Changes in life-style after liver transplantation

Sixty-five pediatric patients who received liver transplants between May 1981 and May 1984 were observed for as many as 5 years and examined for changes in life-style. Children were less frequently hospitalized, spent less time hospitalized, required fewer medications, and generally had excellent liver and renal function after hepatic transplantation as compared with their pretransplantation status. Most children were in age-appropriate and standard school classes or were only 1 year behind. Cognitive abilities remained unchanged. Children improved in gross motor function and patients' behavior significantly improved according to parents' perceptions. Enuresis was more prevalent, however, than in the population of children who had not received liver transplants. Parental divorce rates were no greater than those reported for other families with chronically ill children. Overall, objective changes in life-style as well as parents' perceptions of behavior of children appear to be improved after liver transplantation

Towards meta-interpretive learning of programming language semantics

We introduce a new application for inductive logic programming: learning the semantics of programming languages from example evaluations. In this short paper, we explored a simplified task in this domain using the Metagol meta-interpretive learning system. We highlighted the challenging aspects of this scenario, including abstracting over function symbols, nonterminating examples, and learning non-observed predicates, and proposed extensions to Metagol helpful for overcoming these challenges, which may prove useful in other domains.Comment: ILP 2019, to appea

The Complements of Lower Cones of Degrees and the Degree Spectra of Structures

We study Turing degrees a for which there is a countable structure whose degree spectrum is the collection {x : x ≰ a}. In particular, for degrees a from the interval [0′, 0″], such a structure exists if a′ = 0″, and there are no such structures if a″ \u3e 0‴

What is the evidence for the contribution of forests to poverty alleviation? A systematic map protocol

This is the final version of the article. Available from BioMed Central via the DOI in this record.Background: Forests provide an essential resource that support the livelihoods of an estimated 20% of the global population. Forests are thought to serve in three primary roles to support livelihoods: subsistence, safety nets, and pathways to prosperity. While we have a working understanding of how poor people depend on forests in individual sites and countries, much of this evidence is dispersed and not easily accessible. Thus, while the importance of forest ecosystems and resources to contribute to poverty alleviation has been increasingly emphasized in international policies, conservation and development initiatives and investments- the strength of evidence to support how forests can affect poverty outcomes is still unclear. This study takes a systematic mapping approach to scope, identify and describe studies that measure the effect of forest-based activities on poverty outcomes at local and regional scales. This effort builds upon an existing systematic map on linkages between conservation and human well-being in order to make this process more efficient. We will conduct a refined and updated search strategy pertinent to forests-poverty linkages to glean additional evidence from studies outside the scope of the original map. Results of this study can be used for informing conservation and development policy and practices in global forest ecosystems and highlight evidence gaps where future primary studies and systematic reviews can add value. Methods: We build upon the search strategy outlined in McKinnon et al. (Environ Evid 1-25, 2016) and expand our search to cover a total of 7 bibliographic databases, 15 organizational websites, 8 existing systematic reviews and maps, and evidence gap maps, and solicit key informants. All searches will be conducted in English and encompass all nations. Search results will be screened at title, abstract, and full text levels, recording both the number of excluded articles and reasons for exclusion. Full text assessment will be conducted on all included article and extracted data will be reported in a narrative review that will summarize trends in the evidence, report any knowledge gaps and gluts, and provide insight for policy, practice and future research. The data from this systematic map will be made available as well, through an open access, searchable data portal and visualization tool.We are grateful for funding support from the Program on Forests (PROFOR) (SA, SO, SC, RG) and the USDA National Institute of Food and Agriculture, Hatch Project #1009327 (DM)

Power monitoring in a feedforward photonic network using two output detectors

Programmable feedforward photonic meshes of Mach-Zehnder interferometers are computational optical circuits that have many classical and quantum computing applications including machine learning, sensing, and telecommunications. Such devices can form the basis of energy-efficient photonic neural networks, which solve complex tasks using photonics-accelerated matrix multiplication on a chip, and which may require calibration and training mechanisms. Such training can benefit from internal optical power monitoring and physical gradient measurement for optimizing controllable phase shifts to maximize some task merit function. Here, we design and experimentally verify a new architecture capable of power monitoring any waveguide segment in a feedforward photonic circuit. Our scheme is experimentally realized by modulating phase shifters in a 6 x 6 triangular mesh silicon photonic chip, which can non-invasively (i.e., without any internal "power taps ") resolve optical powers in a 3 x 3 triangular mesh based on response measurements in only two output detectors. We measure roughly 3% average error over 1000 trials in the presence of systematic manufacturing and environmental drift errors and verify scalability of our procedure to more modes via simulation

Multiple splice defects in ABCA1 cause low HDL-C in a family with Hypoalphalipoproteinemia and premature coronary disease

<p>Abstract</p> <p>Background</p> <p>Mutations at splice junctions causing exon skipping are uncommon compared to exonic mutations, and two intronic mutations causing an aberrant phenotype have rarely been reported. Despite the high number of functional <it>ABCA1 </it>mutations reported to date, splice variants have been reported infrequently. We screened DNA from a 41 year-old male with low HDL-C (12 mg/dL [0.31 mmol/L]) and a family history of premature coronary heart disease (CHD) using polymerase chain reaction single-strand conformation polymorphism (SSCP) analysis.</p> <p>Methods</p> <p>Family members with low levels of HDL-C (n = 6) were screened by SSCP for mutations in <it>ABCA1</it>. Samples with altered SSCP patterns were sequenced directly using either an ABI 3700 or ABI3730Xl DNA Analyzer. To screen for splicing defects, cDNA was isolated from the proband's RNA and was sequenced as above. A series of minigenes were constructed to determine the contribution of normal and defective alleles.</p> <p>Results</p> <p>Two novel splice variants in <it>ABCA1 </it>were identified. The first mutation was a single base pair change (T->C) in IVS 7, 6 bps downstream from the exon7/intron7 junction. Amplification of cDNA and allelic subcloning identified skipping of Exon 7 that results in the elimination of 59 amino acids from the first extracellular loop of the ABCA1 protein. The second mutation was a single base pair change (G->C) at IVS 31 -1, at the intron/exon junction of exon 32. This mutation causes skipping of exon 32, resulting in 8 novel amino acids followed by a stop codon and a predicted protein size of 1496 AA, compared to normal (2261 AA). Bioinformatic studies predicted an impact on splicing as confirmed by <it>in vitro </it>assays of constitutive splicing.</p> <p>Conclusion</p> <p>In addition to carnitine-acylcarnitine translocase (CACT) deficiency and Hermansky-Pudlak syndrome type 3, this represents only the third reported case in which 2 different splice mutations has resulted in an aberrant clinical phenotype.</p

PCBs Exert an Estrogenic Effect through Repression of the Wnt7a Signaling Pathway in the Female Reproductive Tract

Polychlorinated biphenyls (PCBs) have been proposed to have a weak estrogenic activity and therefore pose a risk as potential environmental endocrine disruptors to the perinatal development of the female reproductive tract. Perinatal exposure to high concentrations of the potent synthetic estrogen diethylstilbestrol (DES) induces abnormal development of the female reproductive tract via a mechanism that acts through the down-regulation of Wnt7a (wingless-type MMTV integration site family, member 7A). To test the hypothesis that PCBs act as weak estrogens, we injected neonatal mice with a commercial PCB mixture (Aroclor 1254) or with low levels of DES and measured effects of exposure on Wnt7a expression and uterine morphology. We report here that neonatal PCB or low-level DES exposure resulted in the down-regulation of Wnt7a expression. In addition, both PCB and low-level DES exposure induced changes in the uterine myometrium and gland formation. These data reveal that weak estrogens such as the PCBs act through a Wnt7a-dependent pathway and suggest that Wnt7a regulation is a sensitive biomarker for testing weak estrogenic candidate compounds. The morphologic changes that were elicited by PCBs and DES were different immediately after exposure, suggesting that Wnt7a-independent pathways are also activated by one or both of these compounds. Although Wnt7a down-regulation is transient after estrogenic exposure, subsequent morphologic changes became more pronounced during postnatal and adult life, suggesting that the female reproductive tract is permanently reprogrammed after exposure even to weak estrogenic compounds. In addition, Wnt7a heterozygous mice were more sensitive to PCB exposure, revealing an important genetic predisposition to risks of environmental endocrine disruptors

Diffusion of particles moving with constant speed

The propagation of light in a scattering medium is described as the motion of a special kind of a Brownian particle on which the fluctuating forces act only perpendicular to its velocity. This enforces strictly and dynamically the constraint of constant speed of the photon in the medium. A Fokker-Planck equation is derived for the probability distribution in the phase space assuming the transverse fluctuating force to be a white noise. Analytic expressions for the moments of the displacement $$ along with an approximate expression for the marginal probability distribution function $P(x,t)$ are obtained. Exact numerical solutions for the phase space probability distribution for various geometries are presented. The results show that the velocity distribution randomizes in a time of about eight times the mean free time ($8t^*$) only after which the diffusion approximation becomes valid. This factor of eight is a well known experimental fact. A persistence exponent of $0.435 \pm 0.005$ is calculated for this process in two dimensions by studying the survival probability of the particle in a semi-infinite medium. The case of a stochastic amplifying medium is also discussed.Comment: 9 pages, 9 figures(Submitted to Phys. Rev. E

In Vitro Primary-Indirect Genotoxicity in Bronchial Epithelial Cells Promoted by Industrially Relevant Few-Layer Graphene

Few-layer graphene (FLG) has garnered much interest owing to applications in hydrogen storage and reinforced nanocomposites. Consequently, these engineered nanomaterials (ENMs) are in high demand, increasing occupational exposure. This investigation seeks to assess the inhalation hazard of industrially relevant FLG engineered with: (i) no surface functional groups (neutral), (ii) amine, and (iii) carboxyl group functionalization. A monoculture of human lung epithelial (16HBE14o-) cells is exposed to each material for 24-h, followed by cytotoxicity and genotoxicity evaluation using relative population doubling (RPD) and the cytokinesis-blocked micronucleus (CBMN) assay, respectively. Neutral-FLG induces the greatest (two-fold) significant increase (p 1 µm diameter). The findings of the present study have demonstrated the capability of neutral-FLG and amine-FLG to induce genotoxicity in 16HBE14o- cells through primary indirect mechanisms, suggesting a possible role for carboxyl groups in scavenging radicals produced via oxidative stress