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Biomedical subjects

K Baker

Publications and source records attributed to K Baker.

At least 55 records · Page 3Linked to original sources
PubMed1998

Synthetic combined superoxide dismutase/catalase mimetics are protective as a delayed treatment in a rat stroke model: a key role for reactive oxygen species in ischemic brain injury.

Stroke is a severe and prevalent syndrome for which there is a great need for treatment, including agents to block the cascade of brain injury that occurs in the hours after the onset of ischemia. Reactive oxygen species (ROS) have been implicated in this destructive process, but antioxidant enzymes such as superoxide dismutase (SOD) have been unsatisfactory in experimental stroke models. This study is an evaluation of the effectiveness of salen-manganese complexes, a class of synthetic SOD/catalase mimetics, in a rat focal ischemia model involving middle cerebral artery occlusion. We focus on EUK-134, a newly reported salen-manganese complex demonstrated here to have greater catalase and cytoprotective activities and equivalent SOD activity compared with the previously described prototype EUK-8. The administration of EUK-134 at 3 hr after middle cerebral artery occlusion significantly reduced brain infarct size, with the highest dose apparently preventing further infarct growth. EUK-8 was also protective but substantially less effective. These findings support a key role for ROS in the cascade of brain injury after stroke, even well after the onset of ischemia. The enhanced activity of EUK-134 suggests that, in particular, hydrogen peroxide contributes significantly to this injury. Overall, this study suggests that synthetic SOD/catalase mimetics might serve as novel, multifunctional therapeutic agents for stroke.

Animals↗
PubMed1998

Ventricular myxoma presenting as acute visual loss.

We report a case of left ventricular myxoma with embolization to the left posterior cerebral artery, causing acute visual loss. The tumor was successfully resected and a follow-up echocardiography after 21 months revealed no evidence of tumor recurrence. The patient also had a past history of testicular seminoma. We believe that this is the first case report of an association of cardiac myxoma and testicular seminoma.

Heart Neoplasms↗
PubMed1997

Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors.

TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.

Amino Acid Sequence↗
PubMed1997

Defective "pacemaker" current (Ih) in a zebrafish mutant with a slow heart rate.

At a cellular level, cardiac pacemaking, which sets the rate and rhythm of the heartbeat, is produced by the slow membrane depolarization that occurs between action potentials. Several ionic currents could account for this pacemaker potential, but their relative prominence is controversial, and it is not known which ones actually play a pacemaking role in vivo. To correlate currents in individual heart cells with the rhythmic properties of the intact heart, we have examined slow mo (smo), a recessive mutation we discovered in the zebrafish Danio rerio. This mutation causes a reduced heart rate in the embryo, a property we can quantitate because the embryo is transparent. We developed methods for culture of cardiocytes from zebrafish embryos and found that, even in culture, cells from smo continue to beat relatively slowly. By patch-clamp analysis, we discovered that a large repertoire of cardiac currents noted in other species are present in these cultured cells, including sodium, T-type, and L-type calcium and several potassium currents, all of which appear normal in the mutant. The only abnormality appears to be in a hyperpolarization-activated inward current with the properties of Ih, a current described previously in the nervous system, pacemaker, and other cardiac tissue. smo cardiomyocytes have a reduction in Ih that appears to result from severe diminution of one kinetic component of the Ih current. This provides strong evidence that Ih is an important contributor to the pacemaking behavior of the intact heart.

Animals↗
PubMed1997

Correction of the Bloom syndrome cellular phenotypes.

Bloom syndrome (BLM) is a genetic disorder associated with predisposition to cancer and chromosome instability. However, the most readily recognized clinical feature of the syndrome is growth retardation. Introduction of the previously cloned BLM gene into BLM cells yielded correction of the chromosome instability and slow growth phenotypes. Additionally, asynchronous cultures of complemented clones revealed a lower percentage of cells in S-phase than uncomplemented BLM cells. These results support the notion that BLM is a defect in which short stature, chromosome instability and cancer predisposition are all associated with an error in DNA replication.

Adenosine Triphosphatases↗
PubMed1997

Merger motorway. Giving staff the tools to reengineer.

Mergers and health care agencies' response to mergers dominate current conversations in this evolving managed care environment. Hospitals are rapidly learning to adjust to declining occupancy rates and deceased utilization of resources. A business model to guide mergers was adapted to assist staff with the people, structural, cultural and political issues of organizational change. Creating successful new work environments, moving from a "We-they" mentality to unity and decreasing use of resources are outcomes described in this article.

Adaptation, Psychological↗
PubMed1997

Comparison of actual and recommended ENT endoscope disinfection practices, by geographical regions in the United States.

Endoscopy of the aerodigestive tract, a commonly performed procedure in ENT practice, is not without risk of disease transmission. Review of the nursing literature reveals concern regarding endoscopy of the GI tract, but little has been published regarding disease transmission from ENT endoscopy. The ENT nursing literature does not offer specific practice guidelines for high level disinfection (HLD) of ENT endoscopes. This lack of practice guidelines and recognized confusion regarding clinical practice led to the need for a national survey of ENT nurses to examine what reprocessing practices are being performed. Questionnaires were sent to 150 nurse members of the Society of Otorhinolaryngology-Head and Neck Nurses (SOHN) to gather information about actual endoscope cleaning practices and whether there were any regional differences. Eighty completed forms were returned. The results were tabulated and compared to the AORN recommended method of achieving HLD by glutaraldehyde soak. Results indicate SOHN nurses use a variety of methods to clean and disinfect endoscopes; some nurses use methods not recommended for HLD; results do not demonstrate a universal understanding of the requirements to achieve HLD; regional differences were not obvious; and SOHN nurses may benefit from use of a professionally endorsed disinfection protocol.

Disinfection↗
PubMed1996

Unexplained hepatitis C virus antibody seroconversion in established blood donors.

BACKGROUND: Understanding of the epidemiology and natural history of hepatitis C virus (HCV) infection is incomplete without reference to the early phase of infection. The prevalence of HCV infection is well documented in numerous reports. The seroconversion pattern in previously antibody-negative blood donors provides a model for the study of the incidence and transmission of HCV infection. STUDY DESIGN AND METHODS: Records of HCV antibody tests at the West Midlands Blood Transfusion Centre were reviewed to determine the seroconversion rate in 1994 among previously anti-HCV-negative blood donors. Seroconverting donors were counseled to investigate the possible routes of infection. RESULTS: In 1994, blood donations (n = 256,935) were collected from 149,370 donors; 24 donors (0.016%; 1/6224) were positive in the screening enzyme-linked immunosorbent assay (ELISA) and the third-generation recombinant immunoblot assay (RIBA-3). Two donors previously negative for HCV antibody in ELISA were positive in both tests in 1994. Four donors positive in ELISA and indeterminate in RIBA-3 in 1993 reacted positively in both tests in 1994. One donor negative for HCV antibody on previous screening reacted positively in ELISA and was indeterminate in RIBA-3 in 1994 and has become positive in both tests in 1995. A further 43 donors negative for HCV antibody on previous screening reacted positively in ELISA and were indeterminate in RIBA-3 in 1994. CONCLUSION: Documented seroconversion can take place in the absence of exposure to recognizable risk factors for the infection. The index donation or the donation immediately preceding seroconversion may be positive for HCV RNA in the polymerase chain reaction.

Blood Donors↗
PubMed1995

Inhibition of cysteine proteinases by Carica papaya cystatin produced in Escherichia coli.

A papaya cystatin (Cst)-encoding cDNA clone was isolated from a papaya leaf cDNA library and the active protein produced in Escherichia coli. The amino-acid sequence reveals a protein of 11,262 Da with over 40% identity to other published plant Cst. Unique features of the papaya Cst include a single Cys residue, variation in the papain-binding region, and the first reported inhibition of papaya proteinase IV by a Cst.

Base Sequence↗
PubMed1995

Comparison of experimental and theoretical parameters of the Moolgavkar-Venzon-Knudson incidence function for the stages of initiation and promotion in rat hepatocarcinogenesis.

Mathematical descriptions of complex biological phenomena, such as cancer, require an experimental format that faithfully recapitulates the biological process. In addition, the biological process must dictate the parameters in the mathematical formula. Evidence from the epidemiology of several human cancers and from experimental carcinogenesis in several organ systems indicates that cancer is a multistage process. The initiation-promotion-progression format of experimental carcinogenesis mimics the development of cancer in humans and other animals. In rats, the altered hepatic focus model of hepatocarcinogenesis has been well characterized and, coupled with the method of quantitative stereology, permits accurate determination of the number and the volume fraction of such altered foci per liver. The placental isozyme of glutathione S-transferase (PGST) is reportedly the best single marker of preneoplasia in the rat liver. Recently, single hepatocytes expressing PGST have been proposed as putatively initiated cells. Quantitation of individual hepatic cells and altered hepatic foci expressing PGST in the livers of rats subjected to an initiation-promotion protocol permits determination of the congruence of the Moolgavkar-Venzon-Knudson (MVK) model with experimental data. The best fit of the MVK model for the preneoplastic stages of hepatocarcinogenesis assumes that all hepatocytes are susceptible and that single hepatocytes expressing PGST are the initiated cell population for the focal lesions that express PGST. Further refinement of the initiation-promotion-progression model to permit accurate quantitation of early malignant conversion should allow a more complete analysis of the congruence of the MVK model for human cancer risk determination. In addition, the MVK model may be extended to other model systems and to human cancers in which early preneoplasia can be quantitated. Furthermore, the use of a more biologically based risk-assessment protocol, such as the MVK model rather than the stochastic one-hit model presently used, would permit incorporation of the present knowledge on the pathogenesis of cancer. To apply experimental data to a mathematical model that reflects the biological processes underlying human cancer development will require integration of the cell kinetics and experimental data to a mathematical model that reflects the biological processes underlying human cancer development including the pharmacokinetic and pharmacodynamic properties of the treatment chemicals.

Animals↗