Miracle-dz/UniFAR-FTUs huggingface dataset:
Energy balance in obesity

The current epidemic of human obesity implies that whilst energy balance appears to be regulated, the extent of this regulatory process is being overwhelmed in large numbers of the population by environmental changes. Clearly, the shift towards positive energy balance reflects both alterations in energy intake and decreases in physical activity. Increased energy intake and, in particular, the rising proportion of energy from fat is linked with obesity. However, on a population level reduced levels of activity probably play the predominant role. It is apparent that individual susceptibility to weight gain varies enormously. The factors underlying this susceptibility are an area of intense research interest. Variations in BMR from that predicted appear to be linked to the propensity to gain weight. The genes responsible for this variation may include uncoupling proteins-2 and -3, with a number of studies showing a link with obesity. However, in vivo studies of these proteins have not yet demonstrated a physiological role for them that would explain the link with obesity. Non-exercise activity thermogenesis may also protect from weight gain, but the regulation of this type of thermogenesis is unclear, although the sympathetic nervous system may be important. A profusion of hormones, cytokines and neurotransmitters is involved in regulating energy intake, but whilst mutations in leptin and the melanocortin-3 receptor are responsible for rare monogenic forms of obesity, their wider role in common polygenic obesity is not known. Much current work is directed at examining the interplay between genetic background and environmental factors, in particular diet, that both lead to positive energy balance and seem to make it so hard for many obese subjects to lose weight.
Inhibition of indoleamine 2, 3‐dioxygenase‐mediated tryptophan catabolism accelerates crescentic glomerulonephritis

Immunomodulatory enzyme indoleamine 2, 3‐dioxygenase (IDO) is one of the initial and rate‐limiting enzymes involved in the catabolism of the essential amino acid tryptophan. Via catalysing tryptophan degradation, IDO suppresses adaptive T cell‐mediated immunity and plays an important role in various forms of immune tolerance. Its role in T helper type 1 (Th1)‐directed, cell‐mediated crescentic glomerulonephritis (GN) is still unclear. Therefore, we investigated the activity and role of IDO in crescentic GN using a model of nephrotoxic serum nephritis (NTN), and IDO activity was inhibited by 1‐methyl‐tryptophan (1‐MT) in vivo. Our results showed that activity of IDO, as determined by high performance liquid chromatography analysis of the kynurenine/tryptophan ratio, was increased markedly in the serum and renal tissue of NTN mice, and immunohistochemistry revealed that expression of IDO was up‐regulated significantly in glomeruli and renal tubular epithelial cells during NTN. Treatment with 1‐MT resulted in significantly exacerbated kidney disease with increased glomerular crescent formation, accumulation of CD4+T cells and macrophages in renal tissue, and augmented renal injury compared with phosphate‐buffered saline‐treated NTN mice, which was associated with enhanced Th1 responses and intrarenal cellular proliferation. These findings suggest that the development of NTN was regulated negatively by increased IDO activity, and IDO might play an important role in the pathogenesis of crescentic GN.
Monitoring microarray-based gene expression profile changes in hepatocellular carcinoma.

AIM To find out key genes responsible for hepatocarcinogenesis and to further understand the underlying molecular mechanism through investigating the differential gene expression between human normal liver tissue and hepatocellular carcinoma (HCC). METHODS DNA microarray was prepared by spotting PCR products of 1 000 human genes including 445 novel genes, 540 known genes as well as 12 positive (housekeeping) and 3 negative controls (plant gene) onto treated glass slides. cDNA probes were prepared by labeling normal liver tissue mRNA and cancer liver tissue mRNA with Cy3-dUTP and Cy5-dUTP separately through reverse transcription. The arrays were hybridized against the cDNA probe and the fluorescent signals were scanned. The data obtained from repeated experiments were analyzed. RESULTS Among the 20 couple samples investigated (from cancerous liver tissue and normal liver tissue), 38 genes including 21 novel genes and 17 known genes exhibited different expressions. CONCLUSION cDNA microarray technique is powerful to identify candidate target genes that may play important roles in human carcinogenesis. Further analysis of the obtained genes is helpful to understand the molecular changes in HCC progression and ultimately may lead to the identification of new targets for HCC diagnosis and intervention.
Pipeline Pressures and Sectoral Inflation Dynamics

In a production network, shocks originating in individual sectors do not remain confined to individual sectors but permeate through the pricing chain. The notion of “pipeline pressures” alludes to this cascade effect. In this paper we provide a structural definition of pipeline pressures to inflation and use Bayesian techniques to infer their presence from quarterly U.S. data. We document two insights. (i) Due to price stickiness along the supply chain, we show that pipeline pressures take time to materialize which renders them an important source of inflation persistence. (ii) As we trace their origins to 35 disaggregate sectors, pipeline pressures are docu- mented to be a key source of headline/disaggregated inflation volatility. Finally, we contrast our results to the dynamic factor literature which has traditionally inter- preted the comovement of price indices arising from pipeline pressures as aggregate shocks. Our results highlight the role of sectoral shocks – joint with the production architecture – to understand the micro origins of disaggregate/headline inflation persistence/volatility.
Receptor autoradiographic mapping of the mesial motor and premotor cortex of the macaque monkey

This study analyzes regional and laminar distribution patterns of neurotransmitter binding sites in the motor areas of the macaque mesial frontal cortex. Differences in distribution patterns are compared with the cytoarchitectonic parcellation. Binding sites were analyzed with quantitative in vitro receptor autoradiography in unfixed brains of five macaque monkeys. Alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxalone propionic acid (AMPA), kainate, and N‐methyl‐D‐aspartate (NMDA) binding sites were labeled with [3H]AMPA, [3H]kainate, and [3H]MK‐801, respectively, muscarinic binding sites with [3H]pirenzepine or [3H]oxotremorine‐M, noradrenergic binding sites with [3H]prazosin or [3H]UK‐14304, γ‐aminobutyric acid (GABA)A binding sites with [3H]muscimol, and serotoninergic binding sites with [3H]ketanserine. Adjacent sections were stained with a modified Nissl method for cytoarchitectonic analysis. In the motor areas F1, F3, and F6, [3H]AMPA, [3H]pirenzepine, and [3H]oxotremorine‐M binding was maximal in layers II, III, and V, and [3H]kainate binding was maximal in layers V and VI. Clear‐cut changes in laminar distribution patterns of [3H]AMPA, [3H]kainate, and [3H]oxotremorine‐M binding sites very closely matched corresponding cytoarchitectonic borders. Mean areal binding densities of all ligands to F1, F3, and F6 were plotted as polar plots for each area. A polygon was obtained for each area (“neurochemical fingerprint”) when all the density values belonging to one area were connected with each other. The “neurochemical fingerprints” of F1, F3, and F6 were virtually identical in shape but increased in size from F1 to F6. This result reflects the functional similarity of these motor‐related areas and possibly correlates with their differential involvement in motor control. Areas F1, F3, and F6 can thus be grouped into one “neurochemical family” of areas. J. Comp. Neurol. 397:231–250, 1998. © 1998 Wiley‐Liss, Inc.
An update on celiac disease histopathology and the road ahead.

CONTEXT Celiac disease (CD) is a common immune-mediated disorder that occurs in genetically predisposed individuals (carriers of HLA-DQ2 and DQ8 haplotypes) on consumption of wheat (gluten). It is characterized by inflammation of the small-intestinal mucosa and myriad gastrointestinal and systemic manifestations. Celiac disease is common in the general population (prevalence, 0.5%-1%). Currently, small-bowel biopsy is considered the gold standard for diagnosing CD. However, the role of serologic testing in the diagnosis of CD has evolved, from being a supportive test to supplanting intestinal biopsies in certain patient populations. OBJECTIVE To summarize key aspects of histopathologic assessment, discuss the benefit of standardized pathology reports, impact of the site and number of small-bowel biopsy samples on diagnosis, and recommendations regarding serologic testing. DATA SOURCES Literature review of publications on CD and experience with histopathologic review of biopsies at the Department of Pathology and Cell Biology, Columbia University Medical Center, New York-Presbyterian Hospital, New York. CONCLUSIONS Intraepithelial lymphocytosis in the context of villous atrophy is considered a characteristic histologic finding of CD; however, it is a rather nonspecific finding. A growing list of publications has also indicated that the detection of intraepithelial lymphocytosis in the absence of villous atrophy has rather low specificity for CD. Therefore, communication between pathologists and gastroenterologists is paramount, as is knowledge regarding the pertinent clinical and laboratory data, in distinguishing between CD and other disorders with similar histopathologic and clinical manifestations.
Preclinical diagnosis of familial hypertrophic cardiomyopathy by genetic analysis of blood lymphocytes.

BACKGROUND The clinical diagnosis of familial hypertrophic cardiomyopathy is usually made on the basis of the physical examination, electrocardiogram, and echocardiogram. Making an accurate diagnosis can be particularly difficult in children, who may not have cardiac hypertrophy until adulthood. Recently, we demonstrated that mutations in the cardiac myosin heavy-chain genes cause familial hypertrophic cardiomyopathy in some families. We report a diagnostic test for familial hypertrophic cardiomyopathy that relies on the detection of mutations in the beta myosin heavy-chain gene in circulating lymphocytes that we used to evaluate three generations of a family, including the children. METHODS AND RESULTS Using the polymerase chain reaction, we found that normal and mutant beta cardiac myosin heavy-chain genes are transcribed in circulating lymphocytes. This allowed us to examine beta cardiac myosin heavy-chain messenger RNA from blood lymphocytes, even though ordinary expression of the gene is virtually restricted to the heart. Base sequences amplified from this messenger RNA were analyzed with a ribonuclease protection assay to identify small deletions, abnormal splicing, or missense mutations. Using this technique we identified a novel missense mutation in a patient with familial hypertrophic cardiomyopathy. We evaluated 15 of the patient's adult relatives and found perfect agreement with the clinical diagnosis (8 affected and 7 not affected). Clinical analysis of 14 of the children (age, 1 to 20 years) of these affected family members revealed 1 child with echocardiographic findings diagnostic of familial hypertrophic cardiomyopathy. However, genetic analyses showed that six other children had also inherited the missense mutation and might later manifest the disease. CONCLUSIONS Transcripts of beta cardiac myosin heavy-chain gene can be detected in blood lymphocytes and used to screen for mutations that cause familial hypertrophic cardiomyopathy. This approach makes practical the identification of mutations responsible for this disorder and may be applicable to other diseases in which direct analysis is difficult because the mutated gene is expressed only in certain tissues. Preclinical or prenatal screening in an affected family will make it possible to study the disease longitudinally and to develop preventive interventions.
Task‐irrelevant visual letters interact with the processing of speech sounds in heteromodal and unimodal cortex

Letters and speech sounds are the basic units of correspondence between spoken and written language. Associating auditory information of speech sounds with visual information of letters is critical for learning to read; however, the neural mechanisms underlying this association remain poorly understood. The present functional magnetic resonance imaging study investigates the automaticity and behavioral relevance of integrating letters and speech sounds. Within a unimodal auditory identification task, speech sounds were presented in isolation (unimodally) or bimodally in congruent and incongruent combinations with visual letters. Furthermore, the quality of the visual letters was manipulated parametrically. Our analyses revealed that the presentation of congruent visual letters led to a behavioral improvement in identifying speech sounds, which was paralleled by a similar modulation of cortical responses in the left superior temporal sulcus. Under low visual noise, cortical responses in superior temporal and occipito‐temporal cortex were further modulated by the congruency between auditory and visual stimuli. These cross‐modal modulations of performance and cortical responses during an unimodal auditory task (speech identification) indicate the existence of a strong and automatic functional coupling between processing of letters (orthography) and speech (phonology) in the literate adult brain.
Interaction Between Atypical Antipsychotics and the Gut Microbiome in a Bipolar Disease Cohort

The atypical antipsychotic (AAP) class is often associated with metabolic disease, but the mechanistic underpinnings of this risk are not understood. Due to reports linking gut bacteria function to metabolic disease, we hypothesize that AAP treatment in adults results in gut dysbiosis potentiating metabolic criteria. This report describes recent findings linking AAP treatment with differences in gut microbiota communities in a human cohort with bipolar disorder (BD).
The association between fibrinogen haplotypes and myocardial infarction in men is partly mediated through pleiotropic effects on the serum IL‐6 concentration

Background and objectives. Fibrinogen haplotypes have been associated with risk of myocardial infarction (MI), independently of plasma fibrinogen concentration, and experimental data indicate that fibrinogen exerts pleiotropic effects on interleukin 6 (IL‐6) production. Also, the coagulation factor XIII (gene symbol F13A1) Val34Leu haplotype tag single nucleotide polymorphism (htSNP) has been reported to exert pleiotropic effects on serum IL‐6 concentration and to be associated with risk of MI. Therefore, in the present case–control study (a substudy to the Stockholm Heart Epidemiology Program), the effects of the fibrinogen gamma (FGG) 9340T>C [rs1049636], fibrinogen alpha (FGA) 2224G>A [rs2070011] and F13A1 Val34Leu [rs5985] htSNPs on concentrations of plasma fibrinogen and serum IL‐6 and risk of MI were assessed.
Exploiting WSSUS Multipath for GNSS Ranging

We propose a low-dimensional parameter estimation scheme for satellite-based ranging in the presence of an attenuated line-of-sight (LOS) signal and a time-varying number of multipath signals. This is of interest for landmobile users of global navigation satellite systems in diverse scattering environments with limited satellite visibility (e.g., a car moving through an urban canyon). Conventional ranging techniques, which rely solely on estimation of LOS parameters, ignore or suppress multipath and thus sacrifice available information; on the other hand, exhaustive approaches involving detection and estimation of each time-variant echo are too cumbersome in terms of parameter dimension. We suggest an unconditional maximum likelihood estimator (U-MLE) for joint estimation of LOS synchronization parameters and a small set of multipath distribution parameters. Our key assumptions are Gaussian wide-sense stationary uncorrelated scattering (WSSUS) and a known structure of the power delay profile. The proposed estimator uses as input data only a few complex-valued correlator outputs, which are provided by conventional navigation receivers, and its complexity is independent of the actual number of present echoes. Simulations demonstrate that the U-MLE improves accuracy and robustness of LOS synchronization for various model-matched and -mismatched multipath settings, including standardized and approved urban scenarios.
Alcohol Dehydrogenase 3 and Risk of Squamous Cell Carcinomas of the Head and Neck

In order to examine the association between alcohol dehydrogenase 3 (ADH3) genotypes and risk of head and neck squamous cell carcinomas (HNSCC), we conducted a hospital based case-control study including 348 cases and 330 controls. DNA isolated from exfoliated cells from the oral cavity were genotyped for ADH3 polymorphisms using PCR followed by SspI digestion. Odds ratios (OR) and hazards ratios (HR) were done by unconditional logistic regression and Cox regression. Relative to ADH32-2 carriers, ADH31-1 [OR, 0.7; 95% confidence interval (CI), 0.4-1.1] and ADH31-2 (OR, 0.8; 95% CI, 0.5-1.2) had a nonsignificant reduced risk of HNSCC. ADH1-2 smokers of >30 pack-years were at decreased risk of oral cavity squamous cell carcinomas compared with ADH32-2 (OR, 0.3, 0.1-0.9), whereas ADH31-1 smokers were not. After adjustment, those with ADH31-2 had significantly worse overall survival compared with ADH31-1 (HR, 0.3, 0.2-0.6) or ADH32-2 (HR, 0.4, 0.2-0.9) and increased recurrence (ADH31-1, 0.2, 0.1-0.6; ADH32-2, 0.6, 0.2-1.3). Our data did not show that ADH3 genotypes had a significantly independent effect on the risk of HNSCC, nor did they modify the risks increased by alcohol or tobacco consumption and high-risk human papillomavirus infection. However, participants with ADH31-2 genotype were associated with poorer survival compared with those who had the other two ADH3 genotypes and a higher rate of recurrence than participants with ADH31-1 genotype.
Modeling Volatility for Conventional and Islamic Stock Market Indices

This study aims to investigate the volatility between Conventional and Islamic stock market by deploying Autoregressive Conditional Heteroskedastic (ARCH) model and Generalized ARCH (GARCH) models along with their variants, Power ARCH (PARCH), Threshold ARCH (TARCH) and Exponential GARCH (EGARCH) on comparable stock market index. Karachi Stock Exchange 30 index (KSE-30) was cross examined with the volatility of KSE Meezan Index (KMI-30) and Dow Jones Islamic Market Index (DJIMI) with Dow Jones Industrial Average (DJIA) to determine the existence of correlation and impact in the volatility of indices. Time effect is being analyzed in the study where the response time to external factors of growing Islamic Market Index is compared to that of a mature Conventional Market Index by applying lags and testifying the ARCH effect on the stationary data, arrived through Augmented Dickey Fuller test, including daily closing prices from 2012 to 2016. The results assess the most appropriate model for each index to be applied for the purpose of forecasting on the basis of volatility. It also established the relationship between comparable index volatility with identifying common denoting factor either the type of the index, that is, Islamic and Conventional or the Geographical Boundaries of the index.
CpG hypermethylation of promoter region and inactivation of E‐cadherin gene in human bladder cancer

Several studies have shown that E‐cadherin expression is lost during malignant transformation. We hypothesized that CpG methylation in the promoter region may inactivate the expression of the E‐cadherin gene in human bladder cancer. Normal and bladder cancer samples from 51 patients were compared in terms of E‐cadherin gene expression and methylation status by immunohistochemistry, methylation‐specific polymerase chain reaction (MSP), and bisulfite genome‐sequencing techniques. Ten different CpG sites (nt 863, 865, 873, 879, 887, 892, 901, 918, 920, and 940) in the promoter region were studied. Thirty‐five of 51 (69%) bladder cancer samples lacked E‐cadherin expression, whereas only six of 51 (12%) normal bladder samples lacked E‐cadherin immunoreactivity. MSP analysis of bladder cancer samples suggested that 43 of 51 (84%) showed methylation of the promoter region, whereas only 12 of 51 (24%) normal bladder samples showed hypermethylation. Sodium bisulfite genome‐sequencing analysis revealed that of 10 CpG sites, two sites (nt 892 and nt 940) showed 100% methylation in all the cancer samples analyzed. Other CpG sites were partially methylated (47–91%). Normal tissue showed only 12% methylation (range, 1–33%) on various CpG sites. Also supporting these data, E‐cadherin–negative bladder cancer cell lines restored expression of the E‐cadherin gene after treatment with the demethylating agent 5‐aza‐2′‐deoxycytidine. The present study showed that CpG hypermethylation was an important mechanism of E‐cadherin gene inactivation in bladder cancer and also that specific CpG sites consistently presented higher methylation levels than others. These findings may provide a better strategy for the diagnosis and management of bladder cancer. © 2002 Wiley‐Liss, Inc.
The influence of short sellers on negative press coverage and price discovery

In this paper we empirically address two questions: (1) Do short sellers influence the extent to which negative news is reported by the business press? ; and (2) Do reduced short selling constraints bring more arbitrage capital and informed trading pressure to bear on negative business press coverage, increasing the speed and intensity with which negative news reports are impounded into stock price. Exploiting the randomized Regulation SHO experiment to identify effects of short-sale constraints, we find that following reduction in short selling costs the sentiment of pilot firms’ press coverage tilts significantly more negative and the probability of their receiving negative news coverage increases. This result holds for media-initiated articles, but not for firm-initiated press releases, and is more pronounced for more opaque firms where short sellers are likely to have greater scope for relative information advantage. Consistent with shortsale constraints limiting arbitrage activities, we find that following relaxation of short selling constraints stock returns become more sensitive to negative news reports, more arbitrage capital is allocated to news sentiment-based trading strategies and such trading strategies earn lower abnormal returns.