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Put simply, ‘spoofing’ is a means of controlling the reported position and time of a GNSS receiver. Spoofing has now been well demonstrated in the experimental context, but until a few years ago it was regarded as “…a bit like UFOs: much speculation, occasional alarms at suspected instances, but little real-world evidence of its existence” (Ref. 1). In the intervening years spoofing has transformed from a research laboratory into an emerging threat. In this paper we focus on radio-frequency attack as the primary method of spoofing. However there is also the possibility of cyber-attack on GNSS systems, in which there is interception and modification of computed position between the receiver and application. It had perhaps previously been considered that the technology and know-how “barrier to entry” to produce an effective spoofer was itself a significant deterrent. However, the commercial availability of inexpensive (sub £250) software defined radio systems, low-cost computing and open-source GNSS signal generator software has all but eliminated this barrier. This paper will consider various methods of spoofing, means of detecting spoofing through analysis of signal anomalies and also mitigation of spoofing at the physical layer via the antenna and signal processing and at the software application layer through the detection of anomalies.

INTRODUCTION Mini-incision focused parathyroidectomy (MI-FP) is advocated as an alternative to bilateral neck exploration (BNE), owing to its reduced morbidity. The site and side of the affected gland is identified preoperatively using a combination of ultrasound and sestamibi scans. However, the acceptable degree of inter-scan concordance required to prompt MI-FP without compromising accuracy is undetermined. METHODS Accuracy of preoperative imaging was determined both individually and in combination for all parathyroidectomies (2007–2014). A grading system (excellent, good, poor) was devised to describe the interscan concordance, which was validated by the operative and histological findings. RESULTS Eighty-nine patients (17 male, 68 female) underwent parathyroidectomy (MI-FP 44, BNE 45). The accuracy of scans interpreted individually was 53% for ultrasound and 60% for sestamibi, with no difference according to surgical technique (P = 0.43, P = 1, respectively). The proportion of interscan concordance was: excellent – 35%, good – 40%, poor 25%. Combined accuracy was 100% for both excellent and good grades but only 13% for those graded poor. Similar rates of normocalcaemia were observed for MI-FP and BNE, while postoperative hypocalcaemia was five times higher in those undergoing BNE. CONCLUSIONS Reduction in the inter-scan concordance from excellent to good does not compromise accuracy. MI-FP could be successfully performed in up to 75% of patients – 25% higher than recommended in national guidelines. Focused parathyroidectomy does not compromise surgical and endocrinological outcomes but boasts a far superior complication rate.

An assessment is presented that examines a number of prominent factors from the professional literature describing the background and clinical characteristics of paraphilic individuals and sex offenders. The factors include sexual history and preference, substance abuse, mental illness, personality and defensiveness, history of violence, neuropsychological impairment, and biological problems. The reliability and validity of measures in use are reviewed with suggestions for a battery of measures that offer some index of dangerousness and targets for treatment.

The expression of Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) is essential for the activation and immortalization of human B lymphocytes by EBV. EBNA3C consists of 992 amino acids and includes a potential bZIP motif and regions rich in acidic, proline, and glutamine residues. Thus, EBNA3C resembles several trans regulators of gene expression. It has recently been shown that a fragment of EBNA3C can activate reporter gene expression when fused to the DNA-binding domain of GAL4 (D. Marshall and C. Sample, J. Virol. 69:3624-3630,1995). Although EBNA3C binds DNA, a specific site for EBNA3C binding has not been identified; to test the ability of full-length EBNA3C to regulate transcription, EBNA3C (amino acids 11 to 992) was fused to the DNA-binding domain of GAL4. We show that this fusion protein does not transactivate but rather is a potent repressor of reporter gene expression. Repression is dependent on the dose of GAL4-EBNA3C and on the presence of GAL4-binding sites within reporter plasmids. Repression is not restricted to B cells nor is it species or promoter specific. Repression is independent of the location of the GAL4-binding sites relative to the transcription start site. A fragment of EBNA3C (amino acids 280 to 525) which represses expression in a manner which is nearly identical to that of the full-length protein has been identified; this fragment is rich in acidic and proline residues. A second, less potent repressor region located C terminal to amino acids 280 to 525 has also been identified; this domain is rich in proline and glutamine residues. We also show binding of EBNA3C, in vitro, to the TATA-binding protein component of TFIID, and this suggests a mechanism by which EBNA3C may communicate with the basal transcription complex.

From measurements of airway and esophageal pressures and flow, we calculated the elastance and resistance of the total respiratory system (Ers and Rrs), chest wall (Ecw and Rcw), and lungs (EL and RL) in 11 anesthetized-paralyzed patients immediately before cardiac surgery with cardiopulmonary bypass and immediately after chest closure at the end of surgery. Measurements were made during mechanical ventilation in the frequency and tidal volume ranges of normal breathing. Before surgery, frequency and tidal volume dependences of the elastances and resistances were similar to those previously measured in awake seated subjects (Am. Rev. Respir. Dis. 145: 110–113, 1992). After surgery, Ers and Rrs increased as a result of increases in EL and RL (P < 0.05), whereas Ecw and Rcw did not change (P > 0.05). EL and RL exhibited nonlinearities (i.e., decreases with increasing tidal volume) that were not seen before surgery, and RL showed a greater dependence on frequency than before surgery. The changes in RL or EL after surgery were not correlated with the duration of surgery or cardiopulmonary bypass time (P > 0.05). We conclude that 1) frequency and tidal volume dependences of respiratory system properties are not affected by anesthesia, paralysis, and the supine posture, 2) open-chest surgery with cardiopulmonary bypass does not affect the mechanical properties of the chest, and 3) cardiac surgery involving cardiopulmonary bypass causes changes in the mechanical behavior of the lung that are generally consistent with those caused by pulmonary edema induced by oleic acid (J. Appl. Physiol. 73: 1040–1046, 1992) and decreases in lung volume.

Summary: Aspartate transport in Rhizobium meliloti was found to be mediated by at least two transport systems. High rates of aspartate uptake, necessary for growth on aspartate as a carbon source, required the dicarboxylate transport (Dct) system, which also transports succinate, fumarate and malate. The apparent K m for aspartate transport by this system was about 10 mm, compared to 15 μm for succinate. This difference in affinity was also apparent in competitive inhibition studies, which showed that succinate effectively inhibits aspartate transport. Although aspartate was not a preferred substrate, it was a very efficient inducer of the Dct system. Both the Dct system and a second aspartate transport system were capable of supplying aspartate for use as a nitrogen source. The second system had a lower apparent K m for aspartate transport (1.5 mm), and was competitively inhibited by glutamate. This aspartate-glutamate system was regulated independently from the Dct system, since it functioned in mutants lacking the Dct system regulatory genes dctB and dctD, and its induction did not coactivate the Dct system. Uptake kinetics in cultures growing on aspartate as nitrogen source showed rapid substrate exchange between extracellular and internal aspartate. R. meliloti was shown to be able to selectively activate the two uptake systems, and also regulated its metabolism as required to utilize aspartate as either carbon or nitrogen source.

In Rhizobium meliloti, an aspartate aminotransferase (AspAT) encoded within a 7.3-kb HindIII fragment was previously shown to be required for symbiotic nitrogen fixation and aspartate catabolism (V. K. Rastogi and R.J. Watson, J. Bacteriol. 173:2879-2887, 1991). A gene coding for an aromatic aminotransferase located within an 11-kb HindIII fragment was found to complement the AspAT deficiency when overexpressed. The genes encoding these two aminotransferases, designated aatA and tatA, respectively, have been localized by subcloning and transposon Tn5 mutagenesis. Sequencing of the tatA gene revealed that it encodes a protein homologous to an Escherichia coli aromatic aminotransferase and most of the known AspAT enzymes. However, sequencing of the aatA gene region revealed two overlapping open reading frames, neither of which encoded an enzyme with homology to the typical AspATs. Polymerase chain reaction was used to selectively generate one of the candidate sequences for subcloning. The cloned fragment complemented the original nitrogen fixation and aspartate catabolism defects and was shown to encode an AspAT with the expected properties. Sequence analysis showed that the aatA protein has homology to AspATs from two thermophilic bacteria and the eukaryotic tyrosine aminotransferases. These aminotransferases form a distinct class in which only 13 amino acids are conserved in comparison with the well-known AspAT family. DNA homologous to the aatA gene was found to be present in Agrobacterium tumefaciens and other rhizobia but not in Klebsiella pneumoniae or E. coli.

We have examined parameters that affect sequence-specific interactions of the mouse c-myb protein with DNA oligomers containing the Myb-binding motif (CA/CGTTPu). Complexes formed between these oligomers and in vitro translated c-myb proteins were analysed by electrophoresis on non-denaturing polyacrylamide gels using the mobility-shift assay. By progressive truncation of c-myb coding sequences it was demonstrated that amino acids downstream of a region of three imperfect 51-52 residue repeats (designated R1, R2 and R3), which are located close to the amino terminus of the protein, had no qualitative or quantitative effect on the ability to interact specifically with this DNA motif. However, removal of only five amino acids of the R3 repeat completely abolished this activity. The contribution of individual DNA-binding domain repeats to this interaction was investigated by precisely deleting each individually: it was demonstrated that a combination of R2 and R3 was absolutely required for complex formation while the R1 repeat was completely dispensible. c-myb proteins showed quantitatively greater interaction with oligomers containing duplicated rather than single Myb-binding motif, in particular where these were arranged in tandem. Moreover, it was observed that c-myb protein interacted with these tandem motifs as a monomer. These findings imply that a single protein subunit straddles adjacent binding sites and the implications for c-myb activity are discussed.

The expression of genes required for progression through the cell cycle is highly modulated through a regulatory axis containing the E2F transcription factor and retinoblastoma tumour suppressor protein families. One of the genes regulated through this mechanism encodes the B-Myb transcription factor, which has been shown to be critically required for early embryonal development in the mouse. Transcriptional activity of B-Myb is substantially enhanced in S phase through modification by cyclin A/cdk2, and the evidence points squarely to the major role being played by B-Myb during this phase of the cell cycle. We discuss in this review recent findings suggesting that B-Myb is a multifunctional protein that has, in addition to its transcriptional properties, the ability to interact directly with other regulators of the cell cycle.

The paper presents a model for combining meteorological radar data in overlapping regions, along with results from a short dual Doppler study of a convective event observed in the Po Valley region of northern Italy. To perform any kind of quantitative analysis between two overlapping radars, whether spaceborne or ground based, it is useful to adopt a common coordinate system on which to view the data. The volume weighting model presented overcomes some of the problems intrinsic to distance weighted interpolation schemes. The results of a short, dual Doppler study of a convective event observed from two operational radars are presented. The data used for the study were collected under the European Union funded Polarisation and Doppler Radar Experiment (PADRE).

We have undertaken fine-wire localization and biopsy of 130 impalpable breast lesions identified by mammography and considered suspicious of malignancy. Histologically 22 of these lesions were invasive carcinomas and 24 were in situ carcinomas (35 per cent malignant). Twenty-nine per cent of the lesions were identified during the screening of asymptomatic women. In the remainder, the presenting symptoms bore no relation to the eventual histological diagnosis. Clusters of micro-calcification were more often malignant than were abnormal soft-tissue masses. Malignancy in the absence of microcalcification was almost always invasive.

We have previously shown in mouse NIH3T3 fibroblasts that transcription of the B-myb gene, which encodes a transcription factor required for S phase entry, is repressed through a promoter E2F site in G0/early G1. Transcription repression at this stage of the cell cycle was correlated with binding of a specific p107/E2F complex to this site. We report here, however, that transfection of cells with the known components of this complex, p107, E2F-4 and DP-1, did not repress the B-myb promoter in cycling NIH3T3 cells, although p107 inhibited transcription transactivation by E2F-4/DP-1. To establish definitively the contribution of E2F to repression, the effects of further mutations within and surrounding the E2F site were examined. It was evident that E2F binding and repression were closely correlated, lending greater weight to the contention that E2F itself is implicated in this activity. These studies also identified a closely linked site, designated the downstream repression site (DRS), which was not required for E2F binding or transactivation but which was necessary for repression. These findings indicated that E2F-dependent repression and activation are independently regulated phenomena and suggest that repression involves additional interactions determined by the promoter context.

Introduction The “Hawthorne Effect” is the phenomenon in which subjects modify practice as a consequence of the knowledge that they are being observed. This is a potential confounder during periods of national endosocopy audit and may result in spuriously improved outcome reporting during audit periods. We aimed to investigate whether the Hawthorne Effect influences colonoscopy practice. We also aimed to ascertain if the national colonscopy audit could result in a change in practice, and whether any such change was maintained. Methods The Unisoft endoscopy database at Whipps Cross University Hospital was interrogated to determine patient demographics, sedation rates, quality of bowel preparation, diagnoses and therapeutic interventions during 5 2-week time periods; The national colonoscopy audit period (t), t−1 year, t−2 weeks, t+2 weeks and t+3 months. Results were compared to determine whether there was a statistically significant difference in measurable indices of clinical practice that may be due to the Hawthorne Effect. Time periods following the audit period were included to establish whether there was any evidence of a “washout period” of improved outcomes following the national audit—that is, if the process of observed audit results in a lasting improvement in clinical practice. The null hypothesis was suggested that all periods would be similar, and tested to a 95% confidence level. Results Colonoscopies performed during the national colonoscopy audit period (t) were compared with 2-week periods t−1 year, t−2 weeks, t+2 weeks and t+3 months. Similar numbers of procedures were carried out during the five time periods. Basic patient demographics were similar, as were the numbers of male and female patients. No statistically significant differences were found in the sedative dose, ceacal or TI intubation rates between the audit period and any other time period. Moreover, polyp detection and retrieval was likewise also not statistically significantly different when the four time periods were compared with the fortnight of the national colonscopy audit. Small differences were noted in the colonscopists assessment of bowel preparation—there was more likely be a comment on poor bowel preparation during the audit period than any of the other time periods. Conclusion Data from Whipps Cross University Hospital demonstrate that observation of colonoscopists during the recent BSG national colonoscopy audit does not alter significantly the clinical practice or interpretation of findings when compared to time periods before or after the audit period. This validates the national colonoscopy audt findings; the data are indeed a true reflection of “normal” colonsocopy practice—colonoscopists are apparently not affected by the “Hawthorne Effect”. Competing interests None declared.

The binding of (1)-[3H]vesamicol was characterized in several subcellular fractions and brain regions of the rat. Binding to a lysed P2 fraction from the rat cerebral cortex reached equilibrium within 4 min at 37 degrees C and was reversible (dissociation half-time 4.9 min). At least two binding affinities were found in P2 fractions from the cerebral cortex (Kd: 21 nM and 980 nM), striatum (Kd: 28 nM and 690 nM), and cerebellum (Kd: 22 nM and 833 nM). High affinity Bmax values were highest in striatum (1.17 pmol/mg protein), followed by cerebellum (0.67 pmol/mg protein), and cerebral cortex (0.38 pmol/mg protein). Low affinity Bmax values were highest in cerebellum (5.2 pmol/mg protein), with similar values for cerebral cortex (3.7 pmol/mg protein) and striatum (3.8 pmol/mg protein). High affinity but not low affinity binding in each brain region was stereospecific. Another inhibitor of vesicular ACh-transport also displaced 1-vesamicol binding potently (IC50: 17 nM) and efficaciously (over 90%). Both high affinity and low affinity Bmax values for [3H]vesamicol-binding were highest in a partially purified synaptic vesicle fraction, followed by purified synaptosomes, crude membranes and P2 fractions. Specific binding was not observed in a mitochondria-enriched fraction. Crude membrane preparations of primary, neuron-enriched whole brain cultures also exhibited high (64 nM) and low affinity (1062 nM) [3H]vesamicol binding. Isoosmotic replacement of 0.18 M KCl in the binding-buffer with NaCl had no effect on binding. These results suggest that at least some high affinity [3H]vesamicol binding in rat brain preparations may be associated with synaptic vesicles, some of which may not be cholinergic in origin.

We have isolated five specialized transducing lambda bacteriophages (lambda dpyrE spoT) carrying the pyrE and spoT genes of Escherichia coli. A fragment from one of these phages was used as the source of DNA to clone the spoT and pyrE genes on a multicopy plasmid, pBR322. Insertions and deletions in this plasmid were obtained. These plasmids were used to transform a minicell-producing strain, and the gene products synthesized were determined. Our experiments demonstrate that the spoT and pyrE genes are separated by about 4 magadaltons and suggest that the spoT gene product is a protein whose molecular weight is 80,000. The strain in which the spoT+ allele is carried on a plasmid produced nine times more spoT gene activity than a normal spoT+ strain when assayed in crude extracts. This strain was used to prepare partially purified gene product, guanosine 5'-diphosphate, 3'-diphosphate pyrophosphatase. The enzyme has the following characteristics. (i) It hydrolyzes pyrophosphate from the 5'-pyrophosphate of guanosine 5'-diphosphate, 3'-diphosphate, yielding GDP and pyrophosphate. (ii) Its activity is strongly stimulated by Mn2+ and slightly stimulated by salt. (iii) Its activity is inhibited by uncharged tRNA. There are also two additional activities in the cell extract which degrade guanosine in 5'-diphosphate, 3'-diphosphate in vitro but which are not specified by the spoT gene.

We describe the molecular cloning of a 9-kilo-base-pair BamHI fragment from human placental DNA containing a sequence homologous to the transforming gene (v-mos) of Moloney murine sarcoma virus. The DNA sequence of the homologous region of human DNA (termed humos) was resolved and compared to that of the mouse cellular homolog of v-mos (termed mumos) [Van Beveren, C., van Straaten, F., Galleshaw, J.A. & Verma, I.M. (1981) Cell 27, 97-108]. The humos gene contained an open reading frame of 346 codons that was aligned with the equivalent mumos DNA sequence by the introduction of two gaps of 15 and 3 bases into the mumos DNA and a single gap of 9 bases into the humos DNA. The aligned coding sequences were 77% homologous and terminated at equivalent opal codons. The humos open reading frame initiated at an ATG found internally in the mumos coding sequence. The polypeptides predicted from the DNA sequence to be encoded by humos and mumos also were found to be extensively homologous, and 253 of 337 amino acids were shared between the two polypeptides. The first five NH2-terminal and last two COOH-terminal amino acids of the humos gene product were in common with those of mumos. In addition, near the middle of the polypeptide chains, four regions ranging from 19 to 26 consecutive amino acids were conserved. However, we have not been able to transform mouse cells with transfected humos DNA fragments or with hybrid DNA recombinants containing humos and retroviral long terminal repeat (LTR) sequences.

A retrospective study was performed of 163 patients aged 65 years and over with a diagnosis of duodenal ulceration admitted to one Health District over a period of six years. Eighty per cent of the patients were admitted with acute complications, 50% bled and 30% were perforated. A large proportion of these patients were currently taking anti-inflammatory agents. Patients managed surgically for their complications had a high mortality rate but this was even higher for those managed conservatively. Giant ulcers were found to occur frequently in this age group which had a tendency to severe bleeding. It is concluded that early diagnosis and prompt surgical intervention is essential in the management of complications associated with duodenal ulceration in the elderly.

We have established that in the Becker strain of pseudorabies virus (PRV), the glycoprotein gIII gene is not essential for growth in cell culture. This was accomplished by construction and analysis of viral mutants containing two defined deletion mutations affecting the gIII gene. These mutations were first constructed in vitro and introduced into Escherichia coli expression plasmids to verify structure and protein production. Each mutation was then crossed onto PRV by cotransfection of plasmid DNA and parental viral DNA by using gIII-specific monoclonal antibodies as selective and screening reagents. One resultant virus strain, PRV-2, contained an in-frame deletion of a 402-base-pair (bp) SacI fragment contained within the gIII gene. Another virus strain, PRV-10, contained a deletion of a 1,480-bp XhoI fragment removing 230 bp of the upstream, putative transcriptional control sequences and 87% of the gIII coding sequence. The deletion mutants were compared with parental virus by analysis of virion DNA, gIII specific RNA, and proteins reacting with gIII specific antibodies. Upon infection of PK15 cells, the deletion mutants did not produce any proteins that reacted with two gIII specific monoclonal antibodies. However, two species of truncated glycosylated proteins were observed in PRV-2 infected cells that reacted with antiserum raised against bacterially produced gIII protein. PRV-10 produced no detectable gIII-specific RNA or protein. PRV-10 could be propagated without difficulty in tissue culture. Virus particles lacking gIII were indistinguishable from parental PRV virus particles by analysis of infected-cell thin sections in the electron microscope. We therefore conclude that expression of the gIII gene was not absolutely essential for PRV growth in tissue culture.

A collection of symbiotically defective mutants of Rhizobium meliloti JJ1c10 was derived by Tn5 mutagenesis using the suicide vector pGS9. They include two Nod− and about 250 Fix− mutants. The mutants were found to be heterogenous in acetylene reduction activity and in the morphology and ultrastructure of the nodules which they induced. Over 90% were found to contain bona fide Tn5 insertions in a variety of DNA restriction fragments. When Tn5-carrying DNA segments cloned from 24 of the mutants were introduced into the equivalent location in the genome of the wild-type strain by recombination-mediated replacement, only eight produced a symbiotically defective phenotype similar to that of the original mutant. This result indicated that many of the symbiosis mutations were not directly caused by Tn5 insertion. DNA segments apparently containing mutated fix genes but not containing Tn5 were found in eight mutants by identifying cosmids carrying wild-type DNA which complemented their symbiosis defects. Probing of the DNA of these mutants with their complementing cosmids revealed no detectable physical alteration of the homologous DNA. A segment of DNA including the hsn and nifHDK genes was favoured for these non-Tn5 mutations. Three regions of the genome in which Tn5 caused fix mutations were identified. One of these was the known megaplasmid nod-nif region. The other two regions, designated fix-e5 and fix-h21, were found to be chromosomal. Mutants in one of these chromosomal regions fluoresced more intensely on calcofluor plates than the wild type.

Mouse c-myb gene transcripts in various cells of haemopoietic origin were analysed using S1 nuclease and RNase mapping techniques and by Northern blotting. It was found that the prevalent 3.8-kb c-myb mRNA present in thymocytes, T cell leukaemias, myelomonocytic leukaemias, erythroleukaemias and myeloid stem cells was initiated at several cap sites mapping within a region 97-244 bp upstream from the protein coding sequence. Utilization of additional cap sites mapping further upstream was also observed in certain cells, most notably thymocytes, and this gave rise to RNA species (4.3-5.6 kb) larger than the presumptive mRNA. In contrast, myeloma cell c-myb transcripts, which are much less abundant than those in more immature haemopoietic cells, were found to be initiated at a restricted set of cap sites mapping 244-277 bp upstream of the coding sequence. Hence, these data suggest that the abundance of the c-myb mRNA may be regulated by a process involving selective utilization of mRNA cap sites. Sites hypersensitive to DNase I were associated with mRNA cap sites in cells that expressed c-myb.

The deconvolution process is widely used to enhance seismic data by suppressing distortions of the shot pulse caused by such things as reverberations and ghosts. The process consists of estimating the correlation function from the data, determining the inverse filter using the Levinson algorithm, and applying the inverse filter to the data. This paper is concerned with the estimation problem. Certain conclusions about the estimation problem are suggested by the theory of power spectra developed by Tukey and others. By means of a Monte Carlo simulation of the deconvolution process, we have tested these conclusions: (1) Severely distorted data should be prewhitened. (2) Tructors (lag windows) with the same number of degree of freedom yield the same error. (3) There is an optimum number of degree of freedom for a fixed data window. (4) Due to time variance in the data, there is an optimum length of data window. Monte Carlo simulation can be used to estimate the optimum values (3) and (4) and so improve the performance sof the deconvolution process.

This paper presents some of the background prior to the actual survey, the functioning of the “Technical Committee” and its relationship to the contractors. A brief outline is also presented covering the various technical phases of the operation together with some of the inherent hazards of the area and how they were handled. A summary of recommended changes in equipment and procedure arising from the experience of this survey is given.

A seismogram may be treated as the sum of a primary wave train, a secondary wave train, and noise. Assuming the secondary has the same wave form as the primary and arrives at time Δt behind it with a relative strength R, a deconvolved seismogram which is an estimate of the primary seismogram can be found for every Δt. It is postulated that at Δt's close to the values of real secondaries, especially pP, the deconvolved seismogram will be simplified. A test based on the decrease in energy represented by the deconvolved seismogram is proposed with empirical justification by which such times can be determined. This method of recognizing secondaries is tested on 14 seismograms of the May 10, 1963, Ecuador earthquake and on 14 nuclear-blast seismograms. Although it picks out secondaries, it finds many other pulses besides pP; however, it does not always find pP.

Using optimum filter theory as a starting point, we describe a method for the design of practical multi-trace seismic data processing systems. We assume the inputs to be the superposition of signal, coherent noise, and incoherent noise. The signal and coherent noise moveouts are described statistically by their probability densities. Our approach is to split the system into two stages. The first stage achieves optimum noise suppression but distorts the signal. The signal distortion is reduced in the second stage by an optimum finite memory inverse filter. The system that is obtained using our method of design depends upon the form of the probability density functions. We show two examples, ghost suppression and velocity filtering. In ghost suppression we choose a model with moveouts known exactly, which corresponds to delta functions for the probability densities. In velocity filtering the signal and coherent noise moveouts are equally probable within non-overlapping ranges. The resulting system in each case is both simple and effective. In ghost suppression a simple shift and subtract cancels the coherent noise. The signal distortion is reduced by an inverse filter. The velocity filter system consists of differentiated moving averages applied to each trace, followed by a 90° phase shift and a low pass filter.

Multiple reflections constitute an important source of “noise” on seismograms. Because multiples are related to the primary reflectivity function r(t) in a very complicated way, the suppression of all multiple reflections on a single seismic trace is unlikely without a detailed knowledge of the reflectivity function itself. This paper describes a series of approximations in which multiple reflections are decomposed into component subsets. For certain types of velocity functions, one or two of these subsets form a sufficiently good approximation to the complete multiple process to at least predict the strongest multiples present on a field seismogram. The subset approximations to the complete multiple function include the first‐order surface multiples, i.e., three‐bounce multiples having a second reflection at the surface. The expression for this set of multiples is [Formula: see text], where the * stands for convolution, and [Formula: see text] is the surface reflection coefficient. Computations of this set are compared with the complete multiple function for logs from Alberta, Canada, and southern Mississippi. A further approximation, called the [Formula: see text], is valid in areas where a few reflection coefficients, r⁁(t), are responsible for the bulk of the multiple noise. [Formula: see text] consists of all first‐order surface multiples which have a contribution from the r⁁(t) zone. The above‐mentioned velocity logs are used to illustrate the [Formula: see text] approximation. The [Formula: see text] function is compared with the complete first‐order surface multiple function for the two logs. A method for suppressing the multiples described by the approximations is proposed. The technique is illustrated for the [Formula: see text] approximation but can be extended to higher‐order approximations. It consists of a positive feedback circuit in which a reflectivity function is simulated along with appropriate time‐variant gain adjustments. In order to realize the computation, it is necessary to find the time and amplitude of the reflection coefficients responsible for the large‐amplitude multiple reflections. Several methods for providing this information are discussed and a correlation search technique is illustrated with examples. Finally, the suppression technique is illustrated with live seismic data on two record sections from two different areas showing data before and after multiple suppression. In both cases the [Formula: see text] approximation was adequate.

A herpes simplex virus type 1 strain isolated from a recurrent lesion of the nose reacted with monoclonal antibodies recognizing a type 2-specific site on glycoprotein D but not with monoclonal antibodies recognizing other type 2-specific sites. DNA sequence analysis of the glycoprotein D gene of the isolate revealed a single nucleotide alteration which changed the codon for asparagine to one encoding histidine at amino acid 97 in the protein. Histidine is located at this position in glycoprotein of herpes simplex virus type 2; thus, the monoclonal antibody 17 beta A3 recognizes an epitope located at this region of the protein.

The existence of interfacial turbulence associated with mass transfer of uranyl nitrate, plutonium (IV) nitrate and nitric acid from an aqueous solution to an organic phase containing tri-butyl phosphate is described. The conclusion is drawn that because such interfacial activity can affect interdroplet interactions, single droplet studies will not correctly represent the behaviour of multi-droplet extraction systems.

We have looked for conserved DNA sequences between four herpes simplex virus type 1 (HSV-1) glycoprotein genes encoding gB, gC, gD, and gE and pseudorabies virus (PRV) DNA, HSV-1 DNA fragments representing these four glycoprotein-coding sequences were hybridized to restriction enzyme fragments of PRV DNA by the Southern blot procedure. Specific hybridization was observed only when HSV-1 gB DNA was used as probe. This region of hybridization was localized to a 5.2-kilobase (kb) region mapping at approximately 0.15 map units on the PRV genome. Northern blot (RNA blot) analysis, with a 1.2-kb probe derived from this segment, revealed a predominant hybridizing RNA species of approximately 3 kb in PRV-infected PK15 cells. DNA sequence analysis of the region corresponding to this RNA revealed a single large open reading frame with significant nucleotide homology with the gB gene of HSV-1 KOS 321. In addition, the beginning of the sequenced PRV region also contained the end of an open reading frame with amino acid homology to HSV-1 ICP 18.5, a protein that may be involved in viral glycoprotein transport. This sequence partially overlaps the PRV gB homolog coding sequence. We have shown that the PRV gene with homology to HSV-1 gB encoded the gII glycoprotein gene by expressing a 765-base-pair segment of the PRV open reading frame in Escherichia coli as a protein fused to beta-galactosidase. Antiserum, raised in rabbits, against this fusion protein immunoprecipitated a specific family of PRV glycoproteins of apparent molecular mass 110, 68, and 55 kilodaltons that have been identified as the gII family of glycoproteins. Analysis of the predicted amino acid sequence indicated that the PRV gII protein shares 50% amino acid homology with the aligned HSV-1 gB protein. All 10 cysteine residues located outside of the signal sequence, as well as 4 of 6 potential N-linked glycosylation sites, were conserved between the two proteins. The primary protein sequence for HSV-1 gB regions known to be involved in the rate of virus entry into the cells and cell-cell fusion, as well as regions known to be associated with monoclonal antibody resistance, were highly homologous with the PRV protein sequence. Furthermore, monospecific antibody made against PRV gII immunoprecipitated HSV-1 gB from infected cells. Taken together, these findings suggest significant conservation of structure and function between the two proteins and may indicate a common evolutionary history.

A minigene containing a cDNA encoding the normal mouse p80c-myb protein under strong promoter control was used to transfect Friend erythroleukaemia cells. Expression of the transfected gene was found to result in elevated levels of p80c-myb which were not subject to rapid down-modulation by inducers of Friend cell differentiation as was the product of the endogenous c-myb gene. Continued synthesis of p80c-myb was found to be associated with a marked decrease in differentiation of Friend cells and we concluded that normal down-regulation of c-myb expression may be a necessary event in differentiation of these cells.

The control of c-myb mRNA abundance was examined in three representative cell lines, (the erythroleukaemia F4-12B2, the myeloma MOPC-31C and the fibroblast NIH3T3), which display abundant, low and undetectable levels of this transcript, respectively. We observed a small difference in half-life between F4-12B2 and MOPC-31C c-myb mRNA (175 min and 105 min, respectively) insufficient to account for the approximately 20-fold lower levels of this transcript in myelomas. Using the run-on transcription assay we found that c-myb transcripts were initiated at similar rates in all three cell types and were elongated at this relatively high rate to a site approximately 2 kilobases into the first intron. NIH3T3 c-myb transcripts did not proceed detectably beyond this pause/attenuation site, while in F4-12B2 cells transcription of regions 3' of this site occurred at a rate approximately 12-fold greater than in MOPC-31C. We have concluded that this transcriptional arrest mechanism, together with small differences in RNA turnover, were sufficient to account for the spectrum of c-myb mRNA abundance observed. Despite evidence of transcript initiation, we were unable to detect c-myb mRNA in fibroblasts, even under conditions (e.g. serum stimulation) which induced high c-myc mRNA levels. However, a novel 3.0 kilobase transcript with homology to c-myb was detected in cycloheximide-treated NIH3T3 cells.

Nuclear and cytoplastic transcripts, synthesized in cells infected with six DNA-negative temperature-sensitive (ts) mutants of HSV-1 (ts B, ts D, ts E, ts K, ts S and ts T) under non-permissive conditions, were isolated and hybridized to unlabelled fragments of HSV-1 DNA, generated by restriction endonuclease digestion and immobilized on to nitrocellulose membranes by the method of Southern (1975). In this way it has been possible to map those regions of the HSV-1 genome represented by stable transcrips in cells infected with these mutants and compare them with those regions transcribed in cells infected with the wild-type virus at early and late times post infection (before and after viral DNA replication) and in the presence of DNA- and protein-synthesis inhibitors. Viral transcription in ts D, ts T and ts K-infected cells is restricted, the patterns of hybridization being similar, but not identical to that observed with immediate early RNA. Since these three mutants fall into two complementation groups, these experiments suggest that at least two viral products are required for the switch-on of early transcripts. In contrast, transcript mapping with the other early mutants (ts B, ts E and ts S) has shown a much less restricted transcriptional pattern, the pattern obtained resembling that with early, rather than late RNA.

The intralobular stroma of the resting human mammary gland was studied by thin-sectioning transmission electron microscopy on tissue obtained from reduction mammoplasty or adjacent to fibroadenomas. The arrangement of delimiting fibroblasts around the epithelium and their possession of contacts as shown by earlier studies were confirmed. Observations on other ultrastructural aspects show these cells to have abundant rough endoplasmic reticulum, a well developed Golgi apparatus and vesicles considered to contain collagen-precursor, and conflict with earlier data. The fine structure of those fibroblasts without close epithelial proximity has been described for the first time and was similar to that of delimiting fibroblasts. Other features applicable to both categories of fibroblast included: variation in overall staining intensity, structures resembling hemi-desmosomes, simple junctions, and close juxtapositions of cell surfaces forming 'contacts' with other fibroblasts as well as with mononuclear cells (lymphocytes, plasma cells, mast cells, macrophages). These cell contacts have not been documented previously. Contacts were structurally undifferentiated, forming spaces 20-50 nm wide which were occluded by lanthanum nitrate. Intralobular stromal cells were therefore organised into a kind of reticulum. The possible functions of this network are discussed. The concept of the epithelial-stromal junction is re-assessed in the light of these observations.

We have examined the structures of two herpes simplex virus type 1 immediate-early (IE) RNAs (IE mRNA-4 and IE mRNA-5) which map at the junctions of the unique (Us) and reiterated regions (TRs/IRs) of the virus DNA short component. Hybrids between IE cytoplasmic RNA and herpes simplex virus type 1 DNA restriction fragments were digested with single-strand-specific nucleases S1 and exonuclease VII, and the products were analyzed by agarose gel electrophoresis. Data obtained with the nuclease digestion technique were confirmed by electron microscopy of R-loop structures formed with polyadenylated IE RNA and virus DNA fragments. It was found that both IE mRNA-4 and IE mRNA-5 contained a 260-base 5'-terminal cotranscript which mapped at equivalent loci within TRs/IRs. These 5'-terminal sequences were shown to be spliced to 3'-terminal cotranscripts of 1,450 bases (for IE mRNA-4) and 1,540 bases (for IE mRNA-5). The 3'-terminal cotranscripts contained sequences encoded by both TRs/IRs and opposite ends of Us, indicating that the introns contained by the IE mRNA-4 and IE mRNA-5 genes, found to be approximately 150 base pairs in size, mapped entirely within the reiterated sequences. The data suggest that these genes may contain common and unique components, and the implications of this model are discussed.