The authors developed a biodegradable polymer that releases an antibiotic (nalidixic acid) slowly and continuously, for prevention of catheter-induced infection during drainage of cerebrospinal fluid. We investigated the in vitro antibiotic releasing characteristics and bacterial killing effects of the new polymer against E. coli. The novel fluoroquinolone polymer was prepared using diisopropylcarbodiimide, poly (e-capro-lactone) diol, and nalidixic acid. FT-IR, mass spectrometry, and elemental analysis proved that the novel antibacterial polymer was prepared successfully without any side products. Negative MS showed that the released drug has a similar molecular weight (M.W.=232, 350) to pure drug (M.W.=232). In high pressure liquid chromatography, the released drug and drug-oligomer showed similar retention times (about 4.5-5 min) in comparison to pure drug (4.5 min). The released nalidixic acid and nalidixic acid derivatives have antibacterial characteristics against E. Coli, Staphylococcus aureus, and Salmonella typhi, of more than 3 months duration. This study suggests the possibility of applying this new polymer to manufacture drainage catheters that resist catheter-induced infection, by delivering antibiotics for a longer period of more than 1 month.
Anti-Bacterial Agents/*administration & dosage ; Biodegradation ; Biofilms ; Catheterization/*adverse effects ; Cerebrospinal Fluid/*physiology ; Chromatography, High Pressure Liquid ; Drainage/*adverse effects ; *Drug Delivery Systems ; Humans ; Nalidixic Acid/*administration & dosage ; Polymers/administration & dosage ; Research Support, Non-U.S. Gov't ; Spectrum Analysis, Mass

Carcinoma of lung is classified by histologic cell type, this is based on predominant major cell population by tissue specimen. But in fact a range of 13% to 63% of lung cancer has been appeared to be heterogeneous cell type at the light microscopic level. After treatment of the mixed lung cancer and/or with time there are reports that cell type is changed. Because it is possible that the tumor were pleomorphic and that the antitumor therapy eliminated the more sensitive cell population and permitted the subsequent emergence of the more resistant cell population. The authors reported here, a case of 32 year old female patient with mixed lung cancer composed of three cell type, and this is the first case in Korea.
Adult ; Female ; Humans ; Korea ; Lung ; Lung Neoplasms ; Population Characteristics

The pathogenesis of antiepileptic drug (AED) resistance is multifactorial. However, most candidate gene association studies typically assess the effects of candidate genes independently of each other, which is partly because of the limitations of the parametric-statistical methods for detecting the gene-to-gene interactions. A total of 200 patients with drug-resistant epilepsy and 200 patients with drug-responsive epilepsy were genotyped for 3 representative the single nucleotide polymorphisms (SNPs) of the voltage-gated sodium channel genes (SCN1A, SCN1B, and SCN2A) by polymerase chain reaction and direct sequencing analysis. Besides the typical parametric statistical method, a new statistical method (multifactor dimensionality reduction [MDR]) was used to determine whether gene-to-gene interactions increase the risk of AED resistance. None of the individual genotypes or alleles tested in the present study showed a significant association with AED resistance, regardless of their theoretical functional value. With the MDR method, of three possible 2-locus genotype combinations, the combination of SCN2A-PM with SCN1B-PM was the best model for predicting susceptibility to AED resistance, with a p value of 0.0547. MDR, as an analysis paradigm for investigating multi-locus effects in complex disorders, may be a useful statistical method for determining the role of gene-to-gene interactions in the pathogenesis of AED resistance.
Adolescent ; Adult ; Alleles ; Anticonvulsants/*therapeutic use ; Case-Control Studies ; Child ; Child, Preschool ; Data Interpretation, Statistical ; Drug Resistance ; Epilepsy/drug therapy/*genetics ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Infant ; Male ; Polymorphism, Single Nucleotide ; Sodium Channels/*genetics

BACKGROUND: Acute adaptive vascular remodeling occurs in active and unstable inflammatory plaques. It has been suggested that the adaptive coronary vascular remodeling, in patients with acute coronary syndrome (ACS), may be systemic and may show similar vascular remodeling in the carotid arteries. We investigated the ultrasonographic features of the common carotid artery (CCA) to determine whether the arterial expansive remodeling found in the coronary artery occurs in the carotid arteries of patients with ACS. METHODS: We measured lumen diameter (LD), interadventitial diameter (IAD) and intima media thickness (IMT) using a B-mode ultrasound in both common carotid arteries in patients with ACS (N=74) and chronic stable angina (CSA) (N=31). Positive remodeling was arbitrarily defined as an IMTmax >1 mm and IAD >8 mm and negative remodeling as an IMTmax >1 mm and IAD <7 mm. Other values were defined as "no remodeling" RESULTS: There were no significant differences in LD IAD and maximal IMT of the right CCA and the left CCA in comparisons between the ACS and the CSA patient groups. There were no differences for number of cases with no remodeling or differences in positive and negative remodeling in the right common carotid artery and left common carotid artery in comparisons between the ACS and CSA patient groups. . Presence of plaque in both common carotid arteries showed similar frequency in the ACS and CSA patient groups. The characteristics of carotid artery plaques were not different in the two groups. The remodeling index (IAD/LD) was correlated with IMTmax (right CCA r=0.797, p<0.001; left CCA r=0.860, p<0.001). CONCLUSIONS: The common carotid arterial structure of ACS patients was not different from that of CSA patients. Therefore, these results suggest that the expansive arterial remodeling, due to coronary inflammatory plaques, appears to take place locally rather than systemically.
Acute Coronary Syndrome* ; Angina, Stable* ; Carotid Arteries* ; Carotid Artery, Common ; Carotid Stenosis ; Coronary Vessels ; Humans ; Ultrasonography

BACKGROUND: The measurement of perfusion is very important to understanding the physiology in the ischemic and reperfused tissue. However, no studies have been reported using a beating heart with a real time-continuous perfusion measurement system (QFlow(TM)400) to check local tissue perfusion so far. In this study, the changes in hemodynamics and local myocardial perfusion (LMP) after coronary reperfusion with nicardipine (a calcium channel blocker) administration were evaluated. METHODS: A total of 10 mongrel dogs were divided into two groups; group I (control group, n = 5), group II (nicardipine group, n = 5). After femoral arterial, pulmonary arterial and left ventricular catheterization, a left thoracotomy was performed. Next, the left anterior descending coronary artery (LAD) was exposed, and a thermal diffusion microprobe was inserted in the myocardium to measure LMP. RESULTS: In group II, blood pressure and systemic vascular resistance after LAD reperfusion were significantly decreased compared to group I. Cardiac output and stroke volume were more rapidly increased in group II, while left ventricular stroke work was decreased in group II. In group I, the LMP after LAD reperfusion did not recover to the baseline level, but the LMP did recover 20 minutes after LAD reperfusion and was increased more compared to the baseline level at 30 minutes after LAD reperfusion in group II. There were no significant differences in dP/dt between the two groups. CONCLUSIONS: We found that the LMP did not recover to the baseline level in the early state of LAD reperfusion; however, nicardipine administration increased the LMP after the early reperfusion period. Cardiac output and stroke volume were also more rapidly increased when nicardipine was administrated.
Animals ; Blood Pressure ; Calcium Channels ; Cardiac Output ; Catheterization ; Catheters ; Coronary Vessels ; Dogs* ; Heart ; Hemodynamics* ; Myocardial Reperfusion* ; Myocardium ; Nicardipine* ; Perfusion* ; Physiology ; Reperfusion ; Stroke ; Stroke Volume ; Thermal Diffusion ; Thoracotomy ; Vascular Resistance

Drugs for acute blood pressure control are often required during a cardiovascular operation. Hypertension frequently occurs in an off-pump coronary artery bypass graft. The purpose of this study was to evaluate the effect of nicardipine on hemodynamic change. Twenty adult patients were studied. Anesthesia was induced intravenously with thiopental (4 mg/kg), vecuronium (1 mg/kg), and fentanyl (4microgram/kg), and maintained with 100% O2 and isoflurane 1 1.5 Vol%. When systolic blood pressure rose above 150 mmHg, nicardipine 1 mg was administrated intravenously. Immediately after the nicardipine bolus injection, nicardipine was infused continuously 0.5 4microgram/kg/min. Thereafter, hemodynamic data was recorded. Systolic blood pressure decreased, but cardiac index significantly increased after an intravenous administration of nicardipine and was maintained during the study. There was no incidence of tachycardia. It was concluded that acute blood pressure control using nicardipine could be suitable and safe in patients with an off-pump CABG.
Administration, Intravenous ; Adult ; Anesthesia ; Blood Pressure ; Coronary Artery Bypass, Off-Pump* ; Fentanyl ; Hemodynamics* ; Humans ; Hypertension* ; Incidence ; Isoflurane ; Nicardipine* ; Tachycardia ; Thiopental ; Transplants* ; Vecuronium Bromide

During the prostate cancer (PCa) development and its progression into hormone independency, androgen receptor (AR) signals play a central role by triggering the regulation of target genes, including prostate-specific antigen. However, the regulation of these AR-mediated target genes is not fully understood. We have previously demonstrated a unique role of HOXB13 homeodomain protein as an AR repressor. Expression of HOXB13 was highly restricted to the prostate and its suppression dramatically increased hormone-activated AR transactivation, suggesting that prostate-specific HOXB13 was a highly potent transcriptional regulator. In this report, we demonstrated the action mechanism of HOXB13 as an AR repressor. HOXB13 suppressed androgen-stimulated AR activity by interacting with AR. HOXB13 did neither bind to AR responsive elements nor disturb nuclear translocation of AR in response to androgen. In PCa specimen, we also observed mutual expression pattern of HOXB13 and AR. These results suggest that HOXB13 not only serve as a DNA-bound transcription factor but play an important role as an AR-interacting repressor to modulate hormone-activated androgen receptor signals. Further extensive studies will uncover a novel mechanism for regulating AR-signaling pathway to lead to expose new role of HOXB13 as a non-DNA-binding transcriptional repressor.
Passive Cutaneous Anaphylaxis ; Prostate ; Prostate-Specific Antigen ; Prostatic Neoplasms ; Receptors, Androgen ; Staphylococcal Protein A ; Transcription Factors ; Transcriptional Activation

No abstract available.
Aneurysm, False

BACKGROUND: The beta2 adrenergic receptor (beta2 AR) polymorphisms occurring at amino acid position 16 (Arg to Gly), 27 (Gln to Glu), 34 (Val to Met), and 164 (Thr to Ile) are known to be functionally relevant and also disease-modifying in subjects with asthma. However the contribution of these polymorphisms to the development of the asthmatic phenotype or other markers for allergic disease remains to be established. METHODS: 109 patients with bronchial asthma and 42 healthy person were included. Serum total IgE, allergen specific IgE, and skin prick test were performed to all of the subjects. beta2 AR polymorphisms were checked by mutated allele specific amplification (MASA) method. RESULTS: The results were as follows. The frequencies of beta2 AR polymorphisms in asthmatic patients and healthy person were not statistically different(p>0.05). There was no association between beta2 AR polymorphisms of amino acid position 16, 27, 34 and the existence of atopy among asthmatic patients (p>0.05). Between asthmatic patients with or without elevated IgE level and beta2 AR polymorphisms of amino acid position 16, 27, 34, there was no statistically significant association(p>0.05). CONCLUSION: There was no difference in frequency of the beta2 AR polymorphism between asthmatic patients and healthy person. In the bronchial asthma, association of beta2 AR polymorphism and atopy/serum total IgE was not found.
Alleles ; Asthma ; Humans ; Immunoglobulin E* ; Phenotype ; Receptors, Adrenergic ; Receptors, Adrenergic, beta-2 ; Skin

BACKGROUND: Persistent nonproductive cough is a major adverse effect encountered with ACE inhibitor treatment and the most frequent reason for withdrawal of the drug. The mechanism of cough was postulated to be associated with accumulation of bronchial irritants which are substrates of ACE. It has been speculated that occurrence of this adverse effect is genetically predetermined; in particular, variants of the genes encoding ACE. To investigate this relationship, we determined ACE gene Insertion/Deletion polymorphism in subjects with and without a history of ACE inhibitor-induced cough. METHODS: Among the 339 patients with ACE inhibitor treatment, subjects who developed cough that resolved when not taking medication were designated to cough group and other subjects who did not complain cough were designated to non-cough group. Clinical characteristics of the patients were collected by review of medical records. ACE genotypes were determined by PCR amplification of DNA from peripheral blood RESULTS: 37 patients complained of dry cough(cough group) and 302 patients did not complained of cough(non-cough group). The incidence of ACE inhibitor induced dry cough was 10.9%. There was a preponderance of females in the cough group (M:F=24.3%:75.7%) compared to the non-cough group(M:F=49.7%:50.3%, p=0.004). There was no significant difference in mean age, underlying diseases, and kinds and frequencies of ACE inhibitors and their mean dosage between the both groups. ACE genotypic frequencies were I/I : I/D : D/D = 16.2%:18.9%:64.9% in the cough group and 18.9%:18.2%:62.9% in the non-cough group which showed no significant difference between the both groups(p=0.926). Allelic frequencies were I : D = 25.7%:74.3% and 28.0%:72.0% in the cough and non-cough group respectively and the difference was not significant(p=0.676). CONCLUSION: The incidence of ACE inhibitor-induced cough are 10.9%, and women are more susceptible to ACE inhibitor-induce cough. ACE inhibitor induce dry cough is not associated with ACE gene Insertion/Deletion polymorphism.
Angiotensin-Converting Enzyme Inhibitors ; Cough* ; DNA ; Female ; Genotype ; Humans ; Incidence ; Irritants ; Medical Records ; Polymerase Chain Reaction