• Tuberculosis and Respiratory Diseases
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• v.70 no.2
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• pp.105-112
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• 2011

Pneumonia is frequently encountered in the clinical fields, both as a cause for admission and as a complication of the underlying disorder or as the course of treatment. Pneumonia is the second most common hospital-acquired infection and is associated with the highest morbidity and mortality rates among hospital-acquired infections. The guidelines for the management of hospital-acquired pneumonia by the American Thoracic Society include identifying individuals who have recently received antibiotics therapy or have been in medical facilities; these individuals are at higher risk for infection with multiple drug resistant organisms. Individuals, who have acquired pneumonia according to this clinical scenario, have what is known as healthcare-associated pneumonia (HCAP). Patients with HCAP should be considered to have potentially drug-resistant pathogens and should receive broad spectrum empiric antibiotic therapy directed at the potentially resistant organisms. In this paper, the diagnosis, risk factors, and treatment of HCAP are discussed.

• Archives of Pharmacal Research
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• v.21 no.3
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• pp.286-290
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• 1998

The abuse of zipeprol, an antitussive agent, was found to be most prevalent among young people in Korea. Because abusers take large doses of this drug for its hallucinogenic effects, fatalities from zipeprol overdose abuse have been on the rise since 1991. Since 1991, a total of 69 zipeprol-related deaths have occurred throughout the nation. A demographic study shows that in ninety six percent of cases involving zipeprol alone, the victims were in their teens and twenties. The mate/female ratio in zipeprol related death was 3.5:1. Most of these zipeprol-associated deaths occurred in the larger cities of Seoul and Inchon. The blood concentration of zipeprol ranged from 0.8 to $38.3{\mu}g/mL $in single drug involved deaths, while zipeprol varied from to 35.3 $0.1{\mu}g/mL $in zipeprol and dextromethorphan victims.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2285-2289
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• 2012

Multidrug resistance (MDR) is a main cause of failure in the chemotherapeutic treatment of malignant disorders. One of the well-known genes responsible for drug resistance encodes the multidrug resistance-associated protein (MRP1). The association of MRP1 with clinical drug resistance has not systematically been investigated in Iranian pediatric leukemia patients. We therefore applied real-time RT-PCR technology to study the association between the MRP1 gene and MDR phenotype in Iranian pediatric leukemia patients. We found that overexpression of MRP1 occurred in most Iranian pediatric leukemia patients at relapse. However, no relation between MRP1 mRNA levels and other clinical characteristics, including cytogenetic subgroups and FAB subtypes, was found.

• Korean Journal of Clinical Pharmacy
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• v.16 no.2
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• pp.155-164
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• 2006

Great inter-variability in drug response and adverse drug reactions is related to inter-variability of drug bioavailability, drug interaction and patient's disease and physyological state that cause change in absorption, distribution, metabolism and excretion of drugs. However, these alone do not sufficiently predict and explain inter-variability in drug response. In recent studies, it is reported that inter-variability in drug response and adverse drug reactions may largely resulted from genetically determined differences in drug absoption, distribution, metabolism and drug target proteins. Especially, the major human drug-metabolizing enzymes such as CYP450, N-acetyl tranferase, thiopurine S-methyl transferase, glutathione S-transferase are identified as the major gene variants that cause inter-individual variability in drug's response and adverse drug reactions. These variations may have most significant implications for those drugs that have narrow therapeutic index and serious adverse drug reactions. Therefore, the genetic variation such as polymorphisms in drug metabolizing enzymes can affect the response of individuals to drugs that are used in the treatment of depression, psychosis, cancer, cardiovascular disorders, ulcer and gastrointestinal disorders, pain and epilepsy, among others. This review describes the pharmacogenomics of the drug metabolizing enzymes associated with the drug response and its clinical applications.

• Bulletin of the Korean Chemical Society
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• v.34 no.4
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• pp.1131-1136
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• 2013

Parabens, the esters of p-hydroxybenzoic acid, have been widely used as antimicrobial preservatives in cosmetic products, drugs, and processed foods and beverages. However, some parabens have been shown to have weak estrogenic effects through in vivo and in vitro studies. Because such widespread use has raised concerns about the potential human health risks associated with exposure to parabens, we developed a simultaneous analytical method to quantify 4 parabens (methyl, ethyl, propyl, and butyl) in human urine, by using solid-phase extraction and high-performance liquid chromatography coupled with triple quadrupole mass spectrometry. This method showed good specificity, linearity ($R^2$ > 0.999), accuracy (92.2-112.4%), precision (0.9-9.6%, CV), and recovery (95.7-102.0%). The LOQs for the 4 parabens were 1.0, 0.5, 0.2, and 0.5 ng/mL, respectively. This method could be used for quick and accurate analysis of a large number of human samples in epidemiological studies to assess the prevalence of human exposure to parabens.

• Molecules and Cells
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• v.38 no.6
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• pp.562-572
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• 2015

We previously reported the role of histone deacetylase 3 (HDAC3) in response to anti-cancer drugs. The decreased expression of HDAC3 in anti-cancer drug-resistant cancer cell line is responsible for the resistance to anti-cancer drugs. In this study, we investigated molecular mechanisms associated with regulation of HDAC3 expression. MG132, an inhibitor of proteasomal degradation, induced the expression of HDAC3 in various anti-cancer drug-resistant cancer cell lines. Ubiquitination of HDAC3 was observed in various anti-cancer drug-resistant cancer cell lines. HDAC3 showed an interaction with SIAH2, an ubiquitin E3 ligase, that has increased expression in various anti-cancer drug-resistant cancer cell lines. miRNA array analysis showed the decreased expression of miR-335 in these cells. Targetscan analysis predicted the binding of miR-335 to the 3'-UTR of SIAH2. miR-335-mediated increased sensitivity to anti-cancer drugs was associated with its effect on HDAC3 and SIAH2 expression. miR-335 exerted apoptotic effects and inhibited ubiquitination of HDAC3 in anti-cancer drug-resistant cancer cell lines. miR-335 negatively regulated the invasion, migration, and growth rate of cancer cells. The mouse xenograft model showed that miR-335 negatively regulated the tumorigenic potential of cancer cells. The down-regulation of SIAH2 conferred sensitivity to anti-cancer drugs. The results of the study indicated that the miR-335/SIAH2/HDAC3 axis regulates the response to anti-cancer drugs.

• Journal of Periodontal and Implant Science
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• v.54 no.4
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• pp.224-235
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• 2024

Purpose: This systematic review investigated whether drug use is associated with the presence of oral lesions and periodontitis. Methods: A search was performed for studies that analyzed the presence of periodontitis and/or oral lesions in users of crack, cocaine, and/or marijuana in the PubMed, Scopus, and Web of Science databases. Observational studies in English, Spanish, or Portuguese, without limitation of year, age, and sex, were included. Studies that did not evaluate periodontitis and oral lesions according to the eligibility criteria were excluded. Two authors independently performed study selection and data extraction using a standardized form. The risk of bias of studies included in the meta-analysis was assessed using the Joanna Briggs Institute Critical Appraisal Checklist. The meta-analysis included studies that investigated the association of drug use with the outcome. Results: The initial search resulted in 9,279 articles, from which 16 studies with 15,434 participants were included in the review and 8 studies were included in the meta-analysis. Most studies that evaluated periodontitis in drug users and non-users found a positive association in users. Most studies that analyzed oral lesions reported a higher prevalence, association, or risk of oral lesions in drug users than in non-users. A critical evaluation identified a need to improve the control and reporting of confounding factors in studies on this topic. An association was found between periodontitis and the use of crack, cocaine, and/or marijuana (odds ratio [OR], 1.84; 95% confidence interval [CI], 1.04-3.27; P=0.04) and between oral lesions and the use of these drugs (OR, 2.13; 95% CI, 1.58-2.86; P<0.001). Conclusions: Drug users are more likely to develop oral lesions and periodontitis than nonusers. However, the results should be interpreted with caution, considering the heterogeneity and quality of the studies included in the analysis.

• Korean Journal of Clinical Pharmacy
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• v.18 no.2
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• pp.75-83
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• 2008

Purpose: Currently lung cancer ranks second in cancer for incidence rate and is a disease that ranks first for a death rate by cancerous growth because it is already advanced at the time of diagnosis. The purpose of this paper was to analyze the factors that affect the effectiveness of and rash occurrence by Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR TKI) in patients with non-small cell lung cancer. Methods: A retrospective chart review of 100 patients, who took EGFR TKI (erlotinib, gefitinib) among patients who were diagnosed with non-small cell lung cancer in a Hospital in Korea between May 2005 and February 2008, was conducted. The drug effectiveness was evaluated by Response Evaluation Criteria In Solid Tumor. Results: EGFR mutation was the only factor associated with drug response (complete response and partial response). When stable disease was added to drug response as the evaluation parameter, ECOG and rash as well as EGFR mutation were found to be important factors. Survival, however, was not affected by EGFR mutation. The factors influenced on survival were older age (${\geq}65$), low ECOG ($1{\sim}2$), adenocarcinoma and rash. In the case of rash, group with EGFR mutation or low ECOG showed significantly higher chance of occurrence. There was no significant difference in rash occurrence between gefitinib and erlotinib groups. Conclusions: Based on the results, EGFR mutation positive and low ECOG ($1{\sim}2$) were significantly important factors for both effectiveness of EGFR TKI and rash occurrence. Also, rash itself was found to be an independently significant factor for the disease control and survival. Therefore, while administering EGFR TKI, patients who have the factors associated with rash occurrence should be closely monitored for effective and safe drug therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5619-5625
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• 2012

Gastric carcinoma is a leading cause of cancer death in the world and multi-drug resistance (MDR) is an essential aspect of gastric carcinoma chemotherapy failure. Recent studies have shown that integrin-linked kinase (ILK) is involved in metastasis of human tumors, expression silencing of ILK inhibiting the metastasis of several types of cultured human cancer cells. However, the role and potential mechanism of ILK to reverse the multi-drug resistance in human gastric carcinoma is not fully clear. In this report, we focused on roles of expression silencing of ILK in multi-drug resistance reversal of human gastric carcinoma SGC7901/DDP cells, including increased drug sensitivity to cisplatin, cell apoptosis rates, and intracellular accumulation of Rhodamine-123, and decreased mRNA and protein expression of multi-drug resistance gene (MDR1), multi-drug resistance-associated protein (MRP1), excision repair cross-complementing gene 1 (ERCC1), glutathione S-transferase -${\pi}$ (GST-${\pi}$) and RhoE, and transcriptional activation of AP-1 and NF-${\kappa}B$ in ILK silenced SGC7901/DDP cells. We also found that there was a decreased level of p-Akt and p-ERK. The results indicated that ILK might be used as a potential therapeutic strategy to combat multi-drug resistance through blocking PI3K-Akt and MAPK-ERK pathways in human gastric carcinoma.

• 대한임상약리학회:학술대회논문집
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• 2006.11a
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• pp.43-44
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• 2006