Kimberly Whatley and Lawrence Harrison, Jr. in a Joint Senior Recital

This is the program for the joint senior voice recital of soprano Kimberly Carol Whatley and tenor Lawrence Wayne Harrison, Jr. Pianist Jay Crowder assisted Harrison. The recital took place on February 2, 1989, in the Mabee Fine Arts Center Recital Hall

UK experience of liver transplantation for erythropoietic protoporphyria

Erythropoietic protoporphyria (EPP) is characterised by excess production of free protoporphyrin from the bone marrow, most commonly due to deficiency of the enzyme ferrochelatase. Excess protoporphyrin gives rise to the cutaneous photosensitivity characteristic of the disease, and in a minority of patients leads to end-stage liver disease necessitating liver transplantation (LT). There is limited information regarding the timing, impact and long-term outcome of LT in such patients, thus we aimed to identify the indications and outcomes of all transplants performed for EPP in the UK using data from the UK Transplant Registry. Between 1987 and 2009, five patients underwent LT for EPP liver disease. Median follow-up was 60 months, and there were two deaths at 44 and 95 months from causes unrelated to liver disease. The remaining recipients are alive at 22.4 years, 61 months and 55 months after transplant. A high rate of postoperative biliary stricturing requiring multiple biliary interventions was observed. Recurrent EPP-liver disease occurred in 4/5 (80%) of patients but graft failure has not been observed. Given the role of biliary obstruction in inducing EPP-mediated liver damage, we suggest that consideration should be given for construction of a Roux loop at the time of transplant. Thus we demonstrate that although EPP liver transplant recipients have a good long-term survival, comparable to patients undergoing LT for other indications, biliary complications and disease recurrence are almost universal, and bone marrow transplantation should be considered where possible

RECIPROCAL RECURRENT SELECTION FOR 21-DAY LITTER WEIGHT OF CROSSBRED GILTS. II. REPRODUCTIVE PERFORMANCE OF PUREBRED FEMALES PRODUCING PUREBRED AND TWO-WAY CROSS LITTERS AND PERFORMANCE OF PUREBRED AND CROSSBRED PIGS

This paper reports estimates of correlated genetic change in reproductive performance of purebred gilts producing two-way cross litters and purebred sows producing purebred litters as well as postweaning performance of two-way cross and purebred pigs produced during reciprocal recurrent selection (RRS) between Line 8 (Duroc) and Line 9 (Beltsville No. 1) for 21-d litter weight production of crossbred gilts. A randomly mated control line developed from a crossbred foundation was maintained to monitor environmental change. Data were adjusted for age of dam, inbreeding of dam, inbreeding of litter (or pig) and linear and quadratic effects of day born within season. The traits evaluated were: litter size, litter weight and average pig weight/litter at birth and weaning (42 d); postweaning average daily gain; age at 90.7 kg and backfat thickness at 90.7 kg. Two data sets were analyzed; the first set included seven seasons of data with purebred gilts producing two-way cross litters, and the second set included seven seasons of data with purebred sows producing purebred litters. No estimates of environmental trend were significant in either set of data. In the first data set, only the estimate of genetic change in backfat thickness of two-way cross pigs was significant and it was in the desired direction. All other estimates were small and did not approach significance. In the second data set, estimates of genetic trend were greater in Line 9 than in Line 8. Estimates of genetic trend in Line 9 were significant for average pig weight at birth, age at 90.7 kg and backfat probe at 90.7 kg, and approached significance for litter size at weaning and average daily gain. The estimates were undesirable for preweaning traits and desirable for postweaning traits. The estimates of genetic trend in Line 8 were of the same sign as those in Line 9, but only the estimate for backfat thickness was significant. The decrease in size of purebred litters in Line 9, and to some degree Line 8, suggests an accelerated accumulation of homozygosity beyond that accounted for by adjustment for pedigree inbreeding. The fact that Line 9 showed a greater decrease than Line 8 suggests that most of the increase in level of reproduction of crossbred gilts may have resulted from genetic change in Line 9 rather than Line 8, or that favorable alleles were being fixed in Line 8 and unfavorable alleles in Line 9

RECIPROCAL RECURRENT SELECTION FOR 21-DAY LITTER WEIGHT OF CROSSBRED GILTS. I. SELECTION APPLIED AND GENETIC CHANGE IN REPRODUCTION OF CROSSBRED GILTS

Six cycles of reciprocal recurrent selection (RRS) between Line 8 (Duroc) and Line 9 (Beltsville No. 1) were completed at the Fort Reno Livestock Research Center, E1 Reno, Oklahoma. A randomly mated control line was maintained. Each cycle of selection required three seasons. Selection of purebred pigs (born in the second season) was based on the mean 21-d litter weight of their maternal and paternal half-sib crossbred gilts that were born in the first season and farrowed in the third season (XB21DLWT). On the average, 5.8 maternal and paternal half-sib gilts contributed to the mean XB21DLWT for each purebred individual. The average potential selection differential for XB21DLWT was 5.64 kg, but only 70.2% of this value was realized in the initial selection (3.95 kg). Disease problems and unsoundness were the primary reasons for this discrepancy. The potential, initial, final and weighted final standardized selection differentials for females averaged 61, 60, 55 and 47%, respectively, of the corresponding differentials for males. Standardized selection differentials were similar for Line 8 and Line 9. The estimate of realized heritability for XB21DLWT was .076 ± .319 for the average of 8 x 9 and 9 x 8 gilts. Environmental trends, estimated from control data, were not significant for any of the traits evaluated. The genetic change in reproductive ability of 8 x 9, 9 x 8 and their unweighted average was estimated by regressing the deviation of the line mean from the control mean on generation number. In general, estimates of genetic change for litter size, litter weight and average pig weight/litter at 0, 21 and 42 d of age were not significant, but all estimates were favorable. The estimated genetic change for 21-d litter weight was 1.04 ± 1.25 kg/cycle of selection. Based on these results and considering the complexity of RRS, the increase in generation interval and the expected decline in purebred performance that theoretically should accompany successful RRS, it seems doubtful that RRS can be more beneficial than selection based on purebred performance as a method to improve productivity of crossbred gilts

Tamoxifen and the Rafoxifene analog LY117018: their effects on arachidonic acid release from cells in culture and on prostaglandin I(2 )production by rat liver cells

BACKGROUND: Tamoxifen is being used successfully to treat breast cancer. However, tamoxifen also increases the risk of developing endometrial cancer in postmenopausal women. Raloxifene also decreases breast cancer in women at high risk and may have a lower risk at developing cancer of the uterus. Tamoxifen has been shown to stimulate arachidonic acid release from rat liver cells. I have postulated that arachidonic acid release from cells may be associated with cancer chemoprevention. METHODS: Rat liver, rat glial, human colon carcinoma and human breast carcinoma cells were labelled with [(3)H] arachidonic acid. The release of the radiolabel from these cells during incubation with tamoxifen and the raloxifene analog LY117018 was measured. The prostaglandin I(2 )produced during incubation of the rat liver cells with μM concentrations of tamoxifen and the raloxifene analog was quantitatively estimated. RESULTS: Tamoxifen is about 5 times more effective than LY117018 at releasing arachidonic acid from all the cells tested. In rat liver cells only tamoxifen stimulates basal prostaglandin I(2 )production and that induced by lactacystin and 12-O-tetradecanoyl-phorbol-13-acetate. LY117018, however, blocks the tamoxifen stimulated prostaglandin production. The stimulated prostaglandin I(2 )production is rapid and not affected either by preincubation of the cells with actinomycin or by incubation with the estrogen antagonist ICI-182,780. CONCLUSIONS: Tamoxifen and the raloxifene analog, LY117018, may prevent estrogen-independent as well as estrogen-dependent breast cancer by stimulating phospholipase activity and initiating arachidonic acid release. The release of arachidonic acid and/or molecular reactions that accompany that release may initiate pathways that prevent tumor growth. Oxygenation of the intracellularly released arachidonic acid and its metabolic products may mediate some of the pharmacological actions of tamoxifen and raloxifene

Control of the growth of human breast cancer cells in culture by manipulation of arachidonate metabolism

<p>Abstract</p> <p>Background</p> <p>Arachidonate metabolites are important regulators of human breast cancer cells. Production of bioactive lipids are frequently initiated by the enzyme phospholipase A2 which releases arachidonic acid (AA) that is rapidly metabolized by cyclooxygenases (COX) or lipoxygenases (LO) to other highly potent lipids.</p> <p>Methods</p> <p>In this study we screened a number of inhibitors which blocked specific pathways of AA metabolism for their antiproliferative activity on MCF-7 wild type and MCF-7 ADR drug resistant breast cancer cells. The toxicity of these inhibitors was further tested on human bone marrow cell proliferation.</p> <p>Results</p> <p>Inhibitors of LO pathways (specifically the 5-LO pathway) were most effective in blocking proliferation. Inhibitors of platelet activating factor, a byproduct of arachidonate release, were also effective antiproliferative agents. Curcumin, an inhibitor of both COX and LO pathways of eicosanoid metabolism, was 12-fold more effective in blocking proliferation of the MCF-7 ADR^scells compared to MCF-7 wild type (WT) cells. These inhibitors that effectively blocked the proliferation of breast cancer cells showed varying degrees of toxicity to cultures of human bone marrow cells. We observed greater toxicity to bone marrow cells with inhibitors that interfere with the utilization of AA in contrast to those which block utilization of its downstream metabolites. MK-591, MK-886, PCA-4248, and AA-861 blocked proliferation of breast cancer cells but showed no toxicity to bone marrow cells.</p> <p>Conclusion</p> <p>These inhibitors were effective in blocking the proliferation of breast cancer cells and may be potentially useful in human breast cancer therapy.</p