A demographic study based upon income, age and education variables as related to the willingness or unwillingness to accept foster children

The research problem in this thesis can be briefly stated as a study of a general population to test certain demographic variables, in particular those of income, age and education, which may or may not have a significant relationship to an expressed willingness to care for foster children; and to further examine whether certain special characteristics of a child, in particular those of increased age, physical handicap, minor emotional problems or mental retardation, further increase unwillingness to care for foster children. The sample was selected by a two- stage cluster sampling taken from the Southeast catchment area of metropolitan Portland, Oregon. From this sample of 787 individuals, the survey was conducted by trained interviewers, using a questionnaire and personal interview. The data used in this research project were then extracted from the larger survey, and computed to determine the relationship of age, income and education to willingness to care for foster children. The data were extracted on the basis of the chosen variables of income, age and education and five questions relating specifically to willingness to care for foster children. As had been anticipated, the findings showed that the general population is not willing to care for foster children. However, certain significant findings were related to willingness to care for foster children. A significant relationship was found between income and willingness to care for foster children in that those respondents with incomes between $4,000-$20,000 expressed the most willingness to care for foster children while there was significant underrepresentation in both the highest and lowest income groupings to express a willingness to care for foster children with an almost lineal relationship of decreasing age with increasing willingness to care for foster children. There is no significant relationship, it was found, between education of the respondent and willingness to care for foster children. There is a lineal relationship of increasing willingness to care for foster children with increasing age of the foster child. Of those individuals expressing a willingness to care for foster children, there is no significant decrease in willingness because of physical disability, minor emotional problems or mental retardation. The results of this study have certain implication for recruitment and selection of foster parents. The findings indicate the need for further research to explore why more individuals in the population do not express a willingness to care for foster children, how such an interest can be encouraged and what criteria can be used in recruitment and selection

Determination of citric acid in urine and in serum

Peer Reviewe

Walking performances and muscle oxygen desaturation are increased after supervised exercise training in Takayasu arteritis: a case report and a review of the literature.

Takayasu arteritis (TAK) is a rare chronic inflammatory vasculitis predominantly affecting the aorta and its main branches. Takayasu arteritis has been shown to increase cardiovascular risk. Supervised exercise training (SET) is a well-recognized and effective therapeutic tool improving walking performances in patients with chronic atherosclerotic disease; however, the effects of SET, and the underlying mechanisms, remain poorly documented in TAK patients. We reviewed the literature and investigated the effects of a 12-week SET programme on walking performances, physical function, and calf muscle oxygen saturation (StO <sub>2</sub> ; assessed by near-infrared spectroscopy) during exercise in a 28-year-old man with TAK and symptoms of arterial lower limb claudication. The literature review evidences only two recent publications suggesting that exercise training is effective and well-tolerated in patients with arteritis. The treadmill pain-free (+22%) and maximal (+273%) walking distance, 6-min walking distance (+66%), and physical function of lower extremities (+20%) following SET were significantly improved in our patient. Moreover, we observed a greater muscle oxygen desaturation (increased oxygen extraction) during exercise. Following SET, the increased oxygen extraction may be related to improved microvascular milieu leading to a better match between muscle oxygen supply and demand during exercise. These new results may contribute to mechanistic insights in peripheral adaptations following exercise training in TAK patients and may help to explain, at least partly, the increased walking performances. Although more studies are needed to better explore the impact of exercise training, these results suggest that exercise should be recommended in TAK patients

A new measurement of the neutron detection efficiency for the NaI Crystal Ball detector

We report on a measurement of the neutron detection efficiency in NaI crystals in the Crystal Ball detector obtained from a study of single p0 photoproduction on deuterium using the tagged photon beam at the Mainz Microtron. The results were obtained up to a neutron energy of 400 MeV. They are compared to previous measurements made more than 15 years ago at the pion beam at the BNL AGS

Measurements of double-polarized compton scattering asymmetries and extraction of the proton spin polarizabilities

The spin polarizabilities of the nucleon describe how the spin of the nucleon responds to an incident polarized photon. The most model-independent way to extract the nucleon spin polarizabilities is through polarized Compton scattering. Double-polarized Compton scattering asymmetries on the proton were measured in the Δ(1232) region using circularly polarized incident photons and a transversely polarized proton target at the Mainz Microtron. Fits to asymmetry data were performed using a dispersion model calculation and a baryon chiral perturbation theory calculation, and a separation of all four proton spin polarizabilities in the multipole basis was achieved. The analysis based on a dispersion model calculation yields γE1E1=−3.5±1.2, γM1M1=3.16±0.85, γE1M2=−0.7±1.2, and γM1E2=1.99±0.29, in units of 10−4  fm4

Optimizing Nervous System-Specific Gene Targeting with Cre Driver Lines: Prevalence of Germline Recombination and Influencing Factors.

The Cre-loxP system is invaluable for spatial and temporal control of gene knockout, knockin, and reporter expression in the mouse nervous system. However, we report varying probabilities of unexpected germline recombination in distinct Cre driver lines designed for nervous system-specific recombination. Selective maternal or paternal germline recombination is showcased with sample Cre lines. Collated data reveal germline recombination in over half of 64 commonly used Cre driver lines, in most cases with a parental sex bias related to Cre expression in sperm or oocytes. Slight differences among Cre driver lines utilizing common transcriptional control elements affect germline recombination rates. Specific target loci demonstrated differential recombination; thus, reporters are not reliable proxies for another locus of interest. Similar principles apply to other recombinase systems and other genetically targeted organisms. We hereby draw attention to the prevalence of germline recombination and provide guidelines to inform future research for the neuroscience and broader molecular genetics communities

The degradation of p53 and its major E3 ligase Mdm2 is differentially dependent on the proteasomal ubiquitin receptor S5a.

p53 and its major E3 ligase Mdm2 are both ubiquitinated and targeted to the proteasome for degradation. Despite the importance of this in regulating the p53 pathway, little is known about the mechanisms of proteasomal recognition of ubiquitinated p53 and Mdm2. In this study, we show that knockdown of the proteasomal ubiquitin receptor S5a/PSMD4/Rpn10 inhibits p53 protein degradation and results in the accumulation of ubiquitinated p53. Overexpression of a dominant-negative deletion of S5a lacking its ubiquitin-interacting motifs (UIM)s, but which can be incorporated into the proteasome, also causes the stabilization of p53. Furthermore, small-interferring RNA (siRNA) rescue experiments confirm that the UIMs of S5a are required for the maintenance of low p53 levels. These observations indicate that S5a participates in the recognition of ubiquitinated p53 by the proteasome. In contrast, targeting S5a has no effect on the rate of degradation of Mdm2, indicating that proteasomal recognition of Mdm2 can be mediated by an S5a-independent pathway. S5a knockdown results in an increase in the transcriptional activity of p53. The selective stabilization of p53 and not Mdm2 provides a mechanism for p53 activation. Depletion of S5a causes a p53-dependent decrease in cell proliferation, demonstrating that p53 can have a dominant role in the response to targeting S5a. This study provides evidence for alternative pathways of proteasomal recognition of p53 and Mdm2. Differences in recognition by the proteasome could provide a means to modulate the relative stability of p53 and Mdm2 in response to cellular signals. In addition, they could be exploited for p53-activating therapies. This work shows that the degradation of proteins by the proteasome can be selectively dependent on S5a in human cells, and that this selectivity can extend to an E3 ubiquitin ligase and its substrate

Experimental evidence for temporal uncoupling of brain Aβ deposition and neurodegenerative sequelae

Brain A beta deposition is a key early event in the pathogenesis of Alzheimer ' s disease (AD), but the long presymptomatic phase and poor correlation between A beta deposition and clinical symptoms remain puzzling. To elucidate the dependency of downstream pathologies on A beta, we analyzed the trajectories of cerebral A beta accumulation, A beta seeding activity, and neurofilament light chain (NfL) in the CSF (a biomarker of neurodegeneration) in A beta-precursor protein transgenic mice. We find that A beta deposition increases linearly until it reaches an apparent plateau at a late age, while A beta seeding activity increases more rapidly and reaches a plateau earlier, coinciding with the onset of a robust increase of CSF NfL. Short-term inhibition of A beta generation in amyloid-laden mice reduced A beta deposition and associated glial changes, but failed to reduce A beta seeding activity, and CSF NfL continued to increase although at a slower pace. When short-term or long-term inhibition of A beta generation was started at pre-amyloid stages, CSF NfL did not increase despite some A beta deposition, microglial activation, and robust brain A beta seeding activity. A dissociation of A beta load and CSF NfL trajectories was also found in familial AD, consistent with the view that A beta aggregation is not kinetically coupled to neurotoxicity. Rather, neurodegeneration starts when A beta seeding activity is saturated and before A beta deposition reaches critical (half-maximal) levels, a phenomenon reminiscent of the two pathogenic phases in prion disease. The poor correlation between brain A beta deposition and clinical symptoms in Alzheimer ' s disease remains puzzling. Here, the authors show a temporal dissociation of A beta deposition and neurodegeneration

CP-31398, a putative p53-stabilizing molecule tested in mammalian cells and in yeast for its effects on p53 transcriptional activity

BACKGROUND: CP-31398 is a small molecule that has been reported to stabilize the DNA-binding core domain of the human tumor suppressor protein p53 in vitro. The compound was also reported to function as a potential anti-cancer drug by rescuing the DNA-binding activity and, consequently, the transcription activation function of mutant p53 protein in mammalian tissue culture cells and in mice. RESULTS: We performed a series of gene expression experiments to test the activity of CP-31398 in yeast and in human cell cultures. With these cell-based assays, we were unable to detect any specific stimulation of mutant p53 activity by this compound. Concentrations of CP-31398 that were reported to be active in the published work were highly toxic to the human H1299 lung carcinoma and Saos-2 cell lines in our experiments. CONCLUSION: In our experiments, the small molecule CP-31398 was unable to reactivate mutant p53 protein. The results of our in vivo experiments are in agreement with the recently published biochemical analysis of CP-31398 showing that this molecule does not bind p53 as previously claimed, but intercalates into DNA