An analysis of code mixing used in the novel Long Distance Hearts 2 by @LongDistance_R

This research concern with a sociolinguistics study. It is focused on thecode mixing theory. Nowadays some people often use code mixing in their dailycommunication. Code mixing becomes familiar in among, teenanger, old human even child. Most of them speak using code mixing. They used code mixing toavoid missunderstanding, this is also to show that code mixing can increase their ability to speak more than one languange. In this research, the researcher wants to analysis code mixing which exist in the novel entitled “Long Distance Hearts 2”The aims of this research is to describe the forms of code mixing used in the novel of Long Distance Hearts 2 and explain the reason of using code mixingin the novel of Long Distance Hearts 2.This research used descriptive qualitative method. This method used to explore and understanding the meaning individuals or group about the form ofcode mixing and the reason of using code mixing based on the data that gainedthrough reading the novel then selecting the form which exist in those novel. The last, explain the reason of using code mixing in the novel.The result of this research show that there are six forms which appear in the novel, they are insertion of word, insertion of phrase, insertion of hybrid,insertion of word reduplication, insertion of idiom and the last insertion of clause.Meanwhile, the reason of using code mixing are talking about particular topic,interjection, repetition used for clarification,intention of clarifying the speechcontent for interlocutor. Three reasons that are quoting somebody else, expressinggroup identity and being emphatic about something did not found in those novel. The researcher hopes this research can give the benefit to everyone especially to the reader and English Department student. The researcher alsohopes this research can increase the knowledge and can apply in the society sothat they have a bilingual speech

Influence of handgrip strength in oxidative stress in children

El ejercicio físico puede producir estrés oxidativo en el individuo lo que pueden condicionar el riesgo cardiovascular en niños y adolescentes. Este estudio pretende analizar el estrés oxidativo según la fuerza muscular isométrica de las extremidades superiores en la edad pediátrica. Se estudiaron 70 niños sanos con edades entre 10 y 14 años, y se analizaron en saliva los lipoperóxidos (LPO), el glutatión reducido (GSH), la ratio GSH/LPO y la catalasa, como marcadores de estrés oxidativo. La muestra se dividió en dos grupos según una condición física superior o inferior medida a través de dinamometría manual (TKK 5110); se diferenció la serie en sujetos prepuberales y puberales. Se encontraron niveles significativamente inferiores de GSH y GSH/LPO en el grupo de niños con fuerza superior, y en los puberales con la mismas características; estos resultados podrían indicar la existencia de un mayor estrés oxidativo en esta situación. En conclusión, los mayores niveles de fuerza músculo esquelética, medida a través de dinamometría manual, posiblemente pueden estar asociados a un mayor estrés oxidativo en niños púberes con condición física musculoesquelética superior.Physical exercise can produce oxidative stress, this situation could contribute cardiovascular risk in children and adolescents. The following study tries to evaluate the oxidative stress produced according to the handgrip strength in infancy. 70 healthy male subjects, ages 10 to 14 years, were studied. In the saliva samples, lipoperoxides (LPO), reduced glutathione (GSH), glutathione/lipoperoxides ratio and catalase were analyzed as biomarkers of oxidative stress. Children were divided into two groups according to their handgrip strength (high or low) measured by handgrip strength (TKK 5110). The groups were also divided into prepubertal and pubertal subjects. We found GSH’s significantly low levels and of GSH/LPO in pubertal group with high handgrip strength. We could possibly conclude that the higher levels of handgrip strength could be associated with more oxidative stress in pubertal group with high fitness

Influencia de la fuerza muscular isométrica de las extremidades superiores en el estrés oxidativo en niños. (Influence of handgrip strength in oxidative stress in children).

<b>Resumen</b><p align="justify">El ejercicio físico puede producir estrés oxidativo en el individuo lo que pueden condicionar el riesgo cardiovascular en niños y adolescentes. Este estudio pretende analizar el estrés oxidativo según la fuerza muscular isométrica de las extremidades superiores en la edad pediátrica. Se estudiaron 70 niños sanos con edades entre 10 y 14 años, y se analizaron en saliva los lipoperóxidos (LPO), el glutatión reducido (GSH), la ratio GSH/LPO y la catalasa, como marcadores de estrés oxidativo. La muestra se dividió en dos grupos según una condición física superior o inferior medida a través de dinamometría manual (TKK 5110); se diferenció la serie en sujetos prepuberales y puberales. Se encontraron niveles significativamente inferiores de GSH y GSH/LPO en el grupo de niños con fuerza superior, y en los puberales con la mismas características; estos resultados podrían indicar la existencia de un mayor estrés oxidativo en esta situación. En conclusión, los mayores niveles de fuerza músculo esquelética, medida a través de dinamometría manual, posiblemente pueden estar asociados a un mayor estrés oxidativo en niños púberes con condición física musculoesquelética superior.</p><b>Abstract</b><p align="justify">Physical exercise can produce oxidative stress, this situation could contribute cardiovascular risk in children and adolescents. The following study tries to evaluate the oxidative stress produced according to the handgrip strength in infancy. 70 healthy male subjects, ages 10 to 14 years, were studied. In the saliva samples, lipoperoxides (LPO), reduced glutathione (GSH), glutathione/lipoperoxides ratio and catalase were analyzed as biomarkers of oxidative stress. Children were divided into two groups according to their handgrip strength (high or low) measured by handgrip strength (TKK 5110). The groups were also divided into prepubertal and pubertal subjects. We found GSH’s significantly low levels and of GSH/LPO in pubertal group with high handgrip strength. We could possibly conclude that the higher levels of handgrip strength could be associated with more oxidative stress in pubertal group with high fitness.</p>doi:10.5232/ricyde2011.0220

Antigenotoxicity and Tumor Growing Inhibition by Leafy Brassica carinata and Sinigrin

Cruciferous vegetables are well known and worldwide consumed due to their health benefits and cancer prevention properties. As a desirable cruciferous plant, Ethiopian mustard (Brassica carinata A. Braun) and its glucosinolate sinigrin were tested in the in vivo Drosophila melanogaster (SMART) and the in vitro HL60 (human promyelocytic leukaemia cell line) systems. High performance liquid chromatography (HPLC) analysis of plant samples confirmed the presence of sinigrin as principal B. carinata glucosinolate. SMART was performed by feeding D. melanogaster larvae either with different concentrations of plant/compound samples or combining them with hydrogen peroxide (a potent oxidative mutagen) being both antimutagenics. HL60 assays showed the tumoricidal activity of plant samples (IC50 = 0.28 mg·mL−1) and the breakdown products of sinigrin hydrolysis (IC50 = 2.71 μM). Our results enhance the potential of B. carinata as health promoter and chemopreventive in both systems and the leading role of sinigrin in these effects

Gαq activation modulates autophagy by promoting mTORC1 signaling.

The mTORC1 node plays a major role in autophagy modulation. We report a role of the ubiquitous Gαq subunit, a known transducer of plasma membrane G protein-coupled receptors signaling, as a core modulator of mTORC1 and autophagy. Cells lacking Gαq/11 display higher basal autophagy, enhanced autophagy induction upon different types of nutrient stress along with a decreased mTORC1 activation status. They are also unable to reactivate mTORC1 and thus inactivate ongoing autophagy upon nutrient recovery. Conversely, stimulation of Gαq/11 promotes sustained mTORC1 pathway activation and reversion of autophagy promoted by serum or amino acids removal. Gαq is present in autophagic compartments and lysosomes and is part of the mTORC1 multi-molecular complex, contributing to its assembly and activation via its nutrient status-sensitive interaction with p62, which displays features of a Gαq effector. Gαq emerges as a central regulator of the autophagy machinery required to maintain cellular homeostasis upon nutrient fluctuations.We thank Paula Ramos, Susana Rojo-Berciano, and Laura López for helpful technicalassistance. Dr. Marta Cruces (Universidad Autónoma de Madrid, Spain) for herinvaluable help regarding the liver explants experiments, Dr. Badford Berk (University ofRochester, NY, USA) for providing the GFP-Flag-PB1-p62 plasmid, Drs. Stefan Offer-manns and Nina Wettschureck (Max-Planck-Institute for Heart and Lung Research,Germany) for providing Tie2-CreERT2; Gnaq f/f; Gna11−/−[EC-q/11-KO) mice, andDr. Guzmán Sánchez for scientific advice. We thank also Ricardo Ramos from theGenomic facility of Fundación Parque Científico de Madrid (Universidad Autónoma deMadrid, Spain) and Gemma Rodríguez-Tarduchy from the Genomic facility of theInstituto de Investigaciones Biomédicas“Alberto Sols”for their help with cell linesauthentication. The help from CBMSO Animal Care, Flow Cytometry, Electron andOptical and Confocal Microscopy facilities is also acknowledged. This work was sup-ported by Ministerio de Economía; Industria y Competitividad (MINECO) of Spain(grant SAF2017-84125-R to F.M.), (grant BFU2017-83379-R to A.M.A.), Instituto deSalud Carlos III (PI18/01662 to CR, co-funded with European FEDER contribution),CIBERCV-Instituto de Salud Carlos III, Spain (grant CB16/11/00278 to F.M., co-fundedwith European FEDER contribution), Fundación Ramón Areces (to C.R. and F.M.) andPrograma de Actividades en Biomedicina de la Comunidad de Madrid-B2017/BMD-3671-INFLAMUNE to F.M. and NIH grants AG021904 and AG038072 to A.M.C. Wealso acknowledge the support of a Contrato para la Formación del Profesorado Uni-versitario (FPU13/04341) and (FPU14/06670), an EMBO short-term fellowship (ASTF600-2016). We also acknowledge institutional support to the CBMSO from FundaciónRamón Areces.S

Antigenotoxicidad y citotoxicidad de alimentos

Los alimentos de origen vegetal son unos firmes candidatos para ser considerados como alimentos funcionales y jugar un papel en prevención y tratamiento de enfermedades degenerativa. Se han estudiado aceites de uso alimentario y esenciales, bebidas, plantas medicinales, plantas de consumo como Borago officinalis, Brassica carinata o Raphanus sativus cuya capacidad para acumular metales es bien conocida, y ciertos componentes activos de los alimentos citados. Se ha utilizado el sistema de Mutaciones y Recombinaciones Somáticas en células en proliferación de discos imaginales alares de Drosophila melanogaster (SMART) para determinar su seguridad alimentaria así como su papel en la protección del daño de ADN. Al mismo tiempo se analiza la potencia tumoricida en líneas celulares promielocíticas humanas (HL- 60) de las sustancias que previamente han sido detectadas como antimutagénicas frente a genotoxinas de tipo oxidativo. Se relacionan las respuestas antimutagénicas y citotóxicas de las sustancias ensayadas con su contenido en fenoles, glucosinolatos e isotiocianato

Protective role of chaperone-mediated autophagy against atherosclerosis

Chaperone-mediated autophagy (CMA) contributes to regulation of energy homeostasis by timely degradation of enzymes involved in glucose and lipid metabolism. Here, we report reduced CMA activity in vascular smooth muscle cells and macrophages in murine and human arteries in response to atherosclerotic challenges. We show that in vivo genetic blockage of CMA worsens atherosclerotic pathology through both systemic and cell-autonomous changes in vascular smooth muscle cells and macrophages, the two main cell types involved in atherogenesis. CMA deficiency promotes dedifferentiation of vascular smooth muscle cells and a proinflammatory state in macrophages. Conversely, a genetic mouse model with up-regulated CMA shows lower vulnerability to proatherosclerotic challenges. We propose that CMA could be an attractive therapeutic target against cardiovascular diseases

In Vivo Remodeling of Altered Autophagy-Lysosomal Pathway by a Phosphopeptide in Lupus

The phosphopeptide P140/Lupuzor, which improves the course of lupus disease in mice and patients, targets chaperone-mediated autophagy (CMA), a selective form of autophagy that is abnormally upregulated in lupus-prone MRL/lpr mice. Administered intravenously to diseased mice, P140 reduces the expression level of two major protein players of CMA, LAMP2A and HSPA8, and inhibits CMA in vitro in a cell line that stably expresses a CMA reporter. Here, we aimed to demonstrate that P140 also affects CMA in vivo and to unravel the precise cellular mechanism of how P140 interacts with the CMA process. MRL/lpr mice and CBA/J mice used as control received P140 or control peptides intravenously. Lysosome-enriched fractions of spleen or liver were prepared to examine lysosomal function. Highly purified lysosomes were further isolated and left to incubate with the CMA substrate to study at which cellular step P140 interacts with the CMA process. The data show that P140 effectively regulates CMA in vivo in MRL/lpr mice at the step of substrate lysosomal uptake and restores some alterations of defective lysosomes. For the first time, it is demonstrated that by occluding the intralysosome uptake of CMA substrates, a therapeutic molecule can attenuate excessive CMA activity in a pathological pro-inflammatory context and protect against hyperinflammation. This recovery effect of P140 on hyperactivated CMA is not only important for lupus therapy but potentially also for treating other (auto)inflammatory diseases, including neurologic and metabolic disorders, where CMA modulation would be highly beneficial