung cancer accompanied with lipoma. Endobronchial lipoma can cause irreversible parenchymal lung damage if not diagnosed and treated early. Therefore, it should initially be treated by fiberoptic bronchoscopy or surgery depending on the status of distal parenchymal lung damage. Bronchiolitis obliterans with organizing pneumonia (BOOP) is a pathological syndrome that is defined by the presence of buds of granulation tissue consisting of fibroblasts and collagen within the lumen of the distal air spaces. BOOP is caused by drug intoxication, connective tissue disease, infection, obstructive pneumonia, tumors, or an unknown etiology. We encountered a 58 year-old male patient with endobronchial lipoma, causing the collapse of the right middle and lower lobes, and BOOP due to obstructive pneumonia.
Background: Anticancer agents induce a variety of adverse effects when administered to cancer patients. Busulfan is a known antileukemia agent. When administered for treatment of leukemia in young patients, busulfan could cause damage to the male reproductive system as one of its adverse effects, resulting in sterility. Methods: We investigated the effects of Korean Red Ginseng extract (KRGE) on busulfan-induced damage and/or dysfunction of the male reproductive system. Results: We found that administration of busulfan to mice: decreased testis weight; caused testicular histological damage; reduced the total number of sperm, sperm motility, serum testosterone concentration; and eventually, litter size. Preadministration of KRGE partially attenuated various busulfan-induced damages to the male reproductive system. These results indicate that KRGE has a protective effect against busulfan-induced damage to the male reproduction system. Conclusion: The present study shows a possibility that KRGE could be applied as a useful agent to prevent or protect the male reproductive system from the adverse side effects induced by administration of anticancer agents such as busulfan.
Lee, Jung Hyun;Yeom, Hyungseon;Kim, Hyeon Chang;Suh, Il;Kim, Mi Kyung;Shin, Min-Ho;Shin, Dong Hoon;Koh, Sang-Baek;Ahn, Song Vogue;Lee, Tae-Yong;Ryu, So Yeon;Song, Jae-Sok;Choe, Hong-Soon;Lee, Young-Hoon;Choi, Bo Youl
Journal of Preventive Medicine and Public Health
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v.49
no.5
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pp.275-287
/
2016
Objectives: C-reactive protein (CRP), an inflammatory biomarker, has been widely used as a preclinical marker predictive of morbidity and mortality. Although many studies have reported a positive association between CRP and mortality, uncertainty still remains about this association in various populations, especially in rural Korea. Methods: A total of 23 233 middle-aged participants (8862 men and 14 371 women) who were free from cardiovascular disease, cancer, and acute inflammation (defined by a CRP level ${\geq}10mg/L$) were drawn from 11 rural communities in Korea between 2005 and 2011. Blood CRP concentration was analyzed as a categorical variable (low: 0.0-0.9 mg/L; intermediate: 1.0-3.0 mg/L; high: 3.1-9.9 mg/L) as well as a continuous variable. Each participant's vital status through December 2013 was confirmed by death statistics from the National Statistical Office. Cox proportional hazard models were used to assess the independent association between CRP and mortality after adjusting for other risk factors. Results: The total quantity of observed person-years was 57 975 for men and 95 146 for women, and the number of deaths was 649 among men and 367 among women. Compared to the low-CRP group, the adjusted hazard ratio for all-cause mortality of the intermediate group was 1.17 (95% confidence interval [CI], 0.98 to 1.40) for men and 1.27 (95% CI, 1.01 to 1.61) for women, and the corresponding values for the high-CRP group were 1.98 (95% CI, 1.61 to 2.42) for men and 1.41 (95% CI, 1.03 to 1.95) for women. Similar trends were found for CRP evaluated as a continuous variable and for cardiovascular mortality. Conclusions: Higher CRP concentrations were associated with higher mortality in a rural Korean population, and this association was more prominent in men than in women.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
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v.26
no.6
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pp.581-590
/
2000
Alterations in the cellular genome affecting the expression or function of genes controlling cell growth and differentiation are considered to be the main cause of cancer. Over 30 oncogenes can be activated by insertional mutagenesis, single point mutations, chromosomal translocations and gene amplification. The ras oncogenes have been detected in $15{\sim}20%$ of human tumors that include some of the most common forms of human neoplasia and are known to acquire their transforming properties by single point mutations in two domains of their coding sequences, most commonly in codons 12 and 61. The ras gene family consists of three functional genes, N-ras, K-ras and H-ras which encode highly similar proteins of 188 or 189 amino acid residues generically known as P21. ras proteins have been shown to bind GTP and GTP, and possess intrinsic GTPase activity. Experimental study was performed to observe the mutational change of the ras gene family and apply the results to the clinical activity. 36 Golden Syrian Hamster each weighing $60{\sim}80g$ were used and painted with 0.5% DMBA by 3 times weekly on the right buccal cheek(experimental side) for 6, 8, 10, 12, 14 and 16 weeks. Left buccal cheek (control side) was treated with mineral oil as the same manner of the right side. The hamsters were sacrificed on the 6, 8, 10, 12, 14 & 16 weeks. Normal and tumor tissues from paraffin block were completely dissected by microdissection and DNA from both tissue were isolated by proteinase K/phenol/chloroform extraction. Segments of the K-ras and H-ras gene were amplified by PCR using the oligonucleotide primers corresponding to the homologous region (codon 12 and 61) of the hamster gene, and then confirmational change of ras genes was observed by SSCP and autosequencing analysis. The results were as follows : 1. Malignant lesion could be found in the experimental side from the experimental six weeks. 2. One hamster among six showed point mutation of the H-ras codon 12($G{\rightarrow}A$ transition) at the experimental 10 and 14 weeks. 3. One of six at 6 weeks, two of six at 8 weeks and one of six at 12 weeks revealed the confirmational change of the H-ras codon 61($A{\rightarrow}T$ transversion). 4. The incidence of point mutation of H-ras codon 12 and 61 were 5.5%(2 of 36) and 11%(4 of 36) respectively. 5. Point mutation of the K-ras could not be seen during the whole experimental period. Form the above results, these findings strongly support the concept that H-ras oncogenes may have the influence of the DMBA induced carcinoma of hamster buccal pouch.
Choi, Sungim;Choi, Heun;Park, Seong Yeon;Kwak, Yee Gyung;Song, Je Eun;Shin, So Youn;Baek, Ji Hyeon;Shin, Hyun-IL;Oh, Hong Sang;Kim, Yong Chan;Yeom, Joon-Sup;Han, Jin-Hee;Kim, Min Jae
Parasites, Hosts and Diseases
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v.60
no.1
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pp.39-43
/
2022
Plasmodium vivax exhibits dormant liver-stage parasites, called hypnozoites, which can cause relapse of malaria. The only drug currently used for eliminating hypnozoites is primaquine. The antimalarial properties of primaquine are dependent on the production of oxidized metabolites by the cytochrome P450 isoenzyme 2D6 (CYP2D6). Reduced primaquine metabolism may be related to P. vivax relapses. We describe a case of 4 episodes of recurrence of vivax malaria in a patient with decreased CYP2D6 function. The patient was 52-year-old male with body weight of 52 kg. He received total gastrectomy and splenectomy 7 months before the first episode and was under chemotherapy for the gastric cancer. The first episode occurred in March 2019 and each episode had intervals of 34, 41, and 97 days, respectively. At the first and second episodes, primaquine was administered as 15 mg for 14 days. The primaquine dose was increased with 30 mg for 14 days at the third and fourth episodes. Seven gene sequences of P. vivax were analyzed and revealed totally identical for all the 4 samples. The CYP2D6 genotype was analyzed and intermediate metabolizer phenotype with decreased function was identified.
Xerostomia and xerophthalmia are delicate or serous side effects, occuring when the radiotherapy is administered to the head and neck cancer patient. It is known that the cause of the above side effect is radiosensitivity of serous cells. In this study, the ultrastructural features of the parotid glands of the X-irradiated rats were observed. Sprague-Dawley rats weighing 200-250g each were anesthetized with sodium thiopental, and placed on the Mitsubishi linear accelerator. Only the head and neck areas of animals were exposured at the distance of 80cm, within the area of $30X30cm$, in the depth of 1cm, with the speed of 200R/min. Total doses applied were 3,000R or 6,000R depending on the experimental groups. Animals were sacrificed on the 6th hour, 2nd day and 6th day after the irradiation. Parotid glands were fixed in the 2.5% glutaraldehyde-1.5% paraformaldehyde solution, and followed by refixation in the 1% osmium tetroxide solution. Dehydrated blocks were embedded in araldite mixture, and ultrathin sections were cut. Sections were contrasted with the solution of uranyl acetate and lead citrate, and observed with JEM 100 CX-II electron microscope. The results were as follows: 1. Normal parotid acinar cells are two types; the light and the dark acinar cells. The light acinar cell contains dense secretory granules, whereas dark acinar cells contains granules of medium density with some darker spots within them, or other cells contain granules of medium density with darker rims. 2. Six hours after the irradiation, many acinar cells were degenerated showing variable stages of cytolytic bodies, light bodies, or dense degenerations. Within the acinar cell, Golgi apparatus and granular endoplasmic reticula were most severely altered elements. Granules showed more contrasting densities and irregularities. 3. Two days after the irradiation, some cytolytic bodies, and focal lucent degeneration of cytoplasm, and fine granular alteration of cytoplasmic matrix were pronounced. But other elements including secretory granules are rather looked unlatered. 4. Six days after the irradiation, most severe alterations were seen. Many intracellular canaliculi (or secretion figures), quanta of cytoplasm containing secretion antecedants, severely irregular luminal border, and again contrasting density of secretory granules showing tigroid spots or dense rims were noted. And myoepithelial degenerations were observed not uncommonly. 5. Irregular densities of secretory granules were interpreted as abnormal components of protein or carbohydrate portion are synthesized or abnormally metabolized under severe X-irradiation. 6. Myoepithelial degeneration and related alteration of nerve endings, etc., were suggested as the other causes of xerostomia following X-irradiation. 7. It is requested that radiation doses should be arranged, considering in mind not only the sensitivity of acinar cells but also the myoepithelial and neural functions.
Background: To develop a novel treatment strategy for hepatitis B virus infection, a major cause of liver chirosis and cancer, we aimed to make human monoclonal antibodies inhibiting RNase H activity of P protein playing in important role in HBV replication. In this regard, phage display technology was employed and demonstrated as an efficient cloning method for human monoclonal antibody. So this study analysed the usability of human monoclonal antibody as protein based gene therapy. Methods: RNase H of HBV was expressed as fusion protein with maltose binding protein and purified with amylose resin column. Single chain Fv (scFv) phage antibody library was constructed by PCR cloning using total RNAs of PBMC from 50 healthy volunteers. Binders to RNase H were selected with BIAcore 2000 from the constructed library, and purified as soluble antibody fragment. The affinity and sequences of selected antibody fragments were analyzed with BIAcore and ABI automatic sequencer, respectively. And finally RNase H activity inhibiting assay was carried out. Results: Recombinant RNase H expressed in E. coli exhibited an proper enzyme activity. Naive library of $4.46{\times}10^9cfu$ was screened by BIAcore 2000. Two clones, RN41 and RN56, showed affinity of $4.5{\times}10^{-7}M$ and $1.9{\times}10^{-7}M$, respectively. But RNase H inhibiting activity of RN41 was higher than that of RN56. Conclusion: We cloned human monoclonal antibodies inhibiting RNase H activity of P protein of HBV. These antibodies can be expected to be a good candidate for protein-based antiviral therapy by preventing a replication of HBV if they can be expressed intracellularly in HBV-infected hepatocytes.
Chemotherapy-induced side effects affect the quality of life and efficacy of treatment of cancer patients. Current approaches for treating the side effects of chemotherapy are poorly effective and may cause numerous harmful side effects. Therefore, developing new and effective drugs derived from natural nontoxic compounds for the treatment of chemotherapy-induced side effects is necessary. Experiments in vivo and in vitro indicate that Panax ginseng (PG) and its ginsenosides are undoubtedly non-toxic and effective options for the treatment of chemotherapy-induced side effects, such as nephrotoxicity, hepatotoxicity, cardiotoxicity, immunotoxicity, and hematopoietic inhibition. The mechanism focus on anti-oxidation, anti-inflammation, and anti-apoptosis, as well as the modulation of signaling pathways, such as nuclear factor erythroid-2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1), P62/keap1/Nrf2, c-jun Nterminal kinase (JNK)/P53/caspase 3, mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinases (ERK), AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR), mitogen-activated protein kinase kinase 4 (MKK4)/JNK, and phosphatidylinositol 3-kinase (PI3K)/AKT. Since a systemic review of the effect and mechanism of PG and its ginsenosides on chemotherapy-induced side effects has not yet been published, we provide a comprehensive summarization with this aim and shed light on the future research of PG.
Kim, Byung-Su;Kim, Soo-Kyoung;Kim, Jae-Moon;Moon, Heui-Soo;Park, Kwang-Yeol;Park, Jeong Wook;Sohn, Jong-Hee;Song, Tae-Jin;Chu, Min Kyung;Cha, Myoung-Jin;Kim, Byung-Kun;Cho, Soo-Jin
Journal of the Korean neurological association
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v.36
no.4
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pp.294-301
/
2018
Background: Neuroimaging can play a crucial role in discovering potential abnormalities to cause secondary headache. There has been a progress in the fields of headache diagnosis and neuroimaging in the past two decades. We sought to investigate neuroimaging findings according to headache disorders, age, sex, and imaging modalities in first-visit headache patients. Methods: We used data of consecutive first-visit headache patients from 9 university and 2 general referral hospitals. The International Classification of Headache Disorders, third edition, beta version was used in headache diagnosis. We finally enrolled 1,080 patients undertook neuroimaging in this study. Results: Among 1,080 patients (mean age: $47.7{\pm}14.3$, female: 60.8%), proportions of headache diagnosis were as follows: primary headaches, n=926 (85.7%); secondary headaches, n=110 (10.2%); and cranial neuropathies and other headaches, n=43 (4.1%). Of them, 591 patients (54.7%) received magnetic resonance imaging (MRI). Neuroimaging abnormalities were found in 232 patients (21.5%), and their proportions were higher in older age groups and male sex. Chronic cerebral ischemia was the most common finding (n=88, 8.1%), whereas 76 patients (7.0%) were found to have clinically significant abnormalities such as primary brain tumor, cancer metastasis, and headache-relevant cerebrovascular disease. Patients underwent MRI were four times more likely to have neuroimaging abnormalities than those underwent computed tomography (33.3% vs. 7.2%, p<0.001). Conclusions: In this study, the findings of neuroimaging differed according to headache disorders, age, sex, and imaging modalities. MRI can be a preferable neuroimaging modality to identify potential causes of headache.
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