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Biomedical subjects

T Davis

Publications and source records attributed to T Davis.

At least 91 records · Page 5Linked to original sources
PubMed1995

An overview of the CERC ARTEMIS project.

The basic premise of this effort is that health care can be made more effective and affordable by applying modern computer technology to improve collaboration among diverse and distributed health care providers. Information sharing, communication, and coordination are basic elements of any collaborative endeavor. In the health care domain, collaboration is characterized by cooperative activities by health care providers to deliver total and real-time care for their patients. Communication between providers and managed access to distributed patient records should enable health care providers to make informed decisions about their patients in a timely manner. With an effective medical information infrastructure in place, a patient will be able to visit any health care provider with access to the network, and the provider will be able to use relevant information from even the last episode of care in the patient record. Such a patient-centered perspective is in keeping with the real mission of health care providers. Today, an easy-to-use, integrated health care network is not in place in any community, even though current technology makes such a network possible. Large health care systems have deployed partial and disparate systems that address different elements of collaboration. But these islands of automation have not been integrated to facilitate cooperation among health care providers in large communities or nationally. CERC and its team members at Valley Health Systems, Inc., St. Marys Hospital and Cabell Huntington Hospital form a consortium committed to improving collaboration among the diverse and distributed providers in the health care arena. As the first contract recipient of the multi-agency High Performance Computing and Communications (HPCC) Initiative, this team of computer system developers, practicing rural physicians, community care groups, health care researchers, and tertiary care providers are using research prototypes and commercial off-the-shelf technologies to develop an open collaboration environment for the health care domain. This environment is called ARTEMIS--Advanced Research TEstbed for Medical InformaticS.

Computer Communication Networks↗
PubMed1994

The effect of naltrindole on spinal and supraspinal delta opioid receptors and analgesia.

The relationship between changes in binding for delta 1 (DPDPE) and delta 2 (DSLET) selective ligands were compared to potency changes for these ligands following naltrindole (NTI) in mice. Mice were injected s.c. with NTI (1 or 20 mg/kg) or saline and 1 hr later sacrificed for binding studies ([3H]DSLET, [3H]DPDPE) using whole brain or spinal cord. Other mice were injected s.c. with NTI (1 or 20 mg/kg) or saline and then injected IT or ICV with DSLET or DPDPE and were tested for analgesia using the tailflick test. In saturation binding studies, NTI decreased specific binding of [3H]DPDPE and [3H]DSLET in brain and spinal cord, but had no selective effect on either ligand. In contrast, in functional studies, NTI decreased analgesic potency of spinally and supraspinally administered DSLET more than DPDPE. Thus in functional studies NTI produced a selective effect on the delta 2 agonist DSLET; but in binding studies, NTI had no selective effect on the binding of [3H]DSLET and [3H]DPDPE.

Analgesia↗
PubMed1994

Spinal and supraspinal effects of pertussis toxin on opioid analgesia.

The effects of in vivo pertussis toxin (PTX) treatment on the functional effects of opioid agonists were examined in the mouse. Mice were injected intracerebroventricularly (ICV), or intrathecally (IT), or IT and ICV with PTX, and dose-response studies of the antinociceptive action of systemic (SC) morphine, fentanyl, and etorphine were conducted 10 days later. IT PTX decreased the potency (approximately 4.5-fold) of morphine more than ICV administration (approximately 1.5-fold), whereas the combination of IT and ICV administration produced an additive effect. When PTX was administered spinally and supraspinally, the potency of morphine, fentanyl, and etorphine was reduced similarly (approximately 5-7-fold), indicating that the effect of PTX does does not vary considerably among agonists of different intrinsic efficacies. These studies indicate that in vivo PTX can reduce the potency of opioid agonists with different intrinsic efficacies, and that spinal mechanisms appear to be more sensitive to PTX treatment.

Analgesics↗
PubMed1994

Opioid antagonist-induced receptor upregulation: effects of concurrent agonist administration.

The present study examined whether opioid antagonist-induced receptor upregulation could be antagonized by simultaneous treatment with opioid agonists. Mice were treated concurrently with opioid agonists (morphine, fentanyl, etorphine) and antagonists (naloxone, naltrexone) over a period of 7-8 days. Concurrent morphine (1 or 4, 75 mg SC implanted pellets), fentanyl (5.0 mg/kg/day, infusion) or etorphine (0.25 mg/kg/day, infusion) administration were unable to inhibit upregulation of mu opioid (DAMGO) receptors by either naloxone (1 mg/kg/day, infusion) or naltrexone (15 mg or 2 mg SC implanted pellet). Only a very high infusion dose of etorphine (10 mg/kg/day) inhibited upregulation by naltrexone (2mg SC implanted pellet). These results indicate that antagonist-induced upregulation is a robust, receptor-mediated phenomenon.

Animals↗
PubMed1994

Human tissue kallikrein induces hypotension in transgenic mice.

We investigated the role of the kallikrein-kinin system in blood pressure control by developing transgenic mice overexpressing human tissue kallikrein. Two lines of transgenic mice carrying the human tissue kallikrein gene under the control of the mouse metallothionein metal-responsive promoter were established. Human tissue kallikrein was identified in pancreas, salivary gland, kidney, liver, and spleen of the transgenic mice by a specific radioimmunoassay for human tissue kallikrein. The immunoreactive human tissue kallikrein reached high levels in the circulation. The linear displacement curves for the transgenic product were parallel with the human tissue kallikrein standard curve, indicating their immunologic identity. The expression of human tissue kallikrein transcript in the transgenic mice was further confirmed by Northern blot analysis and by reverse transcription-polymerase chain reaction followed by Southern blot. Both lines of transgenic mice had significantly lowered blood pressure (86.4 +/- 13.5 mm Hg [mean +/- SD], n = 8 and 78.9 +/- 12.4 mm Hg, n = 8) compared with control mice (100.9 +/- 5.0 mm Hg, n = 8). Induction with zinc did not lower the blood pressure further despite elevated expression of the transgene. Administration of aprotinin, a potent tissue kallikrein inhibitor, restored the blood pressure of the transgenic mice but had no significant effect on control littermates. Our findings raise the possibility of tissue kallikrein being a powerful modulator of blood pressure and provide a new animal model for the study of blood pressure regulation.

Animals↗
PubMed1994

Cat-transmitted fatal pneumonic plague in a person who traveled from Colorado to Arizona.

Plague, primarily a disease of rodents and their infected fleas, is fatal in 50% of infected humans if untreated. In the United States, human cases have been concentrated in the southwest. The most common modes of plague transmission are through flea bites or through contact with infected blood or tissues; however, primary pneumonic plague acquired from cats has become increasingly recognized. We report on the case investigation of a patient, presumably exposed to a plague-infected cat in Colorado, who presented with gastrointestinal symptoms, and subsequently died of primary pneumonic plague. Public health officials should be vigilant for plague activity in rodent populations, veterinarians should suspect feline plague in ill or deceased cats, and physicians should have a high index of suspicion for plague in any person who has traveled to plague enzootic areas.

Adult↗
PubMed1993

CD30 antigen, a marker for Hodgkin's lymphoma, is a receptor whose ligand defines an emerging family of cytokines with homology to TNF.

CD30 is a surface marker for neoplastic cells of Hodgkin's lymphoma and shows sequence homology to members of the tumor necrosis factor (TNF) receptor superfamily. Using a chimeric probe consisting of the extracellular domain of CD30 fused to truncated immunoglobulin heavy chains, we expression cloned the cDNA cognate from the murine T cell clone 7B9. The encoded protein is a 239 amino acid type II membrane protein whose C-terminal domain shows significant homology to TNF alpha, TNF beta, and the CD40L. Cross-hybridization to an induced peripheral blood T cell cDNA library yielded the human homolog, which is 72% identical at the amino acid level. The recombinant human ligand enhances the proliferation of CD3-activated T cells yet induces differential responses, including cell death, in several CD30+ lymphoma-derived clones. The human and murine genes map to 9q33 and the proximal region of chromosome 4, respectively.

Amino Acid Sequence↗