No abstract available.

In order to understand the role of mec regulator genes in the evolution of methicillin-resistant S. aureus (MRSA), the distribution of the mec regulator genes among the 66 clinical isolates of MRSA was analysed. And also the correlation between gene mutation and degree of phenotypic expression of resistance was studied. Fifty strains carried whole mec regulator region, while the mecI gene and nearly half of the 3'-end of the mecR#l gene were deleted in fifteen strains. The mecRl MS gene was detected among all of the mecA carried strains, but the mecRl PB gene was carried by 77% of the MRSA strains. At least a portion of the 5'-end region of the mecRl gene was carried by all MRSA strains tested. Forty-seven strains were finally confirmed to have mecI gene and each mecI gene of above strains was sequenced for identification of the relationship between repressor function of mecI gene on mecA transcription and MIC level of methicillin. Point mutations were detected in 11 strains of 47 strains. In 8 strains, there was one nucleotide substitution (C to T at position 202) that produced a new termination codon at position 201. In 3 strains, one nucleotide substitution from G to T at position 43 caused an amino acid substitution from Val to Phe. The MIC of methicillin of strains carrying mutated mecI genes ranged 256 ug/ ml to 1024 ug/ml. Transcription level of amplified cDNA corresponding to mecA was determined by the method of RT-PCR of extracted RNA. Total RNA was extracted from two strains with mutated mecI gene and a strain with intact mecI gene. Deletional loss or the mutational inactivation of the mecI gene did not affect the level of mecA transcription. Role of mecI gene as a strong repressor function on mecA gene seemed to be skeptical.
Amino Acid Substitution ; Codon, Terminator ; DNA, Complementary ; Genes, Regulator* ; Methicillin Resistance ; Methicillin* ; Methicillin-Resistant Staphylococcus aureus ; Point Mutation ; RNA

ICAM-l(Intercellular adhesion molecule-1) is an important early marker of immune activation and response. ICAM-1 is expressed on varous cell types and observed in a variety of diseases, including patients with asthma, melanoma, prostatic cancer, ovarian and colon cancer. Some authors demonstrated the expression of ICAM-1 protein in high-grade intraepithelial squamous neoplasia of cervix by immunohistochemistry and suggested that the expression was related to human papillomavirus infection. The aim of this study was to determine the serum levels of soluble intercellular adhesion molecule-1(sICAM-1) in patients with squamous cell carcinoma of the cervix, Serum levels of sICAM-1 were measured by enzyme-linked immunosorbent assay(ELISA), We evaluate invasive squamous cell carcinoma of the cervix (40), carcinoma in situ (16) and control (15) patients. Serum levels of sICAM-1 in healthy volunteers, in parients with carcinoma in situ and invasive cervical cancer were 150.1+/-41.3, 182.7+/-105.9, 189.8+/-60.0 ng/ml, respectively. Although the serum levels of sICAM-1 in patients with carcinoma in situ did not increase, serum levels of ICAM-1 in patients with invasive cervical cancer were significantly increased (control vs invasive cervical cancer, p < 0,05). From the above results, sICAM-1 is shed from the cancerous tissue in patients with squamous cell carcinoma of the cervix.
Asthma ; Carcinoma in Situ ; Carcinoma, Squamous Cell ; Cervix Uteri ; Colonic Neoplasms ; Enzyme-Linked Immunosorbent Assay ; Female ; Healthy Volunteers ; Humans ; Immunohistochemistry ; Intercellular Adhesion Molecule-1 ; Melanoma ; Papillomavirus Infections ; Prostatic Neoplasms ; Uterine Cervical Neoplasms*

No abstract available.
Candidiasis* ; Humans ; Infant, Newborn ; Infant, Premature*

To evaluate the lipid-lowering effect of lovastatin(Mevacor(R)), lovastatin was administered to 38 patients with non-familial hypertcholesterolemia(>220mg/dl). The analysis of the effect was made with 25 patients(58.2+/-7.5 years ; 13 male, 12 female)who had received lovastatin more than 12 weeks. The drug was administered as a single dose with evening meal 20mg at the begining and adding another 20mg if the total cholesterol level was persistently higher than 200mg/dl at the end of each 4 week-period. 1) Total cholesterol level was decreased from 256.6+/-36.9mg/dl to 20932+/-50.1mg/dl at the end of the 4th week, 201.9+/-44.2mg/dl the 8th week and 203.6+/-39.6mg/dl the 12th week (p<0.001), respectively). 2) Triglyceride level was decreased from 196.4+/-104.1mg/dl to 163.4+/-74.4mg/dl at the end of the 4th week(p<0.05) but no significant change at the end of the 8th week showing 169.8+/-73.2mg/dl and 162.7+/-54.8mg/dl the 12th week(p<0.05). 3) High density lipoprotein cholesterol(HDL-C) level was not significantly changed with the drug during the 12 week treatment period. 4) Low density lipoprotein cholesterol(LDL-C) level was decreased remarkably similar to that of total cholesterol. 5) Total cholesterol/HDL-C ratio was decreased from 5.05+/-0.92 to 4.06+/-1.40 at the end of the 4th week(p<0.05), 3.89+/-0.99 the 8th week(p<0.001). 4.20+/-1.10 the 12th week(p<0.01). 6) LDL-C/HDL-C ratio was decreased from 3.24+/-0.94 to 2.43+/-1.21 at the end of the 4th week(p<0.05), 2.23+/-0.86 the 8th week(p<0.001) and 2.54+/-0.98 the 12th week(p<0.05). 7) There was no significant side effect on lovastatin therapy of 12 weeks duration. 8) The laboratory findings including liver function test, uric acid, creatinine, creatine phosphokinase and blood glucose were not changed significantly. From above results we concluded that lovastatin is safe and effective hypocholesterolemic agent in its clinical use.
Blood Glucose ; Cholesterol ; Creatine Kinase ; Creatinine ; Humans ; Hypercholesterolemia* ; Lipoproteins ; Liver Function Tests ; Lovastatin ; Male ; Meals ; Triglycerides ; Uric Acid

We had experienced 2 cases of acute subdural hematoma due to vitaimin K(vit. K) deficiency. They were 44-and 42-day-old. After the adminstration of vit.K1, prolonged prothrombin time(PT) and activated partial thromboplastin time(APTT) were corrected, so the surgical treatment ws performed. We supposed the predisposing factors were breast feeding and unknown hepatic pathology. No complication remained to one infant but the other multiple cerebral infarctions. The etiology, pathogenesis, diagnosis, prevention are discussed. We insist on neonatal administration of vit. K1 for the prevention of bleeding tendency. If intracranial hemorrhage develops, we must keep in mind that the early neurosurgical intervention may be needed.
Breast Feeding ; Causality ; Cerebral Infarction ; Diagnosis ; Hematoma, Subdural, Acute* ; Hemorrhage ; Humans ; Infant* ; Intracranial Hemorrhages ; Partial Thromboplastin Time ; Pathology ; Prothrombin ; Prothrombin Time ; Thromboplastin ; Vitamin K Deficiency ; Vitamins*

We have experienced two cases of Wernicke's encephalopathy associated with hypere-mesis gravidarum. Delay in it's diagnosis caused a protracted illness and persisting neurol-ogic deficits. Because of its association with chronic alcoholism, possibility of Wernicke's encephalopathy may not be considered in early stage of disease. The clinical feature, the principle of management and the prevention of Wernicke's encephalopathy are discussed.
Alcoholism ; Diagnosis ; Female ; Hyperemesis Gravidarum* ; Pregnancy ; Wernicke Encephalopathy*

No abstract available.
Peptic Ulcer*

No abstract available.
Diabetes Mellitus* ; Hearing* ; Humans

No abstract available.
Tibia*