| 1. |
- Aida, Azusa, et al.
(författare)
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Using mHealth to Provide Mobile App Users With Visualization of Health Checkup Data and Educational Videos on Lifestyle-Related Diseases : Methodological Framework for Content Development
- 2020
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Ingår i: JMIR mHealth and uHealth. - : JMIR Publications Inc.. - 2291-5222. ; 8:10
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The number of people with lifestyle-related diseases continues to increase worldwide. Improving lifestyle behavior with health literacy may be the key to address lifestyle-related diseases. The delivery of educational videos using mobile health (mHealth) services can replace the conventional way of educating individuals, and visualization can replace the provision of health checkup data. OBJECTIVE: This paper aimed to describe the development of educational content for MIRAMED, a mobile app aimed at improving users' lifestyle behaviors and health literacy for lifestyle-related diseases. METHODS: All videos were based on a single unified framework to provide users with a consistent flow of information. The framework was later turned into a storyboard. The final video contents were created based on this storyboard and further discussions with leading experts and specialist physicians on effective communication with app users about lifestyle-related diseases. RESULTS: The app uses visualization of personal health checkup data and educational videos on lifestyle-related diseases based on the current health guidelines, scientific evidence, and expert opinions of leading specialist physicians in the respective fields. A total of 8 videos were created for specific lifestyle-related diseases affecting 8 organs: (1) brain-cerebrovascular disorder, (2) eyes-diabetic retinopathy, (3) lungs-chronic obstructive pulmonary disease, (4) heart-ischemic heart disease, (5) liver-fatty liver, (6) kidneys-chronic kidney disease (diabetic kidney disease), (7) blood vessels-peripheral arterial disease, and (8) nerves-diabetic neuropathy. CONCLUSIONS: Providing enhanced mHealth education using novel digital technologies to visualize conventional health checkup data and lifestyle-related diseases is an innovative strategy. Future studies to evaluate the efficacy of the developed content are planned.
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| 2. |
- Franzen, Stephanie, et al.
(författare)
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Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes
- 2014
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Ingår i: American Journal of Physiology-Renal Physiology. - : American Physiological Society. - 1931-857X .- 1522-1466. ; 306:10, s. F1171-F1178
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Tidskriftsartikel (refereegranskat)abstract
- One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic nephropathy in four commonly used and commercially available mouse strains with type 1 diabetes to determine the suitability of each strain. Type 1 diabetes was induced in C57Bl/6, NMRI, BALB/c, and 129Sv mice by alloxan, and conscious glomerular filtration rate, proteinuria, and oxidative stress levels were measured in control and diabetic animals at baseline and after 5 and 10 wk. Histological alterations were analyzed using periodic acid-Schiff staining. Diabetic C57Bl/6 displayed increased glomerular filtration rate, i.e., hyperfiltration, whereas all other parameters remained unchanged. Diabetic NMRI developed the most pronounced hyperfiltration as well as increased oxidative stress and proteinuria but without glomerular damage. Diabetic BALB/c did not develop hyperfiltration but presented with pronounced proteinuria, increased oxidative stress, and glomerular damage. Diabetic 129Sv displayed proteinuria and increased oxidative stress without glomerular hyperfiltration or damage. However, all strains displayed intras-train correlation between oxidative stress and proteinuria. In conclusion, diabetic C57Bl/6 and NMRI both developed glomerular hyperfiltration but neither presented with histological damage, although NMRI developed low-degree proteinuria. Thus these strains may be suitable when investigating the mechanism causing hyperfiltration. Neither BALB/c nor 129Sv developed hyperfiltration although both developed pronounced proteinuria. However, only BALB/c developed detectable histological damage. Thus BALB/c may be suitable when studying the roles of proteinuria and histological alterations for the progression of diabetic nephropathy.
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| 3. |
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| 4. |
- Friederich-Persson, Malou, et al.
(författare)
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Kidney Hypoxia, Attributable to Increased Oxygen Consumption, Induces Nephropathy Independently of Hyperglycemia and Oxidative Stress
- 2013
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Ingår i: Hypertension. - : American Heart Association. - 0194-911X .- 1524-4563. ; 62:5, s. 914-919
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Tidskriftsartikel (refereegranskat)abstract
- Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult to determine the role of kidney hypoxia, per se, for the development of nephropathy. We tested the hypothesis that kidney hypoxia, without confounding factors such as hyperglycemia or elevated oxidative stress, results in nephropathy. To induce kidney hypoxia, dinitrophenol (30 mg per day per kg bodyweight by gavage), a mitochondrial uncoupler that increases oxygen consumption and causes kidney hypoxia, was administered for 30 consecutive days to rats. Thereafter, glomerular filtration rate, renal blood flow, kidney oxygen consumption, kidney oxygen tension, kidney concentrations of glucose and glycogen, markers of oxidative stress, urinary protein excretion, and histological findings were determined and compared with vehicle-treated controls. Dinitrophenol did not affect arterial blood pressure, renal blood flow, glomerular filtration rate, blood glucose, or markers of oxidative stress but increased kidney oxygen consumption, and reduced cortical and medullary concentrations of glucose and glycogen, and resulted in intrarenal tissue hypoxia. Furthermore, dinitrophenol treatment increased urinary protein excretion, kidney vimentin expression, and infiltration of inflammatory cells. In conclusion, increased mitochondrial oxygen consumption results in kidney hypoxia and subsequent nephropathy. Importantly, these results demonstrate that kidney tissue hypoxia, per se, without confounding hyperglycemia or oxidative stress, may be sufficient to initiate the development of nephropathy and therefore demonstrate a new interventional target for treating kidney disease.
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| 5. |
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| 6. |
- Nordquist, Lina, et al.
(författare)
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Activation of Hypoxia-Inducible Factors Prevents Diabetic Nephropathy
- 2015
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Ingår i: Journal of the American Society of Nephrology. - : American Society of Nephrology. - 1046-6673 .- 1533-3450. ; 26:2, s. 328-338
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Tidskriftsartikel (refereegranskat)abstract
- Hyperglycemia results in increased oxygen consumption and decreased oxygen tension in the kidney. We tested the hypothesis that activation of hypoxia-inducible factors (HIFs) protects against diabetes-induced alterations in oxygen metabolism and kidney function. Experimental groups consisted of control and streptozotocin-induced diabetic rats treated with or without chronic cobalt chloride to activate HIFs. We elucidated the involvement of oxidative stress by studying the effects of acute administration of the superoxide dismutase mimetic tempol. Compared with controls, diabetic rats displayed tissue hypoxia throughout the kidney, glonnerular hyperfiltration, increased oxygen consumption, increased total mitochondrial leak respiration, and decreased tubular sodium transport efficiency. Diabetic kidneys showed proteinuria and tubulointerstitial damage. Cobalt chloride activated HIFs, prevented the diabetes-induced alterations in oxygen metabolism, mitochondrial leak respiration, and kidney function, and reduced proteinuria and tubulointerstitial damage. The beneficial effects of tempol were less pronounced after activation of HIFs, indicating improved oxidative stress status. In conclusion, activation of HIFs prevents diabetes-induced alteration in kidney oxygen metabolism by normalizing glomerular filtration, which reduces tubular electrolyte load, preventing mitochondrial leak respiration and improving tubular transport efficiency. These improvements could be related to reduced oxidative stress and account for the reduced proteinuria and tubulointerstitial damage. Thus, pharnnacologic activation of the HIF system may prevent development of diabetic nephropathy.
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| 7. |
- Palm, Fredrik, et al.
(författare)
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Uremia induces abnormal oxygen consumption in tubules and aggravates chronic hypoxia of the kidney via oxidative stress
- 2010
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Ingår i: American Journal of Physiology - Renal Physiology. - : American Physiological Society. - 0363-6127 .- 1522-1466 .- 1931-857X. ; 299:2, s. F380-F386
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Tidskriftsartikel (refereegranskat)abstract
- In addition to causing uremic symptoms, uremic toxins accelerate the progression of renal failure. To elucidate the pathophysiology of uremic states, we investigated the effect of indoxyl sulfate (IS), a representative uremic toxin, on oxygen metabolism in tubular cells. We demonstrated an increase in oxygen consumption by IS in freshly isolated rat and human proximal tubules. Studies utilizing ouabain, the Na-K-ATPase inhibitor, and apocynin, the NADPH oxidase inhibitor, as well as the in vivo gene-silencing approach to knock down p22(phox) showed that the increase in tubular oxygen consumption by IS is dependent on Na-K-ATPase and oxidative stress. We investigated whether the enhanced oxygen consumption led to subsequent hypoxia of the kidney. An increase in serum IS concentrations in rats administered indole was associated with a decrease in renal oxygenation (8 h). The remnant kidney in rats developed hypoxia at 16 wk. Treatment of the rats with AST-120, an oral adsorbent that removes uremic toxins, reduced serum IS levels and improved oxygenation of the kidney. Amelioration of hypoxia in the remnant kidney was associated with better renal functions and less histological injury. Reduction of serum IS levels also led to a decrease in oxidative stress in the kidney. Our ex vivo and in vivo studies implicated that uremic states may deteriorate renal dysfunction via dysregulating oxygen metabolism in tubular cells. The abnormal oxygen metabolism in tubular cells by uremic toxins was, at least in part, mediated by oxidative stress.
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| 8. |
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| 9. |
- Sivertsson, Ebba, et al.
(författare)
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Lowering plasma levels of protein-bound uremic toxins improves cardiac output and renal oxygenation in a rat model of chronic kidney disease
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Chronic kidney disease (CKD) is an increasing health problem which is closely associated with cardiac dysfunction. In CKD uremic toxins accumulate as kidney function declines. Indoxyl sulfate is a uremic toxin that induces kidney tissue hypoxia, proteinuria and kidney damage. Furthermore, high salt intake is a growing health issue worldwide. In this study, we investigated the effect of reducing plasma indoxyl sulfate in a rat model of CKD challenged with high salt intake and compared the effects to that of conventional treatment using an angiotensin converting enzyme inhibitor (ACEI). In rats, the right kidney and 2/3 of the left kidney were surgically removed (5/6 nephrectomy). Animals were fed a normal salt containing diet for four weeks and randomized to either vehicle or chronic treatment with either the oral absorbent AST-120 or the ACEI enalapril. Thereafter, kidney function was measured before and after a week of high salt intake. Cardiac output was measured at the end of the study period. A reduction of plasma levels of indoxyl sulfate by AST-120 improved cardiac output as well as urinary oxidative stress and proteinuria. ACEI reduced oxidative stress in kidney tissue and significantly improved proteinuria and the glomerular filtration rate in response to the high salt intake. Both interventions improved intrarenal oxygen availability.In conclusion, decreasing circulating levels of protein bound uremic toxins, e.g. indoxyl sulfate, improves cardiac output, reduces urinary oxidative stress and proteinuria in experimental CKD. Reduced angiotensin II signaling has direct reno-protective effects by decreasing intrarenal oxidative stress, protecting renal reserve and increasing urinary Na+ excretion during high salt intake. Both treatments had striking effects on cortical oxygen availability. A dual strategy, to reduce indoxyl sulfate and angiotensin II signaling simultaneously, could be an efficient strategy to target both cardiac and renal dysfunction in CKD, to further slow progression of disease.
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| 10. |
- 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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