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Translation, Editing/proofreading, Subtitling
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Specializes in:
Medical (general)
Science (general)
Medical: Cardiology
Medical: Pharmaceuticals
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English to Spanish - Standard rate: 0.06 USD per word Spanish to English - Standard rate: 0.06 USD per word
English to Spanish: Mechanism of Disease COPD General field: Medical Detailed field: Medical (general)
Source text - English Chronic obstructive pulmonary disease (copd) is a major cause of
illness and death throughout the world. It affects about 10% of the general
population,1 but its prevalence among heavy smokers can reach 50%.2 COPD
is the fourth leading cause of death in most industrialized countries, and it is projected
to be the third leading cause of death worldwide by 2020.1 Tobacco smoking
is the primary risk factor for the development of COPD, but other factors, such as
burning biomass fuels for cooking and heating, are important causes of COPD in
many developing countries.3,4
A principal feature of COPD is a limitation of airflow that is not fully reversible
and is associated with an abnormal inflammatory response in the small airways
and alveoli. The principal abnormalities in small airways are the presence of an
inflammatory cellular infiltrate and a remodeling that thickens the airway wall,
thereby reducing the airway diameter and increasing resistance to flow5 (Fig. 1).
Additional features are prominent inflammatory infiltrates in the alveolar walls,
destruction of alveoli, and enlargement of air spaces. These anatomical hallmarks
of emphysema reduce the elastic pressure that generates expiratory flow6 (Fig. 2).
Chronic bronchitis, a condition that according to some authors has little to do
with the development of airflow obstruction,7 develops in approximately 50% of
smokers.
Several mechanisms may contribute to these abnormalities. In 1964, researchers
reported that a deficiency of alpha1-antitrypsin was associated with emphysema.8
A few years later, neutrophil elastase was reported to be the target of alpha1-antitrypsin.
9 These findings, together with the observation of increased numbers of
neutrophils and macrophages in the lungs of smokers, pointed to a connection between
neutrophil elastase and macrophage proteinases as the primary effectors of
lung destruction in COPD, a premise that still prevails.10,11 Other, complementary
mechanisms have been proposed more recently, including oxidative stress due to
cigarette smoking or to the increase in activated neutrophils and macrophages,12 as
well as apoptosis of endothelial and epithelial cells. The apoptosis results in part
from the down-regulation of vascular endothelial growth factor (VEGF), which is
required for the growth and survival of endothelial and alveolar cells. These events
interfere with lung maintenance and repair, which are necessary to overcome the
sustained injury imposed by cigarette smoke.13 In addition, residual apoptotic debris
can promote further inflammation and an immune reaction.14 Another possible
mechanism involves viral infections, which are common in smokers. Viruses can
add to the inflammatory milieu promoted by smoking.7,15 Age-related alterations,
such as epigenetic changes, low-grade chronic inflammation, and cell senescence, can
also contribute to the development of emphysema by enhancing inflammation and
impairing tissue repair.16 All these mechanisms point to a central role of the inflammatory
response to inhaled particles and pollutants in the pathogenesis of COPD.
Translation - Spanish Enfermedad Pulmonar Obstructiva Crónica (EPOC) es una causa importante de enfermedad y muerte en todo el mundo. Afecta aproximadamente 10% de la población general, pero su prevalencia en fumadores crónicos puede alcanzar hasta un 50%. EPOC es la cuarta causa más frecuente de muerte en países industrializados y se proyecta que en el año 2020 será la tercera causa más frecuente de muerte en el mundo. El fumar es el factor de riesgo más importante en el desarrollo de EPOC, pero otros factores, como el uso de combustibles sólidos para cocinar y la calefacción, también son causas de EPOC en muchos países en vía al desarrollo.
Una característica principal de EPOC es una limitación del flujo aéreo que no es completamente reversible y que es asociada a una respuesta inflamatoria anormal en las vías aéreas pequeñas y los alveolos. Las principales anormalidades encontradas en las vías aéreas pequeñas son la presencia de un infiltrado celular inflamatoria y un remodelamiento que aumenta el grosor de la pared de la vía aérea, y por ende, reduce el diámetro de la vía aérea aumentado así la resistencia al flujo. Otras características son infiltrados inflamatorios prominentes en la pared alveolar, destrucción alveolar y aumento de tamaño de los espacios aéreos. Estos hallazgos anatómicos del enfisema reduce la presión elástica la cual en condiciones normales genera el flujo espiratorio. Bronquitis crónica, una condición que según algunos autores tiene poco que ver con el desarrollo de obstrucción aérea, se desarrolla en aproximadamente 50% de los fumadores.
Diferentes mecanismos pueden contribuir a estas anormalidades. En 1964, investigadores reportaron que una deficiencia de la alfa 1-antitripsina estaba asociada al enfisema. Unos años después se reportó que la alfa 1-antitripsina actuaba sobre la elastasa neutrófila. Estos hallazgos, juntos con la observación de cifras aumentadas de neutrófilos y macrófagos en los pulmones de fumadores, señalaban una conexión entre la elastasa neutrófila y la proteinasa macrófaga como los efectores principales de destrucción pulmonar en EPOC, una premisa que todavía prevalece. Recientemente se han propuesto otros mecanismos complementarios, incluyendo el estrés oxidativo debido al fumado de cigarros o al aumento de actividad neutrófila y macrófaga, también el apoptosis de células endoteliales y epiteliales. El apoptosis en parte resulta de la reducción en el número de receptores del factor de crecimiento endotelial vascular (VEGF), lo cual es necesario para el crecimiento y sobrevivencia de células alveolares y endoteliales. Estos eventos interfieren con el mantenimiento y reparación pulmonar necesaria para superar las lesiones constantes del humo de cigarro. Además, desechos residuales de la apoptosis pueden provocar más inflamación y una reacción inmunitaria. Otro mecanismo posible involucra infecciones víricas, las cuales son comunes en los fumadores. Los virus pueden agregar al entorno inflamatorio promovido por el fumar. Alteraciones relacionadas a edad, como cambios epigenéticos, inflamación crónica de bajo grado y senescencia celular también pueden contribuir al desarrollo de enfisema, aumentando la inflamación e inhibiendo la reparación del tejido. Todos estos mecanismos apuntan a un rol central de la respuesta inflamatoria a las partículas y contaminantes inhaladas en la patogénesis del EPOC.
Spanish to English: Fisiopatología de la insuficiencia renal crónica General field: Medical Detailed field: Medical (general)
Source text - Spanish Introducción
La insuficiencia renal crónica (IRC) es un síndrome con manifestaciones
clínicas muy variadas que afecta a la mayor parte de órganos y sistemas
(Tabla 1), lo cual es un reflejo de la complejidad de las funciones que el
riñón desempeña en condiciones fisiológicas, así como de las severas
consecuencias que comporta la disfunción renal.
La insuficiencia renal es un proceso que expresa la pérdida de capacidad
funcional de las nefronas, con tendencia a empeorar y ser irreversible. En
este artículo se revisan sucintamente los mecanismos involucrados en su
progresión y las principales alteraciones fisiopatológicas que produce la
pérdida de la función renal.
Funciones del riñón
El riñón tiene tres tipos de funciones: depuradora, de regulación
hidroelectrolítica y del equilibrio ácido base, y también hormonales y
metabólicas.
El riñón juega un papel preeminente en la regulación del medio interno.
Los productos de deshecho del metabolismo son excretados por la orina.
Asimismo, gran parte de medicamentos se metabolizan por vía renal.
La composición del organismo ha de mantenerse constante dentro de
estrechos márgenes en cuanto a volumen, osmolaridad, concentración
iónica y acidez de los espacios extra e intracelular, para lo cual el riñón
ajusta el balance diario entre los aportes y la eliminación por la orina de
agua, Na , K , Cl-, Ca , Mg , PO4
-, CO3H- e H .
Translation - English Introduction
Chronic Kidney Disease is a syndrome with many different clinical manifestations that affects most of the organs and systems (Table 1). This not only shows the complexity of the different renal functions in physiological conditions, but also the severe consequences of renal dysfunction.
Renal failure is a process in which nephrons lose the functional capacity. This nephron dysfunction tends to be irreversible. This article briefly reviews the mechanisms involved in its progression and the principal pathophysiological alterations that renal function loss produces.
Renal Functions
The kidney has three types of functions: a filter regulating water, electrolytes, and acid base homeostasis, hormonal functions, and metabolic functions.
The kidney plays an essential role in regulations of the internal medium. The metabolic waster products are excreted in the urine. Likewise, many drugs are metabolized in the kidney.
The composition of the organism must remain stable within small margins in terms of volume, osmolarity, ionic concentration, and pH for extracellular and intracellular fluids. The kidney adjusts the daily balance between contributions and urine elimination of water, Na , K , Cl-, Ca , Mg , PO4
-, CO3H- e H .
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Experience
Years of experience: 24. Registered at ProZ.com: Dec 2009.
I am a freelance translator (English-Spanish and Spanish-English) with years of experience in the field.. I believe my translating skills, business and medical background, and multinational upbringing give me the experience and knowledge needed to meet the unique challenges facing your translation project. Pertinent experience and skills for translation include:
• Several years of freelance Spanish-English and English-Spanish translating. My American parents raised me in Nicaragua from a very young age allowing me to be a native speaker in both English and Spanish. I also have studied at a university level in both USA (Messiah College) and Nicaragua (UNAN-Leon), making me comfortable with formal and academic language use in both languages. This has naturally led me to have entered the field of freelance translating where I have worked translating medical journal articles, legal documents, advertising materials, company bylaws, and government documents.
• Current Medical Student: I have spent 4 plus years in medical school here in Nicaragua, using medical jargon in Spanish while doing most of my studying in English due to the availability of information. My contacts in the Facultad de Ciencias Médicas have allowed me to interact with doctors for whom I have worked translating up to date medical articles into Spanish. Also, I have worked with the University of Pittsburgh on a kidney research project translating Spanish language medical articles and findings into English.
• Hands on experience in marketing. When I started my own small language school in Nicaragua I created and administrated a marketing campaign that quickly enabled the business to expand its student body. This included materials for brochures and radio advertising scripts in both English and Spanish.
• Working as part of a team: I have enjoyed working as a member of a team, whether it be in-person or long distance, or whether it be in the business environment or the medical field. My business background in Nicaragua has allowed me to adapt marketing campaigns with my associates to reach our targeted audience. My work with medical professors and students from University of Pittsburgh enriched my ability to perform precise scientific Spanish to English medical translations.
My CV includes a more detailed list of relevant experience and education and references from different sectors. More references and my portfolio are available upon request. You may contact me at this email (translations.bert.baltodano@gmail.com) or call me at country code 505 8-698-8877. I look forward to hearing from you.
Sincerely,
Philip John Bert
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