Based on minimal excretion of other phenothiazine derivatives, it appears that occasional short-term use of promethazine for the treatment of nausea and vomiting poses little risk to the breastfed infant. With repeated doses, observe infants for excess sedation. Because promethazine can lower basal prolactin secretion, promethazine might interfere with the establishment of lactation if given during labor before lactation is well established or with a sympathomimetic such as pseudoephedrine. An antiemetic without potent histamine blocking action is preferred in nursing mothers.

The objective of this study was to evaluate the effect of supplementation with bee pollen (BP) and propolis (PRO) on productive performance, Eimeria oocyst counts in feces, blood metabolites, and the meat quality of growing rabbits. A total of 160 hybrid rabbits (California × New Zealand) of 30 days of age and 643 ± 8.0 g body weight (BW) were assigned to four treatments with 10 replicates each (four rabbits/replicate). The treatments were as follows: (1) CON: rabbits fed basal diet and not supplemented with BP or PRO; (2) BP500: CON + BP (500 mg/kg BW); (3) PRO50: CON + PRO (50 µL/kg BW); and (4) BP + PRO: CON + BP (500 mg/kg BW) + PRO (50 µL/kg BW). Higher daily weight gain (p = 0.04) and lower feed conversion rate (p = 0.03) were observed in rabbits supplemented with PRO50. In addition, supplementation with PRO50 and BP + PRO reduced the amount of Eimeria oocysts per gram of feces (p < 0.05). Most hematological and serum biochemical parameters were similar in rabbits of all treatments. Protein content, collagen, and meat color were similar between treatments. In conclusion, propolis supplementation (50 µL/kg BW) can prevent coccidiosis and act as a natural growth promoter in rabbits without affecting animal health and meat quality.

Colon cancer is the fourth and third most common cancer, respectively in men and women worldwide and its incidence is on the increase. Stress response has been associated with the incidence and development of cancer. The catecholamines (CA), adrenaline (AD) and noradrenaline (NA), are crucial mediators of stress response, exerting their effects through interaction with α- and β-adrenergic receptors (AR). Colon cancer cells express β-AR, and their activation has been implicated in carcinogenesis and tumor progression. Interest concerning the efficacy of β-AR blockers as possible additions to cancer treatment has increased. The aim of this study was to investigate the effect of several AR agonists and β-blockers following cell proliferation of HT-29 cells, a human colon adenocarcinoma cell line. For this purpose, HT-29 cells were incubated in the absence (control) or in the presence of the AR-agonists, AD, NA and isoprenaline (ISO) (0.1-100 µM) for 12 or 24 h. The tested AR agonists revealed proliferative effects on HT-29 cells. In order to study the effect of several β-blockers following proliferation induced by AR activation, the cells were treated with propranolol (PRO; 50 µM), carvedilol (CAR; 5 µM), atenolol (ATE; 50 µM), or ICI 118,551 (ICI; 5 µM) for 45 min prior, and simultaneously, to incubation with each of the AR agonists, AD and ISO, both at 1 and 10 µM. The results suggested that adrenergic activation plays an important role in colon cancer cell proliferation, most probably through β-AR. The β-blockers under study were able to reverse the proliferation induced by AD and ISO, and some of these blockers significantly decreased the proliferation of HT-29 cells. The elucidation of the intracellular pathways involved in CA-induced proliferation of colon cancer cells, and in the reversion of this effect by β-blockers, may contribute to identifying promising strategies in cancer treatment.

Understanding the relationship between energy nutrients compositions in a diet and appetite-controlling substances is essential for providing sound advice to anyone attempting to control body weight. Appetite is known to be affected by various hormones, ghrelin and peptide tyrosine-tyrosine (PYY), which are related to the compositions of a diet. The purpose of this study was to investigate the effects of compositions of energy nutrients in the diet on the levels of postprandial appetite-related hormones and satiety in healthy adult women. Ten subjects (BMI: 18.5-22.9 kg/m(2)) were recruited and assigned to three iso-coloric breakfast meals with different compositions of energy nutrients, regular meal (RM, CHO: 60%, Pro: 20%, Fat: 20%), high protein meal (HPM, CHO: 30%, Pro: 50%, Fat: 20%), and high fat meal (HFM, CHO: 30%, Pro: 20%, Fat: 50%). Blood levels of ghrelin, PYY, insulin and leptin and satiety were assessed at baseline, 30, 60, 90, 120, and 180 min following the consumption of each meal. There was no significant difference in the fasting blood hormones among the subjects taking each meals at baseline. Blood levels of ghrelin and insulin changed significantly following the consumption of each meal (p<0.05) over time, however no significant difference was shown between experimental meals until 180 min. Blood levels of PYY and leptin were not changed following the ingestion of each meals. In conclusion, the composition of energy nutrients in a diet had no effect on the postprandial plasma levels of ghrelin, PYY, insulin and leptin as well as satiety in healthy adult women.

Nocardioides sp. strain JS614 grows on the C(2) alkenes ethene (Eth), vinyl chloride, and vinyl fluoride as sole carbon sources. The presence of 400-800 microM ethene oxide (EtO) extended the growth substrate range to propene (C(3)) and butene (C(4)). Propene-dependent growth of JS614 was CO(2) dependent and was prevented by the carboxylase/reductase inhibitor 2-bromoethanesulfonic acid, sodium salt (BES), while growth on Eth was not CO(2) dependent or BES sensitive. Although unable to promote growth, both propene and propene oxide (PrO)-induced expression of the genes encoding the alpha subunit of alkene monooxygenase (etnC) and epoxyethane CoM transferase (etnE) to similar levels as did Eth and EtO. Propene was transformed by Eth-grown and propene-grown/EtO-induced JS614 to PrO at a rate 4.2 times faster than PrO was consumed. As a result PrO accumulated in growth medium to 900 microM during EtO-induced growth on propene. PrO (50-100 microM) exerted inhibitory effects on growth of JS614 on both acetate and Eth, and on EtO-induced growth on Eth. However, higher EtO concentrations (300-400 microM) overcame the negative effects of PrO on Eth-dependent growth.

Elevated concentrations of unconjugated bilirubin (UCB) are responsible for neonatal jaundice and can eventually lead to kernicterus or death. The molecular mechanism of UCB toxicity is incompletely elucidated. The purpose of this study was to analyze changes in gene regulation mediated by UCB to determine novel pathways that contribute to UCB-mediated toxicity. We employed microarray analysis to determine changes in gene regulation mediated by UCB at both pro- (50 microM) and antioxidant (70 nM) concentrations in Hepa 1c1c7 cells at 1 and 6 h. The changes observed in select genes were validated with qPCR. Using immunoblot analysis, we validated these changes at the protein level for select genes and documented the activation of two proteins involved in the endoplasmic reticulum (ER) stress pathway, eIF2 alpha and PERK. Following treatment with 50 microM UCB, microarray analysis revealed the upregulation of many genes involved in ER stress (ATF3, BiP, CHOP, Dnajb1, and Herp). We demonstrate that upregulation of the proapoptotic transcription factor CHOP results in increased intracellular protein content. It was determined that activation of proteins involved in ER stress was an early event in UCB toxicity as eIF2 alpha and PERK were both phosphorylated and activated by 1 h posttreatment. We also demonstrate that procaspase-12 content, a proposed initiator caspase in ER stress-mediated apoptosis, is decreased by 4 h posttreatment. In conclusion, this study demonstrates that elevated concentrations of UCB (50 microM) are able to activate select components of the ER stress pathway in Hepa 1c1c7 cells, which may contribute to UCB-mediated apoptosis.

We evaluated the effects of five clinically used antimuscarinic agents for overactive bladder (OAB) treatment on in vivo muscarinic receptor binding in rat brain by quantitative autoradiography. There was a dose-related decrease in in vivo specific +N-[11C]methyl-3-piperidyl benzilate ([11C](+)3-MPB) binding in each brain region of rats 10 min after i.v. injection of oxybutynin, propiverine, solifenacin, and tolterodine. Rank order of the i.v. dose for 50% receptor occupancy (RO(50)) of antimuscarinic agents in rat brain regions was propiverine > solifenacin > tolterodine, oxybutynin. There was a good linear relationship between in vivo (pRO(50) values in the rat hippocampus) and in vitro (pK(i) values in human M(1) receptors) receptor binding activities of propiverine, solifenacin, and tolterodine. The observed RO(50) value of oxybutynin was approximately five times smaller than the predicted in vitro K(i) value. The dose ratios of antimuscarinic agents for the brain receptor occupancy (RO(50)) to the inhibition of carbachol- and volume-induced increases in intravesical pressure (ID(50)), which reflects in vivo selectivity for the urinary bladder over the brain, were greater for solifenacin, tolterodine, and propiverine than oxybutynin. Darifenacin displayed only a slight decrease in specific [11C](+)3-MPB binding in the rat brain regions, and it was not dose-related. In conclusion, in vivo quantitative autoradiographic analysis of brain muscarinic receptor occupancy may provide fundamental basis for managing central nervous system (CNS) side effects in antimuscarinic therapy for OAB. It is suggested that in the treatment of OAB, CNS side effects can be avoided by antimuscarinic agents with high selectivity for the urinary bladder over the brain.

Venous or arterial thrombosis, abortion, and the presence of antiphospholipid antibodies (aPL) define the criteria for the antiphospholipid syndrome (APS). A heterogeneous group of antibodies against phospholipids and plasma proteins may influence several coagulation pathways and lead to thrombophilia. We investigated the presence of antibodies to thrombin (Thr) in patients with aPL and reviewed their clinical manifestations. IgG and IgM titers of aPL were measured by ELISA (Aesku.Diagnostics, Wendelsheim, Germany). Lupus anticoagulants (LA) were measured according to the criteria of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis. One hundred twenty patients were identified with LA or anticardiolipin (aCL). Of the 120 patients, 98 (82%) had primary APS and 22 (18%) had secondary APS. Further, 76/120 (63%) were suffering from thromboembolic manifestations, mostly venous thrombosis. Anti-thrombin-IgG was detected in 20%, and anti-thrombin-IgM was detected in 23% of the patients. The presence of anti-thrombin antibodies was closely related to the presence of anti-beta(2)-glycoprotein-I (beta(2)-GP-I) (96%), aCL (97%), and LA (87%), and less well to the presence of anti-phosphatidylserine/prothrombin (Ser/Pro) antibodies (71%) or anti-prothrombin antibodies (Pro) (50%). Sixty-seven percent of the patients with anti-Thr-IgG suffered from thromboembolic complications, mostly arterial thrombosis. The rate of thrombosis was higher for these patients than for patients with anti-beta(2)-GP-I antibodies (37/60, 62%), LA (50/79, 63%), or anti-Ser/Pro antibodies (18/28, 64%). Anti-thrombin antibodies were found in 20% of patients with aPL; 67% of these patients were admitted with thrombotic manifestations of APS. The presence of anti-thrombin antibodies was closely associated with the presence of aCL and anti-beta(2)-GP-I antibodies. The sensitivity of the test for anti-thrombin antibodies for the diagnosis of APS was higher than the sensitivity of the anti-prothrombin assay and similar to the sensitivity of the anti-Ser/Pro assay.