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The gender composition of U.S. dental schools has changed dramatically over the past 25 years. While women represent less than 10 percent of the practicing dental population, the dramatic increase in dental school enrollment by women will be reflected in a much larger percentage of female dental practitioners in the near future. It is not clear how this trend will affect the structure and organization of the dental profession or the delivery of dental care. This study examined gender differences among recent dental graduates' professional commitment, choice of practice arrangements, and income. The data consist of a random sample of 1979, 1980, and 1981 graduates of U.S. dental schools with an adjusted response rate of 77.6 percent (n = 2,648 males and 346 females). Findings include statistically significant gender differences in mean annual income from private practice, administration, or teaching of dentistry; total family income before taxes; employment status in private practice; marital status, and the number of children under 18 years of age. A gender difference of fewer than four hours worked per week, while statistically significant, is less than previous reports in the literature. Gender remained as a statistically significant predictor of income when controlling for practice ownership, hours per week worked, background, and family/social variables. These findings have policy implications for dental resource planning, organized dentistry, dental education, and the delivery of dental care.

The effects of supplementing a wheat/animal protein diet with copper (nil, 125 or 250 ppm), zinc (nil or 150 ppm) and iron (nil or 150 ppm) were studied in a 2 x 2 x 2 x 3 factorial experiment with 48 pigs. The diet was restrictively and individually fed to barrows and gilts between 18 and 73 kg liveweight. Daily rate of gain, feed conversion ratio and carcase score were not affected by the supplementary minerals. Supplementary copper increased the storage of manganese, zinc and copper in the liver. Although liver copper levels were greater in both sexes at 250 than at 125 ppm copper, barrows stored more copper than gilts at the higher level. Adding 150 ppm zinc at the same time as 250 ppm copper reduced liver copper storage in the barrows to the level of that in gilts given the same amount of copper. The iodine number, i.e, softness, of backfat in barrows was increased to that of gilts by 250 ppm copper; gilts were unaffected. Zinc supplementation also increased backfat softness in barrows but not in gilts. Despite this, 150 ppm zinc partially reduced the effect of 250 ppm copper on backfat in barrows.

A 2 x 2 x 3 x 3 factorial experiment with 72 growing pigs examined the effect of adding salt, calcium and phosphorus (Ca + P) and trace minerals (TM-manganese, zinc, iron and copper) to a wheat/soybean meal diet. Gilts and barrows were individually fed at restricted intakes from 20 kg liveweight. Pigs required both salt and Ca + P to reach slaughter at 73 kg. Without these minerals they stopped growing; lameness and broken bones were also common. All pigs fed salt plus the higher level of Ca + P (0.84 and 0.57 per cent, respectively) completed the experiment but only half those fed salt plus the lower level (0.42 and 0.29 per cent Ca + P, respectively) did so. There was a response to salt within three weeks. In the first four weeks, 0.125 per cent added salt improved growth by 26.5 per cent and feed conversion ratio by 21 per cent. The results indicated that growing pigs require less sodium than currently estimated (Agricultural Research Council). A response to both levels of supplementary Ca + P was seen after about seven weeks with salt and nine weeks without salt. In the first eight weeks of the experiment there were no differences in performance between the two levels of added Ca + P when salt was also used. Between 8 and 12 weeks, pigs fed the higher level grew 17 per cent faster. Although 0.84 + 0.57 per cent Ca + P increased rib Ca and P levels, foot and joint abnormalities showed that these levels were insufficient for normal bone development. This suggests that the Agricultural Research Council estimates of Ca and P requirements for restrictively fed growing pigs are low. TM supplementation did not affect performance when both salt and Ca + P were added to the diet.

The response of growing pigs to supplementation with minerals, vitamins, or both, when fed diets bassd on barley, oats, sorghum or maize was examined in six factorial experiments involving 192 pigs. In two of these experiments meat-and-bone meal (with some fish meal up to 32 kg liveweight) was used as a protein concentrate with barley and oats. In the other four experiments, soybean meal (SBM) was used with each grain. A base supplement of vitamins A and D3 was added to all diets, The pigs were restrictively and individually fed between 18 and 73 kg. Mineral supplementation of the animal protein (AP) diets did not affect pig performance, but improved that of pigs fed the SBM diets. Lack of supplementary minerals in the SBM diets caused slow growth, broken bones, foot abnormalities and failure of many pigs to reach slaughter weight. Some results indicated there were differences in mineral availability between grains. Vitamin supplementation, over and above vitamins A and D3 did not affect performance of pigs fed AP diets. Despite a number of apparent vitamin deficiencies in the SBM diets, there was little or no response to vitamin supplementation. The lack of response suggests the vitamin requirements of growing pigs currently estimated by the Agricultural Research Council are high for restrictively fed pigs.

Two factorial experiments examined the effects of mineral and or vitamin supplementation on the performance of 64 growing pigs. The wheat-based diets contained either meat-and-bone meal (with some fish meal up to 32 kg liveweight) or solvent-extracted soybean meal (SBM). A basal supplement of vitamins A and D2 was added to all diets. The pigs were individually fed at restricted intakes between 18 and 73 kg liveweight and housed as mixed treatment groups. In a third factorial experiment, 32 growing pigs were restrictively fed a wheat/SBM diet from 20 kg liveweight to 75 kg or for 20 weeks. The pigs were individually housed to prevent cross-transfer of vitamins from supplemented to unsupplemented pigs by way of the faeces (cross-coprophagy). Mineral supplementation of the wheat/animal protein diet (experiment 1) did not affect pig performance, but improved the growth rate and feed conversion ratio of pigs fed the SBM diet (experiment 2) by 45 and 32 per cent respectively. Omitting the mineral supplement from the SBM diet caused loss of appetite, soft bones, joint and foot abnormalities and lameness in many pigs; 5 out of 16 pigs did not reach slaughter weight. Gilts fed the SBM diet were less tolerant of mineral deficiencies than barrows. They also stored less calcium in their bones when minerals were added to the diet. There was no response to vitamin supplementation even though both diets, but especially the SBM diet, were apparently deficient in a number of vitamins. The SBM diet provided 76, 83 and 53 per cent respectively of the pigs' estimated requirements for riboflavin, pantothenic acid and vitamin B12. In experiment 3 the SBM diet supplied 64, 80 and 28 per cent of the pigs' riboflavin, pantothenic acid and vitamin B12 requirements. As in experiment 2, there was no response to vitamin supplementation. Cross-coprophagy was thus most unlikely to have caused the lack of response to vitamin supplementation in the group-housed pigs of experiment 2. Mineral supplementation improved growth rate by 108 per cent and feed conversion ratio by 40 per cent.

Angiogenesis is an essential requirement for tumour growth and metastasis and is regulated by a complex network of factors produced by both stromal cells and neoplastic cells within solid tumours. The cytokine tumour necrosis factor alpha (TNF-alpha) and the enzyme thymidine phosphorylase (TP) are two factors known to promote tumour angiogenesis. We have demonstrated recently that high numbers of tumour-associated macrophages (TAMs) are significantly associated with increased tumour angiogenesis and poor prognosis in invasive carcinoma of the breast. We have also shown that TAMs are a major source of TNF-alpha in invasive breast carcinomas, and that macrophage-like stromal cells as well as tumour cells synthesize TP in such tumours. However, little is known of the factors that regulate the production or activity of these factors in the tumour microenvironment. As TNF-alpha has been shown to up-regulate TP expression in tumour cells in vitro we performed an immunohistochemical study to investigate the possibility that TNF-alpha may be involved in the regulation of TP expression by malignant breast epithelial cells in vivo. To do this, we used a cocktail of non-neutralizing monoclonal anti-TNF-alpha antibodies to visualize both TNF-alpha-expressing macrophages and TNF-alpha bound to its receptors on tumour cells and endothelial cells in a series of 93 invasive carcinomas of the breast. A semiquantitative grading system was then used to compare these staining patterns with that for TP in the same biopsies. TNF-alpha immunoreactivity was also compared with various important tumour variables known to relate to outcome in this disease (microvessel density, node status, grade, stage, receptor status and macrophage infiltration), as well as relapse-free and overall survival data for these patients. Our data show significant positive correlations between TNF-alpha bound to its receptors on tumour cells and: (1) TP protein production by tumour cells, and (2) axillary lymph node status (i.e. metastasis). These results suggest that tumour cell responsiveness to TNF-alpha produced by neighbouring TAMs may play a part in the regulation of TP expression by tumour cells as well as their metastatic behaviour. This may explain, in part, the relationship between increased macrophage infiltration and angiogenesis in breast cancer, and further supports the contention that TAMs may represent an important target for future anti-angiogenic therapies.

Numerous interactions between malignant and stromal/inflammatory cells take place within solid human tumours, which are mediated, in part, by the release of signalling proteins called cytokines. In the present study, we have compared the secretion of two important immunomodulatory cytokines, IFN-gamma and IL-4 by individual, immunophenotyped NK cells freshly isolated from either malignant tumour biopsies, or peripheral blood samples from patients with ductal invasive breast cancer. Due to the marked heterogeneity amongst cells isolated from these clinical samples, we have employed a technique called the reverse haemolytic plaque assay to identify and enumerate cytokine-secreting cells at the single cell level. Our data indicate that NK cells isolated directly from the tumour site secrete more IFN-gamma and IL-4 than NK cells from the blood of the same patients. However, a greater proportion of CD16+ cells from both sources in breast cancer patients secreted IFN-gamma than of those from the blood of healthy donors. We also show that factors secreted by the human breast cell lines, MCF-7 and MDA-231 PN9, were able to mimic the stimulatory influence of the tumour microenvironment on secretory activity of NK cells.

The purpose of this study was to explore longitudinal observational analysis of insurance claims data with goal of graphically demonstrating that effective dental care leads to the diminished use of services in subsequent time intervals. Using the Rand HIE claims data, definitions of the best patients for whom claims data would be profiled and the best parameters to use in rate calculations for the time series graphs were empirically derived. Profiles using these definitions were found to be very similar to a conceptual model of such profiles.

The expression of tumour necrosis factor alpha (TNF-alpha) and its two distinct receptors, TNF-R p55 and TNF-R p75, was assessed by immunocytochemistry in 28 primary breast cancer and three reduction mammoplasty specimens ('normal' breast tissue). Expression of TNF-alpha or TNF-R p75 was not detectable in normal breast tissue or in non-malignant breast tissue adjacent to the tumours. By contrast, TNF-R p55 was expressed by occasional stromal cells in normal tissue. TNF-alpha was expressed focally in 50% of the tumours studied, being largely localised to macrophage-like cells in the stroma. TNF-R p55 was expressed by a population of stromal cells in all the tumours examined, and a varying proportion of neoplastic cells in 75% of these tissues. TNF-R p75 was detected in about 70% of the tumours, immunoreactivity being confined mainly to cells in the stroma. In this preliminary study there was no association between the above cytokine parameters and such measures of tumour biology as lymph node status, tumour grade, proliferative activity or degree of angiogenesis. However, there was a correlation between the expression of TNF-R p55 by blood vessels and the number of leucocytes present.

The effects of tumour necrosis factor-alpha (TNF alpha) on the growth and DNA synthesis of the human breast cell line, T47D, were studied. A dose-dependent, reversible inhibition of thymidine incorporation and cell growth was observed in the range of 0.1 ng ml-1 to 100 ng ml-1 of TNF alpha. Cell viability was not impaired in any of the experiments. Flow-cytometric DNA analysis demonstrated that after 24 h exposure to TNF alpha, T47D cells accumulated in the G1 phase of the cell cycle, and were depleted in the G2/M and S phases, suggesting a block in the progression of the G1/S transition. The involvement of protein kinases (PK) and protein phosphatases in TNF alpha-induced signal transduction was also investigated. A transient and rapid 2-fold increase in total cellular protein kinase C (PKC) activity was detected after 10 min exposure to TNF alpha. To study the role of the observed PKC activation in the cytostatic effect of TNF alpha, T47D cells were exposed to the cytokine in the presence of the potent PKC inhibitor, H7. The inhibitory effect of TNF alpha on thymidine incorporation was not affected by exposure to H7 at concentrations sufficient to block the stimulation of thymidine up-take induced by the PKC agonist, phorbol-12-myristate-13-acetate (PMA). The involvement of other signalling pathways was addressed using the cyclic nucleotide-dependent PK inhibitor, H8; the calmodulin-dependent PK inhibitor, W7; and the inhibitor of protein phosphatases PP1 and PP2B, okadaic acid. Exposure of T47D cells to these enzyme inhibitors failed to antagonise the inhibition of thymidine incorporation by TNF alpha. Taken together, these results indicate that the cytostatic effect of TNF alpha on T47D cells occurs at the G1/S transition of the cell cycle, and is mediated by an intracellular pathway which does not involve the activity of protein kinases C and A, nor protein phosphatases PP1, PP2B.

Soil, pasture and grazing dairy cattle with calves were monitored at two locations on the North Coast of New South Wales for insecticide residues from 1972-1 975, after soil incorporation of dieldrin and heptachlor at the recommended rate of 1.1 kg/ha before sowing to control pasture weevil pests. The soil and pasture types were: Wollongbar clay loam sown with tropical legumes and grass at Wollongbar (dieldrin), and black alluvial sown with temperate legumes and grass, at Duck Creek substation, near Ballina (dieldrin and heptachlor). After the treatments, persistent residues were found in soil and pasture, and grazing stock, although residues declined over the trial period. Stock residues in many cases exceeded the 0.15 and 0.2 g/g maximum residue limits recommended by the National Health and Medical Research Council for the fat of milk and meat, and similar residues were found in additional cattle introduced after fifteen months. In view of the long-term risks for grazing stock, the pre-sowing soil treatment with dieldrin and heptachlor for the control of pasture pests is no longer recommended by the New South Wales Department of Agriculture.