SwePub - search: WFRF:(Lindahl Anders)

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1.	King, Carina, et al. (author) COVID-19—a very visible pandemic 2020 In: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 396:10248, s. 15-15 Journal article (peer-reviewed)
2.	Lindahl, Anders, et al. (author) Analysmetoder 2002 In: Keramik i Sydsverige : en handbok för arkeologer. - 9197305715 ; 2, s. 45-49 Book chapter (other academic/artistic)
3.	Lindahl, Anders, et al. (author) Glasyr, Bränningsmetoder 2002 In: Keramik i Sydsverige: en handbok för arkeologer. - 9197305715 ; Monographs on Ceramics 2, s. 29-35 Book chapter (other academic/artistic)
4.	Lindahl, Anders, et al. (author) Kärlets form och bruk 2002 In: Keramik i Sydsverige: en handbok för arkeologer. - 9197305715 ; Monographs on Ceramics 2, s. 38-43 Book chapter (other academic/artistic)
5.	Thorfve, Anna, 1982, et al. (author) Hydroxyapatite coating affects the Wnt signaling pathway during peri-implant healing in vivo 2014 In: Acta Biomaterialia. - : Elsevier BV. - 1742-7061 .- 1878-7568. ; 10:3, s. 1451-1462 Journal article (peer-reviewed)abstract Owing to its bio- and osteoconductivity, hydroxyapatite (HA) is a widely used implant material, but its osteogenic properties are only partly evaluated in vitro and in vivo. The present study focused on bone healing adjacent to HA-coated titanium (Ti) implants, with or without incorporated lithium ions (Li+). Special attention was given to the Wnt signaling pathway. The implants were inserted into rat tibia for 7 or 28days and analyzed ex vivo, mainly by histomorphometry and quantitative real-time polymerase chain reaction. HA-coated implants showed, irrespective of Li+ content, bone-implant contact (BIC) and removal torque significantly higher than those of reference Ti. Further, the expressions of OCN, CTSK, COL1A1, LRP5/6 and WISP1 were significantly higher in implant-adherent cells of HA-coated implants, with or without Li+. Significantly higher β-catenin expression and significantly lower COL2A1 expression were observed in peri-implant bone cells from HA with 14ngcm-2 released Li+. Interestingly, Ti implants showed a significantly larger bone area in the threads than HA with 39ngcm-2 released Li+, but had a lower BIC than any HA-coated implant. This study shows that HA, with or without Li+ is a strong activator of the Wnt signaling pathway, and may to some degree explain its high bone induction capacity.
6.	Thorfve, Anna, et al. (author) Hydroxyapatite Coating with Li+ Affects the Wnt Signaling Pathway in vivo 2013 Conference paper (peer-reviewed)
7.	Vukusic, Kristina, 1979, et al. (author) The Atrioventricular Junction: A Potential Niche Region for Progenitor Cells in the Adult Human Heart 2019 In: Stem Cells and Development. - : Mary Ann Liebert Inc. - 1547-3287 .- 1557-8534. ; 28:16, s. 1078-1088 Journal article (peer-reviewed)abstract A stem cell niche is a microenvironment where stem cells reside in a quiescent state, until activated. In a previous rat model, we combined 5-bromo-2-deoxy-uridine labeling with activation of endogenous stem cells by physical exercise and revealed a distinct region, in the atrioventricular junction (AVj), with features of a stem cell niche. In this study, we aim to investigate whether a similar niche exists in the human heart. Paired biopsies from AVj and left ventricle (LV) were collected both from explanted hearts of organ donors, not used for transplantation (N = 7) and from severely failing hearts from patients undergoing heart transplantation (N = 7). Using antibodies, we investigated the expression of stem cell, hypoxia, proliferation and migration biomarkers. In the collagen-dense region of the AVj in donor hearts, progenitor markers, MDR1, SSEA4, ISL1, WT1, and hypoxia marker, HIF1-alpha, were clearly detected. The expression gradually decreased with distance from the valve. At the myocardium border in the AVj costaining of the proliferation marker Ki67 with cardiomyocyte nuclei marker PCM1 and cardiac Troponin-T (cTnT) indicated proliferation of small cardiomyocytes. In the same site we also detected ISL1(+)/WT1(+)/cTnT cells. In addition, heterogeneity in cardiomyocyte sizes was noted. Altogether, these findings indicate different developmental stages of cardiomyocytes below the region dense in stem cell marker expression. In patients suffering from heart failure the AVj region showed signs of impairment generally displaying much weaker or no expression of progenitor markers. We describe an anatomic structure in the human hearts, with features of a progenitor niche that coincided with the same region previously identified in rats with densely packed cells expressing progenitor and hypoxia markers. The data provided in this study indicate that the adult heart contains progenitor cells and that AVj might be a specific niche region from which the progenitors migrate at the time of regeneration.
8.	Abrahamsson, Lena, et al. (author) Industriell ekonomi och organisering : IE 2016 Book (peer-reviewed)
9.	Andersson, Henrik, et al. (author) Assaying cardiac biomarkers for toxicity testing using biosensing and cardiomyocytes derived from human embryonic stem cells 2010 In: JOURNAL OF BIOTECHNOLOGY. - : Elsevier Science B.V., Amsterdam.. - 0168-1656 .- 1873-4863. ; 150:1, s. 175-181 Journal article (peer-reviewed)abstract Human embryonic stem cell (hESC) derived cardiomyocytes are in the present study being used for testing drug-induced cardiotoxicity in a biosensor set-up. The design of an in vitro testing alternative provides a novel opportunity to surpass previous methods based on rodent cells or cell lines due to its significantly higher toxicological relevance. In this report we demonstrate how hESC-derived cardiomyocytes release detectable levels of two clinically decisive cardiac biomarkers, cardiac troponin T and fatty acid binding protein 3, when the cardiac cells are exposed to the well-known cardioactive drug compound. doxorubicin. The release is monitored by the immuno-biosensor technique surface plasmon resonance, particularly appropriate due to its capacity for parallel and high-throughput analysis in complex media.
10.	Asp, Julia, 1973, et al. (author) Cardiomyocyte clusters derived from human embryonic stem cells share similarities with human heart tissue. 2010 In: Journal of molecular cell biology. - : Oxford University Press (OUP). - 1759-4685 .- 1674-2788. ; 2:5, s. 276-83 Journal article (peer-reviewed)abstract Cardiotoxicity testing is a key activity in the pharmaceutical industry in order to detect detrimental effects of new drugs. A reliable human in vitro model would both be beneficial in selection of lead compounds and be important for reducing animal experimentation. However, the human heart is a complex organ composed of many distinct types of cardiomyocytes, but cardiomyocyte clusters (CMCs) derived from human embryonic stem cells could be an option for a cellular model. Data on functional properties of CMCs demonstrate similarities to their in vivo analogues in human. However, development of an in vitro model requires a more thorough comparison of CMCs to human heart tissue. Therefore, we directly compared individually isolated CMCs to human fetal, neonatal, adult atrial and ventricular heart tissues. Real-time qPCR analysis of mRNA levels and protein staining of ion channels and cardiac markers showed in general a similar expression pattern in CMCs and human heart. Moreover, a significant decrease in beat frequency was noted after addition of Zatebradine, a blocker to I(f) involved in regulation of spontaneous contraction in CMCs. The results underscore the similarities of CMCs to human cardiac tissue, and further support establishment of novel cardiotoxicity assays based on the CMCs in drug discovery.
11.	Batra, Gorav, et al. (author) Atrial fibrillation in patients undergoing coronary artery surgery is associated with adverse outcome 2019 In: Upsala Journal of Medical Sciences. - : Taylor & Francis. - 0300-9734 .- 2000-1967. ; :1, s. 70-77 Journal article (peer-reviewed)abstract BACKGROUND: The aim was to determine the association between atrial fibrillation (AF) and outcome in patients undergoing coronary artery bypass grafting (CABG).METHODS: All patients undergoing CABG between January 2010 and June 2013 were identified in the Swedish Heart Surgery Registry. Outcomes studied were all-cause mortality, cardiovascular mortality, myocardial infarction, congestive heart failure, ischemic stroke, and recurrent AF. Patients with history of AF prior to surgery (preoperative AF) and patients without history of AF but with AF episodes post-surgery (postoperative AF) were compared to patients with no AF using adjusted Cox regression models.RESULTS: Among 9,107 identified patients, 8.1% (n = 737) had preoperative AF, and 25.1% (n = 2,290) had postoperative AF. Median follow-up was 2.2 years. Compared to no AF, preoperative AF was associated with higher risk of all-cause mortality, adjusted hazard ratio with 95% confidence interval (HR) 1.76 (1.33-2.33); cardiovascular mortality, HR 2.43 (1.68-3.50); and congestive heart failure, HR 2.21 (1.72-2.84). Postoperative AF was associated with risk of all-cause mortality, HR 1.27 (1.01-1.60); cardiovascular mortality, HR 1.52 (1.10-2.11); congestive heart failure, HR 1.47 (1.18-1.83); and recurrent AF, HR 4.38 (2.46-7.78). No significant association was observed between pre- or postoperative AF and risk for myocardial infarction and ischemic stroke.CONCLUSIONS: Approximately 1 in 3 patients undergoing CABG had pre- or postoperative AF. Patients with pre- or postoperative AF were at higher risk of all-cause mortality, cardiovascular mortality, and congestive heart failure, but not of myocardial infarction or ischemic stroke. Postoperative AF was associated with higher risk of recurrent AF.
12.	Bentham, J, et al. (author) A double-staining technique for detection of growth hormone and insulin-like growth factor-I binding to rat tibial epiphyseal chondrocytes. 1993 In: The Journal of endocrinology. - 0022-0795. ; 137:3, s. 361-7 Journal article (peer-reviewed)abstract In the present study a double-staining technique was developed to investigate simultaneous GH and insulin-like growth factor-I (IGF-I) binding to chondrocytes in a monolayer cell culture. Rat tibial epiphyseal chondrocytes were isolated by enzymatic digestion and cultured in monolayer. GH and IGF-I were labelled with biotin. The affinity of the biotin-labelled ligands was compared with unlabelled ligands in a radioreceptor assay. To study the distribution of GH and IGF-I binding in the monolayer, chondrocytes were incubated with biotinylated ligands with or without an excess of unlabelled ligands, followed by incubation with Vectastain ABC complex, which was then reacted with diaminobenzidine (DAB). Double staining was accomplished by carrying out the first reaction with DAB in the presence of nickel ammonium sulphate to give a black precipitate, followed by incubation with the second ligand, then ABC complex and finally DAB in the absence of nickel ammonium sulphate to give a brown stain. The presence of type-II collagen was demonstrated by immunohistochemistry and used as a marker for differentiated chondrocytes. Biotin-labelled GH and biotin-labelled IGF-I exhibited dose-dependent displacements of 125I-labelled GH and 125I-labelled IGF-I respectively from the chondrocytes in a radioreceptor assay. The displacement curves were identical to those of unlabelled ligands indicating that the affinity was unaltered. Binding of biotinylated GH to cells was seen throughout the culture in regions where there was little or no type-II collagen staining. IGF-I binding was predominantly localized to cells at high density; areas which also showed a high degree of staining for type-II collagen.(ABSTRACT TRUNCATED AT 250 WORDS)
13.	Brittberg, Mats, 1953, et al. (author) Autolog broskcellstransplantation. Smärtlindring och återställd ledfunktion är målet : Autologous cartilage cell transplantation. The goal is pain relief and restored joint function 1995 In: Nordisk medicin. - 0029-1420. ; 110:12, s. 330-4 Journal article (peer-reviewed)abstract Chondral and osteochondral damage is a common result of trauma to the joints. The capacity of cartilage to heal such damage is poor, and repetitive wear on joint surfaces that do not heal results in impaired joint function, which can culminate in full blown arthrosis. Thus, it is important to improve our knowledge of cartilage regenerative potential, and develop methods to forestall progression to arthrosis by promoting the early healing of cartilage damage. Autologous cartilage cell transplantation may be a mean of healing cartilage damage. A method of cultivating autologous chondrocytes for transplantation in the treatment of isolated damage to articular cartilage of the knee is presented in the article.
14.	Brittberg, Mats, 1953, et al. (author) [Autologous chondrocyte transplantation. Pain relief and restored joint function is the target] 1995 In: L?kartidningen. - 0023-7205. ; 92:37, s. 3315-20 Journal article (peer-reviewed)
15.	Brittberg, Mats, 1953, et al. (author) Cellular aspects on treatment of cartilage injuries. 1993 In: Agents and actions. Supplements. - 0379-0363. ; 39, s. 237-41 Journal article (peer-reviewed)abstract Cellular aspects on articular cartilage growth and development are discussed. Cells with chondrogenic potential are described and current treatment models for cartilage injuries are considered. A rabbit model for treatment of articular cartilage defects with autologous cultured and transplanted chondrocytes for treatment of knee cartilage defects in humans are discussed.
16.	Brittberg, Mats, 1953, et al. (author) Rabbit articular cartilage defects treated with autologous cultured chondrocytes. 1996 In: Clinical orthopaedics and related research. - 0009-921X. ; :326, s. 270-83 Journal article (peer-reviewed)abstract Adult New Zealand rabbits were used to transplant autologously harvested and in vitro cultured chondrocytes into patellar chondral lesions that had been made previously and were 3 mm in diameter, extending down to the calcified zone. Healing of the defects was assessed by gross examination, light microscope, and histological-histochemical scoring at 8, 12, and 52 weeks. Chondrocyte transplantation significantly increased the amount of newly formed repair tissue compared to the found in control knees in which the lesion was solely covered by a periosteal flap. In another experiment, carbon fiber pads seeded with chondrocytes were used as scaffolds, and repair significantly increased at both 12 and 52 weeks compared to knees in which scaffolds without chondrocytes were implanted. The histologic quality scores of the repair tissue were significantly better in all knees in which defects were treated with chondrocytes compared to knees treated with periosteum alone and better at 52 weeks compared to knees in which defects were treated with carbon scaffolds seeded with chondrocytes. The repair tissue, however, tended to incomplete the bonding to adjacent cartilage. This study shows that isolated autologous articular chondrocytes that have been expanded for 2 weeks in vitro can stimulate the healing phase of chondral lesions. A gradual maturation of the hyalinelike repair with a more pronounced columnarization was noted as late as 1 year after surgery.
17.	Brittberg, Mats, 1953, et al. (author) Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. 1994 In: The New England journal of medicine. - 0028-4793. ; 331:14, s. 889-95 Journal article (peer-reviewed)abstract BACKGROUND. Full-thickness defects of articular cartilage in the knee have a poor capacity for repair. They may progress to osteoarthritis and require total knee replacement. We performed autologous chondrocyte transplantation in 23 people with deep cartilage defects in the knee. METHODS. The patients ranged in age from 14 to 48 years and had full-thickness cartilage defects that ranged in size from 1.6 to 6.5 cm2. Healthy chondrocytes obtained from an uninvolved area of the injured knee during arthroscopy were isolated and cultured in the laboratory for 14 to 21 days. The cultured chondrocytes were then injected into the area of the defect. The defect was covered with a sutured periosteal flap taken from the proximal medial tibia. Evaluation included clinical examination according to explicit criteria and arthroscopic examination with a biopsy of the transplantation site. RESULTS. Patients were followed for 16 to 66 months (mean, 39). Initially, the transplants eliminated knee locking and reduced pain and swelling in all patients. After three months, arthroscopy showed that the transplants were level with the surrounding tissue and spongy when probed, with visible borders. A second arthroscopic examination showed that in many instances the transplants had the same macroscopic appearance as they had earlier but were firmer when probed and similar in appearance to the surrounding cartilage. Two years after transplantation, 14 of the 16 patients with femoral condylar transplants had good-to-excellent results. Two patients required a second operation because of severe central wear in the transplants, with locking and pain. A mean of 36 months after transplantation, the results were excellent or good in two of the seven patients with patellar transplants, fair in three, and poor in two; two patients required a second operation because of severe chondromalacia. Biopsies showed that 11 of the 15 femoral transplants and 1 of the 7 patellar transplants had the appearance of hyaline cartilage. CONCLUSION. Cultured autologous chondrocytes can be used to repair deep cartilage defects in the femorotibial articular surface of the knee joint.
18.	Carey, J. L., et al. (author) Autologous Chondrocyte Implantation as Treatment for Unsalvageable Osteochondritis Dissecans: 10- to 25-Year Follow-up 2020 In: American Journal of Sports Medicine. - : SAGE Publications. - 0363-5465 .- 1552-3365. ; 48:5, s. 1134-1140 Journal article (peer-reviewed)abstract Background: An unsalvageable osteochondritis dissecans (OCD) fragment has been defined as one that cannot be saved. Unsalvageable OCD lesions have been treated with various techniques, including fragment excision, microfracture, osteochondral autograft transfer, fresh osteochondral allograft transplantation, and autologous chondrocyte implantation (ACI). Hypothesis: Patients who underwent ACI as treatment for unsalvageable OCD more than 10 years ago would maintain satisfactory patient-oriented outcome measures and have a low need for additional open surgery, especially arthroplasty. Study Design: Case series; Level of evidence, 4. Methods: All Swedish and Norwegian patients (59 patients with 67 OCD lesions) who underwent ACI for OCD under the direction of the senior author between 1990 and 2005 were identified through manual chart review. Features of the patient, OCD lesion, and surgery were extracted from the medical record and intraoperative photographs. Patients were sent questionnaires to assess the Knee injury and Osteoarthritis Outcome Score, Tegner-Wallgren activity score, and Lysholm score. In addition, patients were asked whether they had to undergo further surgery, including knee replacement, of the knee that underwent ACI. They were asked whether they would have the surgery again if in the same situation. Results: A total of 55 patients (93%) with 61 OCD lesions (91%) responded. The median follow-up duration was 19 years (range, 10-26 years) and the median age at follow-up was 43 years (range, 28-69 years). Subsequent arthroscopy was performed in the majority of cases, although many of these were scheduled “second looks” as part of a study. With respect to other subsequent surgery, 12 knees (20%) underwent any additional open surgery, but only 2 knees (3%) underwent arthroplasty. Eight knees (13%) underwent revision ACI. Most patients reached their preinjury activity level (62%) and would undergo ACI again if in the same situation (85%). If failure is defined as revision of the graft or conversion to arthroplasty, then survivorship after ACI for OCD in the current study would be 87% at 10 years, 85% at 15 years, and 82% at 20 years. Conclusion: ACI for OCD provides a durable treatment option. At a median follow-up of 19 years, there was a very low (~3%) conversion to total knee arthroplasty. © 2020 The Author(s).
19.	Eklund, Anders, 1965-, et al. (author) A catheter tactile sensor for measuring hardness of soft tissue : measurement in a silicone model and in an in vitro human prostate model 1999 In: Medical and Biological Engineering and Computing. - 0140-0118 .- 1741-0444. ; 37:5, s. 618-624 Journal article (peer-reviewed)abstract Tissue hardness is related to tissue composition, and this is often changed by disease. It is therefore of interest to measure the hardness in an objective and non-invasive way. A tactile sensor based on a vibrating piezoelectric ceramic element in a feedback loop is described. When the sensor touches an object it produces a frequency shift related to the hardness of the object. The aim of this study was to develop an in vitro hardness measurement method using a catheter type version of the sensor. The method was evaluated in an established silicone tissue model and on human prostate tissue in vitro. A linear relationship was found with a high degree of explanation (R2 = 0.98) between a cone penetration hardness standard (DIN ISO 2137) applied to the silicone model and the corresponding frequency shift. The results from measurements on a human prostate tissue sample, fixed with formalin, showed that the relative hardness measured with the tactile sensor correlated (R = -0.96, p < 0.001, N = 60) with the proposed hardness related to the histological composition of the prostate tissue. The results indicated that hardness of prostate tissue, and maybe hardness of human tissue in general, can be expressed according to the cone penetration standard and that the hardness can be measured with this tactile sensory system. These findings hold the promise of further development of a non-invasive tool for hardness measurement in a clinical situation
20.	Eklund, Anders, et al. (author) A resonator sensor for evaluation of prostate tissue composition and hardness 1999 In: Proceedings of the 11th Nordic-Baltic conference on biomedical engineering.. ; , s. 181-182 Conference paper (other academic/artistic)
21.	Eklund, Anders, et al. (author) Vibrationssensor för värdering av vävnadsmjukhet 1998 In: Program & sammanfattningar. [55]. - Stockholm : Svenska läkaresällskapet. ; , s. 259- Conference paper (other academic/artistic)
22.	Ekström O,, et al. (author) Performance of Industrial Buildings – Pilot study in Bilprovningen plant Aröd 1994 Reports (other academic/artistic)
23.	Fröidh, Oskar, et al. (author) Färdplan för ökad forskning och innovation inom underhåll av järnvägsfordon 2015 Reports (other academic/artistic)abstract KTH, Chalmers och Handelshögskolan vid Göteborgs universitet har av Trafikverket fått uppdraget att ta fram ett dokument om forskningen inom underhåll av järnvägsfordon. Det är föreliggande färdplan som ingår i Trafikverkets satsning Morgondagens depåer. Färdplanen ska ligga till grund för en strategi och förslag på utveckling för kostnadseffektivt fordonsunderhåll med de förutsättningar som råder i Sverige, med avreglering och många aktörer i branschen likväl som speciella klimatförutsättningar. Trafikverket har uppmärksammat att frågor om depåer och fordonsunderhåll inte alltid hanteras på ett bra sätt för att utveckla järnvägssystemet. Tidigare hade Banverket ett sektorsansvar men det avskaffades i och med att Trafikverket bildades. Det behövs dock ett övergripande systemansvar och incitament för att leda processen framåt mot en stabil utveckling genom forskning, utveckling och innovation i den fortsatta omreglering som sker av den svenska järnvägssektorn. Hur kan en effektiv samverkan mellan universitet, näringsliv och offentlig sektor utformas för att bidra till en säker och pålitlig tågtrafik i Sverige? En litteraturgenomgång har genomförts för att visa var den internationella forskningsfronten står. Det tycks dock som att det samlade greppet inom underhåll av järnvägsfordon inte är ett genomarbetat forskningsområde, utan det kan bli ett svenskt ”pionjärområde” där universitet, högskolor och institut i samarbete med branschen kan skapa forskningsresultat och kunskapsutveckling. Denna färdplan föreslår ett antal olika områden som skulle behöva ökad forskning för större kunskap och kompetens. Var ska depåer för person- respektive godsfordon mest effektivt lokaliseras, centralt eller perifert i jämförelse med trafiksystemet och respektive omlopp? Hur ska de utformas mest effektivt med tanke på fordonstyper, reservdelar och personalutnyttjande? Hur ska infrastrukturen till och internt i depåerna utformas för effektivt arbete? Detta ska ske i en avreglerad järnvägssektor med olika operatörer, vagnägare, depåägare samt underhållsleverantörer på olika långa kontrakt. Hur ska detta organiseras på ett stabilt sätt med långsiktig ekonomisk bärkraft för samtliga parter? Arbetet går att dela upp i avhjälpande och förebyggande underhåll; i depå eller mobilt, med säkerhets-, drifts- eller komfortrelaterat underhåll. På vilka olika sätt går det att utvärdera samt utveckla modeller för att prognostisera behovet av underhåll enligt ovan nämnda variabler? Målet är att ta fram vetenskapliga metoder för att effektivisera fordonsunderhåll för järnvägstrafiken på ett optimalt sätt. I färdplanen rekommenderas en strategi för fordonsunderhåll: Trafikverket ska verka för att efterfrågad funktion i det svenska järnvägssystemet uppnås, inkluderande kostnadseffektivt underhåll av både infrastruktur och fordon. Hög driftsäkerhet är attraktivt för resenärer och godskunder och har ett värde och motiverar ett samhällsekonomiskt synsätt på underhåll av järnvägsfordon. Tillståndsövervakning och relaterad prediktering ges en viktigare roll för förebyggande underhåll. Öka synergin mellan infrastruktur- och fordonsbaserad tillståndsövervakning, inte minst av den dynamiska samverkan mellan infrastruktur och fordon. Utred hur ”intelligensen” hos infrastruktur och fordon bäst fördelas och utvecklas för ett mera kostnadseffektivt underhåll av järnvägssystemet. Detta innefattar att man vet vad man skall mäta och att uppmätta storheter kan länkas till framtida nedbrytning av fordon och infrastruktur. Utred flödet och ”flaskhalsar” i dagens system av fordonsunderhåll (kritiska aspekter). Utveckla distinktionen av säkerhetsnödvändigt underhåll och komfortrelaterat underhåll. Verka för tydliga och rimliga ”spelregler” för aktörer inom fordonsunderhåll. Förbättra nätverket bland dessa aktörer, inte minst kring tekniska frågor. Skapa ytterligare incitament för effektivt fordonsunderhåll genom att se över kostnader och intäkter i intressentkedjan mellan de primära kunderna och de som kan åtgärda problemen. Lyft fram goda exempel (best practice) på väl fungerande fordonsunderhåll. Låt universitet och högskolor få en viktig och neutral roll i den kunskapsbaserade utvecklingen. Detta bör ske genom att skapa ett forsknings- utvecklings- och demonstrations (FUD)-program inom området underhåll för järnvägsfordon. I denna färdplan föreslås även ett antal olika forskningsprojekt och -områden som skulle kunna utvecklas i ett sammanhållet forskningsprogram.
24.	Fröidh, Oskar, et al. (author) Färdplan för ökad forskning och innovation inom underhåll av järnvägsfordon 2015 Reports (other academic/artistic)abstract KTH, Chalmers och Handelshögskolan vid Göteborgs universitet har av Trafikverket fått uppdraget att ta fram ett dokument om forskningen inom underhåll av järnvägsfordon. Det är föreliggande färdplan som ingår i Trafikverkets satsning Morgondagens depåer. Färdplanen ska ligga till grund för en strategi och förslag på utveckling för kostnadseffektivt fordonsunderhåll med de förutsättningar som råder i Sverige, med avreglering och många aktörer i branschen likväl som speciella klimatförutsättningar.Trafikverket har uppmärksammat att frågor om depåer och fordonsunderhåll inte alltid hanteras på ett bra sätt för att utveckla järnvägssystemet. Tidigare hade Banverket ett sektorsansvar men det avskaffades i och med att Trafikverket bildades. Det behövs dock ett övergripande systemansvar och incitament för att leda processen framåt mot en stabil utveckling genom forskning, utveckling och innovation i den fortsatta omreglering som sker av den svenska järnvägssektorn. Hur kan en effektiv samverkan mellan universitet, näringsliv och offentlig sektor utformas för att bidra till en säker och pålitlig tågtrafik i Sverige?En litteraturgenomgång har genomförts för att visa var den internationella forskningsfronten står. Det tycks dock som att det samlade greppet inom underhåll av järnvägsfordon inte är ett genomarbetat forskningsområde, utan det kan bli ett svenskt ”pionjärområde” där universitet, högskolor och institut i samarbete med branschen kan skapa forskningsresultat och kunskapsutveckling.Denna färdplan föreslår ett antal olika områden som skulle behöva ökad forskning för större kunskap och kompetens. Var ska depåer för person- respektive godsfordon mest effektivt lokaliseras, centralt eller perifert i jämförelse med trafiksystemet och respektive omlopp? Hur ska de utformas mest effektivt med tanke på fordonstyper, reservdelar och personalutnyttjande? Hur ska infrastrukturen till och internt i depåerna utformas för effektivt arbete? Detta ska ske i en avreglerad järnvägssektor med olika operatörer, vagnägare, depåägare samt underhållsleverantörer på olika långa kontrakt. Hur ska detta organiseras på ett stabilt sätt med långsiktig ekonomisk bärkraft för samtliga parter? Arbetet går att dela upp i avhjälpande och förebyggande underhåll; i depå eller mobilt, med säkerhets-, drifts- eller komfortrelaterat underhåll. På vilka olika sätt går det att utvärdera samt utveckla modeller för att prognostisera behovet av underhåll enligt ovan nämnda variabler? Målet är att ta fram vetenskapliga metoder för att effektivisera fordonsunderhåll för järnvägstrafiken på ett optimalt sätt.I färdplanen rekommenderas en strategi för fordonsunderhåll:Trafikverket ska verka för att efterfrågad funktion i det svenska järnvägssystemet uppnås, inkluderande kostnadseffektivt underhåll av både infrastruktur och fordon.Hög driftsäkerhet är attraktivt för resenärer och godskunder och har ett värde och motiverar ett samhällsekonomiskt synsätt på underhåll av järnvägsfordon.Tillståndsövervakning och relaterad prediktering ges en viktigare roll för förebyggande underhåll.Öka synergin mellan infrastruktur- och fordonsbaserad tillståndsövervakning, inte minst av den dynamiska samverkan mellan infrastruktur och fordon.Utred hur ”intelligensen” hos infrastruktur och fordon bäst fördelas och utvecklas för ett mera kostnadseffektivt underhåll av järnvägssystemet. Detta innefattar att man vet vad man skall mäta och att uppmätta storheter kan länkas till framtida nedbrytning av fordon och infrastruktur.Utred flödet och ”flaskhalsar” i dagens system av fordonsunderhåll (kritiska aspekter).Utveckla distinktionen av säkerhetsnödvändigt underhåll och komfortrelaterat underhåll.Verka för tydliga och rimliga ”spelregler” för aktörer inom fordonsunderhåll.Förbättra nätverket bland dessa aktörer, inte minst kring tekniska frågor.Skapa ytterligare incitament för effektivt fordonsunderhåll genom att se över kostnader och intäkter i intressentkedjan mellan de primära kunderna och de som kan åtgärda problemen.Lyft fram goda exempel (best practice) på väl fungerande fordonsunderhåll.Låt universitet och högskolor få en viktig och neutral roll i den kunskapsbaserade utvecklingen.Detta bör ske genom att skapa ett forsknings- utvecklings- och demonstrations (FUD)-program inom området underhåll för järnvägsfordon. I denna färdplan föreslås även ett antal olika forskningsprojekt och -områden som skulle kunna utvecklas i ett sammanhållet forskningsprogram.
25.	Hulander, Mats, et al. (author) Gradients in surface nanotopography used to study platelet adhesion and activation 2013 In: Colloids and Surfaces B-Biointerfaces. - : Elsevier BV. - 0927-7765 .- 1873-4367. ; 110, s. 261-269 Journal article (peer-reviewed)abstract Gradients in surface nanotopography were prepared by adsorbing gold nanoparticles on smooth gold substrates using diffusion technique. Following a sintering procedure the particle binding chemistry was removed, and integration of the particles into the underlying gold substrate was achieved, leaving a nanostructured surface with uniform surface chemistry. After pre-adsorption of human fibrinogen, the effect of surface nanotopography on platelets was studied. The use of a gradient in nanotopography allowed for platelet adhesion and activation to be studied as a function of nanoparticle coverage on one single substrate. A peak in platelet adhesion was found at 23% nanoparticle surface coverage. The highest number of activated platelets was found on the smooth control part of the surface, and did not coincide with the number of adhered platelets. Activation correlated inversely with particle coverage, hence the lowest fraction of activated platelets was found at high particle coverage. Hydrophobization of the gradient surface lowered the total number of adhering cells, but not the ratio of activated cells. Little or no effect was seen on gradients with 36 nm particles, suggesting the existence of a lower limit for sensing of surface nano-roughness in platelets. These results demonstrate that parameters such as ratio between size and inter-particle distance can be more relevant for cell response than wettability on nanostructured surfaces. The minor effect of hydrophobicity, the generally reduced activation on nanostructured surfaces and the presence of a cut-off in activation of human platelets as a function of nanoparticle size could have implications for the design of future blood-contacting biomaterials.
26.	Isaksson, Olle, 1943, et al. (author) Regulation of cartilage growth by growth hormone and insulin-like growth factor I. 1991 In: Pediatric nephrology (Berlin, Germany). - 0931-041X. ; 5:4, s. 451-3 Journal article (peer-reviewed)abstract A number of studies have shown that growth hormone (GH) and insulin-like growth factor-I (IGF-I) have important regulatory roles for skeletal growth. However, it has been a matter of controversy whether GH acts directly on cells in the growth plate or if the growth-promoting effects of GH are mediated by liver-derived (endocrine-acting) IGF-I. With the recognition that GH regulates the production of IGF-I in multiple extra-hepatic tissues, autocrine and paracrine functions of IGF-I have been suggested as important components of GH action. This review focuses on recent developments in our understanding of the cellular mechanisms by which GH promotes longitudinal bone growth and the inter-relationship between GH and IGF-I in the growth plate.
27.	Jalkanen, Ville, et al. (author) Detektering av förändringar i prostatavävnad mha resonanssensor 2002 In: Program & sammanfattningar. [59]. - Stockholm : Svenska läkaresällskapet. ; , s. 231- Conference paper (other academic/artistic)
28.	Jonsson, Marianne, 1962, et al. (author) Novel 3D culture system with similarities to the human heart for studies of the cardiac stem cell niche. 2010 In: Regenerative medicine. - : Future Medicine Ltd. - 1746-076X .- 1746-0751. ; 5:5, s. 725-36 Journal article (peer-reviewed)abstract AIMS: The aim of this study was to develop a 3D culture system with similarities to the human heart, which was suitable for studies of adult cardiac stem or progenitor cells. MATERIALS & METHODS: Dissociated cells from human cardiac biopsies were placed in high-density pellet cultures and cultured for up to 6 weeks. Gene and protein expressions, analyzed by quantitative real-time PCR and immunohistochemistry, and morphology were studied in early and late pellets. RESULTS: Cells cultured in the 3D model showed similarities to human cardiac tissue. Moreover, markers for cardiac stem and progenitor cells were also detected after 6 weeks of culture, in addition to markers for signaling pathways active in stem cell niche regulation. CONCLUSIONS: The described 3D culture model could be a valuable tool when studying the influence of different compounds on proliferation and differentiation processes in cardiac stem or progenitor cells in cardiac regenerative research.
29.	Karlsson, Anna, et al. (author) The effect of tinzaparin on biomarkers in FIGO stages III-IV ovarian cancer patients undergoing neoadjuvant chemotherapy - the TABANETOC trial : study protocol for a randomized clinical multicenter trial 2024 In: Acta Oncologica. - : Medical Journals Sweden. - 0284-186X .- 1651-226X. ; 63, s. 581-585 Journal article (peer-reviewed)abstract Background: Tinzaparin, a low-molecular weight heparin (LMWH), has shown anti-neoplastic properties in animal models and in in vitro studies of human cancer cell lines. The reduction of CA-125 levels during neoadjuvant chemotherapy (NACT) in patients with epithelial ovarian cancer (EOC) co-varies with the prognosis; the larger the decrease in CA-125, the better the prognosis.Purpose: This study aims to evaluate the potential anti-neoplastic effects of tinzaparin by investigating changes in serum CA-125 levels in advanced EOC patients who receive NACT.Material and methods: This is an open randomized multicenter pilot trial. Forty patients with EOC selected to receive NACT will be randomized 1:1 to receive daily addition of tinzaparin or no tinzaparin. The processing and treatment of the patients will otherwise follow the recommendations in the Swedish National Guidelines for Ovarian Cancer. Before every cycle of chemotherapy, preoperatively, and 3 weeks after the last cycle of chemotherapy, a panel of biomarkers, including CA-125, will be measured.Patients: Inclusion criteria are women aged 18 years or older, World Health Organization performance status 0–1, histologically confirmed high-grade serous, endometrioid or clear cell EOC, International Federation of Gynecology and Obstetrics (FIGO) stages III-IV. In addition, a CA-125 level of ≥ 250 kIE/L at diagnosis. Exclusion criteria are contraindications to LMWH, ongoing or recent treatment with unfractionated heparin, LMWH, warfarin or non-vitamin K antagonist oral anticoagulants.Interpretation: This study will make an important contribution to the knowledge of the anti-neoplastic effects of tinzaparin in EOC patients and may thus guide the planning of a future study on the impact of tinzaparin on survival in EOC.
30.	Karlsson, Anna, 1985-, et al. (author) The effect of tinzaparin on biomarkers in FIGO stages III-IV ovarian cancer patients undergoing neoadjuvant chemotherapy – the TABANETOC trial: study protocol for a randomized clinical multicenter trial 2024 In: Acta Oncologica. - Uppsala : Medical Journals Sweden. - 0284-186X .- 1651-226X. ; 63, s. 580-585 Journal article (peer-reviewed)abstract Background: Tinzaparin, a low-molecular weight heparin (LMWH), has shown anti-neoplastic properties in animal models and in in vitro studies of human cancer cell lines. The reduction of CA-125 levels during neoadjuvant chemotherapy (NACT) in patients with epithelial ovarian cancer (EOC) co-varies with the prognosis; the larger the decrease in CA-125, the better the prognosis.Purpose: This study aims to evaluate the potential anti-neoplastic effects of tinzaparin by investigating changes in serum CA-125 levels in advanced EOC patients who receive NACT.Material and methods: This is an open randomized multicenter pilot trial. Forty patients with EOC selected to receive NACT will be randomized 1:1 to receive daily addition of tinzaparin or no tinzaparin. The processing and treatment of the patients will otherwise follow the recommendations in the Swedish National Guidelines for Ovarian Cancer. Before every cycle of chemotherapy, preoperatively, and 3 weeks after the last cycle of chemotherapy, a panel of biomarkers, including CA-125, will be measured.Patients: Inclusion criteria are women aged 18 years or older, World Health Organization performance status 0–1, histologically confirmed high-grade serous, endometrioid or clear cell EOC, International Federation of Gynecology and Obstetrics (FIGO) stages III-IV. In addition, a CA-125 level of ≥ 250 kIE/L at diagnosis. Exclusion criteria are contraindications to LMWH, ongoing or recent treatment with unfractionated heparin, LMWH, warfarin or non-vitamin K antagonist oral anticoagulants.Interpretation: This study will make an important contribution to the knowledge of the anti-neoplastic effects of tinzaparin in EOC patients and may thus guide the planning of a future study on the impact of tinzaparin on survival in EOC.
31.	Lind, Lars, et al. (author) Growth-differentiation factor-15 is an independent marker of cardiovascular dysfunction and disease in the elderly : results from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) Study 2009 In: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 30:19, s. 2346-2353 Journal article (peer-reviewed)abstract AIMS: Growth-differentiation factor-15 (GDF-15) is emerging as an independent prognostic biomarker in patients with cardiovascular (CV) disease. Little is known about the pathophysiological basis for the close association of GDF-15 to future CV events. We hypothesized that GDF-15 is related to underlying CV pathologies. METHODS AND RESULTS: To relate the levels of GDF-15 to indices of CV dysfunction and disease in elderly individuals, serum levels of GDF-15 were measured in 1004 subjects aged 70 years from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. Carotid intima-media thickness and plaque burden, and left ventricular (LV) geometry and function were assessed by ultrasound. Endothelial function was evaluated in forearm resistance vessels and in the brachial artery by venous occlusion plethysmography and ultrasound imaging, respectively. Elevated levels of GDF-15 were related to several CV risk factors (male gender, current smoking, body mass index, waist circumference, diabetes, fasting glucose, triglycerides, and low HDL cholesterol). After adjustment for CV risk factors, increased levels of GDF-15 were associated with reduced endothelium-dependent vasodilation in resistance vessels, plaque burden, LV mass and concentric LV hypertrophy, reduced LV ejection fraction, and clinical manifestations of coronary artery disease and heart failure. CONCLUSION: GDF-15 carries information on CV dysfunction and disease that is not captured by traditional CV risk factors in elderly individuals.
32.	Mejtoft, Thomas, Universitetslektor, 1976-, et al. (author) Kan en branschspecifik innovationsmodell öka ”success rate” för medicintekniska innovationer? 2019 Conference paper (other academic/artistic)
33.	Mejtoft, Thomas, Universitetslektor, 1976-, et al. (author) Medtech innovation guide : an empiric model to support medical technology innovation 2022 In: Health and Technology. - : Springer. - 2190-7188 .- 2190-7196. ; 12:5, s. 911-922 Journal article (peer-reviewed)abstract Innovation has become increasingly important for most industries to cope with rapid technological changes as well as changing societal needs. Even though there are many sectors with specific needs when it comes to supporting innovation, the medical technology sector is facing several unique challenges that both increases the lead-time from idea to finished product and decreases the number of innovations that are developed. This paper presents a proposed innovation guide that has been developed and evaluated as a support for the innovation process within medical technology research. The guide takes the unique characteristics of the medical technology sector into account and serves as a usable guide for the innovator. The complete guide contains both a structure for the process and a usable web application to support the journey from idea to finished products and services. The paper also includes a new readiness level, Sect. 4.2 to provide support both when developing and determining the readiness for clinical implementation of a medical technology innovation.
34.	Mälarstig, Anders, et al. (author) Raised Interleukin-10 is an Indicator of Poor Outcome and Enhanced Systemic Inflammation in Patients with Acute Coronary Syndrome 2008 In: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 94:6, s. 724-9 Journal article (peer-reviewed)abstract OBJECTIVES: To re-evaluate the relation between plasma interleukin-10 (IL-10) concentration at hospital admission and outcome and to investigate the impact of single nucleotide polymorphisms (SNP) in the IL-10 gene in patients with non-ST elevation acute coronary syndrome (ACS). DESIGN: Determination of IL-10 plasma concentrations and genotyping of SNPs in the IL-10 gene in a prospective trial of patients with ACS and in a group of healthy controls. PATIENTS: 3179 patients in the Fragmin and fast revascularisation during InStability in Coronary artery disease II (FRISC II) trial and 393 healthy controls. MAIN OUTCOME MEASURES: Mortality and incidence of myocardial infarction (MI) at 12 months. RESULTS: The median and interquartile ranges of IL-10 were 0.8 (0.5-1.0) pg/ml in healthy controls and 1.1 (0.7-1.9) pg/ml in patients (p<0.001). In patients, IL-10 predicted a crude risk increase of death/MI, with the highest risk observed in the fourth quartile (adjusted odds ratio 1.7 (95% confidence interval 1.2 to 2.3)). Adjustment for common risk indicators, including C-reactive protein and interleukin-6, weakened the association to a non-significant level. The 1170 CC genotype weakly predicted increased plasma concentrations of IL-10 in patients (p = 0.04) and in controls (p = 0.03), which was consistent with the modest association of this variant with coronary disease (p = 0.01). CONCLUSION: In contrast with some previous reports, we conclude that IL-10 reflects a proinflammatory state in patients with ACS and we therefore suggest that IL-10 is as effective a biomarker for the risk prediction of future cardiovascular events as other markers of systemic inflammation.
35.	Nilsson, Anders, 1958, et al. (author) Hormonal regulation of longitudinal bone growth. 1994 In: European journal of clinical nutrition. - 0954-3007. ; 48 Suppl 1 Journal article (peer-reviewed)abstract The regulation of postnatal somatic growth is complex. Genetic, nutritional factors and hormones exert regulatory functions. Hormones that have an established role in the regulation include growth hormone (GH), thyroid hormone and sex steroids. GH promotes mainly the growth of the long bones in terms of final height, while the action of the sex steroids and thyroid hormone is less well known. Longitudinal bone growth is the result of chondrocyte proliferation and subsequent endochondral ossification in the epiphyseal growth-plates. The growth-plate is a cartilaginous template that is located between the epiphysis and the metaphysis of the long bones. GH and insulin-like growth factor-I (IGF-I) have different target cells in the epiphyseal growth-plate. GH stimulates the slowly dividing prechondrocytes in the germinative cell layer while IGF-I promotes the clonal expansion in the proliferative cell layer of a GH primed cell. Thyroid hormone blocks the clonal expansion and stimulates chondrocyte maturation. IGF-I mRNA is primarily regulated by GH, and IGF-I is produced in several tissues such as the liver, muscle, fat and epiphyseal growth plates. However, IGF-I mRNA is also increased during compensatory growth of heart and kidneys and by estrogen in the Fallopian tube in the rat. Nutrition, i.e. energy from fat and carbohydrates and proteins, also influences the final height, but the cellular mechanism of action is not known. The aim of this article is to review hormonal action on longitudinal bone growth.
36.	Nilsson, Anders, et al. (author) Ting tar tid. Kommentarer till Utbildning och ekonomisk utveckling 2005 In: Utbildning och ekonomisk utveckling – vad visar den empiriska forskningen om orsakssambanden?. Book chapter (other academic/artistic)
37.	Ohlsson, Claes, 1965, et al. (author) Effect of growth hormone and insulin-like growth factor-I on DNA synthesis and matrix production in rat epiphyseal chondrocytes in monolayer culture. 1992 In: The Journal of endocrinology. - 0022-0795. ; 133:2, s. 291-300 Journal article (peer-reviewed)abstract The influence of various culture conditions was studied on the effect of GH and insulin-like growth factor-I (IGF-I) on DNA and matrix synthesis in epiphyseal rat chondrocytes in monolayer culture. Chondrocytes from enzymatically digested rat tibia epiphyseal growth plates were seeded in 48-well culture plates and precultured for 10 days in Ham's F-12 medium supplemented with 1% (v/v) newborn calf serum and 1% (v/v) of a serum substitute. After preculture, the medium was changed to Ham's F-12 medium supplemented with 1% serum from hypophysectomized rats, and the effect of GH and IGF-I on DNA synthesis ([3H]thymidine incorporation) and matrix production ([35S]sulphate uptake) was studied during an additional 96-h culture period. Isotopes were present during the last 24 h of culture. Both hGH and IGF-I stimulated DNA synthesis in a dose-dependent manner. A maximal effect of GH was seen at a concentration of 25 micrograms/l (60 +/- 11% stimulation over control) and for IGF-I at 10 micrograms/l (162 +/- 12%). The stimulatory effects of the same concentrations of human GH (hGH) and IGF-I on [35S]sulphate uptake were 135 +/- 25 and 320 +/- 42% respectively. In-vitro pulse labelling revealed that GH did not produce a response during the first 3 days of culture (after addition of GH) but was effective during days 4 and 5 of culture. In contrast, IGF-I was effective throughout the culture period. Pretreatment of cells with GH or IGF-I for 2.5 days showed that GH but not IGF-I produced a sustained effect on [3H]thymidine uptake. In order to study the influence of cell density on the effect of GH and IGF-I on DNA synthesis, the effect of added peptides was evaluated after different preculture periods (5-15 days). A maximal stimulatory effect of hGH was seen at a cell density of 150,000-300,000 cells/cm2. GH had no significant effect at a low (less than 100,000 cells/cm2) or a high (greater than 400,000 cells/cm2) cell density. The magnitude of the stimulatory effect of IGF-I was the same at densities between 10,000 and 250,000 cells/cm2, but was reduced at higher cell densities (over 250,000 cells/cm2). Chondrogenic properties of cells that had been cultured for 15 days were verified in vitro by positive alcian blue staining and identification of type II collagen, and in vivo by development of cartilage nodules in nude mice.(ABSTRACT TRUNCATED AT 400 WORDS)
38.	Ohlsson, Claes, 1965, et al. (author) Effects of tri-iodothyronine and insulin-like growth factor-I (IGF-I) on alkaline phosphatase activity, [3H]thymidine incorporation and IGF-I receptor mRNA in cultured rat epiphyseal chondrocytes. 1992 In: The Journal of endocrinology. - 0022-0795. ; 135:1, s. 115-23 Journal article (peer-reviewed)abstract The effects of tri-iodothyronine (T3) and insulin-like growth factor-I (IGF-I) on [3H]thymidine incorporation, alkaline phosphatase (ALP) activity and IGF-I receptor mRNA levels were studied in rat epiphyseal chondrocytes cultured in monolayer. Chondrocytes from enzymatically digested rat tibia epiphyseal growth plates were seeded in monolayer culture and precultured for 7-14 days in Ham's F-12 medium supplemented with 10% (v/v) newborn calf serum and 1% (v/v) of a serum substitute. After preculture the medium was changed to Ham's F-12 medium containing 1% (v/v) serum from hypophysectomized rats, and the effects of T3 and/or IGF-I on DNA synthesis ([3H]thymidine incorporation), ALP activity (a late marker of differentiated epiphyseal chondrocytes) and IGF-I receptor mRNA levels were studied. ALP activity was increased by T3 in a dose-dependent manner with a maximal response at 10 micrograms T3/l (678 +/- 86% compared with control culture). The increase in ALP activity was accompanied by a concomitant decrease in [3H]thymidine incorporation (52 +/- 14% compared with control culture). Human GH (hGH; 50 micrograms/l) and IGF-I (25 micrograms/l) had no stimulatory effect on ALP activity. However IGF-I (10 micrograms/l) exerted an inhibition on the T3 (10 micrograms/l)-induced increase in ALP activity (64 +/- 9% compared with T3-treated culture). T3 (3 micrograms/l) inhibited the increase in [3H]thymidine incorporation caused by 25 micrograms IGF-I/l (51 +/- 13% compared with IGF-I-treated culture). Furthermore, IGF-I receptor mRNA levels were increased by 10 micrograms T3/l (137 +/- 4.2% compared with control culture) while no effect of hGH (50 micrograms/l) or IGF-I (25 micrograms/l) was demonstrated. Both T3 and IGF-I were shown to interact with epiphyseal chondrocytes and both substances seemed to affect cell proliferation and maturation and therefore longitudinal bone growth. Furthermore, the results indicated that IGF-I is important for proliferation of the cells while T3 initiates the terminal differentiation of epiphyseal chondrocytes.
39.	Ohlsson, Claes, 1965, et al. (author) Endocrine regulation of longitudinal bone growth. 1993 In: Acta paediatrica (Oslo, Norway : 1992). Supplement. - 0803-5326. ; 82 Suppl 391 Journal article (peer-reviewed)
40.	Ohlsson, Claes, 1965, et al. (author) Establishment of a growth hormone responsive chondrogenic cell line from fetal rat tibia. 1993 In: Molecular and cellular endocrinology. - 0303-7207. ; 91:1-2, s. 167-75 Journal article (peer-reviewed)abstract Reproducible effects of growth hormone (GH) on primary isolated cells in monolayer are highly dependent on the culture conditions and/or the fraction of GH responsive cells. To study the effect of GH at the cellular level, a homogenous cell line with both GH responsiveness and chondrogenic properties was established. Primary isolated cells from 18-day-old fetal rat tibia were subcultured using a strict protocol for passages (every third day and a seeding density of 15,000/cm2). Of six established cell lines, one fetal tibia cell line No. 5 (FTC 5) expressed adipogenic and chondrogenic properties at a low frequency. Cells from FTC 5 were subcultured in soft agar suspension with the addition of bovine GH (100 ng/ml). After 14 days in culture eight monoclonal cell lines were established from individual large colonies. Two subclones, FTC 5:3 and FTC 5:6, expressed a chondrogenic phenotype as demonstrated by chondrocyte foci, alcian blue staining and production of type II collagen. Further characterization of FTC 5:3 revealed specific binding of bovine GH with an affinity of 1.7 x 10(9) M-1, and approximately 7300 receptors/cell. Northern blot analysis of FTC 5:3 with a 32P-labeled RNA probe complementary to an extracellular part of the rat GH receptor, revealed two major labeled bands (4.0 and 1.2 kilobases). Both GH and insulin-like growth factor-I (IGF-I) stimulated 3H-thymidine uptake in FTC 5:3 (194 +/- 28% and 405 +/- 127% over control, respectively), while proteoglycan synthesis, as measured by [35S]sulphate uptake, was stimulated by IGF-I only (101 +/- 18% over control).(ABSTRACT TRUNCATED AT 250 WORDS)
41.	Ohlsson, Claes, 1965, et al. (author) Growth hormone induces multiplication of the slowly cycling germinal cells of the rat tibial growth plate. 1992 In: Proceedings of the National Academy of Sciences of the United States of America. - 0027-8424. ; 89:20, s. 9826-30 Journal article (peer-reviewed)abstract To study the effect of locally infused growth hormone (GH) or insulin-like growth factor I(IGF-I) on slowly cycling cells in the germinal cell layer of the tibial growth plate, osmotic minipumps delivering 14.3 microCi of [3H]thymidine per day were implanted s.c. into hypophysectomized rats, and GH (1 microgram) or IGF-I (10 micrograms) was injected daily through a cannula implanted in the proximal tibia. The opposite leg served as a control. After 12 days of treatment, the osmotic minipumps were removed, and three rats in each group were given GH (20 micrograms/day, s.c.) for an additional 14 days to chase the labeled cells out of the proliferative layers. Labeled cells remained in the germinal layer, in the perichondrial ring, and on the surface of the articular cartilage close to the epiphyseal plate. GH administered together with labeled thymidine significantly increased the number of labeled cells in the germinal cell layer compared to that in the control leg (ratio = 1.95 +/- 0.13), whereas IGF-I showed no stimulatory effect (ratio = 0.96 +/- 0.04). Therefore GH but not IGF-I stimulates the multiplication of the slowly cycling (label-retaining) cells in the germinal layer of the epiphyseal plate. IGF-I acts only on the proliferation of the resulting chondrocytes.
42.	Peterson, Lars, 1936, et al. (author) Two- to 9-year outcome after autologous chondrocyte transplantation of the knee. 2000 In: Clinical orthopaedics and related research. - 0009-921X. ; :374, s. 212-34 Journal article (peer-reviewed)abstract Autologous cultured chondrocyte transplantation was introduced in Sweden in 1987 for the treatment of large (1.5-12.0 cm2) full thickness chondral defects of the knee. The clinical, arthroscopic, and histologic results from the first 101 patients treated using this technique are reported in this study. Patients were assessed retrospectively using three types of endpoints: patient and physician derived clinical rating scales (five validated and two new); arthroscopic assessment of cartilage fill, integration, and surface hardness; and standard histochemical techniques. Ninety-four patients with 2- to 9-years followup were evaluable. Good to excellent clinical results were seen in individual groups as follows: isolated femoral condyle (92%), multiple lesions (67%), osteochondritis dissecans (89%), patella (65%), and femoral condyle with anterior cruciate ligament repair (75%). Arthroscopic findings in 53 evaluated patients showed good repair tissue fill, good adherence to underlying bone, seamless integration with adjacent cartilage, and hardness close to that of the adjacent tissue. Hypertrophic response of the periosteum or graft or both was identified in 26 arthroscopies; seven were symptomatic and resolved after arthroscopic trimming. Graft failure occurred in seven (four of the first 23 and three of the next 78) patients. Histologic analysis of 37 biopsy specimens showed a correlation between hyalinelike tissue (hyaline matrix staining positive for Type II collagen and lacking a fibrous component) and good to excellent clinical results. The good clinical outcomes of autologous chondrocyte transplantation in this study are encouraging, and clinical trials are being done to assess the outcomes versus traditional fibrocartilage repair techniques.
43.	Sandstedt, Joakim, et al. (author) C-kit+ CD45- cells found in the adult human heart represent a population of endothelial progenitor cells. 2010 In: Basic research in cardiology. - : Springer Science and Business Media LLC. - 1435-1803 .- 0300-8428. ; 105:4, s. 545-56 Journal article (peer-reviewed)abstract Although numerous reports support the existence of stem cells in the adult heart, few studies have been conducted using human cardiac tissue. Therefore, cells from human cardiac atrial biopsies were analyzed regarding progenitor properties. Expression of stem cell markers was analyzed using fluorescence-activated cell sorting. This identified a small population of C-kit+ cells, which could be further subdivided based on expression of CD45. The C-kit+ CD45+ population was determined to be of mast cell identity, while the C-kit+ CD45- population expressed mRNA of the endothelial lineage. Since the number of cells obtainable from biopsies was limited, a comparison between directly isolated and monolayer and explant cultured cells, respectively, was carried out. While both cultures retained a small population of mast cells, only monolayer culture produced a stable and relatively high percentage of C-kit+ CD45- cells. This population was found to co-express endothelial progenitor cell markers such as CD31, CD34, CXCR4, and FLK-1. The mRNA expression profile was similar to the one from directly isolated cells. When sorted cells were cultured in endothelial differentiation medium, the C-kit+ CD45- population retained its expression of endothelial markers to a large extent, but downregulated progenitor markers, indicating further differentiation into endothelial cells. We have confirmed that the human cardiac atrium contains a small C-kit+ CD45- population expressing markers commonly found on endothelial progenitor cells. The existence of an endothelial progenitor population within the heart might have future implications for developing methods of inducing neovascularization after myocardial infarction.
44.	Sandstedt, Joakim, et al. (author) Human C-kit+CD45- cardiac stem cells are heterogeneous and display both cardiac and endothelial commitment by single-cell qPCR analysis. 2014 In: Biochemical and biophysical research communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 443:1, s. 234-238 Journal article (peer-reviewed)abstract C-kit expressing cardiac stem cells have been described as multipotent. We have previously identified human cardiac C-kit+CD45- cells, but only found evidence of endothelial commitment. A small cardiac committed subpopulation within the C-kit+CD45- population might however be present. To investigate this at single-cell level, right and left atrial biopsies were dissociated and analyzed by FACS. Only right atrial biopsies contained a clearly distinguishable C-kit+CD45- population, which was single-cell sorted for qPCR. A minor portion of the sorted cells (1.1%) expressed early cardiac gene NKX2.5 while most of the cells (81%) expressed late endothelial gene VWF. VWF- cells were analyzed for a wider panel of genes. One group of these cells expressed endothelial genes (FLK-1, CD31) while another group expressed late cardiac genes (TNNT2, ACTC1). In conclusion, human C-kit+CD45- cells were predominantly localized to the right atrium. While most of these cells expressed endothelial genes, a minor portion expressed cardiac genes.
45.	Sandstedt, Joakim, et al. (author) Left atrium of the human adult heart contains a population of side population cells. 2012 In: Basic research in cardiology. - : Springer Science and Business Media LLC. - 1435-1803 .- 0300-8428. ; 107:2 Journal article (peer-reviewed)abstract Cardiac "side population" (SP) cells have previously been found to differentiate into both endothelial cells and cardiomyocytes in mice and rats, but there are no data on SP cells in the human adult heart. Therefore, human cardiac atrial biopsies were dissociated, stained for SP cells and analyzed with FACS. Identified cell populations were analyzed for gene expression by quantitative real-time PCR and subjected to in vitro differentiation. Only biopsies from the left atrium contained a clearly distinguishable population of SP cells (0.22±0.08%). The SP population was reduced by co-incubation with MDR1 inhibitor Verapamil, while the ABCG2 inhibitor FTC failed to decrease the number of SP cells. When the gene expression was analyzed, SP cells were found to express significantly more MDR1 than non-SP cells. For ABCG2, there was no detectable difference. SP cells also expressed more of the stem cell-associated markers C-KIT and OCT-4 than non-SP cells. On the other hand, no significant difference in the expression of endothelial and cardiac genes could be detected. SP cells were further subdivided based on CD45 expression. The CD45-SP population showed evidence of endothelial commitment at gene expression level. In conclusion, the results show that a SP population of cells is present also in the human adult heart.
46.	Sandstedt, Joakim, et al. (author) SSEA-4+ CD34- Cells in the Adult Human Heart Show the Molecular Characteristics of a Novel Cardiomyocyte Progenitor Population. 2014 In: Cells, tissues, organs. - : S. Karger AG. - 1422-6421 .- 1422-6405. ; 199:2-3, s. 103-116 Journal article (peer-reviewed)abstract Stage-specific embryonic antigen (SSEA) expression is used to describe the differentiation state of an embryonic stem cell (ESC). In human ESCs, SSEA-3 and SSEA-4 are highly expressed in undifferentiated cells and downregulated upon differentiation. SSEA-4 has also been described as a marker for adult stem cells in various tissues, including human neonatal cardiac tissue. However, there is currently little data on the expression of SSEAs in human adult cardiac tissue. We obtained right and left atrial biopsies from patients undergoing cardiac surgery. These were dissociated, stained for SSEAs and other cardiac stem cell markers and analyzed by flow cytometry. Directly isolated cells expressed variable levels of SSEA-1, SSEA-3 and SSEA-4. The SSEA-1+ population was established as contaminating hematopoietic cells. The SSEA-4+ population, on the other hand, could be subdivided based on the endothelial progenitor marker CD34. The SSEA-4+ CD34- population in the right atrium had a high gene expression of both early (TBX5, NKX2.5) and late (TNNT2) cardiomyocyte markers. The SSEA-4+ CD34+ population, on the other hand, overlapped with previously described C-kit+ CD45- cardiac stem cells. Primary monolayer-cultured cells retained expression of SSEAs while the cardiomyogenic specification in the SSEA-4+ CD34- population was lost. In tissue sections, SSEA-4+ cells could be identified both within and outside the myocardium. Within the myocardium, some SSEA-4+ cells coexpressed cardiomyogenic markers. In conclusion, the results show that the adult human heart expresses SSEAs and that there is a subpopulation of SSEA-4+ CD34- cells that show features of a cardiomyocyte progenitor population. © 2014 S. Karger AG, Basel.
47.	Sandstedt, Mikael, 1990, et al. (author) Intracellular flow cytometry may be combined with good quality and high sensitivity RT-qPCR analysis. 2015 In: Cytometry. Part A : the journal of the International Society for Analytical Cytology. - : Wiley. - 1552-4930. ; 87:12, s. 1079-1089 Journal article (peer-reviewed)abstract Flow cytometry (FCM) has become a well-established method for analysis of both intracellular and cell-surface proteins, while quantitative RT-PCR (RT-qPCR) is used to determine gene expression with high sensitivity and specificity. Combining these two methods would be of great value. The effects of intracellular staining on RNA integrity and RT-qPCR sensitivity and quality have not, however, been fully examined. We, therefore, intended to assess these effects further. Cells from the human lung cancer cell line A549 were fixed, permeabilized and sorted by FCM. Sorted cells were analyzed using RT-qPCR. RNA integrity was determined by RNA quality indicator analysis. A549 cells were then mixed with cells of the mouse cardiomyocyte cell line HL-1. A549 cells were identified by the cell surface marker ABCG2, while HL-1 cells were identified by intracellular cTnT. Cells were sorted and analyzed by RT-qPCR. Finally, cell cultures from human atrial biopsies were used to evaluate the effects of fixation and permeabilization on RT-qPCR analysis of nonimmortalized cells stored prior to analysis by FCM. A large amount of RNA could be extracted even when cells had been fixed and permeabilized. Permeabilization resulted in increased RNA degradation and a moderate decrease in RT-qPCR sensitivity. Gene expression levels were also affected to a moderate extent. Sorted populations from the mixed A549 and HL-1 cell samples showed gene expression patterns that corresponded to FCM data. When samples were stored before FCM sorting, the RT-qPCR analysis could still be performed with high sensitivity and quality. In summary, our results show that intracellular FCM may be performed with only minor impairment of the RT-qPCR sensitivity and quality when analyzing sorted cells; however, these effects should be considered when comparing RT-qPCR data of not fixed samples with those of fixed and permeabilized samples. © 2015 International Society for Advancement of Cytometry.
48.	Sandstedt, Mikael, 1990, et al. (author) Regional transcriptomic profiling reveals immune system enrichment in nonfailing atria as well as all chambers of the failing human heart 2023 In: American Journal of Physiology. Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 325:6, s. H1430-H1445 Journal article (peer-reviewed)abstract The different chambers of the human heart demonstrate regional physiological traits and may be differentially affected during pathologic remodeling, resulting in heart failure. Few previous studies have, however, characterized the different chambers at a transcriptomic level. We therefore conducted whole-tissue RNA sequencing and gene set enrichment analysis of biopsies collected from the four chambers of adult failing (n = 8) and nonfailing (n = 11) human hearts. Atria and ventricles demonstrated distinct transcriptional patterns. Compared to nonfailing ventricles, the transcriptional pattern of nonfailing atria was enriched for a large number of gene sets associated with cardiogenesis, the immune system and bone morphogenetic protein (BMP), transforming growth factor beta (TGF beta), MAPK/JNK and Wnt signaling. Differences between failing and nonfailing hearts were also determined. The transcriptional pattern of failing atria was distinct compared to that of nonfailing atria and enriched for gene sets associated with the innate and adaptive immune system, TGF beta/SMAD signaling, and changes in endothelial, smooth muscle cell and cardiomyocyte physiology. Failing ventricles were also enriched for gene sets associated with the immune system. Based on the transcriptomic patterns, upstream regulators associated with heart failure were identified. These included many immune response factors predicted to be similarly activated for all chambers of failing hearts. In summary, the heart chambers demonstrate distinct transcriptional patterns that differ between failing and nonfailing hearts. Immune system signaling may be a hallmark of all four heart chambers in failing hearts, and could constitute a novel therapeutic target.
49.	Svanborg, Anders, 1770-1812 (author) Micha Latine versus et notis philologicis illustratus. Quem ... præside A. Svanborg, ... pro gradu philosophico Ambrosius Ludovicus Lindahl, stip. Flodin. Ostrogothus. In audit. Gustav. die XVIII april. MDCCCXII ..., P. 6 1812 Doctoral thesis (other academic/artistic)
50.	Synnergren, Jane, et al. (author) Transcriptional sex and regional differences in paired human atrial and ventricular cardiac biopsies collected in vivo 2020 In: Physiological Genomics. - : American Physiological Society. - 1094-8341 .- 1531-2267. ; 52:2, s. 110-120 Journal article (peer-reviewed)abstract Transcriptional studies of the human heart provide insight into physiological and pathophysiological mechanisms, essential for understanding the fundamental mechanisms of normal cardiac function and how they are altered by disease. To improve the understanding of why men and women may respond differently to the same therapeutic treatment it is crucial to learn more about sex-specific transcriptional differences. In this study the transcriptome of right atrium and left ventricle was compared across sex and regional location. Paired biopsies from five male and five female patients undergoing aortic valve replacement or coronary artery bypass grafting were included. Gene expression analysis identified 620 differentially expressed transcripts in atrial and ventricular tissue in men and 471 differentially expressed transcripts in women. In total 339 of these transcripts overlapped across sex but notably, 281 were unique in the male tissue and 162 in the female tissue, displaying marked sex differences in the transcriptional machinery. The transcriptional activity was significantly higher in atrias than in ventricles as 70% of the differentially expressed genes were upregulated in the atrial tissue. Furthermore, pathway- and functional annotation analyses performed on the differentially expressed genes showed enrichment for a more heterogeneous composition of biological processes in atrial compared with the ventricular tissue, and a dominance of differentially expressed genes associated with infection disease was observed. The results reported here provide increased insights about transcriptional differences between the cardiac atrium and ventricle but also reveal transcriptional differences in the human heart that can be attributed to sex.

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