Since Senoo and Lincicome (1951) first have brought up for attention to the existence of malayan filariasis in Korea, several reports on the epidemiological investigations of the disease had already been made by many workers. However it is little known what kind of mosquitoes are involved as the major vectors in main endemic areas. In Cheju-Do, known as one of main endemic areas in Korea, Aedes togoi is most likely suspected as an important vector because of their abundant collections and vigorous biting attack to human. As a part of studies on filariasis in Korea, an essential preliminary is to determiine whether this mosquito, Aedes togoi collected in the above areas is receptive to the microfilariae of B. malayi. Therefore, the present paper is concerned chiefly with the development of B. malayi in A. togoi. It is also hoped that the studies on the larval morphology in the mosquito host and the structure of microfilariae will provide the base line data required for later investigation of the different vector hosts. The studies were summarized as follows: The measurements of the fixed points in percentage of the body length of microfilariae from the Giemsa stained thick films were made, and they showed that cephalic space was 8 percent,cephalic space length to width, 1.3:1, nerve ring, 21.2 percent, excretory pore, 30.8 percent, excretory cell, 36.5 percent, R1 cell, 66. 5 percent, anus 80.4 percent and body length 202 micrometer(l81-228 micrometer) maximun width 7.6 micrometer. A study on the development of microfilaria malayi in the mosquito, Aedes togoi was carried out at room temperature (24-30 C). Mosquitoes used in this experiment were reared from larvae collected from the tide water rock pool in the coastal areas of Cheju-Do and they were fed with a blood meal of carrier donors whose microfilaria densities were in the range from 0.5 to 0.7 per cmm of blood. All of the microfilariae ingested by mosquito exsheathed in stomach, penetrated into the body cavity and then migrated into the thoracic muscles of the mosquitoes within 10 hours, after two moults in the mosquito host, the length of the developing 3rd stage larvae reached in size of 1.3-1.7 mm x 23-32 microns with anal ratio, 2.6 to 3.6. The first appearance of 3rd stage larvae in the mosquito host in this experiment was in 8th day after infection. The larvae were observed in the various cavities of mosquito, such as head, thoracic cavity, abdomen, halters, eye and legs. During the larval development in larval development in the host, the shortening of body length was first observed and then elnongation was followed until becoming 3rd stage larvae. Aedes togoi was proved to be the most suitable host for this species of microfilaria malayi in the above endemic areas.
parasitology-helminth-nematoda-Brugia malayi ; filariasis ; epidemiology ; mosquito ; life cycle ; vector

Epstein-Barr virus (EBV) has been linked to a spectrum of neoplastic conditions, including Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, lymphoepithelioma-like carcinomas and malignant lymphomas in immunocompromised state. To determine the prevalence and the subtype of EBV in gatrointestinal malignancies, fifty cases of adenocarcinomas and seventeen cases of malignant lymphomas were analyzed by EBERs in situ hybridization and polymerase chain reaction using primers for EBNA-1, EBNA-2A and EBNA-2B, on the paraffin sections. In addition, immunohistochemical stain for p53 protein was performed to investigate the potential role of EBV infection on tumor suppressor gene, p53, during tumorigenesis. EBER was detected in 6 of 26 gastric adenocarcinomas, 2 of 24 colon adenocarcinomas, and 8 of 17 malignant lymphomas. EBER was more prevalent in malignant lymphoma arising in the intestine (6/6) than in the stomach (2/11), and was detected in both B and T cell phenotypes. EBNA-1 was positive in 11 of 16 EBER positive cases and the subtyping was possible in 8; both type 1 and 2 were detected in gastric cancers, whereas only type 2 was found in intestinal neoplasms. In adenocarcinomas the high rate of p53 protein overexpression was found in both EBER positive (8/8) and negative cases (32/42), whereas the positive rate was higher in EBER positive cases (7/8) than in EBER negative cases (4/9) of malignant lymphomas. From the results, it can be concluded that EBV infection and the p53 tumor suppressor gene are independently associated in a significant portion of the gastrointestinal malignancies, but the mechanism of action remains to be elucidated.
Adenocarcinoma* ; Burkitt Lymphoma ; Carcinogenesis ; Colon ; Epstein-Barr Virus Infections ; Gastrointestinal Tract ; Genes, Tumor Suppressor ; Herpesvirus 4, Human* ; Hodgkin Disease ; In Situ Hybridization ; Intestinal Neoplasms ; Intestines ; Lymphoma* ; Paraffin ; Phenotype ; Polymerase Chain Reaction ; Prevalence ; Stomach ; Stomach Neoplasms

No abstract available.
Hyperplasia*

No abstract available.
Drug Eruptions* ; Imatinib Mesylate*

No abstract available.
Hand ; Hyperplasia

No abstract available.
Adult ; Hidradenitis ; Humans

A fluorescence bronchoscope system has been developed for detecting early lung cancer including dysplasia and carcinoma in situ. To determine the histologic findings and genetic alterations of the lung tissues, which were biopsied by the fluorescence bronchoscope, we analyzed 104 specimens from 62 heavy smokers for their histopathology, cell proliferation index, and genetic mutations of p53 and K-ras. We used immunohistochemistry for MIB-1 and p53, and PCR-SSCP and direct DNA sequencing for p53 and K-ras. The histology was variable from reactive conditions to invasive cancers, and consisted of basal cell hyperplasia (26.9%), dysplasia (4.8%), carcinoma in situ (1.9%), squamous cell carcinoma (7.7%), adenocarcinoma (4.8%), and small cell carcinoma (10.6%). The cellular proliferation index of the lesions increased as their aggressiveness increased. p53 and K-ras mutations were detected in 33.7% and 14.4% of all tissues, respectively. In dysplasia, p53 and K-ras mutations were observed in 3 of 5 and in 2 of 5 tissues, respectively. However, these genetic alterations were not found in carcinoma in situ. Interestingly, 28.6% of basal cell hyperplasia showed p53 mutations. In conclusion, these data suggest that the biopsy specimens using fluorescence bronchoscopy show variable histologic findings, ranging from reactive conditions to invasive cancers. In addition, some of the dysplastic lesions are related to p53 and K-ras mutations, although these genetic alterations are also seen in basal cell hyperplasia.
Adenocarcinoma ; Biopsy* ; Bronchoscopes ; Bronchoscopy* ; Carcinoma in Situ ; Carcinoma, Small Cell ; Carcinoma, Squamous Cell ; Cell Proliferation ; Fluorescence* ; Hyperplasia ; Immunohistochemistry ; Lung ; Lung Neoplasms ; Sequence Analysis, DNA

Lack of exercise may be one of the main causes of obesity in the recent modernized society. With the rapid increase of obese population worldwide, the economic costs of overweight have become a great burden in many countries. The costs of obesity may be divided into the direct costs to the health system and the indirect or social costs to the individuals and the community (for example, sick days and individuals' expenditure on weight loss). The direct costs depend on the main part of the diseases caused by obesity and the cost of these diseases. Some diseases thathave been included in the calculation are Type 2 diabetes, heart disease, hypertension, endometrial cancer, arthritis and colorectal cancer. One of the problems in this assessment is the relative risk of the diseases in different communities and ethnic groups. Several methods have been used to calculate these costs and produceda wide range of results from different countries. One of the latest estimates ofcosts of obesity is from the United States and was 10.2% of the total health care cost. Little data is yet available in Asian countries; however, the Korean Obesity Society reported a total cost of obesity estimated at about 0.11 % of GDP or about 2.13% of the total health care cost. It is now necessary to develop a strategy for life style modifications at the nationwide level.
Arthritis ; Asian Continental Ancestry Group ; Colorectal Neoplasms ; Endometrial Neoplasms ; Energy Metabolism ; Ethnic Groups ; Female ; Guanosine Diphosphate ; Health Care Costs ; Health Expenditures ; Heart Diseases ; Humans ; Hypertension ; Life Style ; Obesity ; Overweight ; Sick Leave ; United States

Despite the advancements in medical sciences, some diseases are becoming epidemic worldwide. One such disease is type 2 diabetes mellitus (T2DM), a chronic disorder linked in part to lifestyle. T2DM is associated with an increased frequency of cardiovascular as well as cerebrovascular diseases, causing significant morbidity and mortality among affected patients. According to recent reports, in Asian countries including Korea, the increasing trends are more significant and the estimated average increases are predicted to surpass the worldwide average. In addition, epidemiological investigations have shown that the onset of disease in Asians is earlier. The complications associated with disease, therefore, occur earlier and the predicted lifespan of affected individuals is known to be shorter. Therefore, improved understanding of the pathophysiology of T2DM is needed for improved prevention, early diagnosis, and disease intervention. However, most of the basic knowledge on the etiology and epidemiology of diabetes is based on reports from Western countries. Thus, they do not reflect the different characteristics of Asian ethnicity, lifestyles, and economics. Several metabolic problems are associated with the development of type 2 diabetes mellitus in a complex manner. In particular, with the deterioration of insulin resistance, the aggravation of the insulin secretory function is understood to play a key role in explaining the pathogenesis of T2DM in our population. In particular, the deterioration of insulin secretion may be an indispensable condition that is inevitable for the development of T2DM in individuals. Even if the insulin resistance of individuals were aggravated limitlessly, a normal glucose tolerance of individuals could be maintained if adequate corresponding compensatory insulin secretion occurs. Further characterization of diabetes in our population is necessary through prospective clinical study.
Asian Continental Ancestry Group ; Diabetes Mellitus, Type 2 ; Early Diagnosis ; Glucose ; Humans ; Insulin ; Insulin Resistance ; Korea ; Life Style ; Precision Medicine

BACKGROUND: In two-kidney one clip Goldbaltt hypertensive rats(2K1C GHR), clipped kidney may be exposed to low pressure and unclipped kidney to high pressure. In addition, both kidneys may have a different amount of adenosine which is increased by ischemia and plays an important role for renin release. The aim of this study was to invstigate the responsmiveness for renin release to adenosine agonists and antagonist in clipped and unclipped kidney of 2K1C GHR. METHODS: Emplying kidney slices from both unclipped and unclipped kidney of 2K1C GHR, the alteration by adenosine agonists and antagonist of renin release was studied. RESULTS: The renal renin content and basal renin release from unclipped kidney slices were suppressed, whereas those from clipped kidney were augmented Adenosine Al receptor agonist, cyclohexyladenosne(CHA), phenylisopropyl adenosine(PIA) and adenosine caused a decrease in renin release from clipped kidney slices. Adenosine A2 receptor agonist, NECA, and nonspecific adenosine receptor aganist, 2-chloroadenosine(CA) caused an increase in renin release from clipped kidney slices. Adenosine receptor antagonist, 8-phenyltheophylline(8-PT) caused an increase in renin release from clipped kidney slices. In unclipped kidney, however, the renin release in response to NECA, CA or 8-PT was reversed and the decreasing effect of renin release to CHA and adenosine was slightly inereased. CONCLUSION: These results suggest that the responsiveness of adenosine receptors, which may participate in renin release is modified in clipped and unclipped kidney of 2K1C GHR.
Adenosine* ; Adenosine-5'-(N-ethylcarboxamide) ; Animals ; Hypertension, Renovascular ; Ischemia ; Kidney ; Rats* ; Receptors, Adenosine A2 ; Receptors, Purinergic P1 ; Renin*