26.9.2005

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Molecular epidemiology of tick-borne encephalitis virus in Ixodes ricinus ticks in Lithuania.

Han, X. Q., A. Juceviciene, N. Y. Uzcategui, H. Brummer-Korvenkontio, M. Zygutiene, A. Jääskeläinen, P. Leinikki and O. Vapalahti.

Journal of Medical Virology. 2005; 77(2): 249-256.

In Lithuania, 171-645 serologically confirmed cases of tick-borne encephalitis occurred annually [Mickiene et al. (2001): Eur J Clin Microbiol Infect Dis 20:886-888] in 1993-1999, and the tick-borne encephalitis virus (TBEV) seroprevalence in the general population was found previously to be 3.0% [Juceviciene et al. (2002):J Clin Virol 25:23-27]. To assess the risk for TBEV virus infection in Lithuania and to characterize the agent a panel of 3,234 ticks combined into 436 pools [Juceviciene et al., 2005] were tested for presence of TBEV RNA by a nested RT-PCR targeting at the NS5 gene. Six pools were confirmed positive and the prevalence of the infected ticks was 0.2% (if one tick per pool [Juceviciene et al., 2005] was considered positive) and the proportion of positive tick pools was 1.4%. The prevalence of the infected ticks in the Panevezys, Siauliai, and Radviliskis regions (in central Lithuania) was 0.1%, 0.4%, and 1.7% corresponding with a higher TBE disease burden in these regions. The 252-nucleotide NS5-region amplicons, and a longer sequence (737 nucleotides) obtained from one sample from the PrM-E gene region, were sequenced. Phylogenetic analysis of the latter showed that all western type TBEV PrM-E sequences, including the Lithuanian strains, were monophyletic, showed no clustering and had very little variation. The NS5 sequences, although identical within one locality, did not show any mutations common to strains from the two Lithuanian regions, nor could any geographical clustering be found among western type TBEV strains from other areas.

Properties of hemagglutination by Prevotella melaninogenica.

Haraldsson, G., J. H. Meurman, E. Kononen and W. P. Holbrook.

Anaerobe. 2005; 11(5): 285-289.

Although Prevotella melaninogenica belongs to the commensal oral microbiota, some strains possess putative virulence factors. For example, we have previously described fimbriated, hemagglutinating strains of P. melaninogenica, isolated from patients with periodontal disease. The aim of this investigation was to compare some chemical and physical properties of hemagglutination (HA) of P. melaninogenica with those of other pigmented gram-negative anaerobes. HA of 13 P. melaninogenica strains proved to be considerably weaker than that of the major periodontal pathogen, Porphyromonas gingivalis. Vigorous shaking reduced HA of shaken cells but the shaken supernatant had the same hemagglutinating activity as non-shaken cells. The hemagglutinating agent on P. melaninogenica seemed to be a protein, which can be separated from the cell and binds to lactose-, galactose-, and raffinose-containing carbohydrates on the erythrocytes. Adherence to epithelial cells did not differ significantly between the hemagglutinating and non-hemagglutinating strains of P. melaninogenica. Although P. melaninogenica is able to agglutinate erythrocytes, this potential virulence factor is of a considerably lower magnitude than that of major periodontal pathogens. (c) 2005 Elsevier Ltd. All rights reserved.

Genetic diversity of JC virus in the Saami and the Finns: Implications for their population history.

Ikegaya, H., H. Y. Zheng, P. J. Saukko, L. Varesmaa-Korhonen, T. Hovi, T. Vesikari, H. Suganami, T. Takasaka, C. Sugimoto, Y. Ohasi, T. Kitamura and Y. Yogo.

American Journal of Physical Anthropology. 2005; 128(1): 185-193.

The JC virus (XV) genotyping method was used to gain insights into the population history of the Saami and the Finns, both speaking Finno-Ugric languages and living in close geographic proximity. Urine samples from Saami and Finns, collected in northern and southern Finland, respectively, were used to amplify a 610-bp JCV-DNA region containing abundant type-specific mutations. Based on restriction site polymorphisms in the amplified fragments, we classified JCV isolates into one of the three superclusters of JCV, type A, B, or C. All 15 Saami isolates analyzed and 41 of 43 Finnish isolates analyzed were classified as type A, the European type, and two samples from Finns were classified as type B, the African/Asian type. We then amplified and sequenced a 583-bp JCV-DNA region from the type A isolates of Saami and Finns. According to type-determining nucleotides within the region, we classified type A isolates into EU-a1, a2, or -b. Most type A isolates from Saami were classified as EU-a1, while type A isolates from Finns were distributed among EU-a1, EU-a2, and EU-b. This trend in the JCV-genotype distribution was statistically significant. On a phylogenetic tree based on complete sequences, most of the type A isolates from Saami were clustered in a single clade within EU-a1, while those from Finns were distributed throughout EU-a1, EU-a2, and EU-b. These findings are discussed in the context of the population history of the Saami and the Finns. This study provides new complete JCV DNA sequences derived from populations of anthropological interest.

Effect of chronic ethanol ingestion and gender on heart left ventricular p53 gene expression.

Jänkälä, H. J., P. C. J. Eriksson, K. Eklund, M. Sarviharju, M. H. Härkonen and T. Mäki.

Alcoholism-Clinical and Experimental Research. 2005; 29(8): 1368-1373.

Background: Although the beneficial effects of mild to moderate ethanol consumption have been implied with respect to heart, alcohol abuse has proven to be a major cause of nonischemic cardiomyopathy in Western society. However, the biochemical and molecular mechanisms, which mediate the pathologic cardiac effects of ethanol, remain largely unknown. The aim of the present study was to explore the effects of chronic ethanol exposure on cardiac apoptosis and expression of some of the genes associated with cardiac remodeling in vivo.

Methods: Alcohol-avoiding Alko Non Alcohol rats of both sexes were used. The ethanol-exposed rats (females, n = 6; males, n = 8) were given 12% (v/v) ethanol as the only available fluid from age of three to 24 months of age. The control rats (females, n = 7; males, n = 5) had only water available. At the end of the experiment, free walls of left ventricles of hearts were immediately frozen. Cytosolic DNA fragmentation, reflecting apoptosis, was measured using a commercial quantitative sandwich enzyme-linked immunosorbent assay kit, and mRNA levels were analyzed using a quantitative reverse transcriptase-polymerase chain reaction method.

Results: Ethanol treatment for two years increased cardiac left ventricular p53 mRNA levels significantly (p = 0.014) compared with control rats. The gene expression was also dependent on the gender (p = 0.001), so that male rats had higher left ventricular p53 mRNA levels than female rats. However, no significant differences in levels of DNA fragmentation were detected.

Conclusions: Chronic ethanol exposure in vivo induces rat cardiac left ventricular p53 gene expression. Expression of p53 is also gender-dependent, males having higher p53 mRNA levels than females. This preliminary finding suggests a role for the p53 gene in ethanol-induced cardiac remodeling. The results might also have some relevance for the known gender-dependent differences in propensity to cardiovascular disease.

Lactase persistence and ovarian carcinoma risk in Finland, Poland and Sweden.

Kuokkanen, M., R. Butzow, H. Rasinperä, K. Medrek, M. Nilbert, S. Malander, J. Lubinski and I. Järvelä.

International Journal of Cancer. 2005; 117(1): 90-94.

Ovarian carcinoma is the fourth most common cause of cancer death in women. The cause and pathogenesis of this disease has remained obscure. Galactose, the hydrolyzing product of the milk sugar lactose, has been hypothesized to be toxic to ovarian epithelial cells and consumption of dairy products and lactase persistence has been suggested to be a risk factor for ovarian carcinoma. In adults, downregulation of lactase depends on a variant C/T-13910 at the 5' end of the lactase gene. To explore whether lactase persistence is related to the risk of ovarian carcinoma we determined the C/T-13910 genotype in a cohort of 782 women with ovarian carcinoma. The C/T-13910 genotype was defined by solid phase minisequencing from 327 Finnish, 303 Polish, 152 Swedish patients and 938 Finnish, 296 Polish and 97 Swedish healthy individuals served as controls. Lactase persistence did not associate significantly with increased risk for ovarian carcinoma in the Finnish odds ratio (OR = 0.77, 95% confidence interval [CI] = 0.57-1.05, p = 0.097), in the Polish (OR = 0.95, 95% Cl = 0.68-1.33, p = 0.75), or in the Swedish populations (OR = 1.63, 95% Cl = 0.65-4.08, p = 0.29). Our results do not support the hypothesis that lactase persistence increases the ovarian carcinoma risk. On the contrary, lactase persistence may decrease the ovarian carcinoma risk at least in the Finnish population. (c) 2005 Wiley-Liss, Inc.

Leg extension power asymmetry and mobility limitation in healthy older women.

Portegijs, E., S. Sipilä, M. Alen, J. Kaprio, M. Koskenvuo, K. Tiainen and T. Rantanen.

Archives of Physical Medicine and Rehabilitation. 2005; 86(9): 1838-1842.

Objective: To investigate the association of asymmetry in leg extension power (LEP) with walking and standing balance. Design: Cross-sectional analysis.

Setting: Research laboratory.

Participants: Healthy female twins (N = 419), ages 63 to 75 years.

Interventions: Not applicable.

Main Outcome Measures: The LEP difference between the stronger and the weaker leg, measured with the Nottingham power rig, was calculated. Ten-meter maximal walking velocity was assessed in a laboratory corridor on a wide (170cm) and narrow (35cm) track, and the ability to maintain tandem stance for 20 seconds was recorded. Results: The mean LEP difference +/- standard deviation between the legs was 15%+/- 9% (P <.001). Those with large LEP difference had lower walking velocity and poorer standing balance than those with small LEP difference, in particular when the LEP of the stronger leg was below the median.

Conclusions: Even in healthy older women, substantial LEP asymmetry between the lower limbs was present, encumbering walking and standing balance. Lower-limb muscle power asymmetry warrants further study in order to develop well-targeted strategies for preventing mobility limitation in older people.

Anthropometric measurements and growth as predictors of low-back pain: a cohort study of children followed up from the age of 11 to 22 years

Poussa, M. S., M. M. Heliövaara, J. T. Seitsamo, M. H. Kononen, K. A. Hurmerinta and M. J. Nissinen.

European Spine Journal. 2005; 14(6): 595-598.

Body height is an alleged risk factor for low-back pain (LBP) in adulthood, but its importance is obscure during childhood and adolescence. We studied growth for its association with the incidence of LBP in a population study of 430 children who were examined five times: at the age 11,12,13,14 and 22 years. Body height and weight and the degrees of trunk asymmetry, thoracic kyphosis and lumbar lordosis were measured at every examination. The history of LBP was obtained by a structured questionnaire at the ages of 14 and 22 years. The incidence of LBP was defined as pain, which occurred on eight or more days during the past year among those 338 children who had been free from LBP until 14 years of age. Growth of body height between 11 years and 14 years of age predicted the incidence of LBP. Adjusted for sex, the odds ratio (with 95% confidence interval) per an increment of one SD (4.3 cm) was 1.32 (1.06-1.65), the P value for trend being 0.03. Growth after 14 years of age was inversely related to the incidence of LBP, but the association did not reach statistical significance (P for trend = 0.06). Other anthropometric measurements or their changes were not found to predict LBP. Our results are not compatible with the old myth that spinal growth actually contributes to LBP. But abundant growth in early adolescence may be a risk factor for subsequent LBP.

Is ethanol a pro-drug? Acetaldehyde contribution to brain ethanol effects.

Quertemont, E., C. J. P. Eriksson, S. M. Zimatkin, P. S. Pronko, M. Diana, M. Pisano, Z. A. Rodd, R. R. Bell and R. J. Ward.

Alcoholism-Clinical and Experimental Research. 2005; 29(8): 1514-1521.

This article presents the proceedings of a symposium at the 2004 meeting of the International Society for Biomedical Research on Alcoholism, held in Mannheim, Germany. The symposium was organized by Etienne Quertemont and chaired by C. J. Peter Eriksson. The presentations were (1) Brain ethanol metabolism and its behavior consequences, by Sergey M. Zimatkin and P. S. Pronko; (2) Acetaldehyde increases dopaminergic neuronal activity: a possible mechanism for acetaldehyde reinforcing effects, by Marco Diana and Milena Pisano; (3) Contrasting the reinforcing actions of acetaldehyde and ethanol within the ventral tegmental area (VTA) of alcohol-preferring (P) rats, by Zachary A. Rodd and Richard R. Bell; (4) Molecular and biochemical changes associated with acetaldehyde toxicity, by Roberta J. Ward; and (5) Role of acetaldehyde in human alcoholism and alcohol abuse, by C. J. Peter Eriksson.

Serum lipids and intake of nutrients in children after kidney transplantion.

Siirtola, A., S. M. Virtanen, M. Antikainen, M. Ala-Houhala, T. Solakivi, T. Lehtimäki, C. Holmberg and M. K. Salo.

Pediatric Transplantation. 2005; 9: 105-105. Meeting Abstract.