Miracle-dz/UniFAR-FTUs huggingface dataset:
Factors influencing spatial patterns on coral reefs around Moorea, French Polynesia

Spatial patterns of 5 components of the macrobenthos [corals, macroalgae, mollusks, sponges, and echinoderms) at 42 stations on 4 reef types were compared in Moorea Fifteen a b ~ o t ~ c and biotic factors were measured and included in Canonical Correspondence Analyses. Macrobenthic communities were dominated by corals and macroalgae. Two major gradients (along the bays, and from the fringing reef to the outer reef slope) were found for corals, macroalgae, and echinoderms. The gradients were realized at a small spatial scale in Moorea [less than 2 km from the fringing reef to the outer reef slope at 35 m depth), while the same type of variation occurs at a large spat~al scale (more than 100 km) on the Great Barrier Reef. Abiotic and biotic factors explained a large amount of the variance in sponge and coral communities, but less for mollusks and markedly less for macroalgae and echinoderms. Some of the factors identified in this study, such as depth, sand coverage, and algal coverage, have been also reported as controlling factors in other coral reefs. In contrast, the high abundance of sea urchins and its impact seem to be characteristic of coral reefs around Moorea.
Does IT Capability and Competitive Actions Shape Firm Profitability?

Research investigating the relationship between information technology (IT) and firm profitability has been a central issue in the information systems (IS) area, and prior studies provided mixed and inconsistent results. To understand the causes of the inconsistent results, we adopted the competitive dynamics theory, which complements and extends other theories such as the resource-based view. This study develops a research model on how IT supports the exercise of competitive actions in the context of rivalry. Specifically, we suggest that IT capability enhances firm profitability by increasing competitive actions of a firm based on 668 firm-year observations in the United States (US). We have found that there is a positive influence of IT on firm performance. The results emphasize the need of considering competitive actions as a key factor to examine the value of IT in developing a firm’s competitiveness.
A comparative evaluation of DIAGNOdent with visual and radiography for detection of occlusal caries: an in vitro study.

BACKGROUND The diagnosis of dental caries is fundamental to the practice of dentistry. Despite the fact that dental caries has declined considerably, it is still a problem of great importance. The reduction in caries prevalence has not occurred uniformly for all the surfaces. The greatest reduction was observed at lesions located on smooth surfaces, so that occlusal caries are most common in children. AIM The purpose of this study is to determine the clinical efficacy of DIAGNOdent in detecting occlusal caries. MATERIALS AND METHODS A total number of 50 teeth were subjected for visual, radiographic, and DIAGNOdent examinations. All the three methods were compared to histology which is a gold standard. RESULTS The result obtained showed that DIAGNOdent is superior to visual and radiographic methods in diagnosing occlusal caries.
Hepatitis B Virus Reverse Transcriptase and ε RNA Sequences Required for Specific Interaction In Vitro

ABSTRACT Initiation of reverse transcription and nucleocapsid assembly in hepatitis B virus (HBV) depends on the specific recognition of an RNA signal (the packaging signal, ε) on the pregenomic RNA by the viral reverse transcriptase (RT). Using an in vitro reconstitution system whereby the cellular heat shock protein 90 chaperone system activates recombinant HBV RT for specific ε binding, we have defined the protein and RNA sequences required for specific HBV RT-ε interaction in vitro. Our results indicated that approximately 150 amino acid residues from the terminal protein domain and 230 from the RT domain were necessary and sufficient for ε binding. With respect to the ε RNA sequence, its internal bulge and, in particular, the first nucleotide (C) of the bulge were specifically required for RT binding. Sequences from the upper portion of the lower stem and the lower portion of the upper stem also contributed to RT binding, as did the base pairing of the upper portion and the single unpaired U residue of the upper stem. Surprisingly, the apical loop of ε, known to be required for RNA packaging, was entirely dispensable for RT binding. A comparison of the requirements for in vitro RT-ε interaction with those for in vivo pregenomic RNA (pgRNA) packaging clearly indicated that RT-ε interaction was necessary but not sufficient for pgRNA packaging. In addition, our results suggest that recognition of some ε sequences by the RT may be required specifically for viral DNA synthesis.
Carnosic acid suppresses colon tumor formation in association with antiadipogenic activity.

SCOPE This study determined the efficacy of carnosic acid (CA) for suppressing colon carcinogenesis associated with excess adiposity. METHODS AND RESULTS Cell growth regulation by CA was evaluated in HT-29 colon adenocarcinoma cells cocultured with 3T3-L1 adipocytes. To determine the in vivo efficacies, male A/J mice were divided into four groups and fed one of the following experimental diets for 11 wk: 15% fat, 45% fat, 45% fat + 0.01% CA, or 45% fat + 0.02% CA. Azoxymethane was administered at the beginning of experimental diet and two cycles of dextran sodium sulfate were supplied 1 wk after the azoxymethane injection. The proliferation of HT-29 cells cocultured with 3T3-L1 cells was significantly higher than proliferation of control cells (p < 0.05). CA treatment suppressed the growth of cocultured HT-29 cells through cell cycle arrest and enhanced apoptosis by inhibiting leptin receptor (Ob-R) signaling, including Akt and extracellular signal-regulated kinase (ERK) phosphorylation. CA supplementation in vivo decreased the number of colon tumors and reduced circulating concentrations of leptin, adiponectin, insulin, and insulin-like growth factor 1. Colonic expression of Ob-R, insulin receptor (IR), p-Akt, p-ERK, B-cell lymphoma extra large (Bcl-xL), and cyclinD1 protein was also suppressed in animals fed CA. CONCLUSION CA appears to alleviate adipocity-related acceleration of colon tumor formation.
Vesicular glutamate transporter 3 (VGLUT3) identifies spatially segregated excitatory terminals in the rat substantia nigra

The excitability of dopaminergic (DA) neurons in the substantia nigra is controlled by the convergent activity of multiple glutamatergic afferents. Here, we show that vesicular glutamate transporter 3 (VGLUT3)‐immunoreactive (ir) terminals segregate to the perisomatic region of DA neurons in the substantia nigra pars compacta, and VGLUT3 decorates a synapse population distinct from those marked by vesicular glutamate transporters 1 and 2. VGLUT3‐ir nerve endings form asymmetric terminals on DA neurons. Retrograde tracing suggests the superior colliculus as an origin of excitatory VGLUT3‐ir afferents. Collectively, our data indicate that VGLUT3 identifies a novel excitatory terminal subset that contributes to the tuning of DA cell excitability in the substantia nigra.
Obesity and dissociable forms of impulsivity in young adults

Objective Obesity is one of the leading causes of preventable morbidity and mortality, and young people are increasingly affected. The aim of this study was to examine relationships between obesity and dissociable forms of impulsivity in young adults. Methods A group of young adults (511) was recruited from city areas in the United States using media advertisements. These young adults were administered careful and extensive clinical and neurocognitive assessment in order to quantify different aspects of impulsivity (behavioral/phenomenological-, cognitive-, and personality-related measures). Associations between obesity and impulsivity were explored using multivariate analysis of variance and discriminant function analysis. Results 10.8% of the sample was obese, and 21.5% was overweight. Compared to controls, subjects with obesity showed significantly elevated rates of maladaptive gambling behaviors, monetary amounts lost to gambling, nicotine consumption, impulsive action (prolonged stop-signal reaction times in the Stop-Signal Test), and impulsive decision-making (reduced modulation of behavior as a function of risk in the Cambridge Gamble Test). Even accounting for potential confounding variables, obesity was significantly predicted by female gender, older age, more maladaptive gambling behaviors, and worse inhibitory control (stop-signal reaction times). Conclusion Obesity is associated with several dissociable forms of impulsivity in young people, especially gambling and impulse dyscontrol. Family doctors should screen for gambling problems in obese young adults. Successful treatment of nicotine dependence in young obese people is likely to require intensive weight management support. Neuropsychological deficits relating to impulsivity occur in obese people in early adulthood, and may represent vulnerability markers rather than being due to chronic untoward metabolic effects on brain function.
Cerebellar control of endpoint position-a simulation model

The ability of a neural network model of the cerebellum to control a nonlinear dynamical model of the neuromuscular system is explored. The cerebellum is represented by adjustable pattern generator (APG) modules capable of commanding movements from arbitrary starting positions to specific endpoints. The network is trained to match endpoints to visual targets using a biologically motivated learning rule. Neural signals recorded from a monkey subject helped to guide realistic simulations. The simulation results illustrate how commanded velocity automatically increases when the initial position of the limb is farther from the target position. The mechanism of this `feedforward' compensation can be traced to a smaller value of limb position input during the preselection period. The decreased excitation serves to increase the number of Purkinje cells that get switched to an off state before the movement begins, and the resultant decrease in loop inhibition leads to a larger commanded velocity. The simulations also demonstrate how limited feedback through the cerebellum can be used, without the threat of instability, to regulate the achievement of a targeted endpoint
Automatic Program Repair Using Genetic Programming

Software quality is an urgent problem. There are so many bugs in industrial program source code that mature software projects are known to ship with both known and unknown bugs [1], and the number of outstanding defects typically exceeds the resources available to address them [2]. This has become a pressing economic problem whose costs in the United States can be measured in the billions of dollars annually [3]. A dominant reason that software defects are so expensive is that fixing them remains a manual process. The process of identifying, triaging, reproducing, and localizing a particular bug, coupled with the task of understanding the underlying error, identifying a set of code changes that address it correctly, and then verifying those changes, costs both time [4] and money, and the cost of repairing a defect can increase by orders of magnitude as development progresses [5]. As a result, many defects, including critical security defects [6], remain unaddressed for long periods of time [7]. Moreover, humans are error-prone, and many human fixes are imperfect, in that they are either incorrect or lead to crashes, hangs, corruption, or security problems [8]. As a result, defect repair has become a major component of software maintenance, which in turn consumes up to 90% of the total lifecycle cost of a given piece of software [9]. Although considerable research attention has been paid to supporting various aspects of the manual debugging process [10, 11], and also to preempting or dynamically addressing particular classes of vulnerabilities, such as buffer overruns [12, 13], there exist virtually no previous automated solutions that address the synthesis of patches for general bugs as they are reported in real-world software. The primary contribution of this dissertation is GenProg, one of the very first automatic solutions designed to help alleviate the manual bug repair burden by automatically and generically patching bugs in deployed and legacy software. GenProg uses a novel genetic programming algorithm, guided by test cases and domain-specific operators, to affect scalable, expressive, and high quality automated repair. We present experimental evidence to substantiate our claims that GenProg can repair multiple types of bugs in multiple types of programs, and that it can repair a large proportion of the bugs that human developers address in practice (that it is expressive); that it scales to real-world system sizes (that it is scalable); and that it produces repairs that are of sufficiently high quality. Over the course of this evaluation, we contribute new benchmark sets of real bugs in real open-source software and novel experimental frameworks for quantitatively evaluating an automated repair technique. We also contribute a novel characterization of
Accelerated Bone Formation in Distracted Alveolar Bone After Injection of Recombinant Human Bone Morphogenetic Protein-2.

BACKGROUND This study evaluates the effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) on the quality and quantity of regenerated bone when injected into distracted alveolar bone. METHODS Sixteen adult beagle dogs were assigned to either the control or rhBMP-2 group. After distraction was completed, an rhBMP-2 dose of 330 μg in 0.33 mL was injected slowly into the distracted alveolar crest of the mesial, middle, and distal parts of the alveolar bone in the experimental group. Histologic and microcomputed tomography analyses of regenerated bone were done after 2 and 6 weeks of consolidation. RESULTS After 6 weeks of consolidation, the vertical defect height in the middle of the regenerated bone was significantly lower in the rhBMP-2 group (2.2 mm) than in the control group (3.4 mm) (P <0.05). Additionally, the width of the regenerated bone was significantly greater in the rhBMP-2 group (4.3 mm) than in the control group (2.8 mm) (P <0.05). The bone density and volume of regenerated bone in the rhBMP-2 group were greater than in the control group after 6 weeks of consolidation (P <0.001). CONCLUSION Injection of rhBMP-2 into regenerated bone after a distraction osteogenesis procedure significantly increased bone volume in the dentoalveolar distraction site and improved both the width and height of the alveolar ridge and increased the bone density.
Timing for Repeated Treatment of Hyperthyroid Disease with Radioactive Iodine After Initial Treatment Failure

Purpose It has been reported that the effect of radioactive iodine (RAI) treatment is complete in 4 to 6 months. This retrospective study evaluated the appropriate time for repeated treatment of hyperthyroid disease with RAI after initial treatment failure. Methods Outcomes of 128 patients treated with RAI for hyperthyroid disease were reviewed retrospectively at 3 and 6 months. Results Eighty patients (group A) were treated successfully with a single dose of RAI. Twenty patients (group B) required a second treatment dose. Twenty-eight patients were lost to follow-up. All patients in group A were clinically improved to various degrees at 3 months and continued to improve at 6 months. All eight patients in group B who showed no improvement at 3 months remained the same at 6 months. The difference between the two groups was statistically significant. Conclusion Patients with hyperthyroid disease who are unimproved at 3 months can be retreated with RAI without further delay.
Emerging roles of TET proteins and 5-hydroxymethylcytosines in active DNA demethylation and beyond

Cytosine methylation is the major epigenetic modification of metazoan DNA. Although there is strong evidence that active DNA demethylation occurs in animal cells, the molecular details of this process are unknown. The recent discovery of the TET protein family (TET1–3) 5-methylcytosine hydroxylases has provided a new entry point to reveal the identity of the long-sought DNA demethylase. Here, we review the recent progress in understanding the function of TET proteins and 5-hydroxymethylcytosine (5hmC) through various biochemical and genomic approaches, the current evidence for a role of 5hmC as an early intermediate in active DNA demethylation and the potential functions of TET proteins and 5hmC beyond active DNA demethylation. We also discuss how future studies can extend our knowledge of this novel epigenetic modification.
Association Between Body Mass Index and Motor Competence in Santal Children of Purulia District, India

ABSTRACT The purpose of this study was to evaluate the relationship between body mass index and motor competence in Santal children 5–12 years old. A total of 816 Santal children were studied. Children's adiposity status was assessed by body mass index (BMI) for age z-score based on World Health Organization reference data. Motor competence was measured using the Bruininks-Oseretsky Test of Motor Competence (BOT-2). There was no significant difference in mean BMI z-score between Santal boys (0.13 ± 0.07) and girls (−0.14 ± 0.07). Healthy weight (HW) children scored higher (p < .05) in some individual motor subtests (bilateral competence, balance, running speed and agility, upper limb competence, and strength) and in total BOT-2 score (p < .05) compared with scores for underweight (UW) and overweight (OW) children. Nonlinear regression analysis showed that BMI is a significant independent predictor of motor competence (p < .01). Motor competence showed a curvilinear relationship with BMI-z-score, with the lowest point motor scores in strength and upper limb competence (p < .05) for both UW and OW children compared to HW children who scored highest. The results also indicated that gross motor skills, but not fine motor skills, were poorer among children who were UW or OW compared with HW children.
Amplification and over‐expression of the EGFR and erbB‐2 genes in human esophageal adenocarcinomas

Esophageal cancer is one of the 10 most prevalent human cancers worldwide. The incidence of esophageal adenocarcinoma is on the rise and patients with this disease typically have very poor prognosis. Informative biomarkers would benefit the clinical management of this disease. We examined 13 cases with esophageal adenocarcinomas and 5 cases with Barrett's esophagus for amplification of the EGFR and erbB‐2 genes. We detected multiple copies of the EGFR gene in 30.8% of the tumors and multiple copies of the erbB‐2 gene in 15.4% of the tumors. Of the cases with amplification of the erbB‐2 gene, co‐amplification of the EGFR gene was found. Multiple copies of the EGFR gene were also found in one case of Barrett's esophagus. Immunohistochemical staining of the tissues revealed increased expression of the erbB‐2 protein in Barrett's mucosa and adenocarcinoma, but no associations between staining intensity and degree of EGFR or erbB‐2 gene amplification, histology, or tumor stage were found. Differential polymerase chain reaction was examined as a method for pre‐operative detection of gene amplification in esophageal tumors and Barrett's mucosa.
Correlated evolution between male ejaculate allocation and female remating behaviour in seed beetles (Bruchidae)

Sperm competition theory suggests that female remating rate determines the selective regime that dictates the evolution of male ejaculate allocation. To test for correlated evolution between female remating behaviour and male ejaculate traits, we subjected detailed experimental data on female and male reproductive traits in seven‐seed beetle species to phylogenetic comparative analyses. The evolution of a larger first ejaculate was positively correlated with the evolution of a more rapid decline in ejaculate size over successive matings. Further, as predicted by theory, an increase in female remating rate correlated with the evolution of larger male testes but smaller ejaculates. However, an increase in female remating was associated with the evolution of a less even allocation of ejaculate resources over successive matings, contrary to classic sperm competition theory. We failed to find any evidence for coevolution between the pattern of male ejaculate allocation and variation in female quality and we conclude that some patterns of correlated evolution are congruent with current theory, whereas some are not. We suggest that this may reflect the fact that much sperm competition theory does not fully incorporate other factors that may affect the evolution of male and female traits, such as trade‐offs between ejaculate expenditure and other competing demands and the evolution of resource acquisition.
Relationship between high-density lipoprotein paraoxonase gene M/L55 polymorphism and carotid atherosclerosis differs in smoking and nonsmoking men.

The enzyme paraoxonase (PON) can eliminate lipid peroxides and is believed to protect against low-density lipoprotein oxidation. A common polymorphism in the PON gene (PON1) causes an amino acid substitution of methionine (M) for leucine (L) at position 55 in the protein, which changes the activity of PON and can affect the risk of atherosclerosis. Because smoking is associated with increased lipid peroxidation, we studied the relationship between PON M/L55 polymorphism and the carotid artery intima-media thickness (IMT) in smokers or previous smokers (n = 112) and nonsmokers (n = 87). IMT was measured at 3 standardized segments by B-mode ultrasonography, and the overall mean IMT value of 199 randomly selected men (mean age 54.2 +/- 3.0 years) was calculated. Subjects with IMT > 1.7 mm in at least 1 standard site were considered to have carotid artery atherosclerotic disease (CAAD). For analysis, L55 homozygotes were compared with the M55 allele carriers. Nonsmoking L55 homozygotes had an 8.9% (95% confidence interval [CI], 1.6 to 16.8) higher overall mean IMT than M55 allele carriers. In smokers, however, the M55 allele carriers tended to have higher overall mean IMT values than L55 homozygotes. There was also a statistically significant interaction between M/L55 genotype and smoking status on CAAD (P =.009) by logistic regression analysis. Among nonsmokers, the L55 homozygotes had an odds ratio of 4.22 (95% CI, 1.06 to 16.8) for CAAD compared with nonsmoking M55 allele carriers. Contrary to nonsmokers, the smoking M55 allele carriers had an odds ratio of 2.22 (95% CI, 0.82 to 6.01) for CAAD when the L55/L55 genotype of smokers was a reference group. These data suggest that in nonsmoking men, a PON L55/L55 genotype may represent a genetic risk factor for CAAD. The reverse effect in smokers implies that the ability of PON to protect against CAAD is influenced by cigarette smoking. The efficiency of this inhibition probably depends on the PON M/L55 genotype.