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Curtis L Lowery

Publications and source records attributed to Curtis L Lowery.

20 records · Page 2Linked to original sources

First magnetomyographic recordings of uterine activity with spatial-temporal information with a 151-channel sensor array.

OBJECTIVE: The purpose of this study was to examine the feasibility of recording the spatial-temporal magnetomyographic activity from the pregnant uterus with the use of the newly developed 151-channel noninvasive device, known as the superconducting quantum interference device array for reproductive assessment. STUDY DESIGN: Uterine magnetomyographic signals were recorded from 10 pregnant subjects with the 151-channel sensor array curved to fit the pregnant abdomen. The recording sessions were 16 minutes in length, with a sampling rate of 250 Hz. RESULTS: Uterine activity bursts were successfully recorded with the superconducting quantum interference device array for reproductive assessment system. By obtaining a contour plot of the magnetic field distribution, we were able to localize the areas of activation over the uterus during a contraction. Also, it was possible to calculate the time delay in the propagation of the activity across the uterus. CONCLUSION: Using superconducting quantum interference device array for reproductive assessment system, we have established the feasibility of recording uterine contractile activity with spatial-temporal resolution that is high enough to determine the regions of localized activation and propagation over the uterus.

Female↗

Defective 3A trophoblast-endometrial cell adhesion and altered 3A growth and survival by human papillomavirus type 16 oncogenes.

Human papillomaviruses (HPVs) are found in trophoblasts of spontaneous abortions and replicate in these cells in culture. We used recombinant adeno-associated viruses (rAAV) to introduce the HPV-16 E6 and E7 oncogenes into 3A trophoblasts. AAV/E7/Neo-infected 3A trophoblasts died rapidly, but AAV/E6/Neo- and AAV/E6-E7/Neo-infected cells grew more rapidly than AAV/Neo-infected 3A cells and parental 3A. After G418 selection, the resulting E6-E7/3A and E6/3A cell lines were found to be highly defective for binding RL95 and HEC endometrial cells compared to Neo/3A and parental 3A. Serum requirements and soft agar colony formation analysis showed that E6-E7/3A had the most malignant phenotype, followed by E6/3A, with parental 3A cells having the lowest. E6/3A and E6-E7/3A were also immortal. Thus, HPV-16 oncogene expression may lead to outright trophoblast death, defective endometrial cell recognition, or a malignant phenotype. Any of these changes might lead to disruption/dysfunction of the trophoblast layer/gestational loss.

Apoptosis↗