Objectives : Smilacis Glabrae Rhizoma (SGR) has been used in traditional medicine for treating diseases related to inflammation and cancer. However, the protective effect of SGR has not been reported in the study of acute pancreatitis (AP). Therefore, this study was performed to evaluate the protective effects of SGR water extract on cerulein-induced AP. Methods : AP was induced by intraperitoneal injection of supramaximal concentrations of stable cholecystokinin analogue cerulein ($50{\mu}g/kg$) 6 times at intervals of one hour in mice. SGR water extract (0.01, 0.05, or 0.1 g/kg) was administrated intraperitoneally 1 h prior to the first injection of cerulein. The mice were sacrificed at 6 h after the final injection of cerulein. Pancreas and lung were rapidly removed for histochemical examination and myeloperoxidase (MPO) assay. In addition, polymerase chain reaction (PCR) was performed to examine mRNA levels of proinflammatory cytokines such as interleukin(IL)-6, $IL-1{\beta}$ and Tumor necrosis $factor(TNF)-{\alpha}$. Results : Administration of SGR water extract significantly inhibited pancreatic weight to body weight ratio. In addition, SGR treatment inhibited the histological damages and increase of MPO activity in both pancreas and lung during AP. Also, mRNA levels of IL-6 but not $IL-1{\beta}$and $TNF-{\alpha}$ were inhibited by SGR water extract against AP. Conclusion : Our results revealed that pre-treatment of SGR water extract reduces the severity of cerulein-induced AP. Therefore, this study suggest that SGR could be used as a drug or agent to prevent AP.
Since mid-1960s the reports from the Surgeon General, the World Health Organization, and other health experts state that there is no risk-free level exposure to smoking and secondhand smoke. Tobacco smoke is made up of more than 7,000 chemicals. Hundreds are toxic, and at least 70 are carcinogens. The chemicals in tobacco smoke reach smoker's lungs quickly every time smoker inhale causing damages immediately. Inhaling even the smallest amount of tobacco smoke can also damage smoker's DNA, which can lead to cancers. Smoking is responsible for more than 87% of lung cancers, but there are a host of other chronic diseases directly related to exposure to tobacco smoke. It's also a major cause of heart disease, stroke, aortic aneurysm, peripheral arterial disease and most of the other diseases. In the United States, each year with more than from 440,000 to 520,000 deaths caused by smoking and exposure to involuntary smoke. They conclude that smoking is the single most important source of preventable morbidity and mortality. The United States of America have about 60-year history of tobacco litigation. Tobacco litigation has been an important tool in tobacco control strategies aimed at limiting the activities of tobacco companies and providing redress to people who have become ill as a result of their use of tobacco products. Tobacco litigation is a kind of tort litigation. Quite often, as in the asbestos and other mass tort litigation episodes, tobacco litigation can play an educational role, warning the public about the magnitude of health risks that might otherwise be less clearly perceived. Tobacco litigation allows smokers, their families or other victims of smoking to sue tobacco companies in order to be compensated for the harm they have suffered. Potential benefits of tobacco litigation include compensation for smoking-related damages, strengthening regulatory activity, publicity, documents disclosure and changing tobacco industry behavior. And also tobacco litigation can limit the political activities of tobacco industry, protect human rights of smokers and non-smokers, increase burden to tobacco price-up and enhance the effects of law and politics in public health.
Asbestos has been used for roofing, walling and the like for the constructions since 60's~70's owing to its excellent fire resistance and heat insulative nature. However, it has banned to be used in major countries all over the world since WHO-affiliated International Agency for Research on Cancer (IARC) stipulated asbestos by a top carcinogen causing lung cancer, malignant mesothelioma and so on in 1986. Therefore, we had prohibited the use of asbestos on brakes for automobile since 2007 and on most of the products other than some cases of having no alternatives such as munitions from 2009. Nevertheless, diseases from asbestos have a long incubation period of 10~40 years, therefore, even if being exposed to asbestos, preliminary prevention is rather more important than instant possible damage as damages can be greater decades later. Accordingly, this thesis has a purpose to seek a plan in order to guarantee the rights of national health from harmfulness of asbestos by comparing and reviewing the policies on asbestos in advanced countries such as France, Japan, Netherlands and such like.
Proceedings of the Korean Society of Toxicology Conference
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2005.05a
/
pp.51-82
/
2005
To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.
Objectives: The lung injuries by exposure to the humidifier disinfectants (HDs) were reported in 2011, Korea. For the HD victims, environmental exposure level and clinical diagnosis were conducted to determine the levels of damage by HDs. Methods: The exposure assessment to the HDs from 1st to 4th questionnaire surveys were carried out for 5,245 victims. And the affecting factors of exposure levels were analyzed by characterizing exposure and demographic information. By using of exposure concentration and cumulative time, exposure levels were classified and compared by percentage of clinical diagnosis classes. The high exposure and low clinical diagnosis rating groups, and low exposure and high clinical diagnosis rating groups were analyzed to overcome the limitation of past exposure assessment such as recall bias. Results: Among the all applicants damaged by the humidifier disinfectants, survivors were 4,028 and the dead were 1,217. And male and female were 2,675, and 2,547, respectively. In case of occurrence age of lung disease, under 10 years was majority age group (1,536) and followed by thirties (917). Pregnant women and fetuses were 339 and 439, respectively. And the damages by exposure to the HDs were concentrated on these susceptible populations in groups with low exposure and high clinical diagnosis rating. On the other hand, the groups classified by high exposure and low clinical diagnosis rating were shown different characterization. Conclusions: The questionnaire survey on past exposure may be uncertain due to recall bias. However, the relationship between classified exposure levels and clinical diagnosis ratings might be shown positive correlation if the exposure assessment errors were analyzed and controlled.
Present study aimed to elucidate the immunosuppressive effect of prednisolone on Naegleria fowlsri infection in mice. N. fowleri was cultured in CGVS medium (Willert and Le Ray, 1973) . White female mice, weighing about 18g, used for experiments were divided into five groups; untreated control group, prednisolone treated groups (before, during and after infection), and only prednisolone treated group. In the prednisolone treated group, the hormone was injected intramuscularly 5 doses of 10 mg/kg every other day. According to designated time of treatment, each mouse was challenged with $1{\times}10^5$ N. fowleri intranasally. Changes of body weights, clinical manifestations and number of dead mouse were observed. Brain and lung tissues of dead mice were cultured in the non-nutrient agar (Kasprzak and Mazur, 1972), or stained with hematoxylin.rosin for the examination of histopathological changes. Results of the experiment are summarized as follows: Mortality among the prednisolone treated groups was higher than that in untreated control group, and among the treated groups, the pretreated group showed shorter survival time. Body weights among untreated control mice showed no significant increase, however, treated groups of mice showed the decrease during the administration and recovery of the weights were observed at 2 to 3 days after the completion of treatment. In the treated control groups, the infected mice began to show the pathologic findings 5 days after infection while, the untreated mice began to show the findings 8 days after infection. Tissue damages in brain and lung occurred due to virulence of amoeba were more severe among treated mice than that in untreated control group. The above mentioned results suggest that the treatment with prednisolone weaken the resistance of mice against N. fowleri infection, and probably induce more severe primary amoebic meningoencephalitis. Especially severe pathological findings were shown in pre-treated group, compared with untreated group.
It studies into viewpoints of 7 doctors of Wenbing studies on macula. The results concerning characteristics, remedy and prevention of macula are as follows; Macule does not protrude on the surface of skin and does not have any color change for external stimulus, but rash out on the surface and becomes white when pushed. It becomes macule when the blood leaks beneath skin as stomach-heat of yangming enters into blood system and damages it. On the other hand, when heat enters lung meridian, penetrates beneath the skin and congeals inside the vessel, it becomes rash. When you combine symptoms of body and pulse with numbers, color, shape and distribution status of macula, you can diagnose the depth of rash, seriousness, the possibility of treatment and prognosis of macula. The remedy for macule consists of cooling heat of yaming, removing heat from the blood and relieving feverish rash, and the one for rash consists of facilitating meridian with aroma, expelling pathogenic factors from muscles with drugs of pungent flavor and cool nature and clearing away heat from the blood systems. It relieves the inhibited functional activities of lung-Ki, and helps extermination of rash as well as clearing heat of the vessel. Also, it is the most important to preserve resin of stomach for every treatment. It is good to avoid expelling pathogenic factors with drugs of pungent flavor and warm nature, raising drugs and invigorating drugs during treating macula. Moreover, the patients should not over dose cold-natured drugs and purgative therapy. There are common clinical symptoms of macula in advance, so right recognition of symptoms can contribute to prevention of macula.
Journal of the Korean Society of Food Science and Nutrition
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v.38
no.12
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pp.1815-1819
/
2009
Based on the soft and rigid extents, tissues are mainly divided into two groups in mammals, soft tissues including heart, lung, kidney and brain, and hard tissues including tendon, cartilage, teeth and bone. Among various tissues, bone, a dynamic rigid organ, is continuously remodeled by the opposing functional activity between bone formation by osteoblasts and bone destruction by osteoclasts. Bone protects the soft tissues and provides mineral reservoirs, which can supply the mineral needs of other soft tissues to normally maintain cellular function. While calcification in bone is an important action to fundamentally support the body and protect the soft tissues, calcification in soft tissues, including the heart, aorta, kidney, lung and spleen, results in severe organ damages, eventually causing sudden death. A growing body of evidence indicates that the osteoporotic patient who are aging, post-menopausal, diabetes and chronic kidney disease simultaneously represent a high clinical incidence of soft tissue calcification, illustrating a link between soft tissue calcification and bone decalcification (osteoporosis). This study will review what is currently known about the connection between bone decalcification and soft tissue calcification.
Objectives : The aims of this study were to exploring the therapeutic effect of Imperatae Rhizoma Extract(IRE) on Asthma. Methods : To investigate biological modulation activities of IRE, we conducted the cell-based assay whether IRE could regulate T helper 2 cells activity with EL4 T cells and mouse splenocytes, and followed animal study to conform the efficacy of their therapeutic potential on OVA-induced asthmatic mouse. Results : In cell study, IRE suppress the nuclear translocation of GATA binding protein-3 protein in phorbol 12-myristate 13-acetate/Ionomycin-stimulated EL4 T cells and Interleukine(IL)-4, IL-5 and IL-13 production in splenocytes at concentration dependent manner. In animal study, IRE-treated groups both 100mg/ml and 200mg/ml improve airway hypersensitibility reaction(AHR) response to methacholine about 30% and 40% with positive control group. Peritoneal blood analysis reveal that eosinophil number and ovalbumin-specific IgE is reduced by IRE treatment. Cell number of eosinophil is also reduced in bronchoalveolar lavage of IRE group like to peritoneal cell and real time-polymerase chain reaction data show that expression levels of IL-4, IL-5 and IL-13 were down regulated in lung tissue. Finally, histological analysis indicate that IRE protect the bronchial tissue damages through the accumulation of inflammatory cells and collagen, and these effect may be cause by interfering Th2 cells activity. Conclusions : Our data represent that IRE potentiates therapeutic activities to the allergic diseases such as asthma by regulating Th2 cells differentiation.
Kim, Eun-Young;Yun, Hye-Jung;Kim, Youn-Jung;Ryu, Jae-Chun
Proceedings of the Korea Society of Environmental Toocicology Conference
/
2003.05a
/
pp.186-186
/
2003
CKD-712, named S-YS49 is a chiral compound derived from higenamine (one component of Aconite spp.) derivatives. To compare the cytotoxicity of CKD-712 between in the absence and in the presence of S9 metabolic activation system, we performed trypan blue dye exclusion assay in Chinese hamster lung (CHL) cell. In CHL cells, the cytotoxicity (IC50) of CKD-712 was 92.9 $\mu\textrm{g}$/ml and 186.1 $\mu\textrm{g}$/ml in the absence and presence of S9 metabolic activation, respectively. And we also investigated the induction of DNA damages in mammalian cells. To perform the single cell gel electrophoresis, we determined optimum concentration in mouse lymphoma L5178Y cells using frypan blue dye exclusion assay Each IC20 of CKD-712 was determined the concentration of 23.4 $\mu\textrm{g}$/ml and 24.8 $\mu\textrm{g}$/ml in the absence and presence of S9 metabolic activation, respectively. In the comet assay, DNA damage was not observed at the concentration range from 23.4 $\mu\textrm{g}$/ml to 5.9 $\mu\textrm{g}$/ml in the absence of S9 metabolic activation system. In the presence of S9 metabolic activation system, DNA damage was not observed at the concentration range from 24.8 $\mu\textrm{g}$/ml to 6.2 $\mu\textrm{g}$/ml. From these results, it is assumed that CKD-712 may be metabolized to less cytotoxic metabolite(s).
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