We describe how the histology course we teach to first-year medical students changed successfully from using glass slides and microscopes to using virtual slides and virtual microscopes. In 1988, we taught a classic medical histology course. Subsequently, students were loaned static labeled images on projection slides to introduce them to their microscope glass slides, and we made laser disks of histological images available in the teaching lab. In 2000, we placed the static labeled images and laboratory manual on the Web. We abandoned the Web-based approach in 2001. Faculty selected specific areas on microscope glass slides in student collections for scanning at a total magnification of 40, 100, 200, or 400. Christopher M. Prince of Petro Image, LLC, scanned the glass slides; digitized, encoded, and compressed (95%) the images; and placed them on CD-ROMs. The scanned images were viewed up to a magnification of 400 using the MrSID viewer (LizardTech software) and the computer as a virtual microscope. This viewer has many useful features, including effective microscope and telescope functions that provide greater versatility for sample study and speed in localizing structures than was possible with the actual microscope. Image detail is indistinguishable from that viewed under the light microscope at equivalent magnifications. Static labeled images were also placed on CD-ROMs to introduce students to the virtual slides. AN OVERVIEW OF TEACHING MEDICAL HISTOLOGY IN THE 20TH CENTURYMedical histology has been a longstanding basic science course in the medical school curriculum worldwide. Changes in histology course materials during the 20th century have reflected improvements in histological techniques and slide preparation as well as developments in light microscopes and associated photomicroscopy. Transmission and scanning electron photomicrographs were used in teaching histology during the second half of the 20th century. Changes in course content during the 20th century initially emphasized new knowledge of structure as observed at the light and electron microscope levels. Faculty members subsequently incorporated more histophysiology and histopathology into their courses to emphasize newly acquired information on the function and clinical relevance of the cells and tissues being studied. The presentation of a significant amount of cell biology also has been incorporated into textbooks and courses. Changes that were incorporated during the 1980s and 1990s have occurred at the same time as an emergence of pressures from the Liaison Committee on Medical Education (LCME) and local university administrators to decompress the curriculum and reduce student-faculty contact hours in courses, including histology. At a significant number of medical schools, financial constraints have resulted recently in only partial replacement of retiring faculty, and the teaching loads of remaining faculty, therefore, have increased.During the latter part of the 20th century and the beginning of the 21st century, there has been a rapi...

No abstract

The environmental toxicant 4-tert-octylphenol (OP) has been shown to exert estrogenic effects on mammalian cells in culture. Recent findings from our laboratories demonstrate clearly that OP administration disrupts reproductive hormone secretion in the adult male rat, quite likely as a result of estrogenic action. In the present study, we investigated the impact of these or other OP-induced changes on male reproductive tissues. Adult male rats were injected with OP (20 or 80 mg) or estradiol valerate (EV; 0.8 or 8 microg) s.c. in oil three times a week for either 1 or 2 mo. We found that an 80-mg dosage of OP for 2 mo or an 8-microg dosage of EV for 1 or 2 mo greatly reduced sperm numbers and adversely influenced the sizes, weights, and histological structures of the testes, epididymides, ventral prostate glands, seminal vesicles, and coagulating glands. The 80-mg dosage of OP for 1 mo reduced epididymal tubule size to a lesser extent than after 2 mo of treatment. Otherwise, treatment with 80 mg OP for 1 mo, 20 mg OP for 1 or 2 mo, or 0.8 microg EV for 1 mo had little or no effect on the histology of the tissues we examined. Additional evaluation of sperm morphology revealed marked increases in the proportions of head and tail abnormalities from animals that had received 80 mg of OP or 8 microg of EV for 1 mo and 20 mg of OP for 2 mo. The head abnormalities consisted mainly of pin heads, detached heads, and the absence of hooks, while tail abnormalities included mainly broken, coiled, and bent tails. Our results clearly demonstrate that OP can severely reduce the size and/or function of all of the male gametogenic and accessory reproductive organs studied. Moreover, the similarity of these cell and tissue changes between rats treated with OP and those treated with EV further suggests that OP may exert its action in an estrogenic-like manner.

Plasma prolactin levels were measured by radioimmuno-assay in free-moving lactating rats bearing heart cannulas. Litters adjusted to 6 pups were returned to the mothers after a separation of 8–12 h from days 6 to 15 postpartum. Blood samples were taken before and 15, 30, 60 and 120 min after suckling had resumed. Lactating mothers were treated at various intervals before the experiment with P-chlorophenylalanine (PCPA), an inhibitor of serotonin (5-HT) synthesis; some animals were treated in addition with 5-hydroxytryptophan (5-HTP), a direct precursor of 5-HT. Blockade of 5-HT biosynthesis completely inhibited the more than 10-fold increase in prolactin levels observed in untreated controls. Inhibition of the prolactin response lasted more than 48 h after administration of PCPA; complete recovery required 120 h. Treatment with 5-HTP, which antagonizes the depletion of 5-HT caused by PCPA, restored the ability of the animals to release prolactin in response to suckling. The basal prolactin levels observed in lactating animals deprived of pups were not significantly affected by either drug at the time of experimentation. The results are consistent with the hypothesis that serotonin-containing neurons have a facilitatory effect on the hypothalamic mechanisms which trigger prolactin release in response to neural inputs involved in the suckling stimulus.

No abstract