It was also reported that DIF influenced crop quality. For example, carbohydrate content de- creased dramatically in Lilium longiflorum under negative DIF (Miller et al. 1993). The sucrose, lupeose and starch content of cucumber leaf sig- nificantly increased under positive DIF (Miao et al. 2009). However, the mechanism by which DIF influenced crop quality was unclear. Endogenous hormones were reported to influence quality of crops. For example, Xie et al. (2003) indicated that endogenous hormones under post-anthesis drought might indirectly affect protein and starch accumulation in grains. Therefore, it was possible that DIF regulated fruit quality through endog- enous hormones.
PCBs also appear to act on a number of endogenous hormones, which in turn could mediate or confound rela- tionships with diabetes. A recent paper of ours examined relationships of PCB exposure at a capacitor manufactur- ing plant with diabetes and endogenous hormones in post -menopausal women . We found inverse associations of PCB levels with levels of sex-hormone binding globulin (SHBG), follicle stimulating hormones (FSH) and dehyr- droepiandrosterone sulfate (DHEAS). PCB exposure was also positively related to diabetes independent of potential confounders and measured hormones and diabetes was significantly and inversely associated with levels of trio- dothyronine (T3) uptake, FSH and DHEAS independent of PCB exposure . This paper explores associations of PCB exposure with diabetes and endogenous hormones in men previously exposed at the same capacitor manufac- turing plant.
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Grape varieties respond to decrease in soil water status by stomatal closure and reduced shoot growth with simultaneous increase in root growth. Most of the water deficit responses are known to be regulated by endogenous hormonal contents like abscissic acid (ABA) and cytokinins. To determine how these endogenous hormones are related to changes in shoot and root morphology, four grape genotypes were grown in pots and subjected to different levels of soil moisture stress for 14 days. None of the genotypes could survive beyond 4 days under 100 % stress conditions. There was an increased accumulation of ABA and corresponding decrease in cytokinins at 50 % stress compared to control (100 % irrigation). Among the genotypes tested Flame Seedless had highest ABA and lowest cytokinin levels and it also had highest root to shoot length ratio and root to shoot dry weight ratio. It is presumed that the reduction in shoot growth and stomatal conductance observed may be due to their ability to synthesize and accumulate ABA with the onset of soil moisture stress.
The effect of seed presoaking with different concentrations of growth bio-regulators (indole acetic acid, gibberellic acid and kinetin) on productivi- ty and some biochemical and physiological aspects of yielded seeds of cowpea ( Vigna sinensis L.) was investigated. Generally, application of growth regula- tors stimulated yield and yield quality of cowpea plants as compared to con- trol plants through inducing a massive increase in number of pods/plants, seed biomass, pod length and number of seeds. In addition, results of this study showed that these growth regulators increased protein content and total soluble sugars in cowpea yielded seeds. Finally, it is evident from the present data that application of kinetin appeared to be the most effective hormone in stimulated productivity endogenous hormones and biochemical aspects in yielded seeds of cowpea plants.
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are vital for the abscission of plant parts. Additionally, evidences supported by their external applications and also the fact that ethylene and polyamines compete for common intermediate S-adenosine methionine (SAM) for the biosynthesis (Kuznetsov and Shevyakova 2007) also point towards the polyamine role in abscission. High temperature has been reported to increase ethylene production and abscisic acid accumulation and alter the levels of other important hormones including polyamines (Huberman et al. 1997, Banowetz et al. 1999, Klueva et al. 2001, Kuznetsov et al. 2006, Wahid et al. 2007, Toh et al. 2008, Cheng et al. 2009). In the present investigation, attempts have been made to study the changes in endogenous hormonal levels and polyamines in floral organs of two capsicum cultivars differing in sensitivity to high temperature with the objective to decipher information on factors linked to the floral abscission induced under high temperature conditions.
measured hemolytic plaque formation (per million splenic leukocytes) of cells which passed through columns of hormone-carrier-Sepharose beads (i.e., those cells that failed to bind). As compared with control (no column) cells, the number of plaque-forming cells was substantially reduced by passage through histamine, epinephrine, isoproterenol, and prostaglandin-E 2 columns. Plaque-forming cells were not significantly reduced by passage through carrier Sepharose (another control) or norepinephrine- and prostaglandin-F 2a - carrier Sepharose columns. Thus, the ability of an insolubilized hormone preparation to subtract plaque-forming cells roughly correlated with the presence of pharmacologic receptors for the corresponding free hormones, as judged by stimulation of cyclic AMP accumulation in the same cells, reported previously. Both 19S and 7S plaque-forming cells were subtracted by columns prepared from pharmacologically active hormones, but none of the insolubilized hormones stimulated accumulation of intracellular cyclic AMP. The cell membrane phenomenon that allows adherence to a given hormone-carrier-bead column may be identical with the cell receptor.
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insolubilizing the hormones and incubating them with the cells. Histamine, norepinephrine, and prostaglandin E 2 (PGE 2 ) were conjugated to either of two types of carrier: (bovine or rabbit) serum albumin or a random copolymer of DL-alanine and L-tyrosine. The conjugates were linked to agarose beads (Sepharose) and the resultant drug-conjugate-beads were incubated with leukocytes. Norepinephrine (when linked to its carrier via glutaraldehyde) and histamine preparations bound the majority of leukocytes. The binding appeared to be specific for the hormones tested. For example, the binding by histamine-rabbit serum albumin-Sepharose was prevented or reversed by high concentrations of histamine and histamine antagonists, but not by catecholamines or their pharmacologic antagonists. Similarly, binding of cells to the norepinephrine conjugate was inhibited by some
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It is still a challenge to estimate the magnitude of the clinical impact of the observed effects on sex hormones, since there are no absolute cut-off values defined that cor- respond with a certain change in future breast cancer risk. Until now, it is assumed that the distributions and rank- ings of sex hormone levels, rather than the absolute values, correspond with breast cancer risk. Observational studies that linked sex hormone levels to breast cancer risk mainly show that women whose hormone levels are in the highest quintiles of the distribution have an up to twofold increased risk when compared with women with levels in the lowest quintiles [12, 33]. However, the abso- lute values corresponding to these quintiles vary largely between studies. For example, the Endogenous Hormones and Breast Cancer Collaborative Group evaluated nine prospective studies that measured sex hormones in post- menopausal breast cancer cases and samples of healthy postmenopausal controls . Median hormone levels varied substantially; for example, estradiol levels differed up to fivefold between the studies, ranging from 22 pmol/l to 101 pmol/l in control women. Besides population het- erogeneity (in ages, BMI, and other determinants of hor- mone levels such as reproductive factors and nutritional habits), the large variation in absolute values is probably mainly caused by differences in laboratory assays [34, 35]. These issues might, in addition to the different interven- tion programs, explain the differences in magnitude of effects across the studies included in this meta-analysis.
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ABSTRACT Testicular cancer is the most common type of malignancy in men aged 15–40 years. Although its incidence has increased over the past 40 years in most countries, the reasons for this rise are unclear. It has been suggested that a relative excess of endogenous estrogens during pre- natal life and/or later exposures to various occupational and environmental estrogenic chemicals such as organochlorine compounds may play a causal role in the etiology of testicular cancer, but the issue is still open to further research. The purpose for this review is to summarize the epidemio- logic literature about hormonal factors, endogenous hormones and environmental xenoestrogens, and testicular carcinogenesis. Future studies need to (a) consider the possible synergistic effect of exposure to environmental xenoestrogens and sex hormones, (b) focus on the most vulnerable life stages of exposure to endocrine disruptors and testicular cancer risk, (c) assess the possible additive role of androgen secretion occurring during puberty in tumor progression, and (d) consider more systematically gene–environment interactions.
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natural conditions, the seeds of Viburnum sargentii are difficult to germinate. 2) Under sand storage for 8 months, the germination rate of untreated seeds was 33%. Puncture and peeling treatment could significantly increase the germination rate, and the germination rate of seeds treated with puncture was 92%, and that treated with peel was 98%. 3) Seed germination was accompa- nied by the decrease in macromolecular substances such as soluble sugar, so- luble starch, and soluble protein. 4) The dynamic changes of hormones dur- ing seed germination conform to the hypothesis of “three factors”. 5) The treatment of puncture and peeling increased the content of endogenous hor- mones promoting germination, decreased the endogenous hormones inhi- biting seed germination, and increased the ratio of (IAA + GA + ZR)/ABA or GA/ABA. The seeds of Viburnum sargentii have obvious dormancy characte- ristics. Under the condition of sand storage, both pricking and peeling treat- ment can effectively promote the process of breaking dormancy, and the ef- fect of peeling treatment is better.
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Our study has both strengths and limitations. This is the largest prospective study to date, although we had limited power in analyses stratified by menopausal status at diagnosis (particularly postmenopausal cases). Our samples were carefully timed in the menstrual cycle. We used highly specific and sensitive assays, and laboratory CVs were excellent. Additionally, we are among the first to present data for premenopausal hormones and breast cancer by tumor hormone receptor status. Although we are limited to samples collected during one menstrual cycle, a prior reproducibility study provides evidence of reasonable stability across a three-year period (follicular estradiol: 0.38 to DHEAS: 0.86), except for luteal proges- terone (ICC = 0.29) . We also used these reproduci- bility data to correct for measurement error and showed that several of the associations may be substantially stronger than observed.
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Another important effect of estrogen relies on renal nitric oxide (NO) synthesis and/or bioavailability. The NO system consists of three distinct NO synthase (NOS) isoforms, encoded by three distinct genes, includ- ing neuronal (nNOS or NOS-1), inducible (iNOS or NOS-2) and endothelial (eNOS or NOS-3) . All of the NO isoforms have been identified in the kidney . NO plays numerous physiological roles in the kidney, including control of renal and glomerular hemodynamics, through interference at multiple physiologically critical steps of nephron function . Estrogens may upregulate eNOS mRNA in renal medullary cells, increase NOS activity and upregulate eNOS protein levels . Corrob- orating these data, Pérez-Torres  demonstrated that in ovariectomized female rats with metabolic syndrome, eNOS expression was significantly lower than in intact animals, indicating that female sex hormones can modu- late the renal synthesis of NO. However, changes in NOS expression do not always correlate with NO bioavailability, superoxide anions react extremely rapidly with NO, gener- ating peroxynitrite. Under physiological conditions, this interaction is minimized by endogenous antioxidant defenses, such as superoxide dismutase activity . Nevertheless, during conditions of increased oxidative stress, such as hypercholesterolemia , these defenses may not be able to compensate and protect the cells against reactive oxygen species (ROS)-induced damage. In our study, ApoE mice present higher levels of DHE fluorescence in the glomerulus, indicating an increased superoxide anion generation. However, in both ovariec- tomized groups, especially in ApoE OVX animals, glomerular oxidative stress was further augmented, indicating a protective role for endogenous female sex hormones on ROS generation. Corroborating our data, Borras et al.  reported that females have greater concentrations of antioxidant enzymes, resulting in lower production of ROS and that ovariectomy increases ROS generation. Strehlow et al.  reported that 17-β estradiol upregulates MnSOD and extracellular SOD expression and activity. Therefore, it seems that increased oxidative stress may be a potential mechanism by which the removal of endogenous female sex hormones resulted in renal dysfunction in ApoE mice.
To our knowledge, this is the first epidemiologic study that directly related adolescent sex hormone levels with adult breast density. Previous studies used sex hormone data collected from middle-aged and older women [6–21]. The association between premenarcheal DHEAS and adult %DBV in our study was nonlinearly positive. In ana- lysis restricted to participants not using hormonal con- traceptives at DISC06 visits when breast density was measured, %DBV increased monotonically across increas- ing quartiles of premenarcheal DHEAS from 16.4 % to 20.9 %, 21.7 %, and 26.2 %. Thus, even though we adjusted for duration of hormone use in our multivariable model, our nonlinear results might be due to residual confound- ing by current hormone use. This positive association is consistent with results from one study of premenopausal women . Our findings for postmenarcheal DHEAS con- centrations are similar to those from most studies in older women that reported relatively flat associations [12–14, 21]. The breast matures mostly before menarche under the influence of sex hormones and growth factors, and DHEAS may have its greatest effect on breast morph- ology at this time of expansion of the breast ductal architecture. DHEAS can be metabolized to estrogens and has been shown to have estradiol-like proliferative effects in a low-estrogen environment , typical of childhood and early puberty . In young girls approaching pu- berty, prior to activation of the hypothalamic-pituitary- ovarian (HPO) axis, adrenal androgens including DHEAS can be metabolized to estrogens in adipose tissue . Peripheral conversion of adrenal androgens to estrogens may explain earlier breast development independent of changes in ovarian hormones in recent birth cohorts  and isolated breast development that occurs without acti- vation of the HPO in some girls . DHEAS is also posi- tively associated with growth factors during adolescence  that may partly regulate breast development [58–60].
Mitochondrial cytopathies, especially Kearns-Sayre and MELAS syndromes, have been reported to be the cause of primary dysthyroidism in several publications, three cases of which were autoimmune hyperthyroidism [8,9,45-48]. Given the frequency of autoimmune dys- thyroidism in the general population, a fortuitous asso- ciation between mitochondrial cytopathies and thyroidopathies cannot be ruled out. Indeed, A3243G mitochondrial mutation does not actually occur signifi- cantly more often in patients with autoimmune diseases. We personally observed one-third of cases with hypothyroidism, 50% of which displayed a goiter or a pituitary component in a series of respiratory deficient patients (unpublished observation). Testing should always be done for both origins. Thyrotropic insuffi- ciency is probably underestimated. Energy defects could impair thyroperoxidase, lowering the production of thyr- oid hormones, which themselves are involved in mito- chondrial metabolism, therefore worsening the mitochondrial dysfunction.
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Many epidemiologic studies have indicated that endo- genous sex hormones, particularly estrogens, play an important role in the etiology of breast cancer . A pooled analysis of nine prospective studies showed that higher estrogens and their androgen precursors were associated with a higher risk of breast cancer in postme- nopausal women . Differences in sex hormone levels among populations might therefore contribute to the variation in breast cancer incidence across countries and regions. Clarification of the difference in sex hormone levels among populations and their determinants might help our understanding of the etiology and prevention of breast cancer.
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Sunflower (Helianthus annuus L.) seeds (Parsun-1) were obtained from National Agriculture Research Center, Islamabad, Pakistan. Seeds were germinated in earthen pots (30 40 cm) having soil contained sand, soil and cow dung (1:1:1) along with chemical fertilizers i.e. Diammonium phosphate and urea. After a week seeds were germinated and at stage of five leaves stage thinning was performed and selected one plant per pot. Plants were watered daily. At five- leaf stage biofertilizers (PSB, Rhizobium and EM Bokashi) were applied to the plants and after a week of this treatment different concentrations of nickel were applied to the plants instead of water and given to plants whenever there was a need of water. Accumulation of nickel was determined at two stages i.e. 65 days after treatment of nickel and 80 days after treatment of nickel while the endogenous level of hormones was determined after 65 days of treatment of nickel. Experiment was a randomized complete block designed performed in green house, three replicate plants were used for each treatment in all experiments. Statistical analyses were performed using M-stat program, analysis of variance were performed to see the significant effect of these treatment and DMRT was performed to distinguish difference among different treatments.
Steroid Occurrence on Feedlot Surfaces. Prior to placement of the cattle in the pens during each year of the study, the soil in the feedlot pens was scraped down to the clay layer and replaced with fresh soil obtained from another location at the research facility. Samples from the fresh soil were collected and analyzed for steroid hormones (Table 2 and SI Table S8, day 0). In 2007, estrone and estriol were detected in the clean soil at maximum concentrations of 0.26 ng/g dw and 6.4 ng/g dw, respectively (Table 2). In 2008, 4-and- rostenedione (max. concentration 1.9 ng/g dw); androsterone (max. concentration 0.82 ng/g dw); α-zearalenol (max. con- centration 0.34 ng/g dw); and progesterone (max. concen- tration 1.7 ng/g dw) were detected in the clean soil. Because the fill soil was obtained from an area of the research facility that had historically had manure applied, it is possible that this is the source of the steroids detected in the fill soil. Alter- natively, the pens utilized in this study have been used for animal production for over 40 years, and although the pens were scraped down to the clay layer, some residual soil may have remained in the pens and been mixed with the back- ground soil. There were no statistically significant differences (p < 0.05; Mann − Whitney test) in the concentration of steroid
Our result showed no statistically significantly correlation between serum estradiol and CRP, a result that mimicked that of Sowers et al. (72) who reported estradiol was not associated with high-sensitivity C-reactive protein (CRP). While our result was not matched with result of Maggio et al. (73) who found that total testosterone, and E2 were all significantly associated with CRP in elderly postmenopausal women. Also Stork et al. (74) `who found a positive association between estradiol and CRP concentrations in postmenopausal women. And mentioned that the source of the CRP from adipose tissue and due to ageing and menopause was a natural protective mechanism reducing the inflammatory potential by decreasing the level of circulating estrogens and androgens and substitution of hormones using hormone replacement therapy may be not be a favorable strategy for improving the cardiovascular risk profile of postmenopausal women. Also Folsom et al. (75) who reported a positive association of estrone levels with CRP concentration in a study on postmenopausal women; however, controlling for obesity attenuated the findings.
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relief corresponds to a difference in VAS of 1.3–2 cm. Only when given at 2 am , did fentanyl cause a small but significant period of hyperalgesia following analgesia. No significant changes were observed for baseline pain, sedation, or the increase in end-tidal CO 2 . The variations in fentanyl’s antinociceptive behavior are well explained by a chronopharmacodynamic effect originating at the circadian clock in the hypothalamus. This may be a direct effect through shared pathways of the circadian and opioid systems or an indirect effect via diurnal variations in hormones or endogenous opioid peptides that rhythmically change the pain response and/or analgesic response to fentanyl.
suppressed with somatostatin and physiologic circulating levels of one or the other hormone were reproduced by exogenous infusion. The interaction of these hormones with insulin was evaluated by performing these studies in juvenile-onset, insulin-deficient diabetic subjects both during infusion of insulin and after its withdrawal. Infusion of glucagon (1 ng/kg-min) during suppression of its endogenous secretion with somatostatin produced circulating hormone levels of approximately 200 pg/ml. When glucagon was infused along with insulin, plasma glucose levels rose from 94 +/- 8 to 126 +/- 12 mg/100 ml over 1 h (P less than 0.01); growth hormone, beta-hydroxy-butyrate, alanine, FFA, and glycerol levels did not change. When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. Thus, under appropriate conditions, physiologic levels of glucagon can stimulate lipolysis and cause hyperketonemia and hyperglycemia in man; insulin antagonizes the lipolytic and ketogenic effects of glucagon more effectively than the hyperglycemic effect. Infusion of growth hormone (1 mug/kg-h) during suppression of its endogenous secretion with
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