848 resultados para Sick Euthyroid Syndrome


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Purpose
– Concern of the deterioration of indoor environmental quality as a result of energy efficient building design strategies is growing. Apprehensions of the effect of airtight, super insulated envelopes, the reduction of infiltration, and the reliance on mechanical systems to provide adequate ventilation (air supply) is promoting emerging new research in this field. The purpose of this paper is to present the results of an indoor air quality (IAQ) and thermal comfort investigation in UK energy efficient homes, through a case study investigation.

Design/methodology/approach
– The case study dwellings consisted of a row of six new-build homes which utilize mechanical ventilation with heat recovery (MVHR) systems, are built to an average airtightness of 2m3/m2/hr at 50 Pascal’s, and constructed without a central heating system. Physical IAQ measurements and occupant interviews were conducted during the summer and winter months over a 24-hour period, to gain information on occupant activities, perception of the interior environment, building-related health and building use.

Findings
– The results suggest inadequate IAQ and perceived thermal comfort, insufficient use of purge ventilation, presence of fungal growth, significant variances in heating patterns, occurrence of sick building syndrome symptoms and issues with the MVHR system.

Practical implications
– The findings will provide relevant data on the applicability of airtight, mechanically ventilated homes in a UK climate, with particular reference to IAQ.

Originality/value
– IAQ data of this nature is essentially lacking, particularly in the UK context. The findings will aid the development of effective sustainable design strategies that are appropriate to localized climatic conditions and sensitive to the health of building occupants.

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INTRODUCTION Rhythm disturbances in children with structurally normal hearts are usually associated with abnormalities in cardiac ion channels. The phenotypic expression of these abnormalities ("channelopathies") includes: long and short QT syndromes, Brugada syndrome, congenital sick sinus syndrome, catecholaminergic polymorphic ventricular tachycardia, Lènegre-Lev disease, and/or different degrees of cardiac conduction disease. METHODS The study group consisted of three male patients with sick sinus syndrome, intraventricular conduction disease, and monomorphic sustained ventricular tachycardia. Clinical data and results of electrocardiography, Holter monitoring, electrophysiology, and echocardiography are described. RESULTS In all patients, the ECG during sinus rhythm showed right bundle branch block and long QT intervals. First-degree AV block was documented in two subjects, and J point elevation in one. A pacemaker was implanted in all cases due to symptomatic bradycardia (sick sinus syndrome). Atrial tachyarryhthmias were observed in two patients. The common characteristic ventricular arrhythmia was a monomorphic sustained ventricular tachycardia, inducible with ventricular stimulation and sensitive to lidocaine. In one patient, radiofrequency catheter ablation was successfully performed. No structural abnormalities were found in echocardiography in the study group. CONCLUSION Common clinical and ECG features suggest a common pathophysiology in this group of patients with congenital severe electrical disease.

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OBJECTIVES Individual mutations in the SCN5A-encoding cardiac sodium channel alpha-subunit cause single cardiac arrhythmia disorders, but a few cause multiple distinct disorders. Here we report a family harboring an SCN5A mutation (L1821fs/10) causing a truncation of the C-terminus with a marked and complex biophysical phenotype and a corresponding variable and complex clinical phenotype with variable penetrance. METHODS AND RESULTS A 12-year-old male with congenital sick sinus syndrome (SSS), cardiac conduction disorder (CCD), and recurrent monomorphic ventricular tachycardia (VT) had mutational analysis that identified a 4 base pair deletion (TCTG) at position 5464-5467 in exon 28 of SCN5A. The mutation was also present in six asymptomatic family members only two of which showed mild ECG phenotypes. The deletion caused a frame-shift mutation (L1821fs/10) with truncation of the C-terminus after 10 missense amino acid substitutions. When expressed in HEK-293 cells for patch-clamp study, the current density of L1821fs/10 was reduced by 90% compared with WT. In addition, gating kinetic analysis showed a 5-mV positive shift in activation, a 12-mV negative shift of inactivation and enhanced intermediate inactivation, all of which would tend to reduce peak and early sodium current. Late sodium current, however, was increased in the mutated channels. CONCLUSIONS The L1821fs/10 mutation causes the most severe disruption of SCN5A structure for a naturally occurring mutation that still produces current. It has a marked loss-of-function and unique phenotype of SSS, CCD and VT with incomplete penetrance.

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Introducción : el síndrome del eutiriodeo enfermo en enfermedades graves es factor de pobre pronóstico. La suplementación con hormona tiroidea mejora la contractibilidad miocardica y estimula la producción de surfactante pulmonar; sin embargo existe controversia debido a las complicaciones secundarias, ausencia de efectos a nivel hemodinámico y de estancia hospitalaria. Objetivo : determinar el efecto de la suplementación oral de hormonas tiroideas en pacientes con choque refractario y necesidad de más de dos inotrópicos con respecto a estabilidad hemodinámica, arritmias, requerimientos de inotrópicos y mortalidad asociada al tratamiento. Metodología : estudio longitudinal observacional de variables repetidas con análisis previo y posterior a la intervención. Realizado en pacientes con choque refractario de la unidad de cuidado intensivo pediátrico del Hospital Simón Bolívar, desde el 1 de enero del 2007 hasta 1 enero del 2009. Resultados: la suplementación tiroidea mostró una disminución significativa en el requerimiento de los inotrópicos adrenérgicos: dopamina, adrenalina y noradrenalina con rangos de [4,78-2.4], [3.92 - 2.98] y [3.58- 2.24] (p <0.001) respectivamente, sin haber diferencia en los vasodilatadores, inodilatadores y diuréticos. No se encontró asociación entre su uso y la presencia de arritmias. Discusión y conclusiones: La hormona tiroidea mostró efecto benéfico en términos de disminución de soporte inotrópico. resultado en concordancia con la literatura y relacionado con la función moduladora de la hormona tiroidea favoreciendo la inotropía miocardica y los índices de contractilidad ventricular izquierda.

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Background: Mycobacterium tuberculosis and human immunodeficiency virus (HIV) are known to cause abnormal thyroid function. There is little information on whether HIV infection aggravates alteration of thyroid function in patients with MDRTB. Objectives: This study was carried out to determine if HIV co-infection alters serum levels of thyroid hormones (T3, T4) and thyroid stimulating hormone (TSH) in patients with MDR-TB patients and to find out the frequency of subclinical thyroid dysfunction before the commencement of MDR-TB therapy. Methods: This observational and cross-sectional study involved all the newly admitted patients in MDR-TB Referral Centre, University College Hospital, Ibadan, Nigeria between July 2010 and December 2014. Serum levels of thyroid stimulating hormone (TSH), free thyroxine (fT4) and free triiodothyronine (fT3) were determined using ELISA. Results: Enrolled were 115 patients with MDR-TB, out of which 22 (19.13%) had MDR-TB/HIV co-infection. Sick euthyroid syndrome (SES), subclinical hypothyroidism and subclinical hyperthyroidism were observed in 5 (4.35%), 9 (7.83%) and 2 (1.74%) patients respectively. The median level of TSH was insignificantly higher while the median levels of T3 and T4 were insignificantly lower in patients with MDR-TB/HIV co-infection compared with patients with MDRT-TB only. Conclusion: It could be concluded from this study that patients with MDR-TB/HIV co-infection have a similar thyroid function as patients having MDR-TB without HIV infection before commencement of MDR-TB drug regimen. Also, there is a possibility of subclinical thyroid dysfunction in patients with MDR-TB/HIV co-infection even, before the commencement of MDR-TB therapy.

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Links between human health and wellbeing, and contact with nature are well understood in the fields of health and psychology, and more recently are gaining attention in the built environment industry. In 1984, E.O. Wilson coined the term ‘biophilia’ to describe the tendency for humans to have an innately emotional response to other living organisms. A growing number of researchers around the world are now exploring the impact of nature in urban environments (i.e. biophilic urbanism) on the human condition, including many indicators of human physical and mental health, recovery and performance. There is also an emergence of research on the potential for biophilic urbanism to address other challenges related to climate change mitigation and adaptation. This paper presents key findings from a review of key literature to date, discussing opportunities for biophilic urbanism to both improve occupant experience and performance, as well as addressing other sustainability objectives including climate change mitigation and adaptation. The paper presents an emerging framework for considering biophilic design opportunities and highlights implications for the built environment industry. This research draws on an Australian project considering biophilic urbanism in the response to climate change, within the Sustainable Built Environment National Research Centre. This includes findings from a literature review, a survey pilot study and two workshops undertaken in Perth and Brisbane with a variety of industry and government stakeholders.

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The built environment has a profound impact on our natural environment, economy, health and productivity. As the majority of the people spent most of their time inside buildings, the environment in which they perform their daily activities will have an impact on their health and productivity. Studies have been conducted about the negative impacts of presence of non-favorable conditions to human health and well being. The term "Sick Building Syndrome" (SBS) is used to describe situations in which building occupants experience acute health and comfort problems that appear to be linked to their time spent in a building. Sustainable infrastructure rating systems have requirements intended to improve occupant productivity and health.While the impact of Sustainable Infrastructure in energy consumption and waste/water reduction can be measured using available tools, the impact on productivity remained as an assumption that is not clearly measured. The purpose of this research is to develop a framework to assess whether the impacts of the incorporation of features intended to improve occupants’ performance and health such as: increased ventilation, lightning and thermal comfort serve their intended purpose.

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Un problema de salud ambiental relevante es la contaminación del aire generado por diferentes factores, uno de ellos es la carga microbiana. El estudio evidencia la presencia de estos contaminantes del aire como son los bioaerosoles cultivables y contables en las áreas de los edificios administrativos estudiados la cual podría afectar la calidad del aire interior. Se realizó un estudio observacional de corte transversal que permitió conocer y establecer las características de la carga microbiana presente relacionada con bioaerosoles cultivables y contables en los sistemas de ventilación mecánica en tres edificios administrativos de la ciudad de Bogotá en el periodo 2012 a 2013 y, la asociación o no entre variables de interés. Los bioaerosoles cultivables y contables encontrados con mayores porcentajes en las muestras tomadas fueron comunes a los tres edificios así: Aspergillus sp. se encontró en el 77,2% (61) de las muestras para el edifico uno, mientras que para el dos fue de 91% (30) de las muestras y para el edificio tres 100% (19) de las muestras tomadas; seguido por el género Penicillium sp. del cual se encontró 60,8% (48) de las muestras para el edificio uno, para el edificio dos 87,9% (29) de las muestras y para el edificio tres 94,7% (18) de las muestras. Otro género encontrado en porcentajes altos en los tres edificios fue el Cladosporium sp. , en el edificio uno 41,8% (33) de las muestras, mientras que para el edificio dos correspondió al 100% (33) de las muestra y finalmente para el edificio tres 84,2% (16) de las muestras analizadas. Los hallazgos se correlacionan con lo reportado por la literatura.

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This paper describes the development and validation of a novel web-based interface for the gathering of feedback from building occupants about their environmental discomfort including signs of Sick Building Syndrome (SBS). The gathering of such feedback may enable better targeting of environmental discomfort down to the individual as well as the early detection and subsequently resolution by building services of more complex issues such as SBS. The occupant's discomfort is interpreted and converted to air-conditioning system set points using Fuzzy Logic. Experimental results from a multi-zone air-conditioning test rig have been included in this paper.

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Buildings affect people in various ways. They can help us to work more effectively; they also present a wide range of stimuli for our senses to react to. Intelligent buildings are designed to be aesthetic in sensory terms not just visually appealing but ones in which occupants experience delight, freshness, airiness, daylight, views out and social ambience. All these factors contribute to a general aesthetic which gives pleasure and affects one’s mood. If there is to be a common vision, it is essential for architects, engineers and clients to work closely together throughout the planning, design, construction and operational stages which represent the conception, birth and life of the building. There has to be an understanding of how patterns of work are best suited to a particular building form served by appropriate environmental systems. A host of technologies are emerging that help these processes, but in the end it is how we think about achieving responsive buildings that matters. Intelligent buildings should cope with social and technological changes and also be adaptable to short-term and long-term human needs. We live through our senses. They rely on stimulation from the tasks we are focused on; people around us but also the physical environment. We breathe air and its quality affects the olfactory system; temperature is felt by thermoreceptors in the skin; sound enters our ears; the visual scene is beheld by our eyes. All these stimuli are transmitted along the sensory nervous system to the brain for processing from which physiological and psychological reactions and judgments are formed depending on perception, expectancies and past experiences. It is clear that the environmental setting plays a role in this sensory process. This is the essence of sensory design. Space plays its part as well. The flow of communication is partly electronic but also largely by people meeting face to face. Our sense of space wants different things at different times. Sometimes privacy but other times social needs have to be satisfied besides the organizational requirement to have effective human communications throughout the building. In general if the senses are satisfied people feel better and work better.

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Ivabradine (IVB) is a heart rate lowering agent that acts via selective inhibition of the pacemaker funny current in sinoatrial nodal P cells, thus, reducing heart rate at rest and during exercise with minimal effect on myocardial contractility, blood pressure, and intracardiac conduction. IVB exerts no effect on external respiratory function parameters and it may also play a role in patients with concurrent chronic obstructive pulmonary disease. This property constitutes an important advantage over β-blockers. IVB acts by reducing the heart rate in a mechanism different from β-blockers, calcium channel blockers or late sodium channel blockers, three commonly prescribed antianginal drugs. As clinical trials have shown, it is remarkably well-tolerated and offers an alternative for patients who cannot take β-blockers. The combination of IVB and atenolol at commonly used doses in patients with chronic stable angina produced additional efficacy with no untoward effect on safety or tolerability. Additionally, side effects are rare and largely limited to a luminous phenomenon or phosphenes. This sensation is thought to be due to a block of Ih in the retina, a current very similar to cardiac If channels. IVB is contraindicated in patients with sick sinus syndrome or sinus node dysfunction and in patients taking hepatic inhibitors of Cytochrome P450 family 3, subfamily A, polypeptide 4 (abbreviated CYP3A4), with exception of omeprazole or lansoprazole. This review briefly summarizes the main studies regarding this drug.

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The cardiac voltage-gated Na(+) channel Na(v)1.5 generates the cardiac Na(+) current (INa). Mutations in SCN5A, the gene encoding Na(v)1.5, have been linked to many cardiac phenotypes, including the congenital and acquired long QT syndrome, Brugada syndrome, conduction slowing, sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy. The mutations in SCN5A define a sub-group of Na(v)1.5/SCN5A-related phenotypes among cardiac genetic channelopathies. Several research groups have proposed that Na(v)1.5 may be part of multi-protein complexes composed of Na(v)1.5-interacting proteins which regulate channel expression and function. The genes encoding these regulatory proteins have also been found to be mutated in patients with inherited forms of cardiac arrhythmias. The proteins that associate with Na(v)1.5 may be classified as (1) anchoring/adaptor proteins, (2) enzymes interacting with and modifying the channel, and (3) proteins modulating the biophysical properties of Na(v)1.5 upon binding. The aim of this article is to review these Na(v)1.5 partner proteins and to discuss how they may regulate the channel's biology and function. These recent investigations have revealed that the expression level, cellular localization, and activity of Na(v)1.5 are finely regulated by complex molecular and cellular mechanisms that we are only beginning to understand.

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The cardiac sodium current (INa) is responsible for the rapid depolarization of cardiac cells, thus allowing for their contraction. It is also involved in regulating the duration of the cardiac action potential (AP) and propagation of the impulse throughout the myocardium. Cardiac INa is generated by the voltage-gated Na(+) channel, NaV1.5, a 2016-residue protein which forms the pore of the channel. Over the past years, hundreds of mutations in SCN5A, the human gene coding for NaV1.5, have been linked to many cardiac electrical disorders, including the congenital and acquired long QT syndrome, Brugada syndrome, conduction slowing, sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy. Similar to many membrane proteins, NaV1.5 has been found to be regulated by several interacting proteins. In some cases, these different proteins, which reside in distinct membrane compartments (i.e. lateral membrane vs. intercalated disks), have been shown to interact with the same regulatory domain of NaV1.5, thus suggesting that several pools of NaV1.5 channels may co-exist in cardiac cells. The aim of this review article is to summarize the recent works that demonstrate its interaction with regulatory proteins and illustrate the model that the sodium channel NaV1.5 resides in distinct and different pools in cardiac cells. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction.