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1.
Gynecol Obstet Invest ; 71(2): 77-86, 2011.
Article in English | MEDLINE | ID: mdl-21150157

ABSTRACT

BACKGROUND: In a university hospital setting, a 25-year-old woman presented with large vaginal and cervical polyps. Past medical history was significant for stage IV endometriosis. Polypectomy was performed and the polyps were histologically consistent with endometriosis. Gene expression was compared with control vaginal tissue to assess if the altered gene expression profile was similar to peritoneal endometriosis. METHODS AND RESULTS: Using quantitative reverse transcription, real-time PCR, estrogen receptor-ß expression was found to be upregulated 10-fold while estrogen receptor-α expression was downregulated 5-fold in the vaginal polyp relative to control vaginal tissue. The estrogen-synthesizing enzyme aromatase was upregulated 8-fold and 3ß-hydroxysteroid dehydrogenase was upregulated 400-fold in the polyp. Immunohistochemical staining revealed altered cell type localization for progesterone receptor in the polyp and increased cell proliferation in polyp stromal cells relative to control. CONCLUSIONS: Increased proliferation in the vaginal polypoid endometriotic tissue may be due to increased local estrogen production. The altered gene expression profile was very similar to the altered gene expression profile seen in peritoneal endometriosis.


Subject(s)
Endometriosis/metabolism , Estrogens/biosynthesis , Gene Expression , Peritoneal Diseases/metabolism , Polyps/metabolism , Vaginal Diseases/metabolism , Adolescent , Adult , Endometriosis/genetics , Endometriosis/pathology , Estrogen Receptor alpha/genetics , Estrogen Receptor alpha/metabolism , Estrogen Receptor beta/genetics , Estrogen Receptor beta/metabolism , Female , Gene Expression Profiling , Humans , Middle Aged , Peritoneal Diseases/genetics , Polyps/pathology , RNA/metabolism , Vaginal Diseases/genetics
2.
J Phys Chem B ; 110(14): 7113-8, 2006 Apr 13.
Article in English | MEDLINE | ID: mdl-16599473

ABSTRACT

Exposing single-walled carbon nanotubes to room-temperature UV-generated ozone leads to an irreversible increase in their electrical resistance. We demonstrate that the increased resistance is due to ozone oxidation on the sidewalls of the nanotubes rather than at the end caps. Raman and X-ray photoelectron spectroscopies show an increase in the defect density due to the oxidation of the nanotubes. Using ultraviolet photoelectron spectroscopy, we show that these defects represent the removal of pi-conjugated electron states near the Fermi level, leading to the observed increase in electrical resistance. Oxidation of carbon nanotubes is an important first step in many chemical functionalization processes. Because the oxidation rate can be controlled with short exposures, UV-generated ozone offers the potential for use as a low-thermal-budget processing tool.


Subject(s)
Nanotubes/chemistry , Ozone/chemistry , Carbon/chemistry , Chemical Phenomena , Chemistry, Physical , Oxidation-Reduction , Photochemistry , Silicon Dioxide/chemistry , Spectrophotometry, Ultraviolet , Spectrum Analysis, Raman , Ultraviolet Rays
10.
Am J Pathol ; 64(2): 405-22, 1971 Aug.
Article in English | MEDLINE | ID: mdl-5142273

ABSTRACT

Optical and electron microscopic evidence is presented to support the finding that sickling of hemoglobin S can be reversed and blocked by urea in invert sugar (UIS). Erythrocytes from subjects having hemoglobin SS, AS or AA were treated with the UIS either before or after deoxygenation with Na(2)S(2)O(5). Light microscopic studies indicated that approximately one-fifth as much urea is required to block sickling as is necessary to reverse sickled poikilocytes to normal forms. Intracellular microfilaments apparent in transmission electron micrographs of sickled erythrocytes were eliminated by treating aliquots of the same deoxygenated erythrocytes with UIS. Scanning electron micrographs showed a reversion of sickled poikilocytes to a normal erythrocyte population of biconcave discs. The use of UIS was deduced from Murayama's hypothesis that the molecular mechanism of sickling clearly involves hydrophobic bonds formed between the number-6 valine substitution of the beta-chain S globins and the alpha-chain globins of interacting hemoglobin molecules. The use of UIS to arrest the formation of such hydrophobic bonds is advocated as an evident and effective therapeutic strategy to treat sickle cell crisis.


Subject(s)
Anemia, Sickle Cell/drug therapy , Erythrocytes, Abnormal/drug effects , Fructose/pharmacology , Glucose/pharmacology , Urea/pharmacology , Anemia, Sickle Cell/pathology , Erythrocyte Count , Erythrocytes, Abnormal/pathology , Fructose/therapeutic use , Glucose/therapeutic use , Hemoglobins, Abnormal/metabolism , Humans , Microscopy, Electron , Microscopy, Electron, Scanning , Time Factors , Urea/therapeutic use
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