No abstract available.
Leiomyoma* ; Scalp*

No abstract available.
Abscess*

We investigated whether the two variant elements of CRE(TGcCGTCA[5'CRE], TGACcTCA[3'CRE]) in the 5'flanking region of the rat TRH gene, which are different from the CRE consensus sequence(5'-TGACGTCA-3') by one base pair, are responsive to cAMP, and whether the one base pair difference is responsible for the degree of cAMP responsiveness of the gene. When CA 77 cells were stimulated with forskolin and isobutylmethylxanthine for 4 hours, the level of TRH mRNA was increased by only two fold. The transient gene expression study using serial 5'deletion of the TRH gene in PC12 cells showed that the region between-113 and-77, which includes 5'CRE, was crucial for the cAMP resonsiveness. When the plasmid, which contains the 30 bp oligonucleotide including either 5'CRE or 3'CRE ligated to the enhancerless RSV promoter, was transfected into PC12 cells, it did not significantly affect not only the basal transcription but cAMP responsiveness. The 65 bp oligonucleotide including both 5'CRE and 3'CRE, however, increased both of the basal transcription and cAMP-stimulated transcription by 2-3 fold. When the sequence of 5'CRE was converted to that of the CRE consensus by replacing one base pair, the cAMP responsiveness was increased by two fold although the basal transcription was not increased. The one base pair mutant of 3'CRE increased both of the basal and cAMP-stimulated transcription by 3-4 fold. These results suggest that there are the two variant CREs in rat TRH gene, which are relatively weak CRE compared to the CREs of other neuropeptide genes and cooperative for the activation of both the basal and cAMP-stimulated transcription. The one base pair difference of the variant CREs from the CRE consensus sequence is responsible for the weak responsiveness to cAMP.
Animals ; Base Pairing ; Colforsin ; Consensus ; Consensus Sequence ; Cyclic AMP ; Gene Expression ; Neuropeptides ; PC12 Cells ; Plasmids ; Rats ; Response Elements ; RNA, Messenger ; Thyrotropin ; Thyrotropin-Releasing Hormone

No abstract available.
Gastrointestinal Hemorrhage ; Intussusception

No abstract available.
Fluorides* ; Osteoblasts*

BACKGROUND: Welders tend to be exposed to a variety of hazards including metal fumes, toxic gases, electricity, heat, noise, and radiation such as ultraviolet and infrared light. Noxious gases generated during welding include carbon monoxide, ozone, and nitrogen oxide. Although the effects of metal fumes have been well studied, few reports have investigated the influence of noxious gas exposure in welders. CASE REPORT: We encountered a patient who developed non-cardiogenic pulmonary edema within a day after fairing up a steel plate with an oxygen/LPG torch. The patient was a 43-year-old female who complained of dyspnea which became exacerbated the following morning. Her chest X-ray and chest CT scan showed an extensive ground glass opacity which was more prominent in the both upper lungs. Both her symptoms and chest X-ray findings improved. We attributed the patient's symptoms to non-cardiogenic pulmonary edema caused by nitrogen dioxide exposure, by reasoning that: 1) the patient's clinical course and radiologic findings suggested pulmonary edema 2) the event happened following fairing work with oxygen/LPG torch that usually induces a high concentration of nitrogen dioxide, and 3) the other possible causes of pulmonary edema could be excluded. CONCLUSION: Nitrogen dioxide-induced pulmonary edema should be considered in oxygen torch contrary to arc welding.
Adult ; Carbon Monoxide ; Dyspnea ; Electricity ; Female ; Gases ; Glass ; Hot Temperature ; Humans ; Lung ; Nitrogen Dioxide ; Nitrogen* ; Noise ; Oxygen* ; Ozone ; Pulmonary Edema* ; Steel ; Thorax ; Tomography, X-Ray Computed ; Welding

Malakoplakia is an uncommon granulomatous disease most frequently found in the bladder or ureter. Howevcr, it has been reyorted in almost every ather organ and structure, the colon is the most common site of malakoplakia outside the urogenital tract and colonic carcinoma is the most commonly associated disease. A case of malakoplakia of the colon in a 54-year-old female is reported. Sigmoidoscopy revealed multiple whiteyellowish nodules simulating polypoid lesion at 10cm from the anal verge. The biopsy showed characteristically comprised submucosal proliferations of histiocyte and chronic inflammatory cells with typical cytoplasmic inclusions known as Michaelis-Gutmann bodies. Intravenous pyelogram showed no evidence of involvement of the urinary system. These nodules were removed by endoscopic polypectomy, So far, this is the first case of isolated colonic malakoplakia in Korea.
Biopsy ; Colon ; Female ; Histiocytes ; Humans ; Inclusion Bodies ; Korea ; Malacoplakia* ; Middle Aged ; Rectum ; Sigmoidoscopy ; Ureter ; Urinary Bladder

BACKGROUND: It is known that bupivacaine induce cell death in several immortalized cells. However, there is no report concerning bupivacaine-induced cell death in the primary cultured cardiomyocytes. We compared the direct cytotoxicity of local anesthetics in cardiomyocytes. Furthermore, the mechanisms of cell death were evaluated. METHODS: The myocardial cells of rat pups were cultured 3 days after seeding. The methyltetrazolium (MTT) assay was employed to quantify differences in cellular viability. To confirm apoptosis, Hoechst-propidium iodide staining, DNA fragmentation by electrophoresis and western blot analysis were performed. And to examine the mechanisms of cell death, intracellular calcium and expression levels of mitogen-activated protein kinases (MAPKs) family members were evaluated. RESULTS: Among the local anesthetics under 1 mM concentration for 18 h, only bupivacaine significantly decreased the MTT activity (P < 0.001). Bupivacaine induced cell death in a dose-responsive and time dependent manner. Cell death showed apoptotic characteristics, such as DNA fragmentation, chromatin condensation, decrease of precursor caspase-3 protein level, increased cleaved PARP, and cytochrome C release into the cytoplasm. Bupivacaine phosphorylated three major MAPKs, i.e. extracellular signal-regulated kinases (ERKs), p38 kinase and c-Jun N-terminal kinases (JNKs) stress-activated protein kinases. Administration of ERK inhibitor increase cell death, whereas inhibitors of p38 kinase and JNK decreased cell death (P < 0.05). In addition, the intracellular calcium level was approximately 4 times higher after the bupivacaine treatment (P < 0.001), which was inhibited by calcium chelators (P < 0.001). Calcium chelators inhibited expression of MAPKs. CONCLUSIONS: In bupivacaine-induced apoptosis in cardiomyocytes, intracellular calcium increase and MAPKs family plays important roles.
Anesthetics, Local ; Animals ; Apoptosis* ; Blotting, Western ; Bupivacaine ; Calcium ; Caspase 3 ; Cell Death ; Chelating Agents ; Chromatin ; Cytochromes c ; Cytoplasm ; DNA Fragmentation ; Electrophoresis ; Extracellular Signal-Regulated MAP Kinases ; Humans ; Mitogen-Activated Protein Kinases ; Myocytes, Cardiac* ; p38 Mitogen-Activated Protein Kinases* ; Phosphotransferases ; Protein Kinases ; Rats

Animals ; Bisphosphonate-Associated Osteonecrosis of the Jaw ; Diphosphonates ; Humans ; Ilium ; Imidazoles ; Macrophages ; Maxillary Sinus ; Membranes ; Osteonecrosis ; Periosteum ; Rabbits ; Sodium Chloride ; Transplants

No abstract available.
Ecological Systems, Closed* ; Osteoblasts* ; RNA, Messenger* ; Sodium Fluoride* ; Sodium*