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Institution

University of Turku

EducationTurku, Finland
About: University of Turku is a education organization based out in Turku, Finland. It is known for research contribution in the topics: Population & Galaxy. The organization has 16296 authors who have published 45124 publications receiving 1505428 citations. The organization is also known as: Turun yliopisto & Åbo universitet.


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Journal ArticleDOI
TL;DR: The results show that although approximately 50% of episodes of the common cold were caused by rhinoviruses, the etiology can vary depending on the epidemiological situation with regard to circulating viruses.
Abstract: Two hundred young adults with common colds were studied during a 10-month period. Virus culture, antigen detection, PCR, and serology with paired samples were used to identify the infection. Viral etiology was established for 138 of the 200 patients (69%). Rhinoviruses were detected in 105 patients, coronavirus OC43 or 229E infection was detected in 17, influenza A or B virus was detected in 12, and single infections with parainfluenza virus, respiratory syncytial virus, adenovirus, and enterovirus were found in 14 patients. Evidence for bacterial infection was found in seven patients. Four patients had a rise in antibodies against Chlamydia pneumoniae, one had a rise in antibodies against Haemophilus influenzae, one had a rise in antibodies against Streptococcus pneumoniae, and one had immunoglobulin M antibodies against Mycoplasma pneumoniae. The results show that although approximately 50% of episodes of the common cold were caused by rhinoviruses, the etiology can vary depending on the epidemiological situation with regard to circulating viruses. Bacterial infections were rare, supporting the concept that the common cold is almost exclusively a viral disease.

720 citations

Journal ArticleDOI
TL;DR: Three lines of evidence are presented that support the notion that, as healthy infants approach the toddler stage, their microbiomes become healthier and more stable, whereas, children who are destined for autoimmunity develop a microbiome that is less diverse and stable.
Abstract: Several studies have shown that gut bacteria have a role in diabetes in murine models. Specific bacteria have been correlated with the onset of diabetes in a rat model. However, it is unknown whether human intestinal microbes have a role in the development of autoimmunity that often leads to type 1 diabetes (T1D), an autoimmune disorder in which insulin-secreting pancreatic islet cells are destroyed. High-throughput, culture-independent approaches identified bacteria that correlate with the development of T1D-associated autoimmunity in young children who are at high genetic risk for this disorder. The level of bacterial diversity diminishes overtime in these autoimmune subjects relative to that of age-matched, genotype-matched, nonautoimmune individuals. A single species, Bacteroides ovatus, comprised nearly 24% of the total increase in the phylum Bacteroidetes in cases compared with controls. Conversely, another species in controls, represented by the human firmicute strain CO19, represented nearly 20% of the increase in Firmicutes compared with cases overtime. Three lines of evidence are presented that support the notion that, as healthy infants approach the toddler stage, their microbiomes become healthier and more stable, whereas, children who are destined for autoimmunity develop a microbiome that is less diverse and stable. Hence, the autoimmune microbiome for T1D may be distinctly different from that found in healthy children. These data also suggest bacterial markers for the early diagnosis of T1D. In addition, bacteria that negatively correlated with the autoimmune state may prove to be useful in the prevention of autoimmunity development in high-risk children.

719 citations

Journal ArticleDOI
Liisa M. Pelttari1, Sofia Khan1, Mikko Vuorela2, Johanna I. Kiiski1, Sara Vilske1, Viivi Nevanlinna1, Salla Ranta1, Johanna Schleutker3, Johanna Schleutker4, Johanna Schleutker5, Robert Winqvist2, Anne Kallioniemi5, Thilo Dörk6, Natalia Bogdanova6, Jonine Figueroa, Paul D.P. Pharoah7, Marjanka K. Schmidt8, Alison M. Dunning7, Montserrat Garcia-Closas9, Manjeet K. Bolla7, Joe Dennis7, Kyriaki Michailidou7, Qin Wang7, John L. Hopper10, Melissa C. Southey10, Efraim H. Rosenberg8, Peter A. Fasching11, Peter A. Fasching12, Matthias W. Beckmann11, Julian Peto13, Isabel dos-Santos-Silva13, Elinor J. Sawyer14, Ian Tomlinson15, Barbara Burwinkel16, Barbara Burwinkel17, Harald Surowy17, Harald Surowy16, Pascal Guénel18, Thérèse Truong18, Stig E. Bojesen19, Stig E. Bojesen20, Børge G. Nordestgaard19, Børge G. Nordestgaard20, Javier Benitez, Anna González-Neira, Susan L. Neuhausen21, Hoda Anton-Culver22, Hermann Brenner17, Volker Arndt17, Alfons Meindl23, Rita K. Schmutzler24, Hiltrud Brauch25, Hiltrud Brauch26, Hiltrud Brauch17, Thomas Brüning27, Annika Lindblom28, Sara Margolin28, Arto Mannermaa29, Jaana M. Hartikainen29, Georgia Chenevix-Trench30, kConFab30, kConFab10, Aocs Investigators31, Laurien Van Dyck31, Hilde Janssen17, Hilde Janssen32, Jenny Chang-Claude17, Anja Rudolph, Paolo Radice, Paolo Peterlongo33, Emily Hallberg33, Janet E. Olson34, Janet E. Olson10, Graham G. Giles34, Graham G. Giles10, Roger L. Milne35, Christopher A. Haiman35, Fredrick Schumacher36, Jacques Simard36, Martine Dumont37, Martine Dumont38, Vessela N. Kristensen37, Vessela N. Kristensen38, Anne Lise Børresen-Dale39, Wei Zheng39, Alicia Beeghly-Fadiel40, Mervi Grip41, Mervi Grip42, Irene L. Andrulis41, Gord Glendon43, Peter Devilee44, Caroline Seynaeve44, Maartje J. Hooning45, Margriet Collée46, Angela Cox46, Simon S. Cross7, Mitul Shah7, Robert Luben17, Ute Hamann17, Ute Hamann47, Diana Torres48, Anna Jakubowska48, Jan Lubinski33, Fergus J. Couch, Drakoulis Yannoukakos9, Nick Orr9, Anthony J. Swerdlow28, Hatef Darabi28, Jingmei Li28, Kamila Czene28, Per Hall7, Douglas F. Easton1, Johanna Mattson1, Carl Blomqvist1, Kristiina Aittomäki1, Heli Nevanlinna 
05 May 2016-PLOS ONE
TL;DR: It is suggested that loss-of-function mutations in RAD 51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.
Abstract: Common variation on 14q24.1, close to RAD51B, has been associated with breast cancer: rs999737 and rs2588809 with the risk of female breast cancer and rs1314913 with the risk of male breast cancer. The aim of this study was to investigate the role of RAD51B variants in breast cancer predisposition, particularly in the context of familial breast cancer in Finland. We sequenced the coding region of RAD51B in 168 Finnish breast cancer patients from the Helsinki region for identification of possible recurrent founder mutations. In addition, we studied the known rs999737, rs2588809, and rs1314913 SNPs and RAD51B haplotypes in 44,791 breast cancer cases and 43,583 controls from 40 studies participating in the Breast Cancer Association Consortium (BCAC) that were genotyped on a custom chip (iCOGS). We identified one putatively pathogenic missense mutation c.541C>T among the Finnish cancer patients and subsequently genotyped the mutation in additional breast cancer cases (n = 5259) and population controls (n = 3586) from Finland and Belarus. No significant association with breast cancer risk was seen in the meta-analysis of the Finnish datasets or in the large BCAC dataset. The association with previously identified risk variants rs999737, rs2588809, and rs1314913 was replicated among all breast cancer cases and also among familial cases in the BCAC dataset. The most significant association was observed for the haplotype carrying the risk-alleles of all the three SNPs both among all cases (odds ratio (OR): 1.15, 95% confidence interval (CI): 1.11-1.19, P = 8.88 x 10-16) and among familial cases (OR: 1.24, 95% CI: 1.16-1.32, P = 6.19 x 10-11), compared to the haplotype with the respective protective alleles. Our results suggest that loss-of-function mutations in RAD51B are rare, but common variation at the RAD51B region is significantly associated with familial breast cancer risk.

715 citations

Journal ArticleDOI
TL;DR: The basis of photosynthetic acclimation and its optical signals is presented, the physical and physiological basis of ChlF is introduced from the molecular to the leaf level and beyond, and PAM and SIF methodology are introduced.
Abstract: subcellular levels. ChlF is now measurable from remote sensing platforms. This provides a new optical means to track photosynthesis and gross primary productivity of terrestrial ecosystems. Importantly, the spatiotemporal and methodological context of the new applications is dramatically different compared with most of the available ChlF literature, which raises a number of important considerations. Although we have a good mechanistic understanding of the processes that control the ChlF signal over the short term, the seasonal link between ChlF and photosynthesis remains obscure. Additionally, while the current understanding of in vivo ChlF is based on pulse amplitude-modulated (PAM) measurements, remote sensing applications are based on the measurement of the passive solar-induced chlorophyll fluorescence (SIF), which entails important differences and new challenges that remain to be solved. In this review we introduce and revisit the physical, physiological, and methodological factors that control the leaf-level ChlF signal in the context of the new remote sensing applications. Specifically, we present the basis of photosynthetic acclimation and its optical signals, we introduce the physical and physiological basis of ChlF from the molecular to the leaf level and beyond, and we introduce and compare PAM and SIF methodology. Finally, we evaluate and identify the challenges that still remain to be answered in order to consolidate our mechanistic understanding of the remotely sensed SIF signal.

714 citations

Journal Article
TL;DR: Cognitive recovery processes seem to be more demanding in partial sleep restriction than in total SD, and studies on its effects on more demanding cognitive functions are lacking.
Abstract: Today, prolonged wakefulness is a widespread phenomenon. Nevertheless, in the field of sleep and wakefulness, several unanswered questions remain. Prolonged wakefulness can be due to acute total sleep deprivation (SD) or to chronic partial sleep restriction. Although the latter is more common in everyday life, the effects of total SD have been examined more thoroughly. Both total and partial SD induce adverse changes in cognitive performance. First and foremost, total SD impairs attention and working memory, but it also affects other functions, such as long-term memory and decision-making. Partial SD is found to influence attention, especially vigilance. Studies on its effects on more demanding cognitive functions are lacking. Coping with SD depends on several factors, especially aging and gender. Also interindividual differences in responses are substantial. In addition to coping with SD, recovering from it also deserves attention. Cognitive recovery processes, although insufficiently studied, seem to be more demanding in partial sleep restriction than in total SD.

704 citations


Authors

Showing all 16461 results

NameH-indexPapersCitations
Kari Alitalo174817114231
Mika Kivimäki1661515141468
Jaakko Kaprio1631532126320
Veikko Salomaa162843135046
Markus W. Büchler148154593574
Eugene C. Butcher14644672849
Steven Williams144137586712
Terho Lehtimäki1421304106981
Olli T. Raitakari1421232103487
Pim Cuijpers13698269370
Jeroen J. Bax132130674992
Sten Orrenius13044757445
Aarno Palotie12971189975
Stefan W. Hell12757765937
Carlos López-Otín12649483933
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023102
2022290
20212,673
20202,688
20192,407
20182,189