Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol (E2) stimulates the proliferation of human endometrial adenocarcinoma cells of the Ishikawa line, which had been previously shown to respond to estrogen by increasing their levels of progesterone receptor and the specific activities of DNA polymerase alpha and alkaline phosphatase. Although E2 (10(-8) M) did not increase rates of proliferation during the initial logarithmic growth period of the cultures under the chosen experimental conditions (MEM with 15% charcoal-treated fetal bovine serum renewed every 2-3 days), it sustained cell proliferation after about day 10, when parallel control cultures had reached plateau cell densities. Cell proliferation in control cultures at plateau levels was resumed when the hormone was added. Growth rates of cultures containing E2 from the time of seeding and the proportion of quiescent cells, estimated by using a simple cell kinetic model, decreased steadily with time. Ornithine decarboxylase and DNA polymerase alpha activities, as well as estrogen receptor levels, also decreased with time in culture. Ishikawa cells formed colonies in soft agar; colony formation efficiencies were higher as the number of cells seeded was increased from 10,000 to 100,000 cells/6 cm dish, were not influenced by the addition of E2 to the medium (10(-9) to 10(-5) M) and were markedly reduced by difluoromethylornithine (10(-2) M), an effect that was counteracted by putrescine (25 X 10(-6) M).
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PMID:Effects of estradiol on proliferation of endometrial adenocarcinoma cells (Ishikawa line). 380 63

The effects of oral contraceptives of varied estrogen/progestin composition on clinical measurements of hepatic, thyroid, and renal function and carbohydrate metabolism were examined in 1,355 women in the Lipid Research Clinics Program Prevalence Study. In general, bilirubin and alkaline phosphatase levels are lower with both oral contraceptives and postmenopausal estrogen use, suggesting an estrogen effect. The least bilirubin reduction is seen with a progestin dominant oral contraceptive. A significant decrement in aspartate aminotransferase is observed in users of one high estrogen dose oral contraceptive and in postmenopausal Premarin users, while aspartate aminotransferase is higher in postmenopausal users of higher dose ethinyl estradiol. Globulins are slightly higher in all hormone use categories, suggesting an estrogen effect on hepatic secretion of this protein class into the circulation. Fasting glucose concentrations are generally slightly lower even in the progestin dominant oral contraceptives, where glucose intolerance has been described. Thyroxine concentrations are generally elevated in all women using oral contraceptives. A relationship to estrogen dose is seen in women with thyroxine concentrations greater than the 99th percentile and in postmenopausal estrogen users. Creatinine concentration is greater with the use of Ovral, a progestin dominant oral contraceptive, and lower with two estrogen dominant oral contraceptives and Premarin, suggesting a competitive effect of estrogen and progestin. Among the clinical laboratory tests considered here, oral contraceptive effects seem to be largely estrogen mediated with a suggestion of competitive effect of estrogen versus progestin only on bilirubin and creatinine levels. These observations differ from lipoproteins where opposing hormonal effects are more clearly reflected in changing lipoprotein concentrations.
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PMID:Effect of estrogen/progestin potency on clinical chemistry measures. The Lipid Research Clinics Program Prevalence Study. 394 98

The effects of 2 oral contraceptives, Ovulen and Norlestrin, were studied in monkeys fed adequate protein and low protein diets. The experiment was carried out in parts. In the first one, the administration of contraceptives was cyclic and similar to that employed in human subjects. In the other experiments, the contraceptives were given continuously and an attempt was made to exaggerate the deleterious effects of the oral contraceptive on the liver by including small doses of a known hepatotoxic agent, aflatoxin (AT). In Experiment 1, 45 female monkeys were divided into 2 groups of 20 and 25 and received an adequate protein (16%) and low protein diet (4%) respectively. Each monkey was fed 1/5 of a tablet of Ovulen or Norlestrin orally for 3 weeks, and then administration was discontinued for 1 week. In Experiment 2, 35 female monkeys were divided into 7 groups of 5 each. All the animals recieved 4% protein diet. 5 groups were tube fed at the rate of 100 cal/kg body weight, while 2 groups were given diet ad libitum. Group I received the diet alone while groups II-V received 10 mcg AT, 25 mcg AT, 10 mcg AT plus 1/5 Ovulen tablets, and 25 mcg AT plus 1/5 Ovulen tablet respectively daily. Groups VI and VII received the diet ad libitum but were orally fed 75 mcg AT and 75 mcg AT plus 1/5 Ovulen tablet respectively. Serum glutamic-oxalacetic transaminase activity and alkaline phosphatase activity were studied at regular intervals after the administation of oral contraceptives in the experiments. Serum proteins and hemoglobin were also determined. Monkeys fed oral contraceptives showed increased serum glutamic-oxalacetic transaminase and alkaline phosphatase activities irrespective of the level of protein in the diet. Livers of animals receiving oral contraceptives were morphologically similar to the controls fed respective diets. The experiments were conducted for a period of almost 2 years.
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PMID:Metabolic effects of oral contraceptives in monkeys fed adequate protein & low proein diets. 420 42

A case report of cholestatic jaundice in a 25 year old woman, who had had jaundice at age 4 years, and had taken Stediril (a combined oral contraceptive) for 1 month, implicates either the pill or a possibly hereditary hyperlipidemia. The jaundice developed in 2 weeks with vomiting, epigastric pain, anorexia, then discolored urine and feces, and intense pruritus. On hospitalization the patient had moderate bilirubinemia (56 mg/1), low alkaline phosphatase (13 U.K.) and slightly high serum glutamate pyruvate transaminase (270 U.W.). There were elevated serum cholesterol (3 gm/1), triglycerides (2.05 gm/1), total lipids (10.6 gm/1), and a definitely increased pre-beta lipoprotein, suggesting hyperlipidemia type IV (Frederickson classification). Liver biopsy showed fibrosis of the portal spaces lymphocytic infiltration, canalicular and intrahepatocytic thrombi. On laparoscopy the liver had a regular lower border, normal volume color and surface. Albumin, prothrombin and flocculation tests were normal. The patient's jaundice lasted about 1 month, then liver function slowly improved, although pruritus remained intense. Probably this jaundice was due to oral contraceptives, in a patient predisposed either by jaundice in childhood or endogenous hyperlipidemia.
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PMID:[Cholestatic icterus due to oral contraceptives]. 426 76

Clinical, serological and lymphocyte studies were done on 435 patients with biopsy proved anaplastic nasopharyngeal carcinoma (NPC) in various clinical status, at the National Taiwan University Hospital, from January 1980 through June 1983. Studies on 134 normal control were also done. Using immunofluorescent antibody method, seropsitive rates of the antibody titers against viral capsid antigens (VCA) and early antigens (EA) of Epstein-Barr (EB) virus were 70.8%-100% for anti-VCA/IgG titers (greater than or equal to 1:640), 81.0%-100% for anti-VCA/IgA titers (greater than or equal to 1:40), 66.7%-93.8% for anti-EA/IgG titers (greater than or equal to 1:160), and 40.0%-87.5% for anti-EA/IgA titers (greater than or equal to 1:40) in NPC patients with disease. They decreased to 10.5%-21.7% in remission patients. In contrast, they were less than 5% in the control. Mean total serum IgG and IgA levels were moderately increased to around 1,500 mg/dl and 300 mg/dl respectively, in all patients. The increase was most remarkable in patients with liver metastases. In control the values were 1,211 mg/dl and 223 mg/dl, respectively. Mean serum IgM, C3 and C4 amounts of NPC patients were not significantly different from those of the normal control, the latter were 129, 80.3 and 43.2 mg/dl, respectively. Serum acid phosphatase and calcium levels of NPC patients were all in the normal range of 0.1-2.0 BU/ml and 2.0-3.0 mmol/dl, respectively. Serum GOT, GPT, alkaline phosphatase, lactate dehydrogenase and mucoprotein were elevated either alone or in combination in some patients before treatment, in many patients with neck recurrence or distant metastases, but in all patients with liver metastases. Using monoclonal antibodies (Ortho Inc., U.S.A.) to define lymphocyte subsets, B lymphocytes comprised about 12% and T lymphocytes about 60% in the patients, whereas they were 11.9% and 73.1% in the control. The helper/suppressor ratio was 1.7 in the control and about 1.0 in NPC patients, and was only 0.8 in remission patients. The lack of correlation between the seropositive rates of anti-VCA antibodies and the helper/suppressor ratio might indicate different manifestations of humoral and cellular immunity in patients with NPC.
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PMID:Humoral and cellular immunity in patients with nasopharyngeal carcinoma. 608 49

Twenty-four surgically menopausal women were randomly allocated to one of two transdermally-administered estrogen replacement therapies (ERT): Group A was administered Estradiol (E2) TTS 0.05 mg/day for 6 months and 0.025 mg/day for the following six months and group B, E2 TTS 0.10 mg/day for the first 6 months and 0.05 mg/day for the following 6 months. For both groups, the treatment regimen was based upon the twice-weekly application of transdermal patches to the lower abdomen for three weeks a month. Serum E2, alkaline phosphatase (AP), osteocalcin (BGP) and urinary hydroxyproline (OHP) excretion levels were measured before the operation, at the beginning of ERT and after 6 and 12 months of treatment. Bone mineral density (BMD) in the distal regions of the forearms was measured by single photon absorptiometry at the start of the study and after 6 and 12 months. In Group A, both mean cortical and trabecular BMD had increased by, respectively, 1.53% and 2.17% after 6 months of therapy; after the second 6 months a significant decrease was observed in both parameters (2.40% and 3.62%, respectively). In Group B, mean cortical and trabecular BMD increased by 1.50% and 2.10%, respectively (significant increase in trabecular bone) after the first 6 months of treatment; after the following 6 months, these values persisted (+0.15 and -0.03%, respectively). Mean AP, OHP and BGP serum levels rose after the operation. In Group A, AP and OHP showed a significant decrease after the first 6 months (-34.90% and -30.90%), followed by an increase at the last evaluation of 22.50% and 35.50%, that reached statistical significance only for OHP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone metabolism changes after transdermal estradiol dose reduction during estrogen replacement therapy: a 1-year prospective study. 796 46

Forty-eight Angus x Hereford steers (initial BW = 336 +/- 8.3 kg) were used in a 56-d study to evaluate growth and endocrine responses to continuous or discontinuous grazing of high-endophyte-infected Kentucky-31 (K; > 57% infestation rate) or low-endophyte-infected Johnstone tall fescue (J; < 1% infestation rate) and implantation with 0 or 24 mg/steer of estradiol-17 beta (E2; Compudose). Steers were allotted by weight to eight 3-ha paddocks (four paddocks of each fescue variety) with six steers per paddock. Two paddocks of each variety were grazed continuously (KK and JJ), whereas steers on the remaining four paddocks were rotated every 14 d from K to J (KJ) or from J to K (JK). Three steers in each paddock were implanted with E2 on d 0. The study extended from May 25, 1988 to July 20, 1988 with steers exposed to potential heat-stress conditions for 52 d of the 56-d study. Body weights were obtained on d 0, 28, and 56, and blood samples were taken on d 28 and 56. Overall ADG, serum prolactin, and serum alkaline phosphatase activity were greater (P < .05) in JJ than in KK steers. Rotation from K to J did not increase overall ADG, prolactin, insulin-like growth factor I (IGF-I), or alkaline phosphatase activity compared with the continuously grazed KK, whereas JK steers had lower (P < .10) ADG, prolactin, and alkaline phosphatase activity than JJ steers. Estradiol-17 beta increased (P < .10) IGF-I in JJ, KJ, and JK steers but not in KK steers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth and endocrine responses of cattle to implantation of estradiol-17 beta during continuous or discontinuous grazing of high- and low-endophyte-infected tall fescue. 846 63

The minimum dosage of transcutaneous hormone replacement therapy (HRT) able to exert protective effects on postmenopausal bone mass, especially in older women, is uncertain. This study investigates the effects of transcutaneous HRT at two different doses of oestradiol [Estraderm 25 and 50 (E25, E50)] over 2 years in 44 postmenopausal women younger than 67 years and 27 of 67 years and older. Circulating biochemical markers of bone and connective tissue turnover, collagen type I (intact PINP, PICP) and type III (PIIINP) propeptides and type I telopeptide (ICTP), osteocalcin (OC) and alkaline phosphatase (AP) were measured. The responses of the biochemical markers in all the groups were very similar, and most of the observed changes occurred within the first year of treatment. E25 had an effect on the bone markers similar to that of E50, and there was little difference in response according to the patient's age. PINP fell markedly after 1 year in all groups to about half the pretreatment level, with a smaller drop in the second year. PICP responded more variably, and mean values were little changed. There was a slight fall at the higher dose in the younger women, and also in the older women (whose baseline level was higher) on the lower dose. The correlation between PINP and PICP was 0.52 at pretreatment and 0.84 after 2 years of treatment. PIIINP showed no changes. OC and AP both fell in all groups by the first year, but less markedly than PINP. Their response was slightly less pronounced in the older women. ICTP fell marginally in the younger women, and only after 2 years, regardless of dose. Postmenopausal serum oestradiol levels increased after HRT and were associated with decreased binding globulin (SHBG) levels in all groups. After E25 patch application individual serum oestradiol levels were variable and peaked between 13 and 36 h with a median value of 83.8 pmol L-1. Our data suggest that low-dose transcutaneous HRT restores circulating oestradiol levels in postmenopausal osteopenic women of all ages as effectively as conventional-dose HRT and is associated with decreased circulating markers of bone and connective tissue turnover.
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PMID:Effects of low- and conventional-dose transcutaneous HRT over 2 years on bone metabolism in younger and older postmenopausal women. 888 38

The effect of short-term estradiol treatment, administered from the time of ovariectomy, on increased bone turnover and subsequent bone loss was studied in the rat. Adult female Sprague-Dawley rats were ovariectomized and administered daily subcutaneous (s.c.) injections of 17 beta-estradiol at 8 micrograms/ kg per day (Low) and 20 micrograms/kg per day (High) or vehicle alone (Veh). Femoral trabecular bone volume (BV/TV) and trabecular number (Tb.N) in the distal femur were transiently increased at 6 days postoperation in a dose-dependent manner following estradiol administration [mean +/- SEM: BV/TV (%), day 0, 6.6 +/- 0.2; day 6, Veh 7.8 +/- 0.4, Low 10.2 +/- 2.2, High 12.8 +/- 1.7 (p < 0.05); Tb.N (/mm), day 0, 2.30 +/- 0.24; day 6, Veh 2.89 +/- 0.33, Low 3.4 +/- 0.7, High 4.39 +/- 0.34 (p < 0.05)]. Estradiol prevented the ovariectomy-induced decrease in BV/TV and Tb.N between 9 and 15 days observed in Veh rats. Both serum alkaline phosphatase and urine hydroxyproline excretion were maintained at preoperative levels or lower from day 6 postoperation with high dose estradiol. Serum osteocalcin, however, rose above preoperative levels with estradiol at days 6 and 9, but returned to these values on days 15 and 21 postoperation. These results suggest that estradiol, administered from the time of ovariectomy, immediately suppressed markers associated with osteoblast proliferation/matrix synthesis and bone resorption. Mineralization does not appear to be so rapidly suppressed by estradiol with relatively high levels immediately following administration, resulting in a transient increase in trabecular bone volume and trabecular number.
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PMID:Estradiol treatment transiently increases trabecular bone volume in ovariectomized rats. 892 43

Lack of consistent information concerning the pathophysiology of corticosteroid-related bone loss may be due to coexisting independent factors that influence bone mineral density (BMD). For example, the disease being treated may increase bone turnover and cause bone loss, and its severity may influence the dose of corticosteroids chosen. Similarly, disease remission due to the treatment or disease progression despite treatment may influence bone turnover and the rate of bone loss. The hormonal changes purportedly responsible for reduced bone formation or increased bone resorption may be the result of the disease, not the corticosteroids. To determine the pathophysiology of corticosteroid-related bone loss, we conducted a controlled, prospective study in men with no systemic illness treated with corticosteroids to reduce antisperm antibodies. We measured BMD using dual x-ray absorptiometry and circulating biochemical and hormonal determinants of bone turnover in 9 men before and during prednisolone treatment and in 10 age-matched controls. The results were expressed as the mean +/- SEM. There were no differences in BMD between the two groups at baseline. The patients received 50 mg prednisolone daily for 3.7 +/- 0.6 months (range, 1-6). BMD decreased by 4.6 +/- 0.8% at the lumbar spine (P = 0.0007), by 2.6 +/- 0.6% at the trochanter (P = 0.004), and by 4.8 +/- 1.9% at the Ward's triangle (P < 0.04). The decrease in lumbar spine BMD correlated with the cumulative dose of corticosteroids (r = -0.49; P = 0.03). Serum osteocalcin and skeletal alkaline phosphatase decreased by 28.5 +/- 15.5% (P = 0.08) and 24.2 +/- 8.6% (P < 0.03), respectively. The decrease in lumbar spine BMD correlated with the decrease in osteocalcin (r = -0.48; P < 0.02). Serum testosterone and sex hormone-binding globulin decreased by 28.6 +/- 4.4% (P < 0.003) and 28.5 +/- 8.3% (P < 0.007), respectively. The testosterone/sex hormone-binding globulin ratio did not change. The decrease in total testosterone correlated with the decrease in osteocalcin (r = -0.40; P = 0.05). There were no detectable changes in urinary C-telopeptide, serum PTH, or serum calcium. Estradiol decreased by 23.5 +/- 11.4% (P < 0.003). Corticosteroid therapy results in rapid bone loss, probably due to reduced bone formation. Neither increased bone resorption nor secondary hyperparathyroidism appears to contribute to the rapid bone loss. Whether the reduction in bone formation may be partly mediated by changes in sex steroids remains unclear.
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PMID:Corticosteroid-induced bone loss in men. 950 31


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