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

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*

Patients with type 2 diabetes mellitus are associated with insulin resistance and/or impaired insulin secretion. Previous observations indicate that patients with type 2 diabetes tend to have an impaired insulin response after a glycemic load. Recently it has been reported that hyperglycemia after a glucose load is itself a risk factor for the development of cardiovascular complications in the absence of elevated fasting plasma glucose. There are several points to be addressed for the application of new pathogenesis to diabetes treatment. One of them is the association between postprandial hyperglycemia and mortality from cardiovascular diseases. For the management of postprandial hyperglycemia inhibitors ofglucosidase and rapidacting insulin secretagogues have beneficial effects. Alphaglucosidase inhibitors in combination with diet therapy ameliorate insulin resistance and reduce the blood sugar level. A rapidly acting insulin secretagogue, such as repaglinide, lowers postprandial glucose levels without asignificant gain of body weight. These drugs may protect pancreaticcells from postprandial glucose toxicity and prevent the progression of diabetes. Both metformin and thiazolidinedione derivative (TZDs) improve insulin resistance, the major pathogenetic background of type 2 diabetes, and decrease blood glucose levels without stimulating, insulin secretion. Metformin inhibits glucose output from the liver, while TZDs increase glucose utilization in the peripheral tissues. In addition, it has been indicated that these agents ameliorate the metabolic syndrome beyond lowering the glucose level. Molecular targets for these agents have recentl been revealed ; AMPactivated protein kinase for metfOrnin and adiponectin, while PPAR for TZDs that induce gene expression of adipocyte glycerol kinase and adiponectin. Insulin-sensitizing agents are clinically useful for obese diabetic patients with insulin resistance. However, periodical examinations are necessary to avoid serious adverse effects such as lactic acidosis, although rare, by metformin and liver injury by TZDs. The advantage of insulin therapy for type 2 diabetic patients is still controversial. However, in many intervention studies, the intensive insulin therapy provided promising effects on preventing cardiovascular diseases. Moreover, insulin has been shown to stimulate nitric oxide production by cultured endothelial cells and to suppress the expression of intercellular adhesion molecule1 at least in vitro. In view of this antiinflammatory effect, longterm insulin therapy may potentially have an antiatherogenic effect.
Acidosis, Lactic ; Adipocytes ; Adiponectin ; Blood Glucose ; Body Weight ; Cardiovascular Diseases ; Clinical Trial ; Diabetes Mellitus ; Diabetes Mellitus, Type 2 ; Diet Therapy ; Endothelial Cells ; Fasting ; Gene Expression ; Glucose ; Glycerol Kinase ; Humans ; Hyperglycemia ; Insulin ; Insulin Resistance ; Intervention Studies ; Liver ; Metformin ; Mortality ; Nitric Oxide ; Peroxisome Proliferator-Activated Receptors ; Protein Kinases ; Risk Factors

One hundred and thirty trimethoprim-resistant R plasmids derived from of Escherichia coli isolated from clinical specimens and feces of healthy collegians were examined for incompatibility, EcoRI endonuclease restriction fragment pattern, and Southern hybridization with DHFR I, II, III, V, and VII probe. 1. Most trimethoprim-resistant R plasmids were resistant to ampicillin, tetracycline, chloramphenicol, gentamicin, and kanamycin, and showed multiple drug resistance and various antimicrobial resistance patterns. 2. Trimethoprim-resistant R plasmids ranged from 90 to 50 kilobase and 42.3% of R plasmids tested were classified to incompatibilty group Inc FI, Inc FII or Inc FIV, 3. Among 48 random selected R plasmids from various origin, 14 R plasmids (including 9 of 14 Inc FII plasmids and 3 of 14 Inc FI plasmids) hybridized with DHFR VII oligonucleotide probe but others did not respond to any of DHFR probes used. 4. Most R plasmids showed various EcoRI endonuclease fragments and different reaction sites by Southern hybridization. Six plasmids showed identical or nearly identical molecular weight, EcoRI endonuclease fragment patterns and different sites of Southern hybridization. But 2 Inc FII plasmids derived from urine and feces showed identical pattern. These findings, if confirmed by further studies, suggest that normal flora E. coli can act as reservoir of resistant genes and, consequently, as a factor in the dissemination of these genes among enteric pathogens and need to be examined further.
Ampicillin ; Chloramphenicol ; Deoxyribonuclease EcoRI ; Drug Resistance, Multiple ; Escherichia coli* ; Escherichia* ; Feces ; Gentamicins ; Immunodeficiency Virus, Feline ; Kanamycin ; Molecular Biology* ; Molecular Weight ; Plasmids ; R Factors ; Tetracycline ; Trimethoprim Resistance* ; Trimethoprim*