Miracle-dz/UniFAR-FTUs huggingface dataset:
Transcriptional Program of Mouse Osteoclast Differentiation Governed by the Macrophage Colony-stimulating Factor and the Ligand for the Receptor Activator of NFκB*

Cytokines macrophage colony stimulating factor (M-CSF) and the receptor activator of NFκB ligand (RANKL) induce differentiation of bone marrow hematopoietic precursor cells into bone-resorbing osteoclasts without the requirement for stromal cells of mesenchymal origin. We used this recently described mouse cell system and oligonucleotide microarrays representing about 9,400 different genes to analyze gene expression in hematopoietic cells undergoing differentiation to osteoclasts. The ability of microarrays to detect the genes of interest was validated by showing expression and expected regulation of several osteoclast marker genes. In total 750 known transcripts were up-regulated by ≥2-fold, and 91% of them at an early time in culture, suggesting that almost the whole differentiation program is defined already in pre-osteoclasts. As expected, M-CSF alone induced the receptor for RANKL (RANK), but also, unexpectedly, other RANK/NFκB pathway components (TRAF2A, PI3-kinase, MEKK3, RIPK1), providing a molecular explanation for the synergy of M-CSF and RANKL. Furthermore, interleukins, interferons, and their receptors (IL-1α, IL-18, IFN-β, IL-11Rα2, IL-6/11R gp130, IFNγR) were induced by M-CSF. Although interleukins are thought to regulate osteoclasts via modulation of M-CSF and RANKL expression in stromal cells, we showed that a mix of IL-1, IL-6, and IL-11 directly increased the activity of osteoclasts by 8.5-fold. RANKL induced about 70 novel target genes, including chemokines and growth factors (RANTES (regulated on activation, normal T cell expressed and secreted), PDGFα, IGF1), histamine, and α1A-adrenergic receptors, and three waves of distinct receptors, transcription factors, and signaling molecules. In conclusion, M-CSF induced genes necessary for a direct response to RANKL and interleukins, while RANKL directed a three-stage differentiation program and induced genes for interaction with osteoblasts and immune and nerve cells. Thus, global gene expression suggests a more dynamic role of osteoclasts in bone physiology than previously anticipated.
Protein synthesis and degradation in flight muscles of adult crickets (Gryllus bimaculatus)

The development and degeneration of the flight muscles in adult crickets, Gryllus bimaculatus, were studied (1) by determination of the total protein content, (2) by SDS one-dimensional polyacrylamide gel electrophoresis (SDS­PAGE) of muscle protein and (3) by in vitro culturing of the muscle. The total protein content of the dorso-longitudinal muscle (DLM) and metathoracic dorso-ventral muscle (DVM) increased during the early days of adult life in both sexes. This high protein content was maintained for at least a further 10 days in some individuals, while in others it declined to a low level. Mesothoracic DVMs in males also showed an increase in protein content after adult emergence but did not undergo histolysis, whereas those in females showed no significant temporal change in protein content. Removal of hind wings or artificial de-alation was found to be useful in inducing degeneration of DLMs and metathoracic DVMs. This treatment also stimulated ovarian development in females. An analysis by SDS­PAGE provided no evidence for new protein synthesis prior to or during flight muscle degeneration. A high rate of [3H]- or [35S]methionine incorporation was observed in DLMs taken from newly emerged adults, but, in intact crickets, the rate declined rapidly during the first 3 days of adult life, a pattern consistent with that obtained from the measurement of total protein content. Compared with DLMs removed from intact crickets, DLMs taken from de-alated crickets showed reduced rates of protein synthesis during in vitro culturing. This, together with the onset of protein degradation, appears to cause the rapid decrease in total protein content of the muscle in de-alated crickets.
An Attempt to Evaluate Mental Workload Using Wavelet Transform of EEG

An attempt was made to evaluate mental workload using a wavelet transform of electroencephalographic (EEG) signals. Participants performed a continuous matching task at three levels of task difficulty. EEG signals during the task were recorded continuously from Fz, Cz, and Pz. The reaction time increased as the difficulty of the task increased. The percentage correct decreased as the task became more difficult. In accordance with this, the rating score on the NASA-Task Load Index tended to increase with increased task difficulty. The EEG signals were analyzed using wavelet transform to investigate time-frequency characteristics. The total power at θ, α, and β frequency bands and the time that the maximum power appeared for the three frequency bands were extracted from the scalogram. Increasing cognitive task difficulty seems to delay the time at which the central nervous system works most actively. These measures were found to be sensitive indicators of mental workload and could differentiate three cognitive task loads (low, moderate, and high) with high precision. Actual or potential applications of this research include a method that is relatively quick and accurate, compared with traditional methods, for the evaluation of mental workload.
Thyroid Abnormalities in Lithium-Treated Patients with Bipolar Affective Disorder

The thyroid functions of 42 subjects with bipolar affective disorder receiving regular lithium therapy were analysed and their thyroid glands were examined by ultrasonography. Following the receipt of lithium therapy (duration 4–156 months), three subjects displayed subclinical hypothyroidism (7.1%), three subclinical hyperthyroidism (7.1%) and one hyperthyroidism (2.4%). Moreover, goitre was detected in 16 (38.1%) subjects. An increase in the conversion of free thyroxine (T4) to free tri-iodothyrosine (T3), which is an indication of mild thyroid dysfunction, was identified in 20 (47.6%) subjects, and was mostly seen in male subjects under 40 years of age and in those having weight gain. In conclusion, some thyroid dysfunctions were observed in the patients treated with lithium.
[Analysis for the impact of adulthood and childhood socioeconomic positions and intergenerational social mobility on adulthood health].

OBJECTIVES There are at least three conceptual models for the effects of the childhood social environment on adult health: the critical period model, the social mobility model, and the cumulative risk model. However, few studies have investigated all three different models within the same setting. This study aims to examine the impact of childhood and adulthood socioeconomic positions and intergenerational social mobility over the life course on the health in adulthood based both on the critical period model and the social mobility model. METHODS This study was conducted on 9583 adults aged between 25 and 64 years old and they were the respondents to the Korea Welfare Panel Study (2006). A multivariate logistic regression analysis was carried out, using the critical period model and the social mobility model out of the life course approaches, to look into the impact of childhood and adulthood socioeconomic positions and intergenerational social mobility on the health status in adulthood. RESULTS Household income and occupation out of the adulthood socioeconomic position indicators had an independent influence on the adulthood health status. The childhood socioeconomic position indicators, except for the place of childhood residence, affected the adulthood health status even after adjustment for the adulthood socioeconomic position. The effect of intergenerational social mobility was also statistically significant even after adjusting for the adulthood socioeconomic position, but it became insignificant when the childhood socioeconomic position was additionally adjusted for. CONCLUSIONS Adulthood health is indeed affected by both the childhood and adulthood socioeconomic positions as well as intergenerational social mobility. This result shows that a life course approach needs to be adopted when dealing with health issues.
Prader-Willi syndrome: intellectual abilities and behavioural features by genetic subtype.

BACKGROUND Studies of chromosome 15 abnormality have implicated over-expression of paternally imprinted genes in the 15q11-13 region in the aetiology of autism. To test this hypothesis we compared individuals with Prader-Willi syndrome (PWS) due to uniparental disomy (UPD--where paternally imprinted genes are over-expressed) to individuals with the 15q11-13 deletion form of the syndrome (where paternally imprinted genes are not over-expressed). We also tested reports that PWS cases due to the larger type I (TI) form of deletion show differences to cases with the smaller type II (TII) deletion. METHOD Ninety-six individuals with PWS were recruited from genetic centres and the PWS association. Forty-nine individuals were confirmed as having maternal UPD of chromosome 15 and were age and sex matched to 47 individuals with a deletion involving 15q11-13 (32 had the shorter (T II) deletion, and 14 had the longer (TI) deletion). Behavioural assessments were carried out blind to genetic status, using the Autism Diagnostic Observation Schedule (ADOS), the Autism Diagnostic Interview (ADI), the Autism Screening Questionnaire (ASQ), the Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS), the Vineland Adaptive Behaviour Scales (VABS), and measurements of intellectual ability, including the Wechsler and Mullen Scales and Raven's Matrices. RESULTS UPD cases exhibited significantly more autistic-like impairments in reciprocal social interaction on questionnaire, interview and standardised observational measures. Comparison of TI and TII deletion cases revealed few differences, but ability levels tended to be lower in the TI deletion cases. CONCLUSIONS Findings from a large study comparing deletion and UPD forms of Prader-Willi syndrome were consistent with other evidence in indicating that paternally imprinted genes in the 15q11-13 region constitute a genetic risk factor for aspects of autistic symptomatology. These genes may therefore play a role in the aetiology of autism. By contrast with another report, there was no clear-cut relationship between the size of the deletion and the form of cognitive and behavioural phenotype.
Is Aortic Impedance Altered in Dwarf Mice?

Dwarf mouse (deficient in growth hormone and insulin-like growth factor-1) lives about 30% longer than wild type mice. However, very little is known about their cardiovascular physiology. We examined the aortic input impedance in dwarf mice and their wild-type littermates to evaluate any differences. Aortic impedance was determined using pressure and velocity signals which are independent of body size. Significant differences were observed in the body weight, aortic systolic, diastolic and mean pressures, and peak and mean aortic flow velocities. No differences were observed in impedance parameters of peripheral resistance, impedance at first harmonic, and characteristic impedance between the two groups. However, the impedance curve in the dwarf mice was higher at low frequency and decreased gradually with increasing frequencies but in the wild type mice the impedance curve oscillated around the characteristic impedance
Prospective multicentric randomized phase III study of imatinib in patients with advanced gastrointestinal stromal tumors comparing interruption versus continuation of treatment beyond 1 year: the French Sarcoma Group.

PURPOSE Imatinib is the standard treatment of advanced GI stromal tumors (GISTs). It is not known whether imatinib may be stopped in patients in whom disease is controlled. METHODS This prospective, randomized, multicentric phase III study was designed to compare continuous (CONT) compared with interrupted (INT) imatinib beyond 1 year of treatment in patients with advanced GIST. The primary end point was progression-free survival. Secondary end points included overall survival, response rate after reinitiation of imatinib, and quality of life. Early stopping rules in cases of rapid progression of disease were defined, with preplanned interim analyses. RESULTS Between May 2002 and April 2004, 182 patients with advanced GIST were enrolled. Between May 2003 and April 2004, 98 patients in response or stable disease under imatinib reached more than 1 year of follow-up. Forty were not eligible for randomization, and 58 patients were randomly assigned, 32 and 26 patients in the INT and CONT arms, respectively. As of October 15, 2005, eight of 26 patients in the CONT group and 26 of 32 patients in the INT group had documented disease progression (P < .0001). Twenty-four of 26 patients with documented progression in the INT arm responded to imatinib reintroduction. No differences in overall survival or imatinib resistance were observed between the two arms. Quality of life evaluated 6 months after random assignment using the 30-item Quality of Life Questionnaire was not significantly different between the two groups of randomly assigned patients. CONCLUSION Imatinib interruption results in rapid progression in most patients with advanced GIST, and cannot be recommended in routine practice unless patient experience significant toxicity
Individual income, income inequality, health, and mortality: what are the relationships?

OBJECTIVE To examine the pathways between income inequality, self-rated health, and mortality in the United States. DATA SOURCE The first National Health and Nutrition Examination Survey and Epidemiologic Follow-up Study. DESIGN This was a longitudinal, multilevel study. DATA COLLECTION Baseline data were collected on county income inequality, individual income, age, sex, self-rated health, level of depressive symptoms, and severity of biomedical morbidity from physical examination. Follow-up data included self-rated health assessed in 1982 through 1984 and mortality through 1987. PRINCIPAL FINDINGS After adjustment for age and sex, income inequality had a modest independent effect on the level of depressive symptoms, and on baseline and follow-up self-rated health, but no independent effect on biomedical morbidity or subsequent mortality. Individual income had a larger effect on severity of biomedical morbidity, level of depressive symptoms, baseline and follow-up self-rated health, and mortality. CONCLUSION Income inequality appears to have a small effect on self-rated health but not mortality; the effect is mediated in part by psychological, but not biomedical pathways. Individual income has a much larger effect on all of the health pathways.
Targeting of Endothelial Nitric-oxide Synthase to the Cytoplasmic Face of the Golgi Complex or Plasma Membrane Regulates Akt- Versus Calcium-dependent Mechanisms for Nitric Oxide Release*

The heterogeneous localization of endothelial nitricoxide synthase (eNOS) on the Golgi complex versus the plasma membrane has made it difficult to dissect the regulation of each pool of enzyme. Here, we generated fusion proteins that specifically target the plasma membrane or cytoplasmic aspects of the Golgi complex and have assessed eNOS activation. Plasma membrane-targeted eNOS constructs were constitutively active, phosphorylated, and responsive to transmembrane calcium fluxes, yet were insensitive to further activation by Akt-mediated phosphorylation. In contrast, cis-Golgi complex-targeted eNOS behaved similarly to wild-type eNOS and was less sensitive to calcium-dependent activation and highly responsive to Akt-dependent phosphorylation compared with plasma membrane versions. In plasma membrane- and Golgi complex-targeted constructs, Ser1179 is critical for NO production. This study provides clear evidence for functional roles of plasma membrane- and Golgi complex-localized eNOS and supports the concept that proteins thought to be regulated and to function exclusively in the plasma membrane of cells can indeed signal and be regulated in internal Golgi membranes.
Competitive Advantages of the Adoption and Use of Technological Systems in Hospitality Marketing: The Case Study of Croatia

Variable economic conditions, new forms of customer buying behavior and in particular new technology is likely to cause the emergence of new or growing existing hospitality markets. In developed European economies, all the more attention is paid to studying the role of new technologies in the field of hospitality marketing. Research focus will be directed towards the usage of technological systems in marketing of hospitality. Internet, as one of the most significant technological phenomena of our time, provides hotel managers completely new competitive opportunities, of which the most significant opportunity to provide immediate and always open access to information throughout the world. According to latest researches, Croatian hotel managers usually use these technological systems: Own web site, System to access the Internet, Points of sale (POS), System of calculating the telephone calls, Local area network (LAN), Uniform system of accounts for lodging Industry (USALI), Intranet system, Central reservation system (CRS), Marketing information system (MIS) and. Object management system (PMS). Modern hotel managers want to achieve automation of marketing strategies and interactive communication with potential guests. However, certain hotels are still not developed a marketing strategy through the Internet pages. Adjustment trends must be timely and possible, so it is necessary to intensify investment in that direction. As a result, it is assumed that the possibility of information and purchase via the Internet to stimulate the future purchase of tourists and change their previous spending habits. To make hotel companies improve their e-marketing strategy, the research shows insufficient usage of the following Web 2.0 tools in Croatian hospitality market: Instant Messaging, Internet Relay Chat, Internet Forums, Social Network Services, Social Guides, Social Bookmarking, Social Reputation Network, Web logs, Social Citations, Peer-to-peer Social Networks, Virtual Presence, Virtual Worlds & Massively Multiplayer Online Games, VOIP -- Internet Telephony and Mobile Internet. Establishing relationships and technological innovations significantly affect the shortening of business cycles and thus the importance of creating competitive advantages in the hospitality industry of Croatia.
Are there ethnic disparities in risk of preterm birth among infants born with congenital heart defects?

BACKGROUND Birth defects and preterm birth (PTB) are leading causes of infant morbidity and mortality in the United States. Infants with birth defects are more likely to be born preterm (<37 weeks), yet the roles of maternal ethnicity and fetal growth in this relationship are unclear. This study aimed to assess the risk of PTB among non-Hispanic (NH) Black, NH-White, and Hispanic infants with congenital heart defects (CHD), adjusting for fetal growth. METHODS Florida Birth Defects Registry data were used to conduct a retrospective cohort study on 14,319 live-born infants with CHDs born January 1, 1998 to December 31, 2002. ORs and 95% CIs were computed for each growth category (small-for-gestational age [SGA], appropriate-for-gestational-age [AGA], and large-for-gestational-age [LGA]) by ethnicity and adjusted for maternal and infant covariates using logistic regression. RESULTS After adjusting for potential confounders, SGA and AGA NH-Black infants with CHDs had increased risk of PTB compared to NH-White infants with CHDs (OR 1.79; 95% CI: 1.40, 2.30 and OR 1.89; 95% CI: 1.68, 2.13, respectively). Hispanic SGA, AGA, and infants with CHDs had no increased risk of PTB compared to NH-White infants. CONCLUSIONS The increased risk of PTB among SGA and AGA NH-Black infants with CHDs is not explained by the overall disparities in risk of PTB between NH-Blacks and NH-Whites. Additional studies are needed to determine the specific subtypes of CHD for which these relationships are present and if these findings are seen among infants with other birth defects.
Synthesis of Messenger Ribonucleic Acid After Bacteriophage T1 Infection

Synthesis of host-specific and phage-specific messenger ribonucleic acid (mRNA) was studied in bacteria infected by unmodified (T1 · B) or modified [T1 · B(P1)] bacteriophage T1. In a “standard” infection of Escherichia coli B by T1 · B (no host-controlled modification involved), the rate and amount of T1 mRNA synthesis was intermediate between those values reported for infections by a virulent phage such as T4 or a temperate phage such as lambda. The initial rate of mRNA synthesis was slightly increased after T1 · B(P1) infection of E. coli B in comparison with T1 · B infection of the same host. Little or no phage mRNA synthesis could be detected in T1 · B infection of E. coli B(P1). Phage mRNA synthesis in T1 · B(P1)-infected E. coli B(P1) cells was approximately the same in amount as that seen in T1 · B(P1) infection of E. coli B. Synthesis of host-specific mRNA continued throughout the latent period in all infections studied. However, the enzyme β-galactosidase could not be induced, except after T1 · B infection of E. coli B(P1). In an attempt to understand the apparent differences in mRNA synthesis after infection of E. coli B by phages T1 · B or T1 · B(P1), the effect of altered T1 deoxyribonucleic acid (DNA) methylation on mRNA synthesis was studied. Methyl-deficient T1 DNA, made in cells infected with ultraviolet-irradiated phage T3, inhibited 14C-uridine incorporation more strongly than normal T1. One passage of methyl-deficient T1 through E. coli B restored uracil incorporation rates to those seen with ordinary T1. This suggests that methylation of T1 DNA can influence the rate of phage mRNA synthesis. However, attempts to relate the difference in mRNA synthesis seen between T1 · B and T1 · B(P1) in E. coli B to the activity of the P1 modification gene were not conclusive.