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Implementing a Black feminist perspective, this ethnographic research examines the seemingly contradictory circumstances in which respectable heterosexual Afrodescendant Creole men of Bluefields are involved in familial relationships based on Christian love and simultaneously engage in intimate partner violence and child sexual abuse. The findings reveal that Creoles’ gender politics are rooted in heteropatriarchal ideology, strongly influenced by Christian respectability. The construction of Creole manhood is based on a complex process characterized by inculcation, emulation, and socialization regulated under strict childrearing practices controlled by men. Regarding their self-perception, within an antiblack multicultural patriarchal context, Creole men define themselves are exceptional benevolent patriarchs. Their perspectives of Creole men’s enactment of intimate partner violence and child sexual abuse connote denial, evasion, minimization, diffusion, and rationalization. Nevertheless, a close examination unveils that Creole men abuse power and enact various forms of gender violence and that they recur to dissemblance to shield the negative aspect of their behavior. Hence, victim-blaming and the belief that perpetrators suffer from mental illness are the primary rationales for explaining perpetrators’ behavior. Nevertheless, it is demonstrated these rationales are rooted in patriarchal ideology. Moreover, patriarchy establishes men to exert power and control over women and children and enables the coexistence of love and gender violence. Notably, Creole men reject all forms of feminist stances and yearn for women to remain submissive; this posture reveals patriarchal nostalgia in the era of women’s liberation. Simultaneously, they advocate for men to practice benevolent patriarchy. To end child sexual abuse, men suggest that both parents and children are to be trained in how to identify sexual predators and avoid them. Lastly, the study reveals that education on gender equality, combined with women’s financial emancipation, is critical to disrupting patriarchy. It also suggests the need to demystify the belief related to benevolent patriarchy, gender complementarity, and love.

Este manual de sustancias químicas es elaborado con el fin de informar y evitar que ocurran accidentes laborales en el área de laboratorio , se da a conocer los diferentes tipos de sustancias peligrosas para la salud de las personas, su reacción e inhalación. INTRODUCCIÓN.............................................................................................................................8 2. OBJETIVOS..................................................................................................................................9 2.2 OBJETIVO GENERAL ................................................................................................................................9 2.3 OBJETIVO ESPECÍFICOS...........................................................................................................................9 3. MARCO REFERENCIAL ......................................................................................................... 10 3.1 MARCO LEGAL...................................................................................................................................10 3.1 .1 ley 9 de 1979 congreso de la república .............................................................................................10 3.1.2 Resolución 2400 de 1979 ministerio de trabajo y seguridad social ....................................................10 3.2 MARCO CONCEPTUAL.............................................................................................................................11 3.2.1 Agentes de riesgos físicos: se consideran agentes de riesgos físicos aquellos que son de factor ambiental es decir que están en la naturaleza. Estos provocan daños y afectaciones a la salud por la intensidad y la concentración que tienen. (SURATEP S.A., 1997)................................................................11 3.2.2 Agentes de riesgos biológicos: son microorganismos que están en el ambiente y que pueden ocasionar enfermedades en las personas cuando tienen contacto con estos. (DISPOSICIONES GENERALES, 1997)..........................................................................................................................................................11 3.2.3 Agentes de riesgos químicos: son todas aquellas sustancias químicas orgánicas que pueden ser manipuladas, almacenadas o transportadas por vías respiratorias y que pueden causar daños en la salud de las personas. Estas sustancias entran en contacto con nuestro cuerpo por medio de la ingestión, inhalación, o absorción. (SURATEP S.A., 1997) ..........................................................................................11 3.2.4 Accidente químico: es un entorno peligroso para la salud humana o el medio ambiente, se da por medio de sucesos como incendios, explosiones, fugas o liberaciones de sustancias toxicas que pueden provocar enfermedad, lesión. Invalidez o muerte en las personas. (SURATEP S.A., 1997)..........................11 3.2.5 Emergencia: se considera una situación la cual no está planeada sino que sucede y se da por un evento no deseado (SURATEP S.A., 1997)..................................................................................................11 3.2.7 Residuo peligroso: se considera aquellos tipos de residuos que pueden ser riesgosos para la salud de las personas y del medio ambiente. (SANCHEZ, 2007)...............................................................................11 4. METODOLOGÍA...................................................................................................................... 20 4.1 ESCENARIO DE ESTUDIO.......................................................................................................................20 4.2 TIPO DE ESTUDIO..................................................................................................................................21 4.3 POBLACIÓN, TIPO DE MUESTREO Y CÁLCULO DEL TAMAÑO DE LA MUESTRA ......................................25 4.4 MÉTODOS E INSTRUMENTOS DE RECOLECCIÓN DE DATOS ..................................................................25 4.5 PROCEDIMIENTO PARA LA RECOLECCIÓN DE INFORMACIÓN...............................................................27 4.6 PLAN PARA LA TABULACIÓN Y ANÁLISIS DE DATOS..............................................................................28 5. RESULTADOS.......................................................................................................................... 29 ETIQUETA...................................................................................................................................................29 PRODUCTOS EXPLOSIVOS ..........................................................................................................................31 6. CONCLUSION........................................................................................................................... 42 BIBLIOGRAFÍA............................................................................................................................ 43 8. ANEXOS..................................................................................................................................... 45 Pregrado Administrador(a) en Salud Práctica Empresarial

BackgroundAround 15–20% of primary breast cancers are characterized by HER2 protein overexpression and/or HER2 gene amplification. Despite the successful development of anti-HER2 drugs, intrinsic and acquired resistance represents a major hurdle. This study was performed to analyze the RANK pathway contribution in HER2-positive breast cancer and anti-HER2 therapy resistance.MethodsRANK and RANKL protein expression was assessed in samples from HER2-positive breast cancer patients resistant to anti-HER2 therapy and treatment-naive patients. RANK and RANKL gene expression was analyzed in paired samples from patients treated with neoadjuvant dual HER2-blockade (lapatinib and trastuzumab) from the SOLTI-1114 PAMELA trial. Additionally, HER2-positive breast cancer cell lines were used to modulate RANK expression and analyze in vitro the contribution of RANK signaling to anti-HER2 resistance and downstream signaling.ResultsRANK and RANKL proteins are more frequently detected in HER2-positive tumors that have acquired resistance to anti-HER2 therapies than in treatment-naive ones. RANK (but not RANKL) gene expression increased after dual anti-HER2 neoadjuvant therapy in the cohort from the SOLTI-1114 PAMELA trial. Results in HER2-positive breast cancer cell lines recapitulate the clinical observations, with increased RANK expression observed after short-term treatment with the HER2 inhibitor lapatinib or dual anti-HER2 therapy and in lapatinib-resistant cells. After RANKL stimulation, lapatinib-resistant cells show increased NF-κB activation compared to their sensitive counterparts, confirming the enhanced functionality of the RANK pathway in anti-HER2-resistant breast cancer. Overactivation of the RANK signaling pathway enhances ERK and NF-κB signaling and increases lapatinib resistance in different HER2-positive breast cancer cell lines, whereas RANK loss sensitizes lapatinib-resistant cells to the drug. Our results indicate that ErbB signaling is required for RANK/RANKL-driven activation of ERK in several HER2-positive cell lines. In contrast, lapatinib is not able to counteract the NF-κB activation elicited after RANKL treatment in RANK-overexpressing cells. Finally, we show that RANK binds to HER2 in breast cancer cells and that enhanced RANK pathway activation alters HER2 phosphorylation status.ConclusionsOur data support a physical and functional link between RANK and HER2 signaling in breast cancer and demonstrate that increased RANK signaling may contribute to the development of lapatinib resistance through NF-κB activation. Whether HER2-positive breast cancer patients with tumoral RANK expression might benefit from dual HER2 and RANK inhibition therapy remains to be elucidated.

Additional file 6: Figure S6. A. Relative number of living (relative survival) SKBR3 RANK cells stimulated with RANKL in the presence or absence of denosumab (DNS) and incubated for 4 days with the indicated concentrations of lapatinib. Cells were seeded in growth media with/without denosumab (1 μg/ml), lapatinib was added after 24 h stimulation with 100 ng/ml RANKL, and cell viability was analyzed with CCK8 as detailed in methods. Determinations were done in triplicates, mean values from n ≥ 2 independent experiments and SD are depicted. B. Western blot analyses of total levels of p65, ERK1/2 and HER2 in whole lysates from SKBR3, BT474 and HCC1954 cells stably transduced with control (empty) or RANK overexpressing (RANK) vectors as depicted in Fig. 5d. Before collecting the cells, they were cultured in media without FBS for 12 h, pretreated with/without lapatinib for 2 h followed by 10 min stimulation with RANKL. Tubulin was used as a loading control. C. Table depicting the relative phospho-protein levels of the indicated proteins from the western blots shown in Fig. 5d and Fig. S6B determined by densitometry analyses with Image J.

Additional file 3: Figure S3. RANK and RANKL expression in breast cancer samples from the PAMELA clinical trial. A. Expression of RANK and RANKL across the intrinsic molecular subtypes from the PAMELA study. P values were calculated by comparing mean values across all groups. B. Scatter plots of RANK and RANKL expression versus ERBB2 expression for baseline samples in the PAMELA study. Solid line in each figure represents the regression line. Pearson correlation coefficient (r) with significance (p value) is presented in each figure. C. Pearson correlation between single genes and gene expression signatures evaluated in baseline samples from the PAMELA study.

Additional file 5: Figure S5. A. Relative number of living (relative survival) SKBR3 and SKLR control cells incubated for 4 days with the indicated concentrations of lapatinib and stimulated with RANKL. Cells were seeded in growth media, 100 ng/ml RANKL were added 24h after seeding, lapatinib was added 24 h later and cells were analyzed with CCK8 as detailed in methods. Determinations were done in triplicates, mean values are depicted from n = 5 independent experiments and SD and p-value (**) calculated by one-way ANOVA is depicted (p ≤ 0.05 for SKBR3 vs SKLR and SKLR +RANKL, SKBR3 +RANKL vs SKLR and SKLR +RANKL; n.s. for SKBR3 vs SKBR3 +RANKL and SKLR vs SKLR +RANKL). Significance of relative survival was calculated for each concentration using two-tailed p values for one sample t test. RANKL significantly increased survival of SKLR cells at 0.018 μM of lapatinib (p = 0.019). B. Western blot showing the total levels of IκB, p65, ERK1/2, AKT and HER2 in SKBR3 control, SKLR control and SKLR sh#3 cells treated with RANKL or lapatinib as depicted in Fig. 4c. Cells were serum starved for 12 h and then treated with lapatinib (2 h) or RANKL (10 min) before processing them. Tubulin was used as a loading control. C. Table depicting the relative phospho-protein levels of the indicated proteins from the western blots shown in Fig. 4c and Fig. S5B determined by densitometry analyses with Image J.

Additional file 7: Figure S7. Western blot analyses of HER2 (p-HER2, p-ERK1/2) and NF-κB (p-p65) pathway activation in SKBR3, BT474 and HCC1954 cells stably transduced with empty or RANK overexpressing (RANK) vectors. Cells were cultured in media without FBS for 12 h, followed by stimulation with EGF (100 ng/ml) (upper panels) or heregulin (HRG 10 ng/ml) (lower panels) for the indicated times. Tubulin was used as a loading control.

Background: A quadrivalent split-virion inactivated influenza vaccine (VaxigripTetre (TM), Sanofi Pasteur; IIV4) containing two A strains (H1N1 and H3N2) and B strains from both lineages (Victoria and Yamagata) was approved in Europe in 2016 for individuals aged >= 3 years. This study examined the efficacy and safety of IIV4 in children aged 6-35 months. Methods: This was a phase III randomised controlled trial conducted in Latin America, Asia, Africa, and Europe during the Northern Hemisphere 2014/2015 and 2015/2016 and Southern Hemisphere 2014 and 2015 influenza seasons. Healthy children aged 6-35 months not previously vaccinated against influenza were randomised to receive two full doses 28 days apart of IIV4, placebo, the licensed trivalent splitvirion inactivated vaccine (IIV3), an investigational IIV3 containing a B strain from the alternate lineage. The primary objective was to demonstrate efficacy against influenza illness caused by any strain or vaccine-similar strains. Results: The study enrolled 5806 participants. Efficacy, assessed in 4980 participants completing the study according to protocol, was demonstrated for IIV4. Vaccine efficacy was 50.98% (97% CI, 37.36-61.86%) against influenza caused by any A or B type and 68.40% (97% CI, 47.07-81.92%) against influenza caused by vaccine-like strains. Safety profiles were similar for IIV4, placebo, and the IIV3s, although injection-site reactions were slightly more frequent for IIV4 than placebo. Conclusions: IIV4 was safe and effective for protecting children aged 6-35 months against influenza illness caused by vaccine-similar or any circulating strains. (C) 2018 The Authors. Published by Elsevier Ltd.