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Case report A 4-year-old neutered male Rhodesian Ridgeback dog with right-sided Horner's syndrome, bilateral laryngeal paralysis, neck pain and bilateral hindlimb ataxia was euthanased following deterioration of its neurological status. Necropsy examination revealed an off-white retropharyngeal neoplastic mass (100 × 30 × 30 mm) attached to the base of the skull on the right side and macroscopic nodular metastases in the spleen and three vertebral bodies (C6, C7 and T6), including a nodule attached to the dura at C7. Histological evidence of neuroblastic tumour was detected in these macroscopic lesions, a regional lymph node, bone marrow of a femur and all 15 vertebral bodies (C1-T8) examined, including the three with macroscopic metastases, and in the lumens of small blood vessels in the lungs and liver. Ganglion cell differentiation was detected only in the primary retropharyngeal mass, one splenic nodule and the C7 dural nodule. Neoplastic cells were immunoreactive to neurofilament protein (ganglion cells only), vimentin and synaptophysin, and were negative for S100 protein, GFAP, CD3 and Pax5. Conclusion The diagnosis was disseminated peripheral neuroblastoma, differentiating subtype (International Neuroblastoma Pathology Classification), with likely primary involvement of the right cranial cervical ganglion. This appears to be the first report of neuroblastoma in a dog with widespread occult haematogenous metastasis to bone marrow.

High-grade glioma is the most common brain tumor in adults, and the prognosis for patients diagnosed with this type of cancer is still poor. The biological behavior of the tumors is correlated to t ...

An autosomal recessive form of cerebellar abiotrophy occurs in Australian Kelpie dogs. Clinical signs range from mild ataxia with intention tremor to severe ataxia with seizures. A whole-genome mapping analysis was performed using Affymetrix Canine SNP array v2 on 11 affected and 19 control dogs, but there was no significant association with disease. A homozygosity analysis identified a three megabase region likely to contain the disease mutation. The region spans 29.8-33 Mb on chromosome 3, for which all affected dogs were homozygous for a common haplotype. Microsatellite markers were developed in the candidate region for linkage analysis that resulted in a logarithm of odds score suggestive of linkage. The candidate region contains 29 genes, none of which are known to cause ataxia.

The neuronal ceroid lipofuscinoses (NCLs, Batten disease) are a group of fatal recessively inherited neurodegenerative diseases of humans and animals characterised by common clinical signs and pathology. These include blindness, ataxia, dementia, behavioural changes, seizures, brain and retinal atrophy and accumulation of fluorescent lysosome derived organelles in most cells. A number of different variants have been suggested and seven different causative genes identified in humans (CLN1, CLN2, CLN3, CLN5, CLN6, CLN8 and CTSD). Animal models have played a central role in the investigation of this group of diseases and are extremely valuable for developing a better understanding of the disease mechanisms and possible therapeutic approaches. Ovine models include flocks of affected New Zealand South Hampshires and Borderdales and Australian Merinos. The ovine CLN6 gene has been sequenced in a representative selection of these sheep. These investigations unveiled the mutation responsible for the disease in Merino sheep (c.184C>T; p.Arg62Cys) and three common ovine allelic variants (c.56A>G, c.822G>A and c.933_934insCT). Linkage analysis established that CLN6 is the gene most likely to cause NCL in affected South Hampshire sheep, which do not have the c.184C>T mutation but show reduced expression of CLN6 mRNA in a range of tissues as determined by real-time PCR. Lack of linkage precludes CLN6 as a candidate for NCL in Borderdale sheep.

In 1997, neuronal ceroid lipofuscinosis (NCL) was identified for the first time in Merino sheep in Australia. A homozygosity mapping approach localized the disease gene in Merino sheep to the same region on chromosome 7 in which NCL was recently mapped in South Hampshire sheep. This region shows conserved synteny with the region on human chromosome 15 in which the human late infantile NCL variant CLN6 was mapped. NCL in Merino and South Hampshire sheep are therefore potential animal models for the human late infantile variant CLN6.

An autosomal recessive form of cerebellar abiotrophy occurs in Australian Kelpie dogs. Clinical signs range from mild ataxia with intention tremor to severe ataxia with seizures. A whole-genome mapping analysis was performed using Affymetrix Canine SNP array v2 on 11 affected and 19 control dogs, but there was no significant association with disease. A homozygosity analysis identified a three megabase region likely to contain the disease mutation. The region spans 29.8-33 Mb on chromosome 3, for which all affected dogs were homozygous for a common haplotype. Microsatellite markers were developed in the candidate region for linkage analysis that resulted in a logarithm of odds score suggestive of linkage. The candidate region contains 29 genes, none of which are known to cause ataxia.

The brains of 21 rhesus monkeys inoculated with SIVMAC251 were examined after intervals ranging from 3 to 27 months and compared with five uninoculated controls. Eighteen animals became infected and individually exhibited several distinct patterns of disease. Nine (50%) had largely intramural leptomeningeal venous infiltrates (LMVI) without multinucleate giant cells (MGC) or foamy macrophages. Three (17%) had only MGC lesions, involving the cerebral parenchyma. One had both patterns and five (33%) neither. The controls had sparse and tiny LMVI only, similar to three inoculated animals that did not become infected. Immunohistochemistry showed the predominance of T and B lymphocytes in LMVI and choroid plexus mononuclear lesions but a predominance of macrophages over lymphocytes in the MGC lesions. Specific disease patterns differed in their association with the humoral immune response. Animals with LMVI were all hypergammaglobulinaemic when killed compared to pre-inoculation levels, and the size of the change in serum immunoglobulin concentration was positively correlated with a quantitative index of LMVI density. Furthermore, their post-mortem lymph node histology was hyperplastic. In contrast, animals found at autopsy to have MGC brain lesions were hypogammaglobulinaemic compared to preinoculation. The results are consistent with two phases in SIV-associated disease: one characterized by LMVI and hypergammaglobulinaemia and another featuring MGC and hypogammaglobulinaemia.

The pathological changes associated with ageing and simian immunodeficiency virus (SIV) infection in groups of immature, adult and ageing Rhesus monkeys were studied. Eighty three per cent (5 of 6) of uninfected ageing animals had hyperplasia of the prostate, 33 per cent (2 of 6) had mild prostatitis and in 66 per cent (4 of 6) there were calcified concretions in the seminal vesicles. The testes were normal and showed active spermatogenesis. In the SIV-infected animals, two types of lesion occurred; the most common, in 81 per cent (18 of 22 monkeys), was the presence of focal lymphoid infiltrations in the epididymis, prostate or seminal vesicles. The other was hypospermatogenesis (23 per cent, 4 of 17) with degeneration of seminiferous tubules. Immunocytochemical staining demonstrated that the lymphoid masses contained approximately equal numbers of B and T lymphocytes, but the majority of diffusely scattered cells were T lymphocytes. Staining for SIV antigen identified small numbers of positive lymphocytes and macrophages in all tissues.

The host range of SIVmac was investigated in three monkey species. Blood-borne and cell-adapted virus inocula obtained from a rhesus macaque infected with SIVmac251 were compared. African green monkeys were not susceptible to infection, whereas baboons and rhesus macaques became persistently infected and showed similar patterns of seroconversion. However, in contrast to the macaques, no clinical or histopathological evidence of disease was seen in the baboons 2 years after virus inoculation. Thus baboons could be used as an alternative to macaques in vaccine development studies with this particular isolate of SIVmac. Furthermore, this system may be useful for the investigation of factors responsible for disease progression.

Cardiomyopathy and woolly haircoat syndrome (CWH) of Poll Hereford cattle is a lethal, autosomal recessive disorder. Cardiac and haircoat changes are congenital, neonatal ocular keratitis develops in some cases and death usually occurs within the first 12 weeks of life. We undertook a homozygosity mapping approach to identify the chromosomal location of the causative gene. Seven candidate genes were examined for homozygosity in affected animals: desmoplakin and junction plakoglobin (both previously implicated in human cardiocutaneous syndromes), desmocollin 2, desmoglein 2, plakophilin 2, nuclear factor kappa B (NFKB1) and NFkappaB interacting protein 1 (PPP1R13L, also known as NKIP1). Homozygosity in 13 affected animals was observed at the PPP1R13L locus, located on bovine chromosome 18. Subsequent sequence analysis revealed a 7-bp duplication (c.956_962dup7) in exon 6 of this 13-exon gene. This frameshift variant is predicted to result in the substitution of three amino acids and the introduction of a premature stop codon at position 325 of the protein product (p.Ser322GlnfsX4). PPP1R13L interacts with NFkappaB, a family of structurally related transcription factors that regulate genes controlling inflammation, immune responses and cell proliferation and survival. CWH represents a large-animal model for cardiocutaneous disorders caused by a mutation in the PPP1R13L gene. The identification of this bovine mutation also indicates that PPP1R13L and other genes affecting NFkappaB activity may be candidate genes in the study of human cardiovascular disease.

Objective To characterise neuronal ceroid lipofuscinosis (NCL) in Merino sheep. Design A prospective clinical, pathological, biochemical and genetic study. Procedure NCL cases were studied from a medium-wool Merino flock, the stud of origin of its replacement rams, and an experimental flock established at the University of Sydney. Results Behavioural changes and visual impairment were first detected at 7 to 12 months of age and progressed, with associated motor disturbances and at later stages seizures, to premature death by 27 months of age. At necropsy there was severe cerebrocortical atrophy associated with neuronal loss, astrocytosis and the presence in neurons of eosinophilic intra-cytoplasmic storage bodies with the characteristics of a lipopigment. In the retina there was progressive loss of photoreceptor cells. Storage bodies isolated from fresh brain, liver and pancreas formed electron-dense aggregates and coarse multilamellar and fine fingerprint profiles ultrastruc-turally, and consisted mainly of the hydrophobic protein, subunit c of mitochondrial ATP synthase. A homozygosity mapping approach localised the gene causing the disease in Merino sheep to the chromosomal region (OAR7q13–15) associated with NCL in South Hampshire sheep. Conclusion NCL in Merino sheep is a subunit c-storing disease, clinically and pathologically similar to NCL in South Hampshire sheep. We propose that the disease in both breeds represents mutation at the same gene locus in chromosomal region OAR7q13–15.

Objective To investigate the seroprevalence ofNeosporacaninum infection in a commercial dairy cattle herd, 15months after detection of an abortion outbreak.Procedure Sera from the whole herd (n=266) were exam-ined for N caninum antibodies by indirect fluorescent antibodytest (IFAT) and immunoblot analysis. Herd records werereviewed to collate serological results with abortion history,proximity to calving, and pedigree data. Results The seroprevalence of N caninuminfection was24% (63/266) for IFAT titre ≥160, 29% (78/266) forimmunoblot positive (+ve), and 31% (82/266) for IFAT≥ 160and/or immunoblot +ve; 94% (59/63) of animals with IFAT≥160were immunoblot +ve. The association between seropositivity(IFAT ≥ 160 and/or immunoblot +ve) and history of abortionwas highly significant (P < 0.001); the seroprevalence was86% (18/21) in aborting cows, compared with 30% (50/164) innon-aborting animals. The abortion rate for seropositive cowswas 26% (18/68) compared with 3% (3/117) for seronegativeanimals. IFAT titres of infected cows were higher within 2months of calving than at other times (P < 0.001). The associ-ation between seropositivity in dams and daughters washighly significant (P = 0.009).Conclusions The abortions were associated with N caninuminfection and there was evidence of reactivation of latentinfection close to calving and congenital transmission of infec-tion. Immunodominant antigens identified by immunoblotsmay prove useful for improved diagnostic tests.

Streptococcus suis was recovered from 9 outbreaks of septicaemia and meningitis in weaned pigs between 1979 and 1983. Fifteen isolates from 7 outbreaks were identified as S. suis type 9, and 3 isolates from 2 outbreaks as S. suis type 2. Three further isolates of S. suis type 2 and an isolate of S. suis type 3 were recovered from cases of bronchopneumonia in weaned pigs from 4 other piggeries.

There is strong evidence that patients with AIDS have loss of cortical neurons. In this study we have examined the hippocampus of rhesus monkeys infected with simian immunodeficiency virus (SIV) to determine whether neuronal damage occurs in this model of human AIDS and to investigate its time course. Twenty-eight infected monkeys (23 young [9 years] and five elderly [16 years]) were compared with 11 controls (six young and five elderly). Numbers of nucleolated neurons per unit area of section and mean pyramidal cell diameters were measured in each CA sub-field of each animal. There was neuronal atrophy in all regions examined, as early as 3 months following inoculation. An initial apparent increase in neuronal density at 3 months did not reach statistical significance. In younger animals, however, there was a later, significant association between the reduction in neuronal density and duration of infection. Elderly animals were only examined at a single, early time point. These results show that there is neuronal pathology following infection with SIV and that there is probably subsequent neuronal death.

Constitutive host factors that influence progression to AIDS are understood poorly. In the macaque model for AIDS, 35 animals infected with simian immunodeficiency virus (SIV) were analyzed for major histocompatibility complex class II antigen expression on blood monocytes and B cells by immunostaining and flow cytometry. Expression varied widely between animals but was constant with time. Level of expression and the proportion of monocytes and B cells that expressed class II were not affected by SIV infection. Significantly more animals developed AIDS in the group with low class II expression than in the group with high expression (P < .001). Progression to disease was faster in animals that expressed poorly (P < .01), and opportunistic pathogens were more common (P < .05). Thus, the constitutive level of class II antigen expression may be a useful prognostic indicator for human immunodeficiency virus disease in humans and may be an important factor in the design of vaccine trials.

SUMMARY The epidemiological, clinical and pathological features of a disease syndrome in adult cattle grazing woolly-pod vetch (Vicia villosa ssp dasycarpa) or popany vetch (V benghalensis) are reported. Outbreaks of toxlcosis occurred between midwinter and midsummer in 3 dairy and 6 beef herds on the north coast of New South Wales, between 1982 and 1992. Friesian, Angus, Murray Grey, Guernsey and Hereford breeds were affected. Mean morbidity and case fatality rates in affected herds were 7% (65 of 889) and 69%, respectively. Signs of pruritic dermatitis, illthrift and death were associated with an eosinophilic granulomatous inflammation of many organs, particularly involving the renal cortex, dermis, myocardium, adrenal glands, lymph nodes and hepatic portal triads.

Hens were exposed to small-particle aerosols containing different concentrations of Salmonella enteritidis phage type 4. They developed a systemic infection and some birds were still excreting the organism in the faeces when killed 28 days after infection. S enteritidis was present for a similar period in a wide range of alimentary tract issues and in the ovary and oviduct.

Summary Two Rhesus monkeys infected with simian immunodeficiency virus for 15 and 24 months developed generalized oedema and one became jaundiced. At necropsy, the liver and pancreas were hard and irregular and the gall bladder was thickened. Histopathologieal examination showed extensive fibrosis of the pancreas, loss of exocrine acini and marked proliferation of ductules. Numerous cryptosporidia were present on the duct epithelium. The liver of both animals had widespread cirrhosis, bile duct proliferation and cholangitis. Cryptosporidia were found in many bile ducts and on the hyperplastic gall bladder epithelium. Lymph nodes and spleen of both animals showed depletion of cortical and paracortical elements characteristic of advanced immunodeficiency virus infection.

Pneumocystis carinii pneumonia occurred in 6 of 17 rhesus monkeys infected with simian immunodeficiency virus and was studied by immunohistochemistry and by scanning and transmission electron microscopy. A monoclonal antibody/streptavidin-biotin-peroxidase staining method was highly sensitive for detecting the organisms in small, early lesions and was much more sensitive and specific than traditional silver impregnation methods. Reprocessing of paraffin wax-embedded lung tissue for scanning electron microscopy and use of a video printer to produce a photographic montage of light microscopic lesions allowed the same areas of tissue to be examined and compared by both methods. The ultrastructural morphology of P. carinii in the rhesus monkey was identical to that in man, as were the histological and electron microscopic lesions, including pulmonary fibrosis. Trophozoites were seen attached to alveolar type I epithelium mainly by intimate apposition to the plasma membrane, but scanning electron microscopy also showed attachment by elongated filopodia. Few macrophages were present in infected alveoli, and though phagocytosis followed by digestion of P. carinii trophozoites was observed, it appeared to occur at a very low level.

The histological lesions were studied in seven rhesus and three cynomolgus monkeys infected with simian immunodeficiency virus for periods ranging from nine weeks to 18 months. Lymphoreticular changes included hyperplasia, follicular involution and depletion, and one animal had amyloidosis of the spleen. Hyperplastic changes also took place in mucosa-associated lymphoid tissue and infiltrations occurred in the vaginal mucosa of one animal, which could be significant in sexual transmission of the infection. The range of opportunistic infections was small compared with that in human AIDS patients, although two monkeys had Pneumocystis carinii pneumonia. Enterocolitis was a common finding and brown adipose tissue was transformed into a large vacuolated type. Lesions of the central nervous system were found in five of nine monkeys, and consisted of foci of glial activity and perivascular and meningeal lymphocytic infiltration. A lymphoma involving the lumbar spinal cord developed in one animal.

Apicomplexan protozoal abortion in cattle is provisionally diagnosed by demonstrating in the aborted foetus characteristic microscopic lesions of multifocal, non-suppurative, necrotising encephalitis, non-suppurative myocarditis, and less frequently, focal non-suppurative inflammation of other organs (Barr et a1 1990); protozoa are not frequently seen in tissue sections. These distinctive foetal lesions, particularly the necrogranulomas in the brain, resemble those caused by the apicomplexan protozoan, Toxoplasma gondii, in sheep (Hartley and Kater 1963). However, an organism similar to Neospora caninum (Dubey ef al 1988) has been implicated, by immunohistochemical staining of affected tissues, as the cause of theselesions in bovinefoetuses(Andersonetal1991; Barretal1991; Thornton el al 1991). An apicomplexan protozoan ultrastructurally similar to N caninum has recently been isolated from the brains of 2 aborted bovine foetuses (Conrad et al 1993a); one of these bovine Neospora isolates has been transplacentally transmitted in cattle to produce foetal infection and death associated with typical foetal lesions, thus confirming its aetiological role in bovine apicomplexan protozoal abortion (Barr et al 1994). N caninum isolated from puppies with congenital encephalomyelitis has also been transplacentally transmitted to produce non-suppurative encephalitis in a bovine foetus (Dubey et a1 1992). Neospora abortion in cattle is an important problem in the USA and New Zealand, and has been reported in Australia, the UK, the Netherlands, Japan, Canada, Mexico and South Africa (Dubey and Lindsay 1993). In Australia, bovine apicomplexan protozoal abortion has been recognised by veterinary pathologists since the midI970s, although it was originally attributed to Sarcocystis infection (Munday and Black 1976; Pass 1977; Jerrett et a1 1984; McCausland et a1 1984). In this paper we review the cases of bovine apicomplexan protozoal abortion diagnosed to July 1994 in northeastern New South Wales, identify the involvement of beef as well as dairy herds, and present immunohistochemical confirmation of Neospora infection in selected foetuses. From January 1982 to July 1994, specimens from 729 aborted bovine foetuses were examined at the Regional Veterinary Laboratory, Wollongbar. Most (90.5%) of the submissions were of whole foetuses; the others were of fresh or formalin-fixed foetal organs. Bovine apicomplexan protozoal abortion was diagnosed by demonstrating the characteristic microscopic lesions in brain and/or heart of 152 (2 I %) of these foetuses (this percentage has been higher in more recent years, Table 1); the laboratory records and histological sections from these 152 cases have been reviewed. Of 126 affected herds, 74 (59%) were dairy and 52 (41 %) were beef enterprises. Cases were diagnosed throughout the full range of gestational ages of foetuses submitted, although few foetuses less than 3 months’ gestation were examined. Two calves that died soon after birth had lesions consistent with apicomplexan protozoal infection but have not been included in this study. Two confirmed TABLE 1 Bovine apicomplexan protozoal (Neospora) abortion in north-eastern New South Wales

SUMMARY The recently described species, Raillietia manfredi was recovered from ears of 24/185 (13%) goats and from 17/23 (74%) herds sampled. Psoroptes cuniculi was recovered from ears of 38/185 (21%) goats and from 5/23 (22%) herds. The youngest goat infested with R. manfredi was 14 days old. Common clinical signs attributed to ear mite infestation included twitching and scratching of ears, and head shaking.

A syndrome in cattle of diarrhoea and death associated with enteric Yersinia pseudotuberculosis infection is described. Outbreaks occurred during winter and early spring in adult cattle grazing pastures waterlogged by recent flooding or persistent heavy rain. Antibiotic therapy was effective early in the course of the syndrome. At necropsy there was severe acute enterocolitis, and bacteria consistent with Y. pseudotuberculosis were observed in the lesions. This organism could usually be isolated from the intestines of affected animals but was recovered less often from other organs. Representative isolates were identified as Y. pseudotuberculosis serotype III. The association of this syndrome with waterlogged pastures and low temperatures suggests that these conditions favour transmission of Y. pseudotuberculosis infection in cattle. The role of Y. pseudotuberculosis as primary pathogen requires confirmation.

Development of the cestode parasite Taenia taeniaeformis in the liver of rats results in gross hyperplastic changes in the stomach and small intestine. In this study we investigated the mechanism by which these lesions are induced. Acutely infected rats were joined surgically to syngeneic noninfected partners in parabiosis. When hyperplastic gastropathy developed in those rats with heavy hepatic infections with cestodes, it also occurred in the uninfected partners of the parabiotic pairs. Gastric changes were usually more severe in the uninfected partner. Duodenal mastocytosis developed in both partners, even when parasite burdens were light in the infected rats. intact chronically infected rats with hyperplastic gastropathy developed markedly elevated serum levels of the hormone, gastrin (approximately 30-fold greater than normal). When rats were antrectomized 24-48 h after infection, gastric hyperplasia still developed, but hypergastrinemia was prevented or was of only moderate degree. There was no correlation between serum gastrin levels and the degree of gastrointestinal change in the intact rats, but hypergastrinemia never developed in infected animals which did not show hyperplasia in the stomach or intestine. When infected rats were bled serially over the first 100 days of infection, hypergastrinemia developed abruptly between 50 and 60 days after infection. These results suggest that the alterations in serum gastrin levels were secondary to the development of hyperplastic changes in the gastrointestinal tract of infected rats. The primary stimuli for both the hyperplasia and the hypergastrinemia remain unknown.

A 10-month-old female, Wire-haired Pointing Griffon dog had a hamartoma of the hypothalamus. Episodes of sudden flaccid collapse had increased in frequency and duration for 7 months. Cerebrospinal fluid pressure was normal. A flat, pedunculated mass, 2.5×3.0×0.9 cm, covered the brain stem between the pituitary gland and pons. Its 1.2-cm-diameter connection to the hypothalamus obliterated the mammillary bodies and extended to the tuber cinereum, distorting the hypothalamus and displacing the third ventricle which also divided the rostral part of the mass. The tissue of the hamartoma resembled gray matter with bullous cytoplasmic vacuolation of many neurons, spongiform change, gemistocytosis and microscopic foci of calcification.

Electrocardiograms were recorded from 4 calves with cardiomyopathy and woolly haircoat syndrome (CWH), a lethal autosomal recessive trait of Poll Hereford cattle and from 9 unaffected calves. Electrocardiograms of calves with CWH were characterised by multifocal ventricular premature contractions which occurred singly, in pairs, in runs and as episodes of ventricular tachycardia. Bigeminal rhythms were recorded occasionally. The frequency of ventricular premature contractions ranged from 5 to 120.min-1. Ventricular premature contractions in calves with CWH were attributed to myocardial degeneration and fibrosis which were observed grossly and microscopically. Electrocardiograms in unaffected calves were characterised by normal sinus rhythm and by variation in the morphology of wave forms between animals. The durations of the various wave forms were less than those previously recorded from adult cattle.

Dermatophilosis was diagnosed in 2 of 13 captive polar bears (Thalarctos maritimus), causing generalized dermatitis of 3 years' and 6 months' duration, respectively. Progressive clinical signs included yellowing and darkening of the hair, pruritus, encrustation of skin, and reluctance to bathe. Dramatic resolution of lesions occurred during 8 weeks of twice-weekly intramuscular treatment with long-acting penicillin.

A method was devised for surgical removal of the pyloric antrum in 3-week-old rats. Contrary to published experiences with older rats, it was found that ligation of right and left gastroepiploic arteries was not necessary in young animals. Erythrocytes and fluids were routinely administered postoperatively, and recovered animals were denied access to water and food for 2 and 3 days, respectively. When the rats were fasted overnight prior to surgery, the recovery rate was 87% (27 of 31 attempted). Surgical sites were intact and showed minimal adhesions 2 months later. When overnight fasting was omitted, only 57% survived (8 of 14 attempted), because extensive manipulations were necessary to remove gastric contents, and this often produced shock.

The properties of low frequency Alfven waves in hot, magnetically confined plasmas are quite unlike those in homogeneous media. Extensive theoretical studies have uncovered the Alfven continuum along with global Alfven eigenmodes (GAE). It has been suggested that such modes may be good candidates for rf heating below the ion cyclotron frequency. We present a unified investigation on PRETEXT of the structure of the global modes. These measurements are made using two phased toroidal antennas. The GAE are predicted to appear as resonances in the antenna loading resistance and have been observed earlier on TCA. We find that in addition to antenna resistance and inductance, signals from magnetic probes at the plasma surface also exhibit this resonant behavior. The plasma parameter dependence (i.e., the amplitude and location) of these resonancces is found in good agreement with the theory. Driven plasma density fluctuations with a rich spatial structure are predicted to develop at these resonances; we have observed this structure using a CO2 lser interferometer. Results from the laser and impedance measurements along with antenna phasing permit assignment of mode numbers. Since the two‐antenna configuration can simultaneously excite more than one mode in the plasma, the resulting interference effects demand careful interpretation of the spatial and temporal mode structures seen. These interference effects provide both a challenge and an opportunity for an optimum antenna design in an Alfven heating experiment.

The Division of Research is considering several proposals from universities and agencies of the government for research reactors. Some of these proposals involve amounts of highly enriched fissionable materials in excess of that which can be loaned under existing law. The Pennsylvania State College, the University of Michigan, and the Watertown Arsenal have plans for reactors (similar to the BSF at Oak Ridge) each requiring about 3.7 Kgs of U-235. In order legally to loan the fissionable material for these reactors, it may be necessary to supply diluted or partially enriched fissionable material instead of the highly enriched material. Although T.H. Johnson has discussed this problem recently in a telephone conversation with A.M. Weinberg, the Research Division would also like written comments representing the opinions of appropriate personnel on the following points.

Many suggestions have been made about the identity of ‘Mr W. H.’ in the Dedication to Shakespeare’s Sonnets. Amongst the candidates occurs the name of William Hervey, third husband of Mary, Countess of Southampton, the mother of Henry Wriothesley, the 3rd Earl. The Countess died in 1607 and the suggestion is that she, the Earl’s mother, would have been a natural collector of the Sonnets addressed to her son and that her husband, William Hervey, sole executor of her will, may have come across the Sonnets amongst her papers and passed them on to Thomas Thorpe. Little is known about Hervey and both Dr Rowse and the D.N.B. are in error; the first of making him a member of a 'good Kent family' and the second by confusing him with two cousins who served in Ireland, Gawen and Roger Hervey. The facts so far published are that he distinguished himself against the Armada in 1588, was knighted at Cadiz in 1596, sailed on the Islands Voyage in 1597, married the Countess of Southampton in 1598 or thereabouts, served in Ireland, remarried in 1608, was raised to a Baronetcy in 1619, was created Baron Hervey of Rosse in Ireland in 1620 and Baron Hervey of Kidbrook in Kent in 1628 and that he died in 1642 and was buried in St Edmund's Chapel in Westminster Abbey.