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Biomedical subjects

D L Davis

Publications and source records attributed to D L Davis.

At least 109 records · Page 6Linked to original sources
PubMed1992

Trends in cancer mortality in 15 industrialized countries, 1969-1986.

BACKGROUND: Assessing trends in cancer provides a means for gauging progress against the disease, estimating future demands for care and treatment, and suggesting clues about shifting causal factors that may account for the more recent changes. PURPOSE: This study was designed to evaluate trends in the major sites of cancer associated with high mortality rates in 15 industrialized countries. To highlight differences among regions, we grouped these countries into six geographic areas: United States, Eastern Europe, Western Europe, East Asia, Oceania, and Nordic countries. In addition, cancer mortality trends in these regions were compared with incidence patterns in the United States. METHODS: Data provided by the World Health Organization were used to evaluate age-specific mortality trends from 1969 through 1986 for lung, breast, prostate, stomach, and colorectal cancers and for all other sites considered as a group. We also assembled and analyzed data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute for the same sites and age groups from 1973 through 1986. RESULTS: Over the period 1969 through 1986, recorded cancer mortality in persons aged 45 years and older in the six regions studied has increased for lung, breast, and prostate cancers in most age groups, while the decline in stomach cancer mortality is substantial. The increase in lung cancer deaths in men aged 45-54 years has slowed greatly or reversed in all areas except Eastern Europe and East Asia. Trends for intestinal cancer vary by age and region. For all other sites considered as a group, increases have occurred for persons older than 64 years in most regions. In Eastern Europe, there are disturbingly high rates and rapid increases for several of the major forms of cancer in persons aged 45-54 years. In general, trends for cancer incidence in the United States parallel those for mortality. For intestinal cancer, however, incidence has increased while mortality has declined. CONCLUSIONS: The trends we report cannot be explained solely by changes in cigarette smoking or aging. Other causes of changes in cancer incidence and mortality need to be determined. IMPLICATIONS: The increasing and decreasing trends in mortality from and incidence of cancer that we found are important for health care planning and may also suggest opportunities for research in cancer prevention.

Age Factors↗
PubMed1992

Neonatal exposure to protoporphyrin-activating lighting as a contributing cause of childhood acute lymphocytic leukemia.

While being a relatively rare disease, acute lymphocytic leukemia (ALL) is the leading form of cancer in children in the developed world today. ALL sharply peaks in incidence at ages three to four years. In the United States there have been persistent, unexplained increases in incidence of ALL in the past two decades. We hypothesize that exposure to photosensitizing lighting immediately after birth may be a contributing cause of ALL. Fluorescent lamps and other light sources with strong illumination, around 400 nanometers, are protoporphyrin-activating. Activation of protoporphyrin produces superoxides and free radicals that can induce breaks in DNA. In newborn nurseries in the US, the intensity of lighting has increased five- to 10-fold over the past two decades. Thus, protoporphyrin-activating light may be a contributing cause of childhood ALL. Additional retrospective and prospective studies should be undertaken of the relationship between exposure of newborns to protoporphyrin-activating illumination and the development of childhood ALL, along with in vitro studies of the hematologic effects of fluorescent lighting. Protoporphyrin-activating lighting is clearly not the sole determinant of ALL, but it could be a completely preventable cause. Inexpensive plastic filters could reduce these exposures substantially.

Humans↗
PubMed1992

Characterization of the epidermal growth factor receptor in preimplantation pig conceptuses.

Embryos recovered from sows on Days 9-13 of pregnancy (Day 0 = first day of estrus) exhibited saturable and time-dependent specific binding of 125I-epidermal growth factor (EGF). The specific binding (pg/mg protein) was greater (P less than 0.001) for Day 13 elongated conceptuses than for conceptuses of earlier stages. Scatchard analyses showed two classes of binding sites (Kd = 7.0 +/- 2.6 x 10(-11) M, Bmax = 6.2 +/- 1.4 fmol/mg protein and Kd = 3.4 +/- 0.2 x 10(-8) M, Bmax = 420 +/- 80 fmol/mg protein). The EGF receptor in Day 13 conceptus membranes is a 170-kDa protein and was phosphorylated in the presence of EGF and adenosine triphosphate. EGF stimulated protein tyrosine kinase activity about 1.6-fold over basal levels. The results show that the preimplantation pig conceptus possesses EGF-binding sites with the properties of functional EGF-receptors.

Amino Acid Sequence↗
PubMed1992

Synthesis of prostaglandins by pig blastocysts cultured in medium containing estradiol or catechol estrogen.

Two experiments were conducted to determine the effects of 2-hydroxy-estradiol-17 beta (2-OH-E2; 0, 50 and 100 microM) and estradiol-17 beta (E2; 0, 25 and 50 microM) on prostaglandin (PG) E and PGF2 alpha synthesis by day-10 pig blastocysts (day 0 is first day of estrus). Blastocysts were incubated in a modified Krebs-Ringer bicarbonate medium, supplemented with bovine serum albumin (4 mg/ml) and the vitamins and amino acids (essential and nonessential) in Minimum Essential Medium (without phenol red or antibiotics). The incubations were conducted at 39 degrees C for three 2-h periods; the second and third periods included an E2 or catechol estrogen treatment. Release of PGF2 alpha into the culture medium decreased (p less than 0.001) linearly with increasing concentrations of 2-OH-E2 in both periods. Release of PGE was not affected by 2-OH-E2, therefore 2-OH-E2 increased (p less than 0.06) the PGE:PGF2 alpha. When E2 was added to the medium, release of PGE was decreased (p less than 0.01) during the second and third periods. Release of PGF2 alpha also was decreased (p less than 0.05) by E2 during period 2, but E2 did not alter the PGE:PGF2 alpha. Content of PGs in blastocysts at recovery was less than 10% of the PGs released in vitro. Therefore, these studies demonstrate effects of both the primary and catechol forms of E2 on the synthesis of PGE and PGF2 alpha. Catechol estrogens and E2 may inhibit PG synthesis and modify the PGE:PGF2 alpha during the establishment of pregnancy in pigs.

Animals↗
PubMed1992

Cell-type specific responses in prostaglandin secretion by glandular and stromal cells from pig endometrium treated with catecholestrogens, methoxyestrogens and progesterone.

The pig conceptus and endometrium possess the ability to convert estrogens into catecholestrogens and catecholestrogens into methoxyestrogens. Experiments were carried out to evaluate the effect of catecholestrogens, methoxyestrogens and progesterone on the secretion of prostaglandin (PG) E and F2 alpha by porcine endometrial glandular and stromal cells in vitro. Both 2-hydroxyestradiol (2-OH-E2, 0-20 microM) and 4-hydroxyestradiol (4-OH-E2, 0-20 microM) increased (P less than .05) PGE and PGF2 alpha secretion by stromal cells in a dose response manner. Two-hydroxyestradiol tended (P less than .1) to decrease PGF2 alpha production by glandular cells. Two-methoxyestradiol (20 microM) suppressed (P less than .05) PGF2 alpha secretion by glandular and stromal cells. Four-methoxyestradiol (20 microM) stimulated (P less than .05) PGE production and PGE:PGF2 alpha ratio. Progesterone (.1 microM) suppressed (P less than .05) PG secretion in both cell types. We conclude that catecholestrogens, methoxyestrogens, and progesterone may participate in the establishment of pregnancy by modulating PG production in the endometrium.

2-Methoxyestradiol↗
PubMed1992

Male-mediated teratogenesis and other reproductive effects: biologic and epidemiologic findings and a plea for clinical research.

This paper reviews biologic and epidemiologic evidence that prefertilization and perifertilization exposures to fathers influence a variety of reproductive outcomes, including fertilization, miscarriage, low birth weight, congenital anomalies, cancer, and neurodevelopmental and other childhood health problems. Males and females bring an equal number of chromosomes to their progeny, but their genomes may affect different aspects of reproduction. While the key male role principally ends at fertilization, there is growing experimental and human evidence that factors relating both to prefertilization and perifertilization exposure also play a role post fertilization. Some negative human epidemiologic findings reflect the fact that routinely gathered information usually generates detailed descriptions of maternal exposures and does not collect records regarding prefertilization paternal exposures. The absence of extensive human evidence should be interpreted as a deficiency in research rather than an absence of male-mediated adverse reproductive outcomes. More than 60 different compounds or industrial processes have been identified as increasing defects in human sperm and possibly increasing the risk to offspring from male-mediated exposures. Further research needs to include better characterizations of both maternal and paternal prefertilization and perifertilization exposures, in order to assess more accurately their relative effects. Pediatricians confronted with adverse pregnancy and antenatal health outcomes should obtain detailed information on relevant prefertilization exposures of both parents.

Abnormalities, Drug-Induced↗
PubMed1992

Epidermal growth factor receptors in porcine endometrium: binding characteristics and the regulation of prostaglandin E and F2 alpha production.

Epidermal growth factor (EGF) and its receptor have been implicated in the control of uterine cell growth and differentiation. The objectives of this study were to determine EGF binding characteristics and effects of EGF on prostaglandin (PG) production in vitro by glandular and stromal cells from porcine endometrium. Endometrial tissues were taken from 10 sows on Day 13 of pregnancy (first day of estrus = Day 0). Glandular and stromal cells were separated by enzymatic dispersion and sieve filtration and cultured for 3 days. EGF-binding assay was carried out at 20 degrees C in the presence of 0.2 nM 125I-EGF with increasing concentrations of unlabeled EGF (0-12 nM). Scatchard analyses revealed one class of high-affinity binding sites in each cell type with apparent equilibrium dissociation constants (n = 6) of 2.96 +/- 0.60 nM and 2.48 +/- 0.50 nM for stromal and glandular cells, respectively. The apparent binding capacities were 199.3 +/- 34.8 fmol/10(6) cells for stromal cells and 40.7 +/- 6.5 fmol/10(6) cells for glandular cells. Effects of EGF on PG production were determined by including 1, 5, 10, or 20 ng/ml EGF in the medium for the final 24 h of the 72-h culture. EGF increased PGE (p less than 0.01) and PGF2 alpha (p less than 0.05) secretion by stromal cells. The highest concentration (20 ng/ml) of EGF increased secretion of PGE and PGF2 alpha by 133% and 64%, respectively, over controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Molecular genetics of steroid 5 alpha-reductase 2 deficiency.

Two isozymes of steroid 5 alpha-reductase encoded by separate loci catalyze the conversion of testosterone to dihydrotestosterone. Inherited defects in the type 2 isozyme lead to male pseudohermaphroditism in which affected males have a normal internal urogenital tract but external genitalia resembling those of a female. The 5 alpha-reductase type 2 gene (gene symbol SRD5A2) was cloned and shown to contain five exons and four introns. The gene was localized to chromosome 2 band p23 by somatic cell hybrid mapping and chromosomal in situ hybridization. Molecular analysis of the SRD5A2 gene resulted in the identification of 18 mutations in 11 homozygotes, 6 compound heterozygotes, and 4 inferred compound heterozygotes from 23 families with 5 alpha-reductase deficiency. 6 apparent recurrent mutations were detected in 19 different ethnic backgrounds. In two patients, the catalytic efficiency of the mutant enzymes correlated with the severity of the disease. The high proportion of compound heterozygotes suggests that the carrier frequency of mutations in the 5 alpha-reductase type 2 gene may be higher than previously thought.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1992

Figuring out cancer.

Cancer continues to increase throughout the industrial world. Aging of the population, smoking habits, and improvements in diagnosis do not account completely for these patterns. About 5 percent of cancers occur in persons under age 45, while 65 percent of all cancers occur in persons over age 65. For this older age group, many of their most common tumors, in addition to those linked with smoking, are not curable and appear to be increasing in incidence as well as mortality in a number of industrial countries. Evaluating cancer causes by looking at an age-adjusted rate obscures important differences that are occurring at different age groups. In order to reduce the cancer burden further, it is important to look for bona fide explanations of recent shifts in cancer patterns, especially those not related to cigarette smoking or other habits.

Adolescent↗
PubMed1992

Regulation of Staphylococcus protease using complement, interferon and immunoglobulin as substrates.

The effects of various agents on the cleavage of serum albumin, interferon, immunoglobulin and complement component C1q by the extracellular protease from Staphylococcus aureus were analysed by SDS-polyacrylamide gel electrophoresis. Arachidonic acid moderately stimulated the proteolysis of serum albumin, interferon and complement component. Phosphatidic acid effectively enhanced the proteolysis of serum albumin and IgG, whereas it inhibited the cleavage of IgM. The proteolysis of IgG was appreciably enhanced by sphingosine. In contrast, phosphatidyl choline and phosphatidyl glycerol were shown to have an inhibitory effect on the proteolysis of IgG and IgM. Phosphatidyl serine, phosphatidyl inositol and phosphatidyl ethanolamine also inhibited the proteolysis of IgG. The failure of any of these agents to exert a persistent effect on the cleavage of all substrates, revealed the complexity of the interactions among the agent, the substrate and the protease.

Complement C1q↗
PubMed1991

Is brain cancer mortality increasing in industrial countries?

This paper analyzes age-specific trends in brain and other central nervous system cancer mortality from 1968 to 1987 in several major industrial countries. It also examines changes in the use of diagnostic confirmation technology and trends in incidence in the U.S. National Cancer Institute, Surveillance, Epidemiology, and End Results (SEER) program from 1973 to 1987 to estimate the influence of diagnostic factors on recent mortality trends. Other sources of error have not been evaluated in this paper. Age-specific analyses of brain and other nervous system cancer mortality show drastic increases in persons ages 75-84 and consistent increases in younger age groups in most countries, although mortality declined in the U.S. in persons 0-24 by 2% annually. In the SEER program, brain cancer incidence increased significantly by 2%, 1%, and 5% annually in persons aged 0-44, 65-74, and 75-84, respectively. Throughout this time period, microscopic or radiographic confirmation occurred in at least 96% of all incident cases of brain and other central nervous system cancers diagnosed before death, with older persons receiving consistently more radiographic tests than younger persons. Changes in diagnoses across populations and over time are unlikely to account completely for these increasing trends which are occurring simultaneously in both males and females in major industrial countries. Additional studies need to be conducted, to exclude artifacts, to assist health care planners in anticipating treatment demands, and to detect preventable causes of these changing trends.

Adult↗
PubMed1991

Prostaglandin E and E2 alpha secretion by glandular and stromal cells of the pig endometrium in vitro: effects of estradiol-17 beta, progesterone, and day of pregnancy.

Prostaglandins (PGs) are believed to play important roles in the establishment of pregnancy. Glandular and stromal cells were isolated from pig endometrium on days 11 through 19 of pregnancy and cultured in the presence of estradiol-17 beta (E2) and progesterone (P4) to determine the effect of day of pregnancy and steroids on the secretion of PGE and PGF2 alpha. Estradiol at concentrations between .01 and 1 microM did not affect PGE and PGF2 alpha secretion into the medium by glandular and stromal cells. Progesterone (.1 microM) suppressed (P less than .001) PGE and PGF2 alpha production from both cell types. Glandular cells secreted more (P less than .01) PGF2 alpha than PGE, whereas stromal cells collected on days 11, 12, 13, and 19 secreted more (P less than .05) PGE than PGF2 alpha. Stromal cells isolated from tissues collected on day 13 of pregnancy produced PGs with higher (P less than .01) PGE:PGF2 alpha ratio than those from tissues harvested on other days of pregnancy. Glandular cells isolated from tissues collected on days 13 and 19 and stromal cells isolated from tissue collected on day 13 of pregnancy secreted more (P less than .05) PGE and PGF2 alpha than cells isolated on other days of pregnancy. We conclude that: 1) P4 has a suppressing effect on PG secretion; 2) endometrial glandular and stromal cells each produce a unique profile of PGs; and 3) endometrial cells harvested on different days of pregnancy secrete different amounts of PGE and PGF2 alpha.

Animals↗
PubMed1991

Chicken vitellogenin gene-binding protein, a leucine zipper transcription factor that binds to an important control element in the chicken vitellogenin II promoter, is related to rat DBP.

We screened a chicken liver cDNA expression library with a probe spanning the distal region of the chicken vitellogenin II (VTGII) gene promoter and isolated clones for a transcription factor that we have named VBP (for vitellogenin gene-binding protein). VBP binds to one of the most important positive elements in the VTGII promoter and appears to play a pivotal role in the estrogen-dependent regulation of this gene. The protein sequence of VBP was deduced from a nearly full length cDNA copy and was found to contain a basic/zipper (bZIP) motif. As expected for a bZIP factor, VBP binds to its target DNA site as a dimer. Moreover, VBP is a stable dimer free in solution. A data base search revealed that VBP is related to rat DBP. However, despite the fact that the basic/hinge regions of VBP and DBP differ at only three amino acid positions, the DBP binding site in the rat albumin promoter is a relatively poor binding site for VBP. Thus, the optimal binding sites for VBP and DBP may be distinct. Similarities between the VBP and DBP leucine zippers are largely confined to only four of the seven helical spokes. Nevertheless, these leucine zippers are functionally compatible and appear to define a novel subfamily. In contrast to the bZIP regions, other portions of VBP and DBP are markedly different, as are the expression profiles for these two genes. In particular, expression of the VBP gene commences early in liver ontogeny and is not subject to circadian control.

Amino Acid Sequence↗
PubMed1991

Mutational studies reveal a complex set of positive and negative control elements within the chicken vitellogenin II promoter.

The endogenous chicken vitellogenin II (VTGII) gene is transcribed exclusively in hepatocytes in response to estrogen. We previously identified two estrogen response elements (EREs) upstream of this gene. We now present an analysis of the VTGII promoter activated by these EREs in response to estrogen. Chimeric VTGII-CAT genes were cotransfected into LMH chicken hepatoma cells along with an estrogen receptor expression vector, and transient CAT expression was assayed after culturing the cells in the absence or presence of estrogen. An analysis of constructs bearing deletions downstream of the more proximal ERE indicated that promoter elements relevant to transcription in LMH cells extend to between -113 and -96. The relative importance of sequences within the VTGII promoter was examined by using 10 contiguous linker scanner mutations spanning the region from -117 to -24. Although most of these mutations compromised VTGII promoter function, one dramatically increased expression in LMH cells and also rendered the VTGII promoter capable of being activated by cis-linked EREs in fibroblasts cotransfected with an estrogen receptor expression vector. Gel retardation and DNase I footprinting assays revealed four factor-binding sites within this promoter. We demonstrate that three of these sites bind C/EBP, SP1, and USF (or related factors), respectively; the fourth site binds a factor that we denote TF-V beta. The biological relevance of these findings is suggested by the fact that three of these binding sites map to sites previously shown to be occupied in vivo in response to estrogen.

Animals↗
PubMed1991

Flushing and altrenogest affect litter traits in gilts.

Gilts (n = 267) were allotted to flushing (1.55 kg/d additional grain sorghum), altrenogest (15 mg.gilt-1.d-1) and control treatments in a 2 x 2 factorial arrangement. Altrenogest was fed for 14 d. Flushing began on d 9 of the altrenogest treatment and continued until first observed estrus; 209 gilts (78%) were detected in estrus. The interval from the last day of altrenogest feeding to estrus was shorter (P less than .05) with the altrenogest + flushing treatment (6.6 +/- .2 d) than with flushing alone (7.6 + .3 d). Ovulation rates (no. of corpora lutea) were higher (P less than .05) in all flushed gilts (14.5 +/- .4 vs 13.4 +/- .4), whether or not they received altrenogest. Flushing also increased the total number of pigs farrowed (.9 pigs/litter; P = .06) and total litter weight (1.43 kg/litter; P = .01), independent of altrenogest treatment. Number of pigs born alive and weight of live pigs were higher for gilts treated with altrenogest + flushing and inseminated at their pubertal estrus than for gilts in all other treatment combinations. In contrast, gilts receiving only altrenogest had greater live litter weight and more live pigs born when inseminated at a postpubertal estrus than when inseminated at pubertal estrus. We conclude that flushing increased litter size and litter weight, particularly for gilts that were inseminated at their pubertal estrus. Increased litter size resulted from increased ovulation rates, which, in nonflushed gilts, limited litter size at first farrowing.

Animal Feed↗