פרסומים

As a mature fruit deriving from a lifelong distinguished scholarly career, Joseph Zeira has written a highly valuable contribution about Israel's economy. His book is original and multidimensional, and is characterized by an intellectually remarkable effort to explain all crucial aspects of Israel's macroeconomy. In the introduction he states: "My involvement attests to my social and political preferences, but I believe that it does not influence my scientific analysis of the Israeli economy, because I am deeply concerned about the need to separate science from personal views." I am writing this review in the hope that I will be able to hold myself apart from my admiration of my excellent and didactic Macroeconomics teacher during my MA studies and from my fruitful collaboration with Joseph in writing empirical papers about Israel's economy. I aim at overcoming this challenge.  

An underlying assumption in computational approaches in cognitive and brain sciences is that the nervous system is an input–output model of the world: Its input–output functions mirror certain relations in the target domains. I argue that the input–output modelling assumption plays distinct methodological and explanatory roles. Methodologically, input–output modelling serves to discover the computed function from environmental cues. Explanatorily, input–output modelling serves to account for the appropriateness of the computed function to the explanandum information-processing task. I compare very briefly the modelling explanation to mechanistic and optimality explanations, noting that in both cases the explanations can be seen as complementary rather than contrastive or competing.

Notwithstanding the significance of a positive bureaucratic reputation, the average bureau functions amidst deep-rooted public hostility. Bureaucracy bashing presumably weakens public sector employees’ commitment to their bureaus, which is known to undermine public sector performance. Motivated by these concerns, this paper investigates whether exogenous signals regarding a bureau’s reputation affect the organizational attachment – identification and commitment – of its employees, and the variation in employee responses. Employing an experiment at an Israeli welfare bureaucracy, we show that the organizational attachment of employees who feel central and influential within the bureau is unshaken, and even reinforced, in response to negative reputation signals. Conversely, employees who feel marginal and powerless are receptive to both negative and positive reputation signals. The implications of these findings are that public organizations can buffer their employees from the detriment

Notwithstanding the significance of a positive bureaucratic reputation, the average bureau functions amidst deep-rooted public hostility. Bureaucracy bashing presumably weakens public sector employees' commitment to their bureaus, which is known to undermine public sector performance. Motivated by these concerns, this paper investigates whether exogenous signals regarding a bureau's reputation affect the organizational attachment – identification and commitment – of its employees, and the variation in employee responses. Employing an experiment at an Israeli welfare bureaucracy, we show that the organizational attachment of employees who feel central and influential within the bureau is unshaken, and even reinforced, in response to negative reputation signals. Conversely, employees who feel marginal and powerless are receptive to both negative and positive reputation signals. The implications of these findings are that public organizations can buffer their employees from the detrimental effects of negative reputation signals, yet by so doing they may shut out justified scrutiny and demands for change.

The aim of this work was to design and characterize a new nanovesicular nasal delivery system (NDS) containing buspirone, and investigate its efficiency in an animal model for the treatment of hot flushes. The presence of multilamellar vesicles with a mean size distribution of 370 nm was evidenced by transition electron microscopy (TEM), cryo-scanning electron microscopy (Cryo-SEM), and dynamic light scattering (DLS) tests. Pharmacodynamic evaluation of the nasal treatment efficacy with the new system was carried out in ovariectomized (OVX) rat—an animal model for hot flushes—and compared with other treatments. We found that the nasal administration of a buspirone NDS resulted in a significant reduction in tail skin temperature (TST). This effect was not observed in the control buspirone-treated groups. Buspirone levels in the plasma and brain of nasally-treated normal rats were quantified and compared with those of rats that had received oral administration by a LC-MS/MS assay. A significantly higher bioavailability was achieved with the new treatment relative to an oral administration of the same drug dose. No pathological changes in the nasal cavity were observed following sub-chronic nasal administration of buspirone NDS. In conclusion, the data of our investigation show that buspirone in the new nanovesicular nasal carrier could be considered for further studies for the development of a treatment for the hot flushes ailment.

During the periovulatory period, the profile of fibroblast growth factor 2 (FGF2) coincides with elevated prostaglandin E2 (PGE2) levels. We investigated whether PGE2 can directly stimulate FGF2 production in bovine granulosa cells and, if so, which prostaglandin E2 receptor (PTGER) type and signaling cascades are involved. PGE2 temporally stimulated FGF2. Accordingly, endoperoxide-synthase2–silenced cells, exhibiting low endogenous PGE2 levels, had reduced FGF2. Furthermore, elevation of viable granulosa cell numbers by PGE2 was abolished with FGF2 receptor 1 inhibitor, suggesting that FGF2 mediates this action of PGE2. Epiregulin (EREG), a known PGE2-inducible gene, was studied alongside FGF2. PTGER2 agonist elevated cAMP as well as FGF2 and EREG levels. However, a marked difference between cAMP-induced downstream signaling was observed for FGF2 and EREG. Whereas FGF2 upregulated by PGE2, PTGER2 agonist, or forskolin was unaffected by the protein kinase A (PKA) inhibitor H89, EREG was significantly inhibited. FGF2 was dose-dependently stimulated by the exchange protein directly activated by cAMP (EPAC) activator; a similar induction was observed for EREG. However, forskolin-stimulated FGF2, but not EREG, was inhibited in EPAC1-silenced cells. These findings ascribe a novel autocrine role for PGE2, namely, elevating FGF2 production in granulosa cells. This study also reveals that cAMP-activated EPAC1, rather than PKA, mediates the effect of PGE2/PTGER2 on the expression of FGF2. Stimulation of EREG by PGE2 is also mediated by PTGER2 but, in contrast to FGF2, EREG was found to be PKA sensitive. PGE2-stimulated FGF2 can act to maintain granulosa cell survival; it can also act on ovarian endothelial cells to promote angiogenesis.