FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2202291808> ?p ?o ?g. }

• W2202291808 abstract "The aims of this study were to investigate the morbidity associated with tick-borne encephalitis (TBE) in the acute stage and at long-term follow-up, to identify the possible host risk factors for development of clinical TBE with special reference to the role of the genetic polymorphism, and to investigate neurochemical changes in the brain induced by TBE virus (TBEV) and their possible role on severity of TBE with special reference to endogenous kynurenic acid (KYNA). Paper I: Of 250 consecutively admitted patients with central nervous system (CNS) infections treated during a 1-year period, all 133 patients with TBE participated in the prospective followup study. TBE presented as mild (meningeal), moderate or severe (encephalitic) forms in 43.6%, 43.6% and 12.8%, respectively. Paralytic disease was observed in 3.8%, and cranial nerve injury in 5.3% of the TBE patients. Permanent CNS dysfunction after 1 year was found in 30.8% of patients; in 8.5% of all TBE cases, severe disabilities required adjustment of daily activities. Cognitive CNS dysfunction was the dominant symptom in patients with more pronounced sequelae. A higher risk for incomplete recovery was seen for the encephalitic form of TBE (odds ratio (OR), 4.066; 95% confidence interval (CI), 1.848–8.947). Papers II and III: A prospectively collected material from patients with TBE (n=129), aseptic meningoencephalitis of non-TBEV aetiology (n=79) and healthy TBEV-naive Lithuanians (n=135) were used in studies on chemokine receptor 5 (CCR5) and Toll-like receptor 3 (TLR3) rs3775291 gene polymorphisms. In addition, children TBE cohort (n=117) and a cohort of adults with severe TBE (n=103) were recruited in Paper III. The prevalence of CCR5∆32 homozygotes was higher among the adults with TBE (2.3%), among children with TBE (2.5%), among adults with severe TBE (1.9%), and in the overall cohort of TBE patients (2.3%) than in controls (0%) (p<0.05). Hence, the CCR5 polymorphism was identified as a significant risk factor for clinical TBE. The CCR5Δ32 allele prevalence was higher in the combined children and adult TBE cohort compared with TBEV-naive individuals, and suggested CCR5Δ32 allele being a risk factor for clinical TBEV infection (OR 1.672; 95% CI 1.005–2.782). The nonfunctional homozygous TLR3 genotype was less prevalent among the combined TBE cohort (11.5%) than among controls (19.9%) (p = 0.025), but did not differ between children TBE and controls. The genotype and allele prevalence of CCR5 and TLR3 did not differ in children nor adult TBE cohorts stratified by disease severity. In adults with severe TBE, homozygous functional TLR3 genotype and wt allele were less prevalent than in adults with the whole disease severity spectrum (44.4% vs 59.8% p = 0.022 and 65.2% vs 76.4% p = 0.009; respectively). Paper IV has shown that cerebrospinal fluid (CSF) KYNA levels were considerably higher in patients with TBE recruited from Paper I (5.3 nmol L) than in control subjects (0.99 nmol L) and increased (p<0.05) with severity of TBE. Conclusion: TBE is the main CNS infection in adults in Lithuania, causing a considerable morbidity with long-lasting sequelae in one-third of patients. Cognitive CNS dysfunction dominates and is the major cause of long-lasting impairment of the quality of life. High levels of KYNA in CSF of TBE patients serve as a marker of severity of TBE. Host genetic polymorphism plays a role in the development of clinical TBE and may even be linked to the disease severity." @default.
• W2202291808 created "2016-06-24" @default.
• W2202291808 creator A5077729859 @default.
• W2202291808 date "2015-11-25" @default.
• W2202291808 modified "2023-10-18" @default.
• W2202291808 title "Tick-borne encephalitis : clinical and pathogenetic aspects" @default.
• W2202291808 cites W128871708 @default.
• W2202291808 cites W141632973 @default.
• W2202291808 cites W1487888547 @default.
• W2202291808 cites W1511903547 @default.
• W2202291808 cites W1514418800 @default.
• W2202291808 cites W1517104951 @default.
• W2202291808 cites W1539680845 @default.
• W2202291808 cites W1542254057 @default.
• W2202291808 cites W1542435349 @default.
• W2202291808 cites W1547937746 @default.
• W2202291808 cites W1567194265 @default.
• W2202291808 cites W1590810109 @default.
• W2202291808 cites W1598356970 @default.
• W2202291808 cites W1607830889 @default.
• W2202291808 cites W163671050 @default.
• W2202291808 cites W166663645 @default.
• W2202291808 cites W1728598174 @default.
• W2202291808 cites W1816614902 @default.
• W2202291808 cites W1833773432 @default.
• W2202291808 cites W1902979788 @default.
• W2202291808 cites W1915162580 @default.
• W2202291808 cites W1954842254 @default.
• W2202291808 cites W1962281618 @default.
• W2202291808 cites W1964256043 @default.
• W2202291808 cites W1964827231 @default.
• W2202291808 cites W1965244206 @default.
• W2202291808 cites W1965477305 @default.
• W2202291808 cites W1965869838 @default.
• W2202291808 cites W1966483902 @default.
• W2202291808 cites W1966928504 @default.
• W2202291808 cites W1969884659 @default.
• W2202291808 cites W1971033371 @default.
• W2202291808 cites W1971486004 @default.
• W2202291808 cites W1972307436 @default.
• W2202291808 cites W1977059937 @default.
• W2202291808 cites W1977131515 @default.
• W2202291808 cites W1977949506 @default.
• W2202291808 cites W1978605261 @default.
• W2202291808 cites W1980409836 @default.
• W2202291808 cites W1980626076 @default.
• W2202291808 cites W1981950171 @default.
• W2202291808 cites W1983153012 @default.
• W2202291808 cites W1983396822 @default.
• W2202291808 cites W1983516658 @default.
• W2202291808 cites W1984143185 @default.
• W2202291808 cites W1984390661 @default.
• W2202291808 cites W1984527935 @default.
• W2202291808 cites W1984584304 @default.
• W2202291808 cites W1984760454 @default.
• W2202291808 cites W1984840308 @default.
• W2202291808 cites W1986994060 @default.
• W2202291808 cites W1988088217 @default.
• W2202291808 cites W1993183064 @default.
• W2202291808 cites W1993267851 @default.
• W2202291808 cites W1993272811 @default.
• W2202291808 cites W1997049965 @default.
• W2202291808 cites W1997191388 @default.
• W2202291808 cites W1997460396 @default.
• W2202291808 cites W1998494157 @default.
• W2202291808 cites W1998970373 @default.
• W2202291808 cites W2000065187 @default.
• W2202291808 cites W2000189636 @default.
• W2202291808 cites W2002139502 @default.
• W2202291808 cites W2002159023 @default.
• W2202291808 cites W2003583308 @default.
• W2202291808 cites W2003746661 @default.
• W2202291808 cites W2004724079 @default.
• W2202291808 cites W2006669012 @default.
• W2202291808 cites W2007510392 @default.
• W2202291808 cites W2009998721 @default.
• W2202291808 cites W2010480258 @default.
• W2202291808 cites W2010875542 @default.
• W2202291808 cites W2013015180 @default.
• W2202291808 cites W2014001082 @default.
• W2202291808 cites W2015004157 @default.
• W2202291808 cites W2015196668 @default.
• W2202291808 cites W2015535769 @default.
• W2202291808 cites W2015773173 @default.
• W2202291808 cites W2016366635 @default.
• W2202291808 cites W2016561811 @default.
• W2202291808 cites W2017579008 @default.
• W2202291808 cites W2019899620 @default.
• W2202291808 cites W2020394679 @default.
• W2202291808 cites W2020735656 @default.
• W2202291808 cites W2021698390 @default.
• W2202291808 cites W2027855919 @default.
• W2202291808 cites W2028117406 @default.
• W2202291808 cites W2029653373 @default.
• W2202291808 cites W2029764494 @default.
• W2202291808 cites W2030481779 @default.
• W2202291808 cites W2030698391 @default.
• W2202291808 cites W2031062821 @default.
• W2202291808 cites W2031354214 @default.
• W2202291808 cites W2031466284 @default.

• next