Identification of 15 novel polymorphic microsatellite loci in pearl oyster (Pinctada fucata).

The pearl oyster Pinctada fucata is a commercially important marine shellfish. As a result, genetic improvement and selective-breeding program have been conducted for this species. Polymorphic microsatellites are effective molecular markers to investigate molecular marker-assisted selection and genetic variance. In this study, microsatellite DNAs were screened and characterized based on the partial genome sequence of P. fucata. We identified 111 microsatellite DNA motifs through mining the published draft genome sequence of P. fucata. Forty-two loci were screened with 8 P. fucata individuals, and 15 were found to be polymorphic and were therefore further evaluated using 40 wild individuals from the Daya Bay, Shenzhen City, Guangdong Province, China. The number of alleles per locus ranged from 3 to 8, with an average of 5.2667 for the 15 polymorphic loci. Observed and expected heterozygosities ranged from 0.1154 to 0.6216 (0.3321 on average) and 0.4950 to 0.8491 (0.6768 on average), respectively. Of the 15 polymorphic loci, 12 loci deviated from Hardy-Weinberg equilibrium after Bonferroni correction (P < 0.0033). Polymorphism information content ranged from 0.44 to 0.83 with a mean value of 0.63. The results suggest that the markers isolated in this study can be used for research on molecular marker-assisted selection and genetic variance of P. fucata.

Effect of montelukast on the expression of interleukin-18, telomerase reverse transcriptase, and Bcl-2 in the brain tissue of neonatal rats with hypoxic-ischemic brain damage.

The aim of this study was to investigate the effect of montelukast on the expression of interleukin (IL)-18, telomerase reverse transcriptase (TERT), and Bcl-2 in the brain tissue of neonatal rats with hypox-ic-ischemic brain damage (HIBD). To establish the model of HIBD, 8% oxygen was applied to rats after the unilateral carotid artery was ligated. Twenty rats were randomly assigned to the control group, while another 40 were used to establish the HIBD model and were randomly divided equally into model group and treatment group. A 0.1 mg/kg dose of montelukast or an equal volume of saline was intraperitoneally injected to the rats in the treatment group and the model group, respectively. Brain tissue from 4 rats in each group was sampled at 0, 6, 12, 24, and 72 h after brain damage, and immunohistochemistry was used to measure IL-18, TERT and Bcl-2 expressions. IL-18, TERT, and Bcl-2 levels increased after 12 h in both the model group and treatment group, peaked after 48 h, and then decreased. Although not statistically significant, IL-18, TERT, and Bcl-2 expressions after 24, 48, and 96 h were all lower in the treatment group than those in the model group. In conclusion, montelukast has a protective effect on the cerebral tissue of neonatal rats with HIBD, and may mediate an increase of TERT and Bcl-2 levels but not of IL-18. Further study is required to elucidate the mechanism of the protective effect of montelukast on HIBD.

Relationship between zinc finger protein 36 (ZFP36) gene polymorphisms and obstructive sleep apnea.

Recent data have indicated that inflammation may have an important correlation with obstructive sleep apnea (OSA). Studies have indicated a relationship between OSA and TNF-α gene polymorphisms. Zinc finger protein 36 (ZFP36) regulates TNF-α mRNAs. However, ZFP36 gene polymorphisms have not been investigated in OSA. Therefore, we conducted the present case-control study to assess whether variances in ZFP36 gene polymorphisms account for differences in TNF-α levels in patients with moderate-to-severe OSA. This case-control study aims to investigate the relationship between genetic variations in the ZFP36 gene and moderate-to-severe OSA. Three common single nucleotide polymorphisms of the ZFP36 gene (rs251864, rs3746083, and rs17879933) were evaluated in a group of patients with moderate-to-severe OSA (N = 408) and in a control group (N = 394) by using TaqMan polymerase chain reaction analysis. The moderate-to-severe OSA group and the control group exhibited significant differences in the distributions of rs251864 and rs17879933 genotypes and alleles (P < 0.05). TNF-α levels were significantly different not only among the three rs251864 genotypes but also between the II genotype and the DD + ID genotypes of rs17879933. However, no significant differences in sleep apnea parameters in the three ZFP36 gene polymorphisms were observed. Logistic regression analyses demonstrated that TNF-α and the three ZFP36 gene polymorphisms were not independently associated with OSA. ZFP36 might be involved in TNF-α regulation. However, ZFP36 gene variants were not independent risk factors for moderate-to-severe OSA.