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Biomedical subjects

D T Brown

Publications and source records attributed to D T Brown.

At least 163 records · Page 9Linked to original sources
PubMed1980

Effect of baricity on spinal anaesthesia with amethocaine.

Amethocaine 1% solution was mixed with equal volumes of water, 0.9% saline or 10% dextrose to prepare respectively, hypobaric, isobaric and hyperbaric solutions which were compared for intradural spinal anaesthesia in 60 patients. Thirty patients received 10 mg and 30 patients received 15 mg of amethocaine. Injections were made with the patients in the lateral recumbent position and the operating table was horizontal during and after injection. Equal numbers of patients and equal numbers of males and females received hypobaric, isobaric and hyperbaric solutions. The mean spread of analgesia after the hyperbaric solution was five dermatomes greater than after the other two solutions, but the extent of analgesia was not significantly different whether amethocaine 10 mg or 15 mg was injected. The mean duration of analgesia after the hyperbaric solution was 285 min compared with 332 min and 360 min after the isobaric and hypobaric solutions respectively. The mean duration of analgesia after amethocaine 15 mg was significantly greater than after 10 mg.

Adult↗
PubMed1980

Delayed adverse responses to both methohexitone and Althesin.

A patient who reacted to both methohexitone and Althesin on separate occasions is described. On each occasion the reaction was delayed following anaesthesia. Underlying chronic infection had sensitised the patient's complement pathway, allowing it to be activated by two unrelated intravenous anaesthetic agents.

Abscess↗
PubMed1980

Intracellular distribution of Sindbis virus membrane proteins in BHK-21 cells infected with wild-type virus and maturation-defective mutants.

The association of Sindbis virus proteins with cellular membranes during virus maturation was examined by utilizing a technique for fractionating the membranes of BHK-21 cells into three subcellular classes, which were enriched for rough endoplasmic reticulum, smooth endoplasmic reticulum, and plasma membrane. Pulse-chase experiments with wild-type (strain SVHR) virus-infected cells showed that virus envelope proteins were incorporated initially into membranes of the rough endoplasmic reticulum and subsequently migrated to the smooth and plasma membrane fractions. Large amounts of capsid protein were associated with the plasma membrane fraction even at the earliest times postpulse, and relatively little was found associated with the other membranes, suggesting a rapid and preferential association of nucleocapsids with the plasma membrane. We also examined the intracellular processing of the proteins of two temperature-sensitive Sindbis virus mutants in pulse-chase experiments at the nonpermissive temperature. Labeled virus proteins of mutant ts-20 (complementation group E) first appeared in the rough endoplasmic reticulum and were then transported to the smooth and plasma membrane fractions, as in wild-type (strain SVHR) virus-infected cells. In cells infected with ts-23 (complementation group D), the pulse-labeled virus proteins appeared initially in the rough membrane fraction and were transported to the smooth membrane fraction, but only limited amounts reached the plasma membrane. Thus, in ts-23-infected cells, the transport of the virus-encoded proteins from the smooth membranes seemed to be defective. In both ts-20- and ts-23-infected cells the envelope precursor polypeptide PE2 was not processed to E2, and no label was incorporated into free virus at the nonpermissive temperature.

Animals↗
PubMed1979

Novel antiviral activity found in the media of Sindbis virus-persistently infected mosquito (Aedes albopictus) cell cultures.

Aedes albopictus (mosquito) cells persistently infected with Sindbis virus for a period of 6 months release into the medium a low-molecular-weight material capable of specifically reducing the yields of Sindbis virus during the "acute phase" of infection in mosquito cells. The antiviral activity was produced in detectable levels at 3 days after infection, and its concentration in the extracellular medium increased thereafter. The antiviral activity was inactivated by treatment with the enzyme protease K and heat. It was not activated by treatment with antibody prepared against extracts of Sindbis virus-infected BHK-21 cells. The antiviral activity differs from interferon produced by vertebrate cells in that it is virus specific as well as cell specific.

Aedes↗
PubMed1979

Tubular subviral structure produced in adenovirus-infected KB cells.

At 40 to 90 h after infection with high multiplicities of adenovirus type 2, 4 to 15% of KB cells produced relatively few intranuclear virions detectable by electron microscopy. The nuclei of these cells were found to contain long tubular structures which were made up at least in part by adenovirus structural proteins. The ends of these tubular structures were frequently terminated by morphologically normal adenovirions in varying degrees of completeness. Circumstantial evidence suggests that the production of these aberrant virus structures results from the malfunction or absence of some essential host-provided function and not from a defect in the infecting virus.

Adenoviruses, Human↗
PubMed1977

Morphogenesis of vesicular stomatitis virus: electron microscope observations with freeze-fracture techniques.

The morphogenesis of vesicular stomatitis virus was examined using freeze-fracture techniques, and the results obtained were compared with those from previously published experiments carried out with influenza viruses and togaviruses. The process of conversion of the host cell plasma membrane into the vesicular stomatitis virus envelope was accompanied by a loss of the intramembranal particles abundant in cell membranes. Frequently a dense accumulation of intramembranal particles could be seen at the base of the developing virion, suggesting that these structures might play some role in the generation of viral envelope. In addition to the viral structures that were seen to develop in the classical fashion, with their long axis perpendicular to the cell surface, structures were also found that suggested the initiation of a process similar to budding, with the long axis of the viral capsid parallel to the plasma membrane. In this situation, as in the "perpendicular" process, intramembranal particles were excluded from the viral structure, and an accumulation of these particles could be seen adjacent to the developing viral membrane.

Cell Line↗
PubMed1977

Envelopments of Sindbis virus: synthesis and organization of proteins in cells infected with wild type and maturation-defective mutants.

The synthesis and organization of Sindbis virus structural proteins was investigated in BHK cells infected with wild-type virus (SVHR) or temperature-sensitive (ts) mutants defective in maturation. Cells infected with ts-23 or ts-20 (complementation groups D and E) were similar in the polypeptides synthesized at the nonpermissive temperature and differed from SVHR-infected cells in that the envelope protein E2 was not cleaved from the PE2 precursor. Data from experiments utilizing pulse-chase procedures or protein synthesis inhibitors indicated that although infectious virions were released from cells infected with these mutants in shift-down experiments, the particles were produced almost exclusively from proteins synthesized after the return to permissive temperature. This suggests that a stable complex may be formed among the structural proteins before budding. A membrane fraction isolated from cells infected with either ts mutants or SVHR contained the PE2, E1, and C polypeptides, whereas E2 was restricted to fractions obtained from SVHR-infected cells. Although equivalent amounts of virus-specific protein were synthesized in cells infected with either mutant and the cells contained qualitatively the same proteins in the isolated membranes, cells infected with ts-23 did not have virus-specific proteins exposed on their surface that could be detected by ferritin-conjugated antibody-labeling procedures or lactoperoxidase-mediated iodination. In contrast, ts-20-infected cells had significant amounts of viral protein, mainly E1, that could be detected on the plasma membrane by either procedure. Iodine was incorporated into E1 and E2 on the surface of SVHR-infected cells in the same relative amounts as seen in iodinated virions. PE2, however, although present in membranes, could not be iodinated on the surface of infected cells under any of the conditions used in this study. We also monitored the relative efficiency with which these viral proteins could be removed from intact cells by dilute solutions of nonionic detergents. The results indicated that E2 was most efficiently removed, followed by E1. PE2 (the precursor to E2) and C remained associated with the cell and could be subsequently isolated in the membrane fraction.

Cell Line↗
PubMed1977

Role of extracellular virus on the maintenance of the persistent infection induced in Aedes albopictus (mosquito) cells by Sindbis virus.

Sindbis virus infection of cultured mosquito cells was found to have no effect on the growth of these cells; instead, a persistent infection of the culture followed an initial acute phase of rapid virus synthesis. Nearly all of the cells in the acute stage of infection were found to actively release virus in an infectious-center assay and to contain significant amounts of virus antigen as determined by immunofluorescence. Cells in the persistent phase of infection released few virions into the media, and only a small percentage of the cultured cells could be demonstrated to contain detectable amounts of virus antigen by immunofluorescence assay. In spite of the fact that nearly 100% of the cells in the persistent phase of infection were found to be virus negative by the two assays described above, the culture as a whole totally excluded the expression of superinfecting virus, as did cells in the acute phase, suggesting that most of the persistently infected cells did, indeed, contain virus information. Prevention of reinfection of the cells in the persistent phase by eliminating extracellular virus resulted in a curing of the culture such that it responded to infection by added virus much as would an uninfected culture.

Aedes↗
PubMed1976

The functional repressor parts of a tetrameric lac repressor-beta-galactosidase chimaera are organized as dimers.

The chimaeric protein repressor-galactosidase, in which fully active lac repressor is covalently linked to the active enzyme beta-galactosidase, was used as a system for probing the quaternary structure of lac repressor. Electron micrographs revealed repressor-galactosidase to be a tetrameric aggregate. When lac repressor, alone, was crosslinked with dimethyl suberimidate, dimers, trimers, tetramers, and oligomers of the protein subunit were produced, whereas crosslinking of the tetrameric repressor-galactosidase resulted in the production of only dimers of the chimaera. Treatment of lac repressor with iodine resulted in the formation of protein dimers; the same result was obtained with repressor-galactosidase. After limited proteolysis of lac repressor, no crosslinking was obtained after treatment with dimethyl suberimidate, whereas iodine still produced a covalent linkage. These results are interpreted as evidence that the lac repressor parts of the tetrameric repressor-galactosidase-chimaera are organized as dimers on the tetrameric-beta-galactosidase core. Because this chimaera has been previously shown to have normal repressor activity [B. Müller-Hill and J. Kania (1974) Nature, 249,561-563], we conclude that lac repressor still is biologically active as a dimeric aggregate.

Bacterial Proteins↗
PubMed1976

Head morphologies in bacteriophage T4 head and internal protein mutant infections.

Escherichia coli infected with phage T4 mutants defective in synthesis of the three major internal proteins found in the phage head, IPI-, IPII-, IPIII-, or IP degrees (lacking all three) were examined in the electron microscope for head formation. Infection with IPI- or IPII- does not appear to induce increased aberrant head formation, whereas IPII- or IP degrees infections result in production of polyheads and viable phage. Multiple mutants of the early head formation genes 20, 21, 22, 23, 24, 31, 40 and IP degrees were constructed. Combination with IP degrees increases polyhead formation when head formation is not blocked at a more defective stage but results in a qualitative shift to lump formation in association with gene 22 mutants. Thin-sectioning studies show morphologically similar cores in amber 21 and 21am IP degrees tau particles. These morphological observations, genetic evidence for interaction between ts mutants in gene 22 and the IP mutants, and analysis of the protein composition of tau particles further support the idea that p22 and the internal proteins form an unstable assembly core necessary for an early stage of head formation (M. K. Showe and L. W. Black, 1973).

Coliphages↗
PubMed1976

Function of gene 49 of bacteriophage T4. II. Analysis of intracellular development and the structure of very fast-sedimenting DNA.

With the exception of mutants in gene 49, all mutants in phage T4 defective in the process of head filling accumulate a normal replicative DNA intermediate of 200S. Mutants in gene 49 produce a very fast-sedimenting (VFS) DNA with s values of greater than 1,000S. The intracellular development of the VFS-DNA generated in gene 49-defective phage-infected cells was followed by sedimentation analysis of crude lysates on neutral sucrose gradients. It was observed that the production of a 200S replicative intermediate is one step in the development of VFS-DNA. After restoring permissive conditions the development of the VFS-DNA can be reversed, but the 200S form is not regenerated under these conditions. The process of head filling can take place from the VFS-DNA under permissive conditions. From the absence of other components in the VFS-DNA complexes, its high resistance to shearing, its resistance against the attack of the single-strand-specific nuclease S1, and from its appearance in the electron microscope, a complex structure of tightly packed DNA is inferred. The demonstration by the electron microscope of branched DNA structures sometimes closely related to partially filled heads is taken in support of the idea that the process of head filling in gene 49-defective phage-infected cells is blocked by some steric hindrance in the DNA. In light of these results, the role of gene 49 is discussed as a control function for the clearance of these structures. A fixation procedure for cross-linking of gene 49-defective heads to the VFS-DNA allowed us to study progressive stages in the process of head filling. Electron microscopic evidence is presented which suggests that during the initial events the DNA accumulates in the vertexes of the head.

Cell Membrane↗