Esophageal reflux and dysmotility as the basis for persistent cervical symptoms.

To examine a possible esophageal basis for cervical symptoms, we studied 63 patients with persistent cervical complaints, 36 patients with gastroesophageal reflux but no cervical symptoms, and ten normal subjects. Patients were evaluated for a history of pyrosis and regurgitation and underwent otolaryngologic examination, barium esophagram, upper endoscopy, esophageal biopsy, standard esophageal manometrics, acid reflux testing, and Bernstein examination, as well as tests of esophageal dysmotility and acid clearance time before and after bethanechol (50 micrograms/kg, two doses). Standard diagnostic examinations usually were normal in patients with cervical symptoms. Pyrosis, regurgitation, and a positive Bernstein examination were uncommon in patients with cervical symptoms. This occurred despite frequent acid reflux (68%) and poor acid clearance (79%). Esophageal dysmotility also was common (63%). Patients with reflux but no cervical symptoms and normal subjects had a normal acid clearance time, and dysmotility was unusual (8%). We conclude that patients with cervical symptoms have diminished esophageal sensitivity despite frequent and long acid exposure. The pathophysiologic significance of this observation is discussed.

Growth inhibition of laryngeal UM-SCC cell lines by tamoxifen. Comparison with effects on the MCF-7 breast cancer cell line.

Six laryngeal squamous cell carcinoma (SCC) cell lines and the MCF-7 breast cancer line, all of which contain estrogen and progesterone receptors, were tested for in vitro growth inhibition by the antiestrogen tamoxifen citrate. Cell line MCF-7 was more sensitive to growth retardation at 1 mumol/L of tamoxifen citrate, but SCC lines showed higher sensitivity than MCF-7 to cytotoxic effects at higher drug concentrations (7 to 10 mumol/L). A cytostatic level of growth inhibition was produced by 5 mumol/L tamoxifen citrate for both types of cell lines. When tamoxifen and estradiol were added to cultures simultaneously, partial reversal of growth inhibition was observed with MCF-7 but not with UM-SCC-5. All of the cell lines recovered from inhibition when tamoxifen was replaced with 0.1 mumol/L estradiol, but laryngeal SCC lines recovered equally well in estradiol-free medium, whereas MCF-7 recovered only partially in the absence of estradiol. These findings indicate that there are at least two tamoxifen receptor sites--one for which estradiol is a competitor and one for which it is not--and that tamoxifen reversibly blocks growth and may synchronize SCC cells.

Lateral neck mass. Sole presenting sign of metastatic thyroid cancer.

Two hundred sixty-eight cases of thyroid cancer treated at the University of Michigan, Ann Arbor, from 1974 to 1984 were evaluated. Thirty-six patients had, as the sole presenting sign, a lateral neck mass that proved to be metastatic thyroid cancer. In every instance, the thyroid gland was clinically normal on initial evaluation. Thyroid scans were found to be of little value in the preoperative evaluation of the lateral neck mass. Surgical treatment consisted of total thyroidectomy and modified or radical neck dissection. Foci of thyroid cancer were found on pathologic evaluation of all thyroid glands removed, supporting the concept of metastatic cancer rather than the lateral aberrant thyroid associated with developmental cell rests.

Effects of bovine serum albumin on normal human lymphocytes.

In the course of other experiments we noted increased tritiated thymidine uptake by normal human peripheral blood lymphocytes (PBL) cultured in medium supplemented with bovine serum albumin (BSA) as compared with human plasmas. We confirmed specific stimulatory effects of BSA and sought evidence supporting antigenicity of BSA for human lymphocytes in culture. The PBL cultured in 0.6%-10% BSA incorporated several fold more [3H]thymidine than did cells in medium alone or in human, dog, rat, or guinea pig serum albumins. Responses were maximal for 1% BSA in 7-day cultures. Nonhuman cells (mouse splenocytes) responded comparably in medium and in human, bovine, dog, rat, andf guinea pig albumins. Human lymphocyte donor plasmas contained agglutinators of sheep red blood cells coated with BSA. Agglutination was inhibited by both BSA and antihuman immunoglobulin. These data established specific in vitro stimulatory effects of BSA and suggested that the explanation for this response is that BSA is antigenic to human PBL. Appreciation of such effects is important in conducting and interpreting tissue culture experimentation.

Effects of acetaminophen on normal human peripheral blood lymphocytes: enhancement of mitogen- and antigen-stimulated incorporation of tritiated thymidine.

This report describes hitherto unrecognized immunoenhancing properties of acetaminophen on cultured human lymphocytes. The addition of acetaminophen (2.5--300 micrograms/ml) significantly enhanced mitogen-induced blastogenesis. The stimulation of cells by Candida albicans, from individuals who were skin-test positive for antigen and two-way responses of mixed lymphocytes, were similarly augmented. Cells stimulated in the presence of acetaminophen were comparably enhanced in cultures lasting for 24--168 hr. Enhancement of stimulated cells was noted only if the drug was added during the first hours of culture. Exposure of cells to acetaminophen before mitogen stimulation did not enhance responses unless tha cells were simultaneously cultured with mitogen and the drug. Cells obtained from normal subjects before, during and after ingestion of therapeutic amounts of acetaminophen for 3 days, were cultured in a medium without acetaminophen, and did not display increased in vitro responses during or after drug consumption. These data indicated: (1) pharmacological concentrations of acetaminophen significantly enhanced lymphocyte responses to specific, non-specific, soluble and insoluble stimulation in vitro; and (2) enhancement by acetaminophen occurred only when the drug was in contact with cells during the early period of cell activation.