Spread of multidrug-resistant Streptococcus pneumoniae in South Korea.
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Biomedical subjects
Publications and source records attributed to J H Song.
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The learned helplessness paradigm was used to test the notion that lesions of a theatrical depression system in the rat will produce antidepression similar to antidepressive medication. Lateral brain stem lesions were effective in producing antidepression and unilateral lesions were as effective as bilateral lesions. Ibotenic acid lesions were not effective, indicating that the effective target site was in a fiber tract and not a cell nucleus.
The peroxidative stability of docosahexaenoic acid (DHA)-containing oils (DHA at 10.7 mol% of the total fatty acids), in the form of phospholipids (PL), triacylglycerols (TG), and ethyl esters (EE) with the same constituent fatty acids, was investigated in the dark at 25 degrees C in a bulk phase, and compared with that of control palm oil (supplemented with 20% soybean oil). The oxygen absorption of the DHA-containing oil was significantly lower in the form of PL than in the form of TG and EE during a 10-week oxidation, and the oxygen absorption of PL was almost equivalent to that of the control oil. A gas chromatographic analysis showed that 90% of initial DHA was retained in the form of PL after the 10-week oxidation, while TG and EE respectively more rapidly decayed with the loss of 97% and 64% of DHA. Tocopherol in the form of TG and EE had also completely decayed after the oxidation, while 37% of the initial tocopherol remained in the form of PL. The peroxide and carbonyl values of TG and EE showed large increases after the oxidation, but no such increase was observed for PL. These results show that DHA-containing oil in the form of PL was more resistant to the oxidative degradation of DHA than that in the form of TG and EE in a bulk phase.
Several studies have suggested that genetic variations of the apolipoprotein (apo) AI-CIII-AIV cluster gene are associated with hyperlipidemia or atherosclerosis. These investigations were carried out mainly with Caucasian groups; there have been few associated studies involving non-Caucasian groups. This study was conducted to elucidate the association between five restriction fragment length polymorphisms (RFLPs) of the apo AI-CIII-AIV cluster gene and Korean hypertriglyceridemic subjects. The rare allele frequencies of the XmnI and SstI polymorphic sites in the patients were significantly higher than those of the control group (P <0.05). These two polymorphic sites had relation to linkage disequilibrium in the hypertriglyceridemic subjects (delta = -0.2733). In addition, S2 allele frequency of the SstI RFLP in Koreans was more frequent than that of Caucasians reported previously. The rare allele of XmnI and SstI polymorphic sites was associated with increased triglyceride concentrations in the hypertriglyceridemic group (P <0.005). Koreans have a much lower prevalence of hyperlipidemia than Caucasians. Nevertheless, this study showed a similar trend with results from Caucasian groups, thereby confirming that genetic variations of the apo AI-CIII-AIV cluster gene are likely to be significant markers for hypertriglyceridemic subjects. Thus, RFLP loci of the apo AI-CIII-AIV cluster gene may be a useful genetic marker for clinical or population studies.
OBJECTIVE: To assess the efficacy of magnetic resonance imaging (MRI) in objectively defining a state of remission in rheumatoid arthritis (RA) after treatment. METHODS: Ten patients with RA involving the wrist were evaluated before treatment with methotrexate and hydroxychloroquine, and then mean 14 mo later with a followup evaluation. Clinical variables, laboratory measurements, and MRI using various techniques (T1 weighted image, T2 weighted image, fat suppression T2 weighted image, postcontrast T1 weighted image, postcontrast dynamic image, postcontrast 3 dimensional image) were observed. Remission was defined by ACR criteria. MRI changes were observed using 3 variables: extent of synovial proliferation; extent of bone marrow edema; and development of new erosion. In 6 of 10 patients, synovial signal intensity time curve changes at 30 s (E30 ratio) were determined for quantitative assessment of synovitis. RESULTS: Four patients achieved remission and 6 did not. All patients in remission showed decrease in extent of synovial proliferation and bone marrow edema with no newly developed erosion after treatment, compared to baseline. Five of 6 patients in nonremission showed newly developed erosions with variable changes in extent of synovial proliferation and bone marrow edema. E30 ratio was determined in 3 patients in the remission group and 3 in the nonremission group, with 48% reduction in the former compared to 9% reduction in the latter. CONCLUSION: MRI is feasible for objectively defining remission and assessing the therapeutic effect of antirheumatic drugs; utility of MRI measures in clinical remission criteria remains to be verified.
The effects of riluzole, a neuroprotective drug, on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in rat dorsal root ganglion neurons were studied using the whole-cell patch clamp technique. At the resting potential, riluzole preferentially blocked TTX-S sodium channels, whereas at more negative potentials, it blocked both types of sodium channels almost equally. The apparent dissociation constants for riluzole to block TTX-S and TTX-R sodium channels in their resting state were 90 and 143 microM, respectively. Riluzole shifted the voltage dependence of activation of TTX-R sodium channels in the depolarizing direction more than that of TTX-S sodium channels. The voltage dependence of the fast inactivation of both types of sodium channels was shifted in the hyperpolarizing direction in a dose-dependent manner, and the apparent dissociation constants for riluzole to block the inactivated channels were estimated to be 2 and 3 microM for the TTX-S and TTX-R sodium channels, respectively, indicating a much higher affinity for the inactivated channels than for the resting channels. Riluzole was equally effective in blocking both types of sodium channels in their slow inactivated state. Since more TTX-S channels are inactivated than TTX-R channels at the resting potential, riluzole blocks TTX-S sodium channels more potently than TTX-R sodium channels. It was concluded that one of the mechanisms by which riluzole exerts its neuroprotective action is to preferentially block the inactivated sodium channel of damaged or depolarized neurons under ischemic conditions, thereby suppressing excess stimulation of the glutamatergic receptors and massive influx of Ca++.
The effects of riluzole, a neuroprotective drug, on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neurons were studied using the whole-cell patch-clamp technique. Riluzole inhibited HVA calcium channel currents in a dose-dependent, time-dependent and reversible manner. The apparent dissociation constants for riluzole inhibition of the transient and sustained components of the current were 42.6 and 39.5 microM, respectively. Riluzole accelerated the activation kinetics of calcium channels without affecting the voltage dependence of activation. It accelerated the fast component of deactivation kinetics without affecting the slow component. It also accelerated fast and slow inactivation kinetics of the HVA channels. However, only one of the two components in the steady-state inactivation curve for the HVA channels was shifted in the hyperpolarizing direction by riluzole, which indicates differential block of the multiple-type HVA channels. By use of the specific blockers nimodipine, omega-conotoxin GVIA and omega-agatoxin IVA, the HVA calcium channels were found to comprise L-type (10%), N-type (63%), P/Q-type (23%) and R-type (9%). Riluzole blocked N- and P/Q-type channels, but not L-type channel, with the order of efficacy of P/Q- > N- >> L-type channels. Riluzole inhibition of N- and P/Q-type calcium channels may result in reduced calcium influx at presynaptic terminals, which thereby decreases excessive excitatory neurotransmitter release, especially glutamate, a mechanism known to cause neuronal death in ischemic conditions.
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Experiments were carried out to investigate the abundance of mRNA for luteotrophic receptors and steroidogenic elements in the ovaries and corpora lutea of mink during the embryonic diapause, peri-implantation and postimplantation pregnancy. The second aim was to determine whether the mink placenta synthesized progesterone. Homologous cDNA probes for the mink LH and prolactin receptors were generated by the polymerase chain reaction. Heterologous cDNA probes for steroidogenic acute regulatory protein (StAR), cytochrome P450 side chain cleavage (P450scc) and 3 beta-hydroxysteroid dehydrogenase-delta 4-delta 5 isomerase (3 beta HSD) were also used. The abundance of mRNA encoding the prolactin receptor was low during the period of embryonic diapause and increased concurrent with circulating progesterone. The abundance of LH receptor message reached peak values during the peri-implantation period followed by maintenance of a steady-state after implantation. The abundance of StAR and P450scc messages appeared not to vary during gestation, while that for 3 beta HSD was correlated with changes in circulating progesterone. There was no evidence of 3 beta HSD activity or transcripts in the placenta. These results indicate that prolactin and LH are necessary for activation of the corpus luteum during the period of embryonic diapause, and for its maintenance during postimplantation gestation. The mink placenta does not synthesize progesterone.
MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclopepten-5,10-imine maleate), a non-competitive NMDA receptor antagonist (0.01-1 micrograms), injected intracerebroventricularly (i.c.v.) dose dependently increased the baseline levels of plasma interleukin-6 in mice. In the 1-h immobilization-stressed animals, MK-801 (1 micrograms) administered i.c.v. produced an additive increase of plasma interleukin-6. NMDA (N-methyl-D-aspartate) (3, 10 ng) administered i.c.v. attenuated dose dependently the 1-h immobilization stress-induced rise in plasma interleukin-6 level. Neither 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) (0.01-0.5 micrograms) nor alpha-methyl-4-carboxyphenylglycine (MCPG) (1-20 micrograms), antagonists of non-NMDA and metabotropic glutamate receptors, respectively, i.c.v. administered, affected the basal and stress-induced plasma interleukin-6 levels. These data indicate that NMDA receptors may be involved in the suppressive regulation of the plasma interleukin-6 levels.
The differential effects of the anticonvulsants phenytoin and carbamazepine on the sodium channels of rat dorsal root ganglion (DRG) neurons were studied using the patch clamp technique. The action potentials from tetrodotoxin-resistant (TTX-R) cells were less sensitive to phenytoin and carbamazepine than those from tetrodotoxin-sensitive (TTX-S) cells. The steady-state inactivation curve for TTX-S sodium channels was shifted by as much as 20.6 mV and 11.4 mV by phenytoin and carbamazepine at 300 microM, respectively, yet the curve for TTX-R sodium channels was shifted only by 6.0 mV and 6.9 mV, respectively. Thus, the differential action potential block of TTX-S and TTX-R cells by phenytoin and carbamazepine is due to different voltage dependence of and differential drug effects on the inactivation kinetics of two types of sodium channels.
Controversies remain over which ion channels are the most sensitive to ethanol. We have found that ethanol potently modulates the neuronal nicotinic acetylcholine receptor-channel at micromolar concentrations with an EC50 of 88.5 microM, which is significantly lower than most values previously reported for other ion channels. Prolonged application of ethanol accelerated the decay phase of acetylcholine-induced currents, caused single-channels to open in bursts, and shortened the mean open time, all of which reflect increased receptor desensitization. However, ethanol slowed the decay phase of the current induced by a brief application of acetylcholine, which may indicate that ethanol manifests its action by causing an increase in the affinity of the receptor for acetylcholine. These results suggest that neuronal nicotinic acetylcholine receptors may be important target sites of ethanol, particularly in the early stages of ethanol intoxication.
The development of less invasive methods to evacuate intracerebral hematomas (ICHs) has improved outcome in patients with traumatic brain injury. Eighteen patients with ICHs underwent surgery via one of two methods: stereotactic endoscopic removal (SER) or stereotactic catheter drainage (SCD). The outcome results were then compared. The patient population was composed of 11 men and seven women with a mean age of 53.3 years (range 33-81 years), all suffering from ICH in the basal ganglia. The mean hematoma volume was 34.4 ml (range 23-105 ml). All patients had major neurological deficits, but showed no sign of transtentorial herniation. Ten patients underwent SCD and eight had SER. All procedures were performed within 24 hours of insult. After local anesthesia was induced in the patient, an intracranial pressure (ICP) monitoring catheter and an Otzuki cannula were placed through separate burr holes in the skull. Using the SER technique, the ICH was removed using suction and forceps through the side window of the cannula until the ICP had decreased significantly. Hemostasis was attained by lesioning with a Nd-YAG laser. In the SCD procedure, we placed a silicone catheter into the hematoma to drain it and then added urokinase. The hematoma was drained for 3 to 5 days in the SER method and 7 to 10 days in the SCD method. Rebleeding occurred in one of the early cases in which we used the SER procedure. At follow-up evaluation, the mortality rate was 13% in the SER group and 10% in the SCD group. The patients in whom outcome was most improved from these treatments were those who had been admitted with an impaired level of consciousness. Stereotactic catheter drainage is a precise, safe, and brief procedure with a very low rebleeding rate, but its outcome effect was more delayed than other procedures. Stereotactic endoscopic removal can easily replace SCD, with a similar mortality rate. Both procedures can be accomplished under direct visualization so as to eliminate any undesirable event or outcome.
Nitromethylene heterocyclic insecticides are known to act on the nicotinic acetylcholine receptor-channel complex. The effects of the nitromethylene heterocycle imidacloprid on the nicotinic acetylcholine receptor of clonal rat pheochromocytoma (PC 12) cells were studied using the single-channel patch clamp technique. Imidacloprid generated single-channel currents of multiple conductance states in PC12 cells. Both acetylcholine and imidacloprid induced single-channel currents of main conductance and subconductance states with conductances of 33.3 and 9.4 pS by acetylcholine and 30.4 and 9.8 pS by imidacloprid. However, the main conductance currents were generated predominantly by acetylcholine, whereas the subconductance currents were generated predominantly by imidacloprid. Partial block of acetylcholine-induced currents by imidacloprid may be explained on the basis of the single-channel behavior.
The differential effects of the pyrethroid tetramethrin on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) single sodium channel currents in rat dorsal root ganglion (DRG) neurons were investigated using the outside-out configuration of patch-clamp technique. Channel conductances were 10.7 and 6.3 pS for TTX-S and TTX-R sodium channels, respectively, at a room temperature of 24-26 degrees C. The single-channel current of TTX-S sodium channels at the test potential of -30 mV was -1.27 +/- 0.25 pA, and was not changed after exposure to 10 microM tetramethrin (-1.28 +/- 0.23 pA). The open time histogram of TTX-S single-channel currents could be fitted by a single exponential function with a time constant of 1.27 ms. After exposure to 10 microM tetramethrin, the open time histogram could be fitted by the sum of two exponential functions with time constants of 1.36 ms (tau fast) and 5.73 ms (tau slow). The percentage of contribution of each component to the population was 62% for the fast component representing the normal channels and 38% for the slow component representing the tetramethrin modified channels. The amplitude of TTX-R single-channel currents was slightly changed from -0.72 +/- 0.14 to -0.83 +/- 0.07 pA by 10 microM tetramethrin. The open time histogram of TTX-R single-channel currents could be fitted by a single exponential function with a time constant of 1.92 ms. In the presence of 10 microM tetramethrin, the open time histogram could be fitted by the sum of two exponential functions with time constants of 2.07 ms (tau fast) and 9.75 ms (tau slow). The percentage of contribution of each component was 15% for the fast, unmodified component and 85% for the slow, modified component. Differential effects of tetramethrin on the open time distribution of single sodium channel currents explains the differential sensitivity of TTX-S and TTX-R sodium channels.
Type I and type II pyrethroids and dichlorodiphenyltrichloroethane (DDT) are known to modulate the sodium channel to cause the hyperexcitatory symptoms of poisoning in animals. However, since the degrees to which neuronal sodium channel parameters are altered differ, a question is raised as to whether these insecticides bind to the same site in the sodium channel. Competition patch-clamp experiments were performed using rat dorsal root ganglion neurons which are endowed with tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels. D-trans-Tetramethrin, S,S-fenvalerate and p,p'-DDT caused a slowly rising and slowly falling tail current to be developed in tetrodotoxin-sensitive sodium channels. In tetrodotoxin-resistant sodium channels, these insecticides, particularly tetramethrin and fenvalerate, generated a large and prolonged tail current upon repolarization. The effects of tetramethrin were reversible after washing with drug-free solution, whereas the effects of fenvalerate and DDT were irreversible. When fenvalerate application was followed by tetramethrin application, the characteristic changes in current by fenvalerate disappeared and the characteristic changes by tetramethrin appeared. After washout, the characteristic current pattern of fenvalerate reappeared. These results can be explained by assuming that the tetramethrin molecule displaces the fenvalerate molecule from the same binding site in the sodium channel protein, or that tetramethrin and fenvalerate bind to separate sodium channel sites which interact allosterically with each other. DDT interacted with fenvalerate and tetramethrin in the same manner.
Our purpose was to compare patients with diffuse three-vessel coronary artery spasm and other types of coronary artery spasm without significant organic stenosis, and to elucidate clinical characteristics and risk factors. Patients were divided into two groups: group I consisted of 26 patients showing other types of coronary artery spasm; group II consisted of 5 patients with diffuse three-vessel coronary artery spasm. The mean age of patients in groups I and II was 52 and 50 years, respectively. The incidence of variant angina was higher in men than in women. The incidence of smoking was high in each group, but not significantly different. Exercise tests showed no significant differences between groups. All mean values of laboratory data, including lipoprotein (a) and low-density lipoprotein cholesterol in the two groups, were within normal ranges. There was no significant difference between groups. The incidence of spontaneous spam was much higher in patients with diffuse three-vessel coronary artery spasm (P < 0.01). Electrocardiographic (ECG) findings before the spasm were almost normal. All 5 patients with diffuse three-vessel coronary artery spasm demonstrated no important ST segment changes with episodes of angina during a coronary angiography on 12-lead ECG, compared to patients with other types of coronary artery spasm (P < 0.01). First, we conclude, diffuse three-vessel coronary artery spasm mostly occurs spontaneously. Second, we emphasize that diffuse three-vessel coronary artery spasm must be considered when 12-lead ECG shows no important ST segment changes with episodes of angina. Third, it is not easy to distinguish diffuse three-vessel coronary artery spasm from other types of coronary artery spasm on the basis of history, laboratory data, or electrocardiographic findings, including exercise tests.