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)

BACKGROUND: The increasing implementation of organ transplantation requires an unequivocal diagnosis of brain death for moral and legal reasons. Among instrumental investigations, angiographic demonstration of absent intracranial blood flow is considered to be the most reliable test in diagnosing brain death. This test should be easily accessible since most brain dead patients are vitally unstable and have various life-supporting equipments besides their beds. To investigate the usefulness of an intracranial CT angiography (CTA) for the diagnosis of brain death, we performed CTA in comatose patients who were either clinically brain dead or not. METHODS: Fourteen comatose patients (11 male and 3 female, aged from 17 to 63 years) with various brain insults were included in this study. Eleven patients were clinically brain dead. Among the remaining three patients, one showed subtle withdrawal movements in one extremity to noxious stimuli with absent brainstem reflexes, and the other two showed multifocal myoclonic seizures. CT scanning was performed with a table speed of 2 mm/sec, twenty seconds after beginning an injection of contrast media. The data were reformatted by maximum intensity projection (MIP) and shaded surface display (SSD) after the reconstruction of a 1 mm interval. A portable electroencephalography (EEG) was also taken serially in clinically brain dead patients except one. RESULTS: Intracranial arterial blood flow was preserved in those who showed either a seizure, abnormal posture or intact brainstem reflexes. On the other hand, intracranial arteries were not visualized in all brain dead patients with electrocerebral silence (ECS) on their EEG with the exception of one patient whose EEG was difficult to determine a ECS due to excessive mechanical artifacts. However, in the clinically brain dead patients, the intracranial arterial flow was preserved in those who suffered from widespread brainstem and cerebellar infarction or whose EEG demonstrated periodic lateralizing epileptiform discharges or a burst suppression pattern. CONCLUSIONS: Intracranial CTA seems to be a safe and noninvasive procedure for the determination of brain death that produces fast, reliable, and easy-to-interpret results. It can be used as an alternative method to the EEG when the EEG is not possible or difficult to interpret due to artifacts.
Angiography* ; Arteries ; Artifacts ; Brain Death* ; Brain Stem ; Brain* ; Coma ; Contrast Media ; Diagnosis ; Electroencephalography ; Extremities ; Female ; Hand ; Humans ; Infarction ; Male ; Organ Transplantation ; Posture ; Reflex ; Seizures ; Tomography, Spiral Computed* ; Tomography, X-Ray Computed ; Transplants

Skip lesion is not uncommon feature in osteosarcoma and considered to be importantly associated with poor prognosis factor, and thus, should be excised with the main mass. The accurate pre-operative evaluation of the intramedullary extent of osteosarcoma is essential, because it determines the level of bone resection. Among the reliable detection methods, bone scan has a drawback of high rate of false negative results and regional MRI has a difficulty to cover the whole involved lesions without clinical suspicion. The authors report a case of osteosarcoma of the distal femur with a proximal skip lesion that was not detected by either regional MR imaging or by bone scan, but which was visualized by FDG-PET/CT.
Complement System Proteins ; Femur ; Neoplasm Metastasis ; Osteosarcoma ; Prognosis

A 25-year-old male patient was received emergency operation, open reduction and tenorrhaphy owing to degloving injury on the dorsum of his left hand, under axillary brachial plexus block using a transarterial approach. Following operation, he revealed the signs and symptoms of brachial plexus injury such as weakness, sensory deficit and tingling sensation on his left forearm and hand. The finding on electromyography (EMG), performed on the 16th postoperative day (POD), was indicative of left incomplete brachial plexus injury, mainly in medial cord and ulnar nerve, and partially median and radial nerve at/above the axillary level. The signs and symptoms were improved slightly on POD 8 and a lot on POD 23. The complete recovery of symptoms and regeneration of injured nerve on EMG were confirmed 3 months following operation. In this case, the causative factors of brachial plexus injury were suggested in stretching of the brachial plexus due to improper positioning of injured arm during or after operation, combined with or without injury due to nerve block or tourniquet compression.
Adult ; Arm ; Brachial Plexus* ; Electromyography ; Emergencies ; Forearm ; Hand ; Humans ; Male ; Nerve Block ; Radial Nerve ; Regeneration ; Sensation ; Tourniquets ; Ulnar Nerve

Prostaglandins have numerous biologic effects on a variety of physiological and pathological activities such as inflammation, platelet aggregation, neurotransmitter release, smooth muscle contraction, and so forth. PGE2 is one of the well-studied inflammatory prostaglandins and causes vasodilatation, edema, fever and pain. Also PGE2 induces the production of matrix metalloproteinases (MMPs) which involve in destruction of tissue. In rheumatoid arthritis, macrophages isolated from patients secrete large amounts of PGE2 and PGE2 promote inflammation and participate in destructive mechanisms of the rheumatoid joint. In addition to its proinflammatory effects, PGE2 acts also as an immunomodulator, promote humoral and Th2-type immune responses and inhibit Th1-type immune responses. Also PGE2 inhibits the production of tumor necrosis factor (TNF-alpha), IL-1beta, IL-8 and IL-12 and stimulates the production of IL-10 by macrophages. Thus PGE2 should be regarded not as proinflammatory molecule but as modulator of immune responses. In this review, we will focus on the current knowledge about PGE2 as the modulator of immune responses and summarize the effects of PGE2 on the immune systems and inflammation.
Arthritis, Rheumatoid ; Dinoprostone* ; Edema ; Fever ; Humans ; Immune System ; Inflammation* ; Interleukin-10 ; Interleukin-12 ; Interleukin-8 ; Joints ; Macrophages ; Matrix Metalloproteinases ; Muscle, Smooth ; Neurotransmitter Agents ; Platelet Aggregation ; Prostaglandins ; Tumor Necrosis Factor-alpha ; Vasodilation

No abstract available.
Animals ; Locomotion* ; Rats* ; Spinal Cord Injuries* ; Spinal Cord*

Cytokines are secreted proteins and interact with their specific cell surface receptors, triggering intracellular signal transduction pathways that activate a number of genes crucial for the biological functions of cytokines. These cytokine signal transduction pathways are tightly regulated processes. The negative regulations of cytokine signaling are achieved by receptor internalization and degradation, dephosphorylation of signaling intermediates, expression of protein inhibitors such as suppressor of cytokine signaling (SOCS) and protein inhibitors of activated STAT (PIAS). The observation that cytokines are central to the inflammatory and destructive process in several autoimmune diseases suggests that interventions targeting the cytokine intracellular signaling will be a new therapeutic strategy in autoimmune diseases. We review the current knowledge about negative regulation of cytokine signal transduction.
Autoimmune Diseases ; Cytokines ; Protein Inhibitors of Activated STAT ; Receptors, Cell Surface ; Signal Transduction* ; Social Control, Formal

No abstract available.
Arthritis, Rheumatoid* ; Humans ; Lung Diseases, Interstitial*

OBJECTIVES: Fibromyalgia is a common rheumatologic disease characterized by chronic myalgia, fatigue, and sleep disturbance. Chronic fatigue syndrome is chracterized by debilitating fatigue of at least 6 months duration accompanied by other symptoms such as fever, pharyngitis, painful lymph nodes, headache, myalgia, sleep disturbances, neurocognitive complaints, and depression. There has reported that 70% of patients with fibromyalgia met the centers for Disease Control and Prevention symptom criteria for chronic fatigue syndrome. The objectives of this study were to determine how frequently patients with fibromyalgia met the criteria for and chronic fatigue syndrome and what symptoms were manifested. METHODS: 34 patients diagnosed with fibromyalgia were participated in the study. The questionnaire made according to the Centers for Disease Control and Prevention criteria was administerd and patients with chronic fatigue syndrome were diagnosed by this questionnaire, physical examination and laboratory tests. RESULTS: 21% (7 patients) of patients with fibromyalgia met the criteria for chronic fatigue syndrome. The symptoms in patients with chronic fatigue syndrome were memory loss/forgetfullness (100%), sore throat (57%), painful lymph node (29%), myalgia (100%), multiple arthralgia (57%), headache (57%), unrefreshing sleep (86%), postexertional malaise (86%). CONCLUSION: 21% of patients diagnosed with fibromyalgia met the criteria for chronic fatigue syndrome. The incidence of chronic fatigue syndrome in our study is low as compared with the previous study (70%) in 1996.
Arthralgia ; Centers for Disease Control and Prevention (U.S.) ; Depression ; Fatigue ; Fatigue Syndrome, Chronic* ; Fever ; Fibromyalgia* ; Headache ; Humans ; Incidence* ; Lymph Nodes ; Memory ; Myalgia ; Pharyngitis ; Physical Examination ; Surveys and Questionnaires

IgA nephropathy can occur rarely as a complication of D-penicillamine treatment, but it is exact pathogenesis remains unclear. If a patients has gross or microscopic hematuria during D-penicillamine treatment, D-penicillamine induced IgA nephropathy should be suspected as a cause of hematuria. In those cases, renal biopsy should be taken for diagnosis and proper management. We experienced a case of IgA nephropathy confirmed by renal biopsy in a 39-years-old female patient with scleroderma during D-penicillamine therapy and report this case with a review of literature.
Biopsy ; Diagnosis ; Female ; Glomerulonephritis, IGA* ; Hematuria ; Humans ; Immunoglobulin A* ; Penicillamine*