Miracle-dz/UniFAR-FTUs huggingface dataset:
Testing executive function models of ADHD and its comorbid conditions: A latent variable approach

Testing Executive Function Models of ADHD and Its Comorbid Conditions: A Latent Variable Approach. (August 2004) Dong Hyung Lee, B.A.; M.A., Chungnam National University, South Korea Chair of Advisory Committee: Dr. Cynthia A. Riccio Current theoretical models of ADHD (i.e., Disinhibition Model: Barkley, 1997; Working Memory Model: Rapport et al., 2001) conceptualize ADHD as the disorder of executive function (EF) with some variation in their emphases on particular components of the broadly-defined EF (e.g., working memory vs. inhibition) and in their postulated relationships with ADHD symptoms. Although these models provide systematic accounts of the manifestation of ADHD, they have not been extensively tested from an empirical standpoint. Moreover, despite the fact that ADHD is highly comorbid with other additional conditions such as learning and behavioral problems and EF deficits are found in individuals with these conditions as well as in those with ADHD, current EF models have not specified the developmental relationship between ADHD and its comorbid conditions. This study was: (1) to examine the extent to which two current models of ADHD are supported in a sample of 102 adults; (2) to present an “integrated” model by combining two current models of ADHD and linking them to recent research findings on two common comorbid conditions with ADHD (i.e., reading difficulty and substance abuse); and (3) to test and revise such an integrated model in the light of data using a latent variable analysis. Major findings provided a strong support for the Working Memory Model with a lesser
Matrix model combinatorics: applications to folding and coloring

We present a detailed study of the combinatorial interpretation of matrix integrals, including the examples of tessellations of arbitrary genera, and loop models on random surfaces. After reviewing their methods of solution, we apply these to the study of various folding problems arising from physics, including: the meander (or polymer folding) problem ``enumeration of all topologically inequivalent closed non-intersecting plane curves intersecting a line through a given number of points" and a fluid membrane folding problem reformulated as that of ``enumerating all vertex-tricolored triangulations of arbitrary genus, with given numbers of vertices of either color".
The Enigma of CDMA Revisited

In this paper, we explore the mystery of synchronous CDMA as applied to wireless and optical communication systems under very general settings for the user symbols and the signature matrix entries. The channel is modeled with real/complex additive noise of arbitrary distribution. Two problems are addressed. The first problem concerns whether overloaded error free codes exist in the absence of additive noise under these general settings, and if so whether there are any practical optimum decoding algorithms. The second one is about the bounds for the sum channel capacity when user data and signature codes employ any real or complex alphabets (finite or infinite). In response to the first problem, we have developed practical Maximum Likelihood (ML) decoding algorithms for overloaded CDMA systems for a large class of alphabets. In response to the second problem, a general theorem has been developed in which the sum capacity lower bounds with respect to the number of users and spreading gain and Signal-to-Noise Ratio (SNR) can be derived as special cases for a given CDMA system. To show the power and utility of the main theorem, a number of sum capacity bounds for special cases are simulated. An important conclusion of this paper is that the lower and upper bounds of the sum capacity for small/medium size CDMA systems depend on both the input and the signature symbols; this is contrary to the asymptotic results for large scale systems reported in the literature (also confirmed in this paper) where the signature symbols and statistics disappear in the asymptotic sum capacity. Moreover, these questions are investigated for the case when not all users are active. Furthermore, upper and asymptotic bounds are derived and numerically evaluated and compared to other derivations.
Ovarian Cancer and BRCA1/2 Testing: Opportunities to Improve Clinical Care and Disease Prevention

Without prevention or screening options available, ovarian cancer is the most lethal malignancy of the female reproductive tract. High-grade serous ovarian cancer (HGSOC) is the most common histologic subtype, and the role of germline BRCA1/2 mutation in predisposition and prognosis is established. Given the targeted treatment opportunities with PARP inhibitors, a predictive role for BRCA1/2 mutation has emerged. Despite recommendations to provide BRCA1/2 testing to all women with histologically confirmed HGSOC, uniform implementation remains challenging. The opportunity to review and revise genetic screening and testing practices will identify opportunities, where universal adoption of BRCA1/2 mutation testing will impact and improve treatment of women with ovarian cancer. Improving education and awareness of genetic testing for women with cancer, as well as the broader general community, will help focus much-needed attention on opportunities to advance prevention and screening programs in ovarian cancer. This is imperative not only for women with cancer and those at risk of developing cancer but also for their first-degree relatives. In addition, BRCA1/2 testing may have direct implications for patients with other types of cancers, many of which are now being found to have BRCA1/2 involvement.
Chemotherapy compared with bone marrow transplantation for adults with acute lymphoblastic leukemia in first remission.

OBJECTIVE To compare efficacy of intensive postremission chemotherapy with allogeneic bone marrow transplantation in adults with acute lymphoblastic leukemia (ALL) in first remission. DESIGN Retrospective comparison of two cohorts of patients. SETTING Chemotherapy recipients were treated in 44 hospitals in West Germany in two cooperative group trials; transplants were done in 98 hospitals worldwide. PATIENTS Patients (484) receiving intensive postremission chemotherapy and 251 recipients of HLA-identical sibling bone marrow transplants for ALL in first remission. Patients ranged from 15 to 45 years of age and were treated between 1980 and 1987. MAIN RESULTS Similar prognostic factors predicted treatment failure (non-T-cell phenotype, high leukocyte count at diagnosis, and 8 or more weeks to achieve first remission) of both therapies. After statistical adjustments were made for differences in disease characteristics and time-to-treatment, survival was similar in the chemotherapy and transplant cohorts: Five-year leukemia-free survival probability was 38% (95% CI, 33% to 43%) with chemotherapy and 44% (CI, 37% to 52%) with transplant. No specific prognostic group had a significantly better outcome with one treatment compared with the other (6% for the difference; CI, -3% to 15%). Causes of treatment failure differed: With chemotherapy, 268 (96%) failures were from relapse and 11 (4%) were treatment-related; with transplants, 43 (32%) failures were from relapse and 92 (68%) were treatment-related. CONCLUSIONS These results suggest that bone marrow transplants currently offer no special advantage over chemotherapy for adults with acute lymphoblastic leukemia in first remission.
Smad-Binding Defective Mutant of Transforming Growth Factor β Type I Receptor Enhances Tumorigenesis but Suppresses Metastasis of Breast Cancer Cell Lines

The role of transforming growth factor β (TGF-β) in carcinogenesis is complex, with tumor suppressor and pro-oncogenic activities depending on the particular tumor cell and its stage in malignant progression. We previously have demonstrated in breast cancer cell lines that Smad2/3 signaling played a dominant role in mediating tumor suppressor effects on well-differentiated breast cancer cell lines grown as xenografts and prometastatic effects on a more invasive, metastatic cell line. Our present data based on selective interference with activation of endogenous Smad2 and Smad3 by stable expression of a mutant form of the TGF-β type I receptor (RImL45) unable to bind Smad2/3 but with a functional kinase again show that reduction in Smad2/3 signaling by expression of RImL45 enhanced the malignancy of xenografted tumors of the well-differentiated MCF10A-derived tumor cell line MCF10CA1h, resulting in formation of larger tumors with a higher proliferative index and more malignant histologic features. In contrast, expression of RImL45 in the more aggressive MCF10CA1a cell line strongly suppressed formation of lung metastases following tail vein injection. These results suggest a causal, dominant role for the endogenous Smad2/3 signaling pathway in the tumor suppressor and prometastatic activities of TGF-β in these cells. Using an in vitro assay, we further show that non-Smad signaling pathways, including p38 and c-Jun NH2-terminal kinase, cooperate with TGF-β/Smads in enhancing migration of metastatic MCF10CA1a cells, but that, although necessary for migration, these other pathways are not sufficient for metastasis.
On the universality of inversion layer mobility in Si MOSFET's: Part I-effects of substrate impurity concentration

This paper reports the studies of the inversion layer mobility in n- and p-channel Si MOSFET's with a wide range of substrate impurity concentrations (10/sup 15/ to 10/sup 18/ cm/sup -3/). The validity and limitations of the universal relationship between the inversion layer mobility and the effective normal field (E/sub eff/) are examined. It is found that the universality of both the electron and hole mobilities does hold up to 10/sup 18/ cm/sup -3/. The E/sub eff/ dependences of the universal curves are observed to differ between electrons and holes, particularly at lower temperatures. This result means a different influence of surface roughness scattering on the electron and hole transports. On substrates with higher impurity concentrations, the electron and hole mobilities significantly deviate from the universal curves at lower surface carrier concentrations because of Coulomb scattering by the substrate impurity. Also, the deviation caused by the charged centers at the Si/SiO/sub 2/ interface is observed in the mobility of MOSFET's degraded by Fowler-Nordheim electron injection. >
Determinants of a transcriptionally competent environment at the GM-CSF promoter

Granulocyte macrophage-colony stimulating factor (GM-CSF) is produced by T cells, but not B cells, in response to immune signals. GM-CSF gene activation in response to T-cell stimulation requires remodelling of chromatin associated with the gene promoter, and these changes do not occur in B cells. While the CpG methylation status of the murine GM-CSF promoter shows no correlation with the ability of the gene to respond to activation, we find that the basal chromatin environment of the gene promoter influences its ability to respond to immune signals. In unstimulated T cells but not B cells, the GM-CSF promoter is selectively marked by enrichment of histone acetylation, and association of the chromatin-remodelling protein BRG1. BRG1 is removed from the promoter upon activation concomitant with histone depletion and BRG1 is required for efficient chromatin remodelling and transcription. Increasing histone acetylation at the promoter in T cells is paralleled by increased BRG1 recruitment, resulting in more rapid chromatin remodelling, and an associated increase in GM-CSF mRNA levels. Furthermore, increasing histone acetylation in B cells removes the block in chromatin remodelling and transcriptional activation of the GM-CSF gene. These data are consistent with a model in which histone hyperacetylation and BRG1 enrichment at the GM-CSF promoter, generate a chromatin environment competent to respond to immune signals resulting in gene activation.
X-linked Alport syndrome caused by splicing mutations in COL4A5.

BACKGROUND AND OBJECTIVES X-linked Alport syndrome is caused by mutations in the COL4A5 gene. Although many COL4A5 mutations have been detected, the mutation detection rate has been unsatisfactory. Some men with X-linked Alport syndrome show a relatively mild phenotype, but molecular basis investigations have rarely been conducted to clarify the underlying mechanism. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS In total, 152 patients with X-linked Alport syndrome who were suspected of having Alport syndrome through clinical and pathologic investigations and referred to the hospital for mutational analysis between January of 2006 and January of 2013 were genetically diagnosed. Among those patients, 22 patients had suspected splice site mutations. Transcripts are routinely examined when suspected splice site mutations for abnormal transcripts are detected; 11 of them showed expected exon skipping, but others showed aberrant splicing patterns. The mutation detection strategy had two steps: (1) genomic DNA analysis using PCR and direct sequencing and (2) mRNA analysis using RT-PCR to detect RNA processing abnormalities. RESULTS Six splicing consensus site mutations resulting in aberrant splicing patterns, one exonic mutation leading to exon skipping, and four deep intronic mutations producing cryptic splice site activation were identified. Interestingly, one case produced a cryptic splice site with a single nucleotide substitution in the deep intron that led to intronic exonization containing a stop codon; however, the patient showed a clearly milder phenotype for X-linked Alport syndrome in men with a truncating mutation. mRNA extracted from the kidney showed both normal and abnormal transcripts, with the normal transcript resulting in the milder phenotype. This novel mechanism leads to mild clinical characteristics. CONCLUSIONS This report highlights the importance of analyzing transcripts to enhance the mutation detection rate and provides insight into genotype-phenotype correlations. This approach can clarify the cause of atypically mild phenotypes in X-linked Alport syndrome.
Essential Roles of the Kar2/BiP Molecular Chaperone Downstream of the UPR Pathway in Cryptococcus neoformans

The endoplasmic reticulum (ER) is a central hub where secreted or membrane-bound proteins are maturated and folded properly in eukaryotes. Maintenance of ER homeostasis is particularly important for human fungal pathogens, such as Cryptococcus neoformans, which encounter a plethora of host-mediated stresses during infection. Our previous study demonstrated that the unfolded protein response (UPR) pathway, composed of the evolutionarily conserved Ire1 kinase and the unique Hxl1 transcription factor, has pleiotropic roles in ER stress response, thermotolerance, antifungal drug resistance, and virulence in C. neoformans. Here, we functionally characterized an ER-resident molecular chaperone, Kar2/BiP, in C. neoformans. Conditional expression of KAR2 by the copper-regulated promoter revealed that Kar2 is essential for the viability of C. neoformans. Constitutive expression of KAR2 by the strong histone H3 promoter partially restores resistance to ER stress, cell wall stress, thermotolerance, and genotoxic stress in ire1Δ and hxl1Δ mutants, suggesting that Kar2 mainly functions downstream of the UPR pathway. Furthermore, Kar2 appears to control azole resistance in C. neoformans downstream of the UPR pathway without regulation of ERG11 or ERG3. Interestingly, we discovered that azole treatment is sensed as ER-stress and subsequently activates the Ire1-dependent Hxl1 splicing event and induction of KAR2 by the UPR pathway. In contrast, the constitutive expression of Kar2 is not sufficient to restore the Ire1-mediated regulation of capsule production in C. neoformans UPR mutants. In conclusion, this study demonstrates that Kar2 is not only essential for vegetative growth but also required for response and adaptation to the environmental stresses and antifungal drugs downstream of the UPR pathway in C. neoformans.
Adverse effects of peroxidized lipid on human spermatozoa

Peroxidation of the sperm cells’ own phospholipids, closely bound up with declining motility, has been demonstrated in human spermatozoa; the rate of peroxidation was determined quantitatively by the reaction with thiobarbituric acid. Immotile or poorly motile spermatozoa from necrospermic or oligospermic semen exhibited a higher rate of peroxidation than highly motile spermatozoa from normal ejaculates. Peroxidized unsaturated fatty acids added to washed sperm suspensions immobilized the spermatozoa rapidly and permanently. Human seminal plasma was found to contain a non-ultrafiltrable factor which effectively prevented, but did not reverse, the toxic effect upon spermatozoa of either endogenous or exogenous lipid peroxides.
High Fat Diet-Induced Skeletal Muscle Wasting Is Decreased by Mesenchymal Stem Cells Administration: Implications on Oxidative Stress, Ubiquitin Proteasome Pathway Activation, and Myonuclear Apoptosis

Obesity can lead to skeletal muscle atrophy, a pathological condition characterized by the loss of strength and muscle mass. A feature of muscle atrophy is a decrease of myofibrillar proteins as a result of ubiquitin proteasome pathway overactivation, as evidenced by increased expression of the muscle-specific ubiquitin ligases atrogin-1 and MuRF-1. Additionally, other mechanisms are related to muscle wasting, including oxidative stress, myonuclear apoptosis, and autophagy. Stem cells are an emerging therapy in the treatment of chronic diseases such as high fat diet-induced obesity. Mesenchymal stem cells (MSCs) are a population of self-renewable and undifferentiated cells present in the bone marrow and other mesenchymal tissues of adult individuals. The present study is the first to analyze the effects of systemic MSC administration on high fat diet-induced skeletal muscle atrophy in the tibialis anterior of mice. Treatment with MSCs reduced losses of muscle strength and mass, decreases of fiber diameter and myosin heavy chain protein levels, and fiber type transitions. Underlying these antiatrophic effects, MSC administration also decreased ubiquitin proteasome pathway activation, oxidative stress, and myonuclear apoptosis. These results are the first to indicate that systemically administered MSCs could prevent muscle wasting associated with high fat diet-induced obesity and diabetes.
Performance Analysis and Power Allocation for Two-Way Amplify-and-Forward Relaying With Generalized Differential Modulation

Differential modulation has been proposed to mitigate the difficulties involved in estimating the channel state information (CSI) in a two-way relay network (TWRN). However, it suffers at least 3-dB performance loss compared with the coherent detection. This work proposes a new differential modulation and detection scheme to close the performance gap for TWRN using amplify-and-forward (AF) protocol. At two source nodes T1 and T2, a block-by-block differential encoder is employed, where each block consists of one reference symbol (RS) and several normal symbols (NSs). After two-way AF (TWAF) relaying, the information bits can be recovered without any knowledge of CSI. The bit-error-rate (BER) performance of the proposed scheme is analyzed, and closed-form expressions for the lower bound of BER and its high signal-to-noise ratio (SNR) approximation are derived. To minimize the lower bound of BER, we also investigate power allocation among the RS and the NSs in each block. Simulation results show that the performance gap between the proposed differential transmission scheme with a block length of 256 and the coherent receiver with perfect CSI is within 0.5 dB in quasi-static fading channels.
Like Is, like, Focus

In these examples (and throughout) I have italicized like for the reader's convenience; but it is important not to mistake the italics for any hint of stress. GRAMMATICAL like can be stressed, as in A whale is like a fish, but it isn't really afish. NONSTANDARD like, to my knowledge, can never be stressed. I will demonstrate, with examples, that nonstandard like is neither random nor mindless. Instead, it functions with great reliability as a marker of new information and focus.
The Human Factor in Quality: Examining the ISO 9000 and Business Excellence Frameworks in Selected Greek Organizations

The aim of this chapter is to theoretically investigate the implications of ISO 9000:2000 and EQA on HR issues in selected Greek industrial organizations in their road to quality improvement. The study sample consists of two selected industrial organizations that were judged as normal, ordinary, and representative. The data gathering was carried out through extensive and in-depth interviews in the two organizations asking several multiple informants. The study shows that organizations approach to quality is of great influence to effective human resource utilization. There is a tendency to avoid the involvement of HR department on either certification or the EQA and also it is clear that HR department status and role is still very traditional. The small sample does not allow making any generalizations for the majority of Greek organizations in all sectors of the economy. This is the first step towards an understanding of the current context and content of HRM in organizations moving towards total quality management implementing ISO 9000:2000 or EQA model. However, further studies needed to investigate similarities and differences in an international basis. The chapter provides a basis for understanding the present status of HRM implementation under ISO 9000 implementation and EQA model of selected Hellenic organizations and the results can be helpful for academics and practitioners. The author suggests that in order to have a reliable and objective depiction of the effect and influence of ISO 9000:2000 and EQA to the context and content of HRM, a thorough examination and analysis of relevant studies should be conducted which will include all the various approaches, practices and perceptions recorded so far in the literature -some of them based on empirical data and some deriving from rhetoric and “good-stories” or “how things ought to be” perspective. DOI: 10.4018/978-1-60566-996-0.ch009