No abstract available.

A case of a third ventricular epidermoid is presented, which was diagnosed by conray ventriculography and computerized tomography. The tumor was subtotally removed through a low parieto-occipital approach and ventriculo-peritoneal shunt was performed. The epidermoid of the third ventricle is extremely rare and only a few cases have been reported in the literatures. It's incidence, preoperative diagnosis, surgical technique and complications are briefly reviewed.
Diagnosis ; Incidence ; Third Ventricle* ; Ventriculoperitoneal Shunt

Tuberculosis is a systemic disease with a world-wide distribution, and its occurance in the oral cavity is well documented in the literature. Disease of oral cavity and jaw caused by Mycobacterium tuberculosis is very rare, so it is often difficult to diagnose tuberculosis in the oral cavity. When granulomatous and ulcerative lesion persists in the oral cavity for a long time, it may be considered a tuberculosis. When differential diagnosis is needed, the most reliable indicators of mycobacterial infection are careful clinical evaluation, skin test, acid-fast staining, biopsy and culture. We report a case of tuberculous osteomyelitis which simultaneously occurred on the maxilla and mandible in a 85 years old man that proved diagnosis difficult, but which responded very well to surgical treatment and chemotherapy.
Aged, 80 and over ; Biopsy ; Diagnosis ; Diagnosis, Differential ; Drug Therapy ; Humans ; Jaw ; Mandible* ; Maxilla* ; Mouth ; Mycobacterium tuberculosis ; Osteomyelitis* ; Skin Tests ; Tuberculosis ; Ulcer

Acute embolic occlusion of the common iliac artery is a rare medical emergency that is not only limbthreatening, but also potentially life-threatening. Several treatment options exist for acute limb ischemia, although no treatment is clearly best. We report a case of acute embolic occlusion of the left common iliac artery in a patient with atrial fibrillation who was treated successfully using mechanical thrombectomy following intra-arterial thrombolysis.
Acute Disease ; Arterial Occlusive Diseases/radiography/*therapy ; Combined Modality Therapy ; Embolism/radiography/*therapy ; Female ; Fibrinolytic Agents/*administration & dosage ; Humans ; *Iliac Artery/radiography ; Middle Aged ; *Thrombectomy ; *Thrombolytic Therapy ; Tomography, X-Ray Computed ; Treatment Outcome ; Urokinase-Type Plasminogen Activator/*administration & dosage

BACKGROUND AND OBJECTIVES: Cilostazol is an anti-platelet and arterial vasodilating drug that inhibits phosphodiesterase type III, an enzyme that breaks down cyclic AMP in platelets, vascular smooth muscle cells, cardiac myocytes and adipocytes. Several animal and human studies have shown that cilostazol has the potential to reduce restenosis after coronary angioplasty, but the precise mechanism by which the inhibition of vascular smooth muscle cell growth occurs from an increase in cyclic AMP is not yet clear. MATERIALS AND METHODS: We investigated the effects of cilostazol on cell proliferation and expression of iNOS and p21 by western blotting with the cultured aortic vascular smooth muscle cells stimulated with platelet-derived growth factor BB. RESULTS: In comparison to the control, treatment with cilostazol significantly inhibited (p<0.05) the increase in cell number. Inducible nitric oxide synthase (iNOS) and p21 expression increased with cilostazol treatment, and these effects of cilostazol were eliminated by simultaneous incubation with the NOS inhibitor, L-NAME. These results indicate that cilostazol increases p21 expression at least partially through an iNOS-dependent pathway in cultured vascular smooth muscle cells stimulated with PDGF-BB. CONCLUSION: These findings suggest that cilostazol has a direct inhibitory effect on abnormal proliferation of vascular smooth muscle cells accompanied by the induction of iNOS-dependent p21 expression, and cilostazol may have potential to prevent restenosis after percutaneous coronary intervention by this mechanism.
Adipocytes ; Angioplasty ; Animals ; Blotting, Western ; Cell Count ; Cell Proliferation ; Cyclic AMP ; Humans ; Muscle, Smooth, Vascular* ; Myocytes, Cardiac ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II ; Percutaneous Coronary Intervention ; Platelet-Derived Growth Factor

Brain abscess is a rare, extremely aggressive, life-threatening infection. It may occur following : infection of contiguous structure, hematogenous spread, or cranial trauma/ surgery. Dental pathology and/or treatment have been linked to a small number of brain abscesses as possible source of infection. 50-year-old male patient was presented with a brain abscess caused by Streptococcus viridans. In the case presented, the significant oral findings were chronic periapical and periodontal infection due to root remnant of lower right 3rd molar. A case history and brief literature review of brain abscess related odontogenic infection was presented after successful treatment with antibiotics and craniotomy.
Anti-Bacterial Agents ; Brain Abscess* ; Brain* ; Craniotomy ; Humans ; Male ; Middle Aged ; Molar ; Pathology ; Viridans Streptococci

Brain abscess is a rare, extremely aggressive, life-threatening infection. It may occur following : infection of contiguous structure, hematogenous spread, or cranial trauma/ surgery. Dental pathology and/or treatment have been linked to a small number of brain abscesses as possible source of infection. 50-year-old male patient was presented with a brain abscess caused by Streptococcus viridans. In the case presented, the significant oral findings were chronic periapical and periodontal infection due to root remnant of lower right 3rd molar. A case history and brief literature review of brain abscess related odontogenic infection was presented after successful treatment with antibiotics and craniotomy.
Anti-Bacterial Agents ; Brain Abscess* ; Brain* ; Craniotomy ; Humans ; Male ; Middle Aged ; Molar ; Pathology ; Viridans Streptococci

BACKGROUND: Vascular lesions are the major cause of morbidity and mortality in hypertensive patients. However, the pathologic characteristics of gradually evolving, chronic hypertension have not been adequately studied and the mechanism by which hypertension accelerates atherosclerosis is still uncertain. This study was undertaken to invertigate the ultrastructural changes of the aorta and the effect of high cholesterol diet in spontaneously hypertensive rats(SHR). METHODS: Spontaneously hypertensive rats (n=80, male, 5 weeks old) and Wistar rats (n=40, male, 5 week old) were used. Forty SHR were fed with 2% cholestrol diete, while the remainder with control diet. Systolic blood pressure was measured weekly until 16 weeks after birth, and then biweekly until 40 weeks after birth. Transmission and scanning electron microscopy were used to evaluate ultrastrucural changes of the aorta. RESULTS: 1) The blood pressure of SHR rose stedily and progressively from the 5 weeks after birth and reached nearly 190mmHG at the 16 weeks after birth. 2) In SHR, the subendothelial component contained finely granular substances, abundant fibrillar collagen and elastin. Infiltration of the mononuclear blood leukocytes into the intima was frequently seen. 3) Endothelium from cholestrol-fed SHR did exhibit numerous pinocytotic vesicles and contained many cytoplasmic filaments. There were a number of large mononuclear lipid-filled cells in the intimal lesions. Blistering of the endothelial plasma membrane was also observed in high cholesterol diet-fed SHR. Later on, adhesion of platelets, febrin, and white blood cells as well as damage of intima shown as multiple small holes were more marked. 4) There was no significant difference in systoloic blood pressure between high cholesterol diet-fed and control diet-fed SHR. CONCLUSION: In the aorta of SHR, the most prominent change was an expansion of the subendothelial space and infiltration of the mononuclear leukocytes into the intima. The present study showed that the SHR was indeed a reliable model for the essential hypertension. In some SHR, high cholesterol diet could induce more pronounced vascular lesions, which were enhanced by hypertension.
Aorta* ; Atherosclerosis ; Blister ; Blood Pressure ; Cell Membrane ; Cholesterol* ; Cytoskeleton ; Diet* ; Elastin ; Endothelium ; Fibrillar Collagens ; Humans ; Hypertension ; Leukocytes ; Leukocytes, Mononuclear ; Male ; Microscopy, Electron ; Microscopy, Electron, Scanning ; Mortality ; Parturition ; Rats, Inbred SHR* ; Rats, Wistar

Helicobacter pylori is a causative agent of type B gastritis and plays a central role in the pathogenesis of gastroduodenal ulcers and gastric cancer. Strategies for the control of H. pylori- induced gastroduodenal diseases based on conventional measures are still of limited utility. Therefore, it seems worthwhile to make a break-through as an alternative strategy by reviewing the host-parasite relationship of H. pylori infection on the basis of genomic structure. In this study, we tried to construct a physical map of H. pylori genome. Chromosomal DNA from a Korean prototype strain, H. pylori 51 was digested with 42 restriction endonucleases to identify restriction patterns suitable for mapping the genome. We identified three enzymes, ApaI, NotI and Sfil, which gave a small number of DNA fragments of higher molecular weight that were well resolved after pulsed-field gel electrophoresis. The H. pylori chromosome contained 7 ApaI fragments ranging from 167 to 311 kb, 7 NotI fragments ranging from 5 to 516 kb and 2 SfiI fragments of 332 and 1,347 kb in size. The genome size of the strain is 1,679 kb. A circular physical map of the H. pylori chromosome was constructed by aligning 3 kinds of restriction fragments by Southern blot analysis of simple ApaI, NotI and SfiI digests or double NotI/ApaI and NotI/SfiI digests with the various probes. When the physical map of H. pylori strain 51 compared with that of strain 26695 of which the cornplete genome sequence was reported, completely different restriction patterns were shown, which suggests the genomic diversity in H. pylori.
Blotting, Southern ; DNA ; DNA Restriction Enzymes ; Electrophoresis, Gel, Pulsed-Field ; Gastritis ; Genome ; Genome Size ; Helicobacter pylori* ; Helicobacter* ; Host-Parasite Interactions ; Molecular Weight ; Peptic Ulcer ; Stomach Neoplasms

To define the genes for production of catalytically active H. pylori urease, we camed out study to elucidate the structure of urease gene transcript, to delineate the genetic region which affected the extent of the expression and the activation of urease structural subunits. UreC and ureD were confirmed not to affect the expression of structural genes and active enzyme production, meaning that these genes are not components of the urease gene cluster of H. pylori. p-independent transcriptional stop signal was found in 12 bp down-stream of ureH stop codon. RNA extension test showed that the transcript starts with 267 bp upstream of ureA start codon. Although accessory genes did not affect the extent of the expression of the structural subunits, they were essential for assembling the active urease in E. coli. E. coli transformants of plasmid clones containing ureAB produced catalytically active urease when they are complemented with the plasmid clones of ureIEFGH or coexisted with ureIEFGH, meaning that accessory gene products could be trans-acting as well as cis-acting. The extent of production of urease structural subunits depended on the region of 241 to 57 bp upstream of ureA start codon. E. coli transformant of pBeloBACII clone containing the urease gene cluster, which is maintained with a single copy in host, did not express the urease. Proteins (60, 38, 30, 29, 27, and 24 kDa) that could hold nickel ions were identified in the cell extract of H. pylori. The results in this study will provide the basis to understand the control mechanism for urease gene expression and formation of the active urease.
Clone Cells ; Codon, Initiator ; Codon, Terminator ; Complement System Proteins ; Gene Expression ; Helicobacter pylori* ; Helicobacter* ; Ions ; Multigene Family ; Nickel ; Plasmids ; RNA ; Urea ; Urease*