Miracle-dz/UniFAR-FTUs huggingface dataset:
Does Maternal Perinatal Probiotic Supplementation Alter the Intestinal Microbiota of Mother and Child?

Objectives: Maternal probiotic supplementation has been shown to prevent the development of atopic dermatitis in the offspring. We aimed to investigate whether probiotics in pregnant and breast-feeding mothers altered the colonization pattern and the diversity of the mothers’ and children's intestinal microbiota. Methods: In a randomized, double-blind trial, women received probiotic milk or placebo from 36 weeks of gestation up to 3 months postnatally while breast-feeding. The probiotic milk contained Lactobacillus rhamnosus GG, L acidophilus La-5, and Bifidobacterium animalis subsp. lactis Bb-12. Stool samples were collected from the mothers at 30 to 36 weeks of gestation and 3 months after birth, and from the child at age 10 days, 3 months, 1 year, and 2 years, and bacteria were analyzed by quantitative polymerase chain reaction. Additionally, stool samples from 3-month-old and 2-year-old children were characterized using 16S ribosomal RNA gene deep sequencing to estimate the bacterial classes and genera, and the &agr;- and &bgr;-diversity. Results: Three months after birth, both the prevalence and the relative abundance of the administered probiotic bacteria were significantly increased among the mothers in the probiotic group compared with among those in the placebo group. Only the Lactobacillus rhamnosus GG bacteria colonized the children at 10 days and at 3 months of age. There were no significant differences in the abundance of the administered probiotic bacteria between the groups at 1 and 2 years of age. For the bacterial classes and genera, and &agr;- and &bgr;-diversity, there were no significant differences between the groups. Conclusions: Different probiotic bacteria seem to have different ability to transfer from the mother to the child. We found no evidence that the probiotics altered the microbial composition or &agr;- and &bgr;-diversity of the children.
A finite-difference technique to incorporate spatial variations in rigidity and planar faults into 3-D models for lithospheric flexure

SUMMARY We present a finite-difference formulation for 3-D elastic flexure of the lithosphere, which is solved by a direct-matrix method. to incorporate the effect of spatial variations in rigidity, additional terms for the bi-harmonic 3-D flexure equation have been derived from a variational displacement formulation as used in finite-element methods. Additionally, planar faults are treated as discontinuities. These are implemented by an additional degree of freedom for fault heave, and a coupled continuum equation for zero-differential tilting across the fault. the 3-D finite-difference results have been tested for line loads, point loads and disc loads by analytical solutions, and for spatial variation in effective elastic thickness (EET) by 2-D finite-difference solutions. Fault-related flexure patterns are compared to the 2-D analytical broken-plate model developed by Vening-Meinesz (1950). We subsequently apply the 3-D fault model to investigate fault controlled 3-D basement geometries in Lake Tanganyika (East Africa). We show that our model is capable of predicting 3-D basement geometries, characteristically observed in rifted basins. the modelling results indicate that fault-controlled upper crustal flexure patterns are associated with low values for EET. A comparison with regional scale-model studies, showing a superposition of high EET flexure effects, supports a multilayered rheological control on continental rifting.
New age constraints for the Ordovician Tyrone Volcanic Group, Northern Ireland

New biostratigraphical evidence and a high-precision isotope dilution thermal ionization mass spectrometry U–Pb zircon age provide refined age constraint for the Ordovician Tyrone Volcanic Group of the Tyrone Igneous Complex. In a graptolite fauna from Slieve Gallion, the presence of Isograptus victoriae lunatus, the index fossil of the victoriae lunatus graptolite zone, indicates a correlation with the Australasian Castlemainian (Ca1) Stage. The U–Pb zircon age of 473 ± 0.8 Ma dates a volcanic arc-related rhyolite body that is stratigraphically below graptolitic mudstones of Slieve Gallion. The U–Pb isotopic and biostratigraphical age constraints closely match an interpolated age for the base of the Middle Ordovician and indicate a Whitlandian age for the upper Tyrone Volcanic Group, which supports the regional correlation with the Ballantrae Complex, Midland Valley Terrane, Scotland.
Psychomotor vigilance performance predicted by Epworth Sleepiness Scale scores in an operational setting with the United States Navy

It is critical in operational environments to identify individuals who are at higher risk of psychomotor performance impairments. This study assesses the utility of the Epworth Sleepiness Scale for predicting degraded psychomotor vigilance performance in an operational environment. Active duty crewmembers of a USA Navy destroyer (N = 69, age 21–54 years) completed the Epworth Sleepiness Scale at the beginning of the data collection period. Participants wore actigraphs and completed sleep diaries for 11 days. Psychomotor vigilance tests were administered throughout the data collection period using a 3‐min version of the psychomotor vigilance test on the actigraphs. Crewmembers with elevated scores on the Epworth Sleepiness Scale (i.e. Epworth Sleepiness Scale >10) had 60% slower reaction times on average, and experienced at least 60% more lapses and false starts compared with individuals with normal Epworth Sleepiness Scale scores (i.e. Epworth Sleepiness Scale ≤10). Epworth Sleepiness Scale scores were correlated with daily time in bed (P < 0.01), sleep (P < 0.05), mean reaction time (P < 0.001), response speed 1/reaction time (P < 0.05), slowest 10% of response speed (P < 0.001), lapses (P < 0.01), and the sum of lapses and false starts (P < 0.001). In this chronically sleep‐deprived population, elevated Epworth Sleepiness Scale scores identified that subset of the population who experienced degraded psychomotor vigilance performance. We theorize that Epworth Sleepiness Scale scores are an indication of personal sleep debt that varies depending on one's individual sleep requirement. In the absence of direct performance metrics, we also advocate that the Epworth Sleepiness Scale can be used to determine the prevalence of excessive sleepiness (and thereby assess the risk of performance decrements).
Fluorescence Resonance Energy Transfer–Based Analysis of cAMP Dynamics in Live Neonatal Rat Cardiac Myocytes Reveals Distinct Functions of Compartmentalized Phosphodiesterases

Cardiac myocytes have provided a key paradigm for the concept of the compartmentalized cAMP generation sensed by AKAP-anchored PKA. Phosphodiesterases (PDEs) provide the sole route for degrading cAMP in cells and are thus poised to regulate intracellular cAMP gradients. PDE3 and PDE4 represent the major cAMP degrading activities in rat ventriculocytes. By performing real-time imaging of cAMP in situ, we establish the hierarchy of these PDEs in controlling cAMP levels in basal conditions and on stimulation with a β-adrenergic receptor agonist. PDE4, rather than PDE3, appears to be responsible for modulating the amplitude and duration of the cAMP response to beta-agonists. PDE3 and PDE4 localize to distinct compartments and this may underpin their different functional roles. Our findings indicate the importance of distinctly localized PDE isoenzymes in determining compartmentalized cAMP signaling.
The Pathogenic Role of Macrophage Migration Inhibitory Factor in Immunologically Induced Kidney Disease in the Rat

Macrophage migration inhibitory factor (MIF) plays a pivotal role in the inflammatory response in endotoxemia and in the delayed-type hypersensitivity response, but its potential as a regulator of immunologically induced disease is unknown. We have addressed this issue by administering a neutralizing anti-MIF antibody in a rat model of immunologically induced crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Six individual experiments using paired inbred littermates were performed. Rats were primed with rabbit immunoglobulin on day −5 and then injection with rabbit anti–rat GBM serum on day 0. Pairs of animals were treated with anti-MIF or a control monoclonal antibody from the time of anti-GBM serum administration until being killed 14 d later. Control antibody-treated animals developed severe proteinuria and renal function impairment with severe histological damage due to marked leukocytic infiltration and activation within the kidney. In contrast, anti-MIF treatment substantially reduced proteinuria, prevented the loss of renal function, significantly reduced histological damage including glomerular crescent formation, and substantially inhibited renal leukocytic infiltration and activation (all P <0.001 compared with control treatment). Inhibition of renal disease by anti-MIF treatment was attributed to preventing the marked upregulation of interleukin-1β, leukocyte adhesion molecules including intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and inducible nitric oxide synthase expression seen in the control antibody-treated animals. This inhibition of progressive renal injury was mirrored by the complete suppression of the skin delayed-type hypersensitivity response to the challenge antigen (rabbit IgG). Interestingly, anti-MIF treatment did not effect the secondary antibody response or immune deposition within the kidney, indicating that MIF participates in cellular-based immunity in this primed macrophage-dependent anti-GBM glomerulonephritis. In conclusion, this study has demonstrated a key regulatory role for MIF in the pathogenesis of immunologically induced kidney disease. These results argue that blocking MIF activity may be of benefit in the treatment of human rapidly progressive glomerulonephritis, and suggest that MIF may be important in immune-mediated disease generally.
Wave Attenuation by Vegetation

The vertically two-dimensional problem of small-amplitude waves propagating over submerged vegetation is formulated using the continuity and linearized momentum equations for the regions above and within the vegetation. The effects of the vegetation on the flow field are assumed to be expressible in terms of the drag force acting on the vegetation. An analytical solution is obtained for the monochromatic wave whose height decays exponentially. The expressions for the wave number and the exponential decay coefficient derived for arbitrary damping are shown to reduce to those based on linear wave theory and the conservation equation of energy if the damping is small. The analytical solution is compared with 60 test runs conducted using deeply submerged artificial kelp. The calibrated drag coefficients for these runs are found to vary in a wide range and appear to be affected by the kelp motion and viscous effects that are neglected in the analysis. The analytical solution is also shown to be applicable to subaerial vegetation, which is predicted to be much more effective in dissipating wave energy.
Novel Demultiplexer for Dense Wavelength-Division-Mutliplexed Millimeter-Wave-Band Radio-Over-Fiber Systems With Optical Frequency Interleaving Technique

We propose a simple demultiplexer for dense wavelength-division-multiplexed (DWDM) milllimeter-wave-band radio-over-fiber (RoF) systems that uses an optical-frequency-interleaving technique, which consists of only a 2 x N arrayed waveguide grating with an optical coupler. In the proposed demultiplexer, a suppression ratio of more than 25 dB against adjacent channels is experimentally obtained. The transmission performance of 12-channel DWDM 60-GHz-band RoF signals with 25-GHz channel spacing over 25-and 2-km standard single-mode fibers via the proposed demultiplexer achieves a bit-error rate of less than 10-9.
Internal Migration in Decline

Internal migration rates in the United States have been steadily declining for at least twenty-five years: In 1984, 6.4 percent of the population moved between counties but by 2006—well before the most significant economic crisis since the Great Depression—annual intercounty migration rates had already declined to 4.7 percent and by 2010 to 3.5 percent. Despite the implications of the migration decline, it is poorly recognized and understood. The analysis shows that over the last thirty years, three broad trends have combined to pull migration rates dramatically lower: an increase in dual-worker couples, increased household indebtedness, and the widespread rise of information and communication technologies (ICTs). The first two are probably linked, as households have responded to decreasing real income over the last quarter-century through greater female labor force participation and maintaining current levels of consumption by borrowing ever more heavily from the equity in their homes. Thus, although this analysis shows that the decline in migration rates is not directly linked to the Great Recession, the migration decline is surely linked to the broader macroeconomic shifts that gave rise to it. With respect to the role of ICTs, it is not surprising that as ICTs have transformed nearly everything else across society, their use has affected migration rates. It is presumed that ICTs are providing new forms of mobility that are substituting for migration.
A ternary complex factor-dependent mechanism mediates induction of egr-1 through selective serum response elements following antigen receptor cross-linking in B lymphocytes

Induction of the primary response gene egr-1 occurs rapidly following antigen receptor cross-linking in B lymphocytes. Antisense studies have demonstrated that this induction is necessary for their subsequent activation to this signal. The present study examines the molecular mechanism whereby the receptor-generated signals interact with the egr-1 promoter to elicit transcription. Deletion mapping and point mutations have indicated that two of the five serum response elements (SREs) in the egr-1 promoter can mediate induction. Of the two critical SREs, both are capable of mediating maximal induction even in the absence of the other SRE. Our results also indicate that adjacent Ets motifs are necessary for induction. Like the c-fos SRE, the egr-1 SRE/Ets sites are occupied by a multiprotein (ternary) complex containing a homodimer of serum response factor and an unidentified member of the Ets family of transcription factors. The identification of a ternary complex-dependent mechanism of egr-1 induction, along with selective utilization of SREs in B lymphocytes, suggests that a complicated array of signaling cascades interacts with unique combinations of regulatory elements in the egr-1 promoter in different cell types.
Disruption of the ASXL1 gene is frequent in primary, post-essential thrombocytosis and post-polycythemia vera myelofibrosis, but not essential thrombocytosis or polycythemia vera: analysis of molecular genetics and clinical phenotypes

Background The myeloproliferative neoplasms, essential thrombocytosis, polycythemia vera and primary myelofibrosis, share the same acquired genetic lesion, but the concept of JAK2 V617F serving as the sole lesion responsible for these neoplasms is under question, and there has been interest in identifying additional mutations that may contribute to disease pathogenesis. Because ASXL1 lesions have been increasingly identified in myeloid neoplasms, we examined the relationships of ASXL1 mutation or deletion to both clinical phenotype and associated molecular features in 166 patients with myeloproliferative neoplasms. Design and Methods Exon 12 of ASXL1 was amplified from neutrophil genomic DNA and bidirectionally sequenced in 77 patients with myelofibrosis (including patients with primary and post-essential thrombocytosis or post-polycythemia myelofibrosis), 42 patients with polycythemia vera, 41 with essential thrombocytosis and 6 with post-myelofibrosis acute myeloid leukemia. Pyrosequencing assays were designed to determine the allele percentages of JAK2 V617F (G5073770T), ASXL1 2475dupA, and ASXL1 2846_2847del in neutrophil genomic DNA samples. Clinical and laboratory characteristics of patients with wild-type and ASXL1 mutations were then compared. Results We identified nonsense mutations or hemizygous deletion of ASXL1 in 36% of the patients with myelofibrosis, but very rarely among those with polycythemia vera or essential thrombocytosis. Among the patients with myelofibrosis, those with ASXL1 lesions were not distinguished from their wild-type counterparts with regard to JAK2 V617F status, exposure to chemotherapy or evolution to leukemia. Myelofibrosis patients with ASXL1 lesions were more likely to have received anemia-directed therapy compared to those without lesions [15/26 (58%) versus 11/39 (23%); P=0.02]. Using serial banked samples and quantitative ASXL1 mutant allele burden assays, we observed the acquisition and accumulation of ASXL1 mutations over time in two patients with post-essential thrombocytosis myelofibrosis. Conclusions ASXL1 haploinsufficiency is associated with a myelofibrosis phenotype in the context of other known and unknown lesions, and disruption of ASXL1 function may contribute to the disease pathogenesis of myelofibrosis.
Estimation of the Exposure of the UK Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake During the Period 1980 to 1996

Although the incidence of variant Creutzfeldt-Jakob disease (vCJD) has declined to 1 since 2012 in the UK, uncertainty remains regarding possible future cases and the size of the subclinical population that may cause secondary transmission of the disease through blood transfusion. Estimating the number of individuals who were exposed to the bovine spongiform encephalopathy (BSE) infectious agent and may be susceptible to vCJD will help to clarify related public health concerns and plan strategies. In this paper, we explore this estimate by describing the probability of potential exposure due to dietary intake throughout the BSE epidemic period from 1980 to 1996 as a stochastic Poisson process. We estimate the age- and gender-specific exposure intensities in food categories of beef and beef-containing dishes, burgers and kebabs, pies, and sausages, separating the two periods of 1980–1989 and 1990–1996 due to the specified bovine offal legislation of 1989. The estimated total number of (living) exposed individuals during each period is 5,089,027 (95% confidence interval [CI] 4,514,963–6,410,317), which was obtained by multiplying the population size of different birth cohorts by the probability of exposure via dietary intake and the probability of survival until the end of 2013. The estimated number is approximately doubled, assuming a contamination rate of . Among those individuals estimated, 31,855 (95% CI 26,849–42,541) are susceptible to infection. We also examined the threshold hypothesis by fitting an extreme-value distribution to the estimated infectious dose of the exposed individuals and obtained a threshold estimate of 13.7 bID50 (95% CI 6.6–26.2 bID50) (Weibull). The results provide useful information on potential carriers of prion disease who may pose a threat of infection via blood transfusion and thus provide insight into the likelihood of new incidents of vCJD occurring in the future.
Further evidence for P59L mutation in GJA3 associated with autosomal dominant congenital cataract

Context: Congenital cataracts are one of the common eye disorders leading to visual impairment or blindness in children worldwide. We found a Chinese family with autosomal dominant pulverulent cataract. Aims: To identify the pathogenic gene mutation in a Chinese family with autosomal dominant inherited pulverulent cataract. Subjects and Methods: After obtained informed consent, detailed ophthalmic examinations were carried out; genomic DNAs were obtained from seven family members in a three-generation Chinese family with three affected. All exons of candidate genes were amplified by polymerase chain reaction and were sequenced performed by bidirectional sequencing. Results: By sequencing the encoding regions of the candidate genes, a missense mutation (c. 176C>T) was detected in gap junction protein alpha 3 genes (GJA3), which resulted in the substitution of highly conserved proline by leucine at codon 59 (p.P59L). The mutation co-segregated with all patients and was absent in 100 normal Chinese controls. Conclusions: The study identified a missense mutation (c. 176C>T) in GJA3 gene associated with autosomal dominant congenital pulverulent cataract in a Chinese family. It gave further evidence of phenotype heterogeneity for P59L mutation in GJA3 associated with congenital cataract.
Ancient DNA Analysis Reveals High Frequency of European Lactase Persistence Allele (T-13910) in Medieval Central Europe

Ruminant milk and dairy products are important food resources in many European, African, and Middle Eastern societies. These regions are also associated with derived genetic variants for lactase persistence. In mammals, lactase, the enzyme that hydrolyzes the milk sugar lactose, is normally down-regulated after weaning, but at least five human populations around the world have independently evolved mutations regulating the expression of the lactase-phlorizin-hydrolase gene. These mutations result in a dominant lactase persistence phenotype and continued lactase tolerance in adulthood. A single nucleotide polymorphism (SNP) at C/T-13910 is responsible for most lactase persistence in European populations, but when and where the T-13910 polymorphism originated and the evolutionary processes by which it rose to high frequency in Europe have been the subject of strong debate. A history of dairying is presumed to be a prerequisite, but archaeological evidence is lacking. In this study, DNA was extracted from the dentine of 36 individuals excavated at a medieval cemetery in Dalheim, Germany. Eighteen individuals were successfully genotyped for the C/T-13910 SNP by molecular cloning and sequencing, of which 13 (72%) exhibited a European lactase persistence genotype: 44% CT, 28% TT. Previous ancient DNA-based studies found that lactase persistence genotypes fall below detection levels in most regions of Neolithic Europe. Our research shows that by AD 1200, lactase persistence frequency had risen to over 70% in this community in western Central Europe. Given that lactase persistence genotype frequency in present-day Germany and Austria is estimated at 71–80%, our results suggest that genetic lactase persistence likely reached modern levels before the historic population declines associated with the Black Death, thus excluding plague-associated evolutionary forces in the rise of lactase persistence in this region. This new evidence sheds light on the dynamic evolutionary history of the European lactase persistence trait and its global cultural implications.
Ratchet Price Mechanism under Currency Changeover: A Natural Housing Market Experiment

This paper examines the effect of a currency changeover on prices. A parsimonious model shows that, during a period of currency changeover, sellers and buyers conversely opt for the currency dominating the negotiation based on exchange rate fluctuations between the preceding and the new currency — potentially affecting the closing price. The currency changeover experienced by the Israeli real estate market in the past decade serves as a unique natural experiment for testing our behavioral model. Results of micro- and macro-level estimation indicate that exchange rate fluctuations associate with an upward ratchet price effect during a currency changeover period. Further, the ratchet price mechanism disappears once the currency changeover phase is completed. Our findings underline the importance of policy measures that are designed to accelerate and truncate the currency transition period.