Age at first child : does education delay fertility timing ? the case of Kenya

Completing additional years of education necessarily entails spending more time in school. There is naturally a rather mechanical effect of schooling on fertility if women tend not to have children while continuing to attend high school or college, thus delaying the beginning of and shortening their reproductive life. This paper uses data from the Kenyan Demographic and Health Surveys of 1989, 1993, 1998, and 2003 to uncover the impact of staying one more year in school on teenage fertility. To get around the endogeneity issue between schooling and fertility preferences, the analysis uses the 1985 Kenyan education reform as an instrument for years of education. The authors find that adding one more year of education decreases by at least 10 percentage points the probability of giving birth when still a teenager. The probability of having one's first child before age 20, when having at least completed primary education, is about 65 percent; therefore, for this means a reduction of about 15 percent in teenage fertility rates for this group. One additional year of school curbs the probability of becoming a mother each year by 7.3 percent for women who have completed at least primary education, and 5.6 percent for women with at least a secondary degree. These results (robust to a wide array of specifications) are of crucial interest to policy and decision makers who set up health and educational policies. This paper shows that investing in education can have positive spillovers on health.Population Policies,Health Monitoring&Evaluation,Adolescent Health,Primary Education,Education For All

Is there a metropolitan bias ? the inverse relationship between poverty and city size in selected developing countries

This paper provides evidence from eight developing countries of an inverse relationship between poverty and city size. Poverty is both more widespread and deeper in very small and small towns than in large or very large cities. This basic pattern is generally robust to choice of poverty line. The paper shows, further, that for all eight countries, a majority of the urban poor live in medium, small, or very small towns. Moreover, it is shown that the greater incidence and severity of consumption poverty in smaller towns is generally compounded by similarly greater deprivation in terms of access to basic infrastructure services, such as electricity, heating gas, sewerage, and solid waste disposal. The authors illustrate for one country -- Morocco -- that inequality within large cities is not driven by a severe dichotomy between slum dwellers and others. The notion of a single cleavage between slum residents and well-to-do burghers as the driver of urban inequality in the developing world thus appears to be unsubstantiated -- at least in this case. Robustness checks are performed to assess whether the findings in the paper are driven by price variation across city-size categories, by the reliance on an income-based concept of well-being, and by the application of small-area estimation techniques for estimating poverty rates at the town and city level.Rural Poverty Reduction,Subnational Economic Development,City Development Strategies,Regional Economic Development

Anti-CD45RC antibody immunotherapy prevents and treats experimental autoimmune polyendocrinopathy-candidiasis- ectodermal dystrophy syndrome

Targeted monoclonal antibody (mAb) therapies show great promise for the treatment of transplant rejection and autoimmune diseases by inducing more specific immunomodulatory effects than broadly immunosuppressive drugs routinely used. We recently described the therapeutic advantage of targeting CD45RC, expressed at high levels by conventional T (Tconv) cells (CD45RC(hi)), their precursors, and terminally differentiated T (TEMRA) cells, but not by regulatory T cells (Tregs; CD45RC(lo/-)). We demonstrated efficacy of anti-CD45RC mAb treatment in transplantation, but its potential has not been examined in autoimmune diseases. Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare genetic syndrome caused by loss-of-function mutations of autoimmune regulator (AIRE), a key central tolerance mediator, leading to abnormal autoreactive T cell responses and autoantibody production. Herein, we show that, in a rat model of APECED syndrome, anti-CD45RC mAb was effective for both prevention and treatment of autoimmune manifestations and inhibited autoantibody development. Anti-CD45RC mAb intervention depleted CD45RC(hi) T cells, inhibited CD45RC(hi) B cells, and restored the Treg/Tconv cell ratio and the altered Treg transcriptomic profile. In APECED patients, CD45RC was significantly increased in peripheral blood T cells, and lesioned organs from APECED patients were infiltrated by CD45RC(hi) cells. Our observations highlight the potential role for CD45RC(hi) cells in the pathogenesis of experimental and human APECED syndrome and the potential of anti-CD45RC antibody treatment.Peer reviewe

CONTROLE DE L'EXPRESSION DES NUCLEOTIDES CYCLIQUES PHOSPHODIESTERASES DE TYPE 4 DANS LE MUSCLE LISSE UTERIN AU COURS DE LA GROSSESSE

PRINCIPALE CAUSE DE MORTALITE ET DE MORBIDITE NEONATALES, LA PREMATURITE DEMEURE UN PROBLEME MAJEUR DE SANTE PUBLIQUE, S'EXPLIQUANT EN PARTICULIER PAR DES STRATEGIES DE PRISE EN CHARGE MEDICALES A LA FOIS LIMITEES ET DECEVANTES. FACE A CETTE SITUATION, NOTRE APPROCHE CONSISTE A DEFINIR AU SEIN DE LA FAMILLE DES NUCLEOTIDES CYCLIQUES PHOSPHODIESTERASES DE TYPE 4 (PDE4), UN SITE D'ACTION SELECTIF ET EFFICACE POUR DE NOUVEAUX AGENTS RELAXANTS DU MUSCLE LISSE UTERIN, LE MYOMETRE. LA FAMILLE PDE4 CATALYSE LA DEGRADATION DE L'AMPC, UN SECOND MESSAGER IMPLIQUE DANS LA RELAXATION DU MYOMETRE. SON INHIBITION ENTRAINE IN VITRO LE RELACHEMENT DU MYOMETRE HUMAIN. CETTE FAMILLE COMPREND DE MULTIPLES ISOFORMES, EXPRIMEES DIFFERENTIELLEMENT SELON LE TYPE CELLULAIRE. AU COURS DE CE TRAVAIL, NOUS AVONS MIS EN EVIDENCE L'INDUCTION DU SOUS-TYPE PDE4B2 DANS LE MYOMETRE HUMAIN A TERME. NOUS AVONS MONTRE QUE LA SYNTHESE ACCRUE DE PDE4B2, MAIS AUSSI DE PDE4D1 ET 4D2, PEUT ETRE LA CONSEQUENCE D'UNE ELEVATION SOUTENUE DE L'AMPC SOUS L'ACTION D'EFFECTEURS DE LA MOTILITE UTERINE TELLE LA PROSTAGLANDINE E 2. CE RETRO-CONTROLE PARTICIPE A LA MISE EN PLACE D'UNE DESENSIBILISATION DE L'ACTIVATION DE LA VOIE DE DE TRANSDUCTION DE L'AMPC EN CAS DE STIMULATION CONTINUE. AINSI, NOUS AVONS OBSERVE DANS LE MYOMETRE A TERME QUE LES PDE4 INTERVIENNENT DANS LE PROCESSUS DE DESENSIBILISATION AUX AGENTS UTERO-RELAXANTS DONT LA TRANSDUCTION DU SIGNAL NECESSITE UNE AUGMENTATION D'AMPC, TELS LES AGONISTES 2-ADRENERGIQUES. NOUS AVONS, DE PLUS, IDENTIFIE QUE LES PDE4 IMPLIQUEES DANS LA CONTRACTION PRESENTENT UNE CONFORMATION DIFFERENTE EN FIN DE GESTATION. L'ENSEMBLE DE CES RESULTATS NOUS PERMETTENT D'ENVISAGER L'UTILISATION DE COMPOSES INHIBITEURS DE PDE4, SELECTIFS D'UN SOUS-TYPE ET/OU D'UNE CONFORMATION DE PDE4 COMME AGENTS UTERO-RELAXANTS, SEULS OU EN ASSOCIATION AVC DES AGONISTES 2-ADRENERGIQUES DANS LE TRAITEMENT DE LA MENACE D'ACCOUCHEMENT PREMATURE.PARIS7-Bibliothèque centrale (751132105) / SudocSudocFranceF

Optical characterization of a single mode Mid Infrared microstructured optical fiber up to 10 μm Potential for supercontinuum generation and applications for QCLs based sensors

International audienc

Highly birefringent chalcogenide optical fiber for polarization-maintaining in the 3-85 µm mid-IR window

International audienceA highly birefringent polarization-maintaining chalcogenide microstructured optical fiber (MOF) covering the 3-8.5 µm wavelength range has been realized for the first time. The fiber cross-section consists of 3 rings of circular air holes with 2 larger holes adjacent to the core. Birefringence properties are calculated by using the vector finite-element method and are compared to the experimental ones. The group birefringence is 1.5x10−3 and fiber losses are equal to 0.8 dB/m at 7.55 µm

Francisella tularensis : FupA mutation contributes to fluoroquinolone resistance by increasing vesicle secretion and biofilm formation

Francisella tularensis is the causative agent in tularemia for which the high prevalence of treatment failure and relapse is a major concern. Directed-evolution experiments revealed that acquisition of fluoroquinolone (FQ) resistance was linked to factors in addition to mutations in DNA gyrase. Here, using F. tularensis live vaccine strain (LVS) as a model, we demonstrated that FupA/B (Fer-Utilization Protein) expression is linked to FQ susceptibility, and that the virulent strain F. tularensis subsp. tularensisSCHU S4 deleted for the homologous FupA protein exhibited even higher FQ resistance. In addition to an increased FQ minimal inhibitory concentration, LVSΔfupA/B displayed tolerance toward bactericidal compounds including ciprofloxacin and gentamicin. Interestingly, the FupA/B deletion was found to promote increased secretion of outer membrane vesicles (OMVs). Mass spectrometry-based quantitative proteomic characterization of vesicles from LVS and LVS∆fupA/B identified 801 proteins, including a subset of 23 proteins exhibiting differential abundance between both strains which may therefore contribute to the reduced antibiotic susceptibility of the FupA/B-deleted strain. We also demonstrated that OMVs are key structural elements of LVSΔfupA/Bbiofilms providing protection against FQ. These results provide a new basis for understanding and tackling antibiotic resistance and/or persistence of Francisella and other pathogenic members of the Thiotrichales class

Effect of Swine Glyco-humanized Polyclonal Neutralizing Antibody on Survival and Respiratory Failure in Patients Hospitalized With Severe COVID-19: A Randomized, Placebo-Controlled Trial

International audienceAbstract Background We evaluated the safety and efficacy of XAV-19, an antispike glyco-humanized swine polyclonal neutralizing antibody in patients hospitalized with severe coronavirus disease 2019 (COVID-19). Methods This phase 2b clinical trial enrolled adult patients from 34 hospitals in France. Eligible patients had a confirmed diagnosis of severe acute respiratory syndrome coronavirus 2 within 14 days of onset of symptoms that required hospitalization for low-flow oxygen therapy (<6 L/min of oxygen). Patients were randomly assigned to receive a single intravenous infusion of 2 mg/kg of XAV-19 or placebo. The primary end point was the occurrence of death or severe respiratory failure between baseline and day 15. Results Between January 12, 2021, and April 16, 2021, 398 patients were enrolled in the study and randomly assigned to XAV-19 or placebo. The modified intention-to-treat population comprised 388 participants who received full perfusion of XAV-19 (199 patients) or placebo (189 patients). The mean (SD) age was 59.8 (12.4) years, 249 (64.2%) individuals were men, and the median time (interquartile range) from symptom onset to enrollment was 9 (7–10) days. There was no statistically significant decrease in the cumulative incidence of death or severe respiratory failure through day 15 in the XAV-19 group vs the placebo group (53/199 [26.6%] vs 48/189 [25.4%]; adjusted risk difference, 0.6%; 95% CI, −6% to 7%; hazard ratio, 1.03; 95% CI, 0.64–1.66; P = .90). In the safety population, adverse events were reported in 75.4% of 199 patients in the XAV-19 group and in 76.3% of 190 patients in the placebo group through D29. Conclusions Among patients hospitalized with COVID-19 requiring low-flow oxygen therapy, treatment with a single intravenous dose of XAV-19, compared with placebo, did not show a significant difference in terms of disease progression at day 15