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Supplementary Figure 2 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Testicular germ cell cancers in young adult men derive from a precursor lesion called carcinoma in situ (CIS) of the testis. CIS cells were suggested to arise from primordial germ cells or gonocytes. However, direct studies on purified samples of CIS cells are lacking. To overcome this problem, we performed laser microdissection of CIS cells. Highly enriched cell populations were obtained and subjected to gene expression analysis. The expression profile of CIS cells was compared with microdissected gonocytes, oogonia, and cultured embryonic stem cells with and without genomic aberrations. Three samples of each tissue type were used for the analyses. Unique expression patterns for these developmentally very related cell types revealed that CIS cells were very similar to gonocytes because only five genes distinguished these two cell types. We did not find indications that CIS was derived from a meiotic cell, and the similarity to embryonic stem cells was modest compared with gonocytes. Thus, we provide new evidence that the molecular phenotype of CIS cells is similar to that of gonocytes. Our data are in line with the idea that CIS cells may be gonocytes that survived in the postnatal testis. We speculate that disturbed development of somatic cells in the fetal testis may play a role in allowing undifferentiated cells to survive in the postnatal testes. The further development of CIS into invasive germ cell tumors may depend on signals from their postpubertal niche of somatic cells, including hormones and growth factors from Leydig and Sertoli cells. [Cancer Res 2009;69(12):5241–50]

Supplementary Table 1 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Supplementary Figure 1 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Supplementary Table 4 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Supplementary Table 3 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Supplementary Figure 3 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

Supplementary Table 2 from Analysis of Gene Expression Profiles of Microdissected Cell Populations Indicates that Testicular Carcinoma In situ Is an Arrested Gonocyte

This work investigates whether the unique low thermal expansion property of Invar (64Fe–36Ni) is retained after processing using the additive manufacturing process selective laser melting (SLM). Using this process, near-full-density components (99.96%) were formed by melting thin (20 μm) layers of powdered Invar (15–45 μm particle size). The mechanical properties of SLM Invar were comparable to that of cold-drawn Invar36®; however, the thermal coefficient of expansion was observed to be a lower value and negative up until 100 °C. This negative value was attributed to residual stress in the as-deposited parts. The low thermal expansion property of Invar was still maintained when processed using a non-conventional layer-based additive manufacturing technique.

The Selective Laser Melting (SLM) process generates large thermal gradients during rapid melting of metallic powdered feedstock. During solidification certain alloys suffer from thermally induced micro-cracking which cannot be eliminated by process optimisation. An alloy’s crack susceptibility may reduce by increasing its Thermal Shock Resistance (TSR), potentially achieved through an increase in tensile strength. This hypothesis is investigated with Hastelloy X, a common nickel-base superalloy of known high crack susceptibility when processing SLM. It is demonstrated that through consideration of the imposed rapid solidification conditions, Hastelloy X can be made to form a supersaturated solid solution in the as deposited state. The fundamental solid solution strengthening (SSS) effect is exploited to generate an increase in lattice stress, by increasing the most potent SSS elements present within the alloy, whilst maintaining specification composition. The modified alloy displayed a 65% reduction in cracking and an increase in elevated temperature tensile strength, lending support to the initial hypothesis and identifying a possible approach for developing further SLM crack resistant versions of well-known alloy compositions.

Genomic integrity of human pluripotent stem cell (hPSC) lines requires routine monitoring. We report here that novel karyotyping assay, utilizing bead-bound bacterial artificial chromosome probes, provides a fast and easy tool for detection of chromosomal abnormalities in hPSC lines. The analysis can be performed from low amounts of DNA isolated from whole cell pools with simple data analysis interface. The method enables routine screening of stem cell lines in a cost-efficient high-throughput manner., Highlights ► We report a novel high-throughput karyotyping assay for human pluripotent cells. ► This assay provides fast and easy tool for detection of chromosomal abnormalities. ► The analysis can be run from low DNA amounts with simple data analysis interface. ► The results are in good concordance with the data from G-banding and SNP arrays. ► The assay enables routine screening of stem cell lines in a cost-efficient manner.

The pluripotent potential of embryonic stem cells has often seen them touted as the future of regenerative medicine. The road to any therapeutic success however, must stretch back to teratocarcinoma, the tumour from which pluripotent stem cells (embryonal carcinoma cells) were first derived. This 2011 meeting in Cardiff acted as a historical perspective from which the impact of embryonal carcinoma cell research on the present pluripotent stem cell landscape could be observed, with many of the early luminaries in this field still very active. The meeting addressed the genetic and epigenetic make-up of pluripotent stem cells, the mechanisms which control their fate, and their relationship to the early embryo proper. With each speaker tasked with revisiting previous questions, this meeting demonstrated how far has been travelled, yet how far is left to go.

The ligand binding site of Cys-loop receptors is dominated by aromatic amino acids. In GABA(C) receptors, these are predominantly tyrosine residues, with a number of other aromatic residues located in or close to the binding pocket. Here we examine the roles of these residues using substitution with both natural and unnatural amino acids followed by functional characterization. Tyr198 (loop B) has previously been shown to form a cation-π interaction with GABA; the current data indicate that none of the other aromatic residues form such an interaction, although the data indicate that both Tyr102 and Phe138 may contribute to stabilization of the positively charged amine of GABA. Tyr247 (loop C) was very sensitive to substitution and, combined with data from a model of the receptor, suggest a π-π interaction with Tyr241 (loop C); here again functional data show aromaticity is important. In addition the hydroxyl group of Tyr241 is important, supporting the presence of a hydrogen bond with Arg104 suggested by the model. At position Tyr102 (loop D) size and aromaticity are important; this residue may play a role in receptor gating and/or ligand binding. The data also suggest that Tyr167, Tyr200, and Tyr208 have a structural role while Tyr106, Trp246, and Tyr251 are not critical. Comparison of the agonist binding site "aromatic box" across the superfamily of Cys-loop receptors reveals some interesting parallels and divergences.

Summary The antigenic profile of human embryonic stem (ES) and embryonal carcinoma (EC) cells has served as a key element of their characterization, with a common panel of surface and intracellular markers now widely used. Such markers have been used to identify cells within the ‘undifferentiated state’, yet it appears that this categorization may be an oversimplification, because a number of sub-states appear to exist within this state. To increase the resolution of the undifferentiated state, we have generated eight novel monoclonal antibodies, all capable of recognizing undifferentiated human ES and EC cells, and herein describe their characterization. The reactivity of these antibodies against a range of cell lines is reported, as well as their developmental regulation, basic biochemistry and reactivity in immunohistochemistry of testicular germ cell tumours. Our data reveal a range of reactivity for all antibodies against both ES and EC cells, suggesting that these markers will afford recognition of unique sub-states within the undifferentiated stem cell compartment.

Prolonged culture of human embryonic stem cells (hESCs) can lead to adaptation and the acquisition of chromosomal abnormalities, underscoring the need for rigorous genetic analysis of these cells. Here we report the highest-resolution study of hESCs to date using an Affymetrix SNP 6.0 array containing 906,600 probes for single nucleotide polymorphisms (SNPs) and 946,000 probes for copy number variations (CNVs). Analysis of 17 different hESC lines maintained in different laboratories identified 843 CNVs of 50 kb-3 Mb in size. We identified, on average, 24% of the loss of heterozygosity (LOH) sites and 66% of the CNVs changed in culture between early and late passages of the same lines. Thirty percent of the genes detected within CNV sites had altered expression compared to samples with normal copy number states, of which >44% were functionally linked to cancer. Furthermore, LOH of the q arm of chromosome 16, which has not been observed previously in hESCs, was detected.

The long-term culture of human embryonic stem (ES) cells is inevitably subject to evolution, since any mutant that arises with a growth advantage will be selectively amplified. However, the evolutionary influences of population size, mutation rate, and selection pressure are frequently overlooked. We have constructed a Monte Carlo simulation model to predict how changes in these factors can influence the appearance and spread of mutant ES cells, and verified its applicability by comparison with in vitro data. This simulation provides an estimate for the expected rate of generation of culture-adapted ES cells under different assumptions for the key parameters. In particular, it highlights the effect of population size, suggesting that the maintenance of cells in small populations reduces the likelihood that abnormal cultures will develop.

Testicular germ cell cancers in young adult men derive from a precursor lesion called carcinoma in situ (CIS) of the testis. CIS cells were suggested to arise from primordial germ cells or gonocytes. However, direct studies on purified samples of CIS cells are lacking. To overcome this problem, we performed laser microdissection of CIS cells. Highly enriched cell populations were obtained and subjected to gene expression analysis. The expression profile of CIS cells was compared with microdissected gonocytes, oogonia, and cultured embryonic stem cells with and without genomic aberrations. Three samples of each tissue type were used for the analyses. Unique expression patterns for these developmentally very related cell types revealed that CIS cells were very similar to gonocytes because only five genes distinguished these two cell types. We did not find indications that CIS was derived from a meiotic cell, and the similarity to embryonic stem cells was modest compared with gonocytes. Thus, we provide new evidence that the molecular phenotype of CIS cells is similar to that of gonocytes. Our data are in line with the idea that CIS cells may be gonocytes that survived in the postnatal testis. We speculate that disturbed development of somatic cells in the fetal testis may play a role in allowing undifferentiated cells to survive in the postnatal testes. The further development of CIS into invasive germ cell tumors may depend on signals from their postpubertal niche of somatic cells, including hormones and growth factors from Leydig and Sertoli cells. [Cancer Res 2009;69(12):5241–50]

Human embryonic stem cells undergo adaptive changes that can increase their growth capacity upon prolonged culture in vitro. This is frequently associated with nonrandom karyotypic changes, commonly involving amplification of genetic material from chromosomes 12, 17, and X. A recent study suggested that the karyotypically abnormal cells can be identified by their expression of CD30, which confers resistance to apoptosis. We have now investigated CD30 expression and apoptosis in karyotypically normal and abnormal sublines of the human ES cell line, H7, but our results were contrary to those previously observed. In this cell line, CD30 expression did not segregate the normal and abnormal cells, and abnormal cells were not protected from apoptosis. These data suggest that culture adaptation can occur through a variety of mechanisms. Disclosure of potential conflicts of interest is found at the end of this article.

The application of human embryonic stem cells (HESCs) to provide differentiated cells for regenerative medicine will require the continuous maintenance of the undifferentiated stem cells for long periods in culture. However, chromosomal stability during extended passaging cannot be guaranteed, as recent cytogenetic studies of HESCs have shown karyotypic aberrations. The observed karyotypic aberrations probably reflect the progressive adaptation of self-renewing cells to their culture conditions. Genetic change that increases the capacity of cells to proliferate has obvious parallels with malignant transformation, and we propose that the changes observed in HESCs in culture reflect tumorigenic events that occur in vivo, particularly in testicular germ cell tumors. Further supporting a link between culture adaptation and malignancy, we have observed the formation of a chromosomal homogeneous staining region in one HESC line, a genetic feature almost a hallmark of cancer cells. Identifying the genes critical for culture adaptation may thus reveal key players for both stem cell maintenance in vitro and germ cell tumorigenesis in vivo.

To circumvent difficulties of isolating pure populations of cancer stem cells (CSCs) for the purpose of identifying malignancy-specific gene expression, we have compared exon-resolution transcriptomic profiles of 5 embryonal carcinoma (EC) cell lines, a histological subtype of germ cell tumor (GCT), to their nonmalignant caricature, specifically 6 human embryonic stem (ES) cell lines. Both cell types are readily accessible, and were purified for undifferentiated cells only. We identified a set of 28 differentially expressed genes, many of which had cancer and stemness roles. Overexpression of the recently discovered pluripotency gene NR5A2 in malignant EC cells revealed an intriguing indication of how WNT-mediated dysregulation of pluripotency is involved with malignancy. Expression of these 28 genes was further explored within 2 publically available data sets of primary EC tumors and normal testis. At the exon-level, alternative splicing events were detected in ZNF195, DNMT3B, and PMF1, and alternative promoters were detected for ASH2L and ETV5. These events were validated by reverse transcriptase-polymerase chain reaction-based methods in EC and ES lines, where the alternative splicing event in the de novo DNA methyltransferase DNMT3B may have functional consequences. In conclusion, we have identified malignancy-specific gene expression differences within a rigorous pluripotent stem cell context. These findings are of particular interest for both GCT and ES cell biology, and, in general, to the concept of CSCs.

The excitement surrounding human ES cell research is indicative of the potential that these cells hold for regenerative therapy. However, realizing this potential requires efficient derivation of the necessary cell type and also a guarantee that the differentiated product poses no threat to the patient. With respect to these prerequisites, robust differentiation protocols have been developed for the generation of several cell types, in particular those of the neural lineage. For example, a culture of approximately 90% neural progenitors can be generated from human ES cells by simply adding dorsomorphin (a selective small molecule inhibitor of bone morphogenetic protein signaling) to a basal growth media (1). Furthermore, the fact that the ES cell–derived neurons possess the characteristics of those found in vivo has prompted clinical trials assessing their potential for therapy. Geron Corp. was among the first to test the waters with the intention of creating tissue to repair spinal cord injury, although financial issues have brought a premature end to this trial. The issue of transplant safety, however, remains a potential stumbling block. Unlike differentiation efficiency, safety is a difficult parameter to quantify, and our knowledge is limited by the lack of data from human recipients. As a result, the stem cell field seems to have drawn a direct correlation between risk and mutation, so that any tissue whose genomic integrity has been compromised is not considered suitable for therapy. Human ES cell research has had to contend with this issue since 2004, when karyotypic changes were first reported in cultured human ES cells (2), although changes in tissue-derived cells have only been sporadically reported. With this in mind, the impact of the report in this issue of the JCI by Varela and colleagues that human ES cell–derived neural stem cells (NSCs) recurrently acquire genetic changes (3) must be considered.

The promise that human embryonic stem (ES) cells hold for regenerative medicine has generated much excitement since their initial derivation. However, before the potential of these cells can be realised, efficient differentiation protocols must be devised, and the cells should be shown to pose no safety risk. Despite initial reports suggesting that human ES cells are karyotypically stable, during the last decade it has become apparent that they do acquire genetic and/or epigenetic changes during culture, reflecting an adaptation to life in vitro. This culture adaptation can affect ES cell growth and differentiation, but of particular concern is the potential link between adaptation and cancer, which would become an issue if the cells are to be used for transplantation. In this chapter we discuss the issues surrounding culture adaptation of ES cells, and the potential impacts, both positive and negative, it may have on the use of these cells for regenerative medicine.

Embryonic stem (ES) cells may acquire genetic and epigenetic changes upon prolonged passage in culture, which can confer on them more robust growth characteristics. The genetic changes are often manifest cytogenetically as nonrandom gains of chromosomal regions that are also typically amplified in embryonal carcinoma (EC) cells, the malignant counterpart of ES cells. Although this raises some concerns for the future use of ES or induced pluripotent stem (iPS) cells in regenerative medicine, or in vitro screening applications, these concerns remain largely hypothetical. It may be that potential problems can be substantially ­mitigated when we understand more about the underlying causes and mechanisms of culture adaptation. At the same time, this phenomenon also provides a tool that can help dissect the mechanisms controlling stem cell behavior, while potentially providing more robust cells for use in some applications.

Nanosecond optical Kerr‐effect (OKE) measurements are reported using a modified apparatus, designed to enable rapid and precise data recording in pure liquids. Careful design of the apparatus enables measurements to be made at several inducing wavelengths without substantial apparatus modifications. The first measurement of the optical Kerr effect for benzene at an inducing wavelength of 532 nm is presented together with novel OKE data for the hitherto unstudied homologous alcohol series from methanol to 1‐dodecanol. Analysis of the results indicates for this series the existence of a linear relationship between the carbon chain length and the optically induced Kerr constant somewhat similar to the behavior previously observed in the n‐alkanes.

The optical Kerr effect, also known as laser-induced birefringence, has been measured for some 21 pure liquids which variously comprise three homologous liquid series of the n-alkanes, 1-alkenes, and 1-alkynes. Birefringence has been induced using nanosecond pulses of laser light at 1064-nm wavelength and detected at 442-nm wavelength. For all liquids, a quadratic dependence was obtained for the observed birefringence upon the inducing laser beam electric vector amplitude

The optical Kerr effect, also known as laser-induced birefringence, has been measured for some 21 pure liquids which variously comprise three homologous liquid series of the n-alkanes, 1-alkenes, and 1-alkynes. Birefringence has been induced using nanosecond pulses of laser light at 1064-nm wavelength and detected at 442-nm wavelength. For all liquids, a quadratic dependence was obtained for the observed birefringence upon the inducing laser beam electric vector amplitude

Vicenzo Calvanese et al..., Developmental genes are silenced in embryonic stem cells by a bivalent histone-based chromatin mark. It has been proposed that this mark also confers a predisposition to aberrant DNA promoter hypermethylation of tumor suppressor genes (TSGs) in cancer. We report here that silencing of a significant proportion of these TSGs in human embryonic and adult stem cells is associated with promoter DNA hypermethylation. Our results indicate a role for DNA methylation in the control of gene expression in human stem cells and suggest that, for genes repressed by promoter hypermethylation in stem cells in vivo, the aberrant process in cancer could be understood as a defect in establishing an unmethylated promoter during differentiation, rather than as an anomalous process of de novo hypermethylation., This work was primarily supported by the European Union (LSHG-CT-2006-018739; ESTOOLS). MFF is funded by the Spanish Ramon & Cajal Programme and the Health Department of the Spanish Government (PI061267). The Cancer Epigenetics group at the CNIO is supported by the Health (FIS01-04) and Education and Science (I+D+I MCYT08-03, FU2004-02073/BMC and Consolider MEC09-05) Departments of the Spanish Government, the European Grant TRANSFOG LSHC-CT-2004-503438, and the Spanish Association Against Cancer (AECC). VC is a recipient of a Fellowship from the FPU Spanish Research Programme. CLL and BSA are supported by the Health Department of the Spanish Government (PI051707). The BACM is supported by the Consejería de Salud de la Junta de Andalucía (0029 and, 0030/2006 to PM) and, the Spanish Ministry of Health to PM (FIS PI070026). CB is supported by the International Jose Carreras Foundation against Leukemia (EDThomas-05) and the ISCIII (FIS 3+3 contract). The Institute of Reconstructive Neurobiology received additional funding from the DFG and the Hertie Foundation. BS, AbH and AnH are supported by the Fundación Progreso y Salud and Instituto de Salud Carlos III-Red Española de Terapia Celular (RD06/0010/0025 ). PWA, NH and HDM are also supported by the MRC.

Teratocarcinomas are a subset of tumours that result from the neoplastic transformation of primordial germ cells. Such germ cell tumours (GCT) are histologically heterogeneous, reflecting a capacity for differentiation (pluripotency) of their embryonal carcinoma (EC) stem cells. However, malignant evolution of these tumours may ultimately correlate with a decrease in pluripotency, because this would tend to increase the propensity of EC cells for self-renewal. Human embryonic stem (ES) cells, derived from early blastocysts, closely resemble EC cells and, on prolonged culture in vitro, acquire progressive genetic changes that show striking similarity to those seen in GCT (e.g. gain of material from chromosome 12). In parallel, these abnormal ES cells show enhanced population growth rates and plating efficiencies, indicative of their adaptation to culture conditions. Understanding the mechanisms that drive such culture adaptation of ES cells may also provide insights into the development and progression of GCT.

We have previously shown, using radioligand binding studies, that N-methyl-d-aspartate (NMDA) NR1 and NR2A receptor subunits density was decreased in the forebrain of morphine-dependent rats. We have now determined if morphine-dependent rats display regional differences in NMDA receptor expression and whether such changes are functionally relevant. In morphine-dependent rats, the expression of NR1 and NR2A subunits protein, as determined by Western blotting with NMDA receptor subunit antibodies, were decreased in frontal cortex and hippocampus but significantly increased in the nucleus accumbens. The expression of the NR2B subunit was unchanged in all regions examined. In separate groups of morphine-dependent rats, MK-801-induced hyperactivity (thought to be mediated via modulation of nucleus accumbens dopamine release) was significantly enhanced in morphine-dependent animals. Similarly, the MK-801-induced increase of dopamine metabolism was significantly increased in the nucleus accumbens of morphine-dependent animals as compared to sham controls. Results provide both biochemical and behavioural evidence to suggest that NMDA receptor function in the nucleus accumbens, at least with respect to an interaction with the limbic dopamine system, is markedly enhanced in morphine-dependent rats. This increase in function may be associated with an enhanced expression of NMDA receptors, particularly those in the nucleus accumbens containing the NR2A subunit. Taken together, these data support several studies in the literature indicating that NMDA receptors in the nucleus accumbens are involved in the process of opiate dependence.

gamma-Aminobutyric acid, type A (GABA(A)) receptors, of which the GABA(C) receptor family is a subgroup, are members of the Cys loop family of neurotransmitter receptors. Homology modeling of the extracellular domain of these proteins has revealed many molecular details, but it is not yet clear how GABA is orientated in the binding pocket. Here we have examined the role of arginine residues that the homology model locates in or close to the binding site of the GABA(C) receptor (Arg-104, Arg-170, Arg-158, and Arg-249) using mutagenesis and functional studies. The data suggest that Arg-158 is critical for GABA binding and/or function; substitution with Lys, Ala, or Glu resulted in nonfunctional receptors, and modeling placed the carboxylate of GABA within 3A of this residue. Substitution of Arg-104 with Ala or Glu resulted in10,000-fold increases in EC(50) values compared with wild type receptors, and modeling indicated a role of this residue both in binding GABA and in the structure of the binding pocket. Substitution of Arg-170 with Asp or Ala yielded nonfunctional receptors, whereas Lys caused an approximately 10-fold increase in EC(50). Arg-249 was substituted with Ala, Glu, or Asp with relatively small ( approximately 4-30-fold) changes in EC(50). These and data from other residues that the model suggested could interact with GABA (His-105, Ser-168, and Ser-243) support a location for GABA in the binding site with its carboxylate pincered between Arg-158 and Arg-104, with Arg-104, Arg-170, and Arg-249 contributing to the structure of the binding pocket through salt bridges and/or hydrogen bonds.

GABA(C) (rho) receptors are members of the Cys-loop superfamily of neurotransmitter receptors, which includes nicotinic acetylcholine (nACh), 5-HT(3), and glycine receptors. As in other members of this family, the agonist binding site of GABA(C) receptors is rich in aromatic amino acids, but while other receptors bind agonist through a cation-pi interaction to a tryptophan, the GABA(C) binding site has tyrosine at the aligning positions. Incorporating a series of tyrosine derivatives at position 198 using unnatural amino acid mutagenesis reveals a clear correlation between the cation-pi binding ability of the side chain and EC(50) for receptor activation, thus demonstrating a cation-pi interaction between a tyrosine side chain and a neurotransmitter. Comparisons among four homologous receptors show variations in cation-pi binding energies that reflect the nature of the cationic center of the agonist.

We have constructed a molecular model of the ligand-binding domain of the GABA(C) receptor, which is a member of the Cys-loop ligand-gated ion channel family. The extracellular domains of these receptors share similar sequence homology (20%) with Limnaea acetylcholine-binding protein for which an X-ray crystal structure is available. We used this structure as a template for homology modeling of the GABA(C) receptor extracellular domain using FUGUE and MODELLER software. FlexX was then used to dock GABA into the receptor ligand-binding site, resulting in three alternative energetically favorable orientations. Residues located no more than 5 A from the docked GABA were identified for each model; of these, three were found to be common to all models with 14 others present only in certain models. Using data from experimental studies, we propose that the most likely orientation of GABA is with its amine close to Y198, and its carboxylate close to R104. These studies have therefore provided a model of the ligand-binding domain, which will be useful for both GABA(C) and GABA(A) receptor studies, and have also yielded an experimentally testable hypothesis of the location of GABA in the binding pocket. [Figure: see text].

Nanocomposite intermediate rare-earth∕high-boron content hard magnetic alloys, having compositions Nd9Fe73B12.6C1.4M4 (M=Ti, V, Cr, Zr, or Nb), have been produced as melt spun ribbon. As for the Ti addition, all the other solutes were effective in modifying the crystallization behavior so that the Nd2Fe14B phase formed rather than the cubic Nd2Fe23B3 phase. The magnetic properties of the V-, Cr-, Zr-, and Nb-containing alloys in the as-spun state and following annealing are compared with those of the Ti-containing alloy. Good combinations of intrinsic coercivity (1020kAm−1) and of maximum energy product (97kJm−3) were obtained for the V-containing alloy, closely comparable with those for the M=Ti alloy, and the Zr addition also yielded a good property combination.

Measurements are reported of the laser-induced Kerr effect for the homologous series of alk-1-enes up to the icosene member. The effect was induced with the electric vector of an Nd : YAG laser beam, pulsed in the nanosecond timescale and operating at either 1064 nm or 532 nm wavelength. On average, values for 532 nm wavelength are some 50% higher than results for 1064 nm. The first recorded measurements on three alkadienes are also reported using an inducing wavelength of 1064 nm. These data indicate that separation of the unsaturated bonds could be an important factor in the magnitude of the effect.