Privatization : problems of implementation in Egypt

This study aims to investigate to what extent the views of the managers of the enterprises to be privatized are a barrier to smooth implementation of privatization as opposed to other problems. Accordingly, the research tackles two main issues: Identification and analysis of the major problems encountered in the implementation of the Egyptian privatization programme and at which level these problems exist while proposing different approaches to tackle them; and views of public sector top and middle-level managers regarding the main issues of privatization. The study relies upon a literature survey, interviews with stakeholders, a survey of managers' attitudes and several illustrative case studies. A model of "good practice" for the smooth and effective implementation of privatization has been designed. Practice in Egypt has then been studied and compared with the "good practice" model. Lack of strictness and firmness in implementing the announced privatization programme has been found to be a characteristic of Egyptian practice. This is partly attributable to the inadequacy of the programme and partly to the different obstacles to implementation. The main obstacles are doubtful desirability of privatization on the part of the managers at different implementation levels, resistance of stakeholders, in adequately of the legal framework governing privatization, redundant labour, lack of an efficient monitoring system allowing for accountability, inefficient marketing of privatization, ineffective communication, insufficient information at different levels and problems related to valuation and selling procedures. A large part of the thesis is concerned with SOE (State Owned Enterprise) managers' attitudes on and understanding of the privatization (appraised through surveys). Although most managers have stated their acceptance of privatization, many of their responses show that they do not accept selling SOEs. They understand privatization to include enterprise reform and restructuring, changing procedures and giving more authority to company executives, but not necessarily as selling SOEs. The majority of managers still see many issues that have to be addressed for smooth implementation of privatization e.g. insufficiency of information, incompleteness of legal framework, restructuring and labour problems. The main contribution to knowledge of this thesis is the study of problems of implementing privatization in developing countries especially managers' resistance to privatization as a major change, partly because of the threat it poses and partly because of the lack of understanding of privatization and implications of operating private businesses. A programme of persuading managers and offsetting the unfavourable effects is recommended as an outcome of the study. Five different phrases and words for the national Index to theses are: Egypt, privatization, implementation of privatization, problems of implementing privatization and managers' attitudes towards privatization.

Calcitonin and calcitonin receptor-like receptors:common themes with family B GPCRs?

The calcitonin receptor (CTR) and calcitonin receptor-like receptor (CLR) are two of the 15 human family B (or Secretin-like) GPCRs. CTR and CLR are of considerable biological interest as their pharmacology is moulded by interactions with receptor activity-modifying proteins. They also have therapeutic relevance for many conditions, such as osteoporosis, diabetes, obesity, lymphatic insufficiency, migraine and cardiovascular disease. In light of recent advances in understanding ligand docking and receptor activation in both the family as a whole and in CLR and CTR specifically, this review reflects how applicable general family B GPCR themes are to these two idiosyncratic receptors. We review the main functional domains of the receptors; the N-terminal extracellular domain, the juxtamembrane domain and ligand interface, the transmembrane domain and the intracellular C-terminal domain. Structural and functional findings from the CLR and CTR along with other family B GPCRs are critically appraised to gain insight into how these domains may function. The ability for CTR and CLR to interact with receptor activity-modifying proteins adds another level of sophistication to these receptor systems but means careful consideration is needed when trying to apply generic GPCR principles. This review encapsulates current thinking in the realm of family B GPCR research by highlighting both conflicting and recurring themes and how such findings relate to two unusual but important receptors, CTR and CLR.

Dynamic spectrum access in heterogeneous unlicensed wireless networks

Existing wireless systems are normally regulated by a fixed spectrum assignment strategy. This policy leads to an undesirable situation that some systems may only use the allocated spectrum to a limited extent while others have very serious spectrum insufficiency situation. Dynamic Spectrum Access (DSA) is emerging as a promising technology to address this issue such that the unused licensed spectrum can be opportunistically accessed by the unlicensed users. To enable DSA, the unlicensed user shall have the capability of detecting the unoccupied spectrum, controlling its spectrum access in an adaptive manner, and coexisting with other unlicensed users automatically. In this article, we propose a radio system Transmission Opportunity-based spectrum access control protocol with the aim to improve spectrum access fairness and ensure safe coexistence of multiple heterogeneous unlicensed radio systems. In the scheme, multiple radio systems will coexist and dynamically use available free spectrum without interfering with licensed users. Simulation is carried out to evaluate the performance of the proposed scheme with respect to spectrum utilisation, fairness and scalability. Comparing with the existed studies, our strategy is able to achieve higher scalability and controllability without degrading spectrum utilisation and fairness performance.

Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells

Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. The inhibition of VEGFR-1 results in a dramatic decrease in the number of capillary connections, indicating that VEGFR-1 ligands promote branching angiogenesis. In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. Together, these findings indicate that PlGF-containing ligands contribute to pathological angiogenesis by prolonging cell survival signals and maintaining vascular networks.

Autonomic nervous system, circadian rhythms, and primary open-angle glaucoma

The etiology of primary open-angle glaucoma (POAG) remains the subject of continuing investigation. Despite the many known risk factors and mechanism of damage, the principal treatment objectives in POAG still consist of reduction of intraocular pressure, which although straightforward in many cases, often leaves the clinician with the question of how far to pursue a sufficiently low pressure to prevent further damage. Other risk factors such as hemodynamic insufficiency due to vascular dysregulation and abnormal blood pressure are often overlooked in the day-to-day practice; their harmful effects for glaucoma are, it seems, more potent at night while the patient sleeps and when clinical investigation is most difficult. Although the status of autonomic nervous system is an important determinant of the systemic hemodynamic parameters, this issue is usually ignored by the clinician in the process of glaucoma diagnosis. Consequently, there is a lack of alternative therapies tailored to address associated systemic risk factors for POAG on a case and chronological basis; this approach could be more effective in preventing the progression and visual loss in selected glaucoma cases. © 2004 Elsevier Inc. All rights reserved.

Stokes waves revisited:exact solutions in the asymptotic limit

The Stokes perturbative solution of the nonlinear (boundary value dependent) surface gravity wave problem is known to provide results of reasonable accuracy to engineers in estimating the phase speed and amplitudes of such nonlinear waves. The weakling in this structure though is the presence of aperiodic “secular variation” in the solution that does not agree with the known periodic propagation of surface waves. This has historically necessitated increasingly higher-ordered (perturbative) approximations in the representation of the velocity profile. The present article ameliorates this long-standing theoretical insufficiency by invoking a compact exact n-ordered solution in the asymptotic infinite depth limit, primarily based on a representation structured around the third-ordered perturbative solution, that leads to a seamless extension to higher-order (e.g., fifth-order) forms existing in the literature. The result from this study is expected to improve phenomenological engineering estimates, now that any desired higher-ordered expansion may be compacted within the same representation, but without any aperiodicity in the spectral pattern of the wave guides.

Familial adrenal hypoplasia syndromes

The adrenal cortex secretes steroid hormones, including glucocorticoids and mineralocorticoids. Glucocorticoids control body homeostasis, stress, and immune responses, while mineralocorticoids regulate the water and electrolyte balance. A spectrum of genetic defects can disrupt the normal adrenal development, causing adrenal hypoplasia and various forms of adrenal insufficiency, which usually present in infancy or childhood with or without mineralocorticoid deficiency and with or without gonadal dysfunction. The genetic causes of adrenal hypoplasia can be broadly categorized into adrenal hypoplasia due to adrenocorticotropic hormone resistance syndromes (i.e., familial glucocorticoid deficiency and triple A syndrome) and adrenal hypoplasia due to primary defects in the development of the adrenal glands (i.e., X-linked adrenal hypoplasia congenita and primary adrenal hypoplasia caused by steroidogenic factor 1 mutations).

Dysregulation of placental cystathionine-β-synthase promotes fetal growth restriction

Fetal growth restriction (FGR) is characterized by the birth weight and body mass below the tenth percentile for gestational age. FGR is a major cause of perinatal morbidity and mortality and babies born with FGR are prone to develop cardiovascular diseases later in life. The underlying pathology of FGR is inadequate placental transfer of nutrients from mother to fetus, which can be caused by placental insufficiency. Hydrogen sulfide (H2S), a gaseous messenger is produced endogenously by cystathionine-lyase (Cth), cystathionine-β-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST), which are present in human placenta. Recently, we demonstrated that the dysregulation of H2S/Cth pathway is associated with preeclampsia and blockade of CSE activity induces preeclampsia-like condition in pregnant mice. We hypothesized that defect in H2S pathways promote FGR and H2S donor restores fetal growth in mice where CBS or CSE activity has been compromised. Western blotting and qPCR revealed that placental CBS expressions were significantly reduced in women with FGR. ELISA analysis showed reduced placental growth factor production (PlGF) from first trimester (8–12 weeks gestation) human placental explants following inhibition of CBS activity by aminooxyacetic acid (AOA). Administration of AOA to pregnant mice had no effects on blood pressure, but caused fetal growth restriction. This was associated with reduced PlGF production. Histological analysis revealed a reduction in the placental junction zone, within which trophoblast giant cells and glycogen cells were less prominent in CBS inhibitor treated mice. These results imply that placental CBS is required for placental development and that dysregulation of CBS activity may contribute to the pathogenesis of FGR but not preeclampsia.

Dysregulation of placental cystathionine-β-synthase impact on fetal growth restriction

INTRODUCTION: Fetal growth restriction (FGR), which causes perinatal morbidity and mortality, is characterized by birth weight and body mass being below 10th percentile for gestational age. FGR babies are prone to develop cardiovascular diseases later in life. Inadequate placental transfer of nutrients from mother to fetus due to placental insufficiency is considered the underlying cause of FGR. Recently, we demonstrated that blockade of cystathionine-γ-lyase (CSE) activity induces preeclampsia-like condition in pregnant mice. We hypothesized that defect in cystathionine-β-synthase (CBS) / H2S pathway may promote FGR. METHODS: Placental CBS expressions were determined in women with FGR (n=9) and normal controls (n=14) by Western blotting and real-time qPCR. ELISA was used to determine angiogenic factors levels in plasma and first-trimester (8–12 weeks gestation) human placental explants. Time pregnant mice were treated with CBS inhibitor, aminooxyacetic acid (AOA). Mean arterial blood pressure (MBP), histological assessments of placenta and embryos were performed. RESULTS: Placental CBS expressions were significantly reduced in women with FGR. Inhibition of CBS activity by AOA reduced PlGF production from first-trimester human placental explants, Administration of AOA to pregnant mice had no effects on blood pressure, but caused fetal growth restriction, which was associated with reduced placental PlGF production. Histological analysis revealed a reduction in the placental junction zone, within which trophoblast giant cells and glycogen cells were less prominent in CBS inhibitor-treated animals. Furthermore, H2S donor GYY4137 treatment restored fetal growth in pregnant mice exposed to high level of sFlt-1. CONCLUSIONS: These results imply that placental CBS is required for placental development and that dysregulation of CBS activity may contribute to the pathogenesis of FGR but not preeclampsia opening up the therapeutic potentials of H2S therapy in this condition.