Incomplete Pairing Research Articles

Evaluating Decision-making Factors Used in Adopting New Farming Technologies—Recomputing Weighting Factors by Incomplete Paired Comparison Method in the Analytical Hierarchy Process

Evaluating Decision-making Factors Used in Adopting New Farming Technologies—Recomputing Weighting Factors by Incomplete Paired Comparison Method in the Analytical Hierarchy Process

Measuring heritable contributions to Alzheimer's disease: polygenic risk score analysis with twins.

The heritability of Alzheimer’s disease estimated from twin studies is greater than the heritability derived from genome-based studies, for reasons that remain unclear. We apply both approaches to the same twin sample, considering both Alzheimer’s disease polygenic risk scores and heritability from twin models, to provide insight into the role of measured genetic variants and to quantify uncaptured genetic risk. A population-based heritability and polygenic association study of Alzheimer’s disease was conducted between 1986 and 2016 and is the first study to incorporate polygenic risk scores into biometrical twin models of Alzheimer’s disease. The sample included 1586 twins drawn from the Swedish Twin Registry which were nested within 1137 twin pairs (449 complete pairs and 688 incomplete pairs) with clinically based diagnoses and registry follow-up (Mage = 85.28, SD = 7.02; 44% male; 431 cases and 1155 controls). We report contributions of polygenic risk scores at P < 1 × 10−5, considering a full polygenic risk score (PRS), PRS without the APOE region (PRS.no.APOE) and PRS.no.APOE plus directly measured APOE alleles. Biometric twin models estimated the contribution of environmental influences and measured (PRS) and unmeasured genes to Alzheimer’s disease risk. The full PRS and PRS.no.APOE contributed 10.1 and 2.4% to Alzheimer’s disease risk, respectively. When APOE ɛ4 alleles were added to the model with the PRS.no.APOE, the total contribution was 11.4% to Alzheimer’s disease risk, where APOE ɛ4 explained 9.3% and PRS.no.APOE dropped from 2.4 to 2.1%. The total genetic contribution to Alzheimer’s disease risk, measured and unmeasured, was 71% while environmental influences unique to each twin accounted for 29% of the risk. The APOE region accounts for much of the measurable genetic contribution to Alzheimer’s disease, with a smaller contribution from other measured polygenic influences. Importantly, substantial background genetic influences remain to be understood.

Combining Paired and Two-Sample Data Using a Permutation Test

This paper presents a permutation test for the incomplete pairs setting. This situation arises in both observational and experimental studies when some of the data are in the form of a paired sample and the rest of the data comprise two independent samples. The proposed method uses the data from the two types of samples to test the difference between the mean responses. Our test statistic combines the observed mean difference for the complete pairs with the difference between the two means of the independent samples. The randomizations are carried out as is typically done with standard permutation tests for paired and independent samples. We show by a simulation study that our statistic performs well in comparison to other methods.

Interspecies RNA Interactome of Pathogen and Host in a Heritable Defensive Strategy

Communication with bacteria deeply impacts the life history traits of their hosts. Through specific molecules and metabolites, bacteria can promote short- and long-term phenotypic and behavioral changes in the nematode Caenorhabditis elegans. The chronic exposure of C. elegans to pathogens promotes the adaptive behavior in the host’s progeny called pathogen-induced diapause formation (PIDF). PIDF is a pathogen avoidance strategy induced in the second generation of animals infected and can be recalled transgenerationally. This behavior requires the RNA interference machinery and specific nematode and bacteria small RNAs (sRNAs). In this work, we assume that RNAs from both species co-exist and can interact with each other. Under this principle, we explore the potential interspecies RNA interactions during PIDF-triggering conditions, using transcriptomic data from the holobiont. We study two transcriptomics datasets: first, the dual sRNA expression of Pseudomonas aeruginosa PAO1 and C. elegans in a transgenerational paradigm for six generations and second, the simultaneous expression of sRNAs and mRNA in intergenerational PIDF. We focus on those bacterial sRNAs that are systematically overexpressed in the intestines of animals compared with sRNAs expressed in host-naïve bacteria. We selected diverse in silico methods that represent putative mechanisms of RNA-mediated interspecies interaction. These interactions are as follows: heterologous perfect and incomplete pairing between bacterial RNA and host mRNA; sRNAs of similar sequence expressed in both species that could mimic each other; and known or predicted eukaryotic motifs present in bacterial transcripts. We conclude that a broad spectrum of tools can be applied for the identification of potential sRNA and mRNA targets of the interspecies RNA interaction that can be subsequently tested experimentally.

Negative emotions influence EEG correlates of inference formation during analogical reasoning

Previous research indicates that negative emotions influence cognitive resource utilization during analogical reasoning. However, no research has yet demonstrated an influence of negative emotions on inference formation during analogical reasoning. For this reason, we used evoked response potentials to investigate how negatively valenced content affects inference formation during analogical reasoning. Participants generated inferences about the missing term of 256 four-term analogies consisting of a first pair (A is to B), a second incomplete pair (as C is to?), and a probe term (D). We manipulated the affective valence of the terms (negative/neutral) forming the first two pairs and the soundness of the analogies. In Experiment 1, the terms were words and the relations were semantic in nature. We recorded the N400 event-related component time-locked to the probe term. The effect of analogy soundness on N400 amplitude was weaker when both pairs of terms were negative than when one or both pairs were neutral. In Experiment 2, we used analogies with negatively or neutrally conditioned symbols as terms, and visuospatial transformations as relations. We recorded the P3b event-related component time-locked to the final term of the analogy. The effect of analogy soundness on P3b amplitude was weaker when the first pair of terms was negatively conditioned than when they were neutrally conditioned. Results of both experiments suggested that negatively valenced content impairs the formation of inferences during analogical reasoning, as indicated by reduced effects of analogy soundness on N400 and P3b in the presence of negatively valenced content.

The Role of the Environment in Overweight and Eating Behavior Variability: Insights from a Multivariate Twin Study.

Research has emphasized the genetic basis of individual differences in body mass index (BMI); however, genetic factors cannot explain the rapid rise of obesity. Eating behaviors have been stipulated to be the behavioral expression of genetic risk in an obesogenic environment. In this study, we decompose variation and covariation between three key eating behaviors and BMI in a sample of 698 participants, consisting of 167 monozygotic, 150 dizygotic complete same-sex female twins and 64 incomplete pairs from a population-based twin registry in the southeast of Spain, The Murcia Twin Registry. Phenotypes were emotional eating, uncontrolled eating and cognitive restraint, measured by the Three Factor Eating Questionnaire and objectively measured BMI. Variation in eating behaviors was driven by nonshared environmental factors (range: 56%-65%), whereas shared environmental and genetic factors were secondary. All three eating behaviors were correlated with BMI (r = .19-.25). Nonshared environmental factors explained the covariations (Emotional eating-Uncontrolled eating: rE = .54, 95% CI [.43, .64]; BMI-Cognitive restraint: rE = .15, 95% CI [.01, .28]). In contrast to BMI, individual differences in eating behaviors are mostly explained by nonshared environmental factors, which also accounted for the phenotypic correlation between eating behaviors and BMI. Due to the sample size, analyses were underpowered to detect contributions of additive genetic or shared environmental factors to variation and covariation of the phenotypes. Although more research is granted, these results support that eating behaviors could be viable intervention targets to help individuals maintain a healthy weight.

Hybrid larval lethality of Drosophila is caused by parent-of-origin expression: an insight from imaginal discs morphogenesis of Lhr pausing rescue hybrids of D. melanogaster and D. simulans

Hybrid males that inherit haploid set of chromosomes along with Hybrid male rescue, (Hmr+) gene from D. melanogaster mother and an autosomal set with Lethal hybrid rescue, (Lhr+) gene from D. simulans father, die at the larval/pupal transition phase due to insufficient growth of imaginal disc tissues. Comparable pattern reminiscent of hybrid F1female lethality was noted when D. melanogaster compound females were crossed with D. simulans males. The lethality is suppressed when the hybrids inherit one mutant allele of hybrid incompatibility gene (either Lhr−, or Hmr−) from either of the parent. In order to better understand the cause of lethality of F1 hybrids at larval stage, the imaginal discs development of lethal hybrids were examined and compared with those of ‘rescued’ hybrids with Lhr− and parental species. The study revealed the following major findings: (a) when hybrid male and female larvae carry only D. melanogaster X chromosome(s) in presence of both Lhr+ and Hmr+ genes, broad-ranging cell death reaction was induced in the disc tissues and eventually death of the hybrid larvae, (b) when hybrid females carry the X chromosome of both species in the background of maternal cytoplasm of D. melanogaster, the frequency of cell death in the discs was reduced significantly and discs were able to metamorphose, (c) when hybrid males and females inherit one set of autosome from Lhr null strain of D. simulans, the frequency of non-apoptotic cell death in the discs was suppressed significantly and discs development were restored, although the discs displayed fluctuating asymmetric of development. To understand the defects in the chromosomal organization associated with abnormal development of the ‘rescued’ hybrids, the functional organization of the polytene chromosomes of the ‘rescued’ hybrids were examined. It was noted that incomplete pairing of the autosomes of two species along with abnormal X chromosomal telomeric structure may have some bearing on developmental defects of the ‘rescued’ hybrids. From the results it is suggested that (1) cell death reaction in the imaginal discs of the larval lethal hybrids may be the result of divergent lineage of maternal and paternal sets of chromosomes in zygote in presences of two species specific mediator genes, Lhr+, and Hmr+, (2) suppression of larval lethality, in absence of Lhr function, indicated that the non-apoptotic type of cell death factor in the disc cells was controlled genetically by the two mediator genes in the disc cells, (3) re-specification of compartmental organization of paternal segment polarity genes in ‘rescued’ hybrid discs might cause non-random tissue damages and eventually the apoptotic type of cell death resulting into asymmetric development of the appendages in hybrids. In sum, our data revealed that cell death reaction in imaginal discs, associated with larval lethality in hybrids was a developmentally controlled program, through incompatible interactions between species specific mediator genes, Lhr+, Hmr+ and D. melanogaster X chromosome and the pattern of cell death reaction in the discs was different from apoptosis.

Differences in blastomere totipotency in 2-cell mouse embryos are a maternal trait mediated by asymmetric mRNA distribution.

It is widely held that the first two blastomeres of mammalian embryos are equally totipotent and that this totipotency belongs to the group of regulative properties. However, this interpretation neglects an important aspect: evidence only came from successful monozygotic twins which can speak only for those pairs of half-embryos that are able to regulate in the first place. Are the frequently occurring incomplete pairs simply an artefact, or do they represent a real difference, be it in the imperfect blastomere’s ability to regulate growth or in the distribution of any compound X that constrains regulation? Using the model system of mouse embryos bisected at the 2-cell stage after fertilization, we present evidence that the interblastomere differences evade regulation by external factors and are already latent in oocytes. Specifically, an interblastomere imbalance of epiblast production persists under the most diverse culture conditions and applies to the same extent in parthenogenetic counterparts. As a result, cases in which twin blastocysts continued to develop in only one member account for 65 and 57% of zygotic and parthenogenetic pairs, respectively. The interblastomere imbalance is related to the subcellular distribution of gene products, as documented for the epiblast-related gene Cops3, using mRNA FISH in super-resolution mode confocal microscopy. Blastomere patterns of Cops3 mRNA distribution are α-amanitin-resistant. Thus, the imbalance originates not from de novo transcription, but from influences which are effective before fertilisation. These data expose previously unrecognized limits of regulative capacities of 2-cell stage blastomeres and point to aspects of cytoplasmic organization of the mouse oocyte that segregate unequally to blastomeres during cleavage.

Proposed Statistical model for Scoring and Ranking Sport Tournaments

A class of modification is proposed for calculating a score for each Player/team in Unbalanced Incomplete paired Comparisons Sports Tournaments. Many papers dealing with Balanced Incomplete Paired Comparison Sports Tournaments with at most one comparison per pair have appeared since 1950. However, little has been written about unbalanced situations in which the player /the team (object) ( j ) plays unequal number of games against the player/the team( m ) in a tournament, and the results of all games can be summarized in a Win-Lose matrix Y = { Yjm } , where Yjm = 1,0,1/2, respectively, according to as the player or the team ( j ) wins, losses or draws against the player or the team (m ). Published papers by Ramanujacharyulu (1964), Cowden, D.J. (1975), and David, H. A.(1988) have concentrated on the problem of converting the results of unbalanced incomplete paired comparison tournaments into rank with little consideration of the main relative ability on each player or team. We suggest (modification) another way of quantifying the outcomes of the games/tournaments, in particular, ratings on a scales, 0 to 5, 1 to 10 .ect. It is important to consider not only the vector Vj(d) or the vectors Sj, in scoring and ranking the k teams in such tournaments, but also the vector Zj, where Zj = Sj + SjRj, to take into account the ratio of the relative ability of each team ( Rj ). The proposed modification helps to introduce these methods for use in comparisons/games (tournaments), where the player/team are quantified on a special scale. e.g. 0-5, 1-10, ..etc. We conclude the following:- The scores stabilized to three decimal places at iteration 2 in Cowden’s method Vj(d) .see table(1.4). The scores stabilized to three decimal places at iteration 2 in David’s method Sj , and it’s modification Zj. The proposed modification (Zj) has the advantage of removing ties from David’s method (Sj), and hence it is the best method.

Revisiting Meiosis in Sugarcane: Chromosomal Irregularities and the Prevalence of Bivalent Configurations.

Traditional sugarcane cultivars (Saccharum officinarum) proved highly susceptible to diseases, and this led breeders to progress to interspecific crosses resulting in disease resistance. A backcrossing program to S. officinarum was then required to boost sucrose content. Clonal selection across generations and incorporation of other germplasm into cultivated backgrounds established the (narrow) genetic base of modern cultivars (Saccharum spp.), which have a man-made genome. The genome complexity has inspired several molecular studies that have elucidated aspects of sugarcane genome constitution, architecture, and cytogenetics. However, there is a critical shortage of information on chromosome behavior throughout meiosis in modern cultivars. In this study, we examined the microsporogenesis of a contemporary variety, providing a detailed analysis of the meiotic process and chromosome association at diakinesis, using FISH with centromeric probes. Chromosomal abnormalities were documented by examining high quality preparations of pollen mother cells (700 in total). Approximately 70% of the cells showed abnormalities, such as metaphase chromosomes not lined up at the plate, lagging chromosomes and chromosomal bridges, and tetrad cells with micronuclei. Some dyads with asynchronous behavior were also observed. Due to the hybrid composition of the sugarcane genome, we suggest that bivalent incomplete pairing may occur in the first prophase leading to univalency. The presence of rod bivalents showing the lagging tendency is consistent with a reduction in chiasma frequency. Finally, the presence of chromatin bridges indicates the indirect occurrence of chromosomal inversions, although chromosome fragments were not clearly recognized. Possible reasons for such meiotic abnormalities and the large prevalence of bivalent formation are discussed.

Chromosomal Studies of the Hybrid between Female &amp;lt;i&amp;gt;Rhodeus ocellatus ocellatus&amp;lt;/i&amp;gt; and Male &amp;lt;i&amp;gt;Rhodeus atremius fangi&amp;lt;/i&amp;gt; in Bitterlings (Teleostei: Cypriniformes: Acheilognathinae)

The chromosome analysis of the masculinized hybrid between female Rhodeus ocellatus ocellatus and male R. atremius fangi in bitterlings (Acheilognathinae) was done. It was presumed that they had intermediate karyotype between the parents, and formed sperms with heteroploidy resulting from the incomplete pairing of homologous chromosomes in meiosis. Due to the abundance of species and the ease of artificial fertilization, the study of the factor of the hybrid sterility in bitterlings would lead to the clarification of the mechanism about species differentiation and karyotype differentiation, and also develop a new variety. And also, it would also be important to make the hybrid various natures clear in environmental preservation.

A study of genetic and environmental contributions to structural brain changes over time in twins concordant and discordant for bipolar disorder

This is the first longitudinal twin study examining genetic and environmental contributions to the association between liability to bipolar disorder (BD) and changes over time in global brain volumes, and global and regional measures of cortical surface area, cortical thickness and cortical volume.A total of 50 twins from pairs discordant or concordant for BD (monozygotic: 8 discordant and 3 concordant pairs, and 1 patient and 3 co-twins from incomplete pairs; dizygotic: 6 discordant and 2 concordant pairs, and 1 patient and 7 co-twins from incomplete pairs) underwent magnetic resonance imaging twice. In addition, 57 twins from healthy twin pairs (15 monozygotic and 10 dizygotic pairs, and 4 monozygotic and 3 dizygotic subjects from incomplete pairs) were also scanned twice. Mean follow-up duration for all twins was 7.5 years (standard deviation: 1.5 years). Data were analyzed using structural equation modeling software OpenMx.The liability to BD was not associated with global or regional structural brain changes over time. Although we observed a subtle increase in cerebral white matter in BD patients, this effect disappeared after correction for multiple comparisons. Heritability of brain changes over time was generally low to moderate.Structural brain changes appear to follow similar trajectories in BD patients and healthy controls. Existing brain abnormalities in BD do not appear to progressively change over time, but this requires additional confirmation. Further study with large cohorts is recommended to assess genetic and environmental influences on structural brain abnormalities in BD, while taking into account the influence of lithium on the brain.

Effects of Anxiety on Caloric Intake and Satiety-Related Brain Activation in Women and Men.

To test the relationship of anxiety to caloric intake and food cue perception in women and men. Fifty-five twins (26 complete, 3 incomplete pairs; 51% women) underwent 2 functional magnetic resonance imaging (fMRI) scans (before and after a standardized meal) and then ate at an ad libitum buffet to objectively assess food intake. State and trait anxiety were assessed using the State-Trait Anxiety Inventory. During the fMRI scans, participants viewed blocks of fattening and nonfattening food images, and nonfood objects. In women, higher trait anxiety was associated with a higher body mass index (BMI) (r = 0.40, p = .010). Trait anxiety was positively associated with kilocalories consumed at the buffet (r = 0.53, p = .005) and percent kilocalories consumed from fat (r = 0.30, p = .006), adjusted for BMI. In within-pair models, which control for shared familial and genetic factors, higher trait anxiety remained associated with kilocalories consumed at the buffet (p = .66, p = .014), but not with BMI. In men, higher state anxiety was related to macronutrient choices, but not to total caloric intake or BMI. FMRI results revealed that women with high trait anxiety did not suppress activation by fattening food cues across brain regions associated with satiety perception after eating a standardized meal (low anxiety, mean difference = -15.4, p < .001; high anxiety, mean difference = -1.53, p = .82, adjusted for BMI). In women, trait anxiety may promote excess caloric consumption through altered perception of high-calorie environmental food cues, placing women with genetic predispositions toward weight gain at risk of obesity. Clinicaltrials.govidentifier:NCT02483663.

Nausea and Vomiting During Pregnancy is Highly Heritable.

Nausea and vomiting during pregnancy (NVP) affects about 70% of all expectant mothers and commonly impacts their physical health and psychosocial functioning. The aim of this study was to estimate the heritability of the presence, duration and severity of NVP. The sample consisted of 1723 women (M age=41.78, SD=11.67) including twins in both complete and incomplete pairs and their sisters from two cohorts participating in the NVP Genetics Consortium. The sample comprised 159 monozygotic and 140 dizygotic complete twin pairs, and 69 twin-sister pairs. We applied an extended twin design using OpenMx and Mx for secondary analysis. Individual differences in NVP were best explained by additive genetic and unique environmental effects. Heritability estimates were 73% (95% CIs=57-84%) for presence, 51% (95% CIs=36-63%) for duration and 53% (95% CIs=38-65%) for severity of NVP. The genetic correlation between duration and severity was almost perfect. Our results show that genes play an important role in different aspects of NVP and justify the importance of searching for genetic variants.

Chromosomal Studies of Masculinized Hybrids in Bitterlings (Teleostei: Cypriniformes: Acheilognathinae)

The chromosome analysis of the masculinized hybrid between female Tanakia limbata and male T. signifer in bitterlings (Acheilognathinae) was done. It was presumed that they had intermediate karyotype between the parents, and formed sperms with heteroploidy resulting from the incomplete pairing of homologous chromosomes in meiosis. Due to the abundance of species and the ease of artificial fertilization, the study of the factor of the hybrid sterility in bitterlings would lead to the clarification of the mechanism about species differentiation and karyotype differentiation, and also to developing a new variety.

Uncovering Direct Targets of MiR-19a Involved in Lung Cancer Progression.

Micro RNAs (miRNAs) regulate the expression of target genes posttranscriptionally by pairing incompletely with mRNA in a sequence-specific manner. About 30% of human genes are regulated by miRNAs, and a single miRNA is capable of reducing the production of hundreds of proteins by means of incomplete pairing upon miRNA–mRNA binding. Lately, evidence implicating miRNAs in the development of lung cancers has been emerging. In particular, miR-19a, which is highly expressed in malignant lung cancer cells, is considered the key miRNA for tumorigenesis. However, its direct targets remain underreported. In the present study, we focused on six potential miR-19a target genes selected by miRNA target prediction software. To evaluate these genes as direct miR-19a target genes, we performed luciferase, pull-down, and western blot assays. The luciferase activity of plasmids with each miR-19a–binding site was observed to decrease, while increased luciferase activity was observed in the presence of anti-miR-19a locked nucleic acid (LNA). The pull-down assay showed biotinylated miR-19a to bind to AGO2 protein and to four of six potential target mRNAs. Western blot analysis showed that the expression levels of the four genes changed depending on treatment with miR-19a mimic or anti-miR-19a-LNA. Finally, FOXP1, TP53INP1, TNFAIP3, and TUSC2 were identified as miR-19a targets. To examine the function of these four target genes in lung cancer cells, LK79 (which has high miR-19a expression) and A549 (which has low miR-19a expression) were used. The expression of the four target proteins was higher in A549 than in LK79 cells. The four miR-19a target cDNA expression vectors suppressed cell viability, colony formation, migration, and invasion of A549 and LK79 cells, but LK79 cells transfected with FOXP1 and TP53INP1 cDNAs showed no difference compared to the control cells in the invasion assay.

Trial Design and Analysis with Incomplete Paired Data

For a clinical trial design with paired data, it often involves missing observations. In such a case, the data from the trial become a mixture of paired and unpaired data. A commonly used approach for the analysis of the trial data is to ignore the incomplete pairs. Such a treatment of missing data is not statistically efficient. We propose a simple method that will allow us to use all data, including the incomplete pairs. The method is optimal in the sense that it minimizes the variance. We will show how to design classical and adaptive trials with the proposed method. The proposed method can also be used for meta-analysis, in which, some trials with paired data and some are not.

Propensity score method for partially matched omics studies.

This paper focuses on the problem of partially matched samples in the presence of confounders. We propose using propensity score matching to adjust for confounding factors for the subset of data with incomplete pairs, followed by integrating the P-values computed from the complete and incomplete paired samples, respectively. Several simulations and a case study on DNA methylation are considered to evaluate the operating characteristics of the proposed method.

Comparative Analysis of Micrornas Expression Between Tumor and Normal Breast Tissue in Patients with Invasive Ductal Carcinoma

INTRODUCTION: MicroRNAs are small non-coding RNAs of 19-22 nucleotides, which regulate gene expression through mechanisms such as incomplete pairing and post-transcriptional gene silencing, repressing the translation of the mRNA target. Although they don’t have the property of coding for protein, such molecules have been recognized as one of the main regulators of genes encoding the human genome. They became part of the RNA-induced silencing complex and repress the translation of RNA by binding to the 3 UTR region homologous in a faulty connection. In recent years, in addition to the identification of microRNAs, about 1000 in humans, increasing information about the target and biological function has been accumulated exponentially. MicroRNAs influence the expression of genes that regulate cell proliferation, migration and apoptosis, acting as oncogene or tumor suppressor. MATERIAL AND METHODS: Were evaluated and compared for expression of microRNAs in paraffin material of 11 samples of tissue (08 being diagnosed with invasive ductal breast carcinoma and 3 of normal breast tissue). The expression analysis was performed using the miScript miRNA PCR System (Qiagen) containing 84 miRNAs for breast cancer. The samples were deparaffinized and extraction of total RNA was performed using MiRNeasy FFPE kit. The next step was convertion into cDNA using the MiScript II RT Kit, followed by PCR amplification with the MiScript SYBR Green PCR Kit. The reactions were packed in specific plates that were analyzed using the 7500 Real Time PCR System (MIHS 90ZA). Statistical analysis was performed using software MIScript miRNA PCR Array Data Analysis Tool. RESULTS: Cases were divided into two groups: tumor and normal breast. 17 microRNAs were overexpressed in tumor tissue and 06 microRNAs were hypoexpressed (p <0. 05). Let - 7g, mir-141, miR-15-A, miR-15-B, miR 16, mir 181 a, mir 181c, mir 193b, mir 199a-5p, mir 200a, mir 200b, mir 21, mir210, mir22, mir 27-A, mir 340, miR 429 were upregulated. Mir 125b, miR-125b-1*, mir 145, miR 204, miR 328, miR 489 were down regulated. DISCUSSION: Previous studies have analyzed the expression of miRNA and the results clearly distinguished the healthy tissue and breast cancer and the most aberrant miRNAs were miR-125b, mir-145, mir-21 and mir-155. CONCLUSION: Our series also evaluated and found overexpression of microRNAs in tumor tissues statistically significant in miR-125b, miR-145 and miR-21. It seems likely that the expression levels of miRNA can be used as new diagnostic markers and can thus provide a new approach for therapeutic intervention.

Body Mass Index and Breast Size in Women: Same or Different Genes?

The objective of the current study was to investigate the heritability of breast size and the degree to which this heritability is shared with BMI. In a sample of 1010 females twins (mean age 35 years; SD = 2.1; range 28-40), self-report data pertaining to bra cup size and body mass index (BMI) was collected in the context of self-report data and an interview relating to disordered eating respectively. In a sample of 348 complete twin pairs who completed data collection (226 MZ pairs and 122 DZ pairs and 360 incomplete pairs (170 MZ and 190 DZ)), we found that the heritability of bra cup size was 56%. Of this genetic variance, one third is in common with genes influencing body mass index, and two thirds (41% of total variance) is unique to breast size, with some directional evidence of non-additive genetic variation. The implications of these findings with respect to previous research linking breast size with reproductive potential are discussed.