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Biomedical subjects

J Vaughan

Publications and source records attributed to J Vaughan.

At least 73 records · Page 4Linked to original sources
PubMed1994

Human maternal uniparental disomy for chromosome 16 and fetal development.

Two severely growth-retarded fetuses found to have maternal uniparental disomy (UPD) for chromosome 16 and trisomy 16 placental mosaicism both had an unfavourable outcome. Antenatally, the first case was complicated by an unexplained raised maternal serum alpha-fetoprotein concentration, preterm premature rupture of the membranes, and growth retardation detectable at 21 weeks' gestation, whilst the other had an unexplained raised maternal serum human chorionic gonadotrophin level, a two-vessel cord on ultrasound, and cessation of growth at 25 weeks. At post-mortem, both babies had an imperforate anus. Fetal maternal UPD may explain the poor outcome that occurs in some cases of confined placental mosaicism for chromosome 16 and is also associated with specific fetal abnormalities.

Adult↗
PubMed1994

Studies of tamoxifen as a promoter of hepatocarcinogenesis in female Fischer F344 rats.

Tamoxifen, an antiestrogen used in the treatment of breast cancer, was assessed for carcinogenic potential in the two-stage model of experimental hepatocarcinogenesis. Groups of female Fisher F344 rats were initiated with a non-necrogenic, subcarcinogenic dose of diethylnitrosamine (DEN; 10 mg/kg, po) and fed tamoxifen at a concentration of 250 mg per kg of AIN-76A diet for 6 or 15 months. The livers of these animals exhibited an increase in size and number of altered hepatic foci compared with those animals which were initiated with DEN but not exposed to tamoxifen. This finding indicates that tamoxifen may have a carcinogenic potential in the rat liver. After 6 months of treatment, neoplastic nodules were observed in 3/8 rats in the DEN-initiated, tamoxifen-treated group. In the initiated group provided with tamoxifen for 15 months, neoplastic nodules were observed in 7/8 rats and hepatocellular carcinomas in 3/8 rats. The serum level of tamoxifen in these rats was 200-300 ng/ml. The ratio of tamoxifen, 4-hydroxy tamoxifen, and N-desmethyl tamoxifen was 1:0.1:0.5-1 in the serum. When adjusted for age-related weight increases, the serum and liver levels of tamoxifen and its N-desmethyl metabolite did not change over the 15 months. In the rat liver, the level of tamoxifen and its N-desmethyl metabolite was 10-29 micrograms/g liver after 6 or 15 months of chronic dietary administration. The ratio of tamoxifen:4-hydroxy tamoxifen:N-desmethyl tamoxifen was 1:0.1.3-3.3 in the liver. Therefore, the liver had 20- to 30-fold more tamoxifen and 4-hydroxy tamoxifen and at least 100-fold more N-desmethyl tamoxifen than the serum (assuming 1 gram of tissue is equivalent to 1 ml of serum). These results indicate that tamoxifen is a promoting agent for the rat liver at serum levels found in patients given the usual therapeutic course of tamoxifen. The high concentrations of tamoxifen attained in the rat liver indicate that actions other than its known estrogenicity for liver could contribute to its promoting action. In addition, these results indicate that the pharmacodynamic differences in tamoxifen metabolism in rats and humans and at low versus high doses should be determined. Thus, the therapeutic indications for tamoxifen should be balanced by the potential risk it may present as a promoting agent in mammalian liver.

Animals↗
PubMed1994

Focal and non-focal hepatic expression of placental glutathione S-transferase in carcinogen-treated rats.

Carcinogenesis develops in stages that have been operationally defined as initiation, promotion and progression. Although morphological end points have been described for detection and quantitation of these stages, to date initiation has been assessed only in the context of clonal growth in response to certain promoting agents. Initiated cells are morphologically indistinguishable from surrounding cells and early changes at the cellular level during initiation have not been clarified. One commonly used end point for the detection of preneoplastic hepatic lesions i their aberrant expression of the placental isozyme of glutathione S-transferase (PGST). Because single hepatocytes expressing PGST have been detected in aged rats and in those administered hepatocarcinogens, it has been suggested that such cells constitute a population of putatively initiated hepatocytes. In order to further elucidate the characteristics of single PGST-positive hepatocytes, we analyzed the number of these cells 2 and 18 weeks after various doses (0-100 mg/kg) of diethylnitrosamine (DEN) and of dimethylbenz[a]anthracene (DMBA). When determined 14 days after carcinogen administration, the number of single hepatocytes expressing PGST was greater after DEN administration (ranging from 0.8 +/- 0.3 per cm2 transection of liver at 1 mg/kg to 33.0 +/- 4.7 at 100 mg/kg) than after DMBA administration (ranging from 0.25 +/- 0.14 at 10 mg/kg to 3.03 +/- 0.5 at 100 mg/kg); none were detected in control rats of the same age. Additional rats were maintained on a basal diet or a basal diet plus phenobarbital for a further 4 month period. Whereas individual PGST-positive hepatocytes were only sporadically detected in rats treated with DMBA and maintained on a basal diet for 18 weeks, those rats placed on phenobarbital for 16 weeks had an even higher number of such PGST-positive hepatocytes than at 2 weeks after DMBA administration. In contrast, the dose-response curve observed for DEN-treated rats 18 weeks after carcinogen administration was similar to that observed 2 weeks after carcinogen treatment for both phenobarbital- and non-phenobarbital-treated rats. In addition, the number of single PGST-positive hepatocytes detected at 2 weeks was directly parallel to the number of altered hepatic foci expressing PGST 18 weeks after DEN administration. The dose-dependent induction of PGST-positive single hepatocytes after treatment with two hepatocarcinogens, the dose-dependent growth of altered hepatic foci (AHF) expressing PGST with phenobarbital administration and the parallel dose-response curve of single hepatocytes expressing PGST and later of AHF expressing PGST argue strongly for a precursor role of single PGST-positive cells in the development of AHF expressing PGST.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

In vitro culture of colony forming unit-megakaryocyte (CFU-MK) in fetal alloimmune thrombocytopenia.

Perinatal alloimmune thrombocytopenia (PAITP) causes intracranial haemorrhage in the fetus and neonate. However, the severity of the thrombocytopenia correlates poorly with maternal anti-platelet antibody titres. To test the hypothesis that reduced platelet production contributes to fetal thrombocytopenia in PAITP, maternal sera from three HPA-1a-negative mothers whose pregnancies were complicated by anti-HPA-1a (two severe cases, one mild case) were added to colony forming unit-megakaryocyte (CFU-MK) cultures from HPA-1a positive and negative individuals. Sera from the two severely affected pregnancies containing anti-HPA-1a caused 66-100% inhibition of HPA-1a-positive fetal and neonatal CFU-MK, whereas CFU-MK from two HPA-1a-negative mothers were not inhibited by the anti-HPA-1a-containing sera. Maternal serum from the case of mild PAITP caused only mild inhibition of HPA-1a-positive cord and adult CFU-MK and did not inhibit HPA-1a-positive fetal CFU-MK. Taken together, these findings suggest that reduced megakaryocyte production contributes to fetal thrombocytopenia due to maternal anti-HPA-1a antibodies and also that the degree of CFU-MK inhibition correlates with severity of fetal thrombocytopenia.

Adult↗
PubMed1994

Prenatal determination of human platelet antigen type using DNA amplification following amniocentesis.

OBJECTIVES: To demonstrate that fetal human platelet antigen (HPA1) type can be determined, without the need for fetal blood sampling, by amplification of fetal DNA from amniotic fluid cells using polymerase chain reaction and allele specific oligonucleotide hybridisation. DESIGN: Oligonucleotide DNA primers were designed to amplify a portion of the platelet glycoprotein GpIIIa gene which spans the site of the single base change which differentiates HPA1a from HPA1b. Specific oligonucleotides were designed to hybridise either to the amplified HPA1a allele or to the HPA1b allele. Amniotic cells were used as the DNA template both directly and following formal isolation of DNA. Fetal HPA1 type, determined by this method in fifteen pregnancies not at risk of perinatal alloimmune thrombocytopaenia, was compared to typing of fetal blood obtained following cordocentesis. The methodology was then used to HPA type the fetus in two pregnancies at risk of the disease. SETTING: Department of Molecular Biology and Centre for Fetal Care, Queen Charlotte's Hospital. SUBJECTS: Fifteen women undergoing amniocentesis and fetal blood sampling for other indications and two women at risk of perinatal allo-immune thrombocytopaenia whose partners were heterozygotes. RESULTS: In the 15 control cases and the two clinical cases, determination of fetal HPA1 type from amniotic fluid cells agreed with typing of fetal blood. There was no difference in the efficiency of amplification from amniotic fluid cells directly or from isolated DNA. CONCLUSIONS: Fetal HPA type may be reliably determined by amplification of DNA from amniotic fluid cells, eliminating the need for fetal blood sampling or immunoglobulin administration when the fetus is HPA1a negative.

Amniocentesis↗
PubMed1994

Clinical and echographic features of in utero cardiac dysfunction in the recipient twin in twin-twin transfusion syndrome.

OBJECTIVE: Fetal twin-twin transfusion syndrome (TTTS) presenting in the second trimester has been associated with almost no perinatal survival until recently, when serial drainage of amniotic fluid has improved the prognosis to 70%-80%. Most recipient twins now survive but develop cardiac dysfunction. The study was undertaken to evaluate the abnormal echocardiographic features and clinical complications of cardiac disease in the recipient twin of TTTS. DESIGN: Antenatal and postnatal echocardiographic and clinical observational study. SETTING: Antenatal studies in a tertiary referral centre. Postnatal management and follow up were performed by the same paediatric cardiologist, either at the obstetric hospital or at the regional referral centre. PATIENTS: Twin pregnancies complicated by TTTS with severe polyhydramnios diagnosed earlier than 25 weeks that proceeded until viability (n = 5). INTERVENTION: Serial fetal echocardiography with colour Doppler. Postnatal echocardiography in the first week and between two and seven months. Serial amnioreduction was performed in all pregnancies. Digoxin treatment, pericardiocentesis, paracentesis, or laser ablation of placental anastomoses was undertaken when there was hydrops. RESULTS: Increased cardiothoracic ratio and tricuspid regurgitation were seen in all recipient twins. High pulmonary artery velocities developed in three. One recipient twin died a week after delivery of endocardial fibroelastosis and infundibular pulmonary stenosis. Two other had balloon dilatation for pulmonary stenosis, one shortly after birth and one at four months. A further twin has apical thickening of the right ventricle at six months. The remaining recipient twin had normal echocardiographic findings at follow up. CONCLUSION: This report characterises for the first time a cardiac disease acquired in utero in the recipient twin in pregnancies complicated by TTTS. Clinical manifestations in utero range from mild to critical pulmonary stenosis or lethal cardiomyopathy. Although perinatal prognosis seems to be related to the severity of dysfunction when first diagnosed in utero, follow up in infancy is recommended in view of the possibility of progressive pulmonary stenosis.

Echocardiography, Doppler↗
PubMed1993

An investigation of fetal growth using serial ultrasound data.

Serial ultrasonic measurements were performed in 67 Caucasian fetuses from 20 weeks' gestation until term to derive reference standards for abdominal circumference (AC) and estimated fetal weight (EFW). The variances of both AC and EFW increased with gestational age. Four mathematical models (linear, quadratic, Gompertz and Rossavik) were fitted to the log(10)(AC) and log(10)(EFW) data from each fetus using least squares regression analysis. The standard deviations of the residual error were greatest for the linear model. The linear model also overestimated the final log(10)(AC) while the linear, Gompertz and Rossavik models all overestimated the final log(10)(EFW) when these data were omitted from the fitting process. The individual quadratic constants were, therefore, used to produce 67 individual growth curves. Values of log(10)(AC) and log(10)(EFW) for each fetus at exact gestational ages between 20 and 40 weeks were derived by interpolation; the mean and standard deviation values were then used to derive centile ranges for abdominal circumference and estimated fetal weight. These standards should prove useful in the assessment of fetal growth.

Journal Article↗
PubMed1993

Immunocytochemical evidence for the presence of inhibin and activin-like proteins and their localization in goldfish gonads.

In previous studies, we have demonstrated that inhibin and activin are stimulatory to goldfish gonadotropin release. In the present study, the distribution of immunoreactive inhibin and activin subunits (alpha, beta A, and beta B) in goldfish gonads was examined with domain-specific antibodies against mammalian inhibin and activin subunits, using the avidin-biotin-peroxidase complex method. In the ovary, follicle cells surrounding the oocyte were heavily stained with anti-porcine beta A and human beta B subunits. The cytoplasm of previtellogenic oocytes, at all stages of the ovarian cycle, also showed strong reactions with anti-beta A and beta B. As ovarian recrudescence progressed, oocytes that started to accumulate cortical vesicles gradually lost their immunoreactivity, with the reaction intensity inversely proportional to the amount of cortical vesicles in the oocyte; when oocytes became full of cortical vesicles, the oocytoplasm was no longer immunoreactive to anti-beta A and beta B. The staining with antiporcine alpha subunit was similar to that with anti-beta A and beta B but the reaction intensity was weaker than that with anti-beta A and beta B. In the testis, the mature sperm in the tubular lumen exhibited a strong immunoreaction to anti-alpha antibody, while the interstitial tissue was completely negative. However, the immunoreactivities with anti-beta A and beta B in the testis were exclusively restricted to the interstitial tissues. These results provide evidence for the presence of inhibin and activin-like molecules in the goldfish and reveal the distribution of these molecules in the goldfish gonads.

Activins↗
PubMed1993

Ultrasonic estimation of fetal weight: use of targeted formulas in small for gestational age fetuses.

OBJECTIVE: To derive a formula for calculating fetal weight in small for gestational age (SGA) fetuses and to determine prospectively whether the use of such a targeted formula reduces birth weight prediction errors. METHODS: Standard ultrasonic measurements were made in 159 SGA fetuses within 7 days of delivery. Three classes of fetal weight formulas (linear, quadratic, and cubic) were fitted to the data using stepwise regression analysis. Birth weight predictions using these three formulas were then compared prospectively with five previously reported formulas in 187 SGA fetuses. RESULTS: R2 was 0.97 for each of the three derived formulas. The 95% prediction intervals were comparable for the three formulas (eg, cubic model -11.6, 17.8%), and none were statistically superior to previous formulas. Each of the formulas evaluated prospectively had a systematic error and, with the exception of the present study's linear formula, all had percentage errors that varied systematically over the range of actual birth weights. CONCLUSION: Clinically useful birth weight predictions can be made in SGA fetuses, although no particular formula estimates birth weight significantly more accurately than any other.

Birth Weight↗
PubMed1993

Fetal blood sampling from intrahepatic vein versus cord insertion: effect on pH and blood gases.

OBJECTIVE: To determine whether venous pH, base excess, and blood gas values collected by antenatal ultrasound-guided sampling from the fetal intrahepatic vein (intra-abdominal umbilical vein, portal sinus, or portal vein) differ from those obtained from the placental cord insertion. METHODS: Retrospective analysis was done of 1053 clinically indicated fetal blood sampling procedures performed between 1988-1992. One hundred sixty-eight appropriate for gestational age (AGA) singleton fetuses were identified after exclusion of those with conditions believed likely to have impaired fetal blood gas status. Fetal venous pH, carbon dioxide pressure, oxygen pressure, and base excess from 52 samplings at the intrahepatic vein were compared cross-sectionally to those from 116 samplings at the placental cord insertion, using analysis of covariance to correct for gestational age. RESULTS: There was no systematic difference in the blood gas or acid-base values between the two sites of fetal venous blood sampling. CONCLUSIONS: Acid-base and blood gas status in AGA fetuses is not affected by the site of sampling. Values obtained at the intrahepatic vein may be interpreted using reference ranges derived from sampling at the placental cord insertion.

Acid-Base Imbalance↗
PubMed1993

Amiodarone given by three routes to terminate fetal atrial flutter associated with severe hydrops.

BACKGROUND: We describe the concurrent administration of amiodarone using three different routes in order to provide: 1) rapid and adequate fetal loading without giving unduly high doses to the mother, and 2) a maintenance dose to the fetus without risking repeated invasive procedures. CASE: Rapid atrial flutter was seen on ultrasound in a fetus with severe hydrops at 27 weeks' gestation. Following failed transplacental therapy with sotalol and flecainide, amiodarone was administered to the fetus via the intravenous, intraperitoneal, and transplacental routes. Conversion to sinus rhythm and resolution of hydrops followed this treatment. CONCLUSION: Combined triple-route administration of amiodarone to the fetus can be effective in treating supraventricular tachycardia and may have a role in the management of life-threatening fetal arrhythmias refractory to transplacental therapy.

Adult↗
PubMed1992

The melanin-concentrating hormone system of the rat brain: an immuno- and hybridization histochemical characterization.

In addition to a nonadecapeptide homologous to the teleost melanin-concentrating hormone (MCH), the amino acid sequence predicted from a rat prepro-MCH (ppMCH) cDNA suggested that at least one (neuropeptide EI, or NEI), and possibly a second (NGE), additional neuropeptide may be encoded by this precursor. Cross-reactivity with epitopes of NEI or NGE can account for reported localization of alpha-MSH, rat CRF, and human GRF in rat dorsolateral hypothalamic neurons. We have used antisera raised against rat MCH and NEI in immunohistochemical studies at the light and electron microscopic levels, along with hybridization histochemical localization of ppMCH mRNA, to define the organization of this system. As expected, ppMCH mRNA is prominently expressed in cells in the lateral hypothalamic area and zona incerta. The MCH and NEI peptides were extensively colocalized in neurons in both of these areas. In addition, smaller cell groups in the olfactory tubercle and pontine tegmentum were also positively hybridized for ppMCH mRNA and immunostained for MCH and NEI. Fibers stained for MCH and NEI were similarly, and very broadly, distributed throughout the central nervous system in patterns that generally conformed with known projection fields of the lateral hypothalamic area and zona incerta. A differential distribution was seen in at least one region, the interanterodorsal nucleus of the thalamus, which contained a prominent terminal field stained for MCH but not NEI. At the electron microscopic level, MCH-stained perikarya displayed a prominent staining associated with the Golgi apparatus; this was not encountered in NEI-stained cells. Both peptides were distributed similarly in terminals in the lateral hypothalamic area and median eminence, with staining associated principally with dense-cored vesicles. The results suggest that ppMCH-derived peptides may serve as neurotransmitters or modulators of prominence in a surprisingly expansive projection field of incerto-hypothalamic neurons. The terminal distributions of this system seem most compatible with functional roles in generalized arousal and sensorimotor integration, processes previously implicated as being subject to modulation by the lateral hypothalamic area.

Animals↗
PubMed1992

Effect of activin A on globin gene expression in purified human erythroid progenitors.

The regulatory control of human erythropoiesis through a purified protein, activin A, was examined. Previous studies using mixed populations of bone marrow cells suggested that activin A has an indirect effect on cellular proliferation and DNA synthesis of erythroid progenitors through the mediation of accessory cells. In present studies, the cultures of purified erythroid progenitors were used to examine the effect of activin A on globin gene expression. Human erythroid burst-forming units (BFU-E) were partially purified from peripheral blood, and after 8 days of culture the cells generated consisted mainly of erythroid colony-forming units (CFU-E). It was found that the subsequent 7-day cultures of these purified progenitors yielded similar numbers and size distributions of erythroid colonies, regardless of the presence of activin A in the cultures. In addition, these erythroid progenitor cells were responsive, in terms of stimulation of DNA synthesis, to the addition of erythropoietin, but not to treatment by activin A. Therefore, once the erythroid progenitors are depleted of accessory cells, activin A has little effect on both the proliferation and the DNA synthesis of these progenitors. However, when these purified erythroid progenitors were cultured in the presence of activin A, the levels of all alpha, beta, and epsilon globin transcripts and hemoglobins were significantly increased. In addition, disuccinimidyl suberate was found to chemically cross-link 125I-activin A to cell surface binding proteins (45 to 54 Kd) in both purified erythroid progenitors and K562 cells. The labeling of these binding proteins was specifically inhibited by the presence of unlabeled activin A, but not transforming growth factor-beta. These results suggest that, in addition to its indirect effect on DNA synthesis and cellular proliferation of erythroid progenitors, activin A directly affects the levels of globin mRNAs and hemoglobins in developing human erythroid cells through its specific surface binding receptor(s).

Activins↗
PubMed1992

Time course of movement planning: selection of handgrips for object manipulation.

A goal of research on the cognitive control of movement is to determine how movements are chosen when many movements are possible. We addressed this issue by studying how subjects reached for a bar to be moved as quickly as possible from a home location to a target location. Ss generally grabbed the bar in a way that afforded a comfortable posture at the target location (the end-state comfort effect) and with the thumb toward the end of the bar that would be aligned with the target (the thumb-toward bias). The data suggested that subjects chose handgrips by retrieving instances of previous reaches, not by carrying out computations that treated candidate reaches as new behavioral events.

Acceleration↗
PubMed1992

Fetal breathing movements in oligohydramnios are not increased by aminoinfusion.

OBJECTIVE: To determine whether fetal breathing movements (FBM) in pregnancies with oligohydramnios change with restoration of amniotic fluid volume. DESIGN: A prospective experimental study. SETTING: Fetal Medicine Unit, tertiary referral hospital. SUBJECTS: 16 women with singleton pregnancies complicated by severe oligohydramnios. INTERVENTIONS: Restoration of amniotic fluid volume by transabdominal amnioinfusion. Controls comprised pregnancies in which infused fluid leaked vaginally, so that oligohydramnios was not corrected. MAIN OUTCOME MEASURES: Change in total breathing movements, change in FBM incidence derived from 40 min recordings immediately before and after amnioinfusion. RESULTS: There was no significant difference in the change in total breathing movements or in the change in incidence of FBM between the 10 pregnancies in which amniotic fluid volume was restored, and the other six in which fluid leaked after infusion and volume was not restored. In both groups, there was no significant change with infusion in number of FBM (mean change -72, 95% CI -218 to +74 in the fluid-retained group and -64, 95% CI -273 to +145 in the fluid-leaked group) and incidence of FBM (median change -2.5%, range -27 to +10 in the fluid retained group and -4.5%, range -34 to +15 in the fluid-leaked group). CONCLUSIONS: This study suggests that restitution of amniotic fluid volume in human pregnancies complicated by severe oligohydramnios does not acutely alter the incidence of FBM. These data support an increasing literature suggesting that impairment of fetal breathing is not the mechanism for oligohydramnios-related pulmonary hypoplasia.

Amnion↗
PubMed1992

Regulation of FSH beta messenger ribonucleic acid levels in the rat by endogenous inhibin.

This study investigated the role of endogenous inhibin in regulating FSH beta mRNA levels subsequent to the gonadotropin surge in the immature, estradiol (E2)-treated female rat. Rats which undergo FSH surges on day 29 have low to undetectable levels of FSH beta mRNA at 0900 h on day 30, whereas those treated simultaneously with E2 and progesterone (P) implants to block these surges have considerably higher levels of FSH beta mRNA. In view of the profound inhibitory effect of inhibin on FSH beta mRNA, we examined the possibility that increased inhibin secretion is responsible for the decline in FSH beta mRNA levels on the morning after the FSH surge by immunoneutralization of endogenous inhibin. Twenty-eight day-old rats which received E2 and blank (B1) or P implants were injected iv with 0.4 ml of a potent anti-rat inhibin serum (anti I alpha, prepared in sheep against rat inhibin alpha (1-26)-Tyr27 coupled to human alpha-globulins) or normal sheep serum at 1700 to 1830 h on day 29 and were killed at 0900 h on day 30. Animals which received the inhibin antiserum showed significantly (P less than 0.001) elevated serum FSH levels (22.9 +/- 1.9 ng/ml [E2 + B1] and 17.1 +/- 0.6 ng/ml [E2 + P]) compared to those which received normal serum (4.4 +/- 0.1 [E2 + B1] and 4.2 +/- 0.1 [E2 + P]). Serum LH was undetectable (less than 0.6 ng/ml) in all groups. Free glycoprotein alpha-subunit was also increased (P less than 0.001) by antiserum to inhibin in E2 + B1-treated rats but was significantly suppressed by P after injection of either normal serum or anti I alpha. Total pituitary RNA was extracted and hybridized to cDNA probes for rat FSH beta, LH beta, and the common alpha-subunit by Northern blot analysis; RNA levels were normalized with beta-actin or cyclophilin probes. As expected, in rats which received normal serum, FSH beta mRNA levels were about 4-fold higher after treatment with E2 + P implants than after treatment with E2 + B1 implants. However, injection with anti-inhibin serum resulted in a striking elevation of FSH beta mRNA levels: 13-fold in animals treated with E2 + B1 implants and 5-fold in animals treated with E2 + P implants. There were no significant differences in levels of LH beta or alpha-subunit mRNAs between rats which received anti-inhibin or normal serum although there was a 30-40% decrease in alpha mRNA after P treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗