Miracle-dz/UniFAR-FTUs huggingface dataset:
Caries Ecology Revisited: Microbial Dynamics and the Caries Process

In this essay we propose an extension of the caries ecological hypothesis to explain the relation between dynamic changes in the phenotypic/genotypic properties of plaque bacteria and the demineralization/remineralization balance of the caries process. Dental plaque represents a microbial ecosystem in which non-mutans bacteria (mainly non-mutans streptococci and Actinomyces) are the key microorganisms responsible for maintaining dynamic stability on the tooth surface (dynamic stability stage). Microbial acid adaptation and subsequent acid selection of ‘low-pH’ non-mutans bacteria play a critical role for destabilizing the homeostasis of the plaque by facilitating a shift of the demineralization/remineralization balance from ‘net mineral gain’ to ‘net mineral loss’ (acidogenic stage). Once the acidic environment has been established, mutans streptococci and other aciduric bacteria may increase and promote lesion development by sustaining an environment characterized by ‘net mineral loss’ (aciduric stage). Hence, high proportions of mutans streptococci and/or other aciduric bacteria may be considered biomarkers of sites of particularly rapid caries progression. This cascade of events may change the surface texture of caries lesions from smooth to rough (enamel) or hard to soft (dentin). These clinical surface features can be reversed at any stage of lesion development provided that the acidogenic/aciduric properties of the biofilm are resolved. From an ecological point of view it is therefore not only important to describe which bacteria are involved in caries, but also to know what the bacteria are doing.
Postpartum psychosis: detection of risk and management.

Mrs. A, a 34-year-old married mother who lived with her husband and their 5year-old daughter, strangled her infant son to death 3 weeks after birth. She had a planned, healthy pregnancy with some depression at 28 weeks’ gestation. She had a normal spontaneous vaginal delivery, giving birth to a healthy boy, “B. ” She began breastfeeding immediately. From postpartum days 2 through 11, her depression worsened. She was unable to sleep but could not get out of bed or attend to her hygiene. She was suspicious that her husband would harm B. On postpartum day 2, she began having obsessional, ego-dystonic images of throwing B out the window. She believed, despite the pediatrician’s reassurances, that she was harming B with her breast milk and that he was losing weight. She was unable to give him a bath, believing that he had “gas” or “something bad” inside and could not be moved.
Pioneering studies on the mechanisms of axonal regeneration

While ultimately, focus must be placed on experimentation using adult systems, vastly important clues to regeneration can be found in the study of the embryonic nervous system. In embryonic systems, axonal regeneration is successful before a critical period, and numerous advances have resulted from the study of isolated cells and tissues in vitro. Studies over many decades from the laboratory of Paul C. Letourneau have probed the cellular and molecular phenomena involved in axon outgrowth and guidance in the embryonic central and peripheral nervous system and have laid the framework for many current advances in regeneration research. Letourneau's pioneering work related to growth cone behavior, guidance, and regeneration has resulted in considerable contributions toward our understanding not only of cellular mechanisms that underlie axon growth, but also of the specific areas of study that require attention to accomplish future breakthroughs. The present article summarizes some of the major contributions from Paul Letourneau and his team in the area of axonal regeneration. © 2011 Wiley Periodicals,Inc. Develop Neurobiol, 2011
Coexistent Non-Hodgkin's Lymphoma and Renal Cell Carcinoma in aPatient with Von Hipple-Lindau Disease: A Case Report

Von Hippel-Lindau (VHL) disease is an autosomal dominant syndrome that, due to loss of tumor suppressor gene function, predisposes affected individuals to various benign and malignant tumors including renal cell cancer. In contrast, lymphomas are a varied group of clonal diseases arising from a lymphocyte progenitor and can affect any site of the lymphatic system. We present the case of a 56 year old female with Von Hippel-Lindau disease and clear cell renal carcinoma (CCRC), who developed a nasopharyngeal mass with cervical and submandibular lymphadenopathy subsequently proven to be a Non Hodgkin’s lymphoma (NHL). Though the association between VHL and renal cell cancer is significant, a mechanism linking these two diseases has previously been unknown. To the best of our knowledge, this is the first reported case of a patient presenting with coexistent VHL and NHL. In an effort to explain this rarity, we propose that a defective VHL allele may serve as a possible link between VHL and RCC, thus leading to an environment that would favour the development of a malignant clone, our patient’s NHL.
Acute administration of metoprolol and enalaprilat reduces insulin‐stimulated thermogenesis and skin blood flow

Tuominen JA, Eriksson JG, Koivisto VA (Department of Medicine, Helsinki University Central Hospital, and National Institute of Public Health, Helsinki, Finland). Acute administration of metoprolol and enalaprilat reduces insulin‐stimulated thermogenesis and skin blood flow. J Intern Med 1996; 239: 399–406.
Economies of Scale in Independent Insurance Agencies

Among the recent developments in the property-liability insurance markets which constitute a potential threat to competition are the erosion of the independent agents' market share and the merger movement among independent agencies. The goal of this study is to provide information to guide regulators in formulating positions with respect to these developments. Specifically, the article reports results of tests for scale economies in the operation of independent agencies. Estimation of short and long-run cost functions provides no evidence of economies of scale. Hence, agency mergers generally cannot be justified on the basis of cost economies. The independent agency system traditionally has been the dominant form of marketing channel in property-liability insurance. Independent agents maintain contacts with several different insurers and are not obligated to place business with any particular one of them. During the past two decades, independent agents have lost a substantial share of the insurance market (particularly in auto and homeowners insurance) to exclusive agents, who deal with a single insurer (such as State Farm or Allstate) and place business only with that insurer. Independent agents are still dominant in the commercial insurance markets, but their preeminence in these markets is being challenged. These developments may have significant implications for the maintenance of competition in the property-liability insurance markets. For many years, a substantial share of the property-liability insurance market has been operated under a cartel-type arrangement whereby most insurers set rates in concert through organizations known as rating bureaus. Regulators have permitted this system to exist because of the argument that pooling J. David Cummins is Associate Professor of Insurance, Wharton School, University of Pennsylvania. He is Research Director of the S. S. Huebner Foundation for Insurance Education. Some of his publications include An Econometric Model of the Life Insurance Sector of the U.S. Economy; Impact of Consumer Services on Independent Insurance Agency Performance (coauthor); and Investment Activities of Life Insurance Companies (editor). He has been a frequent contributor to the Journal of Risk and Insurance and serves as secretary of its editorial board. The research on which this article is based was supported in part by a grant from the IMA Education & Research Foundation. The author is grateful to Steven N. Weisbart, Associate Professor of Insurance at Georgia State University, for his valuable comments and suggestions during the preparation of this article. Of course, the author is solely responsible for any errors or omissions.
Altered Levels of the Soluble IL-1, IL-4 and TNF Receptors, as well as the IL-1 Receptor Antagonist, in Intermittent Allergic Rhinitis

Background: The effects of cytokines are modulated by soluble cytokine receptors (SCR) and receptor antagonists. Therefore, allergic disease may depend on altered proportions between cytokines, their SCR and receptor antagonists, rather than absolute changes in cytokine levels. Little is known about SCR in intermittent allergic rhinitis (IAR). Objective: To examine the concentrations of SCR, i.e. sIL-1R2, sIL-4R, sIL-6R and sTNFR1, as well as the interleukin-1 receptor antagonist (IL-1Ra) in nasal fluids from allergen-challenged patients with IAR and healthy controls. Methods: 30 patients with birch- or grass-pollen-induced IAR and 30 healthy controls were studied. In the patients nasal fluids were obtained before as well as 1 and 6 h after allergen provocation. Results: Both symptom scores and rhinoscopic signs of rhinitis increased in the patients after allergen challenge. Comparisons between patients and controls showed that sIL-4R was lower in patients before and 1 and 6 h after provocation. IL-1Ra was lower before and 1 h after provocation. In addition, lower concentrations of sTNFR1 were found in patients after 1 h, while sIL-1R2 concentrations were higher after 1 h. Comparisons of patients before and after challenge showed that IL-1Ra and sTNFR1 decreased after 1 h, while sIL-1R2 increased. No significant differences were found compared to 6 h. sIL-6R did not significantly differ between the study groups. Conclusions: After allergen challenge, significant changes in the nasal fluid levels of IL-1Ra, sIL-1R2 and sTNFR1 were found. By contrast, sIL-4R remained at lower levels than in controls both before and after challenge. Since sIL-4R modulates IgE synthesis, this may play a role in the pathogenesis of IAR.
Genome scan of schizophrenia.

OBJECTIVE The goal of this study was to identify chromosomal regions likely to contain schizophrenia susceptibility genes. METHOD A genomewide map of 310 microsatellite DNA markers with average spacing of 11 centimorgans was genotyped in 269 individuals--126 of them with schizophrenia-related psychoses--from 43 pedigrees. Nonparametric linkage analysis was used to assess the pattern of allele sharing at each marker locus relative to the presence of disease. RESULTS Nonparametric linkage scores did not reach a genomewide level of statistical significance for any marker. There were five chromosomal regions in which empirically derived p values reached nominal levels of significance at eight marker locations. There were p values less than 0.01 at chromosomes 2q (with the peak value in this region at D2S410) and 10q (D10S1239), and there were p values less than 0.05 at chromosomes 4q (D4S2623), 9q (D9S257), and 11q (D11S2002). CONCLUSIONS The results do not support the hypothesis that a single gene causes a large increase in the risk of schizophrenia. The sample (like most others being studied for psychiatric disorders) has limited power to detect genes of small effect or those that are determinants of risk in a small proportion of families. All of the most positive results could be due to chance, or some could reflect weak linkage (genes of small effect). Multicenter studies may be useful in the effort to identify chromosomal regions most likely to contain schizophrenia susceptibility genes.
Application of a Corticosteroid (Triamcinolon) Protects Inner Ear Function after Surgical Intervention

Hypothesis: Opening of the inner ear during stapes surgery or cochlear implantation may result in trauma to inner ear structures and possible hearing loss. The dual aim of the present study was to evaluate the effectiveness of locally applied Triamcinolon* to protect the inner ear against surgically induced trauma and to exclude possible ototoxic effects. Methods: In an animal model (guinea pig), a corticosteroid (Triamcinolon) was topically applied to the inner ear, either by extracochlear application and diffusion through the round window membrane or by direct intracochlear application via a cochleostomy. Physiological effects of the steroid were investigated by monitoring the hearing of steroid treated animals in comparison to control animals treated with Ringer solution instead of Triamcinolon. Thresholds as well as input/output functions (I/O function) of compound action potentials (CAPs) in response to auditory stimuli were determined before the cochleostomy and at specific intervals up to 4 weeks after application of Triamcinolon. Results: Extracochlear application of Triamcinolon induced only minor shifts of mean CAP thresholds but significantly increased mean maximal amplitudes of I/O function 14 d after application. No detrimental effects on cochlear function were noted; thus, indicating absence of ototoxicity for extracochlear application in the concentrations used. After the surgical trauma of cochleostomy, CAP thresholds increased by 12.5 dB directly after surgery and by 15.8 dB at day 3. Amplitudes of CAPs diminished. Intracochlear application of Triamcinolon resulted in significantly enhanced recovery of CAP thresholds and amplitudes of I/O function from initial loss over a period of 4 weeks. Conclusions: From these results, we conclude that extracochlear topical application of Triamcinolon has no ototoxic effect in the concentrations that were used and that intracochlear application supports an increased recovery of cochlear functions after surgical trauma. Furthermore, the results indicate a protective effect of corticosteroids, partially preventing progressive loss of hearing after cochleostomy over a period of 4 weeks. Intracochlear application of Triamcinolon may be useful to prevent hearing loss after surgical intervention on the inner ear; however, clinical safety and efficacy remain to be proven in clinical studies.
The DRIP Complex and SRC-1/p160 Coactivators Share Similar Nuclear Receptor Binding Determinants but Constitute Functionally Distinct Complexes

ABSTRACT Transcriptional activation requires both access to DNA assembled as chromatin and functional contact with components of the basal transcription machinery. Using the hormone-bound vitamin D3receptor (VDR) ligand binding domain (LBD) as an affinity matrix, we previously identified a novel multisubunit coactivator complex, DRIP (VDR-interacting proteins), required for transcriptional activation by nuclear receptors and several other transcription factors. In this report, we characterize the nuclear receptor binding features of DRIP205, a key subunit of the DRIP complex, that interacts directly with VDR and thyroid hormone receptor in response to ligand and anchors the other DRIP subunits to the nuclear receptor LBD. In common with other nuclear receptor coactivators, DRIP205 interaction occurs through one of two LXXLL motifs and requires the receptor's AF-2 subdomain. Although the second motif of DRIP205 is required only for VDR binding in vitro, both motifs are used in the context of an retinoid X receptor-VDR heterodimer on DNA and in transactivation in vivo. We demonstrate that both endogenous p160 coactivators and DRIP complexes bind to the VDR LBD from nuclear extracts through similar sequence requirements, but they do so as distinct complexes. Moreover, in contrast to the p160 family of coactivators, the DRIP complex is devoid of any histone acetyltransferase activity. The results demonstrate that different coactivator complexes with distinct functions bind to the same transactivation region of nuclear receptors, suggesting that they are both required for transcription activation by nuclear receptors.
Cloning, expression and sequence analysis of the gene encoding the 120kD surface‐exposed protein of Rickettsia rickettsii

Rickettsia rickettsii (R strain) genomic DNA was partially digested and cloned into the lambda expression vector gt11 generating a genomic clone bank. Trans‐formant plaques were screened with antisera generated against the 120 kiloDalton protein of R. rickettsii to detect those phage expressing the recombinant protein. The gene encoding the 120kD protein was localized to a 4.3 kilobase Sphl‐BamHl fragment from the recombinant phage and subcioned into pUC18 and pUC19. Full‐length expression of the recombinant protein was achieved with both orientations. The gene and flanking regions were sequenced. The p120 gene consists of 3900 base pairs coding for 1300 amino acids. A distinguishable promoter region was not identified, although there are several 5′ sequences that resemble classical prokaryotic promoters. Downstream of the termination codon for this gene lies a 726 base pair open reading frame on the opposite strand with the potential to encode a protein of approximately 27 kD. The identity of this putative gene product is unknown. The two open reading frames are separated by a 106 base pair intergenic region that consists of a stretch of dyad symmetry resembling rho‐independent transcriptional terminators.
Markers of Type I and Type III Collagen Turnover, Insulin-Like Growth Factors, and Their Binding Proteins in Cord Plasma of Small Premature Infants: Relationships with Fetal Growth, Gestational Age, Preeclampsia, and Antenatal Glucocorticoid Treatment

Disorders affecting fetal growth are commonly associated with premature birth. IGFs and their binding proteins (IGFBPs) are potent regulators of fetal growth. In vitro evidence suggests that they regulate collagen turnover. Collagen turnover can be monitored by serum markers of type I collagen synthesis (PINP) and degradation (ICTP) and a marker of type III collagen synthesis (PIIINP). We examined whether these markers in fetal circulation reflect intrauterine growth and maturity, and whether any interrelationship exists between them and fetal IGFs and IGFBPs in preterm infants before 32 wk of gestation. Cord plasma PINP, ICTP, PIIINP, IGF-I, IGF-II, IGFBP-1, and IGFBP-3 were determined for 98 preterm infants. To express birth weight in units adjusted for gestational age, a birth weight SD score (SDS) was calculated. Negative correlations existed between gestational age and PINP (r = −0.43;p < 0.0001), ICTP (r = −0.34;p = 0.002), and PIIINP (r = −0.34;p = 0.0001). Positive correlations existed between birth weight SDS and PINP (r = 0.40;p = 0.0002) and ICTP (r = 0.48;p < 0.0001) but not PIIINP. Moreover, birth weight SDS was positively correlated with IGF-I (r = 0.58;p < 0.0001) and IGFBP-3 (r = 0.44;p < 0.0001) and negatively correlated with IGF-II (r = −0.36;p = 0.003) and IGFBP-1 (r = −0.50;p < 0.0001). Gestational age correlated with IGFBP-3 (r = 0.25;p = 0.03). In preeclampsia, IGF-I was lower (p = 0.002) and IGFBP-1 higher (p < 0.0001), also after adjustment for fetal size. The number of antenatal glucocorticoid treatments was associated with lower ICTP (p = 0.04), higher IGF-I (p = 0.002), lower IGF-II (p = 0.02), lower IGFBP-1 (p = 0.05), and higher IGFBP-3 (p = 0.004), also after adjustment for potential confounders. In multiple regression analysis, the factors significantly associated with PINP (R2 = 0.47) were gestational age and IGF-I, and those associated with ICTP (R2 = 0.54) were IGF-I, gestational age, and antenatal glucocorticoid treatment. We conclude that IGF-I may be involved in regulation of type I collagen turnover in the growing fetus. Cord blood PINP and ICTP reflect both fetal growth and maturity and deserve evaluation as potential indicators of postnatal growth velocity in preterm infants, whereas PIIINP reflects fetal maturity.
Financial Asset Accumulation by Poor Adolescents Participating in Child Savings Accounts in Low Resource Communities in Uganda

Financial Asset Accumulation by Poor Adolescents Participating in Child Savings Accounts in Low Resource Communities in Uganda Leyla Karimli This dissertation examined savings attitudes and financial asset accumulation of poor and vulnerable school-going AIDS-orphaned adolescents involved in a subsidized matched child savings program in Uganda and being cared for by a living parent (adolescents who have lost one parent) or by an adult guardian within an extended family (for adolescents who have lost both parents). More specifically, the study tested (1) whether participation in a subsidized matched savings program had an independent effect above and beyond the effect of individual and family characteristics on adolescents' saving attitudes and self-reported financial asset accumulation; (2) whether family characteristics (i.e. family relations, family financial socialization, and household demographics) moderated the effect of participation in a subsidized matched child savings program on adolescents' saving attitudes and self-reported financial asset accumulation; and (3) whether the adolescents’ future orientation and family financial socialization served as mechanisms to transmit the effect of the participation in a subsidized matched child savings program on adolescents' self-reported financial asset accumulation. Grounded in an integrated theoretical framework of classical and behavioral economics, family financial socialization theory, and the institutional theory of saving, this study used longitudinal analyses of data on 346 dyads (adolescents and their guardians) collected in a experimental cluster-randomized controlled trial. The study found that adolescents’ saving attitudes (both reported willingness to save and reported confidence in saving), although not affected by participation in a subsidized matched child savings program, were significantly associated with family relations, family financial socialization, caregiver’s gender, and adolescent’s gender and educational aspirations. Adolescents’ self-reported saving was significantly affected by participation in a subsidized matched child savings program; this effect was direct, and neither moderated nor mediated by any of the family characteristics, nor by adolescent’s future orientation. The adolescents’ self-reported amount saved is significantly affected by participation in a subsidized matched child savings program. This effect is weakened by the number of children in the household: the more children in the household, the weaker the effect. In addition, the effect is potentially mediated by the guardian saving for the adolescent. The findings contribute to the institutional perspective on saving arguing that saving is not only a function of individual characteristics, but also institutional opportunities. Findings may help inform programs and policies facilitating assetbuilding initiatives for youth in developing countries, particularly in sub-Saharan Africa.