Theory-based evaluation of the impact of Master's programmes in development studies: Insights from a mixed-methods and multicultural alumni action research project.

To understand the impact of the international Master's programmes offered at the Institute of Development Policy (University of Antwerp), a theory-based evaluation was undertaken. In the first phase, a Theory of Change (ToC) was elaborated, distinguishing between three levels of impact (individual, organisational and societal), four learning dimensions (knowledge, skills, attitudes and networks) and five implicit pathways (change agent, social network, widening access, academic diversity, international understanding). Given the multifaceted and vague nature of the 'impact' concept under study, we selected an international, gender-balanced, multi-sectoral team of alumni researchers who fostered inclusiveness of different perspectives, at the same time capitalising on their depth of understanding, having gone through the study experience themselves.

Effect of post-warming culture time on the live birth rate after frozen embryo transfer.

Purpose: This study evaluated the influence of post-warming culture time on the live birth rate in day-3 and day-5 frozen embryo transfer (FET) cycles.

Methods: This multicenter, retrospective cohort study was performed at IVFMD, My Duc Hospital and IVFMD Phu Nhuan, My Duc Phu Nhuan Hospital in Vietnam between October 2019 and October 2020. Women who underwent FET cycles with the transfer of ≤2 day-3 or day-5 embryos were included in the study.

Regulation of a Novel Splice Variant of Early Growth Response 4 (EGR4-S) by HER+ Signalling and HSF1 in Breast Cancer.

The zinc finger transcription factor EGR4 has previously been identified as having a critical role in the proliferation of small cell lung cancer. Here, we have identified a novel, shortened splice variant of this transcription factor (EGR4-S) that is regulated by Heat Shock Factor-1 (HSF1). Our findings demonstrate that the shortened variant (EGR4-S) is upregulated with high EGFR, HER2, and H-Ras-expressing breast cell lines, and its expression is inhibited in response to HER pathway inhibitors.

Tafenoquine versus Primaquine to Prevent Relapse of Plasmodium vivax Malaria.

Background: Tafenoquine, a single-dose therapy for Plasmodium vivax malaria, has been associated with relapse prevention through the clearance of P. vivax parasitemia and hypnozoites, termed "radical cure."

Methods: We performed a phase 3, prospective, double-blind, double-dummy, randomized, controlled trial to compare tafenoquine with primaquine in terms of safety and efficacy.

Histone deacetylase activity mediates acquired resistance towards structurally diverse HSP90 inhibitors.

Heat shock protein 90 (HSP90) regulates multiple signalling pathways critical for tumour growth. As such, HSP90 inhibitors have been shown to act as effective anticancer agents in preclinical studies but, for a number of reasons, the same effect has not been observed in the clinical trials to date. One potential reason for this may be the presence of de novo or acquired resistance within the tumours.

Mammographically dense human breast tissue stimulates MCF10DCIS.com progression to invasive lesions and metastasis.

Background: High mammographic density (HMD) not only confers a significantly increased risk of breast cancer (BC) but also is associated with BCs of more advanced stages. However, it is unclear whether BC progression and metastasis are stimulated by HMD. We investigated whether patient-derived HMD breast tissue could stimulate the progression of MCF10DCIS.

Molecular stress-inducing compounds increase osteoclast formation in a heat shock factor 1 protein-dependent manner.

Many anticancer therapeutic agents cause bone loss, which increases the risk of fractures that severely reduce quality of life. Thus, in drug development, it is critical to identify and understand such effects. Anticancer therapeutic and HSP90 inhibitor 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) causes bone loss by increasing osteoclast formation, but the mechanism underlying this is not understood.

The eIF2B-interacting domain of RGS2 protects against GPCR agonist-induced hypertrophy in neonatal rat cardiomyocytes.

The protective effect of Regulator of G protein Signaling 2 (RGS2) in cardiac hypertrophy is thought to occur through its ability to inhibit the chronic GPCR signaling that promotes pathogenic growth both in vivo and in cultured cardiomyocytes. However, RGS2 is known to have additional functions beyond its activity as a GTPase accelerating protein, such as the ability to bind to eukaryotic initiation factor, eIF2B, and inhibit protein synthesis. The RGS2 eIF2B-interacting domain (RGS2(eb)) was examined for its ability to regulate hypertrophy in neonatal ventricular myocytes.

Heat-shock factor 1 both positively and negatively affects cellular clonogenic growth depending on p53 status.

HSF1 (heat-shock factor 1) is the master regulator of the heat-shock response; however, it is also activated by cancer-associated stresses and supports cellular transformation and cancer progression. We examined the role of HSF1 in relation to cancer cell clonogenicity, an important attribute of cancer cells. Ectopic expression or HSF1 knockdown demonstrated that HSF1 positively regulated cancer cell clonogenic growth.

RGS2 is a component of the cellular stress response.

Regulator of G protein signaling (RGS) proteins are GTPase accelerating proteins for heterotrimeric G protein α-subunits. RGS2 has recently been shown to have additional G protein-independent functions including control of ion channel currents, microtubule polymerization, and protein synthesis. Cellular levels of RGS2 mRNA and protein are upregulated in response to various forms of stress suggesting that it may be a stress-adaptive protein; however, direct evidence to support this notion has remained elusive.

The proline-rich N-terminal domain of G18 exhibits a novel G protein regulatory function.

The protein G18 (also known as AGS4 or GPSM3) contains three conserved GoLoco/GPR domains in its central and C-terminal regions that bind to inactive Galpha(i), whereas the N-terminal region has not been previously characterized. We investigated whether this domain might itself regulate G protein activity by assessing the abilities of G18 and mutants thereof to modulate the nucleotide binding and hydrolytic properties of Galpha(i1) and Galpha(o). Surprisingly, in the presence of fluoroaluminate (AlF(4)(-)) both G proteins bound strongly to full-length G18 (G18wt) and to its isolated N-terminal domain (G18DeltaC) but not to its GoLoco region (DeltaNG18).

Translational control by RGS2.

The regulator of G protein signaling (RGS) proteins are a family of guanosine triphosphatase (GTPase)-accelerating proteins. We have discovered a novel function for RGS2 in the control of protein synthesis. RGS2 was found to bind to eIF2Bepsilon (eukaryotic initiation factor 2B epsilon subunit) and inhibit the translation of messenger RNA (mRNA) into new protein.

The Vps4 C-terminal helix is a critical determinant for assembly and ATPase activity and has elements conserved in other members of the meiotic clade of AAA ATPases.

Sorting of membrane proteins into intralumenal endosomal vesicles, multivesicular body (MVB) sorting, is critical for receptor down regulation, antigen presentation and enveloped virus budding. Vps4 is an AAA ATPase that functions in MVB sorting. Although AAA ATPases are oligomeric, mechanisms that govern Vps4 oligomerization and activity remain elusive.

Vps4 regulates a subset of protein interactions at the multivesicular endosome.

During endocytic transport, specific integral membrane proteins are sorted into intraluminal vesicles that bud from the limiting membrane of the endosome. This process, known as multivesicular body (MVB) sorting, is important for several important biological processes. Moreover, components of the MVB sorting machinery are implicated in virus budding.

Repeated quinpirole treatments produce neurochemical sensitization and associated behavioral changes in female hamsters.

Rationale: Repeated stimulation of dopaminergic pathways with dopamine receptor agonists can produce both neurochemical and behavioral sensitization.

Objectives: The present study was designed to examine whether repeated treatment with the D2-like dopamine receptor agonist, quinpirole, would produce neurochemical sensitization of D1 dopamine receptor-mediated processes and associated behavioral changes in female hamsters in a manner analogous to that previously used to sensitize heterologous dopamine signaling pathways in derived cell lines.

Materials And Methods: Female hamsters received two injections of quinpirole (1.

Dexamethasone-induced Ras protein 1 negatively regulates protein kinase C delta: implications for adenylyl cyclase 2 signaling.

We identified dexamethasone-induced Ras protein 1 (Dexras1) as a negative regulator of protein kinase C (PKC) delta, and the consequences of this regulation have been examined for adenylyl cyclase (EC 4.6.1.

D2 dopamine receptor-induced sensitization of adenylyl cyclase type 1 is G alpha(s) independent.

Acute activation of D2 dopamine receptors inhibits adenylyl cyclase (EC 4.6.1.

Dexras1 blocks receptor-mediated heterologous sensitization of adenylyl cyclase 1.

Dexras1/AGS1/RasD1 is a member of the Ras superfamily of monomeric G proteins and has been suggested to disrupt receptor-G protein signaling. We examined the ability of Dexras1 to modulate dopamine D(2L) receptor regulation of adenylyl cyclase (AC) type 1 in HEK293 cells. Acute D(2L) receptor-mediated inhibition of A23187-stimulated AC1 activity (IC50, 4.

A rare case of nasal glioma in the sphenoid sinus of an adult presenting with meningoencephalitis.

Nasal gliomas are rare embryologic development defects that commonly present shortly after birth. Very few cases have ever been reported in adults. Of those presenting in adult life, most were casual findings in patients with no symptoms.

Using molecular tools to dissect the role of Galphas in sensitization of AC1.

Short-term activation of Galpha(i/o)-coupled receptors inhibits adenylyl cyclase, whereas persistent activation of Galpha(i/o)-coupled receptors results in a compensatory sensitization of adenylyl cyclase activity after subsequent activation by Galpha(s) or forskolin. Several indirect observations have suggested the involvement of increased Galpha(s)-adenylyl cyclase interactions in the expression of sensitization; however, evidence supporting a direct role for Galpha(s) has not been well established. In the present report, we used two genetic approaches to further examine the role of Galpha(s) in heterologous sensitization of Ca(2+)-sensitive type 1 adenylyl cyclase (AC1).