WorldCat Identities

Lindahl, T. (Tomas) 1938-

Works: 36 works in 59 publications in 2 languages and 343 library holdings
Roles: Editor, Author, Thesis advisor, Other
Publication Timeline
Most widely held works by T Lindahl
DNA repair, mutagenesis, and other responses to DNA damage : a subject collection from Cold Spring Harbor perspectives in biology( Book )

1 edition published in 2014 in English and held by 131 WorldCat member libraries worldwide

Genetic instability in cancer( Book )

7 editions published in 1996 in English and held by 117 WorldCat member libraries worldwide

DNA repair and recombination( Book )

13 editions published between 1994 and 1996 in English and held by 35 WorldCat member libraries worldwide

Carcinogenesis and DNA repair( Book )

2 editions published in 1985 in English and held by 16 WorldCat member libraries worldwide

On the structure and stability of nucleic acids in solution by T Lindahl( Book )

4 editions published in 1967 in Swedish and English and held by 11 WorldCat member libraries worldwide

DNA deamination in immunity, virology and cancer : papers of a Discussion Meeting held at the Royal Society on 9 and 10 June 2008 by Royal Society (Great Britain)( Book )

2 editions published in 2009 in English and held by 4 WorldCat member libraries worldwide

DNA repair and recombination : Meeting : Papers( Book )

1 edition published in 1995 in English and held by 1 WorldCat member library worldwide

Instability and decay of the primary structure of DNA by T Lindahl( Book )

1 edition published in 1993 in English and held by 1 WorldCat member library worldwide

Biochemical Foundations of Health and Energy Conservation in Hibernating Free-ranging Subadult Brown Bear Ursus arctos by Karen Gjesing Welinder( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Brown bears (Ursus arctos) hibernate for 5-7 months without eating, drinking, urinating, and defecating at a metabolic rate of only 25% of the summer activity rate. Nonetheless, they emerge healthy and alert in spring. We quantified the biochemical adaptations for hibernation by comparing the proteome, metabolome, and hematological features of blood from hibernating and active free-ranging subadult brown bears with a focus on conservation of health and energy. We found that total plasma protein concentration increased during hibernation, even though the concentrations of most individual plasma proteins decreased, as did the white blood cell types. Strikingly, antimicrobial defense proteins increased in concentration. Central functions in hibernation involving the coagulation response and protease inhibition, as well as lipid transport and metabolism, were upheld by increased levels of very few key or broad specificity proteins. The changes in coagulation factor levels matched the changes in activity measurements. A dramatic 45-fold increase in sex hormone-binding globulin levels during hibernation draws, for the first time, attention to its significant but unknown role in maintaining hibernation physiology. We propose that energy for the costly protein synthesis is reduced by three mechanisms as follows: (i) dehydration, which increases protein concentration without de novo synthesis; (ii) reduced protein degradation rates due to a 6 degrees C reduction in body temperature and decreased protease activity; and (iii) a marked redistribution of energy resources only increasing de novo synthesis of a few key proteins. The comprehensive global data identified novel biochemical strategies for bear adaptations to the extreme condition of hibernation and have implications for our understanding of physiology in general
Effects of the oral, direct factor Xa inhibitor apixaban on routine coagulation assays and anti-FXa assays by A Hillarp( )

1 edition published in 2014 in English and held by 1 WorldCat member library worldwide

Counting the platelets: a robust and sensitive quantification method for thrombus formation by Kjersti Claesson( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Flow chambers are common tools used for studying thrombus formation in vitro. However, the use of such devices is not standardised and there is a large diversity among the flow chamber systems currently used, and also in the methods used for quantifying the thrombus development. It was the study objective to evaluate a new method for analysis and quantification of platelet thrombus formation that can facilitate comparison of results between research groups. Whole blood was drawn over a collagen patch in commercial Ibid or in-house constructed PDMS flow chambers. Five percent of the platelets were fluorescently labelled and z-stack time-lapse images were captured during thrombus formation. Images were processed in a Python script in which the number of platelets and their respective x-, y- and z-positions were obtained. For comparison with existing methods the platelets were also labelled and quantified using fluorescence intensity and thrombus volume estimations by confocal microscopy. The presented method was found less sensitive to microscope and image adjustments and provides more details on thrombus development dynamics than the methods for measuring fluorescence intensity and thrombus volume estimation. The platelet count method produced comparable results with commercial and PDMS flow chambers, and could also obtain information regarding the stability of each detected platelet in the thrombus. In conclusion, quantification of thrombus formation by platelet count is a sensitive and robust method that enables measurement of platelet accumulation and platelet stability in an absolute scale that could be used for comparisons between research groups
DNA repair enzymes by T Lindahl( )

1 edition published in 1982 in English and held by 1 WorldCat member library worldwide

Next Generation Sequencing Analysis of Human Platelet PolyA plus mRNAs and rRNA-Depleted Total RNA by Antheia Kissopoulou( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Background: Platelets are small anucleate cells circulating in the blood vessels where they play a key role in hemostasis and thrombosis. Here, we compared platelet RNA-Seq results obtained from polyA+ mRNA and rRNA-depleted total RNA. Materials and Methods: We used purified, CD45 depleted, human blood platelets collected by apheresis from three male and one female healthy blood donors. The Illumina HiSeq 2000 platform was employed to sequence cDNA converted either from oligo(dT) isolated polyA+ RNA or from rRNA-depleted total RNA. The reads were aligned to the GRCh37 reference assembly with the TopHat/Cufflinks alignment package using Ensembl annotations. A de novo assembly of the platelet transcriptome using the Trinity software package and RSEM was also performed. The bioinformatic tools HTSeq and DESeq from Bioconductor were employed for further statistical analyses of read counts. Results: Consistent with previous findings our data suggests that mitochondrially expressed genes comprise a substantial fraction of the platelet transcriptome. We also identified high transcript levels for protein coding genes related to the cytoskeleton function, chemokine signaling, cell adhesion, aggregation, as well as receptor interaction between cells. Certain transcripts were particularly abundant in platelets compared with other cell and tissue types represented by RNA-Seq data from the Illumina Human Body Map 2.0 project. Irrespective of the different library preparation and sequencing protocols, there was good agreement between samples from the 4 individuals. Eighteen differentially expressed genes were identified in the two sexes at 10% false discovery rate using DESeq. Conclusion: The present data suggests that platelets may have a unique transcriptome profile characterized by a relative over-expression of mitochondrially encoded genes and also of genomic transcripts related to the cytoskeleton function, chemokine signaling and surface components compared with other cell and tissue types. The in vivo functional significance of the non-mitochondrial transcripts remains to be shown
Platelet activation via PAR4 is involved in the initiation of thrombin generation and in clot elasticity development by Karin Vretenbrant( )

1 edition published in 2007 in English and held by 1 WorldCat member library worldwide

Thrombin is a pivotal enzyme formed in the coagulation cascade and an important and potent platelet activator. The two protease-activated thrombin receptors on human platelets are denoted PARI and PAR4. The physiological relevance of PAR4 is still unclear, as both aggregation and secretion can be accomplished by PAR1 activation alone. In the present study we have investigated the role of PARS in platelet activation, blood coagulation, clot elasticity and fibrinolysis. Flow cytometry, free oscillation rheometry and thrombin generation measurements were used to analyze blood or platelet-rich plasma from healthy individuals. Maximum PAR1 activation with the peptide SFLLRN gave fewer fibrinogen-binding platelets with lower mean fluorescent intensity than maximum PAR4 activation with AYPGKF. Inhibition of any of the receptors prolonged clotting times. However, PAR1 is more important for fibrinolysis, inhibition of this receptor prolonged all the steps in the fibrinolytic process. Clot elasticity decreased significantly when the PAR4 receptor was inhibited. In the thrombin generation measurements, PAR4 inhibition delayed the thrombin generation start and peak, but did not affect the total amount of thrombin generated. PAR1 inhibition had no significant impact on thrombin generation. We found that PAR4 is most likely activated by low concentrations of thrombin during the initial phase of thrombin generation and is of importance to the clotting time. Furthermore, we suggest that the PAR4 receptor may have a physiological role in the stabilisation of the coagulum
Effects of inhibition of P2Y 1 and P2Y 12 on whole blood clotting, coagulum elasticity and fibrinolysis resistance studied with free oscillation rheometry by Sofia Ramström( )

1 edition published in 2003 in English and held by 1 WorldCat member library worldwide

Introduction : In vivo, initial platelet activation is likely caused by platelet contacts with collagen in the subendothelium or from the small amounts of thrombin formed by the tissue factor/factor VIIa complex. Our aim was to study the coagulative role of ADP released by the platelets after activation with strong stimuli such as collagen and/or thrombin, and the relative importance of the platelet ADP receptors P2Y 1 and P2Y 12 . Materials and methods : We used 10 Hz free oscillation rheometry to measure clotting time, clot elasticity and fibrinolysis resistance of non-anticoagulated whole blood. The platelets were activated with a collagen-related peptide (CRP), with the PAR1 thrombin receptor activating peptide TRAP-6 or by thrombin, the latter generated by small amounts of thromboplastin. To inhibit the platelet ADP receptors, we used the P2Y 1 antagonist MRS2179 and the P2Y 12 antagonist AR-C69931MX. Results : Both antagonists significantly retarded the clotting induced by CRP. The effects were most pronounced with AR-C69931MX. For TRAP-6, the same trend was seen, but the retardation was only significant with AR-C69931MX. Clotting induced by small amounts of thromboplastin was not affected by any ADP-receptor antagonist. Addition of both antagonists did not change the results as compared to samples with AR-C69931MX alone. Nor did the antagonists, one at a time or in concert, effect fibrinolysis or the elastic properties of the clot. Conclusion : We conclude that ADP-receptor inhibition prolongs the clotting time for whole blood activated by CRP, but that it does not affect the properties of the subsequently formed coagulum
Surface plasmon resonance detection of blood coagulation and platelet adhesion under venous and arterial shear conditions by Kenny Hansson( )

1 edition published in 2007 in English and held by 1 WorldCat member library worldwide

A surface plasmon resonance (SPR) based flow chamber device was designed for real time detection of blood coagulation and platelet adhesion in platelet rich plasma (PRP) and whole blood. The system allowed the detection of surface interactions throughout the 6 mm length of the flow chamber. After deposition of thromboplastin onto a section of the sensor surface near the inlet of the flow chamber, coagulation was detected downstream of this position corresponding to a SPR signal of 7 to 8 mRIU (7 to 8 ng/mm2). A nonmodified control surface induced coagulation 3.5 times slower. Platelet adhesion to gold and fibrinogen coated surfaces in the magnitude of 1.25 and 1.66 mRIU was also shown with platelets in buffer, respectively. SPR responses obtained with PRP and whole blood on surfaces that were methylated or coated with von Willebrand factor (vWF), fibrinogen, or collagen, coincided well with platelet adhesion as observed with fluorescence microscopy in parallel experiments. The present SPR detection equipped flow chamber system is a promising tool for studies on coagulation events and blood cell adhesion under physiological flow conditions, and allows monitoring of short-range surface processes in whole blood. © 2007 Elsevier B.V. All rights reserved
The Toll-like receptor 2/1 (TLR2/1) complex initiates human platelet activation via the src/Syk/LAT/PLC gamma 2 signalling cascade by Knut Fälker( )

1 edition published in 2014 in English and held by 1 WorldCat member library worldwide

The specific TLR2/1 complex activator Pam3CSK4 has been shown to provoke prominent activation and aggregation of human non-nucleated platelets. As Pam3CSK4-evoked platelet activation does not employ the major signalling pathway established in nucleated immune cells, we investigated if the TLR2/1 complex on platelets may initiate signalling pathways known to be induced by physiological agonists such as collagen via GPVI or thrombin via PARs. We found that triggering TLR2/1 complex-signalling with Pam3CSK4, in common with that induced via GPVI, and in contrast to that provoked by PARS, involves tyrosine phosphorylation of the adaptor protein LAT as well as of PLC gamma 2 in a src- and Syk-dependent manner. In this respect, we provide evidence that Pam3CSK4 does not cross-activate GPVI. Further, by the use of platelets from a Glanzmanns thrombasthenia patient lacking beta(3), in contrast to findings in nucleated immune cells, we show that the initiation of platelet activation by Pam3CSK4 does not involve integrin beta(3) signalling; whereas the latter, subsequent to intermediate TXA2 synthesis and signalling, was found to be indispensable for proper dense granule secretion and full platelet aggregation. Together, our findings reveal that triggering the TLR2/1 complex with Pam3CSK4 initiates human platelet activation by engaging tyrosine kinases of the src family and Syk, the adaptor protein LAT, as well as the key mediator PLC gamma 2
Whole blood coagulation on protein adsorption-resistant PEG and peptide functionalised PEG-coated titanium surfaces by Kenny Hansson( )

1 edition published in 2005 in English and held by 1 WorldCat member library worldwide

The aim of this study was to investigate whole blood coagulation on low blood plasma protein adsorbing surfaces. For this purpose, the polycationic graft copolymer poly(L-lysine)-g-poly(ethylene glycol) (PLL-g-PEG), PLL-g-PEG grafted with a cell adhesive peptide containing the amino acid sequence -Arg-Gly-Asp- (RGD), and PLL-g-PEG with a control peptide -Arg-Asp-Gly- (RDG) were adsorbed onto titanium (oxide), forming stable monomolecular adlayers through electrostatic attraction. Free oscillation rheometry and complementary techniques were used to measure the coagulation time (CT) and other interactions of the surfaces with native whole blood, recalcified platelet-rich plasma (PRP), and recalcified citrated platelet-free plasma (PFP). The results show that the uncoated titanium surfaces (reference) activated platelets and quickly triggered the coagulation cascade via the intrinsic pathway, whereas the PLL-g-PEG surfaces displayed a prolonged CT, approximately 2-3 times longer compared to uncoated titanium. We hypothesise that blood coagulates outside the vascular system independent of low protein adsorption to or activation by surfaces, due to the absence of an active down-regulation of procoagulative processes by the vascular endothelium
A novel prothrombin time method to measure all non-vitamin K-dependent oral anticoagulants (NOACs) by T Lindahl( )

1 edition published in 2017 in English and held by 1 WorldCat member library worldwide

Background: There is a clinical need for point-of-care (POC) methods for non-vitamin K-dependent oral anticoagulants (NOACs). We modified a routine POC procedure: Zafena's Simple Simon"!PT-INR, a room-temperature, wet-chemistry prothrombin time method of the Owren-type. Methods: To either increase or decrease NOAC interference, two assay variants were devised by replacing the standard 10 æL end-to-end capillary used to add the citrated plasma sample to 200 æL of prothrombin time (PT) reagent by either a 20 æL or a 5 æL capillary. All assay variants were calibrated to show correct PT results in plasma samples from healthy and warfarin-treated persons. Results: For plasmas spiked with dabigatran, apixaban, or rivaroxaban, the 20 æL variant showed markedly higher PT results than the 5 æL. The effects were even more pronounced at room temperature than at +37 °C. In plasmas from patients treated with NOACs (n = 30 for each) there was a strong correlation between the PT results and the concentration of NOACs as determined by the central hospital laboratory. For the 20 æL variant the PT response of linear correlation coefficient averaged 0.90. The PT range was INR 1.1-2.1 for dabigatran and apixaban, and INR 1.1-5.0 for rivaroxaban. Using an INR ratio between the 20 æL and 5 æL variants (PTr20/5) made the NOAC assay more robust and independent of the patient sample INR value in the absence of NOAC. Detection limits were 80 æg/L for apixaban, 60 æg/L for dabigatran, and 20 æg/L for rivaroxaban. Conclusions: A wet-chemistry POC PT procedure was modified to measure the concentrations of three NOACs using a single reagent
Comparison of prothrombin time (INR) results and main characteristics of patients on warfarin treatment in primary health care centers and anticoagulation clinics by Kerstin Arbring( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Background Oral anticoagulant therapy is used to prevent thrombosis in patients with atrial fibrillation (AF), venous thrombosis and prosthetic heart valves. The introduction of new therapies emphasizes the need to discern the best practice for the patients remaining on warfarin treatment. This study compares patient characteristics and therapeutic control in two settings managing warfarin treatment: Swedish primary health care centers (PHCC) and specialized anticoagulation clinics (ACC). Methods Prothrombin time (PT) test results reported as International Normalized Ratio (INR) were collected for five consecutive days from patients on warfarin treatment; 564 PHCC and 927 ACC patients. Therapeutic control was calculated as PT test results in relation to intended therapeutic range (TR). Mann-Whitney Rank Sum Test and Chi 2 test were used for statistical comparisons. Results The PHCC patients were older than the ACC patients, 76 v. 70 years (p<0.01) with a predominance of men in both groups. The reasons for treating differed between the groups. Seventy-two percent of PHCC patients and 66% of ACC patients had a PT-INR within the intended TR (p<0.05). Men generally had better results than women (72% v. 63%, p<0.001) and particularly in the PHCC group v. the ACC group (78% v. 69%, p<0.01). PT-INR above intended TR was significantly more common in the ACC setting, (p<0.05), for women overall (p<0.01), for women in the PHCC setting, and for ACC men (p<0.05). Conclusions In this study both settings achieved good therapeutic control of warfarin treatment with a minor advantage for PHCC over ACC, and better results for men, especially in the PHCC setting. As patient characteristics differ between the PHCC and ACC, it is important to conduct further randomized studies to discern the best practice locally for warfarin management also after the introduction of new drugs
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Audience level: 0.68 (from 0.62 for DNA repair ... to 0.97 for Effects of ...)

DNA repair and recombination
Alternative Names
Lindahl, T. 1938-

Lindahl, Thomas

Lindahl, Tomas 1938-

Thomas Lindahl

Tomas Lindahl

Tomas Lindahl ahli biologi asal Britania Raya

Tomas Lindahl biòleg suec

Tomas Lindahl biologiste, généticien et chimiste suédois

Tomas Lindahl médico, y biólogo sueco

Tomas Lindahl Nobel prize winning Swedish biologist

Tomas Lindahl schwedischer Krebsforscher

Tomas Lindahl schwedischer Krebsforscher und Nobelpreisträger

Tomas Lindahl scienziato svedese

Tomas Lindahl svéd rákkutató

Tomas Lindahl Swedish biologist

Tomas Lindahl Zweeds bioloog

Tomas Robert Lindahl

Линдал, Томас

Линдаль, Томас

Томас Линдал

Томас Линдал шведски биолог

Томас Ліндаль

תומאס לינדל

توماس ليندال

توماس لیندال

ٹامس لینڈال

ٹامس لینڈل

टॉमस लिंडाल

ਟੌਮਸ ਲਿੰਡਾਹਲ

தோமசு லின்டால்

ತೋಮಸ್ ಲಿನ್ದಾಲ್

ටූමස් ලින්ඩෝල්

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