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Objectives Recently, genome-wide associated studies have identified several genetic loci that are associated with elevated blood pressure and could play a critical role in intracellular calcium homeostasis. The aim of this study was to assess the associations of ATP2B1 rs2681472 and CACNB2 rs12258967 gene polymorphisms with high blood pressure (HBP) among Lithuanian children and adolescents aged 12-15 years. Study design and participants This was a crosssectional study of a randomly selected sample of 646 12-15-year-old adolescents who participated in the survey 'The Prevalence and Risk Factors of HBP in 12-15 Year-Old Lithuanian Children and Adolescents (from November 2010 to April 2012)'. Anthropometric parameters and BP were measured. The participants with HBP were screened on two separate occasions. Subjects were genotyped ATP2B1 rs2681472 and CACNB2 rs12258967 gene polymorphisms using real-time PCR method. Results The prevalence of HBP was 36.7%, significantly higher for boys than for girls. In the multivariate analysis, after adjustment for body mass index and waist circumference, boys with CACNB2 CG genotype, CACNB2 GG genotype and CACNB2 CG +GG genotype had higher odds of having HBP in codominant (adjusted OR (aOR)=1.92; 95% CI 1.16 to 3.18, p=0.011; and aOR=2.64; 95% CI 1.19 to 5.90, p=0.018) and in dominant (aOR=2.05; 95% CI 1.27 to 3.30, p=0.003) inheritance models. Girls carrying CACNB2 CG genotype and CACNB2 CG +GG genotype had increased odds of HBP in codominant (aOR=1.82; 95% CI 1.02 to 3.24, p=0.044) and in dominant (aOR=1.89; 95% CI 1.09 to 3.28, p=0.023) inheritance models. Furthermore, significant associations were found in additive models separately for boys (aOR=1.72; 95% CI 1.20 to 2.46, p=0.003) and girls (aOR=1.52; 95% CI 1.05 to 2.20, p=0.027). No significant association was found between ATP2B1 gene polymorphism and the odds of HBP. Conclusions Our results indicate that CACNB2 gene polymorphism was significantly associated with higher odds of HBP in Lithuanian adolescents aged 12-15 years. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to determine the effect of gingivitis and periodontitis on white blood cell (WBC) count and differential WBC count in gingival microvascular blood (GMB) and in venous blood (VB). Material and methods: 102 systemically healthy adult patients - 32 with gingivitis, 36 with periodontitis, and 34 controls - underwent evaluation of the total WBC count, and the count of different types of WBC in VB and GMB. Results: Inflammation of periodontal tissues was persistently associated with a systemic (in VB) elevation of the WBC count (p<0.05 in gingivitis and p<0.01 in periodontitis), compared to that in control group subjects, and with elevated systemic and local lymphocyte counts (p<0.05), compared to the analogous cell count in the control group. Patients with periodontitis were found to have reduced polymorphonuclear leucocyte (PMN) counts in GMB, compared to patients with gingivitis. Conclusion: Persistent chronic bacterial infection affects the systemic elevation of WBC in subjects with gingivitis and periodontitis. A local decrease in PMN in periodontitis patients and a systemic increase in lymphocytes in gingivitis and periodontitis patients may indicate the inability of these patients' organisms to defend against periodontopathic bacteria - and thus susceptibility to disease. [ABSTRACT FROM AUTHOR]

Aim: To examine the MMP-2 (-1306 C/T) gene polymorphism and the phenotype characterized by soft and hard drusen of early age-related macular degeneration (AMD) and geographic atrophy of late AMD form., Methods: The study enrolled 850 investigations (290 AMD patients with soft and hard drusen, 34 with geographic atrophy and a random sample of the population n =526). Early AMD was classified according to the International Classification and Grading System. For geographic atrophy diagnosis the Age-Related Eye Disease Study classification was used. The potential association with single nucleotide polymorphisms on MMP-2 Rs243865 was evaluated for all patients, adjusted for age and sex. The genotyping test of MMP-2 Rs243865 (C-->T) was conducted using the real-time polymerase chain reaction method., Results: MMP-2 (-1306 C/T) C/C genotype was more frequently detected in AMD patients with hard drusen than the soft drusen or control group (66.43% vs 53.74%, vs 54.94%, P =0.047). Logistic regression analysis showed that the MMP-2 (-1306) C/C genotype increased the likelihood to develop hard drusen in AMD patients (OR=1.7, 95% CI: 1.06-2.74; P =0.028). No association between MMP-2 (-1306 C/T) gene polymorphism in patients with atrophic AMD and control group was found (54.94%, 37.64%, 7.41% vs 50%, 38.24%, 11.76%; P =0.6)., Conclusion: The MMP-2 Rs24386 (C-->T) polymorphism is found to be associated with the development of hard drusen in patients with AMD.

Matrix metalloproteinase-3 (MMP-3) degrades extracellular matrix and may lead to development of dilatative pathology of ascending thoracic aorta. Expression of MMP-3 depends upon the 5A/6A polymorphism in the promoter region. An increased number of 5A alleles leads to high expression of MMP-3. Thus, objective of the study was to determine whether the 5A/6A polymorphism in the promoter region of MMP-3 gene is associated with the development of dilatative pathology of ascending thoracic aorta. We studied 76 patients (age ranged from 31 to 81 years; median age, 64 years) who underwent aortic reconstruction surgery due to dilatative pathology of ascending thoracic aorta and a random sample of the population (n=604) aged 25-64 years, all from Lithuania. DNA was analyzed by using real-time polymerase chain reaction to genotype polymorphism 5A/6A at a position -1171 of the MMP3 gene promoter. The prevalence of MMP-3 genotypes was similar in the group of dilatative pathology of ascending thoracic aorta and random sample of population. The frequency of 5A allele did not differ significantly between both groups and was 0.506 and 0.514, respectively. Male carriers of 5A/5A genotype were significantly younger compared with those with the 6A/6A genotype. In conclusion, the frequency of MMP-3 promoter 5A/6A genotypes did not differ between the group of patients with dilatative pathology of ascending thoracic aorta and the random sample of population, but the males with dilatative pathology of ascending thoracic aorta and 5A/5A genotype required aortic reconstruction surgery at the younger age than the males carrying 6A/6A genotype in the MMP-3 promoter region.

Unlabelled: The objective of this study was to examine the effect of chronic exposure to cadmium and zinc on the mice resistance to experimental Listeria monocytogenes infection., Materials and Methods: At the day beginning of experiment outbred mice were injected with suspension of bacteria and 8 weeks were given the following oral intake treatment: control group (n=28) deionized drinking water, Cd- group (n=37) water containing CdCl2 10 mg/l and Cd+Zn- group (n=33) water containing CdCl2 10 mg/l and ZnSO4 100 mg/l. The delayed type hypersensitivity was evaluated by the inflammatory response during so-called "foot" test. Listerial proteins solution was injected under plantare of lower aponeurosis of rear foot of experimental animals. Survival of L. monocytogenes in organs of experimental animals was evaluated by the presence of bacteria colonies after 30 days incubation of livers homogenates in broth medium at +4 degrees C and inoculation on CASO-agar. Kidneys, liver and spleen were used for metals analysis. Differences were significant if the P value was below 0.05., Results: Chronic exposure to Cd or to Cd with Zn for 8 weeks caused influence on survival of mice: Cd- and Cd+Zn groups mice died more rapidly than control group ones. Bacterial growth in organs was observed for all groups until fourth week. From sixth-week, control and Cd+Zn- group's mice more rapidly eliminated bacteria from organs, demonstrating that Zn- treated mice were more resistant to listerial infection than Cd- intoxicated ones. On the other hand, mice from Cd+Zn- group had significantly decreased spleen index (up to 74%, p<0.01) as compared to control group. Chronic poisoning of mice with low doses cadmium and zinc during infection significantly affected (p<0.05) their growth rate from fourth week in both experimental groups. Cadmium and zinc insignificantly decreased the delayed type hypersensitivity response to L. monocytogenes allergens in Cd+Zn- group of mice, and no differences were observed in Cd- group, as compared with control group., Conclusions: 1. Cadmium-exposed mice are more susceptible to Listeria monocytogenes and to other opportunistic infections than not intoxicated mice. 2. Zinc significantly reduces the negative effect of cadmium on the antimicrobial defense of mice. 3. Cadmium and zinc no significantly decrease the delayed type hypersensitivity response to L. monocytogenes allergens as compared with control.

Impact of aluminium ions on the translation process in mice liver, kidney, skeletal muscle and heart was investigated in vivo as well as on the protein synthesis in liver cell-free translation system in vitro. We find that at early stages of intoxication the effect of aluminium ions on protein synthesis in muscle tissues differs qualitatively from that one in liver or kidneys. Most noticeable aluminium-induced changes of protein synthesis in organs in vivo occur within the first 15-20 h after intoxication. We show that aluminium ions activates protein synthesis in liver and kidneys (at 8-16 h) while in skeletal muscle and heart does not. These results indirectly are supported by the data of experiments in vitro, which demonstrate that at low concentration aluminium ions activates protein synthesis in the cell-free translation system prepared from liver.

This study presents evaluation of effects of aluminium ions on the development of experimental infection induced by the injection of Listeria monocytogenes bacteria into growing mice. We show that single exposure of mice to 0.05 LD50 or 0.5 LD50 of aluminium ions does not affect the accumulation of bacteria in liver and spleen of experimental animals. Long-term exposure of mice to aluminium ions (injection of 0.05 LD50 Al3+ every 3 days for totally 6 weeks) did not slow down the increase in weight of animals while in the infected animals aluminium significantly reduced their growth. Animals subjected to chronic aluminium exposure have shown lower accumulation of bacteria in liver 24 h after the initiation of experimental infection as compared to the mice after single injection of 0.05 LD50 Al3+. Also, long-term exposure to aluminium causes more complicated development of experimental infection, which was evidenced by the decreased survival of aluminium-treated animals (77% compared to 83% in control group) as well as by the increase in the fraction of animals carrying infection after 6 weeks (36% versus 5% in control group). In addition, aluminium-exposed animals had significantly lower blood serum agglutination titer to the listeria, and decrease in the delayed type of hypersensitivity to the listeria antigens. Results, presented here, indicate that the long-term exposure to low aluminium doses activates the antibacterial defence in experimental animals while the specific immunity becomes suppressed.