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Field and laboratory studies indicate that utilisation of biological geotextiles constructed from palm-leaves and other selected organic materials are an effective, sustainable and economically viable soil conservation technique. The three-year plus (1 July 2005–28 February 2009) EU-funded BORASSUS Project (contract no. INCO-CT-2005-510745) evaluated the long-term effectiveness of biological geotextiles in controlling soil erosion and assessing their sustainability and economic viability. These studies progressed in ten countries, both in the ‘industrial north’ (in Europe) and in the ‘developing south’ (Africa, South America and South East Asia). The studied countries in the ‘developing south’ included Brazil, China, The Gambia, South Africa, Thailand and Vietnam. The ‘industrial north’ countries included Belgium, Hungary, Lithuania and the UK. The main findings of these studies are summarised in this paper and thematic information is presented in the other four papers in this Special Issue. Biological geotextiles offer potentially novel bioengineering solutions to environmental problems, including technologies for soil conservation, sustainable plant production and use of indigenous plants, improved ecosystem management by decreasing deforestation, improving agroforestry and cost-effective biogeotextile applications in diverse environments. Biogeotextiles may provide socio-economic platforms for sustainable development and the benefits for developing countries may include poverty alleviation, engagement of local people as stakeholders, employment for disadvantaged groups, small and medium enterprise (SME) development, earning hard currency, environmental education and local community involvement in land reclamation and environmental education programmes. These benefits are achieved through: (i) promotion of sustainable and environmentally friendly palm-agriculture to discourage deforestation, promoting both reforestation and agroforestry; (ii) construction of biogeotextiles enabling development of a rural labour-intensive industry, particularly encouraging employment of socially disadvantaged groups and (iii) export of biogeotextiles to industrialised countries could earn hard currency for developing economies, based on the principles of fair trade. Research and development activities of the BORASSUS Project have improved our knowledge on the effect of biogeotextile mats on the micro- and macro-soil environments and at larger scales through controlled laboratory and field experiments in diverse environments. Copyright © 2011 John Wiley & Sons, Ltd.

Coeliac disease (CD) is an immune-mediated enteropathy triggered by gluten in genetically predisposed individuals. Patients with CD have an increased prevalence of other autoimmune disorders, including type 1 diabetes (T1D) and Graves' disease (GD). CD shares with these conditions certain HLA susceptibility alleles. A number of studies have also shown association of autoimmune diseases, including CD, with the CD28-cytotoxic T lymphocyte antigen 4 (CTLA4)-inducible costimulator (ICOS) region of chromosome 2q33, but until recently the precise causal variant has remained unknown. Recently, it was shown that, in GD, CT60 (+6230G>A), a single nucleotide polymorphism (SNP) at the end of the CTLA4 transcript, is associated with an alteration in the ratio of splice forms of the CTLA4 gene and that this ratio affects disease susceptibility. A similar but weaker association was found with T1D. There is also an independent association of GD and T1D with the SNP MH30 (-23 327G>C), which possibly affects promoter region function. Hypothesizing that CT60 and MH30 may be causal variants in other autoimmune disorders, we investigated these SNPs in CD using 149 family trios and 100 unrelated/unaffected controls. No association was detected with either SNP using both the transmission disequilibrium test (TDT) and case-control methods. Our study appears to have good power to detect moderate genetic effects, but possibly these SNPs exert too weak an effect on risk of CD to have been detected in our sample. Alternatively, the previously noted association of CD with the CTLA4 gene region may be due to different causal variants. Unlike T1D and GD, CD is not a true autoimmune disease, and CD has different associations at the CTLA4 exon 1 SNP +49G>A from all other autoimmune disorders. MH30, CT60, and other SNPs in the region may still warrant further investigation in other CD samples.

Purpose: To determine a gene locus for a family with a dominantly inherited vestibulocerebellar disorder characterised by early onset, but not congenital nystagmus. Design: Observational and experimental study. Methods: We carried out a phenotypic study of a unique four generation family with nystagmus. We performed genetic linkage studies including a genome wide search. Results: Affected family members developed vestibulocerebellar type nystagmus in the first two years of life. A higher incidence of strabismus was noted in affected members. Haplotype construction and analysis of recombination events linked the disorder to a locus (NYS4) on chromosome 13q31-q33 with a lod score of 6.322 at θ=0 for D13S159 and narrowed the region to a 13.8 cM region between markers D13S1300 and D13S158. Conclusions: This study suggests that the early onset acquired nystagmus seen in this family is caused by a single gene defect. Identification of the gene may hold the key to understanding pathways for early eye stabilisation and strabismus.

Susceptibility to coeliac disease has a strong genetic component. The HLA associations have been well described but it is clear that other genes outside this region must also be involved in disease development. Two previous genome-wide linkage studies using the affected sib pair method produced conflicting results. Our own family based linkage study of 16 highly informative pedigrees identified 17 possibly linked regions, each of which produced a result significant at p & 0.05 or less. We have now investigated these 17 regions in a larger set of pedigrees using more finely spaced markers. Fifty multiply affected families were studied, comprising the 16 pedigrees from the original genome screen plus 34 new highly informative pedigrees. A total of 128 microsatellite markers were genotyped with an average spacing between markers of 5 cM. Two-point and three-point linkage analysis using classical and model free methods identified five potential susceptibility loci with heterogeneity lod scores > 2.0, at 6p12, 11p11, 17q12, 18q23 and 22q13.3. The most significant was a heterogeneity lod of 2.6 at D11S914 on chromosome 11p11. This marker maps to a position implicated in one of the two previous genome scans and taken together these results provide strong support for the existence of a susceptibility locus in this region.

SummaryGenetic loci for autosomal dominant pure hereditary spastic paraplegia (ADPHSP) have been mapped to chromosomes 2p, 8q, 12q, 14q, and 15q. We undertook a genomewide linkage screen of a large family with ADPHSP, for which linkage at all previously identified ADPHSP loci was excluded. Analysis of markers on chromosome 19q gave a peak pairwise LOD score of 3.72 at D19S420, allowing assignment of a novel ADPHSP locus (which we have termed “SPG12”) to this region. Haplotype construction and analysis of recombination events narrowed the SPG12 locus to a 16.1-cM region between markers D19S868 and D19S902.

SummaryAutosomal dominant pure hereditary spastic paraplegia (ADPHSP) is clinically characterized by slowly progressive lower-limb spasticity. The condition is genetically heterogeneous, and loci have been mapped at chromosomes 2p, 8q, 14q, and 15q. We have performed a genomewide linkage screen on a large family with ADPHSP, in which linkage to all four previously known loci was excluded. Analysis of markers on chromosome 12q gave a peak pairwise LOD score of 3.61 at D12S1691, allowing us to assign a new locus for ADPHSP (a locus that we have designated “SPG10”) to this region. Haplotype construction and analysis of recombination events narrowed the SPG10 locus to a 9.2-cM region between markers D12S368 and D12S83. In addition, our data strongly suggest that there are at least six ADPHSP loci, since we describe a further family in which linkage to all five known ADPHSP loci has been excluded.

Field and laboratory studies indicate that geotextile mats constructed from palm leaves are an effective, sustainable and economically viable soil conservation technique. The three-year (2005–08) EU-funded BORASSUS Project (Contract Number INCO-CT-2005-510745) is evaluating their long-term effectiveness in controlling soil erosion and assessing their sustainability and economic viability. These studies are in progress in 10 countries, both in the ‘industrial north’ (in Europe) and in the ‘developing south’ (Africa, South America and South-East Asia). This paper focuses on agro-environmental applications and potential in the ‘developing south’ (The Gambia, South Africa, Brazil, China, Thailand and Vietnam). Biogeotextiles offer potentially novel bioengineering solutions to environmental problems, including technologies for soil conservation, sustainable plant production and use of indigenous plants, improved ecosystem management, decreasing deforestation, improving agroforestry and cost-effective geotextile applications in diverse environments. Biogeotextiles may provide socio-economic platforms for sustainable development and the benefits for developing countries may include poverty alleviation, engagement of local people as stakeholders, employment for disadvantaged groups, small and medium enterprise (SME) development, earning hard currency, environmental education and local community involvement in land reclamation and environmental education programmes. These benefits are achieved through: (a) promotion of sustainable and environmentally-friendly palm agriculture to discourage deforestation, promoting both reforestation and agroforestry; (b) construction of palm geotextiles enabling development of a rural labour-intensive industry, particularly encouraging employment of socially-disadvantaged groups and (c) export of palm geotextiles to industrialized countries could earn hard currency for developing economies, based on the principles of fair trade.

Field and laboratory studies suggest geotextile mats constructed from palm leaves are an effective, sustainable and economically viable soil conservation technique. The three-year (2005-08) EU-funded BORASSUS Project (Contract number INCO-CT-2005-510745) is evaluating their long-term effectiveness in controlling soil erosion and assessing their sustainability and economic viability in 10 countries in Africa, Europe, South America and South-East Asia. The technique offers potentially novel bioengineering solutions to environmental problems, including technologies for soil conservation, sustainable plant production and use of indigenous plants, improved ecosystem management, decreasing deforestation, improving agroforestry and cost-effective geotextile applications in diverse environments. Palm geotextiles may improve socio-economic foundations for sustainable development and the benefits for developing countries may include poverty alleviation, engagement of local people as stakeholders, employment for disadvantaged groups, small and medium enterprise (SME) development, earning hard currency, environmental education and local community involvement in land reclamation and environmental education programmes. These benefits are achieved through: (a) Promotion of sustainable and environmentally-friendly palm agriculture to discourage deforestation, promoting both reforestation and agroforestry; (b) Construction of palm geotextiles developing into a rural labour-intensive industry, particularly encouraging employment of socially-disadvantaged groups; and (c) Export of palm geotextiles to industrialized countries earns hard currency for rural developing economies, based on the principles of fair trade. In Europe, experiments are in progress in diverse field environments (agricultural and archaeological sites, coastal sand dunes and engineered slopes) and in laboratory simulations of both water and wind erosion processes.

A comprehensive genetic map containing several hundred microsatellite markers resulted from a large microsatellite mapping project. This was the first real study that introduced high throughput methods to the genetic community. This map and the concurrent technological advances, which will briefly be reviewed, led to further numerous mapping investigations of simple and complex diseases. The annotated draft sequence of approximately three billion base pairs (bp) of the human genome has been completed much sooner than many imagined, due to considerable technological advancements and the international enterprise that resulted. This was a major development for the genetics community, but is only the precursor to the next phase of studying and understanding the variation within the human genome. The awareness of the differences may help us understand the effects on the genetics of the variation between individuals and disease. It is these variations at the nucleotide level that determine the physiological differences, or phenotypes of each individual, including all biological functions at the cellular and body level. Single nucleotide polymorphisms (SNPs) will provide the next high density map, and be the genetic tool to study these genetic variations. There are many sources of SNPs and exhaustive numbers of methods of SNP detection to be considered. The focus in this paper will be on the merits of selected, varied SNP typing methodologies that are emerging to genotype many individuals with the required huge number of SNPs to make the study of complex diseases and pharmacogenomics a practical and economically viable option.

Objectives To localize genes influencing the susceptibility three positive regions is conclusively implicated, to Gilles de la Tourette syndrome (GTS) and associated it seems probable that at least one contains a susceptibility chronic multiple tics (CMT). locus. We recommend that association-based studies.Method A single, large, multiple affected pedigree containing 35 subjects diagnosed with GTS and a further 14 with CMT was genotyped for markers spanning the autosomes. Linkage analysis was carried out using classical lod score analysis and model-free lod score analysis. All markers were subjected to two-point analysis, and markers producing a two-point result significant at P

Atrial septal defect is one of the most common forms of congenital heart malformation. We identified a new locus linked with atrial septal defect on chromosome 14q12 in a large family with dominantly inherited atrial septal defect. The underlying mutation is a missense substitution, I820N, in alpha-myosin heavy chain (MYH6), a structural protein expressed at high levels in the developing atria, which affects the binding of the heavy chain to its regulatory light chain. The cardiac transcription factor TBX5 strongly regulates expression of MYH6, but mutant forms of TBX5, which cause Holt-Oram syndrome, do not. Morpholino knock-down of expression of the chick MYH6 homolog eliminates the formation of the atrial septum without overtly affecting atrial chamber formation. These data provide evidence for a link between a transcription factor, a structural protein and congenital heart disease.

Coeliac disease (CD) is a malabsorption disorder characterised by a small intestinal enteropathy that reverts to normal on removal of dietary gluten. Susceptibility to disease has a strong genetic component. Ninety percent of patients in northern Europe have the HLA class II alleles DQA1*0501 and DQB1*0201, which encode the cell surface molecule HLA-DQ2.1 However, haplotype sharing probabilities across the HLA region in affected sib pairs suggest that genes within the MHC complex contribute no more than 40% of the sib familial risk of CD, making the non-HLA linked gene (or genes) the stronger determinant.2 Attempts have been made to identify these loci using genome wide linkage studies. Zhong et al 3 performed an autosomal screen in 45 affected sib pairs from the west coast of Ireland, using 328 microsatellite markers. They found evidence of linkage with lod scores of greater than 2.0 in five areas: 6p23 (separate from HLA), 7q31.3, 11p11, 15q26, and 22cen. A larger genome wide search involving 110 affected Italian sib pairs using 281 markers found no evidence of linkage in these five areas.4 It did, however, propose a novel susceptibility locus at 5qter, important in both symptomatic and silent CD, and another at 11qter, which appeared to differentiate the two forms. In UK families an initial genome wide search,5 followed by a study of 17 candidate regions6 identified five areas with lod scores of greater than 2.0: 6p12, 11p11, 17q12, 18q23, and 22q13. Of these, 11p11 replicates one of the loci identified by Zhong et al 3 and it is likely that this area contains an important non-HLA susceptibility locus. However, in general the results of these studies are disappointingly inconsistent. A number of candidate genes have been investigated in linkage and association studies. Of these, the only region with repeatedly …

Editor—The hereditary spastic paraplegias (HSPs) are clinically characterised by progressive lower limb spasticity. The spasticity may occur in isolation (“pure”) or may be complicated by other major clinical features. Autosomal dominant, autosomal recessive, and X linked recessive inheritance patterns have been described for pure and complicated forms of HSP.1 ,2 There are loci for ADPHSP on chromosomes 2p (SPG4, MIM 182601),3 ,4 8q (SPG8, MIM 603563),5 ,6 14q (SPG3, MIM 182600),7 15q (SPG6, MIM 600363),8and 19q (SPG12).9 In addition, we recently mapped an ADPHSP locus on chromosome 12q13 (SPG10, MIM 604187) in a large UK family, family 4.10 This locus was narrowed to a 9.2 cM region between markers D12S368 and D12S83. Clinical features and diagnostic criteria for family 4 have previously been described.10 ,11 Briefly, subjects were classified as being affected if they had lower limb hyperreflexia in addition to at least one of the following: progressive spastic gait abnormality, bilateral extensor plantar reflex, or bilateral sustained (⩾5 beats) ankle or knee clonus. Subjects were classified as being possibly affected if lower limb hyperreflexia was present without other abnormal signs and as being normal if they had an entirely normal neurological examination. Thirteen members of family 4 are affected by ADPHSP and the family has a relatively young mean age at onset of 10.8 (SD 9.6) years (range 8-40). We have now genotyped additional markers D12S803, D12S390, D12S270, D12S1618, and D12S355 for subjects from family 4, using previously described methods.10 Primer sequences for these markers are available from the Genethon …

The susceptibility to develop coeliac disease (CD) has a strong genetic component, which is not entirely explained by HLA associations. Two previous genome wide linkage studies have been performed to identify additional loci outside this region. These studies both used a sib-pair design and produced conflicting results. Our aim is to identify non-MHC genetic loci contributing to coeliac disease using a family based linkage study. We performed a genome wide search in 16 highly informative multiply affected pedigrees using 400 microsatellite markers with an average spacing of 10 cM. Linkage analysis was performed using lod score and model free methods. We identified two new potential susceptibility loci with lod scores of 1.9, at 10q23.1, and 16q23.3. Significant, but lower lod scores were found for 6q14 (1.2), 11p11 (1.5), and 19q13.4 (0.9), areas implicated in a previous genome wide study. Lod scores of 0.9 were obtained for both D78507, which lies 1 cM from the gammaT-cell receptor gene, and for D2S364, which lies 12 cM from the CTLA4 gene.

The European Collaborative Interspecific Backcross (EUCIB) resource was constructed for the purposes of high-resolution genetic mapping of the mouse genome (Breen et al. 1994). The large Mus spretus/C57BL/6 backcross of 982 progeny has a genetic resolution of 0.3 cM at the 95% confidence level (∼500 kb in the mouse genome). We have used the EUCIB mapping resource to develop a genome-wide high-resolution genetic map incorporating 3368 microsatellites. The microsatellites are distributed among 2302 genetically separated bins with 1.46 markers per bin on average. Average bin separation is 0.61 cM. This high-resolution genetic map will aid the construction of a robust physical map of the mouse genome.

The use of fluorescent end-labeled primers has proved successful for rapid, semiautomated genotyping of microsatellite loci. However, custom synthesis is expensive and costs can be prohibitive when a wide range of markers is to be analyzed for only a few genotypings. This particularly applies to high-resolution genetic mapping in the mouse either in the construction of global maps or in the production of local high-resolution genetic maps for positional cloning. We demonstrate here the use of fluorescent dUTPs for cost-effective, high-throughput microsatellite genotyping in the mouse. This alternative to the use of fluorescent end-labeled primers for semiautomated genotyping is potentially applicable to the construction of linkage maps in other species.

The faecal flora and bacterial antibody levels of 22 patients with active rheumatoid arthritis (RA) were compared with those of 26 patients with osteoarthritis (OA) undergoing comparable treatment with non-steroidal anti-inflammatory drugs (NSAIDs), and a further 22 patients with OA who were not receiving NSAIDs. Faecal counts of Clostridium perfringens were significantly higher in the RA patient group and in those OA patients receiving NSAIDs, compared with those OA patients not taking NSAIDs (P = 0.032, P = 0.0004 respectively). Total aerobic and anaerobic counts were, however, identical in all three groups. Levels of serum IgA antibody to the alpha toxin of Cl. perfringens were higher in the RA group and in the OA group taking NSAIDs than in OA patients not taking NSAIDs (P = 0.011, P = 0.055). Serum IgG antibody to alpha toxin was higher in the RA group than in OA patients both on and off NSAIDs (P = 0.019, P = 0.0072) and also a group of normal controls (P = 0.032). These results suggest that the increased faecal counts of Cl. perfringens together with the associated increased antibody levels seen in this and previous studies are more likely to result from NSAID therapy used to treat the disease than from a disease specific change in bowel flora.

Editor—Benign familial infantile convulsions (BFIC) (OMIM 601764) is a recently recognised idiopathic epilepsy syndrome originally described in families of Japanese ancestry and more recently in Italian families.1-3 It has since been reported in France, Singapore, Sweden, Germany, USA, and Argentina,4-7 but to our knowledge never in the United Kingdom. The onset of seizures in BFIC is between 3 and 12 months old, and they are mostly of a partial type, some with secondary generalisation. These seizures tend to occur in clusters over several days and remit spontaneously at about 18 months. Ictal electroencephalograms (EEG) show diffuse discharge from the centro-occipital region, although the interictal EEG is normal. The course of the disease is benign with ultimately normal psychomotor development. There is considerable evidence that genetic factors are involved in the human epilepsies, although these genetic factors are complex and incompletely understood. One approach to understanding the molecular pathological basis of seizure disorders is to identify the genes involved in defined familial epilepsy syndromes. To date, genes for four autosomal dominant epileptic diseases have been mapped or cloned: benign familial neonatal convulsions at chromosomes 20q13 ( EBN1 ) and 8q24 ( EBN2 ), partial epilepsy with auditory symptoms at chromosome 10q ( EPT ), autosomal dominant nocturnal frontal lobe epilepsy at chromosome 20q13 ( CHRNA4 ), and BFIC at chromosome 19q in five Italian families.6 8 Haplotype mapping suggests that the BFIC locus at 19q is likely to lie in an approximately 6 cM region between D19S49 and D19S251.6This locus has been excluded in a single large Italian BFIC family, strongly suggesting that the condition is genetically heterogeneous.9 We present a family of United Kingdom origin with BFIC. In total, five family members were affected by a seizure disorder. The proband (case III.1, fig 1) was a male child, aged 3 …

Objective: To map the gene responsible for autosomal dominant pure hereditary spastic paraplegia (ADPHSP) in a large affected family. Background: Autosomal dominant pure hereditary spastic paraplegia (ADPHSP) is genetically heterogeneous, and loci have been mapped at chromosomes 2p (SPG4), 14q (SPG3), 15q (SPG6), and recently, in a single family, at chromosome 8q24 (SPG8). Methods: The authors carried out a genomewide linkage screen on a large family with ADPHSP, for which linkage to the chromosome 2, 14, and 15 loci was excluded. Results: Analysis of markers on chromosome 8q24 gave a peak two-point lod score of 4.49 at marker D8S1799. Analysis of recombination events in this family and in the previously published SPG8-linked family narrowed the SPG8 locus from 6.2 cM to a 3.4-cM region between markers D8S1804 and D8S1179. In another four families, linkage to all four known ADPHSP loci was excluded. The SPG8-linked family had a significantly older mean age at onset of symptoms and had significantly more wheelchair-using patients than the four linkage-excluded families. Conclusions: These results contain the presence of an autosomal dominant pure hereditary spastic paraplegia (ADPHSP) locus at chromosome 8q24 and strongly suggest that there are at least five ADPHSP loci. The data provide additional evidence for locus–phenotype correlations in ADPHSP.

Familial hemophagocytic lymphohistiocytosis (FHL), also known as familial erythrophagocytic lymphohistiocytosis and familial histiocytic reticulosis, is a rare autosomal recessive disorder of early childhood characterized by excessive immune activation. Linkage of the disease gene to an approximately 7.8-cM region between markers D9S1867 and D9S1790 at 9q21.3-22 was identified by homozygosity mapping in four inbred FHL families of Pakistani descent with a combined maximum multipoint LOD score of 6.05. This is the first genetic locus to be described in FHL. However, homozygosity by descent across this interval could not be demonstrated in an additional affected kindred of Arab origin, whose maximum multipoint LOD score was -0.12. The combined sample revealed significant evidence for linkage to 9q markers (LOD score with heterogeneity, 5.00). Identification of the gene(s) involved in the pathogenesis of FHL will contribute to an understanding of the control of T-lymphocyte and macrophage activation, which is central to homeostasis in the immune system.

We have previously reported an autosomal recessive form of congenital muscular dystrophy, characterized by proximal girdle weakness, generalized muscle hypertrophy, rigidity of the spine, and contractures of the tendo Achilles, in a consanguineous family from the United Arab Emirates. Early respiratory failure resulting from severe diaphragmatic involvement was present. Intellect and the results of brain imaging were normal. Serum creatine kinase levels were grossly elevated, and muscle-biopsy samples showed dystrophic changes. The expression of the laminin-alpha2 chain of merosin was reduced on several fibers, but linkage analysis excluded the LAMA2 locus on chromosome 6q22-23. Here, we report the results of genomewide linkage analysis of this family, by use of homozygosity mapping. In all four affected children, an identical homozygous region was identified on chromosome 1q42, spanning 6-15 cM between flanking markers D1S2860 and D1S2800. We have identified a second German family with two affected children having similar clinical and histopathological features; they are consistent with linkage to the same locus. The cumulative LOD score was 3.57 (straight theta=.00) at marker D1S213. This represents a novel locus for congenital muscular dystrophy. We suggest calling this disorder "CMD1B." The expression of three functional candidate genes in the CMD1B critical region was investigated, and no detectable changes in their level of expression were observed. The secondary reduction in laminin-alpha2 chain in these families suggests that the primary genetic defect resides in a gene coding for a protein involved in basal lamina assembly.

We have identified a missense mutation in the motor domain of the neuronal kinesin heavy chain gene KIF5A, in a family with hereditary spastic paraplegia. The mutation occurs in the family in which the SPG10 locus was originally identified, at an invariant asparagine residue that, when mutated in orthologous kinesin heavy chain motor proteins, prevents stimulation of the motor ATPase by microtubule-binding. Mutation of kinesin orthologues in various species leads to phenotypes resembling hereditary spastic paraplegia. The conventional kinesin motor powers intracellular movement of membranous organelles and other macromolecular cargo from the neuronal cell body to the distal tip of the axon. This finding suggests that the underlying pathology of SPG10 and possibly of other forms of hereditary spastic paraplegia may involve perturbation of neuronal anterograde (or retrograde) axoplasmic flow, leading to axonal degeneration, especially in the longest axons of the central nervous system.

Two mouse hybridoma antibodies, G6 and H1, with specificity for idiotypic determinants on the heavy chain of human IgM-RF have been produced. Idiotopes recognized by G6 and H1 were expressed on 5/12 and 2/12 RF paraproteins from the Wa idiotype group respectively, but not on paraproteins lacking rheumatoid factor (RF) activity. Inhibition experiments demonstrated that G6 and H1-specific epitopes were located on (or close to) the antibody binding site of RFs, and measurable on the heavy chain but not their light chains. However, it was concluded that the quaternary structure of the antibody-binding site was important for the optimal expression of both idiotopes. The idiotope recognized by G6 was also detected on polyclonal RFs in unfractionated sera from 8/14 patients with rheumatoid arthritis (RA). The results suggest that the G6 idiotope is a highly conserved determinant on the antibody-binding site of RF. These monoclonal antibodies will allow characterization of RF clonality in RA.

Summary The hypothesis that prolactin may play a part in osmoregulation was investigated by giving a hypotonic fluid load to two groups of normal lactating women. No changes in serum prolactin, milk yield, serum or breast milk osmolality were noted, suggesting that encouraging women to drink excessively has no effect upon lacta-tion, either in terms of yield or composition of milk.