• 한국작물학회지
• /
• 제44권4호
• /
• pp.373-381
• /
• 1999

Six soybean cultivars having different SDS susceptibility were planted with sorghum seedinoculum infested with F. solani isolate 171 in the greenhouse. First leaf symptoms appeared on unifoliar leaves at 9 days after inoculation and all cultivars showed the typical leaf symptoms at 13 days after inoculation, when trifoliar leaves emerged. Leaf symptoms development in susceptible cultivars was faster than in resistant cultivars. Leaf symptom severities during the period of 25 to 29 days after inoculation showed a significant difference between cultivars which had SDS resistance and sus ceptibility. In this period, area under the diseaseprogress curve (AUDPC) of Hartz 6686 was the highest and that of PI 520733 was the lowest. SDS caused serious damage to the growth of soybean in all cultivars. Average reductions of growth rate of root fresh weight and dry weight were greater than those of plant tops. Duyu-kong showed less severe leaf symptoms than that of SDS suscetible cultivars; however, average growth rate of plants top and roots of this cultivar was less but not significantly different than those of SDS susceptible cultivars. In all cultivars, as severity of leaf symptoms increased, plant top weight decreased. Root rot symptoms were observed in all cultivars before leaf symptoms appeared. Average proportions of tap root reddish-brown discoloration of all cultivars was up to 75 % at 15 days after inoculati on; however there was no significant differenc between cultivars at each rating date. Appearances of leaf symptoms on leaves varied in each cultivar. SDS resistant cultivars had a significantly higher level of crinkling than susceptible cultivars and SDS susceptible cultivars had a significantly higher level of necrosis than resistant cultivars. Further study will be needed to identify the relationships between the physiological growth rate and SDS severities in soybeans.

• Journal of Dental Anesthesia and Pain Medicine
• /
• 제23권1호
• /
• pp.45-51
• /
• 2023

Andersen-Tawil syndrome (ATS) is a rare genetic disease characterized by a triad of episodic flaccid muscle weakness, ventricular arrhythmias, and physical anomalies. ATS patients have various cardiac arrhythmias that can cause sudden death. Implantation of an implantable cardioverter-defibrillator (ICD) is required when life-threatening cardiac arrhythmias do not respond to medical treatment. An 11-year-old girl underwent surgery for an ICD implantation. For general anesthesia in ATS patients, anesthesiologists should focus on the potentially difficult airway, serious cardiac arrhythmias, such as ventricular tachycardia (VT), and delayed recovery from neuromuscular blockade. We followed the difficult airway algorithm, avoided drugs that can precipitate QT prolongation and fatal cardiac arrhythmias, and tried to maintain normoxia, normocarbia, normothermia, normoglycemia, and pain control for prevention of sympathetic stimulation. We report the successful application of general anesthesia for ICD implantation in a pediatric patient with ATS and recurrent VT.

• The Korean Journal of Legal Medicine
• /
• 제40권2호
• /
• pp.61-64
• /
• 2016

Ehlers-Danlos syndrome type IV (EDS IV) is a hereditary disorder of the connective tissue, characterized by easy bruising, thin skin with visible veins, and spontaneous rupture of the large arteries, uterus, or bowel. EDS IV is caused by mutations of the gene for type III procollagen (COL3A1), resulting in insufficient collagen production or a defect in the structure of collagen. EDS IV can have fatal complications such as the rupture of great vessels or organs, which can cause hemorrhaging and sudden unexpected death. Here, we report a case of a 43-year-old female who collapsed after a struggle with a neighbor. In this patient, the bifurcation of the bilateral common iliac artery ruptured, with no evidence of trauma, inflammation, or atherosclerosis. Genetic analysis of COL3A1 showed the presence of a c.2771G>A (p.Gly924Arg) mutation, which may be associated with EDS IV. The forensic pathologist should consider the possibility that the spontaneous visceral or arterial rupture was caused by EDS IV. Genetic analysis is not currently a routine procedure during autopsy. However, in this case, we suggest that the patient possibly had an underlying EDS IV condition, and we recommended family members of the deceased to seek genetic analysis and counseling.

• Journal of Dental Anesthesia and Pain Medicine
• /
• 제20권3호
• /
• pp.165-171
• /
• 2020

The congenital long QT syndrome (LQTS) is an inherited cardiac disorder characterized by increased QT intervals and a tendency to experience ventricular tachycardia, which can cause fainting, heart failure, or sudden death. A 4-year-old female patient undergoing velopharyngeal correction surgery under general anesthesia suddenly developed Torsades de pointes. Although the patient spontaneously resolved to sinus rhythm without treatment, subsequent QT prolongation persisted. Here, we report a case of concealed LQTS with a literature review.

• Neonatal Medicine
• /
• 제28권1호
• /
• pp.59-63
• /
• 2021

An important, albeit rare, cause of fetal bradycardia is long QT syndrome (LQTS). Congenital LQTS is an ion channelopathy caused by mutations in genes encoding cardiac ion channel proteins. Fetal onset of LQTS imposes high risk of life-threatening tachyarrhythmias and sudden cardiac death. Here, we report the case of a female newborn with fetal onset of bradycardia and a 2:1 atrioventricular (AV) block. After birth, a 12-lead electrocardiogram (ECG) revealed bradycardia with QT prolongation of a corrected QT (QTc) interval of 680 ms and pseudo 2:1 AV block. Genetic testing identified a heterozygous Gly402Ser (c.1204G>A) mutation in CACNA1C, confirming the diagnosis of LQTS type 8 (LQT8). The patient received propranolol at a daily dose of 2 mg/kg. Mexiletine was subsequently administered owing to the sustained prolongation of the QT interval and pseudo 2:1 AV block. One week after mexiletine inception, the ECG still showed QT interval prolongation (QTc, 632 ms), but no AV block was observed. There were no life-threatening tachyarrhythmias in a follow-up period of 13 months.

• 대한한의학방제학회지
• /
• 제11권1호
• /
• pp.57-90
• /
• 2003

The result of Bibliographic studies on the pathological mechanism of the sudden coma, we got the conclusion like this. 1. The sudden coma is an acute syndrome that refers to be a sudden fainting, an unconsciousness, an aphasia or a cold clammy limb, and immediately awakes or dies, and awakes in a short time, and if we awake, it doesn't leave over and above a sequela. 2. The clinical presentation of the sudden coma can be summarized as follows : The 1st is a disease raising the sudden death due to unconsciousness accompanied by wry mouth & sudden syncope with coma. The 2nd is simply the state of cold limbs. The 3rd is the meaning of the physique and symptomes of the six meridians. The last is the ancient method of expression in contrast of the beriberi. 3. The pathological mechanism of the sudden coma consists of the toxoid from outside, Qi and Xie, fatigue, damp phegm, the damage from seven emotions and the damage from five mental elements, especially the mental disorder due to the angry energy, causes the problems when the fleming-up of liver fire and the depressed of liver qi raise the physiological disorder. 4. Therapeutic methods of sudden coma are soothing the liver and remove stasis, soothing depression and circulating of the qi, calming the liver and suppressing yang. When that is early stage, at first, we must checking upward adverse flow of the qi after promoting the circulation of qi and awakening, and then, we must regulate excessive deficiency of yin yang by therapy that is based on differentiated in symptoms according to heat & cold, deficiency & excess, and use invigorating herb medicine for supporting vigour.

• 대한수의학회지
• /
• 제43권3호
• /
• pp.463-469
• /
• 2003

Eight nursery to grower pigs exhibiting weight loss and sudden death were diagnosed as postweaning multisystemic wasting syndrome (PMWS) based on the results of gross findings, histopathology, immunohistochemistry, fluorescent antibody test, virus isolation, PCR, serology, and electron microscopy. Groosly, the pigs had a rough hair coats and were severely emaciated. And moot lymph nodes were pale and enlarged. Lungs were not fully collapsed and exhibited 10 to 40% pale red cranioventral consolidation. Histopathologically, typical lymphohistiocytic interstitial to bronchointerstitial pneumonia, chronic lymphadenitis, severe lymphoid depletion, and basophilic intracytoplasmic inclusions were noted in the most lymphoid tissues. Porcine circovirus panicles were observed in the inguinal lymph node of the pigs by electron microscopy. Porcine circovirus type 2 (PCV2) antigens or viral DNAs were detected in the lesions of all pigs using immunohistochemistry or PCR. Two PCV2 were isolated from a homogenate of pooled lung and lymph node in 2 of the 5 pigs. Additionally, antigens of porcine reproductive and respiratory syndrome virus (PRRSV) and Hemophilus (H.) parasuis were also detected by immunofluorescent antibody test. Serologically, 55% of randomly selected sows and fattening pigs was serum antibody positive to PCV2 by an indirect fluorescent antibody (IFA) test and approximately 18 % of animals in the herd were serologically pooitive by the ELISA kit for PRRSV. To our knowledge, this is the first report of PMWS co-infected with PCV-2, PRRS, and H. parasuis in Korea.

• The Korean Journal of Physiology and Pharmacology
• /
• 제6권1호
• /
• pp.1-7
• /
• 2002

Congenital Long QT syndrome (LQTs) is a relatively rare pathologic disorder but results frequently in sudden cardiac death. Of the six LQTs that have been clinically described, five have been worked out for their genetic and biophysical profile. Most are generated by mutations which cause a loss of function in two delayed $K^+$ currents, $i_{Ks}\;and\;i_{Kr}.$ One syndrome is generated by mutations in the $Na^+$ channel which causes essentially a gain of function in the channel. Clinically the syndromes are characterized by slowed repolarization of the cardiac ventricular action potential and the occurrence of typical arrhythmias with undulating peaks in the electrocardiogram, called Torsade de Pointes. Arrhythmias are initiated by early or delayed afterdepolarizations and continue as reentry. Triggers for cardiac events are exercise (swimming; LQT1), emotion (arousal; LQT2) and rest/sleep (LQT3). ${\beta}-blockers$ have a high efficacy in the treatment of LQT1 and LQT2. In LQT3 their use is questionable. The study of congenital LQTsyndromes is a remarkable example of how basic and clinical science converge and take profit of each other's contribution.

• 한국응급구조학회지
• /
• 제24권3호
• /
• pp.155-160
• /
• 2020

Torsades de pointes refers to polymorphic ventricular tachycardia (PMVT), which is caused by the suppression of potassium channels owing to genetic and electrolytic abnormalities, resulting in the extension of the QT interval. Symptoms range from spontaneous circulation recovery to fainting and sudden death. Defibrillation, magnesium correction, and the use of lidocaine as an antiarrhythmic agent are recommended as treatments for persistent torsades de pointes. Currently, only amiodarone is available in the ambulance; however, torsades de pointes does not respond efficiently to amiodarone because it suppresses potassium channels and increases the refractory period of the myocardium. Lidocaine, in contrast, reduces the relative refractory period of the myocardium caused by suppressing sodium channels; thus, it inhibits the occurrence of and treats arrhythmia. In cases where PMVT did not respond to defibrillation, the administration of lidocaine showed no difference in survival and discharge rates compared to amiodarone. Thus, ambulances must be equipped with provisions to administer lidocaine.

• 대한수의학회지
• /
• 제36권4호
• /
• pp.1013-1016
• /
• 1996

Since 1993, sudden and massive death has occurred among penaeid shrimp, Penaeus orientalis cultured in Korea. We investigated the pathological characterizations on the spontaneously and experimentally infected penaeid shrimp. The major gross findings of the spontaneous cases were 2-6mm sized-white spots on the inside of the carapace and reddish discolorization. Histopathologically, massive necrosis of lymphoid organ, degeneration and necrosis of epithelia of epidermis and foregut were observed in both spontaneous and experimental cases. Amphophilic to basophilic intranuclear inclusion bodies were readly observed epithelia of epidermis, foregut and gills. Electron microscopy revealed enveloped, non-occuluded ellipsoid to rod shaped virus particles, within the nucleus, in the lymphoid organs and interstitial cells of hepatopancreas of both spontaneously and experimentally infected shrimps. The size of the virion was $375{\times}167nm$, and the nucleocapsid was $290{\times}75nm$. The causative agent causing massive death in penaeid shrimps in Korea resembles baculovirus associated with white spot syndrome (WSBV) occurred in Taiwan in virus morphology and gross and histological changes of the shrimps.