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Microsatellite markers from a transcriptome sequence library were initially isolated, and their genetic variation was characterized in a wild population of the mud crab (Scylla paramamosain). We then tested the association between these microsatellite markers and the growth performance of S. paramamosain. A total of 129 polymorphic microsatellite markers were identified, with an observed heterozygosity ranging from 0.19 to 1.00 per locus, an expected heterozygosity ranging from 0.23 to 0.96 per locus, and a polymorphism information content (PIC) ranging from 0.21 to 0.95 per locus. Of these microsatellite markers, 30 showed polymorphism in 96 full-sib individuals of a first generation family. Statistical analysis indicated that three microsatellite markers were significantly associated with 12 growth traits of S. paramamosain. Of these three markers, locus Scpa36 was significantly associated with eight growth traits, namely, carapace length, abdomen width (AW), body height (BH), fixed finger length of the claw, fixed finger width of the claw, fixed finger height of the claw, meropodite length of pereiopod 2, and meropodite length of pereiopod 3 (MLP3) (P<0.05). Locus Scpa75 was significantly associated with five growth traits, namely, internal carapace width, AW, carapace width at spine 8, distance between lateral spine 2 (DLS2), and MLP3 (P<0.05). Locus Spm30 was significantly associated with BH, DLS2, and body weight (P<0.05). Further analysis suggested a set of genotypes (BC at Scpa36, BC and BD at Scpa75, and AC at Spm30) that have great potential in the selection of S. paramamosain for growth traits. These findings will facilitate the development of population conservation genetics and molecular marker-assisted selective breeding of S. paramamosain and other closely related species. [ABSTRACT FROM AUTHOR]

Background: A number of observational studies have been conducted to investigate the association of the IL-10 gene polymorphisms with systemic lupus erythematosus (SLE) susceptibility. However, their results are conflicting. Method: We searched published case-control studies on the IL-10 polymorphisms and SLE in PubMed, EMBASE and Chinese Biomedical Literature Database. A meta-analysis was conducted using a fixed-effect or random-effect model based on between-study heterogeneity. Results: A total of 42 studies with 7948 cases and 11866 controls were included in this meta-analysis. Among Caucasians, the CA27 allele of the IL10.G microsatellites (OR 2.38, 95% CI 1.01–5.62), the G allele of the IL-10 -1082G/A polymorphism (G vs. A: OR 1.21, 95% CI 1.02–1.44; GG vs. AA: OR 1.45, 95% CI 1.16–1.82; GG+GA vs. AA: OR 1.16, 95% CI 1.03–1.29) and its associated haplotype -1082G/−819C/−592C (OR 1.25, 95% CI 1.10–1.42) were associated with increased SLE susceptibility without or with unimportant between-study heterogeneity. Removing studies deviating from Hardy-Weinberg equilibrium (HWE) hardly changed these results. Among Asians, the CA21 allele of the IL-10.G microsatellites (OR 1.28, 95% CI 1.02–1.60) and the -1082G/−819C/−592C haplotype (OR 1.24, 95% CI 1.00–1.53) were associated with increased SLE susceptibility, but with substantial between-study heterogeneity or sensitive to HWE status. Removing studies deviating from HWE also produced statistically significant associations of the IL-10 -1082G/A (GG vs. AA: OR 3.21, 95% CI 1.24–8.28; GG vs. AA+GA: OR 2.85, 95% CI 1.19–6.79) and -592C/A polymorphisms (CC+CA vs. AA: OR 0.69, 95% CI 0.51–0.94) with SLE among Asians. Conclusion: This meta-analysis showed that the IL10.G microsatellites, the IL-10 -1082G/A and -592C/A polymorphisms and the haplotype -1082G/−819C/−592C are associated with SLE susceptibility. Besides, this is the first time to report an association between the CA27 allele of the IL-10.G microsatellites and SLE among Caucasians. Further studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Background: Interleukin-1 beta (IL-1β), a pro-inflammatory cytokine, is emerging as a key mediator of carcinogenesis that characterizes host-environment interactions. Epidemiological studies investigating the association between two polymorphisms of IL-1B (−511C/T and +3954C/T) and cancer susceptibility have shown conflicting results. The aim of this study is to derive a more precise estimation of the relationship. Methods: Related studies were identified through a systematic literature search of PubMed and Web of Science from their inception to September 15, 2012. Summary odds ratios (ORs) and 95% confidence intervals (CIs) for the IL-1B −511C/T and +3954C/T polymorphisms and cancer risk were calculated. Heterogeneity among studies and publication bias were also tested. Results: The meta-analysis included 91 case-control studies in 85 publications, 81 studies for the −511C/T (19547 cases and 23935 controls) and 26 studies for the +3954C/T polymorphisms (8083 cases and 9183). The pooled results indicated that IL-1B +3954C/T (dominant model: OR = 1.15, 95% CI: 1.01–1.30) was significantly associated with increased overall cancer risk, especially among hospital-based case-control studies (dominant model: OR = 1.30, 95% CI: 1.02–1.66). As for −511C/T, we observed an inverse relationship in cervical cancer (dominant model: OR = 1.74, 95% CI: 1.35–2.23) and hepatocellular carcinoma (dominant model: OR = 0.68, 95% CI: 0.47–0.99). Moreover, −511C/T was associated with risk of specific subtypes of gastric carcinoma. Conclusion: This meta-analysis suggested that both the IL-1B –511C/T and +3954C/T polymorphisms might modulate cancer susceptibility. Further well-designed studies based on larger sample sizes should be performed to confirm the findings. [ABSTRACT FROM AUTHOR]

Introduction: Variations in genetic background are the leading cause of differential susceptibility to traumatic infection. Heat shock protein 90 (HSP90), a broadly distributed and conserved molecule, regulates inflammation under stressful and traumatic conditions. However, the relationships between HSP90 genetic polymorphisms, post-traumatic inflammatory responses and organ function remain unknown. Methods: A total of 286 healthy volunteers and patients with severe trauma took part in a single nucleotide polymorphism (SNP)-based analysis of the HSP90beta gene and a clinical association analysis. HSP90beta and TNF-alpha levels were determined using quantitative PCR and western blot. The transcriptional activity of the HSP90beta promoter was assayed using the Dual-Luciferase Reporter Assay System. Results: The minor allele frequencies for the SNP located at −144 bp relative to the HSP90beta transcriptional start site were 28.47% and 28.52% in the normal and trauma populations, respectively; no significant differences were found between these two distributions. However, the results showed that a promoter containing the -144A allele had a higher transcriptional activity than did a promoter containing the wild-type -144C allele. Furthermore, the -144A promoter induced high expression of HSP90beta and low expression of the inflammatory factor TNF-alpha in a lipopolysaccharide-induced inflammatory model. A clinical association analysis showed that the multiple organ dysfunction scores for -144AA genotype carriers were significantly lower than those of -144CC carriers following trauma. No significant correlations were found between the presence of the two alleles and the incidence of sepsis. Conclusions: These results indicate that differences in expression caused by the -144 polymorphism in the HSP90beta promoter are associated with cellular inflammatory responses and the severity of organ injury. These findings will aid in risk assessment and early prevention of complications for patients with severe trauma. [ABSTRACT FROM AUTHOR]

Microsatellite markers from a transcriptome sequence library were initially isolated, and their genetic variation was characterized in a wild population of the mud crab (Scylla paramamosain). We then tested the association between these microsatellite markers and the growth performance of S. paramamosain. A total of 129 polymorphic microsatellite markers were identified, with an observed heterozygosity ranging from 0.19 to 1.00 per locus, an expected heterozygosity ranging from 0.23 to 0.96 per locus, and a polymorphism information content (PIC) ranging from 0.21 to 0.95 per locus. Of these microsatellite markers, 30 showed polymorphism in 96 full-sib individuals of a first generation family. Statistical analysis indicated that three microsatellite markers were significantly associated with 12 growth traits of S. paramamosain. Of these three markers, locus Scpa36 was significantly associated with eight growth traits, namely, carapace length, abdomen width (AW), body height (BH), fixed finger length of the claw, fixed finger width of the claw, fixed finger height of the claw, meropodite length of pereiopod 2, and meropodite length of pereiopod 3 (MLP3) (P<0.05). Locus Scpa75 was significantly associated with five growth traits, namely, internal carapace width, AW, carapace width at spine 8, distance between lateral spine 2 (DLS2), and MLP3 (P<0.05). Locus Spm30 was significantly associated with BH, DLS2, and body weight (P<0.05). Further analysis suggested a set of genotypes (BC at Scpa36, BC and BD at Scpa75, and AC at Spm30) that have great potential in the selection of S. paramamosain for growth traits. These findings will facilitate the development of population conservation genetics and molecular marker-assisted selective breeding of S. paramamosain and other closely related species. [ABSTRACT FROM AUTHOR]