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Biomedical subjects

D Beard

Publications and source records attributed to D Beard.

At least 55 records · Page 3Linked to original sources
PubMed1990

A cost analysis of film image management and four PACS based on different network protocols.

Picture Archive and Communication Systems (PACS), which allow the electronic acquisition, storage, transportation, and viewing of medical images, hold the eventual promise of reduced costs, improved image-management logistics, and ultimately, improved patient care. But at what point in the future will PACS really cost less than film-based image management for a given hospital size; and how are these costs affected by the choice of the digital communication network? To address these questions, a static differential cost model has been constructed. PAC systems based on two high-speed networks (less than 150 megabytes per second Mbps) and two low-speed networks, as well as film, were considered for five different sized hospitals (ranging from 15,000 to 125,000 procedures per year) and two time periods (1995 and 2000). PACS equipment was assumed to have a payoff of five years. The model considered all capital and supply costs and personnel costs for the PACS and for film storage and retrieval. It did not consider any possible cost savings from logistics improvement likely to result from the adoption of a PACS. Based on the assumptions outlined, high-speed-network PACS are less costly than those based on low-speed networks for all scenarios considered. Further, even though all possible PACS cost savings were not considered, high-speed network PACS appear to be less costly than film for hospitals larger than 60,000 procedures in 1995 and larger than 15,000 in 2000, while low-speed-network PACS should cost less than film for 60,000 and 30,000 procedure hospitals in 1995 and 2000 respectively.

Computer Communication Networks↗
PubMed1988

The acute-phase response of the brain-injured patient.

The acute response to injury and infection is manifested by increased synthesis of acute-phase proteins by the liver, an increased white blood cell count, fever, a negative nitrogen balance, and altered serum mineral levels (zinc, iron, and copper). This response is thought to be partially mediated by cytokines such as interleukin-1, but has not been well studied in head-injured patients. In this study, 25 patients were studied for evidence of the acute-phase response extending from hospital admission up to 21 days postinjury. The patients were divided into two groups to determine if severity of injury influenced the response. Group 1 consisted of nine patients with admission peak 24-hour Glasgow Coma Scale (GCS) scores of 4 or less; Group 2 consisted of 16 patients with admission peak 24-hour GCS scores of 8 or greater. All patients demonstrated some evidence of the acute-phase response. Serum alpha-1 acid glycoprotein, ceruloplasmin, and C-reactive protein levels were elevated on admission and throughout the study. Serum albumin and zinc levels were depressed on admission; zinc levels gradually normalized by Day 21 in both groups, but hypoalbuminemia was observed throughout the study period. Serum copper levels were normal on admission but increased to above normal in both groups by Day 11 postinjury. Urinary urea nitrogen excretion was elevated in both groups and peaked on Day 7 for Group 1 and Day 11 for Group 2 patients. The patients with admission GCS scores equal to or less than 4 had overall higher temperatures than were seen in those with GCS scores greater than or equal to 8 (p = 0.009). All patients but one had an elevated white blood cell count on admission. It is concluded that brain-injured patients with admission GCS scores of 3 to 4 and 8 to 14 demonstrate an acute-phase response which lasts for at least 3 weeks postinjury. It is speculated that this response is at least partially mediated by increased intraventricular interleukin-1 activity.

Acute-Phase Reaction↗
PubMed1983

Regional optic nerve blood flow and its autoregulation.

An autoradiographic method (14C-iodoantipyrine autoradiography) was used to measure regional optic nerve blood flow (ONBF) under basal conditions in 11 adult female cats. Flow was measured in six regions of the optic nerve: (1) prelaminar, (2) laminar, (3) 1 mm post-laminar, (4) 4 mm post-laminar, (5) 6 mm post-laminar, and (6) intracranial optic nerve and chiasm. A gradient of flow rates was found with relatively high flow in the prelaminar, laminar, and 1-mm post-laminar optic nerve, and significantly lower flow in the 4- and 6-mm post-laminar nerve and in the intracranial optic nerve and chiasm. Blood flow in the 4- and 6-mm post-laminar nerve and in the intracranial nerve and chiasm was comparable to previously reported values for cerebral white matter in the cat. With alteration of mean arterial blood pressure (MABP), optic nerve blood flow demonstrated autoregulatory compensation in all areas.

Animals↗
PubMed1979

Reverse transcriptase from avian myeloblastosis virus.

From lots of 20 to 30 g of avian myeloblastosis virus RNA-dependent DNA polymerase was obtained in preparations of purity greater than 95% by using a two-step column chromatographic procedure employing DEAE (DE 52) and carboxymethylcellulose (CM 52.). Yields of RNA-dependent DNA polymerase varied from approximately 20,000 to 35,000 U/g of virus. Specific activity of the enzyme was about 35,000 to 60,000 U/mg of protein. Free of detectable RNase activity, the product exhibited a molecular weight of about 160,000, an isoelectric point of 6.5, and approximately 2 mol of fatty acid per mol of enzyme.

Animals↗
PubMed1978

Protein kinase from avian myeloblastosis virus.

A protein kinase associated with purified virions of avian myeloblastosis BAI strain A was partially purified by ion-exchange chromatography and gel filtration. The transfer of phosphate catalyzed by this enzyme required a divalent metal ion and ATP as phosphate donor. GTP could not be substituted for ATP, and the reaction was unaffected by either cyclic AMP or beef-heart protein-kinase inhibitor. Of the virus and nonvirus proteins tested as phosphate acceptors, only acidic proteins were phosphorylated. In particular, purified preparations of reverse transcriptase from avian myeloblastosis virus did not accept phosphate. The enzyme is a basic protein (pI = 9.3), and, on the basis of molecular sieving through Sephadex G-200 and velocity sedimentation on glycerol gradient, the protein kinase has a molecular weight of 45,000.

Adenosine Triphosphate↗
PubMed1976

Renal neoplastic response to leukosis virus strains BAI A (avian myeloblastosis virus) and MC29.

Previous reports described the induction of avian renal neoplasms by leukosis virus strains BAI A [avian myeloblastosis virus (AMV)] and MC29, and illustrated morphological characteristics of the tumors. Continued studies in this work confirm evidence of the origin of the tumors from embryonal cells residual in the posthatched chick. The work further emphasizes differences in histopathology of the neoplasms caused by the two viruses and reveals differences in the histopathogenesis of the respective growths. Embryonal rests may consist of two types of cells, those of epithelial characteristics and a second element of differentiation between nephroblastema (mesenchyme) and epithelium and designated here as nephromesoblastoma. Infection by AMV induces tumors of epithelial characteristics and, in addition, derivatives of nephromesoblastoma consisting of cartilage, bone, areas of keratinization, and sarcoma. Keratinized structures in the nephroblastoma originate from nephromesoblastoma. In contrast, MC29 virus induces only epithelial growths representing principally aberrant and malformed glomerular and tubular structures with occasional cartilage derived from epithelial cells. MC29 tumors are completely lacking in nephromesoblastoma tissue and contain no bone, sarcoma, or keratinized formations. In MC29 tumors, occasional cartilage was derived from epithelium. Tumors caused by AMV exhibit the complex structure of nephroblastoma with all of the features of the growth in humans (Wilms' tumor). The neoplasms induced by both AMV and MC29 exhibit marked aberration, distortion, and malformation in the differentiation of the cells growing out from the embryonal rests representing rare manifestations of cell genetic influence inherent in the primordial growth of nephroblastema. The results thus illustrate fundamental differences in cellular composition and capacity to respond to etiologically different leukosis viruses.

Adenocarcinoma↗
PubMed1975

Transplantation of hepatomas induced in the avian liver by MC29 leukosis virus.

A hepatomatous growth derived from primary liver tumors induced in chickens by i.v. inoculation with MC29 leukosis virus has been established and maintained in the avian host. Hepatoma tissue transplanted into the abdominal cavity in a total of 278 chicks in 35 experiments yielded tumors in 222 animals (80%). The i.m. implantation in 69 birds in 7 experiments resulted in growth in 67 chicks (97%). Tumor tissue introduced inadvertently into the s.c. tissue likewise grew very rapidly. Histological and cytological features of the transplants in all sites showed preservation of the morphological characteristics of the original primary liver tumors through repeated passages. The properties of this first transplantable hepatoma derived from virus-induced primary liver tumors are compared with those of other transplantable hepatomas.

Abdomen↗
PubMed1975

Neoplastic response of the avian liver to host infection with strain Mc29 leukosis verus.

Studies were made on the oncogenic response of 3086 young chicks to i.v. inoculation of MC29 avian leukosis virus from blood plasma of previous-passage birds or the supernatant fluid of cultures of chick embryo cells infected with strain MC29. Among the large variety of neoplasms of other tissues previously described, there occurred a high incidence of primary growths of the liver. Pathomorphology of the growths frequently differed greatly in both different hosts and the same bird, but some uniformity of the types of neoplasms was evident in many animals. Despite much variation in histopathology, the large proportion of growths could be grouped in several distinctive categories. Examinations by light and electron microscopy provided evidence of derivation of the tumors by alteration of hepatocytes originating principally in the portal regions as indicated by forms transitional from the parenchymal cells to the cells of the different types of growths. Neoplastic aspects of the growths were evident by infiltration and invasion of adjacent tissues, penetration of blood vessels, transplantability to other avian hosts (described in another report), and metastasis to distant organs including the lung, kidney, and spleen. There was no evidence of tumors arising from the biliary system, and growths of cells resembling the biliary type could be traced to altered hepatocytes. None of the findings suggested conversion of biliary-type cells to hepatocytes. Continued growth resulted in anaplastic and metaplastic changes in cell morphology and structural organization and in the formation of cartilage, osteoid, and sarcoma-like spindle-cell tumors of probable epithelial origin. Development of the growths wasnot associated with cirrhosis, and necrosis was limited to infrequent disseminated, essentially unicellular changes or necrobiosis of small groups of cells. The marked variations in the type of virus-induced growths demonstrated the remarkable capacity of cells morphologically inidistinguishable from the hepatocytes for the most diverse alterations in cell structure and tissue organization. This neoplastic response of hepatocytes to the MC29 strain constitutes the only demonstration thus far of the specific hepatocarcinogenic activity of an avian tumor virus.

Adenocarcinoma↗
PubMed1970

Mechanism of carcinogenesis by RNA tumor viruses. 3. Formation of RNA, DNA complex and duplex DNA molecules by the DNA polymerase (s) of avian myeloblastosis virus.

DNA polymerase activity can be unmasked in avian myeloblastosis virus (AMV) by treatment with the nonionic detergent Nonidet P-40. Two products are formed: (1) RNA.DNA hybrid molecules and (2) duplex DNA molecules. The kinetics of dTTP incorporation into DNA are biphasic: an initial rapid reaction for 4 min at 37 degrees C with a minimal polymerization rate of 10-20 nucleotides per see, and a second reaction at about half the initial rate. Viral RNA.DNA complexes are detected as early as 30 sec after the initiation of DNA synthesis; DNA free of template is formed subsequently. Most of the free AMV DNA forms an RNA.DNA hybrid when annealed with viral RNA. Over half of the free AMV DNA product is inferred to be double-stranded, since it is retained on hydroxyapatite columns after elution with 0.12 M phosphate buffer, and is resistant to Escherichia coli exonuclease I. Adenovirus or calfthymus DNA added to unmasked AMV stimulates DNA synthesis 4-16 times if there is no treatment with RNase, and 40-130 fold if RNase treatment precedes the enzyme assay. It is possible that two polymerases are present, or that a single enzyme forms both the RNA.DNA hybrid and the double-stranded product.

Alpharetrovirus↗