Polymorphism of the pig-implantation protein 3 (preis3) gene and its association with litter size traits

The pre-implantation protein 3 (prei3), which might play a role in pre-implantation embryogenesis, is one of the promising candidate genes for litter size traits in pigs. In this study, a single nucleotide polymorphism (SNP: T802G) in intron 6 of the pig prei3 gene was detected and a genotyping assay for this SNP was developed. An association study for this SNP with litter size was performed in two independent populations. One population consisted of crossbred sows derived from Landrace, Large White, Chinese Tongcheng and/or Chinese Meishan (Line DIV). The other population constituted of crossbred animals derived from Chinese Qingping and Duroc (QD). Statistical analysis demonstrated that, in first parity, 2.65 more piglets were born and 3.82 more piglets were born alive in sows in Line DIV with genotype TT than with genotype GG. For second and subsequent litters, in both the DIV and QD lines there were significant differences in the number of piglets born alive between TG and GG sows, with the TG sows producing more piglets born alive than the GG sows. These results suggest that the prei3 SNP is significantly associated with litter size in the two populations studied, and could be useful in selection for increasing litter size in pigs. Further investigations on more pig populations with large sample sizes are needed to confirm this. South African Journal of Animal Science Vol. 36(3) 2006: 209-21

Analysis of DNA Methylation in Various Swine Tissues

DNA methylation is known to play an important role in regulating gene expression during biological development and tissue differentiation in eukaryotes. In this study, we used the fluorescence-labeled methylation-sensitive amplified polymorphism (F-MSAP) method to assess the extent and pattern of cytosine methylation in muscle, heart, liver, spleen, lung, kidney and stomach from the swine strain Laiwu, and we also examined specific methylation patterns in the seven tissues. In total, 96,371 fragments, each representing a recognition site cleaved by either or both EcoRI + HpaII and EcoRI + MspI, the HpaII and MspI are isoschizomeric enzymes, were amplified using 16 pairs of selective primers. A total of 50,094 sites were found to be methylated at cytosines in seven tissues. The incidence of DNA methylation was approximately 53.99% in muscle, 51.24% in the heart, 50.18% in the liver, 53.31% in the spleen, 51.97% in the lung, 51.15% in the kidney and 53.39% in the stomach, as revealed by the incidence of differential digestion. Additionally, differences in DNA methylation levels imply that such variations may be related to specific gene expression during tissue differentiation, growth and development. Three types of bands were generated in the F-MSAP profile, the total numbers of these three types of bands in the seven tissues were 46,277, 24,801 and 25,293, respectively

Association of Adiponectin SNP+45 and SNP+276 with Type 2 Diabetes in Han Chinese Populations: A Meta-Analysis of 26 Case-Control Studies

Recently, many studies have reported that the SNP+45(T>G) and SNP+276(G>T) polymorphisms in the adiponectin gene are associated with type 2 diabetes (T2DM) in the Chinese Han population. However, the previous studies yielded many conflicting results. Thus, a meta-analysis of the association of the adiponectin gene with T2DM in the Chinese Han population is required. In the current study, we first determined the distribution of the adiponectin SNP+276 polymorphism in T2DM and nondiabetes (NDM) control groups. Our results suggested that the genotype and allele frequencies for SNP+276 did not differ significantly between the T2DM and NDM groups. Then, a meta-analysis of 23 case-control studies of SNP+45, with a total of 4161 T2DM patients and 3709 controls, and 11 case-control studies of SNP+276, with 2533 T2DM patients and 2212 controls, was performed. All subjects were Han Chinese. The fixed-effects model and random-effects model were applied for dichotomous outcomes to combine the results of the included studies. The results revealed a trend towards an increased risk of T2DM for the SNP+45G allele as compared with the SNP+45T allele (OR = 1.34; 95% CI, 1.11–1.62; P<0.01) in the Chinese Han population. However, there was no association between SNP+276 and T2DM (OR = 0.90; 95% CI, 0.73–1.10; P = 0.31). The results of our association study showed there was no association between the adiponectin SNP+276 polymorphism and T2DM in the Yunnan Han population. The meta-analysis results suggested that the SNP+45G allele might be a susceptibility allele for T2DM in the Chinese Han population. However, we did not observe an association between SNP+276 and T2DM

Detection and verification of malting quality QTLs using wild barley introgression lines

A malting quality quantitative trait locus (QTL) study was conducted using a set of 39 wild barley introgression lines (hereafter abbreviated with S42ILs). Each S42IL harbors a single marker-defined chromosomal segment from the wild barley accession ‘ISR 42-8’ (Hordeum vulgare ssp. spontaneum) within the genetic background of the elite spring barley cultivar ‘Scarlett’ (Hordeum vulgare ssp. vulgare). The aim of the study was (1) to verify genetic effects previously identified in the advanced backcross population S42, (2) to detect new QTLs, and (3) to identify S42ILs exhibiting multiple QTL effects. For this, grain samples from field tests in three different environments were subjected to micro malting. Subsequently, a line × phenotype association study was performed with the S42ILs in order to localize putative QTL effects. A QTL was accepted if the trait value of a particular S42IL was significantly (P < 0.05) different from the recurrent parent as a control, either across all tested environments or in a particular environment. For eight malting quality traits, altogether 40 QTLs were localized, among which 35 QTLs (87.5%) were stable across all environments. Six QTLs (15.0%) revealed a trait improving wild barley effect. Out of 36 QTLs detected in a previous advanced backcross QTL study with the parent BC2DH population S42, 18 QTLs (50.0%) could be verified with the S42IL set. For the quality parameters α-amylase activity and Hartong 45°C, all QTLs assessed in population S42 were verified by S42ILs. In addition, eight new QTL effects and 17 QTLs affecting two newly investigated traits were localized. Two QTL clusters harboring simultaneous effects on eight and six traits, respectively, were mapped to chromosomes 1H and 4H. In future, fine-mapping of these QTL regions will be conducted in order to shed further light on the genetic basis of the most interesting QTLs

MAPK-Activated Protein Kinase 2 Is Required for Mouse Meiotic Spindle Assembly and Kinetochore-Microtubule Attachment

MAPK-activated protein kinase 2 (MK2), a direct substrate of p38 MAPK, plays key roles in multiple physiological functions in mitosis. Here, we show for the first time the unique distribution pattern of MK2 in meiosis. Phospho-MK2 was localized on bipolar spindle minus ends and along the interstitial axes of homologous chromosomes extending over centromere regions and arm regions at metaphase of first meiosis (MI stage) in mouse oocytes. At metaphase of second meiosis (MII stage), p-MK2 was localized on the bipolar spindle minus ends and at the inner centromere region of sister chromatids as dots. Knockdown or inhibition of MK2 resulted in spindle defects. Spindles were surrounded by irregular nondisjunction chromosomes, which were arranged in an amphitelic or syntelic/monotelic manner, or chromosomes detached from the spindles. Kinetochore–microtubule attachments were impaired in MK2-deficient oocytes because spindle microtubules became unstable in response to cold treatment. In addition, homologous chromosome segregation and meiosis progression were inhibited in these oocytes. Our data suggest that MK2 may be essential for functional meiotic bipolar spindle formation, chromosome segregation and proper kinetochore–microtubule attachments

Preconditioning-induced ischemic tolerance: a window into endogenous gearing for cerebroprotection

Ischemic tolerance defines transient resistance to lethal ischemia gained by a prior sublethal noxious stimulus (i.e., preconditioning). This adaptive response is thought to be an evolutionarily conserved defense mechanism, observed in a wide variety of species. Preconditioning confers ischemic tolerance if not in all, in most organ systems, including the heart, kidney, liver, and small intestine. Since the first landmark experimental demonstration of ischemic tolerance in the gerbil brain in early 1990's, basic scientific knowledge on the mechanisms of cerebral ischemic tolerance increased substantially. Various noxious stimuli can precondition the brain, presumably through a common mechanism, genomic reprogramming. Ischemic tolerance occurs in two temporally distinct windows. Early tolerance can be achieved within minutes, but wanes also rapidly, within hours. Delayed tolerance develops in hours and lasts for days. The main mechanism involved in early tolerance is adaptation of membrane receptors, whereas gene activation with subsequent de novo protein synthesis dominates delayed tolerance. Ischemic preconditioning is associated with robust cerebroprotection in animals. In humans, transient ischemic attacks may be the clinical correlate of preconditioning leading to ischemic tolerance. Mimicking the mechanisms of this unique endogenous protection process is therefore a potential strategy for stroke prevention. Perhaps new remedies for stroke are very close, right in our cells

ICAR: endoscopic skull‐base surgery

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