Income inequality in the OECD area: On measuring its possible effects on economic growth

This thesis studies possible effects income inequality might have on economic growth and examines whether it is reasonable to measure these effects in detail with the tools provided by growth econometrics. Recently published research indicates a strong negative effect of net income inequality on growth and this thesis assesses whether these findings can be considered reliable and significant. This objective is accomplished by inspecting recent literature concerning the subject with a detailed emphasis on a particular OECD working paper stating a robust negative effect of net income inequality on growth. Said working paper, Cingano (2014), is constructed on the MRW augmented Solow model, which is introduced and assessed. Moreover, the estimation model and method as well as the data sets used in Cingano (2014) are examined in detail. Furthermore, development of income inequality in the OECD area in recent decades and theoretical channels through which income inequality might affect growth are introduced and discussed. This thesis finds that overly specific conclusions about the strength of the estimated effects should not be made based on growth regressions on the subject. This conclusion is reached because the estimates often lack sufficient data and there are problems concerning the estimation models and methods. This thesis finds considerable difficulties concerning Cingano (2014) that are also linked to other literature addressing the effects of income inequality on growth in general. Based on the findings in this thesis, it seems unreasonable to interpret the findings of the literature in such a detailed manner as they are expressed. However, this thesis does not suggest that the subject and research about it lacks importance, but suggests that the focus ought to be directed to micro-level data and channels where genuine progress could be accomplished

Frågor och responser i samtal i bankens telefonkundtjänst : En samtalsanalytisk studie

Pro Gradu -tutkielmani käsittelee kysymysten ja vastausten muodostamista sekä niiden suhdetta institutionaalisessa puhelinkeskustelussa. Tutkimuksen tavoite on tutkia keskustelun osapuolten kysymysvuoroja keskustelun eri vaiheissa sekä sitä, mitä erilaisilla kysymysmuodoilla tavoitellaan. Tarkastelen kysymysten esiintymistä erilaisissa konteksteissa ja tutkin kysymysten vaikutusta vastauksiin sekä vastausten muodostamista. Kiinnostuksen kohteena on myös selvittää, kumpi osapuolista esittää puhelun aikana enemmän kysymyksiä ja siten johdattelee keskustelua eteenpäin. Tutkimusmateriaali koostuu tallennetuista pankkiasiointipuheluista, joissa asiakas soittaa puhelinpalveluun saadakseen apua maksukortteihin liittyviin ongelmiin. Tutkimusmateriaalini on ainutlaatuinen ja tarjoaa tutkimusalustan, jota aiemmassa keskusteluntutkimuksessa ei juurikaan ole päästy hyödyntämään. Kysymysten ja vastausten tutkimisessa erilaisten kysymystyyppien tunnistamisen lisäksi oleellista on vuorottelu, vierusparien suhde toisiinsa sekä preferenssirakenne. Nämä termit ovat tutkimuksessani perustavanlaatuisia ja ne esitellään keskustelunanalyyttiseen menetelmään perustuen. Tutkimusmenetelmänä keskustelunanalyysi on metodi, jonka avulla tutkitaan luonnollisesti tapahtuvaa keskustelua ääni- tai videonauhoitteiden avulla. Keskustelunanalyysi perustuu pääperiaatteisiin, joiden mukaan vuorovaikutus ei ole kaoottista, vaan pohjautuu sääntöihin. Vuorovaikutuksessa kaikki yksityiskohdat ovat tärkeitä ja relevantteja eikä mitään voida pitää sattumanvaraisena. Keskustelunanalyysissä käytetään pääasiassa laadullisia menetelmiä, mutta tutkimuksessani hyödynnän lisäksi määrällisiä menetelmiä saadakseni vastauksen kaikkiin tutkimuskysymyksiini. Tutkimuksen tulokset osoittavat, että puhelinpalvelun työntekijät toimivat institutionaalisen roolinsa mukaan esittämällä pääosan kysymyksistä asiakkaille, joiden tehtävä on antaa preferoitu vastaus. Asiantuntijat käyttävät erilaisia kysymysmuotoja riippuen siitä, millaista informaatiota he kulloinkin hakevat. Kysymysten asettelussa oleellista on myös niiden suhde edeltäviin ja niitä seuraaviin vuoroihin. Vuorojen sisältämien osien järjestys voi osaltaan lisätä kysymysten tarvetta, mikä myös lisää asiakkaiden esittämien kysymysten määrää. Asiakkaiden kysymykset liittyvätkin usein asiantuntijan ohjeiden tai termien ymmärtämättömyyteen, soiton syynä olevan ongelman esittelyyn sekä keskustelun aikana muuten ilmenneisiin uusiin asioihin. Aineistossani esiintyy neljänlaisia kysymystyyppejä, jotka joko rakenteeltaan tai toiminnaltaan ovat kysymyksiä: hakukysymyksiä, vaihtoehtokysymyksiä, deklaratiivejä sekä kehotuksia. Eri kysymystyypeillä on tietty funktio, ja usein eri tyyppisiä kysymyksiä käytetään erilaisen tiedon saamiseen. Esimerkiksi vaihtoehtokysymyksillä tiedustellaan jonkin lauseen paikkansapitävyyttä, kun taas hakukysymyksillä haetaan tiettyä suljettua tai avointa tietoa

Endogenous sex hormone levels and breast cancer risk

Sex‐steroid hormones are a major determinant of the risk of breast cancer. We evaluated the relationship between obesity and endogenous estrogen levels in 79 healthy, postmenopausal women. Thirty‐nine of the women were siblings of patients with postmenopausal‐onset breast cancer; the remaining women were age matched (± 10 yr) controls. Our hypothesis was that the siblings of the breast cancer patients would weigh more and that this excess weight would lead to higher serum estrone levels. The choice of unaffected family members of breast cancer patients reduces the concern that results may have been influenced by the cancer rather than antecedent to its development. Our findings demonstrated a statistically significant excess estrone level in the siblings compared to the controls (58.9 vs 47.8 pg/ml, P=0.005). The siblings weighed 4.3 kg more than the controls. Matched pairs analysis (sibling—control), adjusting for weight, also showed significant differences in serum estrone levels. These differences were observed despite comparability in dietary intake, medication use, and personal medical history. These findings represent the first time that higher estrogen levels have been measured in siblings of postmenopausal breast cancer patients. This observation may represent an important link in our understanding of the relationship between genetic and environmental risk factors of breast cancer. One approach to subsequent genetic studies of breast cancer may be to focus on the possible biological determinants such as sex‐steroid hormone level receptors, oncogenes, and gene products and not on the “familial aggregation” of breast cancer.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/101821/1/1370040402_ftp.pd

A nongenomic mechanism for progesterone-mediated immunosuppression: Inhibition of K+ channels, Ca2+ signaling, and gene expression in T lymphocytes

The mechanism by which progesterone causes localized suppression of the immune response during pregnancy has remained elusive. Using human T lymphocytes and T cell lines, we show that progesterone, at concentrations found in the placenta, rapidly and reversibly blocks voltage-gated and calcium-activated K+ channels (KV and KCa, respectively), resulting in depolarization of the membrane potential. As a result, Ca2+ signaling and nuclear factor of activated T cells (NF-AT)-driven gene expression are inhibited. Progesterone acts distally to the initial steps of T cell receptor (TCR)-mediated signal transduction, since it blocks sustained Ca2+ signals after thapsigargin stimulation, as well as oscillatory Ca2+ signals, but not the Ca2+ transient after TCR stimulation. K+ channel blockade by progesterone is specific; other steroid hormones had little or no effect, although the progesterone antagonist RU 486 also blocked KV and KCa channels. Progesterone effectively blocked a broad spectrum of K+ channels, reducing both Kv1.3 and charybdotoxin-resistant components of KV current and KCa current in T cells, as well as blocking several cloned KV channels expressed in cell lines. Progesterone had little or no effect on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and Cl- channels. We propose that direct inhibition of K+ channels in T cells by progesterone contributes to progesterone-induced immunosuppression

Human amniotic fluid glycoproteins expressing sialyl Lewis carbohydrate antigens stimulate progesterone production in human trophoblasts in vitro

Background: Progesterone is thought to mediate immune modulator effects by regulating uterine responsiveness. The aim of the study was to clarify the effect of transferrin and glycodelin A (former name PP14) as sialyl Lewis X-expressing glycoproteins on the release of progesterone by trophoblast cells in vitro. Methods: Cytotrophoblast cells were prepared from human term placentas by standard dispersion of villous tissue followed by a Percoll gradient centrifugation step. Trophoblasts were incubated with varying concentrations (50-300 mug/ml) of human amniotic fluid- and serum-transferrin as well as with glycodelin A. Culture supernatants were assayed for progesterone, human chorionic gonadotropin (hCG) and cortisol by enzyme immunometric methods. Results: The release of progesterone is increased in amniotic fluid transferrin- and glycodelin A-treated trophoblast cell cultures compared to untreated trophoblast cells. There is no relation between transferrin and the hCG or cortisol production of trophoblast cells. Conclusion: The results suggest that sialyl Lewis carbohydrate antigen-expressing amniotic fluid glycoproteins modulate the endocrine function of trophoblasts in culture by upregulating progesterone production. Copyright (C) 2004 S. Karger AG, Basel

Immunohistochemical study of osteopontin in boar testis

The expression of osteopontin (OPN) in boar testis was studied. Western blot analysis detected 66- and 32-kDa OPN immunopositive bands in the testes of adult boars. In postnatal piglets, the 66-kDa OPN band was detected in the testes, but not the 32-kDa band. In the newborn testis, OPN immunostaining was seen in gonocytes and in some supporting cells in the seminiferous tubules, as well as in interstitial Leydig cells. In the adult boar testis, OPN immunoreactivity was detected in seminiferous tubules with varying intensities. Intense OPN immunostaining was seen in the residual bodies and acrosomes in the spermatids while, occasionally, OPN immunostaining was seen in spermatogonia and various stage of spermatocytes but in few Sertoli cells in the seminiferous tubules. In addition, Leydig cells in adult boars were weakly immunostained with OPN. These findings suggest that OPN is detected in the majority of germ cells and is involved in spermatogenesis in boar testis

A Nongenomic Mechanism for Progesterone-mediated Immunosuppression: Inhibition of K+ Channels, Ca2+ Signaling, and Gene Expression in T Lymphocytes

The mechanism by which progesterone causes localized suppression of the immune response during pregnancy has remained elusive. Using human T lymphocytes and T cell lines, we show that progesterone, at concentrations found in the placenta, rapidly and reversibly blocks voltage-gated and calcium-activated K+ channels (KV and KCa, respectively), resulting in depolarization of the membrane potential. As a result, Ca2+ signaling and nuclear factor of activated T cells (NF-AT)-driven gene expression are inhibited. Progesterone acts distally to the initial steps of T cell receptor (TCR)-mediated signal transduction, since it blocks sustained Ca2+ signals after thapsigargin stimulation, as well as oscillatory Ca2+ signals, but not the Ca2+ transient after TCR stimulation. K+ channel blockade by progesterone is specific; other steroid hormones had little or no effect, although the progesterone antagonist RU 486 also blocked KV and KCa channels. Progesterone effectively blocked a broad spectrum of K+ channels, reducing both Kv1.3 and charybdotoxin–resistant components of KV current and KCa current in T cells, as well as blocking several cloned KV channels expressed in cell lines. Progesterone had little or no effect on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and Cl− channels. We propose that direct inhibition of K+ channels in T cells by progesterone contributes to progesterone-induced immunosuppression

Effect of castration and sex hormone treatment on survival, anti-nucleic acid antibodies, and glomerulonephritis in NZB/NZW F1 mice.

NZB/NZW F1 mice of both sexes were castrated at 2 wk of age and implanted subcutaneously with silastic tubes containing either 5-alpha-dihydrotestosterone or estradiol-17-beta. Mice receiving androgen showed improved survival, reduced anti-nucleic acid antibodies, or less evidence of glomerulonephritis as determined by light, immunofluorescent, and electron microscopy. By contrast, opposite effects were observed in castrated mice receiving estrogen. Intact male NZB/NZW F1 mice received androgen implants at 8 mo, an age when they develop an accelerated autoimmune disease associated with a decline in serum testosterone concentration. Such treated mice had improved survival and reduced concentrations of antibodies to DNA and to polyadenylic acid (Poly A). Prepubertal castration of male NZB/NZW F1 mice results in an earlier appearance of IgG antibodies to Poly A. This effect of castration was prevented if neonatal thymectomy was also performed

Vitamin D Binding Protein, Total and Free Vitamin D Levels in Different Physiological and Pathophysiological Conditions.

This review focuses on the biologic importance of the vitamin D binding protein (DBP) with emphasis on its regulation of total and free vitamin D metabolite levels in various clinical conditions. Nearly all DBP is produced in the liver, where its regulation is influenced by estrogen, glucocorticoids and inflammatory cytokines but not by vitamin D itself. DBP is the most polymorphic protein known, and different DBP alleles can have substantial impact on its biologic functions. The three most common alleles-Gc1f, Gc1s, Gc2-differ in their affinity with the vitamin D metabolites and have been variably associated with a number of clinical conditions. Although DBP has a number of biologic functions independent of vitamin D, its major biologic function is that of regulating circulating free and total levels of vitamin D metabolites. 25 hydroxyvitamin D (25(OH)D) is the best studied form of vitamin D as it provides the best measure of vitamin D status. In a normal non-pregnant individual, approximately 0.03% of 25(OH)D is free; 85% is bound to DBP, 15% is bound to albumin. The free hormone hypothesis postulates that only free 25(OH)D can enter cells. This hypothesis is supported by the observation that mice lacking DBP, and therefore with essentially undetectable 25(OH)D levels, do not show signs of vitamin D deficiency unless put on a vitamin D deficient diet. Similar observations have recently been described in a family with a DBP mutation. This hypothesis also applies to other protein bound lipophilic hormones including glucocorticoids, sex steroids, and thyroid hormone. However, tissues expressing the megalin/cubilin complex, such as the kidney, have the capability of taking up 25(OH)D still bound to DBP, but most tissues rely on the free level. Attempts to calculate the free level using affinity constants generated in a normal individual along with measurement of DBP and total 25(OH)D have not accurately reflected directly measured free levels in a number of clinical conditions. In this review, we examine the impact of different clinical conditions as well as different DBP alleles on the relationship between total and free 25(OH)D, using only data in which the free 25(OH)D level was directly measured. The major conclusion is that a number of clinical conditions alter this relationship, raising the question whether measuring just total 25(OH)D might be misleading regarding the assessment of vitamin D status, and such assessment might be improved by measuring free 25(OH)D instead of or in addition to total 25(OH)D