• Title/Summary/Keyword: Atrophy of lung

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Study on the Symptom & the Pulse of Jaundice, Intermittent Fever, Carbuncle, Intestines Carbuncle, & c. of the Maek Kyoung Vol. VIII (맥경(脈經) 권제팔(卷第八)의 황달(黃疸). 학질(?疾). 옹종(癰腫). 장옹(腸癰) 등증맥(等證脈)에 대한 연구)

  • Lim, Dong-Kook;Cho, Kyung-Jong;Choi, Kyung-Suk;Du, Ja-Sung;Kim, Jong-Hoe;Jeong, Heon-Young;Keum, Kyung-Soo;Park, Kyung
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.5
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    • pp.1001-1034
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    • 2008
  • This thesis is a study composed of eight chapters from 9. to 16. of the Maek Kyoung(脈經) Vol. VIII. ; the symptom & the pulse of Jaundice(黃疸), Malarial Disease(?疾). Carbuncle(癰腫) Intestines Carbuncle(腸癰), & c. It is as follows : Chapter 9 refers to the symptom, pulse, treatment and prognosis of Jaundice(黃疸) and Malarial Disease(?疾). Chapter 10 refers to the cause, symptom, pulse and treatment of Cardialgia(胸痺), Cardiagra(心痛) and Nephric Accumulation(賁豚). Chapter 11 refers to the symptom, pulse and treatment of Abdominal Fuliness(腹滿), Cold Mounting(寒疝) and Abiding Food(宿食). Chapter 12 refers to the symptom and pulse of Accumulation and Mass of the Five Viscera(五臟積聚). Chapter 13 refers to the cause, pathogenesis, symptom, pulse, treatment and prognosis of Terror and Palpitation due to Fright(驚悸), Hematemesis(吐血), Nasal Hemorrhage(?血), Metrorrhagia(下血) and Extravasated Blood(瘀血). Chapter 14 refers to the cause, pathogenesis, symptom, pulse and treatment of Vomiting(嘔吐), Hiccough(?) and Diarrhea(下利). Chapter 15 refers to the cause, pathogenesis, symptom, pulse and treatment of Atrophy of Lung(肺?), Pulmonary Abscess(肺癰), Lung-distention(咳逆上氣) and Phlegm(痰飮). Chapter 16 refers to the cause, pathogenesis, symptom, pulse. treatment and prognosis of Carbuncle(癰腫), Intestines Carbuncle(腸癰), Wound(金瘡) and Acute Eczema(侵淫瘡). There have been abundant investigations in China. But we couldn't find a clear result yet, and they were written in archaic texts and colloquial Chinese, therefore it is needed to be translated into Korean. And there was only one inaccurate translation with insufficient annotation. So I hope this study will be useful to develope Oriental Medical Diagnostics.

Etiological Studies on the Acute Fatal Disease of Angora Rabbits : The So-Called Rabbit Viral Sudden Death (앙고라 토끼의 급성폐사성질병(急性斃死性疾病)의 병인학적(病因學的) 연구(硏究) : 소위(所謂) 토끼의 바이러스성(性) 급사병(急死病))

  • Lee, Cha-soo;Park, Cheong-kyu
    • Korean Journal of Veterinary Research
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    • v.27 no.2
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    • pp.277-290
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    • 1987
  • This paper dealt with etiological studies on the acute fatal disease of Angora rabbits occurring as a group in Korea. The disease was confirmed as an acute infectious disease caused by virus. The results obtained were summarized as follows: The disease produced a high morbidity in the rearing Angora rabbits and a high mortality in the infected rabbits, and was acute. The infected rabbits died soon without premonitory signs after inappetence. The body temperature of the affected rabbits rose to $40^{\circ}C$ and nearly all deaths occurred within 48 hours after inoculation. In many cases a bloody foam was visible from the nostrils after death. According to the progress of the disease the nervous signs, such as ataxia, paralysis of the legs, and torticollis could be recognized in the some cases. Rabbits that had recovered from the disease were severe emaciation, and bristly and sparse hairs. In macroscopical findings, there were hemorrhage and edema of the lung, hemorrhage or hyperemia of the tracheal and broncheal mucosae, appearance of blood-tinged effusion in the respiratory tract. The principal lesions were found in the liver. Usually the lobular necrosis of the liver cells was progressed, and focal necrosis and hemorrhagic spots of various sizes were often observed in the liver. Liver was as a whole pale. In chronic cases, however, there was a slight liver cirrhosis with the atrophy of the parenchymal cells. The other lesions encountered grossly consisted of swelling and petechiae of the kidney, hyperemia and hemorrhage of the spleen, catarrh of the small intestine, and hyperemia of the brain. The urinary bladder contained a lot of turbid urine or bloody urine and urinary cast, and was distended with the urine. In microscopical findings, the most striking lesions occurred in the liver and may be classified as viral hepatitis. The hepatic lesions were initially characterized by progression from periportal to peripheral necrosis of the lobules with the infiltration of mononuclear cells. Focal necrosis of various sizes, hemorrhage and hyperemia were often observed in the hepatic lobules. In chronic cases, there were intensive infiltration of lymphocytes, proliferation of fibroblasts, appearance of plasmal cells, and atrophy of parenchymal cells in the hepatic tissue. Perivascular lymphocytic infiltration and meningitis were seen in the brain and spinal cord. In the kidney, there were acute glomerulonephritis, hemorrhage, necrosis of the uriniferous tubules, and retention of eosinophilic substance within the renal tubules. Proliferation of fibroblasts and infiltration of mono-nuclear cells were found in the interstitial stroma of the kidney in chronic case. There were also hemorrhage and edema in the lung, hyperemia and hemorrhage in the trachea and bronchus, perivascular lymphocytic infiltration and focal myocardial necrosis in the heart, hyperemia and hemorrhage in the spleen, vacuolization and desquamation of mucous epithelia in the urinary bladder, catarrhal inflammation of the small intestine, hemorrhage in the adrenal cortex and hyperemia in the other organs. In the electron microscopical findings of the hepatic tissue, crystals of viral particles appeared in the cytoplasm of the hepatocytes and the sinusoidal endothelial cells, and the viral particles, were small in size and polygonal. The authors suppose the virus may belong to picornaviridae family of RNA viruses. Also immature virus-like particles, dilated rough endoplasmic reticulum and destruction of nuclear membrane were seen in the hepatocytes. From these results, it is concluded that the sudden death is an acute viral disease characterized by hepatitis and the affected rabbits may be died of viremia.

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Single dose toxicity study of CKD-602, a new camptothecin anticancer agent, in Beagle dogs (개에서 새로운 캄토테신계 항암제 CKD-602의 단회투여독성시험)

  • Kim, Jong-Choon;Shin, Dong-Ho;Park, Seung-Chun;Son, Woo-Chan;Cha, Shin-Woo;Han, Junghee;Bae, Joo-Hyun;Suh, Jeong-Eun;Chung, Moon-Koo
    • Korean Journal of Veterinary Research
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    • v.44 no.1
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    • pp.49-55
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    • 2004
  • The present study was carried out to investigate the potential acute toxicity of CKD-602 by a single intravenous dose in Beagle dogs. The test chemical was administered intravenously to male and female Beagle dogs at dose levels of 0.3, 0.5, or 2.5 mg/kg. Mortalities, clinical findings, and body weight changes were monitored for the 14-day period following the administration. At the end of 14-day observation period, all animals were sacrificed and complete gross postmortem examinations were performed. All males and females of the 2.5 mg/kg dose group were found dead between the fourth and seventh day after the injection. Treatment related clinical signs, including vomiting, anorexia, mucous stool, diarrhea, and no stool were observed. Decrease or suppression of body weight was observed in a dose-dependent manner. In autopsy, dark red discoloration of the gastrointestinal tract, atrophy of the thymus, paleness of the spleen, sporadic dark red spots of the lung and petechia of the heart were observed in dead animals of the 2.5 mg/kg dose group. There were no specific adverse effects on males and females of the 0.3 and 0.5 mg/kg dose groups, except for the transient clinical signs such as anorexia, vomiting, and mucus/no stool. On the basis of the results, it was concluded that a single intravenous injection of CKD-602 to Beagle dogs resulted in increased incidence of abnormal clinical signs and death, decreased body weight, and increased incidence of abnormal gross findings. The absolute toxic dose of this chemical was 2.5 mg/kg for both genders. The $LD_{50}$ value was 1.1 mg/kg (95% confidence limit not specified) for both genders. The no-observed-effect level (NOEL) was considered to be below 0.3 mg/kg for both genders.

Histopathological Study on the Protective Effect of Korean Red Ginseng on TCDD-induced Acute Toxicity in Male Guinea Pig (TCDD 투여로 급성독성을 유도한 웅성 기니픽에 있어 홍삼의 방어 효과에 대한 병리조직학적 연구)

  • Hwang Seock-Yeon;Jeong Hwa-Sook;Wee Jae-Joon;Sung Rohyun;Kim Si-Kwan
    • Journal of Ginseng Research
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    • v.23 no.4
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    • pp.222-229
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    • 1999
  • Histopathological study has been carried out to elucidate the protective effect of Korean red ginseng water extract (KRG-WE) on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced acute toxicity in male guinea pigs. Forty male guinea pigs ($200{\pm}20g$) were divided into 4 groups: normal controls (group 1) received vehicle and saline; group 2 (single TCDD-treated) received TCDD (5 ${\mu}g/kg$, single dose) and saline; group 3 received KRG-WE (200 mg/kg, i.p.) for 2 weeks starting 1 week before TCDD-exposure; group 4 received same dose of KRG-WE for 7 days from the day of TCDD-exposure. Weights of liver, testis, kidney, spleen and lung of the TCDD-exposed guinea pigs were significantly decreased. Thymus was severely shrunken, thereby could not be distinguished from adipose tissue in group 2 animals. Focal interstitial inflammation and fibrosis were observed from the lung parenchyma of group 2 animals. Furthermore, moderate swelling of hepatocyte, diffused aggregates of hemosiderin-laden macrophages from the Prussian blue stained spleen, marked decrease in spermatogenesis, and pyknotic and degenerative changes in the renal tubules were observed from intestinal organs of group 2 animals. On the other hand, histopathological damage was moderately to markedly alleviated in groups 3 and 4, but pretreatment of KRG-WE was more effective than the simultaneous treatment. In particular, TCDD-induced testicular atrophy was significantly attenuated by KRG-WE (p<0.01). From these results, it could be suggested that Korean red ginseng might be a useful herb that prevented TCDD-induced toxicity on liver, testis, kidney and spleen.

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