| 471. |
- Shayesteh, Alexander, et al.
(författare)
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Navigating in the fog : facing delays, rejection and ignorance when seeking help for primary hyperhidrosis
- 2021
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Ingår i: International Journal of Qualitative Studies on Health and Well-being. - : Taylor & Francis. - 1748-2623 .- 1748-2631. ; 16:1
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Tidskriftsartikel (refereegranskat)abstract
- Primary hyperhidrosis (PH) is a disease characterized by focal and excessive sweating.Purpose: The aim of this study was to describe the experiences of men and women with PH when seeking help for their condition.Method: A qualitative interview study with 30 men and women diagnosed with PH was conducted. Data was inductively analysed using manifest and latent content analysis.Results: The analysis resulted in a theme: Navigating in the fog, based on the categories doubtful encounters with health care professionals, helpful encounters with health care professionals, delays due to inadequate knowledge, and supported urge for help.Conclusions: Deficient knowledge and understanding about PH create a sense of resignation in individuals, resulting in delay of seeking treatment. Support from others, life-changing events, and finding information about PH were important motivating factors in seeking help and demanding access to treatment. A holistic approach towards patients with PH is important to reduce stigma and acknowledge the problems that are encountered in their daily lives. Educating health care professionals and students so that patients can be identified and assessed without delay and making information available about PH in schools and pharmacies could improve the general knowledge and facilitate obtaining treatment for individuals with PH.
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| 472. |
- Shirvany, Yazdan, 1980, et al.
(författare)
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Application of particle swarm optimization in epileptic spike EEG source localization
- 2013
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Ingår i: Applied Soft Computing Journal. - : Elsevier BV. - 1568-4946. ; 13:5, s. 2515-2525
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Tidskriftsartikel (refereegranskat)abstract
- Surgical therapy has become an important therapeutic alternative for patients with medically intractable epilepsy. Correct and anatomically precise localization of an epileptic focus is essential to decide if resection of brain tissue is possible. The inverse problem in EEG-based source localization is to determine the location of the brain sources that are responsible for the measured potentials at the scalp electrodes. We propose a new global optimization method based on particle swarm optimization (PSO) to solve the epileptic spike EEG source localization inverse problem. In a forward problem a modified subtraction method is proposed to reduce the computational time. The good accuracy and fast convergence are demonstrated for 2D and 3D cases with realistic head models. The results from the new method are promising for use in the pre-surgical clinic in the future
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| 473. |
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| 474. |
- Shirvany, Yazdan, 1980, et al.
(författare)
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Evaluation of a finite-element reciprocity method for epileptic EEG source localization: Accuracy, computational complexity and noise robustness
- 2013
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Ingår i: Biomedical Engineering Letters. - : Springer Science and Business Media LLC. - 2093-985X .- 2093-9868. ; 3:1, s. 8-16
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSEThe aim of this paper is to evaluate the performance of an EEG source localization method that combines a finite element method (FEM) and the reciprocity theorem.METHODSThe reciprocity method is applied to solve the forward problem in a four-layer spherical head model for a large number of test dipoles. To benchmark the proposed method, the results are compared with an analytical solution and two state-of-the-art methods from the literature. Moreover, the dipole localization error resulting from utilizing the method in the inverse procedure for a realistic head model is investigated with respect to EEG signal noise and electrode misplacement.RESULTSThe results show approximately 3% relative error between numerically calculated potentials done by the reciprocity theorem and the analytical solutions. When adding EEG noise with SNR between 5 and 10, the mean localization error is approximately 4.3 mm. For the case with 10 mm electrode misplacement the localization error is 4.8 mm. The reciprocity EEG source localization speeds up the solution of the inverse problem with more than three orders of magnitude compared to the state-of-the-art methods.CONCLUSIONSThe reciprocity method has high accuracy for modeling the dipole in EEG source localization, is robust with respect to noise, and faster than alternative methods.
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| 475. |
- Shirvany, Yazdan, 1980, et al.
(författare)
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Influence of Different Sources of Noise on Epileptic Spike EEG Source Localization
- 2013
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Ingår i: Progress in Biomedical Optics and Imaging - Proceedings of SPIE. - : SPIE. - 1605-7422. - 9780819494467 ; 8672
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Konferensbidrag (refereegranskat)abstract
- Spike EEG source localization results are influenced by different errors and approximations, e.g., head-model complexity, EEG signal noise, electrode misplacements, tissue anisotropy, tissue conductivity noise as well as numerical errors. For accurate source localization, understanding the affects of these errors on the source localization is very crucial. Six finite element head models are selected for a head-model complexity study. A reference head model is used to create the synthetic EEG signals by placing a dipole inside the model to mimic the epileptic spike activity. To understand the influence of EEG signal noise, tissue conductivity noise and electrode misplacements on the EEG source localization, different level of noises are added to EEG signals, tissue conductivities and electrode positions, independently. To investigate the influence of white matter anisotropy, a realistic head model generated from T1-weighted MRI is used and the conductivity anisotropy for the white matter is calculated from diffusion tensor imaging (DTI). Major findings of the study include (1) the CSF layer plays an important role to achieve an accurate source localization result, (2) the source localization is very sensitive to the tissue conductivity noises, (3) one centimeter electrode misplacement cause approximately 8 mm localization error, (4) the source localization is robust with respect to the EEG signal noise and (5) the model with white matter anisotropy has small source localization error but large amplitude and orientation errors compared to the isotropic head model.
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| 476. |
- Shokrollahi, Azad, et al.
(författare)
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Passive Infrared Sensor-Based Occupancy Monitoring in Smart Buildings : A Review of Methodologies and Machine Learning Approaches
- 2024
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Ingår i: Sensors. - : MDPI. - 1424-8220. ; 24:5
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Forskningsöversikt (refereegranskat)abstract
- Buildings are rapidly becoming more digitized, largely due to developments in the internet of things (IoT). This provides both opportunities and challenges. One of the central challenges in the process of digitizing buildings is the ability to monitor these buildings' status effectively. This monitoring is essential for services that rely on information about the presence and activities of individuals within different areas of these buildings. Occupancy information (including people counting, occupancy detection, location tracking, and activity detection) plays a vital role in the management of smart buildings. In this article, we primarily focus on the use of passive infrared (PIR) sensors for gathering occupancy information. PIR sensors are among the most widely used sensors for this purpose due to their consideration of privacy concerns, cost-effectiveness, and low processing complexity compared to other sensors. Despite numerous literature reviews in the field of occupancy information, there is currently no literature review dedicated to occupancy information derived specifically from PIR sensors. Therefore, this review analyzes articles that specifically explore the application of PIR sensors for obtaining occupancy information. It provides a comprehensive literature review of PIR sensor technology from 2015 to 2023, focusing on applications in people counting, activity detection, and localization (tracking and location). It consolidates findings from articles that have explored and enhanced the capabilities of PIR sensors in these interconnected domains. This review thoroughly examines the application of various techniques, machine learning algorithms, and configurations for PIR sensors in indoor building environments, emphasizing not only the data processing aspects but also their advantages, limitations, and efficacy in producing accurate occupancy information. These developments are crucial for improving building management systems in terms of energy efficiency, security, and user comfort, among other operational aspects. The article seeks to offer a thorough analysis of the present state and potential future advancements of PIR sensor technology in efficiently monitoring and understanding occupancy information by classifying and analyzing improvements in these domains.
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| 477. |
- Sivertsson, Ebba, et al.
(författare)
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Dose-dependent angiotensin II regulation of mitochondrial function – involvement of Uncoupling protein and Adenine nucleotide translocator
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Increased angiotensin II (Ang II) signaling has been implicated in several conditions associated with the development of chronic kidney disease, including hypertension and diabetes. Increased mitochondrial leak respiration has been shown to be a contributing factor to development of intrarenal hypoxia, a unifying mechanism for chronic kidney disease. However, the link between increased Ang II signaling and renal mitochondrial leak respiration is less clear. We therefore investigated how increased Ang II signaling affects leak respiration of kidney cortex mitochondria by focusing on the two main components of regulated leak respiration, i.e. uncoupling protein 2 (UCP2) and adenine nucleotide translocator (ANT).Wild-type and UCP2 deficient mice were randomly assigned to receive either vehicle or Ang II in low dose (400 ng/kg/min) or high dose (1000 ng/kg/min) for 4 weeks via osmotic minipumps. Thereafter, mitochondria function was measured by high resolution respirometry and gene expressions of the different UCP isoforms, superoxide dismutase (SOD) 1-3 and angiotensin receptor isoforms were measured by quantitative real time PCR. Thiobarbituric acids reactive substances (TBARS) was determined in kidney cortex as a marker of oxidative stress status.Low dose Ang II increased overall mitochondria respiration, but only improved respiratory control ratio in UCP2 deficient animals. However, high dose Ang II decreased overall mitochondria respiration, as a result of reduced mitochondrial efficiency for ATP production, independently of genotype. These effects were accompanied by alterations in regulated mitochondrial leak respiration and correlated to oxidative stress status.In conclusion, Ang II dose-dependently effects mitochondrial function and leak respiration. When intact, both ANT- and UCP2-dependent pathways maintain mitochondrial function during moderate Ang II signaling, whereas during high Ang II signaling overall mitochondrial function is compromised independently of ANT- or UCP2-mediated pathways.
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| 478. |
- Sivertsson, Ebba, et al.
(författare)
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Inhibition of mammalian target of rapamycin decreases intrarenal oxygen availability and alters glomerular permeability
- 2018
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Ingår i: American Journal of Physiology - Renal Physiology. - : AMER PHYSIOLOGICAL SOC. - 1931-857X .- 1522-1466. ; 314:5, s. F864-F872
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Tidskriftsartikel (refereegranskat)abstract
- An increased kidney oxygen consumption causing tissue hypoxia has been suggested to be a common pathway toward chronic kidney disease. The mammalian target of rapamycin (mTOR) regulates cell proliferation and mitochondrial function. mTOR inhibitors (e.g., rapamycin) are used clinically to prevent graft rejection. mTOR has been identified as a key player in diabetes, which has stimulated the use of mTOR inhibitors to counter diabetic nephropathy. However, the effect of mTOR inhibition on kidney oxygen consumption is unknown. Therefore, we investigated the effects of mTOR inhibition on in vivo kidney function, oxygen homeostasis, and glomerular permeability. Control and streptozotocin-induced diabetic rats were chronically treated with rapamycin, and the functional consequences were studied 14 days thereafter. In both groups, mTOR inhibition induced mitochondrial uncoupling, resulting in increased total kidney oxygen consumption and decreased intrarenal oxygen availability. Concomitantly, mTOR inhibition induced tubular injury, as estimated from urinary excretion of kidney injury molecule-1 (KIM-1) and reduced urinary protein excretion. The latter corresponded to reduced sieving coefficient for large molecules. In conclusion, mTOR inhibition induces mitochondrial dysfunction leading to decreased oxygen availability in normal and diabetic kidneys. which translates into increased KIM-1 in the urine. Reduced proteinuria after mTOR inhibition is an effect of reduced glomerular permeability for large molecules. Since hypoxia has been suggested as a common pathway in the development of chronic kidney disease, mTOR inhibition to patients with preexisting nephropathy should be used with caution, since it may accelerate the progression of the disease.
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| 479. |
- Sivertsson, Ebba, 1984-, et al.
(författare)
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Thyroid hormone increases oxygen metabolism causing intrarenal tissue hypoxia; a pathway to kidney disease
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- The proposed mechanisms for the development of nephropathy are many, complex and often overlapping. Although recent literature strongly supports a role of kidney hypoxia as an independent pathway to nephropathy, the evidence remains inconclusive since the role of hypoxia is difficult to differentiate from confounding factors such as hyperglycemia, hypertension and oxidative stress. By increasing kidney oxygen consumption using triiodothyronine (T3) and, thus, avoiding these confounding factors, the aim of the present study was to investigate renal hypoxia per se as a causal pathway for the development of nephropathy.Healthy Sprague-Dawley rats were treated with T3 (10 µg/kg/day) and the angiotensin II AT1-receptor antagonist candesartan (1 mg/kg in drinking water) to eliminate effects of T3-induced renin release for 7 weeks after which in vivo kidney function, oxygen metabolism and mitochondrial function were evaluated.T3 did not affect glomerular filtration rate or renal blood flow, but increased total kidney oxygen consumption resulting in cortical hypoxia. Nephropathy, demonstrated as proteinuria and albuminuria developed in T3-treated animals. Mitochondria uncoupling mediated by uncoupling protein 2 and the adenosine nucleotide transporter was demonstrated as a mechanism causing the increased kidney oxygen consumption. Importantly, blood glucose levels, mean arterial blood pressure and oxidative stress levels were not affected by T3. In conclusion, the present study provides further evidence for increased kidney oxygen consumption causing intrarenal tissue hypoxia, as a causal pathway for development of nephropathy.
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| 480. |
- Sivertsson, Ebba, et al.
(författare)
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Thyroid hormone increases oxygen metabolism causing intrarenal tissue hypoxia; a pathway to kidney disease
- 2022
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Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 17:3
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Tidskriftsartikel (refereegranskat)abstract
- The proposed mechanisms for the development of nephropathy are many, complex and often overlapping. Although recent literature strongly supports a role of kidney hypoxia as an independent pathway to nephropathy, the evidence remains inconclusive since the role of hypoxia is difficult to differentiate from confounding factors such as hyperglycemia, hypertension and oxidative stress. By increasing kidney oxygen consumption using triiodothyronine (T-3) and, thus, avoiding these confounding factors, the aim of the present study was to investigate renal hypoxia per se as a causal pathway for the development of nephropathy. Healthy Sprague-Dawley rats were treated with T-3 (10 mu g/kg/day) and the angiotensin II AT(1)-receptor antagonist candesartan (1 mg/kg in drinking water) to eliminate effects of T-3-induced renin release; and compared to a candesartan treated control group. After 7 weeks of treatment in vivo kidney function, oxygen metabolism and mitochondrial function were evaluated. T-3 did not affect glomerular filtration rate or renal blood flow, but increased total kidney oxygen consumption resulting in cortical hypoxia. Nephropathy, demonstrated as albuminuria and tubulointerstitial fibrosis, developed in T-3-treated animals. Mitochondria uncoupling mediated by uncoupling protein 2 and the adenosine nucleotide transporter was demonstrated as a mechanism causing the increased kidney oxygen consumption. Importantly, blood glucose levels, mean arterial blood pressure and oxidative stress levels were not affected by T-3. In conclusion, the present study provides further evidence for increased kidney oxygen consumption causing intrarenal tissue hypoxia, as a causal pathway for development of nephropathy.
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