PE Treatment Research Articles

RBCK1, a Protein Kinase CβI (PKCβI)-interacting Protein, Regulates PKCβ-dependent Function

RBCK1, a Protein Kinase CβI (PKCβI)-interacting Protein, Regulates PKCβ-dependent Function

Prune Extract (Prunus Domestica L.) Suppresses the Proliferation and Induces the Apoptosis of Human Colon Carcinoma Caco-2

Prunes are the dried fruits of certain cultivars of Prunus domestica L., and are recognized as a health food. The separated ethanol fraction from concentrated prune juice by DIAION HP-20 (PE) was investigated for cytotoxic effects on two different cancer cell lines in vitro. PE dose-dependently reduced the viable cell number of Caco-2, KATO III, but does not reduce the viable cell number of human normal colon fibroblast cells (CCD-18Co) used as a normal cell model. PE treatment for 24 h led to apoptotic changes in Caco-2 such as cell shrinkage and blebbed surfaces due to the convolutions of nuclear and plasma membranes and chromatin condensation, but this was not observed in CCD-18Co. PE induced nucleosomal DNA fragmentation typical of apoptosis in Caco-2 after 24 h of treatment. These results show that PE induced apoptosis in Caco-2. Furthermore, by Caco-2 treatment with H2O2 chelator catalase and Ca2+-chelator BAPTA/AM, the PE-induced cytotoxic pathway was completely blocked, and the viable cell number of Caco-2 was not affected.

Anti-obesity Effect of Pinellia ternata Extract in Zucker Rats

Pinellia ternata is known as the herb effective in removing dampness-phlegm, one of the causes of obesity in traditional Korean medicine. Pinellia ternata water extract (PE) was fed to rats after mixing with diet once a day (400 mg x kg(-1)) for 6 weeks. We investigated its effect on the thermogenesis and fatty acids oxidation with obese Zucker rats. We also determined the gene expression of uncoupling protein 1 (UCP1), peroxisome proliferators-activated receptor alpha (PPARalpha), and PPARgamma coactivator 1alpha (PGC1alpha). The PE treatment lowered the levels of triglyceride and free fatty acids (p<0.05) in blood of the obese rats and the body weight was also reduced slightly. It was also observed that PE significantly increased the expression of both UCP1 mRNA in brown adipose tissue (BAT) (p<0.001) and PPARalpha and PGC1alpha mRNA in white visceral adipose tissue (WAT) (p<0.05 and p<0.001, respectively), which may cause a reduction of obesity. These results suggested that PE would be able to affect anti-obesity through thermogenesis and fatty acid oxidation.

PE, a new sulfated saponin from sea cucumber, Exhibits anti-angiogenic and anti-tumor activities in vitro and in vivo

Here, we examined the in vitro and in vivo anti-angiogenesis and anti-tumor activities of PE, a new marine-derived compound. Inhibition of angiogenesis was assessed in vitro using proliferation, migration, adhesion, tube-formation and apoptosis assays in PE-treated HMECs and HUVECs. In vivo, CAM assays were used to assess inhibition effect of PE on physiological angiogenesis, and immunofluorescent microscopy was used to examine tumor microvessel density and apoptosis in PE-treated mouse tumor models. Finally, Western blotting analyses were performed to examine the effect of PE on VEGF signaling in HMECs. The results showed that PE inhibited proliferation of HMECs and HUVECs with IC50 values of 2.22°¿0.31 ?M and 1.98°¿0.32 ?M, induced endothelial cell apoptosis at concentrations < 2 ?M, induced dose-dependent suppression of cell migration, cell adhesion and tube formation in HMECs and HUVECs, and showed anti-proliferative activities against several tumor cell lines (IC50 values of ~ 4 ?M). In vivo, PE (5 nM/egg) suppressed spontaneous angiogenesis in our CAM assay, and induced marked growth inhibition in mouse sarcoma 180 and hepatoma 22 models. Specifically, PE treatment reduced mouse sarcoma 180 tumor volume by triggering apoptosis of both tumor and tumor-associated endothelial cells, preferentially targeting on endothelial cells comparable with tumor cells. Finally, PE treatment suppressed the active (phosphorylated) forms of VEGFR2, Akt, ERK, FAK and paxillin, which are involved in endothelial cell survival, proliferation, adhesion and migration. Our results indicate that PE exerts an anti-angiogenic activity associated with inhibition of VEGFR2 signaling, and an anti-tumor activity associated with decreased proliferation of tumor cells and increased apoptosis of both endothelial cells and tumor cells.

Beyond the manual: The insider's guide to Prolonged Exposure therapy for PTSD

Prolonged Exposure therapy (PE; Foa & Rothbaum, 1998) has strong empirical support for its efficacy in reducing trauma-related psychopathology in individuals with chronic PTSD (Rothbaum, Meadows, Resick, & Foy, 2000) . In the process of providing PE to many clients and in training therapists in a variety of settings in its use, we at the Center for the Treatment and Study of Anxiety have amassed extensive experience with this therapy. This article extends the treatment guidelines provided in the PE treatment manual by sharing the knowledge and wisdom that years of experience have brought us. We emphasize the importance of forging a strong therapeutic alliance and providing a thorough rationale for treatment, discuss ways to implement in-vivo and imaginal exposure so as to promote effective emotional engagement with traumatic memories, and conclude with some recommendations for how therapists who conduct PE for PTSD can take care of themselves while delivering a therapy that is very rewarding and, at times, emotionally challenging.

EFFICACY OF NEW INSECTICIDES AGAINST BOLLWORMS IN BOLLGARD COTTON, 2000

Cotton was planted on 4 May into a Wicham loam soil in 38-inch rows in southeastern North Carolina near Richlands. The fertility and herbicide programs followed extension recommendations for cotton in this region. Temik at 5.0 lb (AI)/acre was used at planting. Plot size was 45 ft x 4 rows with four replications arranged in an RCBD. The early Orthene 97 PE treatment at 0.75 lb (AI)/acre was made on 18 Jul. Additionally, the whole test was oversprayed on 5 Aug with 0.5 lb (AI)/acre Orthene to encourage bollworm survival via destruction of beneficial insects. The remainder of the treatments were made on 8 Aug with a backpack-type, CO2-pressurized sprayer calibrated to deliver 8.0 gpa at 50 psi with a single TX-8 Spray Systems nozzle 18 inches over the row. All treatments were evaluated for boll damage from bollworms and for live bollworms on 21 Aug. Plots were harvested from the middle two rows with a 2-row John Deere 9600 picker on 18 Oct. Seed cotton yields were converted to lint cotton/acre using 40% gin turnout. All data were entered into Gylling’s Pesticide Research Manager 5.0 software and analyzed via ANOVA and LSD (P = 0.05).

Expression of immediate early genes, GATA-4, and Nkx-2.5 in adrenergic-induced cardiac hypertrophy and during regression in adult mice.

Adrenoreceptor agonists induce a hypertrophic phenotype in vitro and in vivo. To investigate the molecular remodeling in chronic cardiac hypertrophy we infused adult male mice with vehicle. isoproterenol, phenylephrine or both agonists for 3, 7 or 14 days. All drugs increased cardiac mass. After minipump removal cardiac mass regressed to control levels within 7 days after PE and ISO treatment whereas ISO + PE treated hearts were incompletely regressed. ANF and beta-MHC, but not alpha-MHC, expression were increased by agonists at all time points. GATA-4, Nkx-2.5, Egr-1, c-jun and c-fos expression were increased after 3, 7 and 14 days of treatment. Expression was greatest after ISO+PE> >ISO>PE>vehicle infusion suggesting a synergistic effect of adrenoreceptor stimulation and indicating a greater effect of beta- than alpha-adrenergic action in vivo. After PE or ISO drug withdrawal the HW/BW was normal and Egr-1, c-jun, c-fos and GATA-4, but not Nkx2.5, expression dropped to control levels. HW/BW regression was incomplete after ISO+PE and elevated levels of Egr-1, c-jun and Nkx2.5 expression remained. A hydralazine-mediated reduction in blood pressure had no effect on the agonist-induced cardiac hypertrophy or gene expression. In conclusion, we found that continued agonist stimulation, and not blood pressure. is responsible for the maintained increase in gene expression. Further, we found the decrease in gene expression in the regression after drug withdrawal was gene specific.

Contractile activity is required for sarcomeric assembly in phenylephrine-induced cardiac myocyte hypertrophy.

Agonist-induced hypertrophy of cultured neonatal rat ventricular myocytes (NRVM) has been attributed to biochemical signals generated during receptor activation. However, NRVM hypertrophy can also be induced by spontaneous or electrically stimulated contractile activity in the absence of exogenous neurohormonal stimuli. Using single-cell imaging of fura 2-loaded myocytes, we found that low-density, noncontracting NRVM begin to generate intracellular Ca2+ concentration ([Ca2+]i) transients and contractile activity within minutes of exposure to the alpha 1-adrenergic agonist phenylephrine (PE; 50 microM). However, NRVM pretreated with verapamil and then stimulated with PE failed to elicit [Ca2+]i transients and beating. We therefore examined whether PE-induced [Ca2+]i transients and contractile activity were required to elicit specific aspects of the hypertrophic phenotype. PE treatment (48-72 h) increased cell size, total protein content, total protein-to-DNA ratio, and myosin heavy chain (MHC) isoenzyme content. PE also stimulated sarcomeric protein assembly and prolonged MHC half-life. However, blockade of voltage-gated L-type Ca2+ channels with verapamil, diltiazem, or nifedipine (10 microM) blocked PE-induced total protein and MHC accumulation and prevented the time-dependent assembly of myofibrillar proteins into sarcomeres. Inhibition of actin-myosin cross-bridge cycling with 2,3-butanedione monoxime (7.5 mM) also prevented PE-induced total protein and MHC accumulation, indicating that mechanical activity, rather than [Ca2+]i transients per se, was required. In contrast, blockade of [Ca2+]i transients and contractile activity did not prevent the PE-induced increase in cell surface area, activation of the mitogen-activated protein kinases ERK1 and ERK2, or upregulation of atrial natriuretic factor gene expression. Thus contractile activity is required to elicit some but not all aspects of the the hypertrophic phenotype induced by alpha 1-adrenergic receptor activation.

Regulation of protein synthesis by alpha 1-adrenergic receptor subtypes in cultured rabbit aortic vascular smooth muscle cells.

To investigate the role of the sympathetic nervous system in maintenance and remodeling of vascular smooth muscle, we have examined regulation of protein synthesis by alpha 1-adrenergic receptors (alpha 1-AR) in cultured rabbit aortic vascular smooth muscle cells (VSMC). Stimulation of postconfluent cultures (passages 2-6) in serum-free growth medium with the alpha-AR agonist phenylephrine (PE, 30 microM) increases protein synthesis, measured as [3H]leucine incorporation into protein (146 +/- 5%, p < or = 0.001) and total protein content (117 +/- 2%, p < or = 0.001). PE treatment does not affect cellular proliferation or [3H]thymidine incorporation into DNA. PE-stimulated protein synthesis is evident within 24 h, sustained over 96 h, concentration-dependent, and saturable. PE-elicited responses are completely inhibited by the alpha 1-AR antagonist prazosin but not by the alpha 2-AR antagonist yohimbine or the beta-AR antagonists propranolol and atenolol; the beta-AR agonist isoproterenol is ineffective. Competition with [3H]prazosin occupancy of alpha 1-AR and agonist-elicited [3H]leucine incorporation by subtype-selective receptor antagonists (WB4101 and 5-methylurapidil, alpha 1A; chloroethylclonidine, alpha 1B) demonstrates that these cells express a majority of alpha 1B-AR (75%) relative to alpha 1A-AR (25%), which elicit protein metabolism in proportion to their relative abundances. These results indicate that alpha 1B-AR predominate in coupling to metabolic responses, in contrast to previous reports that contractile responses in this tissue are preferentially mediated by alpha 1A-AR.

Strategies for Optimized Nitrate Reduction with Primary Denitrification

Full-scale tests carried out for the extension of a 700 000 PE treatment plant are used to show the consequences of advanced denitrification requirements. Three nitrate recirculation strategies were tested: feedback control via the nitrate content at the denitrification zone outflow, control via the redox potential and adaptive control of the recirculated nitrate load in accordance with the input of biodegradable materials, estimated on the basis of a BOD-MS measurement (3 minute BOD). In a situation in which advanced, process-stable primary denitrification has to be carried out in a restricted space, especially in large treatment plants, controlled nitrate recirculation oriented on the requirement for biodegradables is a feasible method. If denitrification is limited by lack of biodegradable substrate, supplements in line with denitrification requirements will be needed. The necessary control can be implemented via a measurement of BOD-M3 in the influent and measurement of nitrate content in the effluent from the activated sludge tank.

The Implementation of Biological Phosphorus and Nitrogen Removal with the Bio-Denipho Process on a 265,000 PE Treatment Plant

A process, called Bio-Denipho, for combined biological phosphorus and nitrogen removal in a combination of an anaerobic tank and two oxidation ditches is described. In this process the anaerobic tank consisting of three sections working in series is followed by two oxidation ditches. These too are working in series, but with both inlet to and outlet from the tanks changing in a cycle. The Bio-Denipho process is described specifically for the process itself and as a case study for the implementation of the process on a 265,000 pe wastewater treatment plant for the city of Aalborg in Denmark. The plant was designed and erected in two stages and the last stage was inaugurated October 31,1989. Lay-out and functions for the plant is described and design loads, plan lay-out and tank volumes are given in this paper together with performance data for the first year in operation.

Plasma Exchange (Pe) Treatment in Drug-Induced Toxic Epidermal Necrolysis (Ten)

Toxic epidermal necrolysis (TEN) or Lyell's syndrome is a rare fulminating skin disease notorious for its rapidly progressive course and high mortality rate. TEN is characterized by the sudden onset of epithelial necrosis of skin with frequently associated involvement of the gastrointestinal, genitourinary tract and bronchopulmonary linings. We describe the clinical course of five patients with severe drug-induced TEN, treated with PE. The suspected drugs were carbamazepine in one patient, paracetamol in one, a combination of paracetamol and mefenamic acid in one, allopurinol in one and ciprofloxacin in one. Three had a skin involvement affecting almost the entire surface of the body. In addition to the skin lesions, mouth, esophagus and lungs were also involved. Steroids proved ineffective. PE was carried out because of the rapid deterioration of the clinical picture. The mean number of PE sessions was 3.22 (range 1-5). Complete remission of the syndrome was achieved in four patients. One patient died due to septic shock. As so far there is no treatment of proven value for this condition, controlled trials should be set up in order to assess the value of PE in TEN.