The goal of this panel is to launch a dialog on women in UX leadership. Despite ongoing progress toward equality, women still haven't reached significant representation in leadership positions in the high-tech industry. Is the field of User Experience an exception to this norm? Does the interdisciplinary nature of UX play a role in making it easier or more difficult for women in our field? Does a career in UX, regardless of gender place a glass ceiling on upward mobility into "C" level positions? Our accomplished panel of UX managers will share their professional journeys, their observations on advantages and disadvantages, and their advice for the next generation.

This panel will discuss the prominent trend of business consolidations in the enterprise software industry and proffer best practice management techniques for user experience teams following a successfully achieved merger or acquisition. Our panelists are UX managers who have experienced multiple mergers or acquisitions and will represent both the acquiring and acquired companies' perspectives. This panel builds on the success of a SIG organized at CH 2010. It will focus in on the UX management aspect post M&A, since this was most interesting to our audience. We will discuss design and technical challenges such as multiple UI technologies and platforms, navigation paradigms and menu structures, interaction behaviors, visual designs, as well as cultural and organizational challenges such as different maturity levels of UX teams, User Centered Design practices, job titles, talent management, geographical distribution and other cultural differences. Our goal is to explore best practice solutions that could help other UX managers facing similar challenges.

Developers worldwide wish to understand what major companies are doing in user-experience development (UXD). UXD comprises activities in user-centered design of user experience, specifically user-interface development (metaphors, mental models, navigation, interaction, and appearance) that is useful for planning, research, analysis, design, implementation, evaluation, and documentation of products/services across a wide number of platforms. This paper reports the results of a survey conducted with six enterprise software companies.

This paper provides a framework to understand the various aspects of creating international enterprise software. These aspects could be used to evaluate and prioritize a software product’s investment in internationalization. The intended audiences for this paper are user experience designers, product managers and other members of the software development product team, interested in creating world ready enterprise software.

Adrenal tumors occur more frequently in women and are the leading cause of Cushing's syndrome during pregnancy. We aimed to evaluate the potential role of sex steroids in the susceptibility of women to adrenocortical tumors. We evaluated the presence of the progesterone receptor (PR), estradiol receptors (ERs), and aromatase in 5 patients with primary pigmented nodular adrenal disease (PPNAD), 15 adrenocortical adenomas (ACAs) and adjacent normal tissues, 12 adrenocortical carcinomas (ACCs), and 3 normal adrenal glands (NA). The expression of PR and ERalpha was evaluated by enzyme immunoassays, real-time RT-PCR, immunohistochemistry, and cytosol-based ligand-binding assays. ERbeta and aromatase levels were evaluated by real-time RT-PCR. ERalpha concentrations were low in NA, in adrenal tissues adjacent to ACA (51+/-33), in ACC (53+/-78), and lower in ACA (11+/-11 fmol/mg DNA). Conversely, PR concentrations were high in NA and adrenal tissues adjacent to ACA, at 307+/-216 fmol/mg DNA, and were even higher in tumors - 726+/-706 fmol/mg DNA in ACA and 1154+/-1586 fmol/mg DNA in ACC - and in isolated PPNAD nodules. Binding study results in four tumors were compatible with binding to a steroid receptor. In patients with PPNAD, a strong positive immunohistochemical signal was associated with the sole isolated nodular regions. ERbeta transcript levels were very high in all samples except those for two ACCs, whereas aromatase levels were low. PR and ERbeta are clearly present in normal adrenal glands and adrenal tumors. Further studies may shed light on the possible pathogenic role of these receptors in adrenal proliferation.

Les récepteurs hormonaux membranaires sont répartis en trois grandes familles : les récepteurs couplés aux protéines G, les récepteurs tyrosine kinase et les récepteurs des cytokines. Chacune de ces familles est caractérisée par des propriétés structurales communes et des mécanismes de transduction du signal particuliers.

The globalization of Oracle's development organization, customer base, and product lines has had an ongoing impact on the evolution of the Oracle UI Group (OUI). It has changed not only the product and user requirements to be met via the UCD process but also the nature of that process. This overview describes some of the internal and external challenges inherent to the globalization of enterprise software and how OUI has attempted to address them by creating deep connections with both its user and developer communities.

Various cellular and molecular alterations of the cAMP pathway have been observed in adrenal Cushing syndrome. We recently reported the loss of cAMP-responsive element-binding protein (CREB) expression in the adrenocortical cancer cell line H295R. CREB is the major nuclear target of the cAMP pathway. This study therefore aimed to analyze the status of the CREB protein in various types of human adrenocortical tumors and normal fetal adrenal cortex. CREB protein status was studied by Western blotting in adrenocortical adenomas (AAs, n = 27) and adrenocortical carcinomas (ACs, n = 24). A decrease of CREB protein was noticed in the majority of the adrenocortical tumors. The dramatic decrease in CREB protein levels was more pronounced in ACs than in AAs. Levels of the phosphorylated form of CREB were also low in adrenocortical tumors, with a greater decrease in ACs than in AAs. EMSAs also showed decreases in the amounts of CREB- containing complexes in nuclear extracts from adrenocortical tumors. The secretory status of adenomas was strongly correlated with CREB levels, significantly lower in nonfunctioning AAs (n = 9) than in functioning AAs (n = 9). CREB levels, determined by Western blotting and immunohistochemistry, were very low in the fetal zone of human fetal adrenal cortex, whereas they were normal in the definitive zone. In tumors, adrenocortical cells in several zones were weakly immunohistochemically stained for CREB, whereas CREB was uniformly detected in nonendocrine cell nuclei (e.g. vascular cells, fibroblasts). These results suggest that the absence of CREB may be linked to the development of a highly aggressive tumor with a dedifferentiated benign (nonfunctioning AA) or malignant (AC) phenotype. These findings highlight the similarities between the normal human fetal adrenal gland and adrenal cancers previously observed in terms of parallelism in IGF-II production.

The cAMP pathway plays a major role in the development of endocrine tissues and various molecular defects of key components of this pathway (G protein, receptors, PKA, etc.) have been observed in endocrine tumors. The ubiquitous transcription factor CREB binds to the cAMP response element (CRE) and after phosphorylation on Ser by PKA stimulates transcription. The CREB family of transcription factor contains three members: CREB, CREM and ATF-1. Targeted expression of dominant negative mutants of CREB in transgenic mice leads to somatotroph or thyroid hypoplasia. GH-secreting adenomas are benign secreting tumors expressing an activated Gas protein (Gsp) in about 40% of cases. In GH adenomas, CREB is always expressed and often highly phosphorylated. The CREM isoform ICER is stimulated by cAMP and its expression is increased in Gsp-harboring tumors. After transfection in pituitary somatotroph cells, activating mutations of Gs protein (Gsp) as well as overexpression of wild type Gs stimulate transcription of various CRE-containing promoters via CREB in a Ser-specific dependent manner. Expression of a dominant negative mutant of the regulatory subunit RIA of PKA (PRKAR1A) observed in a kindred presenting with Carney complex (PRKAR1A Δ184-236)

Abstract: The cAMP pathway plays a major role in the development of endocrine tissues and various molecular defects of key components of this pathway (G protein, receptors, PKA, etc.) have been observed in endocrine tumors. The ubiquitous transcription factor CREB (cAMP‐response element binding protein) binds to the cAMP response element (CRE) and stimulates transcription after phosphorylation on Ser133 by PKA. The CREB family of transcription factors contains three members: CREB, CREM, and ATF‐1. Targeted expression of dominant‐negative mutants of CREB in transgenic mice leads to somatotrophs or thyroid hypoplasia. GH‐secreting adenomas are benign secreting tumors expressing an activated mutant Gαs protein (Gsp) in about 40% of cases. In GH‐secreting adenomas CREB is always expressed and often highly phosphorylated. The CREM isoform ICER is stimulated by cAMP, and its expression is increased in Gsp‐harboring tumors. After transfection in pituitary somatotroph cells, activating mutations of Gs protein (Gsp) and overexpression of wild‐type GαS stimulate transcription of various CRE‐containing promoters via CREB in a Ser133‐specific‐dependent manner. Activation of the cAMP pathway by ACTH is required for adrenal cortex (AdCx) maintenance and steroidogenesis. CREB is expressed in normal AdCx. Alterations of CRE binding proteins with loss of CREB expression and compensatory overexpression of CREMτ is observed in the human adrenocortical cancer cell line H295R. Similar alterations are found at the protein level in human malignant adrenocortical tumors. In conclusion, the CREB family of transcription factors plays an important role in the development, differentiation, and proliferation of endocrine tissues. Various alterations of the CREB family of transciption factors can be observed in endocrine tumors.

The cyclic AMP (cAMP) pathway plays a major role in the development of endocrine tissues and various molecular defects of key components of this pathway (G protein, receptors, PKA, …) have been observed in endocrine tumors. Hypersecretion of adrenocorticotropin hormone (ACTH), the key activator of the cAMP pathway in adrenal cortex, is associated with adrenocortical hyperplasia and cortisol oversecretion (Cushing's syndrome). The best example of « illegitimate » membrane receptors expression reported is the abnormal expression of the adenylyl cyclase activating gastric inhibitory peptide receptor (GIP-R) in ACTH-independent Cushing's syndrome (ACS). We have observed that ectopic expression of the GIP-R is frequent in ACTH-Independent Macronodular Adrenal Hyperplasia (AIMAH), rare in benign adrenal adenoma (AA), but seems absent in Adrenal Cancer (AC). In vivo systematic screening of AIMAH shows at least one abnormal response of cortisol (suggesting « illegitimate » membrane receptor expression) in almost all patients. Somatic and germ line inactivating mutations of PRKAR1 (regulatory subunit R1A of PKA) can be observed in patient with isolated primary pigmented nodular adrenocortical disease (PPNAD) and AA responsible for ACS. At the nuclear level, the cAMP pathway regulates transcription mainly by PKA-dependent phosphorylation of the cyclic AMP response element binding (CREB) family of transcription factors (CREB, CREM, and ATF-1). Cyclic AMP response element binding protein (CREB) is expressed in normal adrenal cortex. Alterations of CRE binding proteins with loss of CREB expression and compensatory overexpression of CREMtau is observed in the human adrenocortical cancer cell line H295R. Similar alterations are found at the protein level in human malignant adrenocortical tumors. In conclusion, various alterations leading to activation or inactivation of key components of the cAMP signaling pathway can be observed in adrenocortical tumorigenesis.

Several companies now provide cost-effective, indefinitely scalable file storage in the cloud. However, the problem of verifying the integrity of data on untrusted storage sites is largely unanswered. Examining Amazon’s Simple Storage Service (S3) as a case study [1], we note that there are no mechanisms incorporated into S3 that would allow a user to detect changes in stored files, due to data corruption or malicious tampering. Naive solutions, such as retaining a copy of each file for comparison, or simply maintaining checksums of each stored file, do not scale well: when dealing with very large amounts of data, even keeping a checksum for each file becomes space intensive, especially for users who seek to outsource their storage needs. In this paper, we examine prior work in developing scalable solutions to the outsourced data integrity problem. Using insights from these works, we propose a refinement of previous techniques that would allow a completely clientside implementation that provides authenticity guarantees at minimal performance and financial cost. Notably, this solution does not require the use of an external authentication server. The paper is structured as follows. In Section 2, we review the authenticated skip list data structure, explain how it can be used for data integrity applications, and review more recent advancements. In Section 3, we present a high-level overview of our new system. In Section 4, we describe our implementation in more detail. In Section 5, we provide initial performance measurements to support the viability of this system and assess the cost of implementation. Finally, in Section 6, we present a roadmap for future work.

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