EEF-CAS: An Effort Estimation Framework with Customizable Attribute Selection

Existing estimation frameworks generally provide one-size-fits-all solutions that fail to produce accurate estimates in most environments. Research has shown that the accomplishment of accurate effort estimates is a long-term process that, above all, requires the extensive collection of effort estimation data by each organization. Collected data is generally characterized by a set of attributes that are believed to affect the development effort. The attributes that most affect development effort vary widely depending on the type of product being developed and the environment in which it is being developed. Thus, any new estimation framework must offer the flexibility of customizable attribute selection. Moreover, such attributes could provide the ability to incorporate empirical evidence and expert judgment into the effort estimation framework. Finally, because software is virtual and therefore intangible, the most important software metrics are notorious for being subjective according to the experience of the estimator. Consequently, a measurement and inference system that is robust to subjectivity and uncertainty must be in place. The Effort Estimation Framework with Customizable Attribute Selection (EEF-CAS) presented in this paper has been designed with the above requirements in mind. It is accompanied with four preparation process steps that allow for any organization implementing it to establish an estimation process. This estimation process facilitates data collection, framework customization to the organization’s needs, its calibration with the organization’s data, and the capability of continual improvement. The proposed framework described in this paper was validated in a real software development organization

Exile Vol. XXXIII No. 2

POETRY Seams by Jennie Dawes 7 The Milky Blue Water by Mark Livengood 8-9 Patchwork by Mark Livengood 10 Belle Epoque by Karen J. Hall 21 Ballad by Zachary Smith 22-23 My Grandmother\u27s House by Karen J. Hall 24 Ghost by Jennie Dawes 27 What\u27s for Dessert? by Jennifer H. Miller 28 Dreams by Kent Lambert 31 Postmarked Fort Hill by Jennifer H. Miller 32 FICTION A Fostoria Tale by Debra Benko 13-18 The Pile by Jeff Montgomery 35-40 ARTWORK untitled by Lauren Kronish (cover) Standing by Heidi Rubin 3 Home, Part I by Heidi Rubin 4 Untitled by Dan Kirk 19 Infra-red (untitled) by Woody Woodroof 26 Florence, Italy (untitled) by Eliza Brown 29 Mwanafunzi by David Bloch 33 Joshua Tree by Susan McLain 41 CONTRIBUTOR\u27S NOTES 43 Editors share equally all editorial decisions. -2 NOTE: the artwork Home, Part I by Heidi Rubin does not appear to have been published, although it is listed in the table of contents for this issue and so is included here

MineXR: Mining Personalized Extended Reality Interfaces

Extended Reality (XR) interfaces offer engaging user experiences, but their effective design requires a nuanced understanding of user behavior and preferences. This knowledge is challenging to obtain without the widespread adoption of XR devices. We introduce MineXR, a design mining workflow and data analysis platform for collecting and analyzing personalized XR user interaction and experience data. MineXR enables elicitation of personalized interfaces from participants of a data collection: for any particular context, participants create interface elements using application screenshots from their own smartphone, place them in the environment, and simultaneously preview the resulting XR layout on a headset. Using MineXR, we contribute a dataset of personalized XR interfaces collected from 31 participants, consisting of 695 XR widgets created from 178 unique applications. We provide insights for XR widget functionalities, categories, clusters, UI element types, and placement. Our open-source tools and data support researchers and designers in developing future XR interfaces.Comment: 17 pages, 18 figures, Proceedings of the 2024 CHI Conference on Human Factors in Computing System

Structure and N-acetylglucosamine binding of the distal domain of mouse adenovirus 2 fibre

15 pags, 8 figsMurine adenovirus 2 (MAdV-2) infects cells of the mouse gastrointestinal tract. Like human adenoviruses, it is a member of the genus Mastadenovirus, family Adenoviridae. The MAdV-2 genome has a single fibre gene that expresses a 787 residue-long protein. Through analogy to other adenovirus fibre proteins, it is expected that the carboxy-terminal virus-distal head domain of the fibre is responsible for binding to the host cell, although the natural receptor is unknown. The putative head domain has little sequence identity to adenovirus fibres of known structure. In this report, we present high-resolution crystal structures of the carboxy-terminal part of the MAdV-2 fibre. The structures reveal a domain with the typical adenovirus fibre head topology and a domain containing two triple ß-spiral repeats of the shaft domain. Through glycan microarray profiling, saturation transfer difference nuclear magnetic resonance spectroscopy, isothermal titration calorimetry and site-directed mutagenesis, we show that the fibre specifically binds to the monosaccharide N-acetylglucosamine (GlcNAc). The crystal structure of the complex reveals that GlcNAc binds between the AB and CD loops at the top of each of the three monomers of the MAdV-2 fibre head. However, infection competition assays show that soluble GlcNAc monosaccharide and natural GlcNAc-containing polymers do not inhibit infection by MAdV-2. Furthermore, site-directed mutation of the GlcNAc-binding residues does not prevent the inhibition of infection by soluble fibre protein. On the other hand, we show that the MAdV-2 fibre protein binds GlcNAc-containing mucin glycans, which suggests that the MAdV-2 fibre protein may play a role in viral mucin penetration in the mouse gut.This research was sponsored by grant BFU2014-53425-P (to M. J. v. R.), coordinated grants CTQ2015-64597-P-C02-01 and CTQ2015-64597-P-C02-02 (to J. J. B. and F. J. C., respectively), grant BFU2015-70052-R (to M. M.) and the Spanish Adenovirus Network (AdenoNet, BIO2015-68990-REDT), all from the Spanish Agencia Estatal de Investigación. Financial support to M. M. from the CIBER of Respiratory Diseases (CIBERES) from the Spanish Institute of Health Carlos III is also acknowledged. These grants are co-financed by the European Regional Development Fund of the European Union. A. K. S. and T. H. N. were recipients of pre-doctoral fellowships from La Caixa and CSIC-VAST, respectively. The expression vectors were designed and created in Hungary, and this was financed by the Hungarian Scientific Research Fund (OTKA K100163). M. K. thanks Enterprise Ireland for a Commercialisation Fund grant (CF/2015/0089), A. K. acknowledges the National University of Ireland for a Cancer Care West Hardiman PhD scholarship and L. J. acknowledges the EU FP7 programme in support of the GlycoHIT consortium (grant no. 260600). This work was supported by R01 AI104920 (to J. G. S.) from the National Institute for Allergy and Infectious Diseases (www.niaid.nih.gov). S. S. W. was also supported by the Helen Riaboff Whiteley Endowment to the University of Washington and by Public Health Service, National Research Service Awards T32 AI083203 from the National Institute for Allergy and Infectious Diseases and T32 GM007270 from the National Institute of General Medical Sciences

Microdeletion del(22)(q12.2) encompassing the facial development-associated gene, MN1 (meningioma 1) in a child with Pierre-Robin sequence (including cleft palate) and neurofibromatosis 2 (NF2): a case report and review of the literature

<p>Abstract</p> <p>Background</p> <p>Pierre-Robin sequence (PRS) is defined by micro- and/or retrognathia, glossoptosis and cleft soft palate, either caused by deformational defect or part of a malformation syndrome. Neurofibromatosis type 2 (NF2) is an autosomal dominant syndrome caused by mutations in the <it>NF2 </it>gene on chromosome 22q12.2. NF2 is characterized by bilateral vestibular schwannomas, spinal cord schwannomas, meningiomas and ependymomas, and juvenile cataracts. To date, NF2 and PRS have not been described together in the same patient.</p> <p>Case presentation</p> <p>We report a female with PRS (micrognathia, cleft palate), microcephaly, ocular hypertelorism, mental retardation and bilateral hearing loss, who at age 15 was also diagnosed with severe NF2 (bilateral cerebellopontine schwannomas and multiple extramedullary/intradural spine tumors). This is the first published report of an individual with both diagnosed PRS and NF2. High resolution karyotype revealed 46, XX, del(22)(q12.1q12.3), FISH confirmed a deletion encompassing <it>NF2</it>, and chromosomal microarray identified a 3,693 kb deletion encompassing multiple genes including <it>NF2 </it>and <it>MN1 </it>(meningioma 1).</p> <p>Five additional patients with craniofacial dysmorphism and deletion in chromosome 22-adjacent-to or containing <it>NF2 </it>were identified in PubMed and the DECIPHER clinical chromosomal database. Their shared chromosomal deletion encompassed <it>MN1</it>, <it>PITPNB </it>and <it>TTC28</it>. <it>MN1</it>, initially cloned from a patient with meningioma, is an oncogene in murine hematopoiesis and participates as a fusion gene (<it>TEL</it>/<it>MN1</it>) in human myeloid leukemias. Interestingly, <it>Mn1</it>-haploinsufficient mice have abnormal skull development and secondary cleft palate. Additionally, <it>Mn1 </it>regulates maturation and function of calvarial osteoblasts and is an upstream regulator of <it>Tbx22</it>, a gene associated with murine and human cleft palate. This suggests that deletion of <it>MN1 </it>in the six patients we describe may be causally linked to their cleft palates and/or craniofacial abnormalities.</p> <p>Conclusions</p> <p>Thus, our report describes a <it>NF2</it>-adjacent chromosome 22q12.2 deletion syndrome and is the first to report association of <it>MN1 </it>deletion with abnormal craniofacial development and/or cleft palate in humans.</p

Mutations in HYAL2, Encoding Hyaluronidase 2, Cause a Syndrome of Orofacial Clefting and Cor Triatriatum Sinister in Humans and Mice.

Orofacial clefting is amongst the most common of birth defects, with both genetic and environmental components. Although numerous studies have been undertaken to investigate the complexities of the genetic etiology of this heterogeneous condition, this factor remains incompletely understood. Here, we describe mutations in the HYAL2 gene as a cause of syndromic orofacial clefting. HYAL2, encoding hyaluronidase 2, degrades extracellular hyaluronan, a critical component of the developing heart and palatal shelf matrix. Transfection assays demonstrated that the gene mutations destabilize the molecule, dramatically reducing HYAL2 protein levels. Consistent with the clinical presentation in affected individuals, investigations of Hyal2-/- mice revealed craniofacial abnormalities, including submucosal cleft palate. In addition, cor triatriatum sinister and hearing loss, identified in a proportion of Hyal2-/- mice, were also found as incompletely penetrant features in affected humans. Taken together our findings identify a new genetic cause of orofacial clefting in humans and mice, and define the first molecular cause of human cor triatriatum sinister, illustrating the fundamental importance of HYAL2 and hyaluronan turnover for normal human and mouse development

Capsaicin-Induced Changes in LTP in the Lateral Amygdala Are Mediated by TRPV1

The transient receptor potential vanilloid type 1 (TRPV1) channel is a well recognized polymodal signal detector that is activated by painful stimuli such as capsaicin. Here, we show that TRPV1 is expressed in the lateral nucleus of the amygdala (LA). Despite the fact that the central amygdala displays the highest neuronal density, the highest density of TRPV1 labeled neurons was found within the nuclei of the basolateral complex of the amygdala. Capsaicin specifically changed the magnitude of long-term potentiation (LTP) in the LA in brain slices of mice depending on the anesthetic (ether, isoflurane) used before euthanasia. After ether anesthesia, capsaicin had a suppressive effect on LA-LTP both in patch clamp and in extracellular recordings. The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice. The specific antagonist of cannabinoid receptor type 1 (CB1), AM 251, was also able to reduce the inhibitory effect of capsaicin on LA-LTP, suggesting that stimulation of TRPV1 provokes the generation of anandamide in the brain which seems to inhibit NO synthesis. After isoflurane anesthesia before euthanasia capsaicin caused a TRPV1-mediated increase in the magnitude of LA-LTP. Therefore, our results also indicate that the appropriate choice of the anesthetics used is an important consideration when brain plasticity and the action of endovanilloids will be evaluated. In summary, our results demonstrate that TRPV1 may be involved in the amygdala control of learning mechanisms