塔克尔莫乎尔沙漠银沙槐群落主要植物的种间关系

根据野外调查的样地数据资料,运用2×2列联表的Fisher精确检验、Pearson相关系数和Spearman秩相关系数检验,并结合DCA排序,分析塔克尔莫乎尔沙漠银沙槐群落主要植物种群之间的种间关系。结果表明:Fisher精确检验有3个种对呈显著正关联,3个种对呈显著负关联;Pearson相关系数检验有1个种对呈显著正相关,12个种对呈显著负相关;Spearman秩相关系数检验,有14个种对存在显著相关,其中负相关13对,占所有种对数的14.29%,正相关1对,占所有种对数的1.1%。银沙槐群落种间关系相对松散,反映出植物群落随着环境变化其物种组成也发生相应变化,正向着相对稳定独立的无关联方向发展。     

A Problem With the Correlation Coefficient as a Measure of Gene Expression Divergence

The correlation coefficient is commonly used as a measure of the divergence of gene expression profiles between different species. Here we point out a potential problem with this statistic: if measurement error is large relative to the differences in expression, the correlation coefficient will tend to show high divergence for genes that have relatively uniform levels of expression across tissues or time points. We show that genes with a conserved uniform pattern of expression have significantly higher levels of expression divergence, when measured using the correlation coefficient, than other genes, in a data set from mouse, rat, and human. We also show that the Euclidean distance yields low estimates of expression divergence for genes with a conserved uniform pattern of expression.IT is now possible to measure the expression levels of thousands of genes in multiple tissues at multiple times. This has led to investigations into the evolution of gene expression and how the pattern of expression changes on a genomic scale. In some analyses, the evolution of expression is considered only within one tissue, but in many studies the evolution across multiple tissues is investigated. In this latter case, the evolution of an expression profile—a vector of expression levels of a gene across several tissues—is considered.Several different statistics have been proposed to measure the divergence between gene expression profiles. The two most popular measures are the Euclidean distance (Jordan et al. 2005; Kim et al. 2006; Yanai et al. 2006; Urrutia et al. 2008) and Pearson''s correlation coefficient (Makova and Li 2003; Huminiecki and Wolfe 2004; Yang et al. 2005; Kim et al. 2006; Liao and Zhang 2006a,b; Xing et al. 2007; Urrutia et al. 2008). The correlation coefficient is often subtracted from one, so that the statistic varies from zero, when there has been no expression divergence, to a maximum of two; we refer to this statistic as the Pearson distance. Here we describe a significant shortcoming of the Pearson distance that is not shared by the Euclidean distance.To investigate properties of these two measures of expression divergence, we compiled a data set of 2859 orthologous genes from human, mouse, and rat for which we had microarray expression data from nine homologous tissues: bone marrow, heart, kidney, large intestine, pituitary, skeletal muscle, small intestine, spleen, and thymus). The expression data for rat came from Walker et al. (2004), the mouse data from Su et al. (2004), and the human data from Ge et al. (2005). Each tissue experiment had two replicates in mouse, a varying number of replicates in rat, and one in humans; some genes were also matched by multiple probe sets. To obtain an average across experiments and probe sets we processed the data as follows:

1. Raw CEL files of gene expression levels were obtained from the NCBI Gene Expression Omnibus database (http://www.ncbi.nlm.nih.gov/projects/geo/).
2. The results from the mouse, rat, and human arrays were normalized separately using both the MAS5 (Affymetrix 2001) and the RMA algorithms (Irizarry et al. 2003) as implemented in Bioconductor (Gentleman et al. 2004). The results are qualitatively similar for the two normalization procedures, although recent analyses suggest that MAS5 normalization is generally better (Ploner et al. 2005; Lim et al. 2007).
3. The expression of each gene within a tissue was averaged across experiments and probe sets.

We computed expression distances (ED) between orthologous gene expression profiles, for each of the three species comparisons, rat–mouse, rat–human, and mouse–human, according to the two different distance metrics, the Euclidean distance and the Pearson distance:(1)Here x_ij is the expression level of the gene under consideration in species i in tissue j, and is the average expression level of the gene in species i across tissues. Expression levels are known in a total of k tissues.Because expression levels are measured on different microarray platforms in the three species, we compute relative abundance (RA) values, before calculating the Euclidean distance (Liao and Zhang 2006a). The RA is the expression of a gene in a particular tissue divided by the sum of the expression values of that gene across all tissues. We calculated RA values to remove “probe” effects (the tendency for a gene to bind its probe set on one platform more efficiently than on another platform). Because of probe effects it is not easy to distinguish absolute changes in expression and differences in binding efficiency. Calculating RA values removes this problem from the Euclidean distance. Pearson''s distance does not change under such a rescaling and so this is unnecessary.In some analyses the logarithm of the expression or RA values are used (e.g., Makova and Li 2003; Kim et al. 2006; Xing et al. 2007), and in others the expression values are used without this transformation (e.g., Huminiecki and Wolfe 2004; Jordan et al. 2005; Yang et al. 2005; Liao and Zhang 2006a,b; Yanai et al. 2006; Urrutia et al. 2008). We calculated both the Pearson and the Euclidean distances on log-transformed and untransformed expression values. The results are qualitatively similar so here we present only the results obtained using the logarithm of the expression or RA values.It is natural to expect the two measures of expression divergence to be positively correlated with one another; however, the Euclidean and Pearson distances are almost completely uncorrelated (MAS5 normalization, mouse–rat correlation coefficient = 0.06, human–rat r = 0.13, human–mouse r = 0.10; RMA normalization, mouse–rat correlation coefficient = −0.12, human–rat r = −0.00, human–mouse r = −0.08; Figure 1). This could, plausibly, be because the two statistics measure different aspects of divergence. However, irrespective of this, there is a potential problem associated with the Pearson distance. Imagine that we have a gene that is expressed at identical levels in all tissues in two species (i.e., expression levels are uniform between tissues and also between species). We quite reasonably assume that measured expression levels contain noise. Thus each measured expression level (x_ij) is the sum of the (assumed) uniform expression level and an independent random number representing noise. In this case there is no real divergence in the expression profile between the species. However, the two measures of divergence may differ greatly in this case. The Euclidean distance reflects only the noise present in the data and hence will be small if the noise is small. By contrast, the Pearson distance will have a value close to 1 since the second term in PeaD in Equation 1 will be close to zero, reflecting the fact that the noise components of different expression levels are independent. Thus the Pearson distance will give the impression that expression divergence is great, but all this apparent divergence is noise. This will be a problem with Pearson''s distance whenever measurement error is of the same magnitude as the differences in expression between tissues. This will therefore tend to be a problem for lowly expressed genes, where measurement error can be large relative to the true value.Open in a separate windowFigure 1.—The correlation between the Euclidean and Pearson distances for (a) mouse–rat, (b) human–rat, and (c) human–mouse. Only the results from MAS5 normalization are shown; qualitatively similar results were obtained with RMA.The above example is unrealistic because real gene expression profiles are rarely perfectly uniform. To investigate whether this shortcoming of the Pearson distance is a problem in real data sets, we determined genes with a relatively uniform pattern of expression in all three species considered above. To do this we computed the entropy of a gene''s expression, which is a measure of uniformity in expression across tissues (Schug et al. 2005): the higher the value of the entropy, the more uniform is the expression. We calculated the entropy for each gene in each of the three species, averaged these across species, and then took those genes in the upper quartile of mean entropy values as a data set of genes with a relatively conserved pattern of uniform expression.It is natural to expect those genes with a conserved uniform pattern of expression to have relatively low expression divergence; however, on average these genes have significantly higher Pearson distances than other genes (Figure 2; supporting information, Figure S1 and Figure S2). By contrast, the Euclidean distance shows the pattern one would anticipate; all of the conserved uniform genes have low expression divergence. It therefore seems likely that the Pearson distance is sensitive to measurement error and hence may not be a good measure of expression divergence.Open in a separate windowFigure 2.—The distribution of expression divergence values for those genes with a uniform pattern of expression that is conserved across species vs. the distribution for all genes for (a) Pearson and (b) Euclidean distances for mouse–rat. We present similar values for human–mouse and human–rat in Figure S1 and Figure S2. Only the results from MAS5 normalization are shown; qualitatively similar results were obtained with RMA.

TABLE 1

The median expression divergence for genes that have a conserved uniform pattern of expression (upper quartile of mean entropy values) vs. all other genes

Single-step genomic evaluation improves accuracy of breeding value predictions for resistance to infectious pancreatic necrosis virus in rainbow trout

The aim of this study was to compare the accuracy of breeding values (EBVs) predicted using the traditional pedigree based Best Linear Unbiased Prediction (PBLUP) and the single-step genomic Best Linear Unbiased Prediction (ssGBLUP) for resistance against infectious pancreatic necrosis virus (IPNV) in rainbow trout. A total of 2278 animals were challenged against IPNV and 768 individuals were genotyped using a 57?K single nucleotide polymorphism array for rainbow trout. Accuracies for both methods were assessed using five-fold cross-validation. The heritabilities were higher for PBLUP compared to ssGBLUP. The ssGBLUP accuracies outperformed PBLUP in 7 and 11% for days to death and binary survival, respectively. The ssGBLUP could be an alternative approach to improve the accuracy of breeding values for resistance against infectious pancreatic necrosis virus in rainbow trout, using information from genotyped and non-genotyped animals.     

新城疫病毒HN基因的遗传变异与HI相关性的研究

选取国内1999~2004年分离的新城疫野毒10株,经CEF蚀斑纯化和SPF鸡胚增殖,对其血凝素-神经氨酸酶(HN)基因分别进行克隆和测序,结合在GenBank中发表的LaSota、F48E9和Clone30等参考序列,对其氨基酸序列进行遗传变异分析,绘制系统发育树。利用SPF鸡在隔离器中分别制备上述NDV毒株的单因子阳性血清,进行血凝抑制(HI)交叉试验,计算NDV不同株之间的HI相关系数(r)。利用统计学软件SPSS8.0对NDV不同株之间的HN氨基酸同源率和HI相关系数(r)进行相关比较。结果表明:NDV野毒间氨基酸高度同源,同源性为96.5%~99.8%,而与LaSota、F48E9和Clone30同源率仅为87.4%~89.9%;所有野毒均缺乏1个潜在的糖基化位点;HN基因的氨基酸同源性与HI相关系数显著相关(P<0.01,r=0.55)。     

Use of natural molecules as anti-angiogenic inhibitors for vascular endothelial growth factor receptor

Angiogenesis refers to the formation of new blood vessels, controlled by certain chemicals, which on stimulation repairs damaged cells or form new ones. Other chemicals, called angiogenesis inhibitors, signal the process to stop, having only mild side effects and are non toxic to most healthy cells. In our study, attempt was made to find potent anti-angiogenic inhibitor (pazopanib was considered as a reference drug) for vascular endothelial growth factor receptor (VEGFR-1/FLT-1), which served as a molecular target, using natural agents targeting biological processes important in cancer. Hundreds of natural molecules were initially screened based on lipinski''s rule of five and the satisfying ones were taken for receptor-ligand interaction study using docking tools like HEX and quantum. Around fifteen molecules were taken as lead molecule and their binding pocket on VEGF was analyzed using SwissPDBviewer and Q-site finder. The investigational drug pazopanib was found to be interacting with leucine 32 and glutamine 30 in terms of hydrogen bond with the distance of 1.86 and 2.49 A0 respectively. Ames test for the molecules was predicted for probability of mutagenicity on molecular systems such as blood, cardiovascular system, gastrointestinal system; kidney, liver and lung were considered for further screening of the molecules. The natural molecules curcumin, epigallocatechin gallate (EGCG), barrigtozenol and finasteride were showing reliable interaction with VEGFR and their pharmacokinetics parameters were comparatively good than the pazopanib. The dietary product curcumin and EGCG can be cancer chemopreventive agents and the natural molecules barringtozenol and finasteride can be effective inhibitors for VEGFR.     

Effect of amyloids on the vesicular machinery: implications for somatic neurotransmission

Certain neurodegenerative diseases are thought to be initiated by the aggregation of amyloidogenic proteins. However, the mechanism underlying toxicity remains obscure. Most of the suggested mechanisms are generic in nature and do not directly explain the neuron-type specific lesions observed in many of these diseases. Some recent reports suggest that the toxic aggregates impair the synaptic vesicular machinery. This may lead to an understanding of the neuron-type specificity observed in these diseases. A disruption of the vesicular machinery can also be deleterious for extra-synaptic, especially somatic, neurotransmission (common in serotonergic and dopaminergic systems which are specifically affected in Alzheimer''s disease (AD) and Parkinson''s disease (PD), respectively), though this relationship has remained unexplored. In this review, we discuss amyloid-induced damage to the neurotransmitter vesicular machinery, with an eye on the possible implications for somatic exocytosis. We argue that the larger size of the system, and the availability of multi-photon microscopy techniques for directly visualizing monoamines, make the somatic exocytosis machinery a more tractable model for understanding the effect of amyloids on all types of vesicular neurotransmission. Indeed, exploring this neglected connection may not just be important, it may be a more fruitful route for understanding AD and PD.     

Relationships Between Kendall's Coefficient of Concordance and a Nonparametric Measure of Phenotypic Stability with Implications for the Consistency in Rankings as Affected by Variance Components

For a two-way classification with rows (= genotypes) and columns (= environments) relationships between Kendall's coefficient of concordance W and a nonparametric measure of phenotypic stability S (= variance among the ranks over the environments) are presented. This provides an analogy between Wricke's ecovalence and the sum of squares of genotype-environment interactions on the parametric side and S and Kendall's W on the nonparametric side: S is a genotype's contribution to the discordance (1 — W) in the data set, while Wricke's ecovalence is a genotype's contribution to the genotype-environment interaction sum of squares. Genotype x environment interactions may lead, but must not necessarily lead to non-identical rank orders of the genotypes in different environments (crossover versus noncrossover interactions). When does interaction become rank interaction? The similarity of the rank orders (measured by W) can be approximately expressed by the ratio of the genotypic variance and sum of genotypic variance plus residual variance. For the consistency of rankings this relation leads to an approximate test of significance which is based on variance components. Finally, a numerical example is given using grain yield data of 20 genotypes (varieties) of winter wheat in 10 environments (locations) from German registration trials.     

Divergence with gene flow as facilitated by ecological differences: within-island variation in Darwin's finches

Divergence and speciation can sometimes proceed in the face of, and even be enhanced by, ongoing gene flow. We here study divergence with gene flow in Darwin''s finches, focusing on the role of ecological/adaptive differences in maintaining/promoting divergence and reproductive isolation. To this end, we survey allelic variation at 10 microsatellite loci for 989 medium ground finches (Geospiza fortis) on Santa Cruz Island, Galápagos. We find only small genetic differences among G. fortis from different sites. We instead find noteworthy genetic differences associated with beak. Moreover, G. fortis at the site with the greatest divergence in beak size also showed the greatest divergence at neutral markers; i.e. the lowest gene flow. Finally, morphological and genetic differentiation between the G. fortis beak-size morphs was intermediate to that between G. fortis and its smaller (Geospiza fuliginosa) and larger (Geospiza magnirostris) congeners. We conclude that ecological differences associated with beak size (i.e. foraging) influence patterns of gene flow within G. fortis on a single island, providing additional support for ecological speciation in the face of gene flow. Patterns of genetic similarity within and between species also suggest that interspecific hybridization might contribute to the formation of beak-size morphs within G. fortis.     

The neural and cognitive correlates of aimed throwing in chimpanzees: a magnetic resonance image and behavioural study on a unique form of social tool use

It has been hypothesized that neurological adaptations associated with evolutionary selection for throwing may have served as a precursor for the emergence of language and speech in early hominins. Although there are reports of individual differences in aimed throwing in wild and captive apes, to date there has not been a single study that has examined the potential neuroanatomical correlates of this very unique tool-use behaviour in non-human primates. In this study, we examined whether differences in the ratio of white (WM) to grey matter (GM) were evident in the homologue to Broca's area as well as the motor-hand area of the precentral gyrus (termed the KNOB) in chimpanzees that reliably throw compared with those that do not. We found that the proportion of WM in Broca's homologue and the KNOB was significantly higher in subjects that reliably throw compared with those that do not. We further found that asymmetries in WM within both brain regions were larger in the hemisphere contralateral to the chimpanzee's preferred throwing hand. We also found that chimpanzees that reliably throw show significantly better communication abilities than chimpanzees that do not. These results suggest that chimpanzees that have learned to throw have developed greater cortical connectivity between primary motor cortex and the Broca's area homologue. It is suggested that during hominin evolution, after the split between the lines leading to chimpanzees and humans, there was intense selection on increased motor skills associated with throwing and that this potentially formed the foundation for left hemisphere specialization associated with language and speech found in modern humans.     

A novel method for estimating the number of species within a region

Ecologists are often required to estimate the number of species in a region or designated area. A number of diversity indices are available for this purpose and are based on sampling the area using quadrats or other means, and estimating the total number of species from these samples. In this paper, a novel theory and method for estimating the number of species is developed. The theory involves the use of the Laplace method for approximating asymptotic integrals. The method is shown to be successful by testing random simulated datasets. In addition, several real survey datasets are tested, including forests that contain a large number (tens to hundreds) of tree species, and an aquatic system with a large number of fish species. The method is shown to give accurate results, and in almost all cases found to be superior to existing tools for estimating diversity.     

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

We have generated a novel, neuro-specific ncRNA microarray, covering 1472 ncRNA species, to investigate their expression in different mouse models for central nervous system diseases. Thereby, we analyzed ncRNA expression in two mouse models with impaired calcium channel activity, implicated in Epilepsy or Parkinson''s disease, respectively, as well as in a mouse model mimicking pathophysiological aspects of Alzheimer''s disease. We identified well over a hundred differentially expressed ncRNAs, either from known classes of ncRNAs, such as miRNAs or snoRNAs or which represented entirely novel ncRNA species. Several differentially expressed ncRNAs in the calcium channel mouse models were assigned as miRNAs and target genes involved in calcium signaling, thus suggesting feedback regulation of miRNAs by calcium signaling. In the Alzheimer mouse model, we identified two snoRNAs, whose expression was deregulated prior to amyloid plaque formation. Interestingly, the presence of snoRNAs could be detected in cerebral spine fluid samples in humans, thus potentially serving as early diagnostic markers for Alzheimer''s disease. In addition to known ncRNAs species, we also identified 63 differentially expressed, entirely novel ncRNA candidates, located in intronic or intergenic regions of the mouse genome, genomic locations, which previously have been shown to harbor the majority of functional ncRNAs.     

Intranuclear Aggregation of Mutant FUS/TLS as a Molecular Pathomechanism of Amyotrophic Lateral Sclerosis

Dominant mutations in FUS/TLS cause a familial form of amyotrophic lateral sclerosis (fALS), where abnormal accumulation of mutant FUS proteins in cytoplasm has been observed as a major pathological change. Many of pathogenic mutations have been shown to deteriorate the nuclear localization signal in FUS and thereby facilitate cytoplasmic mislocalization of mutant proteins. Several other mutations, however, exhibit no effects on the nuclear localization of FUS in cultured cells, and their roles in the pathomechanism of fALS remain obscure. Here, we show that a pathogenic mutation, G156E, significantly increases the propensities for aggregation of FUS in vitro and in vivo. Spontaneous in vitro formation of amyloid-like fibrillar aggregates was observed in mutant but not wild-type FUS, and notably, those fibrils functioned as efficient seeds to trigger the aggregation of wild-type protein. In addition, the G156E mutation did not disturb the nuclear localization of FUS but facilitated the formation of intranuclear inclusions in rat hippocampal neurons with significant cytotoxicity. We thus propose that intranuclear aggregation of FUS triggered by a subset of pathogenic mutations is an alternative pathomechanism of FUS-related fALS diseases.     

Identification of ubiquilin, a novel presenilin interactor that increases presenilin protein accumulation

Mutations in the highly homologous presenilin genes encoding presenilin-1 and presenilin-2 (PS1 and PS2) are linked to early-onset Alzheimer's disease (AD). However, apart from a role in early development, neither the normal function of the presenilins nor the mechanisms by which mutant proteins cause AD are well understood. We describe here the properties of a novel human interactor of the presenilins named ubiquilin. Yeast two-hybrid (Y2H) interaction, glutathione S-transferase pull-down experiments, and colocalization of the proteins expressed in vivo, together with coimmunoprecipitation and cell fractionation studies, provide compelling evidence that ubiquilin interacts with both PS1 and PS2. Ubiquilin is noteworthy since it contains multiple ubiquitin-related domains typically thought to be involved in targeting proteins for degradation. However, we show that ubiquilin promotes presenilin protein accumulation. Pulse-labeling experiments indicate that ubiquilin facilitates increased presenilin synthesis without substantially changing presenilin protein half-life. Immunohistochemistry of human brain tissue with ubiquilin-specific antibodies revealed prominent staining of neurons. Moreover, the anti-ubiquilin antibodies robustly stained neurofibrillary tangles and Lewy bodies in AD and Parkinson's disease affected brains, respectively. Our results indicate that ubiquilin may be an important modulator of presenilin protein accumulation and that ubiquilin protein is associated with neuropathological neurofibrillary tangles and Lewy body inclusions in diseased brain.     

Communal range defence in primates as a public goods dilemma

Classic socio-ecological theory holds that the occurrence of aggressive range defence is primarily driven by ecological incentives, most notably by the economic defendability of an area or the resources it contains. While this ecological cost–benefit framework has great explanatory power in solitary or pair-living species, comparative work on group-living primates has always found economic defendability to be a necessary, but not sufficient condition to account for the distribution of effective range defence across the taxon. This mismatch between theory and observation has recently been ascribed to a collective action problem among group members in, what is more informatively viewed as, a public goods dilemma: mounting effective defence of a communal range against intrusions by outgroup conspecifics. We here further develop this framework, and report on analyses at three levels of biological organization: across species, across populations within a single lineage and across groups and individuals within a single population. We find that communal range defence in primates very rarely involves collective action sensu stricto and that it is best interpreted as the outcome of opportunistic and strategic individual-level decisions. Whether the public good of a defended communal range is produced by solitary, joint or collective action is thus the outcome of the interplay between the unique characteristics of each individual, local and current socio-ecological conditions, and fundamental life-history traits of the species.     

Role of radiation therapy in the multidisciplinary management of Ewing's Sarcoma of bone in pediatric patients: An effective treatment for local control

Background

Radiotherapy (RT) plays an important role in the multidisciplinary management of Ewing''s Sarcoma (ES), especially in unresectable cases.

Aim

Assessment of efficacy of RT in terms of local control in pediatric patients with primary ES of bone.

Materials and methods

Thirty-six patients younger than 17 years old with ES treated with combined RT and chemotherapy with (N = 14) or without (N = 22) prior surgery from 1981 to 2008 were retrospectively reviewed. Since 1995, they were all treated according to the Spanish Society of Pediatric Oncology protocol (55.5% cases). Those patients received vincristine, ifosfamide, doxorubicin and etoposide. The TNM classification was as follows: 17 T1, 18 T2 and 1 T3; 36 N0; 29 M0, 5 M1a and 2 M1b. Analysis was stratified by treatment: definitive RT or pre/postoperative RT.

Results

The 36 patients (21 male; 15 female) had a median age of 10 years (range 2–17 years). Median follow-up of living patients was 105 months. The 2-year local control (LC) rate for all patients was 88%. Five-year LC rates for patients treated with definitive and pre/postoperative RT were 91% and 86%, respectively. Two-year overall survival and disease-free survival rates for all patients were 68% and 66%, respectively. Low phosphatase alkaline levels and local and distant recurrences were significantly predictive of worse prognosis (P = 0.021, P = 0.011, P = 0.007, respectively).

Conclusion

Radiotherapy with and without surgery is a highly effective local treatment option in the multidisciplinary management of ES in pediatric patients.     

Antiplatelet antibodies in cases of Glanzmann's thrombasthenia with and without a history of multiple platelet transfusion

Antiplatelet antibodies are known to be present in a wide spectrum of patients, which include chronic Idiopathic Thrombocytopenic Purpura (ITP), infections, etc., including Glanzmann''s thrombasthenia (GT) patients who receive multiple platelet transfusions. The presence of natural antibodies to platelet receptors is not studied in cases of GT. We studied the antiplatelet antibodies in 23 patients with GT, 15 of which had received multiple transfusions and eight that had not received transfusions, along with 50 cases of chronic ITP. The prevalence and specificity of platelet-bound antibodies were detected by inhibition assays using O-group platelets on flow cytometry. The mean antiplatelet antibodies in 15 patients of GT who had not received transfusions and eight patients with multiple transfusions was 8427 + 2131.88 and 9038 + 2856 antibodies/platelet, respectively, while in case of the 50 ITP patients studied, it was 22166 + 5616 antibodies/platelet (Normal Range 1500–3200 antibodies/platelet). We conclude that GT patients who have not received transfusions may develop antiplatelet antibodies to the missing/abnormal receptor. Whether this is due to a molecular mimicry or due to some other mechanism needs to be explored.