In order to find a highly efficient compound against Clonorchis infection, the anthelmintic activity of disophenol, Tremerad (SYD-230), dithiazanine iodide, dehydroemetine-late-release tablets(RO 1-9334/20), niridazole (Ambilhar), hexachlorophene (G-11), Hetol(1, 4-bis-trichloromethylbenzol) and Bilevon (niclofolan) was tested against Clonorchis sinensis experimentally infected rabbits. All drugs showed a progressive increase in efficacy as the dose rate. They were highly efficient against Clonorchis infection if sufficiently high, potentially toxic doses were given. The efficacy was evaluated by the number of detected worms with vital condition at autopsy after the treatment with above drugs. The high efficacy was observed at the following dose rates of each drugs, i.e. disophenol at a single dose of 30 mg/kg, Tremerad at the daily dose of 200 mg/kg for 10 consecutive days, dithiazanine iodide at the daily dose of 50 mg/kg for 6 consecutive days, dehydroemetine at the daily dose of 10 mg/kg for 10 consecutive days, hexachlorophene at the daily dose of 20 mg/kg for 10 to 15 consecutive days, Hetol at the daily doses from 50 to 100 mg/kg for 5 to 10 consecutive days, and Bilevon at a single dose of 8 mg/kg. Moderate effectiveness was shown in niridazole at the dose of 25 mg/kg for 10 days medication. The use of these anthelmintics for the clinical treatment of Clonorchis sinensis infection is discussed.
parasitology-helminth-trematoda ; chemotherapy-Clonorchis sinensis ; clonorchiasis-rabbit ; disophenol ; Tremerad (SYD-230) ; dithiazanine iodide ; dehydroemetine-late-release tablets(RO 1-9334/20) ; niridazole (Ambilhar) ; hexachlorophene (G-11) ; Hetol(1, 4-bis-trichloromethylbenxol) ; Bilevon (niclofolan)

No abstract available.
Kartagener Syndrome*

Thiamine deficiency is generally accepted as the primary etiologic factor for the Wernicke encephalopathy in human and for the similar neurologic symptoms in thiamine depleted experimental animals. Although pyrithiariiineinduced thiamine deficiency has been known to produce histopathologic lesions within many nuclei of the rat brain, the pathogenic mechanisms involved have not been clarified. Furthermore, the effect of thiamine deprivation on the nature and anatomic distribution of neurotransmitter changes has not been fully explored. The present studies were undertaken to investigate - morphological changes of the basal nucleus of Meynert and vestibular nucleus in thiamine deficient rats induced by pyrithiamine and thiamine deficient diet. For this purpose immunohistochemical stain for choline acetyltransferase was performed. Fifty healthy Sprague-Dawley strain rats weighing about 150 gm, were divided into 10 control group and 40 thiamine deficient group. Animals in thiamine deficient group were treated with daily intraperitoneal injection of pyrithiamine( 50 ug/lOOgm of BW/dbLy, Sigma Co.) for 9 days and were continuously given thiamine deficient diet until to be sacrificed. Thiamine deficient rats were subdivided into 3 groups according to different stages of neurologic manifestations ; the early group, the beginning stage of anorexia, hypothermia and weight loss without neurologic manifestations(sacrificed day ; 9th-13th day) the intermediate group, the developing stage of gait ataxia and hypotonia(sacrificed day ; 17th-19th day) the late group, the established stage of tremor, convulsion and back arching(sacrificed day ; 23th-26th day). All animals were anesthetized with sodium pentobarbital(40mg/kg, I.p.) and perfused in vivo through the ascending aorta with 10% neutral buffered formalin or 4% paraformaldehyde-0. 1% glutaraldehyde in PBS, and then brains were removed. Luxol-fast blue and cresyl violet stain was performed according to routine paraffin method for observing morphologic changes in basal nucleus of Meynert and vestibular nucleus. In addition immunohistochemical stains in the same regions were performed by free floating method in cell culture plate. All preparations were observed with a light microscope. The results obtained were as follows ; 1. Sequential changes of the neurologic manifestations in thiamine deficient rats were weight loss, hypothermia and ariorexia on the 9th-10th day, followed by gait ataxia and hypotonia on the 13th-15th day, and then tremor, convulsion and back arching on the 22th-26th day. 2. Glial proliferation was noted in the basal nucleus of the early group but not in the vestibular nucleus. Atrophy and pyknosis of neurons in basal nucleus and vestibular nucleus were shown in the intermediate group and marke neuronal loss and edematous tissue necrosis were noted in the late group. 3. Choline acetyltransferase immurforeactivity in the basal nucleus and vestibular nucleus was markedly positive in the early group as well as control group, moderately positive in the intermediate groupand minimally positive in the late group. It is suggested that the extent of neuronal damage in thiamine deficient rats is proportional to the duration of thiamine depletion. And the data presented here may account for: the regional susceptability and reversibility of certain symptoms in thiamine deficient rats.
Animals ; Anorexia ; Aorta ; Atrophy ; Basal Nucleus of Meynert* ; Brain ; Cell Culture Techniques ; Choline O-Acetyltransferase* ; Choline* ; Coloring Agents ; Diet ; Formaldehyde ; Gait Ataxia ; Glutaral ; Humans ; Hypothermia ; Injections, Intraperitoneal ; Muscle Hypotonia ; Necrosis ; Neurologic Manifestations ; Neurons ; Neurotransmitter Agents ; Paraffin ; Pyrithiamine ; Rats* ; Rats, Sprague-Dawley ; Seizures ; Sodium ; Thiamine Deficiency ; Thiamine* ; Tremor ; Viola ; Weight Loss ; Wernicke Encephalopathy

Quantitative serial measurements of Alpha-fetoprotein (a-FP) and Beta-human chorionic gonadotropin (B-HCG) using radioimmunoassay were performed in a patient with recurrent non-germinomatous germ cell tumor (NGGCT) into CNS during radiotherapy and chemotherapy. When the pineal tumor was initially presented, elevated levels of serum a-FP and B-HCG fell dramatically to normal rage after the completion of cranial irradiation (5,060cGy). Three months later, the patient had a rise in serum and CSF tumor markers coincident with recurrence of tumor into lumbal spinal canal. Serum levels were not changed despite of 15 days of whole spine irradiation (2,000cGy) although decreased remarkably 1 month after the completion of radiotherapy (4,230cGy). At the time of relapse in the suprasella area and the cerebellopontine angle, serum and CSF levels rised again. As a result of two courses of chemotherapy the tumor markers fell markedly, but the tumor was spread to other sites into CNS. We conclude serial measurements of a-FP and B-HCG are useful for the diagnosis of the non-germinomatous germ cell tumor into CNS and for monitoring disease activity.
alpha-Fetoproteins ; Cerebellopontine Angle ; Chorionic Gonadotropin ; Cranial Irradiation ; Diagnosis ; Drug Therapy ; Germ Cells* ; Humans ; Neoplasms, Germ Cell and Embryonal* ; Pinealoma ; Radioimmunoassay ; Radiotherapy ; Rage ; Recurrence ; Spinal Canal ; Spine ; Biomarkers, Tumor*

The etiology of ischemic stroke remains undetermined in nearly 40% of patients despite extensive evaluations. Coagulopathies associated with cerebrovascular ischemia may be familial or acquired and account for 4% of all strokes. The four important naturally occurring circulation proteins that inhibit coagulation are protein C, protein S, antithrombin III, and heparin cofactor II. A carefully balanced interaction between these proteins and normal vascular endothelial cells comprise a major barrier inhibiting thrombosis. The true deficiencies of these proteins are usually inherited although many conditions such as DIC, malignancy, malnutrition, infection, and neutropenia can be associated with acquired deficiencies. Although some data suggest an association between arterial strokes and the deficiency of these proteins in young adults, cerebral venous thrombosis and venous infarcts gave been reported far more commonly with deficiencies of any of these proteins. The understanding of the molecular events underlying coagulation has improved in recent years. This has led to development of specific assays that can identify genetic abnormalities which can cause coagulopathies. Although the technology has improved the fundamental approach to the patient has not changed. A primary care physician requires a basic knowledge of the principles of blood coagulation so as to treat patients with simple problems and refer patients with more unusual or complex disorders on to the specialist. The recognition that hypercoagulable states are sometimes found in ischemic stroke patients has led to testing for these rare conditions. Coagulopathies related to protein C, protein S, or antithrombin III deficiencies, activated protein C resistance, prothrombin gene mutation, anticardiolipin antibodies, or lupus anticoagulant can be evaluated with various coagulation testing strategies.
Activated Protein C Resistance ; Antibodies, Anticardiolipin ; Antithrombin III ; Antithrombin III Deficiency ; Blood Coagulation ; Dacarbazine ; Endothelial Cells ; Heparin Cofactor II ; Humans ; Ischemia ; Lupus Coagulation Inhibitor ; Malnutrition ; Neutropenia ; Physicians, Primary Care ; Protein C ; Protein S ; Prothrombin ; Specialization ; Stroke* ; Thrombosis ; Venous Thrombosis ; Young Adult

Chymopapain was discovered by Jensen in 1941, and in 1963 Smith demonstrated the chondrolytic properties of chymopapain. Since then, many patients have been injected with this agent. Although there are evidences of neurotoxicity to chymopapain in animals, adverse effects in humans have rarely been reported. We present a case delayed onset of paraplegia after chymopapain chemonucleolysis and review the neurotoxicities to chymopapain.
Animals ; Chymopapain ; Humans ; Intervertebral Disc Chemolysis* ; Paraplegia*

Cardiac myxoma is a rare but potentially treatable cause of stroke. The diagnosis is rarely made on typical triad of constitutional, embolic, and obstructive symptoms, and it is difficult because there is no specific history, physical examination, chest X-ray, or electrocardiographic findings, but with the development of echocardiography the correct diagosis is now usualy made. Neurologic manifestation is frequent(25-45%) and presented with embolic infarction, aneurysm formation, intracranial hemorrhage, and distant metastasis. We experienced five patients with cardiac myxoma who presented with these neurologic manifestations. Also we should be considered in the differential diagnosis of cerebral infarction, particularly when multiple cerebral infarction and constitutional or obstructive symptoms are conjoined in young age stroke. We describe five patients who presented with embolic infarction, cerebral metastasis and aneurysm formation.
Aneurysm ; Cerebral Infarction ; Diagnosis ; Diagnosis, Differential ; Echocardiography ; Electrocardiography ; Humans ; Infarction ; Intracranial Hemorrhages ; Myxoma* ; Neoplasm Metastasis ; Neurologic Manifestations* ; Physical Examination ; Stroke ; Thorax

BACKGROUND & PURPOSE: Fibrinoeptide-A (FpA) and D-dimer have been well known as hematologic parameters for activation of the coagulation and the endogeneous fibrinolysis system during acute phase of ischemic stroke. We measured the levels of FpA and D-dimer in acute progressive and non-progressive ischemic strokes to assess whether these markers are valuable as a predictor of stroke progression during acute phase. METHODS: FpA (RIA method) and D dimer (ELISA method) were determined in 54 patients, 9 with acute progressive and 45 with non-progressive within acute stage(< 48 hours of onset) of cerebral infarction. RESULTS: Levels of FpA in patients with acute progressive stroke were significantly higher than those in patients with non-progressive stroke, indicating activation of the coagulation system (P = 0.013). And, levels of D-dimer in patients with acute progressive stroke were also higher than those in patients with non-progressive stroke but statistically insignificant(P-0.071). CONCLUSIONS: These findings suggest that the coagulation system is more enhanced in progressive stroke than non-progressive one during acute stage of ischemic stroke. Higher levels of FpA are thought to be useful markers to predict stroke in progression.
Cerebral Infarction ; Fibrinolysis ; Humans ; Stroke*

BACKGROUND & PURPOSE: Of thalamic stroke syndrome, according to previous reports, the syndrome of hemiataxia and hemisensory loss (thalamic ataxia syndrome) is known to have localizing value confined to the lesion of posterolateral thalamus. And ataxia in thalamic ataxia syndrome is due to interruption of cerebellar outflow pathways. We observed the clinical characteristics of cerebellar manifestations in patients with thalamic ataxia syndrome to clarify intrathalamic cerebellar pathways because it is known that parts of cerebellar efferent fibers do not pass through the thalamus. METHODS: Ten patients with ataxia (5 men, 5 women ; mean age 64), out of 47 thalamic stroke patients admitted to Kyung Hee University Hospital from Jan. 1994 to May. 1995, were selected. The localization of the lesion was based on CT or MR imaging and ataxia was characterized in view of cerebellar functions - coordination of movement, regulation of equilibrium and muscle tone. RESULTS: Out of 10 patients, 4 patients were thalamic hematoma, 4 patients thalamic hematoma with intraventricular hemorrhage, 2 patients thalamic infarction. Four patients were hemiataxia-hemiparesis-hemisensory loss, 4 patients hemiataxia-hemisensory loss, 2 patients hemiataxia-hemiparesis. Posterolateral thalamus was involved in 4 patients, dorsal thalamus in 3 patients, posterolateral and dorsal thalamus in 3 patients. All patients had dysmetria, dysdiadochokinesia, kinetic tremor. Two patient has gait ataxia. Speech and ocular motility disturbances were not noted. CONCLUSION: Thalamic ataxia syndrome appeared in the lesion of posterolateral and dorsal thalamus. Common cerebellar manifestations symptoms of incoordination.
Ataxia* ; Cerebellar Ataxia ; Female ; Gait Ataxia ; Hematoma ; Hemorrhage ; Humans ; Infarction ; Magnetic Resonance Imaging ; Male ; Stroke* ; Thalamus ; Tremor

As, until now, many studies have failed to establish the clinical effect of numerous neuroprotectives, antithrombotic therapy must be emphasized as one of critical options among limited treatment strategies in acute ischemic stroke. Based on the accumulating evidences that platelets and coagulating proteins play an important role in the thrombus formation, antiplatelets and anticoagulants are served as antithrombotics. Recently, major advances have been made in understanding the effects of antiplatelets and anticoagulants. Large randomized clinical trials have highlighted the effectiveness and safety of early and continuous antiplatelet therapy in reducing atherothrombotic stroke recurrence. Urgent anticoagulation has been used often to prevent early recurrent stroke and to improve neurological outcomes, however, its formal use in acute stroke has been the subject of debate even in cardioembolic stroke. That's because anticoagulants also increase the risk of fatal or disabling intracranial hemorrhage and it is difficult to monitor proper anticoagulation. Although early administration of anticoagulants should be considered to prevent the secondary injury and the propagation of thrombosis in patients with atherothrombotic stroke, more evidences are needed especially in patients with infractions secondary to large artery thrombosis or cardioembolism. This review discusses recent advances related to antithrombotic strategies and putative neuroprotectives.
Anticoagulants ; Arteries ; Blood Platelets ; Humans ; Intracranial Hemorrhages ; Organothiophosphorus Compounds ; Proteins ; Recurrence ; Stroke ; Thrombosis