586 research outputs found

    Chronic diseases and labor market outcomes in Egypt

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    By causing a sizeable reduction in employment 6 percent and labor supply 19 percent, chronic diseases are responsible for a major efficiency loss in the Egyptian economy. Furthermore the impact of chronic diseases on the labor market is not uniformly distributed. The older and the less educated suffer a larger drop in the probability of being employed and in their supply of working hours. The authors estimate the reduced form equations of individual employment status, labor supply and the usual wage equation. They control for unobserved ability and individual preferences by means of a within-siblings estimator. Measurement errors in our self-reported health variable have been accounted for.Health Monitoring&Evaluation,Labor Markets,Disease Control&Prevention,Labor Policies,Population Policies

    The relationship between job satisfaction and general happiness

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    Ovaj diplomski rad istražuje povezanost zadovoljstva na poslu i opće životne sreće tj. traži odgovor na istraživačko pitanje jeli opća sreća u životu povezana sa zadovoljstvom na poslu. Rad je rezultat sistematizacije postojeće literature o zadovoljstvu na poslu i opće sreće te anketnog istraživanja u kojemu je sudjelovalo 104 ispitanika (od čega 63 zaposlenika i 41 privremeno zaposlenih studenata). Uz pomoć istraživanja napravljena je usporedba rezultata po pitanju zadovoljstva na poslu i opće sreće. Ispitanici su u prosjeku zadovoljni na poslu (M = 4,2 na ljestvici od 1 do 6) pri čemu su zaposlenici (M = 4,3) zadovoljniji na poslu od studenata (M = 4,0). Također, ispitanici se osjećaju sretnima (M = 5,0 na ljestvici od 1 do 7), pri čemu su također odgovori zaposlenika pozitivniji (M = 5,1) od odgovora zaposlenih studenata (M = 4,8). Ključni nalaz empirijskog istraživanja je dobivena pozitivna korelacija između zadovoljstva na poslu i opće sreće ispitanika, odnosno nalaz da su zaposlenici koji su zadovoljniji na poslu sretniji ljudi i obrnuto.This paper examines the correlation between job satisfaction and general happiness in life i.e. it attempts to answer the research question whether general happiness in life is related to job satisfaction. The paper is a result of systematisation of available literature on job satisfaction and general happiness, as well as the result of a questionnaire survey in which 104 respondents (63 employees and 41 temporary employed students) participated. A comparison is made between the results in terms of job satisfaction and those of general happiness. Respondents are, in average, satisfied at work (M = 4.2 on a scale from 1 to 6), with employees (M = 4.3) being more satisfied at work than students (M = 4.0). Furthermore, respondents feel happy (M = 5.0 on a scale from 1 to 7), with the responses of employees being more positive (M = 5.1) than the responses of employed students (M = 4.8).The main finding of the research is that there is a positive relationship between job satisfaction and overall life happiness, which is in support of the conclusion of this thesis that, in general, employees who are happier at work are also happier people and vice versa

    The relationship between job satisfaction and general happiness

    Get PDF
    Ovaj diplomski rad istražuje povezanost zadovoljstva na poslu i opće životne sreće tj. traži odgovor na istraživačko pitanje jeli opća sreća u životu povezana sa zadovoljstvom na poslu. Rad je rezultat sistematizacije postojeće literature o zadovoljstvu na poslu i opće sreće te anketnog istraživanja u kojemu je sudjelovalo 104 ispitanika (od čega 63 zaposlenika i 41 privremeno zaposlenih studenata). Uz pomoć istraživanja napravljena je usporedba rezultata po pitanju zadovoljstva na poslu i opće sreće. Ispitanici su u prosjeku zadovoljni na poslu (M = 4,2 na ljestvici od 1 do 6) pri čemu su zaposlenici (M = 4,3) zadovoljniji na poslu od studenata (M = 4,0). Također, ispitanici se osjećaju sretnima (M = 5,0 na ljestvici od 1 do 7), pri čemu su također odgovori zaposlenika pozitivniji (M = 5,1) od odgovora zaposlenih studenata (M = 4,8). Ključni nalaz empirijskog istraživanja je dobivena pozitivna korelacija između zadovoljstva na poslu i opće sreće ispitanika, odnosno nalaz da su zaposlenici koji su zadovoljniji na poslu sretniji ljudi i obrnuto.This paper examines the correlation between job satisfaction and general happiness in life i.e. it attempts to answer the research question whether general happiness in life is related to job satisfaction. The paper is a result of systematisation of available literature on job satisfaction and general happiness, as well as the result of a questionnaire survey in which 104 respondents (63 employees and 41 temporary employed students) participated. A comparison is made between the results in terms of job satisfaction and those of general happiness. Respondents are, in average, satisfied at work (M = 4.2 on a scale from 1 to 6), with employees (M = 4.3) being more satisfied at work than students (M = 4.0). Furthermore, respondents feel happy (M = 5.0 on a scale from 1 to 7), with the responses of employees being more positive (M = 5.1) than the responses of employed students (M = 4.8).The main finding of the research is that there is a positive relationship between job satisfaction and overall life happiness, which is in support of the conclusion of this thesis that, in general, employees who are happier at work are also happier people and vice versa

    Membrane protein remodeling in microglia exposed to amyloid peptides

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    Infection, neurodegeneration, and other conditions associated with loss of brain homeostasis, induce changes in microglial morphology, gene expression and function, generally referred to as “activation”. Alzheimer’s disease (AD) is the most common dementia and is characterized by neuroinfammatory changes, including alterations in the morphology and distribution of microglia and astrocytes, and deposition of complement and other infammatory mediators. Our previous observations show that microglial cells challenged in vitro with amyloid peptides clustered and rounded up, dramatically changing their morphology. Besides, in these cells we observed the early acetylation and then the phosphorylation of STAT3 which is required for the expression of the epsilon isoform of 14-3-3, a marker of Abeta-activated microglia (1, 2). We applied afnity partitioning approach combined with high throughput mass spectrometric analysis in order to identify variation of proteins on plasma membrane of BV2 immortalized microglia upon treatment with amyloid peptides. By this method several proteins up- or down-regulated by amyloid treatment were identifed in microglial plasma membrane. Among them annexins (5 and 7), IFITM3 and MARK3. These data have been confrmed in primary microglial cultures. In microglia, plasma membrane plays a relevant role in the cross-talking with the external neuronal environment and in the resulting trophic or infammatory response of these sentinel cells. As such, knowledge of the microglia responsiveness to beta amyloids in term of changes in its plasma membrane proteome is imperative for unveiling the molecular landscape in which AD occurs

    Impairment of the autophagic flux in astrocytes intoxicated by trimethyltin

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    Autophagy is a lysosomal catabolic route for protein aggregates and damaged organelles which in different stress conditions, such as starvation, generally improves cell survival. An impairment of this degradation pathway has been reported to occur in many neurodegenerative processes. Trimethyltin (TMT) is a potent neurotoxin present as an environmental contaminant causing tremors, seizures and learning impairment in intoxicated subjects. The present data show that in rat primary astrocytes autophagic vesicles (AVs) appeared after few hours of TMT treatment. The analysis of the autophagic flux in TMT-treated astrocytes was consistent with a block of the late stages of autophagy and was accompanied by a progressive accumulation of the microtubule associated protein light chain 3 (LC3) and of p62/SQSTM1. Interestingly, an increased immunoreactivity for p62/SQSTM1 was also observed in hippocampal astrocytes detected in brain slices of TMT-intoxicated rats. The time-lapse recordings of AVs in EGFP-mCherry-LC3B transfected astrocytes demonstrated a reduced mobility of autophagosomes after TMT exposure respect to control cells. The observed block of the autophagic flux cannot be overcome by known autophagy inducers such as rapamycin or 0.5mM lithium. Although ineffective when used at 0.5mM, lithium at higher concentrations (2mM) was able to protect astrocyte cultures from TMT toxicity. This effect correlated well with its ability to determine the phosphorylation/inactivation of glycogen kinase synthase-3β (GSK-3β)

    Lithium limits trimethyltin-induced cytotoxicity and proinflammatory response in microglia without affecting the concurrent autophagy impairment

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    Trimethyltin (TMT) is a highly toxic molecule present as an environmental contaminant causing neurodegeneration particularly of the limbic system both in humans and in rodents. We recently described the occurrence of impairment in the late stages of autophagy in TMT-intoxicated astrocytes. Here we show that similarly to astrocytes also in microglia, TMT induces the precocious block of autophagy indicated by the accumulation of the autophagosome marker, microtubule associated protein light chain 3. Consistent with autophagy impairment we observe in TMT-treated microglia the accumulation of p62/SQSTM1, a protein specifically degraded through this pathway. Lithium has been proved effective in limiting neurodegenerations and, in particular, in ameliorating symptoms of TMT intoxication in rodents. In our in vitro model, lithium displays a pro-survival and anti-inflammatory action reducing both cell death and the proinflammatory response of TMT-treated microglia. In particular, lithium exerts these activities without reducing TMT-induced accumulation of light chain 3 protein. In fact, the autophagic block imposed by TMT is unaffected by lithium administration. These results are of interest as defects in the execution of autophagy are frequently observed in neurodegenerative diseases and lithium is considered a promising therapeutic agent for these pathologies. Thus, it is relevant that this cation can still maintain its pro-survival and anti-inflammatory role in conditions of autophagy bloc

    Thrombin regulates the ability of Schwann cells to support neuritogenesis and to maintain the integrity of the nodes of Ranvier

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    Schwann cells (SC) are characterized by a remarkable plasticity that enables them to promptly respond to nerve injury promoting axonal regeneration. In peripheral nerves after damage SC convert to a repair-promoting phenotype activating a sequence of supportive functions that drive myelin clearance, prevent neuronal death, and help axon growth and guidance. Regeneration of peripheral nerves after damage correlates inversely with thrombin levels. Thrombin is not only the key regulator of the coagulation cascade but also a protease with hormone-like activities that affects various cells of the central and peripheral nervous system mainly through the protease-activated receptor 1 (PAR1). Aim of the present study was to investigate if and how thrombin could affect the axon supportive functions of SC. In particular, our results show that the activation of PAR1 in rat SC cultures with low levels of thrombin or PAR1 agonist peptides induces the release of molecules, which favor neuronal survival and neurite elongation. Conversely, the stimulation of SC with high levels of thrombin or PAR1 agonist peptides drives an opposite effect inducing SC to release factors that inhibit the extension of neurites. Moreover, high levels of thrombin administered to sciatic nerve ex vivo explants induce a dramatic change in SC morphology causing disappearance of the Cajal bands, enlargement of the Schmidt-Lanterman incisures and calcium-mediated demyelination of the paranodes. Our results indicate thrombin as a novel modulator of SC plasticity potentially able to favor or inhibit SC pro-regenerative properties according to its level at the site of lesion

    Egas Moniz: 90 years (1927-2017) from cerebral angiography

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    In June 2017 we celebrate the 90th anniversary of the pioneer discovery of cerebral angiography, the seminal imaging technique used for visualizing cerebral blood vessels and vascular alterations as well as other intracranial disorders. Egas Moniz (1874-1955) was the first to describe the use of this revolutionary technique which, until 1975 (when computed tomography, CT, scan was introduced in the clinical practice), was the sole diagnostic tool to provide an imaging of cerebral vessels and therefore alterations due to intracranial pathology. Moniz introduced in the clinical practice this fundamental and important diagnostic tool. The present contribution wishes to pay a tribute to the Portuguese neurosurgeon, who was also a distinguished neurologist and statesman. Despite his tremendous contribution in modern brain imaging, Egas Moniz was awarded the Nobel Prize in Physiology or Medicine in 1949 for prefrontal leucotomy, the neurosurgical intervention nowadays unacceptable, but should rather be remembered for his key contribution to modern brain imaging. KEYWORDS

    Autophagy is differently regulated in astrocytes and microglia exposed to environmental toxic molecules

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    Autophagy is generally considered a degradation pathway involved in many neurodegenerative processes. It can be observed in different stress conditions such as starvation generally improving cell survival. Our previous results described the occurrence of autophagy in neuronal cultures exposed to the toxic compound trimethyltin (TMT) (1). TMT belongs to a family of organotin compounds with wide industrial and agricultural applications, especially as heat stabilizers in PVC production and as biocides. In the nervous system TMT determines the selective destruction of neurons in specific brain regions such as the olfactory bulb and the hippocampus. When this toxic molecule was administered to glial cells we observed in astrocytes a rapid block of the autophagic flux and a consequent increased expression of LC3 and p62 which can be observed both in cultured astrocytes and in the brain of intoxicated animals. Conversely, in microglia autophagy was not impaired in the same conditions and p62 accumulation was not observed neither in vitro primary cultures, nor in brain sections of TMT-treated rats. The protein p62 (also known as SQTM1) is known to be selectively degraded through autophagy and its accumulation activates the transcription factor Nrf2 by sequestering Keap1 (2). To note the block of autophagy has been reported to exert an immunosopressive effect in macrophages (3). Thus, the impairment of autophagy in astrocytes could be related to their limited production of pro-inflammatory cytokines and nitric oxide respect to microglia observed after TMT treatment. This work was supported by grant from Ricerca Scientifica 2013 to L.F
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