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Compared to other areas in nursing, nurses working in A&E Departments encounter a wide range of difficult and specific issues relating to consent to treatment, whether they are acting independently as nurse practitioners or carrying out the treatment prescribed by doctors. The law of consent must be taken into account in our daily practice to avoid a claim of battery or negligence from our patients. Emergency treatment can be given under the doctrine of necessity if an adult patient lacks capacity to give consent, but treatment cannot be imposed on competent adults who refuse it. Assessment of capacity may be difficult. Patients with mental disorders can pose specific consent difficulties, depending on whether the proposed treatment is directly related to the mental disorder. Problems may also arise from adult patients who refuse treatment due to undue influence from others. Obtaining consent to treatment for children depends on their age, maturity and understanding. Specific difficulties may arise if the child's wishes conflict with those with parental consent, or when those with parental responsibility unreasonably refuse to give consent.

Background. The objectives of this study are to explore the effects of the new 1996 guidance requiring explicit demonstration of competencies on the nature of successful MFPHM Part II reports, how successful candidates claimed competency areas in their two reports and the effects of the subject areas of the report on the specific competencies claimed.
Method. The abstracts of candidates who passed the examination from January 1996 to January 1999 were studied. Information was extracted on candidate's region, year of the abstract, examination guidance, subject area, methods and data used, format of the abstract, and level (e.g. national, regional, etc.) for which the work was performed.
Results. Compared with reports submitted under the 1992 guidance, those submitted under the 1996 guidance were more likely to have a structured abstract, and to employ descriptive epidemiological methods and routine data, and were less likely to be case-control or retrospective studies. There were no other significant differences in the level for which the work was performed, the subject area, or the methods and data used. Thirty-nine per cent of candidates under the 1996 guidance claimed at least one identical competency area in both reports, most frequently for health needs assessment and literature review. Each of the four competencies was demonstrated by a significant proportion of reports in each subject areas.
Conclusion. The new examination guidance had only minor effects on the nature of successful Part II reports. Candidates used different strategies for claiming competencies, apparently at the choice of individual trainees and trainers. The competency requirements did not appear to limit the range of work performed.

About half of the familial breast cancer cases are found to bear mutations in the breast cancer susceptibility gene 1 (BRCA1). The majority of BRCA1mutations produce a truncated protein and BRCA1-associated breast tumors exhibit a number of defined tumor phenotypes. The function of BRCA1has been examined in gene knockout mice in which the nullizygous mice die early in utero, but this lethality can be partially rescued by a nullizygous p53mutation. Wild-type BRCA1 protein binds to a number of cellular proteins, including DNA repair protein Rad51, tumor suppressor p53, RNA polymerase II holoenzyme, RNA helicase A, CtBP-interacting protein, c-myc, BRCA1-associated RING domain protein (BARD1), BRCA2 protein, etc. These proteins likely mediate the involvement of BRCA1 in DNA repair, transcriptional transactivation, and cell cycle control. Overall, BRCA1 protein may act as a converging vehicle for cell regulatory proteins to associate with. Therefore, mutations in BRCA1may affect the composition of these complexes on which dysregulation of cellular functions with eventual development of malignancy is expected.

We present the first next-to-leading-order QCD analysis of neutrino charm production, using a sample of 6090?µ- and -induced opposite-sign dimuon events observed in the CCFR detector at the Fermilab Tevatron. We find that the nucleon strange quark content is suppressed with respect to the non-strange sea quarks by a factor ?=0.477-0.053+0.063, where the error includes statistical, systematic and QCD scale uncertainties. In contrast to previous leading order analyses, we find that the strange seax-dependence is similar to that of the non-strange sea, and that the measured charm quark mass,mc=1.70±0.19 GeV/c2, is larger and consistent with that determined in other processes. Further analysis finds that the difference inx-distributions betweenxs(x) and is small. A measurement of the Cabibbo-Kobayashi-Maskawa matrix element |Vcd|=0.232-0.020+0.018 is also presented.

The rate of neutrino- and antineutrino-induced prompt same-sign dimuon production in steel was measured using a sample of µ-µ- events and 25 µ+µ+ events withPµ>9 GeV/c, produced in 1.5 millionvµ and 0.3 million induced charged-current events with energies between 30 GeV and 600 GeV. The data were obtained with the Chicago-Columbia-Fermilab-Rochester (CCFR) neutrino detector in the Fermilab Tevatron Quadrupole Triplet Neutrino Beam during experiments E 744 and E 770. After background subtraction, the prompt rate of same-sign dimuon production is (0.53±0.24)×10-4 pervµ charged-current event and (0.52±0.33)×10-4 per charged-current event. The kinematic distributions of the same-sign dimuon events after background subtraction are consistent with those of the non-prompt background due to meson decays in the hadron shower of a charged-current event. Calculations ofc gluon bremsstrahlung, based on improved measurements of the charm mass parameter and nucleon structure functions by the CCFR collaboration, yield a prompt rate of (0.09±0.39)×10-4 pervµ charged-current event. In this case,c gluon bremsstrahlung is probably not an observable source of prompt same-sign dimuons.

Nick-translated DNA from a recombinant plasmid containing the herpes simplex virus type 1 thymidine kinase gene was used as a probe for the synthesis of thymidine kinase RNA. The recombinant plasmid was generated by inserting the 3.5-kilobase fragment derived by BamHI digestion of herpes simplex virus type 1 DNA into plasmid pBR322. At 8 h after infection, cytoplasmic and nuclear RNA hybridized to 14% and 19% of the recombinant DNA probe, respectively. However, no significant hybridization was found with either nuclear or cytoplasmic RNA extracted from cells infected and maintained in the presence of cycloheximide. This suggests that no thymidine kinase-related RNA was synthesized in the absence of alpha polypeptides, and supports the hypothesis that the alpha polypeptides effect new thymidine kinase RNA synthesis rather than being involved in processing or transport of thymidine kinase RNA. In cells infected and maintained in the presence of the arginine analog canavanine, about 2 to 3% of the plasmid DNA was found to hybridize with cytoplasmic and nuclear RNA. However, when a recombinant plasmid DNA containing only thymidine kinase coding sequences was used, no significant hybridization was found. The inhibition of thymidine kinase transcription by canavanine suggests that thymidine kinase belongs to the beta 2 kinetic class.

To characterize and compare the thymidine (TdR) and deoxycytidine (CdR) kinase isozymes of uninfected and herpesvirus-infected cells: (i) the subcellular distribution of the isozymes has been studied; (ii) a specific assay for CdR kinase has been devised; (iii) the TdR kinase isozymes have been partially purified; and (iv) the purified enzymes have been analyzed by disc polyacrylamide gel electrophoresis, isoelectric focusing, and glycerol gradient centrifugation and by substrate competition and dCTP inhibition studies. The results indicate that there are interesting individual differences with respect to nucleoside acceptor specificity between the cytosol and mitochondrial pyrimidine deoxyribonucleoside kinases of uninfected cells and between the enzymes induced by different herpesviruses. In the cytosol of uninfected mouse, chicken, and owl monkey kidney cells, two different proteins, TdR kinase F and CdR kinase 2, catalyze the phosphorylations of TdR and CdR, respectively. TdR kinase F does not phosphorylate CdR, nor does CdR kinase 2 phosphorylate TdR. A second TdR kinase isozyme present in HeLa(BU25) mitochondria (TdR kinase B) also lacks CdR phosphorylating activity. In contrast, a genetically distinctive deoxypyrimidine kinase (TdR kinase A) of mouse, human, and chick mitochondria catalyzes the phosphorylation of both TdR and CdT. Three herpesviruses, marmoset herpesvirus and herpes simplex virus types 1 and 2, induce in the cytosol fraction of LM(TK-) mouse cells isozymes which share common properties with mitochondrial TdR kinase A, including the ability to catalyze the phosphorylation of both TdR and CdR. However, the herpesvirus-induced deoxypyrimidine kinases differ from mitochondrial TdR kinase A with respect to sedimentation coefficient, sensitivity to dCTP inhibition, and antigenic determinants. The herpesvirus-specific and the mitochondrial deoxypyrimidine kinases exhibit a preference for TdR over CdR as nucleoside acceptor. Pseudorabies virus and herpesvirus of turkeys induce cytosol TdR kinases resembling the other herpesvirus-induced TdR kinases in several properties, but like cellular TdR kinase F, the pseudorabies virus and herpesvirus of turkeys TdR kinases lack detectable CdR phosphorylating activities. Finally, a marmoset herpesvirus nutant resistant to bromodeoxyuridine, equine herpesvirus type 1, and Herpesvirus aotus induces neither TdR nor CdR phosphorylating enzymes during productive infections.

This paper reports on measurements of the total cross section for the inclusive reaction vµ+N, as a function of incident energy. Neutrinos and antineutrinos with energy in the range 30–300 GeV were produced in the 1982 Fermilab narrow-band neutrino beamline. A total of 35 000 neutrino and 7000 antineutrino interactions were recorded in the CCFR detector located in LabE. The incident neutrino flux was determined by methods similar to those used in previous experiments. The rate of increase with energy of the total cross section (s/Ev) in the range 30 to 75 GeV was determined to be 0.659±0.005(stat)±0.039(syst)×10-38 cm2/GeV and 0.307±0.008(stat)±0.020(syst)×10-38 cm2/GeV for incident neutrinos and antineutrinos, respectively. The 5.9% systematic errors are due primarily to uncertainties in the flux intensity measurement. The energy dependence of the cross section in the regionE?=100–300 GeV was found to be linear, as determined by relative normalization techniques. A weighted average of our previous and present measurement for the total ?-N cross section yields: $$\begin{gathered} \sigma (vN) = 0.666 \pm 0.020(statistical \hfill \\ + systematic)E_v 10^{ - 38} cm^2 ; \hfill \\ \sigma (\bar vN) = 0.324 \pm 0.014(statistical \hfill \\ + systematic)E_v 10^{ - 38} cm^2 ; \hfill \\ \end{gathered} $$ .

Using oligodeoxyribonucleotides produced by limited DNase I digestion of calf thymus DNA as a primer, we synthesized complementary DNA (cDNA) from the L and the S RNAs of Pichinde virus. The reaction conditions for in vitro cDNA synthesis were optimized to allow transcription of about 90% of either L or S RNA. No significant hybridization was observed when the L cDNA was hybridized to the S RNA, or when the S cDNA was hybridized to the L RNA. The results indicate that the L and S RNAs of Pichinde virus contain unique nucleotide sequences.

Using hamster anti-Pichinde virus serum, we immunoprecipitated polypeptides from BHK-21 cells infected with Pichinde virus. Seven immunoprecipitable polypeptides exhibited a time- and multiplicity of infection-dependent appearance when the cultures were pulse-labeled with L-[35S]methionine for 1 h. The predominant polypeptide was a nucleoprotein (NP) of 64,000 daltons. Components of 48,000, 38,000, and 28,000 daltons, when analyzed by two-dimensional tryptic peptide mapping, were found to be derived from NP. After a 3-h chase period, polypeptides of 17,000, 16,500, and 14,000 daltons were evident, and peptide mapping revealed that these three polypeptides were also related to NP. During a series of pulse-chase experiments, a 79,000-dalton glycoprotein (GPC) was cleaved to glycoproteins of 52,000 and 36,000 daltons. Radiolabel in a polypeptide of approximately 200,000 daltons (L) did not chase into smaller cleavage products. L, GPC, and NP were found to be unique by two-dimensional tryptic peptide mapping. Comparison of polypeptides immunoprecipitated from infected cells with structural components of purified virus revealed that L protein was evident in both. This is the first report of a high-molecular-weight polypeptide in Pichinde virus particles and infected cells.

Three RNA polymerase activities were found and associated with purified Pichinde virus, a member of the Arenaviridae. A heat-labile polymerase activity which required all four ribonucleoside triphosphates for optimal activity co-sedimented on sucrose gradient centrifugation with the viral ribonucleoprotein complex from detergent-disrupted virus preparations. This enzyme synthesized heteropolymers which represented about 23% of the genome RNA as determined by nucleic acid hybridization. Two relatively heat-stable polymerase activities which differed in their cation requirement and substrate specificity were recovered with the virus-associated ribosomes. These polymerase activities synthesized homopolymers of limited chain length: in the presence of 10 mM Mg2%, polyuridylic acid was made, whereas in the presence of 1 mM Mn2%, polyadenylic acid was made. The addition of complementary RNA synthesized with the viral transcriptase in vitro to the reaction mixture containing the polyadenylic acid polymerase activity resulted in the terminal addition of polyadenylic acid to the complementary RNA. The possible function of the ribosome-associated polymerase activities in the replication of the virus is discussed.

A cistron-specific, enzyme-forming-capacity method was used to study the control of herpes simplex virus (HSV)-specific deoxypyrimidine kinase (dPyK) mRNA synthesis. A virus-specific factor was formed by a primary infecting virus, and this factor effected the transcription of dPyK mRNA of a superinfecting virus in the presence of cycloheximide, suggesting that the factor acted in "trans" and was a diffusible one. After the addition of actinomycin D to prevent further transcription and upon removal of cycloheximide, the dPyK mRNA was allowed to express into dPyK activity. A factor from HSV-1 could effect the transcription of dPyK mRNA of both HSV-1 and HSV-2. Amino acid analogs, canavanine or ethionine, inhibited the action of this factor, suggesting that a protein was involved. This protein factor was shown to belong to the alpha (or immediate-early) group of HSV-Specific polypeptides in preductively infected cells.

A stock of plaque-purified Pichinde virus, prepared under conditions designed to limit the amounts of defective interfering virus, was used to infect BHK cells. At daily intervals after infection, cells were examined for infectious and radiolabeled virus particle production and for the synthesis of virus-specific polypeptides. Quantitative comparisons were also made of the concentrations of genomic Pichinde virus L and S RNAs in the cytoplasm of infected cells on different days after infection. Our results showed that virus particle production, rates of protein synthesis, and the intracellular levels of viral genomic RNAs all increased and decreased with similar kinetics, and that this regulation was independent of the cell growth cycle. We were unable to relate these changes in viral macromolecule and virus production to the appearance of readily identifiable defective interfering particles. Our findings suggest that regulation of virus replication early during the replicative cycle of Pichinde virus may not be dependent upon the generation of defective interfering virus.

Using a modified vector, we developed a method for DNA-mediated transformation of Chlamydomonas reinhardi with increased efficiency. The vector contained the yeast 2 microns origin of replication as a heterologous replicon. The aminoglycoside 3'-phosphotransferase (APH) gene linked to the simian virus 40 early promoter was used as an antibiotic selectable marker. The C. reinhardi transformants were resistant to 12 micrograms of G418 or 150 micrograms of kanamycin per ml. A quick-blot mRNA analysis demonstrated the presence of RNase-sensitive transcripts from the APH gene in the transformants, suggesting that the acquisition of antibiotic resistance was due to the expression of the APH gene. Southern blot analysis revealed the presence of free plasmid DNA in the transformant. The transforming vector was recovered by transforming recipient bacteria with the total DNA extracted from the C. reinhardi transformant.

One hundred and fifteen isolates of herpes simplex virus were recovered from parallel explant cultures of trigeminal and vagus ganglia and trigeminal nerve roots derived from 20 unselected human cadavers. Restriction enzyme patterns of strains recovered from 18 of 20 individuals could be differentiated from individual to individual, although all isolates from a single host were identical. Isolates from two individuals differed among themselves in the number and location of certain restriction enzyme sites.

The Pichinde virus RNA did not possess the following characteristics of eucaryotic mRNA: polyadenylic acid sequence, capped methylated structure, and ability to direct protein synthesis in vitro. Polysomal RNA extracted from cells infected with Pichinde virus reannealed with 32P-labeled virus RNA, protecting about 60% of the latter against RNase degestion. The polyadenylic acid-containing polysomal RNA also reannealed to the 32P-labeled virus RNA to approximately the same extent. These indicate that the major part of the genomic RNA of Pichinde virus is negative stranded.