Lee, Teak Jin;Chun, Jin-Kyong;Kim, Ki Hwan;Kim, Khi Joo;Kim, Dong Soo
Pediatric Infection and Vaccine
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v.15
no.1
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pp.45-51
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2008
Purpose : Better understanding of the epidemiology of Streptococcus pneumoniae affects preventive and therapeutic strategies for children with otitis media. This study was undertaken to examine the prevalence of pneumococcal serotypes causing otitis media in children. Methods : Pneumococcal isolates obtained from the ear discharge of children with otitis media between January 2001 and December 2006 were characterized by serotyping and antibiotic susceptibility testing. Results : There were 54 pneumococcal isolates from 54 children with otitis media. The median age of patients was 13 months, and the proportion of children <5 years old was 81%. The predominant serotypes, in order of decreasing frequency, were 19A (44%), 19F(28%), 6B (7%), 6A (4%), 9V (4%), and 1 (4%); 23 isolates (43%) belonged to types included in the heptavalent pneumococcal conjugate vaccine (PCV7). The proportion of serotype 19A and 19F accounted for 72% of overall pneumococcal isolates, which accounted for 84% of pneumococcal isolates from otorrhea of children <5 years old (vs 20% in children ${\geq}5$ years old, P<0.001). All serotypes isolated from 3 vaccinees of PCV7 were 19A. There was no significant diminution in otitis media caused by pneumococcal vaccine serotypes after the introduction of PCV7. The frequency of nonsusceptibility to penicillin, erythromycin, and trimethoprim-sulfamethoxazole was higher in serotype 19A than in other non-vaccine serotypes, respectively. The frequency of multiple drug resistance was 96% in serotype 19A, compared with 29% in other non-vaccine serotypes (P=0.001). Conclusion : 19A was the most common pneumococcal serotype causing otitis media and represented a large proportion of strains with multiple drug resistance in children younger than 5 years of age.
In order to investigate the classification and antibiotic resistance of Salmonella species,718 isolates were isolated from patient in Seoul from 1996 to 2001. The two hundred and ninety eight isolates (41.5%) were identified as Sal. Enteritidis, followed by Sal. Typhi 218 isolates (30.4%), and Sal. Typhimurium 87 isolates (12.1%). The identified Salmonella species were most resistant to tetracycline (32.7%), followed by streptomycin (28.0%), ticarcillin (18.1%) and ampicillin (12.4%). Among isolates,34.7% of Sal. Enteritidis were resistant to tetracycline, 32.3% to streptomycin,23.2% to ticarcillin,13.5% to ampicillin, respectively. 13.8% of Sal. Typhi were resistant to streptomycin,10.6% to tetracycline, respectively.66.7% of Sal. Typhimurium were resistant to tetracycline, 42.5% to streptomycin, 28.7% to ticarcillin, 26.4% to ampicillin and 17.2% to chloramphenicol, respectively. Of 718 isolates, 324 isolates (45.1%) were resistant to 1 or more drugs and 64 isolates (19.8%) were resistant to 1 drug, 132 isolates (40.7%) were resistant to 2 drugs,50 isolates (15.4%) were resistant to 3 drugs, 27 isolates (8.3%) to 4 drugs,27 isolates (8.3%) to 5 drugs,22 Isolates (6.8%) to 6 drugs. The most prevalent multiple resistant pattern was tetracycline-kanamycin (35.5%), followed by tetracycline-kanamycin-ticarcillin (8.3%), and tetracycline-kanamycin-ticarcillin-ampicillin (7.4%) . Antibiotic resistant rate of Sal. Typhimurium was 73.6%,1311owe4 by Sal. Enteritidis 53.7% and Sal. Typhi 19.3%. Most Sal. Enteritidis was resistant to 1 drug o.2 drugs, whereas Sal. Typhi. and Sal.. Typhunurium were more .resistant to 5 (16.7%) or 6 drugs (26.6%). The old generation antibiotics such as ampicillin, tetracycline, and streptomycin were annually more resistant than the new generation antibiotics such as ceftriaxone, ciprofloxacin or cefoxitin.
In our search for new sources of bioactive secondary metabolites from Streptomyces sp., the ethyl acetate extracts from endophytic Streptomyces SUK 25 afforded five active diketopiperazine (DKP) compounds. The aim of this study was to characterize the bioactive compounds isolated from endophytic Streptomyces SUK 25 and evaluate their bioactivity against multiple drug resistance (MDR) bacteria such as Enterococcus raffinosus, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumanii, Pseudomonas aeruginosa, and Enterobacter spp., and their cytotoxic activities against the human hepatoma (HepaRG) cell line. The production of secondary metabolites by this strain was optimized through Thornton's medium. Isolation, purification, and identification of the bioactive compounds were carried out using high-performance liquid chromatography, high-resolution mass liquid chromatography-mass spectrometry, Fourier transform infrared spectroscopy, and nuclear magnetic resonance, and cryopreserved HepaRG cells were selected to test the cytotoxicity. The results showed that endophytic Streptomyces SUK 25 produces four active DKP compounds and an acetamide derivative, which were elucidated as $cyclo-({\text\tiny{L}}-Val-{\text\tiny{L}}-Pro)$, $cyclo-({\text\tiny{L}}-Leu-{\text\tiny{L}}-Pro)$, $cyclo-({\text\tiny{L}}-Phe-{\text\tiny{L}}-Pro)$, $cyclo-({\text\tiny{L}}-Val-{\text\tiny{L}}-Phe)$, and N-(7-hydroxy-6-methyl-octyl)-acetamide. These active compounds exhibited activity against methicillin-resistant S. aureus ATCC 43300 and Enterococcus raffinosus, with low toxicity against human hepatoma HepaRG cells. Endophytic Streptomyces SUK 25 has the ability to produce DKP derivatives biologically active against some MDR bacteria with relatively low toxicity against HepaRG cells line.
Background: Medical treatment of multiple drug resistant(MDR) pulmonary tuberculosis has been quite unsuccessful. We analyzed our experience to identify the benefits and complications of the pulmonary resection in MDR pulmonary tuberculosis. Material and Method: A retrospective review was performed in 27 patients who unerwent pulmonary resection for MDR pulmonary tuberculosis between January 1994 and March 1998. Mean age was 40 years and the average history of diagnosis prior to surgery was 3.1 years. All had resistance to an average of 4.4 drugs, and received second line drugs selected according to the drug sensitivity test. Most patients (93%) had cavitary lesions as the main focus. Bilateral lesions were identified in 19 patients (70%), however, the main focus was recognized in one side of the lung. Eleven patients (41%) were converted to negative sputum smear and/or culture before surgery. Result: Pneumonectomy was performed in 9 patients, lobectomy in 16 and segmentectomy in 2. There was no operative mortality. Morbidity had occurred in 7 patients (26%), prolonged air leak in 3 patients, reoperation due to bleeding in 2, bronchopleural fistula in 1, and reversible neurologic defect in 1. Median follow up period was 15 months (3-45 months). Sputum negative conversion was initially achieved in 22 patients (82%), and with continuous postopertive chemotherapy negative conversion was achieved in other 4 patients (14%). Only one pneumonectized patient (4%) failed due to considerable contralateral cavity. Conclusion: For patients with localized MDR pulmonary tuberculosis and with adequate pulmonary reserve function, surgical pulmonary resection combined with appropriate pre and postoperative anti-tuberculosis chemotherapy can achieve high success rate with acceptable morbidity.
Treatment with anticancer drugs changes the expression of multiple genes related to cell proliferation, migration, and drug resistance. These changes in gene expression may be connected to regulatory networks for each other. This study showed that doxorubicin treatment induces the expression of oncogenic FosB and decreases the expression of oncogenic SETDB1 in A549 and H1299 human lung cancer cells, which are different in tumor suppressor p53 status. However, a small difference was detected in the quantitative expression of those proteins in the two kinds of cells. To examine the potential regulation of SETDB1 and FosB by p53, we predicted putative p53 binding sites on the genomic DNA of SETDB1 and FosB using a TF motif binding search program. These putative p53 binding sites were identified as 18 sites in the promoter regions of SETDB1 and 21 sites in the genomic DNA of FosB. A luciferase assay confirmed that p53 negatively regulated the promoter activities of SETDB1 and FosB. Furthermore, the results of RT-PCR, western blot, qPCR, and immunostaining experiments indicated that the transfection of exogenous p53 decreases the expression of SETDB1 and FosB in H1299 cells. This indicates that p53 negatively regulates the expression of SETDB1 and FosB at the transcriptional level. Collectively, the downregulation of SETDB1 and FosB by p53 may provide functional networks for apoptosis and for the survival of cancer cells during anticancer drug treatment.
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL/Apo2L) is a recently identified member of the TNF ligand family that can initiate apoptosis through the activation of their death receptors. TRAIL has been paid attention as a potential anti-cancer drug, because it selectively induces apoptosis in tumor cells in vitro and in vivo but not in most normal cells. However, recent studies have shown that some cancer cells including malignant renal cell carcinoma and hepatocellular carcinoma, are resistant to the apoptotic effects of TRAIL. Therefore, single treatment with TRAIL may not be sufficient for the treatment of various malignant tumor cells. Understanding the molecular mechanisms of TRAIL resistance and identification of sensitizers capable of overcoming TRAIL resistance in cancer cells is needed for the establishment of more effective TRAIL-based cancer therapies. Chemotherapeutic drugs induce apoptosis and the upregulation of death receptors or activation of intracellular signaling pathways of TRAIL. Numerous chemotherapeutic drugs have been shown to sensitize tumor cells to TRAIL-mediated apoptosis. In this study, we summarize biological agents and drugs that sensitize tumors to TRAIL-mediated apoptosis and discuss the potential molecular basis for their sensitization.
Park, Seo-Young;Baek, Yeong-Bin;Park, Sang-Ik;Lee, Chang-Min;Kim, Sung-Hak
Journal of Life Science
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v.31
no.2
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pp.248-255
/
2021
Mammary gland tumors are one of the most common cancers in female dogs, and there are various types of cells depending on the tumor type. Complex carcinoma consists of a combination of luminal epithelial and myoepithelial cells with intra-tumoral heterogeneity. However, the origins of these tumor cells and their effects on the malignancies of tumors have not been identified. Recently, it has been reported that cancer stem cells, identified in several types of human tumors, are involved in tumor heterogeneity and may also contribute to malignancies such as tumor recurrence and metastasis. Interestingly, cancer stem cells share several abilities of self-renewal and cell differentiation into multiple types of cancer cells, but they have abnormal genetic mutation and signal transduction pathways to regulate the maintenance of stem cell characters. Moreover, it is known that these cell populations contribute to cell metastasis as well as cell resistance against chemo- and radio-therapeutics that promote tumor recurrence. The existence of cancer stem cells might explain the intra-tumoral heterogeneity and cancer aggressiveness during tumorigenesis in canine mammary gland tumors. This review summarizes the characteristics and types of canine mammary gland tumors, the definition of tumor stem cells, methods of isolation, and clinical significance.
The ubiquitin system uses ligases and deubiquitinases (DUBs) to regulate ubiquitin position on protein substrates and is involved in many biological processes which determine stability, activity, and interaction of the target substrate. DUBs are classified in six groups according to catalytic domain, namely ubiquitin-specific proteases (USPs); ubiquitin C-terminal hydrolases (UCHs); ovarian tumor proteases (OTUs); Machado Joseph Disease proteases (MJDs); motif interacting with Ub (MIU)-containing novel DUB family (MINDY); and Jab1/MPN/MOV34 metalloenzymes (JAMMs). Otubain 1 (OTUB1) is a DUB in the OTU family which possesses both canonical and non-canonical activity and can regulate multiple cellular signaling pathways. In this review, we describe the function of OTUB1 through regulation of its canonical and non-canonical activities in multiple specifically cancer-associated pathways. The canonical activity of OTUB1 inhibits protein ubiquitination by cleaving Lys48 linkages while its non-canonical activity prevents ubiquitin transfer onto target proteins through binding to E2-conjugating enzymes, resulting in the induction of protein deubiquitination. OTUB1 can therefore canonically and non-canonically promote tumor cell proliferation, invasion, and drug resistance through regulating FOXM1, ERα, KRAS, p53, and mTORC1. Moreover, clinical research has demonstrated that OTUB1 overexpresses with high metastasis in many tumor types including breast, ovarian, esophageal squamous, and glioma. Therefore, OTUB1 has been suggested as a diagnosis marker and potential therapeutic target for oncotherapy.
Kim, Eun Kyung;Shim, Tae Sun;Lee, Jung Yeon;Oh, Yeon-Mok;Lim, Chae-Man;Lee, Sang Do;Koh, Younsuck;Kim, Dong Soon;Kim, Won Dong;Kim, Woo Sung
Tuberculosis and Respiratory Diseases
/
v.57
no.3
/
pp.226-233
/
2004
Background : Interferon-gamma (IFN-${\gamma}$) is a critical cytokine in the defense against a Mycobacterium tuberculosis infection. Even though IFN-${\gamma}$ has occasionally been used in the treatment of refractory multidrug-resistant tuberculosis (MDR-TB) with some promising results, there is still some controversy regarding the therapeutic efficacy of IFN-${\gamma}$. This study was performed to examine the effect of subcutaneous IFN-${\gamma}$ in the treatment of MDR-TB patients. Methods : Six patients with refractory MDR-TB were enrolled in this study. Two million IU of IFN-${\gamma}$ was administered subcutaneously three times a week with the concomitant administration of antituberculous drugs for at least for 28 weeks. During the IFN-${\gamma}$ therapy, the sputum smear and culture, radiological and clinical evaluations were performed every 4 weeks throughout the study period. Results : The mean age of the 6 patients was 37 years (ranges, 15-61 years). The drug susceptibility test to standard antituberculous drugs revealed resistance to an average of 6.8 (${\pm}1.2$) agents including isoniazid and rifampicin. An average of 10.8 (${\pm}1.3$) antituberculous drugs were prescribed before IFN-${\gamma}$ therapy. The culture became negative in 2 patients (33%) after initiating IFN-${\gamma}$ therapy; one at 8 weeks, and the other at 24 weeks. Finally, after stopping the IFN-${\gamma}$ therapy after 28 weeks, the culture became positive again in the two patients who were culture-negative. The other 4 patients who failed in the culture conversion are still on antituberculous treatment except for one who died of tuberculosis. Conclusion : Even though 28 weeks of subcutaneous IFN-${\gamma}$ therapy in combination with antituberculous drugs was successful in inducing the culture-negative conversion in some patients with refractory MDR-TB, the culture became positive again after stopping the IFN-${\gamma}$ therapy. This suggests that subcutaneous IFN-${\gamma}$ therapy may have suppressive effect on tuberculosis only during the IFN-${\gamma}$ therapy period in some patients. Further studies will be needed to determine the optimum dose, the administration route, the duration of therapy, and the predicting factors of the response to adjuvant IFN-${\gamma}$ therapy.
Ceftizoxime sodium is a new synthetic ${\beta}$-lactam antibiotic combining potent antibacterial activity with high stability to a wide range of bacterial ${\beta}$-lactamase. This experiment was achieved to evaluate the antibacterial activities of ceftizoxime sodium againist Gram negative enteric bacteria isolated from in outpatient visiting Yeungnam university hospital and to study the emergence of drug induced bacterial varients which resist to ceftizoxime in vitro. The antibacterial activity of the ceftizoxime was compared with that of antibiotics and its effect on population of normal intestinal flora in mice was observed. The results are summarized as follows : 1. Highly effective antibacterial activity of ceftizoxime against Gram negative enteric bacilli was demonstrated and this antibacterial activity was superior to that of ampicillin. 2. Several test strains shows multiple antibiotic resistence. Among 15 strains of Escherichia coli, 1 strain was resistent to ampicillin, cefadroxyl, gentamicin, tetracycline, and 2 strains were resistent to ampicillin, cefadroxyl, tetracycline, five strains of Escherichia coli and Enterobacter cloacae was resistent to amplicillin, tetracycline and Shigella dysenteria was resistent to ampicillin, gentamicin, tetracycline. 3. The frequency of in vitro emergence of resistent varients among ceftizoxime sensitive bacteria in the presence of increasing concentrations of the compound was found to be low. 4. Plasmid was isolated in 6 of 9 strains (6 strains of Escherichia coli, Shigella dysenteriae, Enterobacter cloaceae and Salmonella typhi) That showed different antibiotic resistance. They were 5 strains of Escherichia coli and 1 strain of Shigella dysenteriae. However, plasmid could not be considered as a hallmark for antibiotic resistance by this. Further studies with curing experiment are to be accomplished for this purpose. 5. Changes in the bacterial count of normal intestinal flora following 25mg/kg/day administration of ceftizoxime over S consecutive days were not significant. In conclusion, ceftizoxime appeared to be a drug of choice in the treatment of Gram negative enteric bacilli infection.
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