Early Recanalization After Intravenous Administration of Recombinant Tissue Plasminogen Activator as Assessed by Pre- and Post-Thrombolytic Angiography in Acute Ischemic Stroke Patients

BACKGROUND AND PURPOSE: Recanalization rates after the intravenous (IV) recombinant tissue plasminogen activator (rt-PA) treatment have been poorly studied in acute stroke. METHODS: CT angiography was performed before IV rt-PA in all patients and digital subtraction angiography was undertaken for intra-arterial thrombolysis in cases of no improvement after rt-PA infusion. RESULTS: Forty-five patients were treated with IV rt-PA. Initial CT angiography showed relevant arterial occlusions in 35 patients. Recanalization after rt-PA therapy was demonstrated by digital subtraction angiography in 7 of the 31 patients with the occlusion on initial CT angiography: 2/16 in the internal carotid or proximal middle cerebral artery, 3/11 in the distal middle cerebral artery and 2/4 in the basilar artery occlusion. CONCLUSIONS: The early recanalization rate after IV rt-PA use was very low in cases with large proximal arterial occlusions. CT angiography before IV rt-PA may be useful for the prediction of its efficacy.ope

Clinical Characteristics of Patients with Aortic Plaques In Acute Ischemic Stroke

Background: Transesophageal echocardiography (TEE) is a useful tool for evaluating aortic plaques. Several investigators have reported that the aortic arch atherosclerosis is a potential source of systemic emboli and an independent risk factor for ischemic stroke. But the clinical characteristics and neuroimaging findings of the stroke patients with aortic plaques remain unknown. Methods: From Yonsei Stroke Registry, we reviewed 333 consecutive patients with acute ischemic stroke, who underwent both TEE and vascular imaging studies. We analyzed the risk factor profiles, clinical features, neuroimaging findings, and TEE data of these patients. Based on the TEE findings, the plaques protruding into the lumen≥4 mm, mobile or ulcerated lesions in the proximal aorta were defined as complex aortic plaques (CAP). The possible etiologies of stroke were classified into four groups; CAP only group, potential cardiac sources of embolism (PCSE) only group, relevant artery atherosclerosis (RAA) only group, and more than two etiologies or cryptogenic group (uncertain group). Results: Among the 333patients, aortic plaques were found in 105 (31.5%) patients, Fifty nine patients (17.7%) had the CAP. The patients with CAP were older (p<0.01) and had more frequent history of cigarette smoking (p=0.01) and ischemic stroke (p=0.04) than those without. Total cholesterol level was also higher (p=0.02). The etiologic evaluations revealed CAP only in 31 (9.3%), PCSE only in 68 (20.4%), RAA only in 59 (17.7%), uncertain mechanism in 175 (52.6%) patients. The CAP only group less often had cortical dysfunctions (9.7%, p<0.05), but more likely to have a classic lacunar syndrome (54.8%, <0.01). Less than 1 cm sized lesions were frequently found in CAP only group (55.6%), when compared with PCSE only (19.4%, p<0.01), RAA only (29.8%, p=0.03), or uncertain group (25.0%, p<0.01). Conclusions: Aortic plaques were frequently found in acute stroke patients. The CAPs were closely related with old age, smoking, previous stroke, and hypercholesterolemia. The clinical presentations of CAP patients were characterized by minor stroke symptoms and small lesion sizes.ope

Different role of functional domains of hTR in DNA binding to telomere and telomerase reconstruction

Even if template sequence of hTR played an essential role in telomere binding, a 326 nucleotide fragment of hTR containing template, pseudoknot, and CR4–5 domains is critical for both binding with telomeric DNA and reconstitution of telomerase activity. A functional study with antisense oligonucleotides suggested that targeted disruption of the template region efficiently abrogated both telomeric DNA binding and telomerase activity, whereas disruption of the CR4–5 region induced only loss of telomerase activity. hTR interacts with telomeric DNA via structural region composed of the template, pseudoknot, and CR4–5 domains, however, each structural domain plays a distinct role in telomere binding and telomerase activity reconstitution.ope

시각 특징점의 평면 그룹화를 통한 동시 위치인식 및 지도형성 기법

Docto

Characterization of after-hyperpolarization induced by acetylcholine in male rat major pelvic ganglion neurons

의학과/석사[한글] 수컷 흰쥐의 주 골반 신경절(major pelvic ganglia, MPG)은 교감신경과 부교감신경으로부터 입력을 받고, 방광, 전립선 및 음경 등을 지배하여 배뇨나 발기 현상을 조절하는 자율 신경절이다. 일반적으로 교감 및 부교감 신경 모두 시냅스 흥분전달은 니코틴성 아세틸콜린 수용체에 의해 매개된다고 알려져 있으며, 수용체의 활성화는 빠른 탈분극 현상을 초래하여 절후 신경이 활동전압을 형성케 한다. 하지만 흥분성 시냅스 전위가 끝난 이후의 막전압 변화에 관해서는 중요성에 비해 아직 잘 알려진 바 없다. 따라서 본 실험에서는 수컷 흰쥐 주 골반 신경절 세포에서 니코틴성 수용체 활성화에 따른 막전압의 변화를 관찰하고, 그 전기생리적 기전을 규명하고자 하였다.실험 방법은 효소처리로 분리된 단일 골반 신경절 세포의 막전압을 전류 고정 상태에서 gramicidin-perforated patch clamp 방법으로 측정하였으며, 형광측정장치를 이용하여 세포 내 Na+ 및 Ca2+이온농도를 측정하였다.주 골반 신경절 세포들은 아세틸콜린에 의한 니코틴성 수용체 활성화로 인해 빠른 탈분극을 초래하였으나, 이중 교감신경세포에서는 부교감신경세포와 달리 아세틸콜린 제거 이후 느리게 지속되는 강력한 후과분극(after-hyperpolarization) 현상이 관찰되었다. 이러한 후과분극 현상은 무스카린성 수용체 차단제인 atropine에 의해 영향을 받지 않았다. 한편 아세틸콜린은 세포 내 Na+ 및 Ca2+ 농도를 증가시켰으며, 약물 제거 후 세포 내 Na+ 농도는 Ca2+ 농도에 비해 비교적 느리게 회복되었다. 아세틸콜린에 의한 후과분극 현상은 Na+-K+ ATPase 억제제인 ouabain의 전처치에 의해 현저히 억제되었으며(67.2±5.4%; n=7), 과분극 도중 가하였을 경우는 빠르게 안정막 전위로 회복되었다. 세포 내 Ca2+을 BAPTA-AM으로 제거하거나(29.7±6.9; n=7), Ca2+-activated K+ 통로 차단제 중 하나인 apamin에 의해서도 일부 억제되었으며(27.3±8.6; n=6), ouabain과 같이 BAPTA-AM(88.5±4.4; n=6) 혹은 apamin(87.1±6.3; n=2)을 투여하였을 경우 추가의 억제현상을 관찰하였다.이상의 실험 결과들로 미루어 보아 주 골반 신경절 교감신경세포에서 니코틴성 수용체의 활성화는 세포 내 Na+ 및 Ca2+ 이온농도를 증가시키며, 이들은 각각 Na+-K+ ATPase 및 Ca2+-activated K+ 통로를 활성화시킴으로서 강력한 후과분극을 초래한다. 이러한 후과분극 현상은 시냅스간 흥분 전달에 많은 영향을 미칠 것으로 사료된다 [영문]The major pelvic ganglia (MPG) in male rat are received from sympathetic and parasympathetic inputs and provide autonomic innervation to the bladder, prostate, and penis and physiologically involved in micturition and erectile reflexes. Synaptic transmissions in both sympathetic and parasympathetic neurons are mainly mediated by nicotinic acetylcholine receptor(nAChR). The activation of nAChR induces fast depolarization and action potential in post-synaptic neurons. Despite of its importance, however, the changes in membrane potential after fast depolarization have not been reported yet. Therefore, we investigated the electrophysiological mechanism of membrane potential changes induced by the activation of nAChR in male rat MPG neurons.Under current-clamp mode, we measured the membrane potential of enzymatic-dissociated MPG neuron by using gramicidin-perforated patch clamp method. The concentration of intracellular Na+ ([Na+]i) or Ca2+ ([Ca2+]i) in MPG neuron was measured using fluorescence measurement systemAcetylcholine(ACh) induced a fast depolarization through the activation of nAChR in both sympathetic and parasympathetic MPG neurons. But, a slow, sustained, and strong hyperpolarization followed after the removal of ACh in sympathetic ones only. ACh-induced hyperpolarization was not affected by atropine, a muscarinic receptor blocker. ACh increased both [Na+]i and [Ca2+]i in MPG neurons, however, recovery of [Na+]i was slower than that of [Ca2+]i after removal of ACh. ACh-induced hyperpolarization was blocked by pretreatment of ouabain, an inhibitor of Na+-K+ ATPase (67.2±5.4%; n=7). During hyperpolarization induced by ACh, ouabain elicited fast recovery to resting membrane potential. ACh-induced hyperpolarization was also attenuated by the chelation of [Ca2+]i by BAPTA/AM (29.7±6.9%; n=7) or the selective blockade of small-conductance Ca2+-activated K+ channel by apamin (27.3±8.6%; n=6). The application of ouabain combined with BAPTA/AM (88.5±4.4%; n=6) or apamin (87.1±6.3%; n=2) showed additive blocking effects on ACh-induced hyperpolarization.Taken together, it is concluded that the activation of nAChR increases [Na+]i and [Ca2+]i, which activates the Na+-K+ ATPase and Ca2+-activated K+ channel and consequently strongly hyperpolarizes the membrane potential of sympathetic MPG neuron. The after-hyperpolarization induced by the activation of nAChR may be involved in the regulation of the autonomic synaptic transmission.ope

스트레스에 의한 비뇨생식계를 지배하는 자율신경의 가소성/

Dept. of Medicine/박사Stress is defined as a state of threatened homeostasis, following exposure to extrinsic or intrinsic adverse forces (stressors). In order to re-establish the disturbed equilibrium against an imposed stressor, a repertoire of physiologic and behavioral responses is rapidly mobilized, constituting the adaptive stress response. Hallmarks of the adaptive stress response are the activation of the autonomic nervous system and hypothalamo-pituitary-adrenal (HPA) axis. Stress is known to alter neural, endocrine, immune and cardiovascular functions. To date, studies on stress-induced neural plasticity have focused on the central nervous system, but not the peripheral nervous system. Several studies suggest that stress can impact on the urogenital functions including voiding and erectile reflexes although neural mechanisms underlying this are poorly understood. Thus, the present study was designed to address whether stress can alter synaptic transmission as well as excitability of autonomic major pelvic ganglion (MPG) neurons innervating the urogenital system. In this regard, male Sprague-Dawley rats were immobilized daily for 2 hr in restraint cages. After 7 days, serum level of corticosterone was measured and MPG neurons were enzymatically dissociated for patch-clamp study. Real-time PCR analysis revealed that IMO stress did not alter expression of nicotinic acetylcholine receptor 3 and 4 subunits which mediate cholinergic synaptic transmission in MPG. In consistent with this, Ach-induced currents were not affected by IMO stress. As reported previously, MPG contains both sympathetic and parasympathetic neurons. The sympathetic and parasympathetic neurons show tonic and phasic firing patterns in response to prolonged current injections, respectively. IMO stress significantly reduced spike firing frequency in tonic MPG neurons by increasing afterhyperpolarization (AHP) duration. The effects of IMO stress on spike firing were prevented by adrenalectomy (ADX). RT-PCR analysis showed that STREX, a stress-sensitive splicing variant of large-conductance Ca2+-activated K+ channel (BK) was up-regulated in the MPG neurons of IMO rats. In addition, IMO stress also enhanced expression of SK2 and SK3, small conductance Ca2+-activated K+ channels (BK) isoforms which determine AHP duration and thereby spike firing frequency. Previousl studies have shown that tonic MPG neurons have been found to express T-type Ca2+ channels which are responsible for low-threshold spike firing. IMO stress reduced Ni2+- and mibefradil-sensitive low-threshold spike firing by down-regulation of T-type calcium channel 1H isoform in tonic MPG neurons. Down-regulation of T-type Ca2+ channels was reproduced in corticosterone-treated MPG neurons, indicating that corticosterone is a mediator of the altered gene expression. Finally, IMO stress was also found to down-regulate voltage-gated Na+ channels. Taken together, these data suggest that IMO stress reduces the excitability of autonomic neurons by altering expression of Na+, T-type Ca2+, BK, and SK channels, which might affect functions of target organs such as the bladder, the penis, etc. I studied for the first time effects of short-term stress on functional plasticity of autonomic ganglion neurons. More importantly, I suggest the molecular and cellular mechanisms underlying the stress-induced autonomic plasticity.prohibitio

(A) Study on GVG Construction Using Limited Sensor Data for Mobile Guide Robot

Maste

Efficient SLAM Algorithm with Hybrid Visual Map in an Indoor Environment

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Construction of Hybrid Visual Map for Indoor SLAM

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Robust Navigation Techniques for the GVG-based SLAM in Unstructured Environment

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