| 1. |
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| 2. |
- Ahlgren, Ulf, et al.
(författare)
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Approaches for imaging islets
- 2010
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Ingår i: Advances in Experimental Medicine and Biology. - Dordrecht : Springer Netherlands. - 0065-2598 .- 2214-8019. ; 654, s. 39-57
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Tidskriftsartikel (refereegranskat)abstract
- The establishment of improved technologies for imaging of the pancreas is a key element in addressing several aspects of diabetes pathogenesis. In this respect, the development of a protocol that allows for non-invasive scoring of human islets, or islet beta-cells, is of particular importance. The development of such a technology would have profound impact on both clinical and experimental medicine, ranging from early diagnosis of diabetes to the evaluation of therapeutic regimes. Another important task is the development of modalities for high-resolution imaging of experimental animal models for diabetes. Rodent models for diabetes research have for decades been instrumental to the diabetes research community. The ability to image, and to accurately quantify, key players of diabetogenic processes with molecular specificity will be of great importance for elucidating mechanistic aspects of the disease. This chapter aims to overview current progress within these research areas.
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| 3. |
- Alstermark, Bror, et al.
(författare)
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Premotoneuronal and direct corticomotoneuronal control in the cat and macaque monkey.
- 2002
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 508, s. 281-97
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Tidskriftsartikel (refereegranskat)abstract
- The literature on premotoneuronal and direct corticomotoneuronal (CM) control in the cat and macaque monkey is reviewed. The available experimental findings are not in accordance with a recently proposed hypothesis that direct CM connections have "replaced" the premotoneuronal pathways. Instead, we propose that premotoneuronal CM control plays an important role in motor control also in primates and that the direct CM connection has been added during phylogeny.
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| 4. |
- Bengtsson, Finn
(författare)
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Brain tryptophan/serotonin perturbations in metabolic encephalopathy and the hazards involved in the use of psychoactive drugs
- 1999
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 467, s. 139-154
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Tidskriftsartikel (refereegranskat)abstract
- Several combined pathogenetic factors such as hyperammonemia, different brain tryptophan metabolic disturbancies and serotonin physiological/pharmacological alterations not yet defined in all details, will often give rise to the clinical neuropsychiatric condition known as hepatic encephalopathy (HE). Indeed, to this the probable exposure to novel potent CNS-monoamine acting drugs today may put such patients at certain risk for other pharmacodynamic (PD) responses than usually are expected from these "safe" drugs. Moreover, with a compromised liver function in HE, also pharmacokinetic (PK) features for the drugs are likely changed in these patients. Thus, the ultimate clinical outcome by this probable but unknown PD/PK-deviation for such psychoactive drugs when given to HE-patients needs further clarifrcation. Accordingly, delineation of both PD- and PK-effects in experimental HE should shed light on this issue of relevance for monoamine-active drug safety as well as on some further details in the complex tryptophan/monoamine-related pathophysiology that comes into play in HE.
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| 5. |
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| 6. |
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| 7. |
- Bölükbas, Deniz A., et al.
(författare)
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Current and Future Engineering Strategies for ECMO Therapy
- 2023
-
Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 1413, s. 313-326
-
Bokkapitel (refereegranskat)abstract
- Extracorporeal membrane oxygenation (ECMO) is a last resort therapy for patients with respiratory failure where the gas exchange capacity of the lung is compromised. Venous blood is pumped through an oxygenation unit outside of the body where oxygen diffusion into the blood takes place in parallel to carbon dioxide removal. ECMO is an expensive therapy which requires special expertise to perform. Since its inception, ECMO technologies have been evolving to improve its success and minimize the complications associated with it. These approaches aim for a more compatible circuit design capable of maximum gas exchange with minimal need for anticoagulants. This chapter summarizes the basic principles of ECMO therapy with the latest advancements and experimental strategies aiming for more efficient future designs.
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| 8. |
- Cerenius, Lage, et al.
(författare)
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Crustacean Immunity
- 2010
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Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 708, s. 239-259
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Tidskriftsartikel (refereegranskat)abstract
- This chapter provides a review of recent progress in the elucidation of innate immune mechanisms in crustaceans. Mainly due to the importance of crustacean aquaculture interest in this field is large and the subject for extensive research efforts. Here, we provide detailed data on the molecular characterisation of lectins, antiviral reactions, hemocyte formation and differentiation and on the regulation of innate immune pathways.
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| 9. |
- Chinga-Carrasco, Gary, et al.
(författare)
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Nanocelluloses – Nanotoxicology, Safety Aspects and 3D Bioprinting
- 2022
-
Ingår i: Advances in Experimental Medicine and Biology. - Cham : Springer. - 0065-2598 .- 2214-8019. ; 1357, s. 155-177
-
Tidskriftsartikel (refereegranskat)abstract
- Nanocelluloses have good rheological properties that facilitate the extrusion of nanocellulose gels in micro-extrusion systems. It is considered a highly relevant characteristic that makes it possible to use nanocellulose as an ink component for 3D bioprinting purposes. The nanocelluloses assessed in this book chapter include wood nanocellulose (WNC), bacterial nanocellulose (BNC), and tunicate nanocellulose (TNC), which are often assumed to be non-toxic. Depending on various chemical and mechanical processes, both cellulose nanofibrils (CNF) and cellulose nanocrystals (CNC) can be obtained from the three mentioned nanocelluloses (WNC, BNC, and TNC). Pre/post-treatment processes (chemical and mechanical) cause modifications regarding surface chemistry and nano-morphology. Hence, it is essential to understand whether physicochemical properties may affect the toxicological profile of nanocelluloses. In this book chapter, we provide an overview of nanotoxicology and safety aspects associated with nanocelluloses. Relevant regulatory requirements are considered. We also discuss hazard assessment strategies based on tiered approaches for safety testing, which can be applied in the early stages of the innovation process. Ensuring the safe development of nanocellulose-based 3D bioprinting products will enable full market use of these sustainable resources throughout their life cycle.
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| 10. |
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| 11. |
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| 12. |
- Daşu, Alexandru, et al.
(författare)
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The relationship between vascular oxygen distribution and tissue oxygenation
- 2009
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Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 645, s. 255-260
-
Tidskriftsartikel (refereegranskat)abstract
- Tumour oxygenation could be investigated through several methods that use various measuring principles and can therefore highlight its different aspects. The results have to be subsequently correlated, but this might not be straightforward due to intrinsic limitations of the measurement methods. This study describes an analysis of the relationship between vascular and tissue oxygenations that may help the interpretation of results. Simulations have been performed with a mathematical model that calculates the tissue oxygenation for complex vascular arrangements by taking into consideration the oxygen diffusion into the tissue and its consumption at the cells. The results showed that while vascular and tissue oxygenations are deterministically related, the relationship between them is not unequivocal and this could lead to uncertainties when attempting to correlate them. However, theoretical simulation could bridge the gap between the results obtained with various methods.
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| 13. |
- Daşu, Alexandru, et al.
(författare)
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Theoretical simulation of tumour oxygenation--practical applications
- 2006
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Ingår i: Advances in Experimental Medicine and Biology. - : Springer US. - 0065-2598 .- 2214-8019. ; 578, s. 357-362
-
Tidskriftsartikel (refereegranskat)abstract
- Theoretical simulation of tissue oxygenation is a robust method that can be used to quantify the tissue oxygenation for a variety of applications. However, it is necessary that the relevant input parameters are used for the model describing the tumour microenvironment. The results of the simulations presented in this article suggest that the accuracy of the simulations depends very much on the method of calculation of the effects of the temporal change of the hypoxic pattern due to the opening and the closure of blood vessels. Thus, the use of average oxygenations might lead to dangerous overestimations of the treatment response. This indicates that care should be taken when incorporating hypoxia information into the biological modelling of tumour response.
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| 14. |
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| 15. |
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| 16. |
- Eckerbom, Per, 1974-, et al.
(författare)
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Intravoxel Incoherent Motion MR Imaging of the Kidney : Pilot Study
- 2013
-
Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer New York. - 0065-2598 .- 2214-8019. ; 765, s. 55-58
-
Tidskriftsartikel (refereegranskat)abstract
- MR examinations (Achieva 3 T, Philips, Best, The Netherlands) were performed at five different occasions in a healthy volunteer (male 60 years) and in one renal cancer patient (male 78 years) with normal renal function (creatinine 88 μmol/L). Intravoxel incoherent motion (IVIM) coefficients D + D* were measured using respiratory-triggered diffusion-weighted spin-echo echo-planar imaging. Perfusion data of the patient were acquired using a saturation-recovery gradient-echo sequence and with the bolus of Gd-BOPTA (Multihance). D + D* were computed by monoexponential fitting of MR signal intensity attenuation versus b for b = 0, 50, 100, 150 s/mm2. Perfusion parameters were evaluated with “NordicICE” software. The map of D + D* was compared qualitatively with the perfusion map computed from the Gd scan. D + D* values of the cortex and medulla were in the range 2.3–2.7 and 1.1–1.6 × 10-3 mm2/s, respectively. In conclusion, in this pilot study a good qualitative relation between IVIM variables D + D* and renal perfusion has been found.
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| 17. |
- Edlund, Jenny, et al.
(författare)
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Reduced oxygenation in diabetic rat kidneys measured by T2* weighted magnetic resonance micro-imaging
- 2009
-
Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 645, s. 199-204
-
Tidskriftsartikel (refereegranskat)abstract
- By applying invasive techniques for direct measurements of oxygen tension, we have reported decreased kidney oxygenation in experimental diabetes in rats. However, the non-invasive MRI technique utilizing the BOLD effect provides several advantages with the possibility to perform repetitive measurements in the same animals and in human subjects. In this study, we applied a modified single gradient echo micro-imaging sequence to detect the BOLD effect in kidneys of diabetic rats and compared the results to normoglycemic controls. All measurements were performed on inactin-anaesthetized adult male Wistar Furth rats. Diabetes was induced by streptozotocin (45 mg/kg) 14 days prior to MRI-analysis. Sixteen T2*-weighted image records (B0=1.5 T) were performed using radiofrequency spoiled gradient echo sequence with 2.6 ms step increments of TE (TE1=12 ms), while TR (75 ms) and bandwidth per pixel (71.4 Hz) were kept constant. T2* maps were computed by mono-exponential fitting of the pixel intensities. Relaxation rates R2* (1/T2*) in cortex and outer stripe of the outer medulla were similar in both groups (cortex for controls 22.3 +/- 0.4 vs. diabetics 23.1 +/- 1.8 Hz and outer stripe of outer medulla for controls 24.9 +/- 0.4 vs. diabetics 26.4 +/- 1.8 Hz; n=4 in both groups), whereas R2* was increased in the inner stripe of the outer medulla in diabetic rats (diabetics 26.1 +/- 2.4 vs. controls 18.8 +/- 1.4 Hz; n=4, P<0.05). This study demonstrates that experimental diabetes in rats induces decreased oxygenation of the renal outer medulla. Furthermore, the proposed T2*-weighted MR micro-imaging technique is suitable for detection of regional changes in kidney oxygenation in experimental animal models.
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| 18. |
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| 19. |
- Franzen, Stephanie, et al.
(författare)
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Repetitive Measurements of Intrarenal Oxygenation In Vivo Using L Band Electron Paramagnetic Resonance
- 2014
-
Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer New York. - 0065-2598 .- 2214-8019. - 9781493906208 - 9781493905836 ; 812, s. 135-141
-
Tidskriftsartikel (refereegranskat)abstract
- Intrarenal oxygenation is heterogeneous with oxygen levels normally being highest in the superficial cortex and lowest in the inner medulla. Reduced intrarenal oxygenation has been implied in the pathology of several kidney diseases. However, there is currently no method available to repetitively monitor regional renal oxygenation using minimally invasive procedures. We therefore evaluated implantable lithium phthalocyanine (LiPc) probes, which display a close correlation between EPR line width and oxygen availability. LiPc probes were implanted in the kidney cortex and medulla in the same mouse and sEPR spectra were acquired using a L band scanner during inhalation of air (21 % oxygen) or a mixture of air and nitrogen (10 % oxygen). In order to separate the signals from the two probes, a 1 G/cm gradient was applied and the signals were derived from 40 consecutive sweeps. Peak-to-peak comparison of the EPR line was used to convert the signal to an approximate oxygen tension in MATLAB. Kidney cortex as well as medullary oxygenation was stable over the 45 day period (cortex 56 +/- 7 mmHg and medulla 43 +/- 6 mmHg). However, 10 % oxygen inhalation significantly reduced oxygenation in both cortex (56 +/- 6 to 34 +/- 2 mmHg n = 15 p < 0.05) and medulla (42 +/- 5 to 29 +/- 3 mmHg n = 7 p < 0.05). In conclusion, L band EPR using LiPc probes implanted in discrete intrarenal structures can be used to repetitively monitor regional renal oxygenation. This minimally invasive method is especially well suited for conditions of reduced intrarenal oxygenation since this increases the signal intensity which facilitates the quantification of the EPR signal to absolute oxygenation values.
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| 20. |
- Friederich, Malou, 1983-, et al.
(författare)
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Identification and distribution of uncoupling protein isoforms in the normal and diabetic rat kidney
- 2009
-
Ingår i: Advances in Experimental Medicine and Biology. - New York : Springer. - 0065-2598 .- 2214-8019. - 9780387859972 ; 645, s. 205-212
-
Tidskriftsartikel (refereegranskat)abstract
- Uncoupling protein (UCP)-2 and -3 are ubiquitously expressed throughout the body but there is currently no information regarding the expression and distribution of the different UCP isoforms in the kidney. Due to the known cross-reactivity of the antibodies presently available for detection of UCP-2 and -3 proteins, we measured the mRNA expression of UCP-1, -2 and -3 in the rat kidney in order to detect the kidney-specific UCP isoforms. Thereafter, we determined the intrarenal distribution of the detected UCP isoforms using immunohistochemistry. Thereafter, we compared the protein levels in control and streptozotocin-induced diabetic rats using Western blot. Expressions of the UCP isoforms were also performed in brown adipose tissue and heart as positive controls for UCP-1 and 3, respectively. UCP-2 mRNA was the only isoform detected in the kidney. UCP-2 protein expression in the kidney cortex was localized to proximal tubular cells, but not glomerulus or distal nephron. In the medulla, UCP-2 was localized to cells of the medullary thick ascending loop of Henle, but not to the vasculature or parts of the nephron located in the inner medulla. Western blot showed that diabetic kidneys have about 2.5-fold higher UCP-2 levels compared to controls. In conclusion, UCP-2 is the only isoform detectable in the kidney and UCP-2 protein can be detected in proximal tubular cells and cells of the medullary thick ascending loop of Henle. Furthermore, diabetic rats have increased UCP-2 levels compared to controls, but the mechanisms underlying this increase and its consequences warrants further studies.
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| 21. |
- Friederich, Malou, et al.
(författare)
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Uncoupling protein-2 in diabetic kidneys : increased protein expression correlates to increased non-transport related oxygen consumption
- 2008
-
Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer Berlin/Heidelberg. - 0065-2598 .- 2214-8019. ; 614, s. 37-43, s. 37-43
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Tidskriftsartikel (refereegranskat)abstract
- Diabetic patients have an elevated risk to develop renal dysfunction and it has been postulated that altered energy metabolism is involved. We have previously shown that diabetic rats have markedly decreased oxygen availability in the kidney, resulting from increased oxygen consumption. A substantial part of the increased oxygen consumption is unrelated to tubular transport, suggesting decreased mitochondrial efficiency. In this study, we investigated the protein expression of mitochondrial uncoupling protein (UCP)-2 in kidney tissue from control and streptozotocin (STZ)-induced diabetic rats. Protein levels of UCP-2 were measured in adult male control and STZ-diabetic Wistar Furth as well as Sprague Dawley rats in both the kidney cortex and medulla by Western blot technique. Two weeks of hyperglycemia resulted in increased protein levels of UCP-2 in kidneys from both Wistar Furth and Sprague Dawley rats. Both cortical and medullary UCP-2 levels were elevated 2-3 fold above control levels. We conclude that sustained STZ-induced hyperglycemia increases the kidney levels of mitochondrial UCP-2, which could explain the previously reported increase in non-transport related oxygen consumption in diabetic kidneys. The elevated UCP-2 levels may represent an effort to reduce the increased production of superoxide radicals which is evident during diabetes.
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| 22. |
- Friederich-Persson, Malou, et al.
(författare)
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Angiotensin II Reduces Transport-Dependent Oxygen Consumption but Increases Transport-Independent Oxygen Consumption in Immortalized Mouse Proximal Tubular Cells
- 2014
-
Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer New York. - 0065-2598 .- 2214-8019. - 9781493906208 - 9781493905836 ; 812, s. 157-163
-
Tidskriftsartikel (refereegranskat)abstract
- Oxidative stress is closely associated with renal dysfunction following diabetes and hypertension. Angiotensin II (Ang II) can activate the NADPH-oxidase, increasing oxidative stress that is thought to blunt proximal tubular electrolyte transport and thereby oxygen consumption (QO(2)). We investigated the effect of Ang II on QO(2) in immortalized mouse proximal tubular cells over-expressing the NADPH oxidase subunit p22(phox); a model of increased oxidative stress. Cultured cells were exposed to either Ang II or H2O2 for 48 h. QO(2) was determined during baseline (113 mmol/l NaCl; transport-dependent QO(2)) and during sodium-free conditions (transport-independent QO(2)). Ang II reduced transport-dependent QO(2) in wild-types, but not in p22(phox) which also displayed increased QO(2) at baseline. Transport-independent QO(2) was increased in p22(phox) and Ang II had no additional effect, whereas it increased QO(2) in wild-type. Addition of H2O2 reduced transport-dependent QO(2) in wild-types, but not in p22(phox). Transport-independent QO(2) was unaffected by H2O2. The similar effects of Ang II and H2O2 to reduce transport-dependent QO(2) suggest a direct regulatory role of oxidative stress. In accordance, the transport-dependent QO(2) was reduced in p22(phox) already during baseline. The effects of Ang II on transport-independent QO(2) was not replicated by H2O2, indicating direct regulation via Ang II-receptors independently of oxidative stress. However, the Ang II effect was absent in p22(phox), suggesting that oxidative stress also modulates normal Ang II signaling. In conclusion, Ang II affects both transport-dependent and transport-independent QO(2) in proximal tubular cells and may be an important pathway modulating renal QO(2).
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| 23. |
- Friederich-Persson, Malou, et al.
(författare)
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Increased kidney metabolism as a pathway to kidney tissue hypoxia and damage : effects of triiodothyronine and dinitrophenol in normoglycemic rats.
- 2013
-
Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer-Verlag New York. - 0065-2598 .- 2214-8019. - 9781461474111 - 9781461472568 ; 789, s. 9-14
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Tidskriftsartikel (refereegranskat)abstract
- Intrarenal tissue hypoxia is an acknowledged common pathway to end-stage renal disease in clinically common conditions associated with development of chronic kidney disease, such as diabetes and hypertension. In diabetic kidneys, increased oxygen metabolism mediated by mitochondrial uncoupling results in decreased kidney oxygen tension (PO2) and contributes to the development of diabetic nephropathy. The present study investigated whether increased intrarenal oxygen metabolism per se can cause intrarenal tissue hypoxia and kidney damage, independently of confounding factors such as hyperglycemia and oxidative stress. Male Sprague-Dawley rats were untreated or treated with either triiodothyronine (T3, 10 g/kg bw/day, subcutaneously for 10 days) or the mitochondria uncoupler dinitrophenol (DNP, 30 mg/kg bw/day, oral gavage for 14 days), after which in vivo kidney function was evaluated in terms of glomerular filtration rate (GFR, inulin clearance), renal blood flow (RBF, Transonic, PAH clearance), cortical PO2 (Clark-type electrodes), kidney oxygen consumption (QO2), and proteinuria. Administration of both T3 and DNP increased kidney QO2 and decreased PO2 which resulted in proteinuria. However, GFR and RBF were unaltered by either treatment. The present study demonstrates that increased kidney metabolism per se can cause intrarenal tissue hypoxia which results in proteinuria. Increased kidney QO2 and concomitantly reduced PO2 may therefore be a mechanism for the development of chronic kidney disease and progression to end-stage renal disease.
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| 24. |
- Gaceb, Abderahim, et al.
(författare)
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Pericyte secretome
- 2018
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Ingår i: Pericyte Biology - Novel Concepts. - Cham : Springer International Publishing. - 0065-2598 .- 2214-8019. ; 1109, s. 139-163
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Bokkapitel (refereegranskat)abstract
- The role of pericytes seems to extend beyond their known function in angiogenesis, fibrosis and wound healing, blood-brain barrier maintenance, and blood flow regulation. More and more data are currently accumulating indicating that pericytes, uniquely positioned at the interface between blood and parenchyma, secrete a large plethora of different molecules in response to microenvironmental changes. Their secretome is tissue-specific and stimulus-specific and includes pro- and anti-inflammatory factors, growth factors, and extracellular matrix as well as microvesicles suggesting the important role of pericytes in the regulation of immune response and immune evasion of tumors. However, the angiogenic and trophic secretome of pericytes indicates that their secretome plays a role in physiological homeostasis but possibly also in disease progression or could be exploited for regenerative processes in the future. This book chapter summarizes the current data on the secretory properties of pericytes from different tissues in response to certain pathological stimuli such as inflammatory stimuli, hypoxia, high glucose, and others and thereby aims to provide insights into the possible role of pericytes in these conditions.
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| 25. |
- Golovleva, Irina, et al.
(författare)
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Mutation spectra in autosomal dominant and recessive retinitis pigmentosa in northern sweden.
- 2010
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Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer New York. - 0065-2598 .- 2214-8019. ; 664, s. 255-262
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Tidskriftsartikel (refereegranskat)abstract
- Retinal degenerations represent a heterogeneous group of disorders affecting the function of the retina. The frequency of retinitis pigmentosa (RP) is 1/3500 worldwide, however, in northern Sweden it is 1/2000 due to limited migration and a 'founder' effect. In this study we identified genetic mechanisms underlying autosomal dominant and recessive RP present in northern Sweden. Several novel mutations unique for this region were found. In an autosomal recessive form of RP, Bothnia dystrophy caused by mutations in the RLBP1 gene, bi-allelic mutations R234W, M226K and compound heterozygosity, M226K+R234W was detected.In dominant form of RP mapped to 19q13.42 a 59 kb genomic deletion including the PRPF31 and three other genes was found.These data provide additional information on the molecular mechanisms of RP evolvement and in the future might be useful in development of therapeutic strategies. Identification of the disease-causing mutations allowed introducing molecular genetic testing of the patients and their families into the clinical practice.
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| 26. |
- Hallgren, Jenny, et al.
(författare)
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Mast cell progenitor trafficking and maturation
- 2011
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Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 716:Section II, s. 14-28
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Mast cells are derived from the hematopoietic progenitors found in bone marrow and spleen. Committed mast cell progenitors are rare in bone marrow suggesting they are rapidly released into the blood where they circulate and move out into the peripheral tissues. This migration is controlled in a tissue specific manner. Basal trafficking to the intestine requires expression of alpha 4 beta 7 integrin and the chemokine receptor CXCR2 by the mast cell progenitors and expression of MAdCAM-1 and VCAM-1 in the intestinal endothelium; and is also controlled by dendritic cells expressing the transcriptional regulatory protein T-bet. None of these play a role in basal trafficking to the lung. With the induction of allergic inflammation in the lung, there is marked recruitment of committed mast cell progenitors to lung and these cells must express alpha 4 beta 7 and alpha 4 beta 1 integrins. Within the lung there is a requirement for expression of VCAM-1 on the endothelium that is regulated by CXCR2, also expressed on the endothelium. There is a further requirement for expression of the CCR2/CCL2 pathways for full recruitment of the mast cell progenitors to the antigen-inflamed lung.
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| 27. |
- Hamberg, U, et al.
(författare)
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Human kininogen from Cohns Fraction IV : comparisons of antigenicity and multiple forms
- 1979
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 120B, s. 173-183
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Tidskriftsartikel (refereegranskat)abstract
- Kininogen was isolated from Cohns fraction IV by DEAE-chromatography, gel filtration and ammonium sulphate precipitation. Immunologically pure kininogen was prepared by removal of protein impurities using specific immunoadsorbents with Sepharose-bound antibody. Anti-kininogen serum was raised in rabbits against the pure antigen. Comparison with anti-kininogen sera prepared with the biologically active LMW antigen from whole plasma suggested antigenic identity by double immunodiffusion analysis. The Cohn-kininogen was shown to contain mainly two components (85%) in about equal amounts focusing with peaks at pI 4.2 (42%) and pI 4.3 (43%). These represent apparently structurally altered forms of the native plasma kininogen focusing at pI 4.5-4.6 (54%), which occurred as a minor component (13%).
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| 28. |
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| 29. |
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| 30. |
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| 31. |
- Hanson, Lars A, et al.
(författare)
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Immune system modulation by human milk.
- 2002
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 503, s. 99-106
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Tidskriftsartikel (refereegranskat)
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| 32. |
- Hanson, Lars Åke, 1934, et al.
(författare)
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Immune function
- 2009
-
Ingår i: Advances in experimental medicine and biology. - 0065-2598 .- 2214-8019. ; 639, s. 97-111
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 33. |
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| 34. |
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| 35. |
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| 36. |
- Islam, M. Shahidul
(författare)
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Calcium signaling in the islets
- 2010
-
Ingår i: Advances in Experimental Medicine and Biology. - Dordrecht : Springer Netherlands. - 0065-2598 .- 2214-8019. ; 654, s. 235-259
-
Tidskriftsartikel (refereegranskat)abstract
- Easy access to rodent islets and insulinoma cells and the ease of measuring Ca(2+) by fluorescent indicators have resulted in an overflow of data that have clarified minute details of Ca(2+) signaling in the rodent islets. Our understanding of the mechanisms and the roles of Ca(2+) signaling in the human islets, under physiological conditions, has been hugely influenced by uncritical extrapolation of the rodent data obtained under suboptimal experimental conditions. More recently, electrophysiological and Ca(2+) studies have elucidated the ion channel repertoire relevant for Ca(2+) signaling in the human islets and have examined their relative importance. Many new channels belonging to the transient receptor potential (TRP) family are present in the beta-cells. Ryanodine receptors, nicotinic acid adenine dinucleotide phosphate channel, and Ca(2+)-induced Ca(2+) release add new dimension to the complexity of Ca(2+) signaling in the human beta-cells. A lot more needs to be learnt about the roles of these new channels and CICR, not because that will be easy but because that will be difficult. Much de-learning will also be needed. Human beta-cells do not have a resting state in the normal human body even under physiological fasting conditions. Their membrane potential under physiologically relevant resting conditions is approximately -50 mV. Biphasic insulin secretion is an experimental epiphenomenon unrelated to the physiological pulsatile insulin secretion into the portal vein in the human body. Human islets show a wide variety of electrical activities and patterns of [Ca(2+)](i) changes, whose roles in mediating pulsatile secretion of insulin into the portal vein remain questionable. Future studies will hopefully be directed toward a better understanding of Ca(2+) signaling in the human islets in the context of the pathogenesis and treatment of human diabetes.
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| 37. |
- Islam, M. Shadidul
(författare)
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The islets of Langerhans : Preface
- 2010
-
Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 654, s. vii-viii
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Tidskriftsartikel (refereegranskat)
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| 38. |
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| 39. |
- Johansson, Roland S
(författare)
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Dynamic use of tactile afferent signals in control of dexterous manipulation.
- 2002
-
Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 508, s. 397-410
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Tidskriftsartikel (refereegranskat)abstract
- During object manipulation, humans select and activate neural action programs acquired during ontogenetic development. A basic issue in understanding the control of dexterous manipulation is to learn how people use sensory information to adapt the output of these neural programs such that the fingertip actions matches the requirements imposed by the physical properties of the manipulated object, e.g., weight (mass), slipperiness, shape, and mass distribution. Although visually based identification processes contribute to predictions of required fingertip actions, the digital tactile sensors provide critical information for the control of fingertip forces. The present account deals with the tactile afferent signals from the digits during manipulation and focuses on some specific issues that the neural controller has to deal with to make use of tactile information.
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| 40. |
- Korhonen, Rami K., et al.
(författare)
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Multiscale In Silico Modeling of Cartilage Injuries
- 2023
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 1402, s. 45-56
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Bokkapitel (refereegranskat)abstract
- Injurious loading of the joint can be accompanied by articular cartilage damage and trigger inflammation. However, it is not well-known which mechanism controls further cartilage degradation, ultimately leading to post-traumatic osteoarthritis. For personalized prognostics, there should also be a method that can predict tissue alterations following joint and cartilage injury. This chapter gives an overview of experimental and computational methods to characterize and predict cartilage degradation following joint injury. Two mechanisms for cartilage degradation are proposed. In (1) biomechanically driven cartilage degradation, it is assumed that excessive levels of strain or stress of the fibrillar or non-fibrillar matrix lead to proteoglycan loss or collagen damage and degradation. In (2) biochemically driven cartilage degradation, it is assumed that diffusion of inflammatory cytokines leads to degradation of the extracellular matrix. When implementing these two mechanisms in a computational in silico modeling workflow, supplemented by in vitro and in vivo experiments, it is shown that biomechanically driven cartilage degradation is concentrated on the damage environment, while inflammation via synovial fluid affects all free cartilage surfaces. It is also proposed how the presented in silico modeling methodology may be used in the future for personalized prognostics and treatment planning of patients with a joint injury.
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| 41. |
- Larsson, Lars
(författare)
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Acute Quadriplegic Myopathy : An Acquired "Myosinopathy"
- 2008
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Ingår i: Advances in Experimental Medicine and Biology. - 0065-2598 .- 2214-8019. ; 642, s. 92-98
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Tidskriftsartikel (refereegranskat)abstract
- Acquired neuromuscular disorders have been shown to be very common in critically ill patients receiving prolonged mechanical ventilation in the intensive care unit (ICU). Acute Quadriplegic Myopathy (AQM) is a specific acquired myopathy in ICU patients. Patients with AQM are characterized by severe muscle weakness and atrophy of spinal nerve innervated limb and trunk muscles, while cranial nerve innervated craniofacial muscles, sensory and cognitive functions are spared or less affected. The muscle weakness is associated with altered muscle membrane properties and a preferential loss of the motor protein myosin and myosin-associated thick filament proteins. Prolonged mechanical ventilation, muscle unloading, postsynaptic block of neuromuscular transmission, sepsis and systemic corticosteroid hormone treatment have been suggested as important triggering factors in AQM. However, the exact mechanisms underlying the loss of thick filament proteins are not known, though enhanced myofibrillar protein degradation in combination with a downregulation of protein synthesis at the transcriptional level play important roles.
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| 42. |
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| 43. |
- Lavander, Moa, et al.
(författare)
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Twin arginine translocation in Yersinia
- 2007
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Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer. - 0065-2598 .- 2214-8019. ; 603, s. 258-267
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Tidskriftsartikel (refereegranskat)abstract
- Bacteria utilise Twin arginine translocation (Tat) to deliver folded proteins across the cytoplasmic membrane. Disruption of Tat typically results in pleiotropic effects on e.g. growth, stress resistance, bacterial membrane biogenesis, motility and cell morphology. Further, Tat is coupled to virulence in a range of pathogenic bacteria, including species of Pseudomonas, Legionella, Agrobacterium and Mycobacterium. We have investigated this, for Yersinia, previously unexplored system, and have shown that the Tat pathway is functional and absolutely required for virulence of Yersinia pseudotuberculosis. A range of putative Yersinia Tat substrates have been predicted in silico, which together with the Tat system itself may be interesting targets for future development of antimicrobial treatments. Here we present a brief review of bacterial Tat and discuss our results concerning this system in Yersinia.
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| 44. |
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| 45. |
- Li, Jin-Ping, et al.
(författare)
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Implications of Heparan Sulfate and Heparanase in Amyloid Diseases
- 2020
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Ingår i: Advances in Experimental Medicine and Biology. - Cham : Springer. - 0065-2598 .- 2214-8019. - 9783030345211 - 9783030345204 ; 1221, s. 631-645
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Tidskriftsartikel (refereegranskat)abstract
- Amyloidosis refers to a group of diseases characterized by abnormal deposition of denatured endogenous proteins, termed amyloid, in the affected organs. Analysis of biopsy and autopsy tissues from patients revealed the presence of heparan sulfate proteoglycans (HSPGs) along with amyloid proteins in the deposits. For a long time, HSPGs were believed to occur in the deposits as an innocent bystander. Yet, the consistent presence of HSPGs in various deposits, regardless of the amyloid species, led to the hypothesis that these macromolecular glycoconjugates might play functional roles in the pathological process of amyloidosis. In vitro studies have revealed that HSPGs, or more precisely, the heparan sulfate (HS) side chains interact with amyloid peptides, thus promoting amyloid fibrillization. Although information on the mechanisms of HS participation in amyloid deposition is limited, recent studies involving a transgenic mouse model of Alzheimer’s disease point to an active role of HS in amyloid formation. Heparanase cleavage alters the molecular structure of HS, and thus modulates the functional roles of HS in homeostasis, as well as in diseases, including amyloidosis. The heparanase transgenic mice have provided models for unveiling the effects of heparanase, through cleavage of HS, in various amyloidosis conditions.
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| 46. |
- Lindblom, Emely, et al.
(författare)
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Accounting for Two Forms of Hypoxia for Predicting Tumour Control Probability in Radiotherapy : An In Silico Study
- 2018
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Ingår i: Advances in Experimental Medicine and Biology. - Cham : Springer International Publishing. - 0065-2598 .- 2214-8019. ; 1042, s. 183-187, s. 183-187
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Tidskriftsartikel (refereegranskat)abstract
- The progress in functional imaging and dose delivery has opened the possibility of targeting tumour hypoxia with radiotherapy. Advanced approaches apply quantitative information on tumour oxygenation retrieved from imaging in dose prescription. These do not, however, take into account the potential difference in radiosensitivity of chronically and acutely hypoxic cells. It was the aim of this study to evaluate the implications of assuming the same or different sensitivities for the hypoxic cells. An in silico 3D-model of a hypoxic tumour with heterogeneous oxygenation was used to model the probabilities of tumour control with different radiotherapy regimens. The results show that by taking into account the potential lower radioresistance of chronically hypoxic cells deprived of oxygen and nutrients, the total dose required to achieve a certain level of control is substantially reduced for a given fractionation scheme in comparison to the case when chronically and acutely hypoxic cells are assumed to have similar features. The results also suggest that the presence of chronic hypoxia could explain the success of radiotherapy for some hypoxic tumours. Given the implications for clinical dose escalation trials, further exploration of the influence of the different forms of hypoxia on treatment outcome is therefore warranted.
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| 47. |
- Lindfors, Erno, et al.
(författare)
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Heterogeneous biological network visualization system : case study in context of medical image data
- 2012
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Ingår i: Advances in Experimental Medicine and Biology. - New York, NY : Springer-Verlag New York. - 0065-2598 .- 2214-8019. ; 736, s. 95-118
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Tidskriftsartikel (refereegranskat)abstract
- We have developed a system called megNet for integrating and visualizing heterogeneous biological data in order to enable modeling biological phenomena using a systems approach. Herein we describe megNet, including a recently developed user interface for visualizing biological networks in three dimensions and a web user interface for taking input parameters from the user, and an in-house text mining system that utilizes an existing knowledge base. We demonstrate the software with a case study in which we integrate lipidomics data acquired in-house with interaction data from external databases, and then find novel interactions that could possibly explain our previous associations between biological data and medical images. The flexibility of megNet assures that the tool can be applied in diverse applications, from target discovery in medical applications to metabolic engineering in industrial biotechnology.
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| 48. |
- Lindström, Per
(författare)
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β-cell function in obese-hyperglycemic mice [ob/ob Mice]
- 2010
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Ingår i: Advances in Experimental Medicine and Biology. - Dordrecht : Springer Netherlands. - 0065-2598 .- 2214-8019. ; 654, s. 463-477
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Tidskriftsartikel (refereegranskat)abstract
- This review summarizes key aspects of what has been learned about the physiology of pancreatic islets and leptin deficiency from studies in obese ob/ob mice. ob/ob Mice lack functional leptin. They are grossly overweight and hyperphagic particularly at young ages and develop severe insulin resistance with hyperglycemia and hyperinsulinemia. ob/ob Mice have large pancreatic islets. The beta-cells respond adequately to most stimuli, and ob/ob mice have been used as a rich source of pancreatic islets with high insulin release capacity. ob/ob Mice can perhaps be described as a model for the prediabetic state. The large capacity for islet growth and insulin release makes ob/ob mice a good model for studies on how beta-cells can cope with prolonged functional stress.
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| 49. |
- Liss, Per, et al.
(författare)
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Iodinated contrast media decrease renomedullary blood flow. A possible cause of contrast media-induced nephropathy
- 2009
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Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 645, s. 213-218
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Tidskriftsartikel (refereegranskat)abstract
- The renal medulla has been implicated as a key target for contrast media-induced nephropathy (CIN). Although the effects of contrast media (CM) on whole kidney blood flow are well characterized, the effect of CM on renal medullary blood flow has been controversial. It has been reported that an extremely high dose of a high osmolar CM (iothalamate; 2900 mg I/kg bw) injected rapidly increased the renal outer medullary blood flow (OMBF). However, more clinical relevant doses consistently result in a sustained decrease in medullary blood flow. Furthermore, simultaneous measurements using both laser-Doppler flowmetry and hydrogen washout yield similar results of a decrease in OMBF after CM administration. CM induced a transient 28% decrease in the laser-Doppler signal from the outer medulla, while the hydrogen washout rate in the same region was reduced by approximately 50%. Furthermore, CM administration consistently results in decreased medullary oxygen tension (PO2). The renal medulla works already during normal physiological conditions at the verge of hypoxia, and the majority of the studies published so far are in agreement with the hypothesis that CIN may have its origin in a further reduction in blood flow and/or oxygen availability of this region of the kidney.
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| 50. |
- Lolas, Georgios, et al.
(författare)
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Modeling Proteolytically Driven Tumor Lymphangiogenesis
- 2016
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Ingår i: Advances in Experimental Medicine and Biology. - Cham : Springer-Verlag New York. - 0065-2598 .- 2214-8019. - 9783319420233 - 9783319420219 ; 936, s. 107-136
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Tidskriftsartikel (refereegranskat)abstract
- With the exception of a limited number of sites in the body, primary tumors infrequently lead to the demise of cancer patients. Instead, mortality and a significant degree of morbidity result from the growth of secondary tumors in distant organs. Tumor survival, growth and dissemination are associated with the formation of both new blood vessels (angiogenesis) and new lymph vessels (lymphagenesis or lymphangiogenesis). Although intensive research in tumor angiogenesis has been going on for the past four decades, experimental results in tumor lymphangiogenesis began to appear only in the last 10 years. In this chapter we expand the models proposed by Friedman, Lolas and Pepper on tumor lymphangiogenesis mediated by proteolytically and un-proteolytically processed growth factors (Friedman and Lolas G, Math Models Methods Appl Sci 15(01): 95-107, 2005; Pepper and Lolas G, Selected topics in cancer modeling: genesis, evolution, immune competition, and therapy. In: The lymphatic vascular system in lymphangiogenesis invasion and metastasis a mathematical approach. Birkhauser Boston, Boston, pp 1-22, 2008). The variables represent different cell densities and growth factors concentrations, and where possible the parameters are estimated from experimental and clinical data. The results obtained from computational simulations carried out on the model equations produce dynamic heterogeneous ("anarchic") spatio-temporal solutions. More specifically, we observed coherent masses of tumor clusters migrating around and within the lymphatic network. Our findings are in line with recent experimental evidence that associate cluster formation with the minimization of cell loss favoring high local extracellular matrix proteolysis and thus protecting cancer invading cells from an immunological assault driven by the lymphatic network.
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