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A transient-evoked otoacoustic emission (TEOAE) is a sound originating in the cochlea in response to a brief acoustic stimulus, such as a click. The response is typically a weak (25 dB SPL maximum) signal that lasts 20-40 ms. Analysis of TEOAEs is promising as a noninvasive technique for understanding cochlear function and as a diagnostic tool in identifying hearing loss. A TEOAE database was collected on many subjects, some of which were administered quinine to study the effect of the drug on TEOAE. Historically, FFT techniques have not worked well on TEOAE data because of the nonstationary nature of the signals. We have used a wavelet-like approach in analyzing the data by employing a set of equal-bandwidth filters, which have revealed the emission energy to be concentrated in the 800-2000 Hz range. This type of analysis is shown to be useful in examining the time progression of different frequency bands of the click-evoked emissions in subjects who took quinine.

trans-Diamminedichloroplatinum(II), a paradigm of an inactive platinum compound, exhibited cytotoxic effect against HEP-2 human tumor cells, TA3Ha murine tumor cells, and freshly collected human ovarian carcinoma cells when combined with hyperthermia (43 degrees, 30 min). The heat treatment reduced the D0 of trans-platinum from 56 to 16.5 micrograms/ml in the HEP-2 system and from an undeterminable value at 37 degrees to 8.2 micrograms/ml in the TA3Ha system. Heat treatment before trans-platinum was more cytotoxic than that after trans-platinum in the TA3Ha system (P less than 0.001). TA3Ha cells treated in vitro with 40 micrograms/ml TDDP at 43 degrees failed to form tumors in mice upon subcutaneous implantation into the tails of mice. In contrast, these agents given singly did not alter the tumor-forming ability of TA3Ha cells. In vivo administration of trans-platinum after hyperthermia (43 degrees for 30 min) retarded the growth of TA3Ha tumors compared to either treatment alone. trans-Platinum did not form detectable DNA-interstrand cross-links in the HEP-2 cells treated at 37 degrees or 43 degrees. However, the DNA-protein cross-links were detectable under these conditions. The frequencies of DNA-protein cross-links were higher in the cells treated at 43 degrees than in those treated at 37 degrees, both immediately after and 12 h after the treatment with trans-platinum. Heat alone did not induce the formation of either DNA-interstrand or DNA-protein cross-links. Heat treatment did not appear to enhance the entry of trans-platinum into the cells.

Localized hyperthermia (43 degrees) in single or multiple fractions was applied to mouse mammary adenocarcinoma TA3Ha implanted into the s.c. tail tissue of strain A mice. The effects of heat on the growth of local tumors, on the pattern of metastasis, and on the survival periods of the hosts were studied. Hyperthermia was administered by heating the tumor-bearing tails in a water bath. Multiple 30-min hyperthermia treatments at 5- or 7-day intervals controlled local tumor growth better than did a single 30-min treatment or multiple 30-min treatments at 3-day intervals or at intervals longer than 7 days. Heat treatments that produced cytostatic effects on tumors, sparing the normal tissue, had no effect on either the survival of the hosts or the extent of metastasis to the lungs and the lumbar lymph nodes. However, local treatments reduced the frequency of renal lymph node metastasis, indicating that concurrent metastases in different sites may exhibit differential heat sensitivities.

The factors influencing the growth and metastatic behavior of experimental animal tumors are examined. 10(4) TA3Ha cells were injected intraperitoneally, intravenously, subcutaneously into the flank, and subcutaneously into the tail tissues of syngeneic strain A mice. The tumor takes from these injections were 50/50 (100%), 1/10 (10%), 10/10 (100%), and 7/12 (60%), respectively. The frequency of lung metastasis from these sites was 0, 100, 50, and 100%, respectively. At the time of host death, the flank and tail tumors were, respectively, 2.2 +/- 0.5 cm (geometric mean diameter) and 1.2 +/- 0.3 cm in the TA3Ha and 0.9 +/- 0.1 cm and 0.4 +/- 0.1 cm in the L1210 systems. TA3Ha tumors metastasized regularly to the lymph nodes but the L1210 tumors seldom metastasized to the lymph nodes. Tail implants of TA3Ha tumors behaved similarly in the athymic nude mice and strain A mice. TA3Ha cells inoculated into the Millipore chambers and maintained in mice for greater than 150 days were viable and able to form tumors. The results demonstrate that the anatomic location of the tumor affects the growth and metastatic behavior of the tumors, and that the tumors of different histologic origin metastasize differently even when grown in corresponding locations.

The factors influencing the growth and metastatic behavior of experimental animal tumors are examined. 10(4) TA3Ha cells were injected intraperitoneally, intravenously, subcutaneously into the flank, and subcutaneously into the tail tissues of syngeneic strain A mice. The tumor takes from these injections were 50/50 (100%), 1/10 (10%), 10/10 (100%), and 7/12 (60%), respectively. The frequency of lung metastasis from these sites was 0, 100, 50, and 100%, respectively. At the time of host death, the flank and tail tumors were, respectively, 2.2 +/- 0.5 cm (geometric mean diameter) and 1.2 +/- 0.3 cm in the TA3Ha and 0.9 +/- 0.1 cm and 0.4 +/- 0.1 cm in the L1210 systems. TA3Ha tumors metastasized regularly to the lymph nodes but the L1210 tumors seldom metastasized to the lymph nodes. Tail implants of TA3Ha tumors behaved similarly in the athymic nude mice and strain A mice. TA3Ha cells inoculated into the Millipore chambers and maintained in mice for greater than 150 days were viable and able to form tumors. The results demonstrate that the anatomic location of the tumor affects the growth and metastatic behavior of the tumors, and that the tumors of different histologic origin metastasize differently even when grown in corresponding locations.