Immunotherapy has been considered as secondary strategy of IgE mediated allergic disease. It decreases delayed airway inflammation and blocks irreversible airway change but many controversies still exist despite of its remarkable effect.

The purpose of this study was to estimate clinical effectiveness of immunotherapy in patients with asthma sensitized to house dust mite and to evaluate related factors.

Thirty asthmatic patients visiting allergy clinic of Mock-Dong hospital of Ewha woman university enrolled from March, 1996 to February. All patients were received the D. farinae and D. pteronyssinus standardized extract by a immunotherapy(IT) schedule and we measured clinical parameters.

1) Symptom-medication score was significantly improved after treatment (8.9±0.29 ; before IT vs. 3.4±0.20 ; after IT, p<0.05).

2) Methacholine challenge test demonstrated significant improvement (PC20 0.78± 0.09 before IT vs. 1.l8±0.17 after I year of IT, p<0.05). After we divided patients into two groups, group I that showed more than twice increasing in PC20 after I year IT and group II that did not. There was no significant difference between the groups in pre-treatment PC20s (8.75±2.75mg/ml in group I vs. 7.08±1.84mg/ml in group II, p<0.05).

3) Skin prick test demonstrated no significant change (wheel flare ratio in D. farinae 2.44±0.24 before IT vs. 2.11±0.26 after IT, in D. pteronyssinus 2.33±0.29 before IT vs. 2.22±0.22 after IT, p>0.05).

4) There were no significant correlations for any combination among these three parameters (symptomatic improvement, change of PC20 and disease duration of asthma).

5) In view of side effects, no fatal systemic reaction occurred during treatment period. Only one patient experienced injection-related dyspnea and urticaria that were easily controlled by medication.

This study demonstrated that patients with asthma sensitized to house dust mite benefit from specific immunotherapy through symptomatic improvement and reduced nonspecific bronchial hyperreactivity. As for side reactions immunotherapy might be relatively safe if allergen is carefully administered a controlled and supervised environment.

No abstract available in English.

Alzheimer's disease(AD) is primarily characterized by neurofibrillary tangles, senile plaques, and neurodegeneration. The major component of senile plaques is the beta-amyloid peptide(A β), Which is considered to have a causal role in AD. However, the biological activities of Aβ in AD has not been clearly defined. In this study we have investigated the effects of Aβ 25-35 fragment to neurons using organotypic hippocampal slice culture system which maintained intact hippocampal synaptic circuit and anatomy. Hippocampal slice culture is prepared from rat postnatal 10-old days and after 14 days culture, slices were treated with 10uM Aβ 25-35 fragment. Neuronal death was measured with propidium iodide(PI) uptake and NeuN, neuronal marker, staining. After treatment of Aβ 25-35 fragment for 3days or 7days on hippocampal slice culture, we observed the increased PI uptake and the decreased number of NeuN-stained neuron in CA1 region of hippocampal pyramidal layer or dentate gyrus. These results suggested that Aβ 25-35 fragment exerts the neurotoxicity in hippocampal slice culture.

Bechet's disease(BD) is a chronic inflammatoroy condition involving several organs including gastrointestinal tract. Gastrointestinal tracts involvement in BD has been identified throughout the entire alimentary tract and commonly accompanies ulcerative lesions in the small and large bowel. It is debatable whether BD could be included among seronegative spondyloarthropathy (SPA).SPA usually occurs without overt sign of intestinal inflammation, but significant number of patients have asymptomatic intestinal inflammation, usually affecting ileum. Since most patients with SPA including BD are treated with NSAIDS. However, NSAID may play a role in aggravation or provocation of intestinal inflammation. Special attention to asymptomatic intestinal inflammation is needed, especially when NSAIDs are used for management of arthritic symptom in SpA. We experienced a case of BD which was complicated by a massive small bowel bleeding precipitated by NSAID use.

The granulation tissue, which are found in nonspecific inflammation, occasionally seemed like round mass. We experienced and report four cases in which the granulation tissue presented as endobronchial mass on the bronchoscopy. The masses obstructing lobar or segmental bronchial oriface were round, smooth surfaced and pinkish except whitish one case. The granulation tissue caused by acute or chronic inflammations, should be considered to differentiate endobronchial mass.

Acetaminophen is a mild analgesic and antipyretic agent that is safe and effective when taken in therapeutic doses. Ingestion of overdoses, however, may lead to acute liver failure accompanied by centrilobular degeneration and necrosis. The toxicity of acetaminophen is generally thought to be caused by direct interaction of its reactive metabolites with cellular macromolecules. Cell death, defined as an irreversible loss of vital cellular function and structure, can occur by either necrosis or apoptosis. Until recently, investigation into liver cell death has focused on cell necrosis although it is now appreciated that both apoptosis and necrosis may contribute to liver cell death. The present study examined cultured NCTC-1469 cells for LDH release and DNA laddering and their association with cell death. NCTC-1469 cells were cultured in NCTC-135 medium containing 10% horse serum for 72hr, and changed medium to fresh medium containing acetaminophen(from 0,5mM to 5mM). Cell viability was examined by MTT method and cell necrosis was assessed lactate dehydrogenase leakage. Genomic DNA fragmentation was assessed qualitatively by 1.5% agarose gel electrophoresis. Acetaminophen decreased MTT levels(p<0.05) and increased release of LDH(p<0.05) in dose-dependendent manner. Agarose gel electrophoresis revealed a "ladder" of DNA fragments in all acetaminophen concentration. Cell viability strongly correlated with cell necrosis(r²=0.946). These results show that acetaminophen induced both necrosis and apoptosis in NCTC-1469 cells and cell death mainly attributed to apoptosis.

Corrent information from studies in animal models indicates that perinatal exposure to atcohol produces a variety of damaging consequences in the central nervous system. These mayresult from direct neurotoxic effects of ethanol on the CNS, a system known to be particularlysusceptible to environmental influences during development.

The present study was undertaken to investigate the effects of ethanol on the neuronal viability and neurite outgrowth, one of the critical steps in neuronal differentiation, in primarycultured neuronal and glial cells of rat hippocampus.

Cell cultures were prepared on embryonic day 17 (E17) for treatment with a series ofethanol concentrations (10, 100, 500, and 1000mM). Effect of ethanol was investigated at 0, 18, and 24 hour fo11owing ethanol treatment. To study the changes in proliferation of glialcells, protein content was measured at 7 day in vitro.

The results are as fo11ows :

1) Ethanol did not altered neuronal survival or attachment to the substrate at any of the concentrations that were used.

2) 10 or 100mM ethanol was associated with significant increase in the total neurite length per cell.

3) 10 or 100mM ethanol markedly increased and 1000mM ethanol decreased protein contents on 7 day in vitro.

These findings suggested that ethanol mar have distinct effects on neurite outgrowth andalso indicated that high concentration of ethanol (500~1000mM) and long period of exposure(3~7days) were required to produce toxic effects on neurons and glial cells in this system.

Insulin controls the levels of blood sugar by inhibiting glucose release from liver and by stimulating glucose utilization in muscle and adipose tissues. In addition to its peripheral effects, insulin influences circulating glucose levels by modulating glucose production and its metabolism through central nervous system. But it is presently not well known whether the central effect of insulin on plasma glucose is mediated by directly or indirectly through CNS actions. The autonomic nervous system exerts a dual control over insulin secretion. The parasympathetic nervous system can augment insulin secretion and the sympathetic nervous system can produce a net impairment of insulin release.

In the present study, we measured the changes of blood glucose and pyruvic acid level to examine the effetcs of intracisternally injected insulin. Carbachol and scopolamine in streptozotocin(STZ)-induced diabetic rats.

results are as follows:

1) streptozotocin produced significant increase in blood glucose and pyruvic acid concentrations.

2) Intracisternally injected insulin markedly reduced blood glucose and pyruvic acid concentrations in STZ-induced diabetic rats.

3) Intracisternally injected cholinominetics, carbachol, reduced blood glucose and pyruvic acid concentrations in STZ-induced diabetic rats.

4) Intracisternally injected anticholinergics, scopolamine, increased the concentration of the blood glucose and inhibited the concentration of the blood pyruvic acid in STZ-induced diabetic rats.

Therefore, it is suggested that central parasympathetic nervous system plays an partial role in modulating peripheral blood glucose metabolism and insulin produse hypoglycemic action via central parasympathetic nervous system.